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USMLE step 2 UWORLD NOTES

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Abrupta Placenta - 4
Pt presents with vaginal bleeding, ABDOMINAL PAIN, and uterine tenderness.
The absence of hemorrhage DOES NOT rule out this Dx. DDX:Placenta Previa,
absence of bleeding RULES OUT this dx.\n\n
****Risk factors are
1-HT and preecclampsia, 2-Placental abruption in previous pregnancy, 3-trauma, 4-short umbilical cord, 6-COCAINE abuse. AP is the mcc of DIC in pregnancy, which results from a release of activated thromboplastin from the decidual hematoma in to
maternal circulation.\n\n
****Risk factors
are smoking and,Folate def. It can progress
rapidly so careful monitoring is mandatory. Once dx is made, large-bore IV , as well as Foley cathater is inserted. Pts with AP in LABOR should be managed aggressively to insure rapid vaginal delivery, since this will remove the inciting cause of DIC and hemorrhage. Now if pt is stable tocolysis with MgSO4 is considered, but remmeber Ritordin is CI in pt with HT.\n\n
*** once we dx
next step is Vaginal delivery with augmentation of labor if necessary. Now if mother
and baby are not stable or if there is CI, then Emergency C-section is indicated.
Now if there is Dystocia ( narrowing of the birth passage) then Forcepts can be used.\n\n.
ABCD of Homeostasis
1-Airway 2- breathing 3- circulation \n\n
1-AIRWAY:
An airway is needed for all unconscious pts, in the ER best method is Orotrachial intubation and in the field its needle cricothyroidectomy. For consciouns pt the best airway is chin lift with face mask. \n\n
2-BREATHING:
Cervical spine injury should be analyzed but the first step is to establish ABC. \n\n
3-CIRCULATION:
It needs control of bleeding and restoring the BP. In most
external injuries pressure is enough to stop bleeding but in case of scalp laceration
suturing is needed. Also all pts with hypotension should receive rapid infusion of
isotonic fluid like ringer lactate to prevent life threatening hypotension. If IV line is
not good for adults do saphaneous vein cut down and for children intraosseous
membrane cannulation.\n\n
Absence seizures - 3
Ethosuximide is tx. Now remmeber that Phenytoin and Carbamazapine are first line drug used for primary generalized tonic clonic sezure or partial seizures, both work by blocking Na channels voltage dependent, Phenytoin is a second drug line for myoclonic and tonic clonic seizure, its available in both IV and oral forms. \n\n
Phenytoin SE
is gingivial hypertrophy, lymphadenopathy, hirsutism and rash, Both Phenytoina & Carbamazepine can cause Steven Johnson synd and Toxic Epidermal
Necrolysis.\n\n
*****Absence siezures Tx
is Ethusuxamide or VALPROATE. Classic EEG is symetric
3mhtz spike and wave .\n\n
Acarbose SE
It blocks carbohydrate break down in the intestinal tract. The most significant SE is
GI disturbance due to increased undifested CHO in the stool.\n\n
ACE inhibitor SE, Respira, 6/2
CAPTOPRIL (Cough, Angioedema, Pregnancy, Taste change, hypOtention,
Proteinuria,Rash, Increase renin, Lower AII) and HyperKalemia. \n\n
*****Cough is caused
by accumulation of Kinins possibly by activation of arachadonic acid pathway.
Kinins are degraded by ACE, when there is no ACE they increase. \n\n
*****Angioedema
that is seen in ER. Pt presents with non-inflamatory subcutaneous edema and
laryngeal edema due to bradykinin stimulation.\n\n
Acetaminophen toxicity - 2
Acute alcoholic intake can reduce the risk of hepatic injury by Acetaminophen
because it competes with CYP2E1, so there is less production of toxic metabolites.\n\n
****Chronic alcohol intake
increases risk of hepatic injury by stimulating P450 system
and decreasing the amount of Glutathione (used for metabolism of acetaminophen).\n\n
***Management process
1-4-hr post ingestion AA levels are determined to decide
whether the pt will benefit from NAC or not. 2-On the other hand if the pt has
ingested >7.5 gr AA and levels will not be available w/i 8 hours of ingestion, he
should be given the antidote.\n\n
Acetazolamide Toxicity
Causes normal anion gap metabolic accidosis due to renal loss of bicarbonate. Anion
Gap is 140-(114+116)=10 which is normal anionic gap metabolic acidosis.\n\n
Achalasia - 3
Dx 1-Barium studies, 2-Esopgaguscopy 3-Manometry. ** the CONFIRMATION
test is Manometry. We also need to do Endoscopy to rule out malignancy.\n\n
ACL Injury
It prevents gliding of tibia under femur. Injury is seen after Hyperextension. A
poping sensation is felt at time of injury. Commonly asso with Medial Meniscus and
Medial Colateral Ligament (TRIAD). \n\n
****Lachman test is a test for ACL tear. Flex and
pull tibia.\n\n
flex and pull tibia
**** Drawer sign
also test ACL but its less sensitive. \n\n
****Posterior Drawer sign
tests PCL.\n\n
**** Mc murry's sign
tests Meniscus injury. \n\n
**** Valgus test
is for MCL.\n\n
Acne - 2
1-Comedons (black/white heads): cuase minimal inflamation and tx is topical
retinoids. If reactivation occur add topical Erythromycin or Benzoyl peroxide. 2-
Papular and inflamatory acne: with moderate-severe inflamation: Oral
Doxycycline. 3-Nodular or scaring acne: Oral Isotretinoin.\n\n
Actinomycosis
Cervicofacial actinomycosis presents as slowly progressing , non tender, indurated
mass, which evolves into multiple abscesses, fistula, and draining sinus tracts with
sulfur granules, which appear yellow. \n\n
**** Causitive Agent
Actinomyces israelii , Tx is high
dose IV peniciline for 6-12 weeks. Surgical debrement comes after penicillin
therapy.\n\n
Acute adrenal insufficiency
Acute onset of naseau, vomiting, abdominal pain and hypoglycemia and
hypotension after a stressful event (surgery) in a pt sho is steroid dependant is
typical. \n\n
**** A clue
is preoperative steroid use. Exogenous steroids depress pit-adrenal
axis and a stressful situation can precipitate AAI.\n\n
**** DDX
insulin induced hypoglycemia does not cause naseau and vomit and abdominal pain and
hypotension.\n\n
Acute Alkali ingestion
When a pt takes Lye (alkali substance for suicide), upper GI contrast studies should
be performed as eary as possible, to assess the damage and posible perforation of
esophagus. \n\n
**** Normal x-ray
does not rule out a perforation. Once you know there is noperforation then you can do Diagnostic peritoneal lavage if necessary. But the first
thing is to rule out perforation.\n\n
Acute Appendicitis - 3
Pt who comes to hospital after 5 days of initial symptoms must be hospitalized with
IV hydration and IV Cefotetan. If threre is abcess with CT, percutaneous drainage
is an option.\n\n
****Most pelvic abscesses
are due to perforation of AA. Pt might have a
24 hour RUQ pain that resoves spontaneously and then later on in a few days he
might come with anal abscess symptoms. Drainage of the abscess is tx of
choice. \n\n
****Experiecne has shown
that right hemiclectomy with ileo-transvers
anatomosis has best postoperative results when resection of part of ascending is
requires. And that is when pt has shown gangrenous rupture of appendix with
questionable necrotized colon.\n\n
Acute Bacterial Proctatitis
MCC in young is Chlamydia and Gonococcus, in old E. Coli. To diagnose do culture
of mid-stream urine sample and start empiric therapy. Prostatic massage is
contraindicated due to septecemia chance.\n\n
Acute GI bleeding causes
1-Diverticulosis ; Painless. ruled out with Barium
Enema, 2-Angiodysplasia; Painless. maybe seen as cherry-red spots that maybe
coagulated, dx with labeled erythrocyte scintigraphy. 3-PUD (Painfull. Dx with
endoscopy, if there is Hematochezia, red bright blood,due to lower GI bleed, then
there is no need for endoscopy, the blood is from lower UGI bleeding).\n\n
Acute renal transplant rejection
Renal transplant rejection in the early post-operative stage can be expained by,
ureteral obstruction, Acute rejection, Cyclosporine tox, vascular obstruction and
ATN. \n\n
***To determine the cause
we do US, MRI and Biopsy. If biopsy shows
infiltration of lymphocytes and vasular swelling and there is increase Crt and Bun
and oliguria, then the cause is Acute Rejection. Tx is high dose IV steriods.\n\n
Acute Tubular Necrosis
Prolonged hypotention due to any reason (Hypovolemic shock) can lead to ATN.
Hallmark finding on urine analysis is Muddy brown granular cast.\n\n
***DDX
1:RBC cast,
GN. DDX2:WBC cast, Interstitial Nephritis and Pyelonephritis. DDX3:Fatty cast,
NephrOtic Synd. DDX4:Broad and Waxy cast:Chronic renal failure.\n\n
Acyclovir Toxicity
Can cause crystalluria with renal tubular obstruction during high dose parenteral
therapy, especially in inadequately hydrated pts.\n\n
Addison's Disease - 2
MM-101. Aldosterone def leads to non-anion gap hyperkalemic, hyponatremic
metabolic acidosis. \n\n
***80% of pt have primary adrenal deficiency due to
Autoimmune adrenalitis, mostly in developed country, These pts also present with autoimmune involvement of
other glands as well, like thyroid,parathyroid, ovaries.\n\n
*** Cause In underdeveloped countries
TUBERCULOSIS, Fungal infection and CMV infection are the mcc, TB is the MCC in undeveloped countries. Adrenal Calcification is a
typical feature of TB PAI. \n\n
****Pt presents
with no rise in serum cortisol following
injection of Cosyntropin (ACTH analog), CT shows calcification of adrenal glands.
Tx of TB does not result in normalization of adrenal gland. \n\n
***PAI in HIV pt
is common, mcc is CMV. Sometimes Ketoconazole can cause it. PAI is very rare with adrenal tumor metastasis, even then calcification is not seen. \n\n
Adenomyosis
Is defined as presence of Endometrial glands in the uterine muscle. MF in women
above 49, presents with severe dysmenorrhea, and menorrhagia. The typical exam
reveals enlarged sysmetrical uterus. If Adenomyosis is in one side of uterus then
enlargment is asymetrical.\n\n
*** DDX
includes Myomatous Uterus , Leomyoma,
Endometrial carcioma. For women above 35, its mandatory to perform an
Endometrial curetage or even hysterectomy to rule out endometrial cancer.\n\n
****DDX1
Endometriosis is a benign condition, where foci of endometrial glands are
found OUTSIDE of endometrium. They increase in size throgh out menstrual cycle.
Asso with Adenomyosis occurs in 15% of cases.\n\n

****DDX2 ?? Leomyomas, are difficult to ddx from Adenomyosis, except that consistency of Uterus is softer in Adenomyosis. \n\n
****DDX3
Endometrial Carcinoma, occurs in women after menopause .\n\n
****DDX4
Endometritis manifest with fever, and enlarged and tender uterus, asso with
vaginal discharge . It usually occurs after a septic abortion, and the mc oranism
responsible is Strep.\n\n
ADHD
Short attention span, impulsivity, hyperactivity for >6mo. Tx is Methylphenidate, se
is decreased appetite.\n\n
Adjustment Disorder - 2
Emotional or behavioral symptoms that develop w/I three months of exposure to an
identifiable streesor and raely lasts more than 6 months after the stressor. \n\n
*** Tx of choice
is Conginitve or Psychotherapy, not drugs. \n\n
***DDX
is GAD where pt worries about many thing, AD pt worry about one thing. \n\n
****DDX2
PTSD is when pt relives the trauma that she experienced, nightmare, flashbacks. FOR >1 month.\n\n
**** DDX Acute Stress Disorder
is PTSD but FOR <1 month. \n\n
Adrenal insufficiency, 2ary
Is caused by Pituitary tumor. There is Hypothalamic-Pit failure. \n\n
**There is Glucocorticoid def
weakness, fatigue, depresion,irritability,hypotention,
lymphocytosis,eosinophilia), and Hypothyroidism; cold intolerance,constipation,
dryskin), while Normal K level indicated Aldosterone production is not impaired,
and absence of Hyperpigmentation; characteristic of Primary adrenal insuff, all
suggest 2ary adrenal insufficiency. \n\n
*** Other causes of Primary adrenal insuff
are:Autoimmune destruction,adrenal CMV, adrenal TB and adrenoleukodystrophy. \n\n
CMV , TB
Adrenal insufficiency, Acute
Pt presents with nasea and vomitting, abdominla pain , hypoglycemia and
hypotension. Preoperative steriod use is the main cause. \n\n
Adrenal Tuberculosis: Endo, 6/2
Adrenal insufficiency plus adrenal calcifications. It's the primary cause of Primary
Adrenal insuff in developing countries. In contrast autoimmune adrenalitis is the
mcc of Primary Adrenal insufficiency in developed countries.\n\n
Airway assess
An airway is always patent(SECURE) when a pt is conscious and able to speak. If
he is tachypnea and noisy respiration he needs chin lift and face mask. An airway is
needed in ALL UNCONSIOUS pts. \n\n
***In the FIELD
best option is needle
Crricothyroidectomy. In ER best option is Orotrachial intubation. Nasotracheal is
time consuming. Surgical cricothyroidectomy is a good choice for Apneac pts with
head and spine injury. \n\n
Alcohol withdrawl
It might occur after surgey when pt has not had drink for a few days. Prestns with
fever, HA, N&V and TREMORS. \n\n
***Tx
is Chlordiazepoxide.\n\n
Alcoholic Gastritis
Pt presents with epigastic pain, vomitting dark brown blood after alcohol binge, and
has a hx of PUD. A BUN level >40 in a presence of normal creatine is highly
suggestive of upper GI bleed. \n\n
***its due to
bacterial break down of Hb in the GIT and the resulting absorption of urea.
Another place that causes increase BUN w/o Crt is in administration of steriods.\n\n
Alcoholic liver disease - 2
The three major pathological findings of ALD are: 1-Fatty liver (steatosis). 2-
Alcoholic Hepatitis. 3-Alcoholic Fibrosis/Cirrhosis.\n\n
*** Fatty liver
is the result of short
term alcohol ingestion, where as Hepatitis and Cirrhosis require long,sustain alcohol
use. \n\n
****Alcohol Hepatitis
is manifested by Mallory bodies, infiltration by neutrophils,
liver cell necrosis, and a perivenular distribution of inflamation. Fatty liver, Alcohol
Hepatitis and even early fibrosis can be potentially reversible if the pt stops alcohol
consumption.\n\n
****Females vs males
females are more suseptable to ALD. The most characteristic
manifestation is AST/ALT > 2 . ALT & AST are almost always <500, if >500 this
raises the probability of injury from drugs. \n\n
****Fatty liver exist in
**80% of alcoholics but
only 15-20% develop alcoholic hepatitis, and only 50% of pts w alchoic hepatitis
develop Cirrhosis.\n\n
**** Malory bodies
are NEITHER specific NOR required for dx of
Alcoholc Hepatitis.**** Pts with Alcoholic Cirrhosis should have Esophagoscopy to
prevent varices.\n\n
ALL
Presence of more than 25% lymphoblast in BM and the Positive Periodic Acid Shiff
reaction (PAS) makes the Dx.\n\n
****First symptoms
are non specific, fatigue, palor,
fever, anorexia, petechia and lymphadenopathy. Dx is suggested by
thrombocytopenia and blast cells, but confirmed with BM bioposy.\n\n
*** DDX
1:Hodgkins, presents with painless, firm cervial adenopathy, sign and symptoms
are similar to ALL but LYMPHOBLASTS make ddx of ALL.\n\n
** DDX2
AML, occurs in
adults, main dx is >25% MYELOblasts in BM biopsy. \n\n
**DDX3
Aplastic Anemia, can present lilke ALL BUT lab shows decrease in ALL cell lines
including WBC. \n\n
** DDX4
ITP, children with ITP present with sudden onset of bruising,petechia and
occasional Epistaxis. The only cells that are very low are Platelets and their size is
LARGE. \n\n
***DDX5
Infectious mononucleosis, presents with lymphadenopahty, fever
and pharyngitis, due to EBV. ATYPICAL lymphocyte are seens on peripheral blood
smear and MONOSPOT test is positive. \n\n
***** If parents refusing treatment
obtain
court order for chemotherapy. ****TX meds.\n\n
Allergic Bronchopulmonar Aspergillosis
ABPA is characterized by transient recurrent pulmonary infiltrates, peripheral
eosinophilia, asthma and immediate wheel and flair reaction to Aspergilus
fumigatus and presence of antibodies in serum against AF.\n\n
*** Other characteristics
are Hx of Brownish plug in the sputum and high IgE levels.\n\n
***Tx
Glucocorticoids are used to tx this dis. Whenever an Asthmatic pt is suspected of having ABPA, skin testing with Aspergillos antibody is first dx step, if its negative ABPA is ruled out. If positive serum precipitants agianst Aspergilos and IgE levels are checked. \n\n
***ABPA is excluded if
IgE is <1000, or if serum precipitants against Aspergilus are absent.\n\n
***DDX
1: JOB SYND, a recurrenct bacterial infection and markedly elevated IgE.
Infections are due to Staph and are SKIN infections. Neutrophils exihibit impaired
chemotaxis. Other feaatures are eczema, asthma, allergic rhinitis. Tx is antibiotics. \n\n
***DDX2
Wiskot Aldrich, X-link, Triad of eczema,thrombocytopenia, pyogenic
recurent infections. IgA & IgE are high while IgM is low. \n\n
***DDX 3
Chronic Eosinophilic Pneumonia , is the mc eosinophilic pneumonia in US. Pts presents with systemic signs of fever, malaise, anorexia, weight loss. Eosinophils >40% is suggestive of this dis. TX is Glococorticoid. \n\n
***DDX4
Churg-Strauss is a multisystem vasulitic disorder of unknown etiology that affects skin,kidney, CNS, lungs, GI and heart. There is asthma, , fever, marked Eosinophilia. Tx is glucocorticoids.\n\n
Allergic Conjunctivitis
Is an acute hypersensitivity reaction that is caused by environmental exposure to
allergens. Characterized by intense itching hyperemia, tearing, conjunctivla edema
and eyelid edema.\n\n
Allergic Contact Dermatitis -3
Caused by Nickel and poison IV. Type VI hypersensitivity reaction. It mostly occurs
in adults. \n\n
**DDX1
Atopic Dermatitis, presents as pruritic lesions in infants <6mo.
Prevention is the mainstay of tx. Everywhere is involved but diaper area apears
spared. Give infant warm bath and moisterizers. Acute attack maybe helped with
low dose corticosteriods.\n\n
Allergic Interestitial Nephritis
Its secondary to Nafciline use. It's a type IV hypersensivity reaction. Nephrotoxic
agents are antibiotics; pencilline,cephalosporine, sulanamide, rifampine, cipro),
thiazides, omeprazole, NSAID. Triad of fever,petechial rash and peripherla
eosinophilia in an azotemic (Increased Urea) pt is highly suggestive. \n\n
**DDX
Acute Tubal Necrosis is mostly seen in ischemic or nephrotoxic renal failure. MUDDY brown casts are characteristic.\n\n
Allergic Rhinitis - 2
Dark puffy eyelids is called allergic shiners. The red crease over the nose causes
constant rubbing, called allergic salute. Tx is avoidance and decongestants.\n\n
****If rhinitis is not clear if its allergic or infectious
then next step is Nasal cytology.
Demonstration of neutrophils in nasal secretions suggests infectious cause.
Predominant of Eosinophils suggest allergic cause. \n\n
***Other cause of nasal eosinophilia
include Nasal Polyposis (Aspirin sensitivity).\n\n
Allergy, Drug
for mild reactions just use antihistamines. For systemic reactions, like anaphylactic
use Adrenalin or Steriods. \n\n
Alpha Feto Protein
The mcc of its deficiency is gestational age error.\n\n
*** HIGH levels
are seen in
Gastrochisis and omphalocele, as well as 'false positive' causes like fetal demise,
multiple gestation, inacurate gestational age.\n\n
**** In case of increased MSAFP
should first do US to rule out false positive causes and to detect presence of any anomaly.\n\n
***Afterwards,
**Amniocenthesis must be ordered for confirmation by measuring
amniotic level AFP and AchE. AchE is a protein that increased only in neural tube
defects.\n\n
*** LOW levels of MSAFP
are seen in chromosomal abnormality especially
Down's synd. The screening is more acurate when MSAFP is coupled with b-hCG
and Unconjugated Etridiol (UE3) levels, Its called TRIPLE TEST. Combnation of
Decreased MSAFP + Increased b-hCG + Decreased UE3 is typical for Down's. In
trisomy 18, ALL three are decreased.\n\n
***Likewise,
***US has to be perfomed to rule out
inacurate dates and fetal demise, then amniocenthesis to confirm the Dx. MSAFP
and triple test should be performed by 16-18 week of gestation. \n\n
****AFP is produced
by Yok sac and fetal liver, some passes to maternal circulation.\n\n
*** Other procedures:
CVS- is indicated in women who are known to have genetic
abnormality or previous affected children. Its done 10-12 weeks and offers
advantage of 1st trimester testing. \n\n
Alpha-1 Antitrypsin Deficiency
It's a protease inhibitor synthesized in liver. Pts w homozygous def are at risk of
Panlobular Emphysema in adult life. \n\n
***The mc manifestation in adults
is
Asymptomatic cirrhosis, and maybe complicated by Hepatocellular Carcinoma.
Hepatocytes contain granules that are PAS positive and Diastase resistant. \n\n
***DDX1
Whipple's, which is PAS positive but doesnt cause cirrhosis.\n\n
Alport Synd
Recurent episodes of Hematuria, sensoryneural deafness and a family hx of renal
disease. Alternating areas of thinned and thickened capilary loops with spliting of
GBM.\n\n
Alprazolam
Abrupt cessation is asso with significant withdrawl symptoms like generalized
seizure and confusion. \n\n
ALS - 2
Tx is Riluzole glutamate inhibitor. Side effects are dizziness, nasea, weight loss,
elevated liver enzymes and skeletal weakness.) Both upper (spasticity, bulbar
symptoms, hyperreflexia) and lower motor neuron (Fasciculation) damage. Muscle
wasting of all body muscles. "Tuesdays with Morrie" Jack Lemon. \n\n
Altered Mental status in elderly
Major causes include: 1-Hypo/Hyper natremia. 2-Hypo/Hypercalcemia. 3-
Hypomagnesemia. 4-Hypophosphatemia. 5-Hypoglycemia. 6-Stroke. 7-cardiac
events. 8-infections UTI . \n\n
Alturism
Alturism is minimizing internal fears by helping other who have same problem
(Alcoholic volunteering in AA). DDX: Sublimation, turning unacceptable behavior
to a more acceptable ones. \n\n
Alzheimer's Disease - 4
Diffused cortical atrophy. Tx is Donezapin, Tacrine, rivastigmine, galantamine.\n\n
**** Elderly
gradual memory decline with Apraxia (Loosing the ability to do
routine acts), Aphasia and Agnosia (not recognizing familiar objects). \n\n
*****DDx
it from Picks by MMSE, which is decreased in AD. In picks you need to see more than just one indication of behavior changes(urinating is not enought).\n\n
Amaurosis Fugax
Amorosis Foo-Gacs: Visual loss that is monocular, transient "dropping of the
curtain". Opthalmoscopy reveals zones of whitend, edematous retina, following
retinal artery distribution. \n\n
***Seen in pt with
atherosclerosis and CV disesae. Its
caused by retinal emboli from ipsilateral carotid artery. It last about 15 minutes.\n\n
*** Tx
of atherosclerosis is important to reduce the risk of stroke. Dx is with Duplex of the carotid.\n\n
Amebic (liver) abscess - 2
More common in tropical males. After intestinal infection with Entameba
Histolytica. \n\n
****Transmission
by water or food. Dx of liver abscess is by CT. When
aspirated has "Anchovi-paste" appearance, \n\n
****Tx
is Metroniddazole, orally, given one to two weeks. \n\n
****Hx
of travel to endemic areas followed by dysentry and RUQ
pain with a single Cyst in right lobe of liver is indicative of ALA. \n\n
****Primary infection
is in the colon, but then it goes to portal vein and liver. Dx is made by stool
examination of trophozoit serology and liver imaging.\n\n
****DDX
Hydatid Cyst, caused by Echinococcus acquired by contact with dogs. \n\n
Amenorrhea - 3
1-Secondary Amenorrhea: the first step is to rule out pregnany, then
hyperprolactinoma, then hypothyroidism. \n\n
****The 2nd step
should be determination of
pt's estrogen status with progestine challenge test. A- If pt has adequate estrogen
and a history of intrauterine instrumentation then suspect Asherman's synd
(intrauterine adhesions. A hysterosalpingogram can show). \n\n
***Pts with no such hx
are all anovulatory or oligo-ovulatory. B- If estrogen is inadequate, FSH should be ordered to determine gonadal or central origin.\n\n
****Prolactin production
is
inhibited by Dopamine and stimulated by serotonin and TRH. An increase in TSH
and TRH may lead to Hypothyroidism. Hyperprolactinoma may also affect GnRh
and gonadotropin secretion and thus result in ammenorrhea.\n\n
*** Other causes
are
dopamine antagonist (antipsychotics,TCA), hypothalamic and pituitary tumors. In
the case of ammenorrhea-hyperprolactinoma , first rule out hypothyroidism by
measuring serum TSH.\n\n
***2ary Ammenorhhea in athletes is due to
Estrogen
deficiency because menstruation happens because of Estrogen.******Check out
Table in Q41, Exam 12 0r 13. \n\n
Amiodarone tox - 2
1-Pulmonary, 2-Hepatotox, 3-corneal deposits, 4-skin reactions. *** If a pt needs
rate control but has Restrictive lung disease Amiodarone is CI. \n\n
Amlodipine side effect
WAT.\n\n
Amphetamine intox
pt might act like schizo but HT is not normal. Cocaine is the same as Amphetamine. \n\n
****DDX
is Manic episode that has the mnemonic DIGFAST
(Distractbility,Insomina,Grandiosity,Flight of idea, Activity increase,Speech
talkative,Thoughtlessnes risky actions.).\n\n
*** DDX 2
Herion Tox: Triad of altered
consciousness,respiratory depression and pinpoint pupils. Herion Withdrawl:
muscel and joint pain , N&V, diarrhea,abdominal cramps,
rihnorea,lacrimation,sweating. \n\n
****Amphetamine Withdrwal
depression, increased appetite ,fatig , irritability.\n\n
Amphotericine Toxicity
Hypokalemia.\n\n
Amyloidosis:
In heart is the end stage and next step is Transplantation.\n\n
Anal Fissure
They are most comonly caused by passage of hard, large constipated stool. The mc
symptoms are severe pain and bright red rectal bleeding during defecation. Tx of
both acute and chronic fisures starts with dietry modification (high fiber diet and
lots of fluids) along with stool softner and local anesthetics.\n\n
Analgesic Nephropathy - 2
Clinical senario describes a woman with chronic HA, almost everyday, who presents
for Hematuria. Several years of abuse leads to chronic tubointerstitial damage.
Hematuria is due to Papilary Necrosis. \n\n
**** It's the mc
form of drug induced chronic
renal failure. Most commonly in femlaes . Papilary Necrosis and Tubulointerestitial
nephritis are the mc pathologies seen. \n\n
*** EARLY MANIFESTATION
Polyuria and sterile Pyuria with WBC casts
are early manifestations. In advanved cases you see Proteinuria and hematuria.\n\n
Anaphylactic shock
One HOUR After bee sting in ER the first thing to do is SC Epi, not removing the
sting. If after one minute then first remove the sting.\n\n
Anemia of Prematurity
is the mc anemia in premature and low birth weight infants. Pathology involves a
diminished RBC production, shortened RBC life span. And blood loss. Iron
supplementation doesn't help falling Hb levels and iron def is not the cause of
prematurity.\n\n
Aneurysms
Causes are: 1-TARUMA:Aneurism in a young pt who presents with Desending
Aortic aneurism. Pathophy is acceleration trauma. It might show in Cxr by wide
midiastinum, 10% will have normal cxr so if you suspect it do CT or MRI. Tx is
surgery to prevent rupture. \n\n
***2nd cause
ATHEROSCLEROSIS:Is the mcc of Descending
Aorta aneurism. Pts are older, smokers. They are generaly asymptomatic and are
seen on Cxr. Majority of pts also have significant CAD. \n\n
***3rd cause
MARFAN:nomonic is
'm.A.AR.f.A.n". Pts present with Ascending aneurism of Aorta. Asso findings are
Aortic regurgitation Surgery is required to replace both aortic valve and entire
ascending aorta. They also have a higher chance of Aortic Dissection than genral
population. \n\n
*** 4th cause
MYCOTIC:result from localized infection , Its mc in Femoral artery
and 2mc in Ascending aorta. The mc pathogen is S. Aureus and 2mc is Salmonela.\n\n
****5th cause
SYPHLYTIC: Occur in Ascending Aorta. Pt presens with fever,chills, splinter hemorrhages. CT is dx.\n\n
Angina, Prinzmetal or Variant - 2
Classis picture is a pt with absence of risk factors of CAD, night pain waking her
up, transient ST elevation, absence of Q waves and negative cardiac enzymes. The
disease results from coronary vasospasm of the artery that causes "Transmural
Ischemia" and hence ST elevation on EKG.\n\n
*** Other things to know is
"Subendocardial ischemia" in Angina pectoris causes ST Depression.\n\n
**** "Transmual Infarct" causes
ST elevation followed by development of Q waves and increased cardiac enzymes.\n\n
*** "Subendocardial infarcts cause
ST Depression that are not
followed by Q waves and elevation of cardiac enzymes.\n\n
*** Summary
TM-IS=Elevate ST-Q-Enz. TM-IN=Elevate ST+Q+Enz. SE-IS=Suppresed ST-Q-Enz. and SEIN= Suppresed ST+Q+Enz. \n\n
*** CI for variant Angina
Propranalol and Aspirin are CI in these pts. The
initial tx is with Nitrates and Calcium channel blockers. Second drug is only added
when there is no response to the first drug.\n\n
*** DOC for initial mgmt is Calcium
channel blocker
, Diltiazam.\n\n
Angina, Stable - 4
EKG stress test is the initial test for dx. Rbbb is not a CI. But when a pt has
Lbbb,WPW, ST depression >1mm at rest then stress testing with imaging is done.\n\n
*** Dobutamine stress test is for
those pt who cant exercise sufficiently. Coronary
Angiogram is done if stress test fails. Myocardial Perfusion is for those who are at
risk of develoing complications with excercise or Dobutamine.\n\n
*****Medications that has to be withheld prior to EKG Exercise test are
Anti ischemic medication, Digoxin and medications that slow the heart (B-Blockers, Atenolol).\n\n
**** DOC In pts with stable angina and HT
B-blocker is tx of choice. CCB(Verapamil) is indicated if BBs are CI or dont work. They both have BOTH anti HT and anti anginal effect. Enalapril has ONLY anti HT effect.\n\n
****Stress EKG or an Excercise Echo should
be done for
risk stratification in pts with stable angina. Pharmocological stress
testing is an alternative if pt cant do excercise. Coronary angiography is done when
pt is refractory to medical tx or when excercise tesidentifies pt as high risk.\n\n
Angina, Unstable - 2
Ishcemic chest pain only partially releived by Nitroglycerin, T wave inversion, and
negative cardiac enzymes.\n\n
*** Tx for unstable angina and NON-Q wave infarction
is
with IV heparin, aspirin, B-blobker and nitroglycerin is indicated. Thrombolytic tx
is asso with mortality in these pts. \n\n
***Thrombolytic therpay is indicated
in MI with ST
elevation after sublingual Nitro rules out coronary vasospasm. Another indication
for Thrombolytics is LBBB. \n\n
**** for platlet agg.
Give CLOPIDOGREL not Ticlopidine for platelet
aggregtion.\n\n
Angiodysplasia or Vascular Ectasia
The two mc causes for pianles GI bleeding are diverticulosis and Angiodysplasia. \n\n
***DDX
is that Angiodysplasia is asso w Aortic Stenosis. Other asso is renal failure.
Also Sigmoidoscopy reveal Diverticulosis and not Angiodysplasia.
MERK:Angiodysplasia is an acquired submucosal AVM, which may cause lower GI
bleeding in elderly patients.\n\n
*** When the bleeding is massive,
it is usually from either
angiodysplasia or diverticulosis. Typical angiodysplastic lesions are 0.5 to 1.0 cm,
bright red, flat or slightly raised, and covered by very thin epithelium (see Plate 22-
3). \n\n
***Treatment
is indicated for angiodysplasia that has bled because of its tendency to
cause chronic recurrent hemorrhage. Active, severe bleeding may be controlled
quickly by intra arterial or IV administration of vasopressin when the patient is
stabilized, but results are variable. The lesions then may be treated more definitively
by endoscopic coagulation or surgery.\n\n
**** The most difficult aspect of treatment
is to
eliminate other potential causes for the GI bleeding and to locate all of the
angiodysplastic lesions. If the lesions are not large or numerous, endoscopic
coagulation with hot biopsy forceps or laser photocoagulation is preferred. The
usual surgical treatment is a right hemicolectomy because of the propensity for
angiodysplasia to involve the right colon.\n\n
Angioedema - 2
ACE inhibitors are notorius for producing Angioedema in ER. Pt presents with
non-inflamatory edema and laryngeal edema that could be life threatening.\n\n
** cause of Angioedema
occurs due to proinflamatory action of substance.P which is stimulated by Bradykinin. Bradykinin can be broken down by angiotensinogen converting
enzyme. When an ACE inhibitor blocks this enzyme, the levels of brady kinin
increases leading to angioedema. Tx is Anti histamine.\n\n
Angiofibroma - 3
A benign vascular tumor found in adulescent male. Present with frequent
epistaxis(Epistaxis is the major symptom), nasal obstruction, HA & conductive
hearing loss. In PE hay greyish-red mass in the posterior nasopharynx. CT is Dx,
TX is medical and surgery, depending on stage.\n\n
****Any adulescent boy with epistaxis and has localized mass
with bony erosions on the back of the nose has an Angiofibroma unless proven otherwise.\n\n
Anion Gap Metabolic Acidosis 3
First see pH<7.4, then see HCO3<24 then we know its MA. To calculate
compensation use Winter's Formaula PaCO2= 1.5 (HCO3) + 8, this is what CO2
would be after compensation. Normal AG is b/w 6-12.\n\n
*** MERCK
When metabolic acidosis results from inorganic acids (ie, hyperchloremic or normal anion gap acidosis), HCO3 is required to treat the acid-base disturbance.\n\n
** However
when acidosis results from organic acid accumulation (ie, increased anion gap acidosis), as in lactic acidosis, ketoacidosis, most experts still recommend judicious use of IV sodium bicarbonate in the treatment of severe metabolic acidosis (pH <
7.20)******AG formula is (Na)-(Cl+HCO3), normal is 6-12.\n\n
Ankylosing Spondolytis - 3
Asso with IBD.\n\n
**** TX
regular exercise is the only tx that halts progression of the
disease.\n\n
*** H/P
Pt is young, presents with insidious onset of back pain for more than 3
months, positive family hx, reduced back motion and chest expantion, also HLAB27.
Xray shows scoliosis. NSAID is for pain control. \n\n
***Tx periferal joint
Sulfasalazine is for peripheral
joint involvment. Surgey is recommended when dis is sever and refractory to
medical tx.\n\n
****Dx
cant be made unless there is evisence of sacrolitis. So when pt
has symptoms of AS, the next step is to do Xray of the sacro iliac joint. If Xray is
inconclusive then MRI is done.\n\n
Anorexa Nervosa - 2
Elevated carotene gives the skin a yellow color. Carotene is also elevated in DM and
Hypothyroidism. Pregnant women with current or previous AN are at risk for
Miscarriage, intrauterine growth retardation, hyperemeis gravidarum, premature
birth, cesarean delivery, & post-partum depression. \n\n
***Osteoporosis
is a common
finding in women pregnant or not. Also elevated cholesterol and carotene levels,
euthyroid sick syndrome, cardiac arrythmias (prolonged QT). The FIRST step of
MGMT is Hospitalization.\n\n
****H/P
There Ammenorrhea and body weight is below
normal. In bulemia weight is normal.\n\n
****Once the dx is made the first step
in
managementis hospitalization.\n\n
Anserine Bursitis
Pain over medial tibial plateu, hx is asso with trauma and cxr is normal.\n\n
Anterior Cord Synd
Usually occurs due to motor vehicle accident injury. There is Paralysis and
analgesia below the level of injury and preservation of posterior column function
like position,touch and vibratory.\n\n
**** Pts trearted
with High-dose Methyl prednisone
w.I 8 hrs of injury have significant neuorologiccal improvement. All trauma pt do 2
things, 1-Immobalize, 2-ABC.\n\n
*****Asso with
burst fracture of the vertebra,
characgterized by total loss of motor function (Paraplegia) below the lesion, with
loss of pain and temperature on both sides below the lesion. MRI is the best initial
Dx procedure.\n\n
Anti Psychotc drugs
Work by blocking Dopaminergic receptors. Typical ones are Haloperidol,
Chlorpromazine, Fluphenazine. Atypical ones , add Serotonin blocks as well, so
block EPS SE. Atypical is Clozapine, Risperidone. \n\n
**** SE
Dystonia, an extrapyramidal
SE of Haloperidol is treated with Benztropine or Diphenhydramine.\n\n
Anti-D Ig
After events that are asso with maternal-feto hemorrhage (placenta abruption) the
failure to correct the dose of Anti D can result in maternal Alloimmunization.\n\n
Anti-depressants
Are SSRI, MAO inhbx,TCA. SSRI causes sexual dysfunction. If it does, discontinue
and give Bupriopoin (inhibit Nepi, and dopamine reuptake) it doesn't cause
impotence. \n\n
**** sex dysfunction
TCA also causes sex dysfunction. Trazodone is good for antidepressant in those with Insomnia, but it too causes sex dysfunction.\n\n
*****In pts with terminal dis
when severly depressd with active suicidal thoughts antidepressnt should be given immediately, not lectures about accepting the fact and the feeling being normal and .blahblahlah...\n\n
Antiphospholipid Antibody Synd
Recurrent arerial or venous thrombosis or recurent fetal loses in the presnece of
Antiphopholipid antibodies. There are 3 types of APLA, first one is responsible for
false VDRL, Second is LUPUS and falsly elevates APTT, the Third is
Anticardiolipin. The tx is Heparin+Aspirin.\n\n
Antisocal Personality
Is dx in those older than 18 yo who engage in illegal activites and abuse others. They
show CONDUCT disorder when they are minors.\n\n
Aortic Aneurysm
MCC is ascending aorta and cuase is cystic medial necrosis. Descending aorta is asso
with atherosclerosis.\n\n
Aortic Aneurysm, Abdominal -3
After AAA repair (surgery) , diarrhea and blood in stool should raise the question
of Ischemic Colitis. If CT is inclusive, a sigmoidoscopy/Colonoscopy is
recommended.\n\n
*** DDX
is Pseudomembraneous Colitis due to antibiotics will present
with same symptoms but not the ischemic changes in the colon. CT shows ruptured
aorta and blood around aorta, tx is exploring the abdomen.\n\n
***The study choice
of Dx and folow up is abdominal USG. \n\n
****When pt presents with pulsatile mass and hypotension
a presunptive dx must be entertianed. and pt should be taken directly no surgery, NO USG OR CT. \n\n
***** complication
spinal cord ischemia with lower spastic paraplegia is a rare complication of AAA. Its due to loss of blood during the operation.\n\n
*****When there is ruptured AA confirmed with CT
, then the next step is
Explore abdomen not Laparoscopy (not used in acute conditions).\n\n
Aortic dissection
Htn and BP difference in two arms. First thing to do is admit to ICU, IV
Nitropruside(reduce BP), Beta blocker(Esmolol,reduce heart rate). Any delay
maybe fatal, don't even give pain killer first, just do the above. \n\n
***So first tx is antihypertensive agent, before CT,MRI,TEE or Cxr. Intense retrosternal pain that is radiated to subscapular area, also check for Aortic regurgitation (decresendo
diastolic murmur in the left sternal border, also Hypertension. Dx w TEE.\n\n
...
******The mCC
of AD is HT, if given no info pick this as the cause.\n\n
****Acute AD is a risk factor in
Marfan pts. Tearing pain and raddiation to the back and a difference BP of 30mmhg b/w two arms are impotant clinical clues. TEE or CT ar
the dx studies of choice.\n\n
Aortic Regurgitation
Presents with Water hammer or collapsing heart and pistol shot femoral pulses.
These occur due to hyperdynamic circulation and early diastolic runn off of aortic
insufficincy.\n\n
****Tx
is Diuretics+ACE inhibitors+Digoxin, are given first to releive
congestive sysmtoms for LV dysfuntion and then we need to change valve is
indicated. Pt must undergo Echo for diagnosis.\n\n
Aortic Anreurysm Rupture
should be rulled out in ALL trauma pts with Severe chest trauma,
pulsatile mass and hypotention. Its best done with Cxr. The signs are:1-widening of
mediastinum>8cm, 2-Depresion of L main bronchus >140degrees, 3-Deviation of
nasotracheal tube, 4-Fracture of 1st&2nd rib,sternum,scapula, 5-L apical
hematoma. \n\n
**** TX
Immediate surgery is very important but do confirmatory CT or
angiogram. BUT REMEMBER if question gives you option b/w Surgery and CT go
with surgery.\n\n
Aortic Coarcation:
The tx for RECURRENT AC is Baloon Angiography.\n\n
Aortic Stenosis - 4
Age dependant idiopathic sclero-calcific changes are the mfc of isolated AS in
elderly. Pt presents with exersional syncope. PE shows increased intensity of point of
maximal impulse. Auscultation reveals ejction-type systolic murmur. With radiation
to carotid arteries. \n\n
*** NOTE
Bacterial endocarditis may lead to Aortic insufficiency
not aortic stenosis.\n\n
****Pt presents
with Anginal chest pain, dyspnea or syncope
(The classic triad of symptoms is syncope, angina, and dyspnea on exertion.). Pain is
ischemic in origin and occurs due to increased O2 demand 2ary to LV hypertrophy.
ECHO is the study of choice to Dx AS. Its also used in follow ups. \n\n
****Key to Dx
is Harsh systolic murmur over the right sternal edge, know that only left sided murmurs increase on exspiration. S4 results from forceful atrial contraction against the thick non-compliant ventricle. \n\n
***The classic indication for surgery in pt with AS is
SAD (Syncope, Angina, Dyspnea). Dyspnea results from CHF. Presentation of either
indicates valve replacment surgery. \n\n
*****The indications for Aortic valve replacement are
1-All Symptomatic pts, 2-Pt with severe AS undergoing CABG. 3-Asymptomatic pt with severe AS either poor LV systolic function , LV hypertrophy > 15mm. \n\n
****In ALL AS pt who are SYMPTOMATIC
IE prophylaxis and repeated regular follow
ups are recommended.\n\n
Aplastic Anemia, Acquried
Injury to the bone marrow by drugs, radiation, toxins or insecticide. Pedaitrics
disese. Pallor,fatigue, loss of appetite, easy bruising, petechia, mucosal hemorrhage
and fever. Lab shows, anemia, leukopenia, thrombocytopenia. \n\n
***DX
BM biopsy is essential for Dx and shows hypocellular BM and fatty infiltration. MERCK. \n\n
****Tx
Equine antithymocyte globulin (ATG) has become the treatment of choice for older patients or those without a compatible donor. Combined ATG and cyclosporine is
also effective. \n\n
****Bone marrow transplantation
from an identical twin or an HLAcompatible
sibling is a proven treatment for severe aplastic anemia, particularly in
patients aged < 30.\n\n
***** DDX
Fanconi syndrome, familial, pancytpenia, brown
pigmentation, cafe au lait, short stature, upper limb abnormality, skeletal
abnormality, it starts w thrombocytopenia then neutropenia and then anemia.\n\n
****DDX2
Diamond-Blackfan Anemia, or congenital RBC aplasia presents in the first
three months of life w pallor and poor feeding. WBC and platelet counts are normal.\n\n
Appendicitis:
If a 62 yo on WARFARIN comes in with appendicits and requires emergent
surgery, first step is to reverse the effect of Warfarin not by Vitamin K infusion
(takes 1-2 days for effect), but with infusion of FFP. Then proceed with the surgery. \n\n
****Acute Appendicits may be complicated
by pelvic abscess that presents with
lower abdominal pain, malaise, low grade fever, and tender pelvic mass on rectal
exam. Most of pelvic abscesses are due to perforation of appendix.\n\n
*** Pt could have had appendicits that resolved
with rupture and abscess formation. The diarrhea is reactive due to irritation. Drainage of the abscess is the tx in these cases. \n\n
**** best tx Experience
has shown that right hemicolectomy with ileotransverse
anastomosis has best postoperative results, when resection of part of ascending
colon is required, when hay appendicits with cecum inflammation and
pus.\n\n
******Complicated appendicitis is when
the pain is ignored for days and pt
presents with high fever and localized pain to RLQ. Tx is with IV hydration,
Antibiotics and bed rest. \n\n
****Non-operative management is
curative, CT may reveal abscess that can be drained percutaneously Antibiotics should cover Gram negative
and Anaerobics, Cipro+Vancomycin.\n\n
ARDS - 4
Could happen secondary to Acute pancreatitis. Dx:PaO2/FiO2 must be <200
(PaO2=55, Receiving O2 by mask is 60%) in the setting of absence elevation of left atrial pressure (PCWP<19mmhg). \n\n
*** mcc of ARDS
is sepsis . Other causes are Herion, acute pancreatitis, severe burn
and near drawning.\n\n
****Goal of mechanical ventilation
is to improve oxygenation
and is best doen with increased PEEP. PEEP keeps the alveoli at end expiration and
keeps them open for a longer duration to inprove oxygenation. PEEP is the major
factor in improving oxygenation in ARDS. \n\n
***In a postoperative pt who prsents with dyspnea and tachypnea one must exclude MI,PE,Pneumonia and ARDS. If pt presents with Bilateral fluffy infiltrates on a chest xray and hypoxia with difficulty with oxygenation Its most probabely ARDS. Its not Atelectasis so there is NO FEVER.\n\n
...
Arm Fractures
1-Colles, outstreched hands in elderly. 2-Smith, my injury, 3-Bartion, intraarticular
fraction of distal radius. 4-Chauffer's, fracture of radial styloid process in drivers.
5-Galazzi, isolated fracture anywherea long radius with asso injury to the distal
radial joint.\n\n
Arrest Disorder - 2
Midpelvic contraction which is indicated by prominent ischial spines is an
important cause of Arrest disorder or dialation. DDX:Inlet Dystocia, Descent of the
presenting part at +1 indicates that fetus is engaged, so ID is unlikely.\n\n
****Arrest in dilation
more than 2 hours, and arrest in descent more than 1hour is the definition.\n\n
*** Can be caused
by hypotonic contraction, anesthesia, cephalopelvic malproportion or malpresentation. If arrest is in midpelvic contraction, indicated by prominent ishcial
spines, then the next step is to do a C-section.\n\n
*** Forceps cant be used
until cervix is fully dilated (10cm). Oxytocin might cause uterine rupture due to pelvic prevention of birth. Now in case of Shoulder Dystonia, a last resort tx is 'Zavanelli' maneuver (pushing back the fetus in uterus & doing a C-section.\n\n
Arthritis, Reactive
It's a form of seronegative spondyloarthropahty. Enthesopathy (A disease process
occurring at the site of insertion of muscle tendons and ligaments into bones or joint
capsules ) causes heel pain and sausage digits. Enthesopathy is quite specific to
spondyloarthropathy. \n\n
***Tx of choice
for Reactive Arthritis and Reiter's is NSAIDS.
Tetracycline is added if UTI with Chlamydia is suspected and IM Ceftriaxone if
Gonoccocal is suspected (but NIsseria does not cause RA).\n\n
Asbestosis
The hx of shipyard worker with cxr with pleural plaques is dx. \n\n
***DDX
1:Sillicosis, hx
of glass and pottery making. \n\n
*** DDX2
:Berylliosis, hx of high tech industries.\n\n
Ascending Cholangitis
Characterized by Triad of RUQ pain, Fever and Jaundice (charcot triad). Its an
infection of the CBD, generaly 2ndary to obstruction of CBD with a stone leading to
dilatation of CBD. \n\n
*** 1st step
Broad spectrum antibiotics should be started immediately,
however, its very important to decompress the billiary duct and provide their
drainage. ERCP (Endoscopic Retrograde CholangioPancreatography) is the method
of choice. \n\n
****ERCP can be used to do
a sphingtrectomy with the stone removal and
drain the bile via the sphincter or by placement of a stent. Early drainge can
significantly reduce mortality and morbidity.\n\n
Ascites - 3
Management starts wirh sodium, water and protein restriction, spironolactone,
furesamide. If given a choice for only one drug tx b/w spironolactone and
Furesamide, pick spironolactone.\n\n
*** If that didn't help then
slow tapping of up to 2L of
ascites fluid a day balanced with infusion of 10 gr albumin per liter tapped. \n\n
*** If that didn't work
then do surgery. The vascular shunts are indicated after first bleeding. \n\n
*** Distal spleno-renal shunt
will not improve and it might worsen it. Side to side portocaval shunt might improve the ascites but worsen encephalopathy.\n\n
*** Peritoneum-Jugular shunt
is designed for tx of Ascites only. *If pt 's ascites is so much that is compromising other systems, the next step is Paracentesis which is both therapeutic and diagnostic. \n\n
**** DOC
Spironolactone is the DOC in tx of Cirrhotic Ascites. Tx of
ascites in Cirrhotic pts should be as followes: 1-All the pt shold have Dx
paracentesis done. 2-Salt Restrcited Diet is the coner stone of the therapy, in 10-
20% of pt thats all you need to do. 3-Pts not controlled with SRD, Spironolactone is
next. \n\n
*** why
Its an Aldosterone antagonist, and it works because Ascites is only due to 2ary Hyperaldosteronism. 4-Recalcitrant (difficult to manage) ascites should be tx with
TIPS. 5-Very severe ascites should be tx with paracentesis initially.\n\n
Aspergilosis - 3
An opportunistic infection in South East USA. A mobile cavitary mass in the lung,
which prestns with occasional hemoptysis.\n\n
**** DDX1
Lung abcess, due to anerobic organism, with an AIR FLUID level on Cxr. Medical mgmnt is antibiotics, postural drainage and bronchoscopy.\n\n
***DDX2:
PE, from lower legs, presents with Dyspnea,Tachpnea, Chest pain and collapse. ECG may demonstrate RV Hypertrophy, RBBB, Right Axis and T inversionin antreior leads. Cxr may show decreased pulmonary vascular markings. \n\n
***DDX3
Histoplasmosis:The mc fungal infection in US. Acquired by inhalation. "Calcified Nodes" in lung , mediastenum or spleen. Cxr shows central or target calcification. Ocasionaly causes mediastinal lymph node enlargment.\n\n
***Allergic Broncho Pulmonary Aspergillosis (ABPA),
inding of central bronchiectasis on the cxr and elevated AgE and Eosinophilia is
characteristic. Next do a skin test for Aspergilosis antibody and you have your Dx.\n\n
**Tx
is Prednisone oral. Itraconazole may reduce the need for steriod but its not the
main therapy.
****It occurs
in immunocompromised pt (those taking cyclosporine,
chemotherapy). Pt prestns with fever, cough, hemoptosis, and dyspnea. Cxr may
show cavity lesion. CT shows pulmonary nodule with a 'halo' sign.\n\n
****Aspergiloma is
the "fungus ball" in preexisting cavities, mc presentation is hemoptysis, TX is Lobectomy.\n\n
**** Types and TX
4 types of infection: 1-ABPA (tx is Prednisone), 2-Aspergious
Colonization, 3-Aspergiloma (surgery), 4-Invasive Aspergilosis (tx ix IV
Amphotericine)\n\n
Aspirin intoxication in ADULTS:
Initially increased respiration leads to respiratory alkolosis and then uncouples oxidative phosphorylation and leads to met acidosis. So they have mixed metabolic acidosis and respiratory alkalosis.\n\n
ASprin tox. in CHILDREN
Initially causes Metabolic Acidosis and then compensatory Respiratory Alkolosis. Aspirin can cause acute erosive gastritis and upper GI bleeding. , alcohol can aggrevate this effect.\n\n
Aspirin Sensitivity Synd
Pathogenesis is 'Pseudo-allergic reaction'. Accumulation of leukotriens and changed
leukotrien/progtaglandin balance triggers bronchoconstriction, nasal polyps in
suseptible individuals. Tx are Leukotrien receptor inhibitors(DOC), topical steriods
and aspirin desensitization therapy.\n\n
Asthma - 9
before and after administration of a bronchodialator (Beta-2 agonist). Significant
improvement in FEV1 after bronchodialator indicates reversibility of destruction,
which is more consistant with Asthma.\n\n
****DOC
Mast cell stabalizers (Sodium Cromolyn) are doc for pts who have other allergic disorders, so give this to a boy who started to have night time cough and wheeze with hx of allergic rhinitis.\n\n
**** Exercise induces Asthma
(not to be confused with post excercise asthma) presnts
with chest discomfort, wheezing cough, breathlessness, fatigue and abdominal
discomfort. Beta Agonist and Mast cell stabalizers (Sodium Cromolyn) are the best
tx for these pts.\n\n
**** When an asthmatic pt presents with Subcutaneous Emphysema
which is face becomes all swollen and palpation reveals crepitans all over face and neck, then the first thing to do is to do Cxr to rule out Penumothorax. Once that is rules out just observe the pt, it needs no tx. \n\n
****Inhaled corticosteriods are indicartd in
pt with persistant asthma symptoms. The agents are beclomethasone. In adults SE of low-dose drug are limited to are Dysphonia and Thrush. In high-dose systemic toxicity may occur.\n\n
****Its a common illness in childhood
10% of children come ro ED with un-remitting asthma (continues wheezing despite tx with neubelizers and een steriods). This is called Acute Status Asthmaticus.\n\n
Of these pts 10% require
MECHANICAL VENTILATION, however
hospitalization is mandatory. If on auscultation there is no air entry bilateraly, the
child has 'silent chest' or absent air entry and continues to desaturate despite
Prednisone therapy, therefor the best option is mechanical ventilation and
hospitalization.\n\n
*****For pt who have asthma accompanied with other allergic
disorders
mast cell stabilizers like Sodium Cromolyn are the agent of choice. \n\n
***** DOC
1st neubelizers, 2nd IV steroids, 3rd mech ventilax.Normal PCO2 is one of the indicators of a severe attack. During an attack, pt is tachpneac so he hyperventilates
which should cause decrease in PCO2.\n\n
*** So if PCO2 seems to be normal
that means the obstruction is getting worst or respiratory muscel are getting too tired. Other signs of severity are broken speech, diaphoresis, cyanosis, altered sensorium and silent lung . \n\n
*** Inhaled corticosteriods
improve long term quality of life in
Asthmatics. Initial hypertensive therapy for pt with asthma is Hydrochlorothiazide.\n\n
***To differentiate b/w Asthma and COPD (Emphysema)
the best test is a bronchodialator response test. , its conducted by measuring FEV1.\n\n
Astrocytoma
Occurs in Parietal lobe, supratentorial. It's the mc tumor in both infra and supra
tentorial. \n\n
***2 mc tumor
Medulablastomais the 2nd mc tumor in posterior fossa, 90% occur in
vermis. Craniopharyngioma arise in sella torsica, visual field defect, Its
characterized with cystic structure with calcification.\n\n
Asymptomatic actriuria of pregnancy
When everything is normal but a routin clean catch urine culture grows 100000
colonies of E choli. Untreated pt have increased risk for cystitis and acute
pyelonephritis. So they should be treated with 100mg Nitrofurantoin or Ampicillin
for 7-10 days.\n\n
Atelectasis
its common after surgery in smokers. Bronchoscopy needs to be done to remove
mucus Plug.Pt prestns with tachycardia, tachypnea, low grade fever. Once
Bronchopscopy is done, cxr is repeatd and coughing is encouraged.\n\n
AtheroEmbolic Disease
It immitates Gout, but does not say red toe but its Blue toe. DON'T FALL FOR
GOUT TRICK. Pt has cyanosis and circulation problems like pain in calf, pulses are
fine.\n\n
Athlete foot
Pt presents with sever itching, fissure, thickness of the nail in a swimmer. Best tx is
antifungal medicine, Tolnaftate. \n\n
Atpoic Dermatitis:
Edema and erythema of the skin. Skin is Itchy. Tx is Pimecrolimus, like Tacrolimus,
its MOA is through inhibition of T cell activation. \n\n
Atracurium:
Is the neuromuscular blocking agent of choice for pt with renal and hepatic
problems, because its metabolized in plasma.\n\n
Atrial Fibrillation - 4
Control rate and rhythm.\n\n
**** AF along with WPW tx of choice is
Procainamide or
Disopyramide. \n\n
** CI Drugs
that slow AV conduction (Dixogin, Verapamil) are CI in these
pts, they may lead to malignant arrythmais. \n\n
***Lidocaine
might als worsen the situation. Cardioversion is used in pts that are HemoDynamicaly unstable (very rapid vent rates with hypotension).\n\n
*****When AF absent P waves and irregular
heart rate) is asso with HemoDynamic compromise
tx is only Cardioversion. \n\n
***If AF is not asso with hemodynamic compromise
Amiodarone is used. Amiodarone causes hypotension so its CI with HD compromise (hypotention already in pt), but once
cardioversion stabalizes pt then Amiodarone is an excellent choice to maintain the
pt. Calcium channel blockers are also ONLY excellent choices for AF when there is
no HD compromise.\n\n
Atrial Flutter
shows with saw tooth EKG. Unstable AF is best tx with cardioversion. Acute AF
with stable hemodynamics is tx with cardioversion or rate control. Chronic stable
AF is best tx with rate control with Ca Chanel blocker(VerapamiL) or Betablocker. \n\n
Aut Dom Polycystic Kidney Dis
5-7% asso w. Berry aneurysm. Routine screening is not recommended. \n\n
Autism - 3
Mainstay of tx is special education and behavioral modification techiques. *Have
special interests.Usuallt starts before age 3. \n\n
***DDX
Childhood Disintegrative Disorder, is a rare pervasive developmental disorder, mc in males. Chracterized by a period of NORAML development for atleast 2 yrs, followed by a lost of already acquired skills. They have autism symptoms. Prognosis is poor and they are disabled for life.\n\n
****Rett Synd
characterized by an initial period normal development until 6mo, followed by loss of hand coordination and sterotype hand movments. Almost exclusively in Females. \n\n
Autoimmune Hemoytic Anemia
SEE Spherocytosis. \n\n
Avascular Necrosis of femur
The well known causes of non-traumatic avascular (aseptic) necrosis are chronic
corticosteriod therapy, alcoholism. Pt presents with progressive hip pain w/o
restriction of motion and normal Xray. MRI is the gold standard. \n\n
Avoidant personality:
Shyness and feeling of inferiority, and desire to make friends. \n\n
B12 Deficincy, Hem&Onco, 6/2
DDx b/w Anemia and vegeterian diet is the duration. We store 3-4 years of B12 in
the body, so if you're a vegeterian <3 years and you get B12 def, its due to
Pernicious Anemia not vegy diet. If >4 years then we do Abody test for intrinsic
factor.\n\n
****DDX
b/w Folate and B12 is increase in Methylmalonic level. Folate will
cure anemia but neurological problems will progress. \n\n
Bacillary Angiomatosis:
Is caused by Bartonella species, gram negative bacilli. Cutaneous lesions are round
papules or nodules, vascular and asso with fever malaise and headache. It occurs in
HIV pts.\n\n
Bacterial Meningitis
CSF : elevated protein, decreased glucose, and elevated WBC. Plus skin lesions of
Purpura and petechia. \n\n
****Acute Bacterial Meningitis:
the 3 mf causes in community acquired ABM are S. Pneumonia, H. Inf and Meningococcus.\n\n
***Pneumococci have become resistant to penicillin and cephalos, so empirical therapy in adults and children include Vancomycin in addition to Ceftriaxone.\n\n
...
***Listeria Monocytogenes
is a fc in pt older than 55, so we add Ampiccilin for these pts. Other pts at risk for LM are immunocompromised and lymphoma pts. In children >3 yo, LM is a risk so empiric regimen inclused Ampicillin in addition to Cerotaxime.
*** Now S. Aureus and pseudomona
are agents in meningitis in hospitalized pts, so empiric therapy is with Vancomysin (for aureus) and Ceftazidime (pseudomona).\n\n
Bartter Synd - 2
The DDX of normotensive pt with hypokelemia and metabolic alkolosis include: 1-
Diuretic abuse, 2-Surrepticous vomitting, 3-Bartter synd, 4-Gitelman synd. \n\n
*** Classic Barter usualy presnts early in life
as polyuria,polydupsia,growth and mental
retardation. However this can occur later. The underlying pathology is defective sodium and chloride reabsorption. in the ascendign loop, thereby resulting hypovolemia and consequent activation of renin-angiotensinogen aldosteron system.\n\n
**This then causes
increase in K & H ion secretion leading to hypokalemia and
alkolosis. ?
***DDX
Primary hyperaldosteronism and Renin secreting tumors are charcterized by HT, Met Alk and Hypokalemia. Measurment of Plasma renin activity and aldosterone is used for DDX b/w the two. in Primary hyper Aldosteronism, PRA is suppresed and aldosteron is elevated, but in renin tumors, both PRA and Aldosterone are elevated. \n\n
***Now remember the mcc of Hypokalemia
in clinical practice is Diuretics, which is hard to ddx with Barter.\n\n
Basal Cell Carcinoma - 2
Is the mc malignant tumor of the eyelid. Lesions are slow growing, pearly and
indurated. \n\n
*** histology
Invasive clusters of spindle cells surrounded by palisaded basal cells.\n\n
*** location
It rarely might appear on upper lip but NEVER on the lower lip. The mc location is the lower eyelid. They rarely metastasize.\n\n
** Squamous CC
is much less commn and faster growing, It presents as plaque nodule or inverted wart, its ddx is Actinic Keratosis.\n\n
****sun
is Bad for Basal cell carcinoma. proper clothing coverage is best protection over UV SPF.\n\n
*** Five warning signs
are 1-Open sore tht bleeds, oozes and remain open for >3weeks. 2-Redish patch,3-Shiny bump, scar like area, 5-Pink growth with rolled border. BCC is the mcc of skin in US. \n\n
***Never metastasis
Its removed using by 1-Cauterization(burning), 2-Surgical
(excision with 1-2mm margin). 3-Cryosurgery(freez) and 5-radiation.\n\n
Basilar skull fracture
Signs are rhinorrhea, raccoon eyes (black eye), ecchymosis behined the ear. A way
to see if hay CSF mixed w blood is to drop a drop on a cleansing tissue, if hay csf
there would be a yellowish spreading on the paper.\n\n
*** In this pt head fracture
has to be ruled out w CT of head and spine. Expectant therapy for all uncomplicated cases. Anterior packing is not necessary to control CFS loss. If CSF leak continues for >4 days, spinal drainage and acetazolamide is used to reduce CSF production and reduce ICP.\n\n
Bechet - 2
rare multisystem disorder that affects males <20y, in mediteranean area and
east asia. An AUTOIMMUNE mechanism is suspected. It manifest with Ulcers in
mouth and genital area and asso with Uveitis. Oral lesions are Aphthous like but
genital lesions are more destructive leading to fenesterated vulva. No specific tx yet.\n\n
*** DEF
Multisystemic Inflammatory condition with recurrent oral and genital
ulcers, skin lesions, mc in Turkey, Asian and middle east.Corticosteriods offer releif
but dont prevent progression to Dementia and Blindness.\n\n
Beckwith-Wiedemann synd
Infant with macrosomia, macroglossia, visceromegally, omphalocele, hypoglycemia
& hyperinsulinemia. iT might be asso with duplication of CH 11p, this region has
the gene for IGF-2, which may explain macrosomia. \n\n
***DDX1
congenital hypothyroidism has umbilical hernia instead of omphalocele, and there is no hypoglycemia and hyperinsulinemia. \n\n
***DDX2:
Macrosommia due to maternal diabetes, however these infants dont have the dysmorphic features of omphalocele, prominant occiput and macroglossia. \n\n
*** common congenital problems in these infants are
Caudal progression synd, Transposition of great vessles, Duodenal, atresia and small left colon, Anencephay and neural tube defects. \n\n
***DDX3:WAGR synd, Wilms tumor, Aniridia, Genitourinary anomaly, and mental Retardation. Its related to deletion of CH11 involving the gene WT1.\n\n
...
Bells palsy
PERIPHERAL seventh nerve palsy, Its dx with absence of forehead furrows; however Pts with Central lesion still have
furrows because contralateral motor inervation of forehead rremians intact.\n\n
Benign Intrahepatic Cholestasis
It can develop after a major surgery in which hypotension, extensive blood loss in tissues, and massive blood replacement are noted.
Jaundice develop due to pigment load from transfusion.
*** post op Jaundice
becomes evident 2nd day post operative. Alkaline
phosphatase is markedly elevated but ALT & AST are only mildly elevated.\n\n
**DDX1
Acute hepatic failure, has increased PT, low albumin and neurologic signs
due to hepatoencephalopathy. \n\n
**DDX2
Hepatitis, presents with marked elevation of ALT & AST. \n\n
**DDX3
Halothane Hepatotoxicity, type-1 has mild elevation of liver enzymes and NO jaundice, type-2 is characterized by Acute Liver failure.\n\n
Bernard_SoulierSynd
The hallmark is GIANT platelets.Its auto recessive. There is mild thrombocytopenia
but the major defect is of membrane glycoprotein 1b. \n\n
**This defective membrane \n\n
lacks the receptor for VW atachment so platelet cant adhear to endohtelium. Plateles don't aggregate in presence of normal VWF and Ristocetin.
**8 Vignette presents
a 16 yo girl who's periods last 6-10 days and her brother also had bleeding problems.\n\n
Beta blocker Toxicity
Overdose causes hypotension and bradycardia. Sever overdose may result in
cardiogenic shock.\n\n
*** If bradycardia or AV abnormallity is found
Atropine is indicated
to oppose unopposed vagal tone. \n\n
****If atropine fails
Isoproterenol is given if Atropine fails and if both
of them fails then Glucagon is the DOC. If medication fails then a temp pacemaker
is indicated.\n\n
BIASES: SEE STEP UP book
1-Selection: loss of people to follow up in prospective studies.
2-Observers and Ascertainment: result in misclassification of the outcome due to
flaw of the design of the study.\n\n
*** next
3-Recall: Misclassification of the exposure status, its potential problem for casecontrol.
4-Confounding:
5-Generalizability: when th epopulation you study does not include all the
population where the topic of the research is covering. Like studying just men when
ALL people are targeted.\n\n
***Next
6-Reliability:
7-Validity.
8-Leadtime: Its prolongation of apparent survival in pts whom this test was applied,
w/o changing the prognosis.\n\n
Bicuspid Aortic Valve
Is the mcc of aortic stenosis in middle age adult. Both AS and HCM produce a
midsystolic (Ejection systolic murmur) murmur, however murmur of HCM is best
heard at left lower sternal border and it doesn't radiate to carotids. \n\n
***Valsalva
Attenuates AS murmur but Accenuates HCM murmur. Murmur of AS is best heard right second intercostal space and radiates to the carotids. Slow rising pulse is seen in HCM.\n\n
Billiay Cholic:
Is symptomatic for CheledoCholelithiasis. If there are no signs of acute cholecystitis
(Murphy sing, elevated WBC and fever) then there is no need for hydration,
antibiotics or emergent chlecystectomy.\n\n
** There could be
Emphesematous cholecystitis that presents with gas in gall bladder. DM pts are at increased risk. For an uncomplicated billiary cholic just do spasmolytic and analgesic therapy and elective surgery is done at a later time.\n\n
BioPhysical Profile
BPPis a scoring system to evaluate baby's well being. Its indicated when there is
Decreased movement or a non-reactive NST. It includes NST in addition to 4 things,
1-Fetal tone, 2-Movment, 3-Breathing(30/10min), 4-Amniotic fluid index(5-20).\n\n
*** Each has a score of 2
when present and 0 when absent. 8-10 is normal, and should be repeated once or twice weekly, until term.In presence of OlygoHydramnions
(AFI<5) delivery is considerd. \n\n
****If score is 6 w/o OH
Contraction stress test is ordered. If it gives non-reassuring results then Deliver, if it gives suspicious results then repeat the next day. \n\n
****If its 4 w/o OH
and fetal lung are mature, Delivery is considered. If lungs are not mature, steriods is gven and BPP accessed w/i 24 hrs.
**** If score is <4
deliver now.\n\n
Black widow spider:
Presents with Acute abdomen and best treated with calcium Gluconate and muscle
relaxant. Brown Recluse spider causes skin necrosis localized, resembles pyoderma
gangreosum. Deep skin ulcer develops. \n\n
***TX of choice
Local excision is tx of choice for the ulcer. Dapsone is used for pts with G6PD def.\n\n
Bladder cancer - 2
Up to 80% of pts who go through a urinary diversion procedure, specially an ileal conduit,
can develop hyperchloremic metabolic acidosis due to exchange of Cl for
HCO3 in the intestinal mucosa, leading to loss of HCO3 and increase Chloride.\n\n
Bladder Rupture - 2
Hematuria, suprapubic tenderness, non palbable bladder and lower abdominal and
perineal edema.\n\n
*** The best Dx method
is retrograde cystogram with voiding films.
Remember for Urethral injury we do Retrograde urethrogram. \n\n
****trauma
Intraperitoneal rupture is more common in pts in trauma accidents.\n\n
Blastomycosis - 2
Anyone in Wisconsin, Ohio, Mississippi with chronic respiratory problem is
suspected. Another dx triad is Skin,Lung Cavity and Bone Lytic lesions.\n\n
Blood Transfussion
Femur fracture can acct for 1L blood loss, if Pelvic is also fractured the blood loss
could be several liters. General guidelines are start iv crystalloids initially, 2L in 10
min,\n\n
*** if pt continues sign of hypovolumia
then Blood transfusion is started. So the
best indicator for transfussion is blood loss of >1500ml.\n\n
****Washing of RBC
washes off antigens asso with transfusion. Its used for IgA def pts. Leukoreduced RBC reduces the risk of allosensitization responsible for hyperthermia .\n\n
Blunt Chest Trauma:
When it happens with wide mediastinumon CXR, aortic injury must be suspected.
Either a CT scan or Echo is Dx.\n\n
Body Dysmorphic Disorder
Woman thinks her nose is 'enormous'.\n\n
Boerhaave's Syndrome
Complete tear of distal esophagus that leads to pneumomediastinum, vs incomplete
tear in Malory Weiss and no Pneumomediastinum. \n\n
**** DX
Xray shows subcutaneous emphysema. Dx w barium swallow. Tx give antibiotics and thoracotomy and repair of esophagus immediately.\n\n
Borderline Personality
Spliting characteristic. You are the best and the other doctor was terrible.\n\n
Bordetella Pertusis:
For preventin, all close contacts (houshold and daycare) get 14 day Erythromycin,
regardless of age, immunization or symptoms.\n\n
Botulism - 2
we have two types: 1-Infantile type, organism gains entry through the food and
prduces toxin in the intestinal tract. It's a protease that blocks Ach release. 2-Adult
type the toxin is ingested pesay, produces the effect.\n\n
**** TX of Infntile botulism
tx is supportive only. BUT if Children get it then administer equine derived botulism anti toxin right away.\n\n
Bowel Ischemia
Always consider it as an early complication of operation on the abdominal aorta . Pt
presents with bloody diarrhea and abdominal pain. Its due to infarction of Inferior
Mesenteric artery, 1-2 daya post surgery. \n\n
***DDX
Pseudomembraneous colitis, takes 2-3 weeks after drug therapy. \n\n
****** Unrecognized bowel ischemia
is one of the mc causes of lactic acidosis with severe atherosclerotic disease. Pt complains of abdominal pain after meals.\n\n
Bowel Obstruction
If a pt comes with constipation and no flatulus, even then, unless strangulation or
perforation is suspected, bowel obstruction is treated conservatively. So dont do
surgery first. 1st thing to do afyer IV is nasogastric suction and barium enema.\n\n
Bowel resection:
In pt who goes under bowel resection the mc type of kidney stone is Oxalatedue to
excessive absorption of Oxalate from GI tract. Increased intestinal fat binds calcium
which is then unavailable bind oxalate. Therefore increased absorption of oxalate
occurs in GI and precipitates in kidney.\n\n
BP criteria
BP should be kept below 140/90. But BP in DM and chronic renal pts should be kept
under 130/80 to prevent end-organ damage.\n\n
BPH - 7
Starts in the center of the prostate. Cancer starts in periphery. The mcc of overflow
incontinence in elderly male. Finasteride acts on epihtelium and alpha-1blocker acts
on smooth muscles of prostate.\n\n
**** Alpha blockers (Doxazocin) are prefered in pt with
BPH and dyslipidemia and glucose-intolerance. If Creatinine is elevated do US of kidney, bladder and ureter to check for damages. \n\n
***** Tamsulosin
an Alpha-1 receptor blocker has the least SE of all alpha one blockers used for Tx of BPH.\n\n
****The two initial tests that are recommended
in ALL possible bph pts are
serum creatinin and urine analysis. Urine analysis rules out infection and creatinin
rules out kidney problems.
*****US of the kidney
ureter and bladder should be done in pts whose creatinin level is elevated.\n\n
Brain Abscess
A pt with acute onset of HA and focal neurological symptoms (cant walk right) after
an episode of acute otitis media or sinusitis most likely has brain abscess even if not feverish.\n\n
*** Dx
CT and MRI show ring enhaning lesion. Fever pesents with only 50% of cases so its not a reliable sign.\n\n
Brain death
is defined as irreversible cessation of brain activities. It's a clinical dx. The
characteristic findings are absent cortical and brain stem functions. The spinal cord
may still be functioning, therefore DEEP TENDON REFLEX are intact. \n\n
***EEG
can confirm but is not necessary. In brain dead people, pupilary reaction &
oculovestibular reaction are absent, Atrpine doesnt accelerate heart since vagal is
gone, and there is no spontaneous respiration.\n\n
Brainstem Infarction
1-Medial Medulary Syndrome
Occlusion of vertebral A. Contralateral paralysis of
limbs, contralateral loss of tactile, vabratory and position. Tongue deviated to
affected side. \n\n
***2-Lateral mid-pontine synd
A lesion in Lateral Pons. Impaired
sensory and motor function of CN V trigeminal and limb ataxia.\n\n
**** 3-Medial midpontine Synd
A lesion in Medial Pons. ipsilateral limb ataxia, and contralateral eye deviation and paralysis of the face,arm and leg. \n\n
*** 4-Wallenberg syn
A lesion of laterla Medula. ipsilateral horner synd, loss of pain and temperature of the face, weakness of the palate, pharynx and vocal cords, and cerebellar ataxia. Also loss of pain and temperaturein cotralateral side of the body.\n\n
Breaking Bad News Protocol
1-Comfortable environment
2-Ask pt how much he knows about his symptoms
3-Ask pt how much he wants to know
4- Give him a warning shot ( ie its worst that we thought, do you want someone with you. \n\n
*** Next
5-Break the news if he wants that
6- Tell him of prognosis &the option to make his life comfy
7-Try to explain everything clearly and simple as possible.\n\n
Breast Carcinoma - 4
Inflamatory beast cancer: Erythema and edema of non lactating breast could be due
to locally advanced cancer, biopsy should be done first to rule out that dx. \n\n
*** Tx
is 2-3 weeks of combination chemotherapy to shrink the tumor allowing sybsequent extended resection. \n\n
****Prognosis
Metastatic Breast Cancer has a poor prognosis. with little
chance of cure. Its importnat to choose Local (Surgery) vs Systemic (Systemic
Chemotherapy) tx in pt with metastatic breast cancer. \n\n
****Tumor burden, based on TNM staging
1. single most important prognostic consideration in treating pts with breast cancer.
2. ER+ and PR+ are good prognostic factors.
3. Over expression of Her2/Neu oncogene is worst progosis.\n\n
****Breast cancer is
the leading cause of metastatic skin disease in women. These lesions are erythematous that present as erosions covered by necrotic skin. \n\n
****Tx
is palliative radiation therapy with aggressive wound care. \n\n
*****Two proibitions
when hay breast cancer in pregos: No
chemo in 1st trimester, and no Radiotherapy anytime in pregnancy. Also
Lumpectomy is not a good choice for 1st trimester cuase it needs Radiation
afterwards. So the only Tx for 1st trimester is Modified Radical Mastectomy.\n\n
Breech presentation
If prior to 37 must be left alone. After that External cephalic version may be
attempted PRIOR TO onset of labor, given no CI (Hypertension).\n\n
Bronchiectasis - 2
An irrevesible widening of medium size airways in the lung. Characterized by
destruction of bronchial walls and chronic bacterial infection. They might have life
threating Hemoptysis. Bronchiectasis is due to formation of large collateral vessels,
which have a very fragile wall. Hemoptysis could be very extensive and ALL pt
should be admited. \n\n
****Any pt with fever, night weats, copious foul smelling
sputum
1-Bronchiectasis
2-Lung Abscess
3-Anerobic Pneumonia. "Copious foul smelling" sputum is the KEY word. \n\n
**Cxr shows
characteristic "Tram Track Appearance" (increased vascular markings) ring shadows, peribeonchial thickening. CT is the confirmatory investigation, it has
REPLACED Bronchography. After that Sputum for AFB is done.\n\n
Bronchiolitis:
Is defined as the first episode of wheezing asso with an URT infection. The infection
is usually caused by CMV and is common in winter. In affects 50% of children in
the first two years of life especially those prone to airway reactivity, and there is an
increased inidence for Asthma later in life. \n\n
*** Dx
WBC in nl and Cxr shows air trapping
or atelectais. Tx is supportive care and humidified oxygen and bronchodilators.\n\n
Bronchogenic Carcinoma. Pulm. 6/3
BGC is the mc lung cancer asso with asbestos exposure, while Malignant
Mesothelioma is almost exclusively asso with asbestos exposure but its not the mc
malignancy after asbestos exposure.\n\n
*** hallmark
Pleural involvment is HALLMARK of asbestos exposure. Cigarete smoking acts synergicaly with asbestos exposure in increasing risk factor for BGC.\n\n
Brown Sequard synd
Asso with damage to lateral spinohtalamic tract, causing contralateral loss of pain
and temperature beginning TWO LEVELS BELOW the lesion. Therefore, a lesion
of right sided Laterla SPT at T10 will result in left sided loss of pain and
temperature at beginng at T12.\n\n
Bruton's Agamaglubinemia
X-linked. MERCK: Panhypogammaglobulinemia of male infants
characterized by levels of IgG < 100 mg/dL and other Ig levels low or absent, low or
absent B cells. onset of infections sometime after age 6 mo. \n\n
*** H/P
These infants have recurrent pyogenic infections of the lungs, sinuses, and bones with such organisms as pneumococcus, haemophilus, and streptococcus. \n\n
*** defect
A defect of the Btk (Bruton's tyrosine kinase) gene at Xq22 prevents differentiation of pre-B cells to B cells. Lifelong IG given IM or IV in the lowest dose that prevents recurrent infection is essential.\n\n
Bud Chiari Syndrome
WAT \n\n
Buergers disease
Triad of occlusive dis of arteries, migratory superficial
thrombophlebitis[Thrombi+Phlebe(vein)+Itis(inflamation)], and Reynaud
phenomenon in a smoke male.
*** DDX
w atherosclerotic disease is that in those Pulses are normal.\n\n
Bulimia Nervosa - 2
Outpatient tx include: SSRI antidepressant, cognitive therapy, interpersonal
pshychotherapy, family and group therapy. If pt failed this and/or has metabolic
problems or is suicidal then Hospitalize. \n\n
** H/P
Pt bing eat and then feel guilty. They might even feel sad about their situation. But they maintian their BMI and are NOT Amenorrheic. They bing eat at least TWICE per WEEK. If they dont do that, they are dx as "Eating disorder, not otherwise specified".\n\n
Bullous Pemphigoid- Dermo, 6/3
Is characterized by tense blisters in the flexural areas. Commonly in elderly (>60).
The precipitating factors are ultra violet rays, NSAIDS, antibiotics. Autoantibodies
are formed against basement membrane.\n\n
*** DX
Immunofloresence microscopy reveals diagnostic findings of IgG & C3 at the epidermal-dermal junction and Prednisones are tx of choice. In Pemphigus vulgaris IgG deposits are intercellulary in the dermis.\n\n
***In Herpes there is C3 at
the basement membrane zone.\n\n
Bupropion - 2
Its used for Major depression, ADHD, cigaret craving. It ma be used in conjunction
with Nicotin patches, but such combination requires frequent BP monitering. It
reduces weigh gain that comes with cigarett smoking. Although it might cause
seizure, you dont stop the drug due to this rare SE, unless pt has a Hx of seizures.\n\n
***Pt has hx of epilespy
and wants Bupropion, Dont give him Bupropion its CI for
his Hx of epilepsy, give SSRI \n\n
Burns
Tx of superficial and deep burns. * For inhalation injury which may take a few days
to manifest, Dx is best done with bronchoscopy. \n\n
*****For calculations only consider
2nd and 3rd degree burns. Kids: head=18, lower ext 27. *****when circumferencial
full thickness burns involving extremities or chest is present, Escharectomy maybe
the best option.\n\n
*****Parkland formula
for ressecitation is 4ml/kg/ % of body
burned, half in 8hrs and rest in 16hrs.\n\n
****Early excision therapy is indicated for
extensive partial thickness and full thickness burns.\n\n
*****mcc of death in burn pts in
hospital
is infection.\n\n
*****Inhalation injury
is commonin burn pts and may take
several days to manifest. \n\n
*** Dx
is best done with a bronchoscopy. Beta agonists along
with steroids, endotrachial intubation and antibiotics have all been used in pt with
inhalation injury.\n\n
*****1st degree
confined to epidermis, erythomatous skin. Heals
w/o scarring. Example is sun burn. \n\n
***2nd degree
Involves entire epidermis, red and blisters. Its partial thickness burn. \n\n
***3rd degree
is full thick ness burn, epidermis and dermis completey destroyed. Not painful. Debridment and grafting is required.\n\n
Calcanium Fracture: Surgery 6/2
If due to fall, evaluate for other injury, plain film of head, neck, abdominal, lumbar
& pelvic. Its asso with compression fracture of thoracic spine.\n\n
Cancer Drugs
1-Anorexia: doc for anorexia asso w cancer is Megesterol Acetate. 2-
Nausea&Vomit: Metoclopropamide and ondansentron\n\n
Carcinoid syndrome
Triad of flushing, diarrhea and valvular heart disease. Its asso with carcinoid
tumors and hepatic metastasis. Isolated tumors w/o metastasis do not produce
carcinoid syndrome. \n\n
*** These tumors produce
serotonin. Elevated serotonin and its
metabolite (5HIAA) are in plasma and urine. Tryptophan is the precursor of
Serotonin . Tryptophan is the aa used in synthesis of Niacin. \n\n
***Pts of Carcinoid synd
are at risk of Niacin deficiency due to increased formation of serotonin from tryptophan. As a result supply of tryptophan is decreased and 3 Ds of Niacin def (Diarhhea, dementia, dermatitis) of Pellagra develops. \n\n
****Carcinoid tumor
when symptomatic is in Small bowel, when asymptomatic its in Appendice.\n\n
***Triad of
flushing,diarrhea and wheezing.\n\n
Cardiac Contusion
Is asso with arrythmias, so the first thing to do if you suspect it, is Continues ECG
NOT Echo.\n\n
Cardiac Temponade - 2
Characterized by 1-hypotension, 2-Sinus tachycardia. 3-Pulsus paradoxus. 4-
Prominent JVD with 'Y' descent. US shows blood in pericardial sac. \n\n
***DDX
is Medicastinal hemorrhage, which is the same as CT except that US shows no blood in pericardium and the blood is in mediastinum. It could happen in pts who are
taking warfarin and cause coagulation abnormality.\n\n
Cardiomyopathy, Dialated - 3
Characterized by 1-Impaired systolic function of left and right ventricle leading to
progressive cardiac enlargement. 2-Cxr shows marked or moderate enlagemnt of
cardiac silouette. 3-Echo shows systolic dysfunction and left ventricle dilatation with
Normal wall thickness. \n\n
***Pt should
refrain from drinking alcohol. Viral infection is
the mcc of myocarditis that results in DCM, and the mc virus is Coxsackie virus.\n\n
****DCM
is the end result of myocardial damage produced by toxic, infectious, or
metabolic agents. Viral or idiopathic cause is mc by Coxsackie virus. \n\n
***The dx
is by Echo, shows dilated ventrilces with diffuse hypokinesia resulting in low EF (systolic dysfunction and CHF). Concentric Hypertrophy is seen in Aortic stenosis. Eccentric in Valvular regurgitation. \n\n
*** Hypokinesia
is due to MI inferior wall. MS has Left atrial hypertrophy. HCM shows Asymetric vent septum hypertrophy.\n\n
Cardiomyopathy, Hyper - 5
Characterized by 1-Asymetric left ventricular hypertrophy. 2-Harsh systolic
Diamond shape murmur best heard at the left sternal border. 3-Cxr shows mild
enlargement of cardiac silouette. 4-Echo shows vigorous systolic function Asymetric
septal hypertrophy and Systlic anterior motion of the mitral valve. 5-Due to
hypertrophy of left ventricul there is Diastolic dysfunction.\n\n
*** DOC
Beta blockers are the tx of choice for isolated ventricular diastolic dysfunction. \n\n
*** MERCK:
Systolic murmurs are usually present, but patients with apical and symmetric hypertrophic cardiomyopathy may have no murmur. Most common is a crescendo-diminuendo ejection-type murmur that does not radiate to the neck; it is best heard at the left sternal edge in the 3rd or 4th intercostal space. \n\n
***This murmur is caused by
obstruction of left ventricular ejection (produced in systole when the hypertrophied interventricular septum and the anterior leaflet of the mitral valve approach each other). \n\n
*** 2/2
mitral regurgitation murmur due to distortion of the mitral apparatus is
heard in some patients. It has a characteristic blowing quality and is best heard at
the apex, radiating toward the left axilla. \n\n
***Rarely
early or midsystolic clicks are heard. In some patients with right ventricular outflow tract narrowing, a systolic ejection murmur is heard in the second interspace at the left sternal border. \n\n
*** extra sound
An S4, almost always present, indicates a forceful atrial contraction against a poorly compliant left ventricle in late diastole. Mitral regurgitation is as a result of anteriormotion of the mitral valve leaflet. \n\n
*** Mitral regurgitation in "Infective endocarditis" or
"trauma" is caused
by rupture of chordae tendinae. \n\n
****Mitral degeneration in "elderly women" can be caused
by mitral annulus calcification.\n\n
**** Mitral valve prolapse is the mcc
for "isolated mitral trgurgitaion" in north america. \n\n
*** Dx of choice
Echo is dx of choice, shows asymetrical ventricle septal hypertrophy. \n\n
**** in 25% of HCM pt
there is obstruction of LV ourflow tract (echo shows anterior motion of mitral valve) , because of this filling preffure is furthur elevated and out is compromised. \n\n
*** This outflow gradient is incresed
by manuvers that reduce cavity size of left ventricle. Valsava and standing after squatting, decrease LV Vol thus increasing the gradient and intensify the murmur. ??
*** Handgrip
increases systemic arterial resistence and so decreases gradient and the murmur. Leg elevation also decreases the murmur.because it increases LV vol. \n\n
*****To screen young athlets
for HCM Echo is non sensitive. Do detailed personal,family Hx and PE. \n\n
****Tx
for HCM is Beta blockers. \n\n
***HCM
is Auto DOMINANT. Pt is young, dyspnea on exertion, harsh
diamond shape systolic murmur at the left lower sternal border.Echo shows
Asymetrical septal hypertrophy.\n\n
Cardiomyopathy, Restrictive - 4
Characterized by 1-Severe Diastolic dysfunction due to a stiff ventricular wall. 2-
Echo shows symetrical thickening of the ventricular wall. 3-Kussmal sign. 4-Apical
impluse palpable. \n\n
*** DDX
: Constrictive pericarditis no no 4, cxr shows calcification,
and normal thickness of ventricular wall. \n\n
****Tx of most causes
of RCM is useless except Hemochromatosis, Phlebotomy and Iron chelation with subcunatous defroxamine may result in substantial improvement. \n\n
*****Since heart cant relax
filling is compromised so both Liver and Lung are congested.****Xray shows mild
cardiac slouette. Echo shows symetricly thickened vent wall and near normal
systolic function. "Speckled Pattern" is specific for Amyliodosis .\n\n
Caroli Syndrome
Is a rare congetnital disorder characterized by intrahepatic dialatation of billiary
tree, asso wi APKD.\n\n
Carotid Artery Stenosis & Endarterectomy
Asymp pt with 66-99% are considered for surgery, 100% is CI for surgery.\n\n
Carpal tunnel syndrome - 2
most likely location of pathologic process is the wrist. Pt presents with pain and
burning sensation of the first three fingres and atrophy of thenar eminence, poor 2-
point discrimination over the thumb, and they keep dropping things. \n\n
****Its seen in asso
with RA, Myxedema, Sarcoidosis, amyloidosis and Leukemia. Most specific test is Nerve conduction study. \n\n
*****Tinel test
(tapping on Median nerve) Phalen test (90 degree flextion of both wrist and pushing them together dorsally), \n\n
*** Carpel compression test
(applying pressure over carpal tunnel) are not specific.\n\n
Cat Bite - 2
Should be tx prophylacticaly with Amoxicillin/Calvulanate for 5 days, due to fear
from Pasturela Multicoida. \n\n
****organism
1-Pasturella Multicoida, occurs after cat or dog bite,
and there is an intense inflamatory reaction w/I 24 hrs of the bite. Pain, swelling,
purulent discharge are features. \n\n
****OR
2-Bartonella Hensalae, occurs after cat scratch or
bites. Clinical features occur after 3-10 DAYS. . They include papular or vesicular
lesion, at the site of injury and proximal Lymphadenpathy.\n\n
Cat Scratch Disease
By Bartenella Hensalea. It most commonly presents with localized cutanous and
lymph node disorder near the site of inioculation. A local skin lesion evolves through
vesicular erythematous and papular phases, but can be postular or papular. \n\n
*** Dx
is by clinically and antibody to B. Hensale or a positive Warthin-Stary stain on the tissue specimen.Most people resolve gradualy w/o therapy. However, tender
lymphadenopathy and systemic symptoms require five days of Azithromycin.\n\n
Cataract congenital
Its due to progresively thickening of the lens. In "Congenital cataract" the retina
CAN'T be visulized properly, exam reveals bilateral white reflex, the mcc of white
reflex in the pediatric population is Congenital Cataract. Tx is extraction of the lens.\n\n
Caustic Poisoing - 2
Upper GI Endoscopy is the dx study of choice when a person comes in with
ingestion of Alkali (oven cleaner) in the first 24 hr to assess the damage.\n\n
Cavernous sinus thrombosis.
Presents with severe headache, followed by fever and periorbital edema. Also CN
involvements in the form of opthalmoplegia, lateral gaze palsy, ptosis and dilated
pupils. \n\n
*** labs
Nasal discharge and blood should be cultured. CT scans of the cavernous
and air sinuses, orbit, and brain should be performed. \n\n
*** Treatment
with high-dose IV antibiotics, nafcillin or cefuroxime should be started, pending culture results. \n\n
**Surgical drainage if
of the infected air sinus may be indicated, especially if there is no response to the antibiotics in 24 h. \n\n
***The prognosis
is grave; the mortality rate
remains about 30%, despite antibiotic therapy. \n\n
*** DDX
Orbital Cellulitis:Its unilateral, and more common in children. Presents w abrupt onset of fever, proptosis, restriction of extraocular movements and swollen red eyelids. there is NO CN dysfunction or visual disturbances in the early stages unless it spreads to cavernous sinus. \n\n
***Treatment
with antibiotics, cephalexin should be started, pending culture results. Incision and drainage are indicated if suppuration is suspected or if the infection does not respond to antibiotics.\n\n
Celiac dis - 2 .
Pt present swith malabsorption, loss of muscle or subcutanous fat, pallor due to iron
def anemia, bone pain due to osteomalasia, easy bruising due to vitK def and
Hyperkeratosis due to VitA def. Hay fatigue and weight loss. \n\n
** Dx
is with ELISA for IgA antibodies to gliadin and immunoflorescence for IgA antibodies to endosomysium. ALso antibodies against rtansglutaminase. But CONFIRMATION is small intestine biopsy. \n\n
****H/P
A 15mo old girl with dermatitis herpitiformis (erythematous vesicles symetrically distributed over the extensor surfaces of elbows and knees.) and chronic non-bloddy diarrhea with malabsorption (foul smelling stool) and distended stomach, is suggestive of CD.\n\n
Cellulitis - 2.
Is an inflamation of skin that could extend into deeper tissues. In majority of pt is
caused by Strep hemolytic or Staph aureus. \n\n
***Clinical symptoms
can be Systemic as well as Local. Local findings are swelling, erythema, warm and tender and less well demarcated than Erysipela. The systemic signs are high grade fever chills and rigors, malise and confusion. When systemic signs are present IV Nafcilin or Cefazolin is preffered. \n\n
**** History
The senario is usually a lady with painful leg \n\n
*** DDX
1-Cellulitis, high fever and chills. 2-DVT, cellulitis of calf is the one when there
is high fever and no risk of DVT. 3-Necrotizing facitis is a deep seated cellulitis,
suspect it in pt with bulla or crepitus. 4-Erysipelas, is a superficial cellulitis, it
usually attacks cheeks, area is erythematous, painful and raised, with vesicles or
bullae. No lymphangitis. 5-Erysipeloid is an edematous, purplish plaque with
central clearing. Its caused by Erysipelothrix incidiosa. Usually at hands of
fishermen and meat heandlers, its not as painful as cellulitis and there is no fever.\n\n
Central Cord Syndrome:
Characterized by burning pain and paralysis in the upper extremities with relative
sparing of lower extremities. It is commonly seen in elderly 2ndary to forced
hyperextension of the neck.\n\n
Central line complication:
Include pneumothorax, sesis and temponade occurs in 1-5% of pts. Cxy confirms
that the tip is proximal to cardiac silhouette. \n\n
Central retinal Artery occulsion
Sudden painless loss of vision in one eye, however opthalmoscopy reveals pallor of
the optic disk, cherry red fovea, cotton woolspots, retinal hemorrhages.\n\n
Central retinal Vein occulsion 2.
Sudden painless loss of vision in one eye, however opthalmoscopy reveals disk
swelling venous dilation, tortuosity, retinal hemorrhage and cotton wool spots.\n\n
Cephalohematoma
Is a benign bleeding of newborn's scalp. It's a sub-periosteal hemorrhage. It shows
like a swelling. No tx is necessary. DDX:Caput succedaneum is a diffuse and
ecchymotic swelling of the scalp. It may extend across the midline.\n\n
Cerebral Hemorrhage
If its due to excess warfarin (PT is icreased) then FFP reverses the effect.Pt on
anticoagulants should be on INR measure check. So if 1-INR <5, no significant
bleeding DO omit next warfarin dose. 2-INR is 5-9 and no significant bleeding DO
stop warfarin temporarily. 3-INR >9 DO stop warfarin and give oral VitK. Pts with
serious intracranial bleeding cant wait for VitK, give them FFP right away to bring
INR<1.5. Now to reverse Heparin give Protamine sulfate.\n\n
Cerebral infarction
Hypodense on CT- white area over the cerebral surface.\n\n
Cervical cancer
Risk factors: Young age at first coitus (<20). Young age at marriage and first
pregnany. High parity, multiple sex partners, smoking, and low socioeconomic
status. \n\n
****If pap is dysplasia
perform colposcopy. If it shows inflamatory Atypia
then repeat after 4-6 weeks. \n\n
****If pt comes in with spotting
and you see the cervix
having a gross lesion that bleeds by touching, dont even bother for PAP, go straight
to Punch biopsy to rule out cancer. \n\n
**** Once pt had the cancer check
for cytology every year not every 2 year for normal people.\n\n
Cervical Spondylosis
It affects 10% of people >50. Hx of neck pain is typical. Osteophytes are the mc
findings in cervical radiography in pt with CS. Bony spurs are the mc findings.\n\n
CGD
A defect of phagocytic cells Due to NADPH oxidase def. Leading to recurrent
infection with catalase positive organism, Aureus, seratia, Klebsiela, Aspergillosis.
Not suseptible to catalase neg (strep, influenza, Pyogenes). \n\n
**The MC clinical findings
are lymphadenopathy, hypergamaglobolenemia, hepato and splenomegaly, anemia of chronic causse, short, gingavitis and dermatitis. NitroBlueTetrazolin is dx. \n\n
**Tx
is prevention with trimeta-sulfa and Gamma interferone 3 times a week. BMT is
curative. \n\n
**DDX1
:Wiskot aldrich:Eczema,thrombocytopenia,recurent infection with
encapsulted organism. Manifest at birth, petechia, bruises, circumcision bleeding,
bloody stools. \n\n
DDX2:
Chediak Higashi, decreased granulation,chemotaxis and
granulopoesis.Finding of neutropenia, ginat Lysosome in neutrophil will confirm
Dx. tx includes prevention with Trimeta-Slfa and daily ascorbic acid. \n\n
DDX3:
Jobs syn (Hyper IgE), chronic pruritic dermatitis, recurent staph infection, marked elevated IgE, eosinophilia and coarse facial features.\n\n
Chaga's dis
Caused by insect borne Trypanosoma Cruzi which is a common form of carditis in
Centerl and South America. Pt presetns with Cardiomegally, conduction anomalies.
Almost all pts have a hx of Megacolon or Megaesophagus.\n\n
Chalazion
a small swelling NODULE of the eyelid. It results from obstruction of the glands in
the eyelid. First try to cure it by putting hot compress on it if it comes back again
and again then do histopathology. It often requires surgery. \n\n
** Recurrent chalazion
requires histopathologic exam because there is a risk of underlying Squamous cell
carcinoma. DDX Hordeulom(Stye). Occurs at the edge of the eyelid(pretty red) \n\n
CHD risk factors:
Age (men>45, Women>55. Family Hx of premature CAD (<55 in first degree male
parent, <65 in females relatives). Hypertension up to or equal to 140/90 even
controlled w medication. Cigarret smoking. DM. HDL <35. HDL up to or equal to
60 negates one risk factor.\n\n
Risk factor LDL goal LSM Meds
CHD or Equiv <100 >=100 >=130
> or =2 <130 >=130 >=160
0 or 1 <160 >=160 >=190\n\n
Chediack Higashi:
Is a storage granulocyte abnormality resulting in hepatosplenomegaly,
lymphadenopathy, anemia, thrombocytopenia, and susceptibility to infection in
childood.\n\n
CHF - 6
CHF is a common cause of Pleural Effusion. Pleural analysis is consistant with
transudate effusion. The effusion caused as a result of systemic factors (CHF) is
Transudate. The effusions caused as a result of local factors is Exudate effusion. \n\n
Diff exudate
Existence of at least one of the following indicates exudate, if non exist its a
transudate. 1-Pleural/Serum Protein is >0.5, 2-Pleural/Serum LDH is >0.6. The
determination of pH is important in parapneumonic effusion in which a value of
<7.2 requires a chest tube aspiration to prevent empyema. Pleural fluid pH<7.3
indicates pleural inflamation. \n\n
**** If CHF is exacerbated due to develpement of Atrail fibrillation
then tx of choice for that is Adding Digoxin. \n\n
******Measurement of
serum B-type Natriuretic Peptide (BNP) can help ddx CHF from other causes of Dyspnea (COPD). A value of >100 is dx for CHF. BNP is like ANP but BNP is released from Ventricles vs ANP from Atria. \n\n
**Also remember in CHF pt sodium is reabsorped in kidneys in response to renin-angiotensinogen -Aldosterone system, therefre sodium in urine would be low . \n\n
...
**** drugs that increase survival
ACE inhibitors increase survival rate in
CHF pts, so cosider it in a pt with E<40%. Also out of all diuretics, Spironolactone
is the only one that improves survival. \n\n
*** Drugs that improve survival
are Bblocers,
Spironolactone, ACE inhibitors (Captopril and Losartan), and Aspirin.
Digoxin helps the situation but NOT survival.\n\n
Child Abuse steps
A19-\n\n
Choanal Atresia
Suspect it in a infant who presnts with cyanosis that is aggrevated by feeding and
releived by crying. Failure to pass a cathater through the nose is sugestive of dx. Dx
is confirmed by CT with intranasal contrast. \n\n
***TX
The first step in mgmnt consist of placing an oral airway and lavage feeding. Definite tx is repairing the obstruction with surgery.\n\n
Cholecystitis, Acute - 3
Dx stages: 1-USG(initial workup), 2-HIDA (very specific, for
confirmation. Its particulary useful in dx of Acalculus cholecystitis). \n\n
****Triad of acute RUQ
pain, fever and leukocytosis. Pain radiates to scapula. Billirubin is normal and Murphy (pain on deep inspiration) exist. Its most commnly 2ary to gallstones. , in these pts it mc due to impaction of stones in a cystic duct. \n\n
**The inflamatory response results from any of the following,
1-Mechanical(increased
intraluminal pressure), 2-Chemical(release of tissue factors) 3-Bacteria(2ary to
stasis), this occurs in 50-70% of cases. \n\n
*** REMEMBER
although in 50-70 of cases
there is infection due to bactreia, but the cause for AC is mc due to impaction of the
stone in cystic duct. \n\n
**** If pt still has pain after cholecystectomy
and ERCP shows
sphincter of Oddi dysfucntion, then ERCP with sphincterectomy is the procedure of
choice. \n\n
**** After ERCP and shingterectomy,
if pt has normal LFT and no dilation
of biliary tree with US, then Oddi and CBD can be ruled out and pt is having
FUNCTIONAL PAIN. Give analgesics and reassurance. \n\n
**** Acalculus Cholecystitis occurs in
CRITICALLY ill pts and imagin studies show thickening of gall blader wall and presence of pericholesistic fluid. Etiology might be stasis of bile ducts and ISCHEMIA of the gall bladder (after accident with loss of blood).\n\n
Cholecystectomy: Hepatology, 6/2
Post cholecystectomy pain most commonly is due to either Common bile duct stone,
Sphincter of oddi or Functional pain. \n\n
*** If LFT is normal
and no dilatation of biliary
tree then its functional pain, tx is symptomatically with analgesics and assurance. \n\n
*** If pt has abnormal Alkaline phosphatase
and dialation of billiary tree on US, then we do ERCP to confirm and treat, by stone removal or sphincterectomy.\n\n
Choledochal Cyst
congenital abnormalities of the billiary tree characterized by dialation of intra and
extra hepatic billiary ducts. Presentation vary with age. An infant presents with
jaundice and passage of acholic stools. \n\n
*** In children
it causes abdominla pain, jaundice and attakcs of recurrent pancreatitis, which maybe evident by increase in amylase and lipase. \n\n
***Adults
present with vague epigastric or RUQ pain or Cholangitis. Choledochal cyst could degenerate into cholangiocarcinoma. Initial investigation of choice is US followed by CT or MRI. \n\n
***DDX1:Caroli's Synd,
congenital disorder of intrahepatic dialation of bile ducts. \n\n
*** DDX2:
Biliary Atresia presents in infancy with marked obstructive jaundice and acholic stool.\n\n
Cholelithiasis
Tx: 1-Asymptomatic pt, leave it alone. 2-Symptomatic pt, if ok with surgery choice
is Laparoscopic Cholesystectomy, if surgery is CI or pt declines surgery then
Ursodeoxycholic acid 10 mg/kg/day reduces biliary secretion of cholesterol and
decreases the cholesterol saturation of bile, resulting in gradual dissolution of
cholesterol-containing stones in 30 to 40% of patients. \n\n
****There are 3 types:
1- Cholestrol, 2-Pigment stones(mostly calcium bilirubinate, 20%) and 3-Mixed stones. Water insoluble cholestrol is secreted in bile where its converted into soluble miscles by bile acids and phospholipids. \n\n
*** If too much cholestrol and too little bile
then cholestrol crystals precipitate. \n\n
***Predisposing factors
are Fat,Femlae,Forty,Fertile(OCP), cloFibrate. Remember 80% of stones are radiolucent so xray cant see them.\n\n
Cholesteatoma, ENT 6/2
Causes acquired conducting hearing loss in CHILDREN .Its not a tumor. Its an
Epithelial Cyst that contain desqumated Keratin. It could be acquired secondary to
Otitis media or Eustachian tube dysfunction. \n\n
*** org.
Infection is usally due to Pseudomona. Pt presnts with recurrent infection. MC sign is drainage and granulation tissue and debris unresponsive to antibiotics & marginal tympanic perforation. \n\n
**** compl.
They destroy bone. CT can detect defected bone. Tx is surgical removal. DDX Chronic Otitis media where there is no debris and granulation.\n\n
Cholesterol embolizarion
Or Atheroembolic disease, follows surgical or manipulation of arterial tree ( ie
Angiography), due to showering of cholesterol from aorta or other major arteries.
Its mc seen in elderly pt with evidence of diffused Atherosclerotic dis.. Renal failure,
Livedo reticularis, sstemic eosinophilia, and low complement levels, should make you
think of this. \n\n
**Tx
is conservative, antocoags should be stoppedsince it may prevent
healing of the ruptures Plaque. Physical exam shows painless, redish blue mottling
of the skin of the extremities.\n\n
Cholesterol lipid profile
For CHILDREN the recommendation is: A child with a parental hx of elavated total
cholesterol (>240mg/dl) or a chld with risk factors for CAD should be screened for
total cholesterol level. \n\n
*** If its >200mg/dl
then we do a fasting lipid profile test. For
screening we use HDL and Total Cholesterol. For Tx guidelines we use LDL levels.\n\n
Cholestyramine:
A bile acid sequesterant that lowers LDL and mostly increase HDL when combined
with statin. In addition to binding bile acids in gut it also binds other drugs and
reduces their bioavailibility so the pt needs higher doses ( ex hypothyrism ). \n\n
Chorioamnionitis
Pts present with fever >38, uterine tenderness, irritability, elevated WBC and fetal
tachycardia.Its asso with preterm or prolonged rupture of membrane. Fetal tachy
could also be caused by Beta-2 agonist for tocolysis. \n\n
*** caused
Elevation of WBC could also be caused by steriods admin. \n\n
*** dx
Amniotic fluid cultures are gold for Dx (Nitrazine paper test). Once Dx is established samples are taken for culture . \n\n
** tx
and then Ampicciline and Gentamcin are given. Labor should be induced. If cervix is unfavorable C-section is done.\n\n
Choriocarcinoma
It's a malignant tumor of the trophoblastic tissue. Clasically prestns w Hemoptosis,
but it could also present with shortness of breath and chest pain. In any postpartum
female you should suspect Choriocanrinoma. \n\n
**** dx
Quantitative Beta HCG is important
in Dx. So once you have postpartum woman with hemoptosis chest pain and
shortness of breath then we need to do Cxr, pelvic exam and BetaHCG.\n\n
Chronic Liver Disease
Do Merck. Asso with respiratory alkolosis.\n\n
Chronic Mesenteric Ischemia
suspect it in pt with chronic abdominal crampy pain, weight loss and people who
don't eat food because of pain and other malabsorptive symptoms. Evidence of
Atherosclerotic dis is present. Abdominla exam might reveal bruit in 50% of pts. Dx
needs angiography and Doppler US.\n\n
Chronic renal failure - 2
Secondary hyperparathyroidism with resultant renal osteodystrophy (loose calcium
and retain phosphate) is almost universal in CRF. \n\n
**** eitiology
Normochromic normocytic
anemia due to eryhtropoetin def is a very common I pt with End Stage Renal
Failure. \n\n
** tx
Recombinant Eryhtropoetin is the tx of choice, however, Iron supplemnt
should be given BEFORE erythropeitin. All Chronic Renal Failre pts hct<30,
Hb<10 are canditetes for Erythropetin after Iron def has been ruled out. \n\n
** SE
of Ertythropoetin therapy is 1-Worserning HT ( about 30% of pts. SC toute less
common than IV route). Tx would be removing fluid with Dialysis and B-blockers.
2-HA, 3-Flulike symp, 4-Red cell aplasia. \n\n
****Factors that improve prognosis
in CRF are Protein restreiction and ACE inhibitors. ACE inhibitors are more likely to worsen RF when serum Creatinin are >3-3.5 mg/dl.\n\n
Churg Strauss
A20. MERCK:Its one of the group of diseases of known or unknown etiology
characterized by eosinophilic pulmonary infiltrates and, commonly, peripheral
blood eosinophilia.allergic granulomatosis (Churg-Strauss syndrome), a variant of
polyarteritis nodosa with a predilection for the lungs.\n\n
Circumstantiality
is a thought disorder that answers in un-necassary details that deviate form the
topic but eventually goes back to the topic. DDX is Tangentiality which is an abrupt
permanent deviation from the topic. DDX2:Loose asso which there is no asso b/w
sentences.\n\n
Cirrhosis - 3
Could happen 2ary to alcoholism. Pt has ascites, and esophageal varices 2ary to
portal hypertension. Prophylactic tx of pt wth large varices who have never bled
with propranolol significantly decrese the risk of futur bleeding. \n\n
* In a pt with refractory ascites
, refractory hydrothorax, and recurrent variceal bleeding, TIPS (Transjugular Intrahepatic Portosystemic Shunt). is used. \n\n
****MCC
Alcoholism is the mcc of cirrhosis in US. 33% alcoholics, 10% HBV, 20-30% HCV(the mcc of liver transplant in US). \n\n
****Pts
with cirrhosismay have upper GI bleding due to : Erosve
gastritis, PUD, Mallory-Weiss tear. Sclerotherapy isindicated for first varices, but
not prophylactically. For PUD do consertavie mngmnt, if that didnt work then we
do surgey, Excision of ulcer and vagotomy and pyloroplasty.\n\n
Clavicle Fracture
In bew borns it presents with irregularity,crepitus and fulness over the fracture site
and decreased movemnt of the arm. Predisposing factors ar shoulder dystonia,
traumatic delivery, large infant. No tx is needed \n\n
.***For Adults do a figure of 8 bandage. ****Clavicle fractures that are displaced can damage subclavian artery, Artriogram is needed to rule out injury. Next step would be nerve donduction studies to rule out Brachial plxes injury. \n\n
...
*** If fracture
is in distal third then may require open reduction and internal fixation. Proximal and middle third are treated with closed reduction and figure of eight brace.\n\n
CLL (Chronic Lymphocytic Leukemia - 3
MC Leukemia in Western countries. In older pts. Mostly asymptomatic and
discovered accidentaly. Smudge cells. In general don't need to do lympb node
biopsy to confirm dx, but if you want to a highly specific biospy is available to
confirm dx. \n\n
****DDX
:CML, presents with LEUKOcytosis with left shift
Imyelocytes, neutrophils) not LYMPHOcytosis. \n\n
**** Labs
Smodge cells (leukocytes that break down because of theri greater fragility) are charcteristic. Staging is directly related to prognosis, stage 0= Lymphocytosis only, Good; \n\n
** Stages
I=Lymphocytosis+Adenopathy, Fair; StageII=Splenomegally present, Fair;
StageIII=Anemia present, Intermediate; StageIV=Thrombocytopenia,Poor. Mean
survival is 8-10 years.*****To CONFIRM dx do lymph node biopsy.\n\n
Clomiphene Citrate
Is an antiestrogen acts by competitive blocking of receptors of hypothalamous,
inhibiting the negative feedback that estrogenhas on GnRH and consequently
insreasing Lh & FSH and improving ovulation. Along with hMg and hCG
itsindicated for chronic ovulation. \n\n
** SE
are hot flashes, breast discomfort, spotting.
DANAZOL is an androgen derivative that has gonadotropin inhibitory effect . Its
indicated in Endometriosis, Fibroids and Fibrocystic breast disease.\n\n
Clonazepam toxicity
Clonazepam is used for insomnia. In elderly pt it could cause memory disruption.
The next step in mngmt is to discountinue it.\n\n
Clozapine se
Agranulocytsis.\n\n
Club foot
Or Talipus Equinovarus. Calcaneum and talus are in equines and varus position.
Initial mgmnt involves non-surgical methods (stretching and manipulation of the
foot, followed by serial plaster casts, splint or taping). Surgical tx is indicated if that
didn't work , its performed b/w 3 and 6 month of age.\n\n
Cluster headache - 2
Tx for acute attack is 100% oxygen & subcutaneous Sumatriptan. *Presents with
acute , sever retroorbital pain that wakes pt up at night. Maybe accompanied with
redness of ipsilateral eye, tearing , runny nose, and Ispilateral HORNER synd
(Ptosis, Myosis, Anhydrosis). Prophylaxis is key to mgmt, with verapamil, lithium
and ergotamine.\n\n
CML
There is increased mature granulocytes like segmented neutrophils and band forms.
BM shows hypercellularity with prominent granlocyte hyperplasia. When pt is in
Crisis phase, IMATINIB is DOC. It's a tyrosine kinase inhibitor that block signals
w/I cancer cells. SE are mild naseau, diarrhea, leg cramps and swelling of the face
and itchy rash. It has chenged the prognosis with CML.\n\n
CMV Pneumonitis
Is seen in 15-20% of Bone Marrow Transplants with case fertality of 84-88%. Pt
presents with dypnea, cough and fever. \n\n
Dx
Cxr shows multifocal diffused pathy infiltrates, and ground glass attenuation, parenchymal opacification or multiple small nodules on high res CT. BAL is dx in most cases. IT IS NOT SEEN IN IMMEDAITE post transplant period \n\n
*** ddx
wich is DDX with bacterial and fungus pneumonitis. PCP is also seen in immediate post transplant but its occurance has decreased dramatically due to routine prophylactic use of tri.sulfa in pre-transplant period.\n\n
Coarcation of Aorta
Present with rib notching (the 3 sign). HA is a presenting sign. Hay HT in upper
extremity. Cxr shows dilatated ascending aorta and subvlavian artery. Indentation
of aorta at site of coarcation and pre and post stenting dilation is called the '3' sign.\n\n
Cocaine Tox - 3
Pt presents with EKG abnormality of st depresion (ischemia and infarction), HT
and excrutiating chest pain. Tx is Benzodiazepine, Nitrate and aspirine.If pt has MI
then first line is Cathaterization. \n\n
****Fetuses exposed to cocain abuse
exhibit intracranial hemorhage., nerotizing enterocolitis and cardaic defets and GU malformations. \n\n
****Could cause MI due to causing vasospasm, threre is blood in
narises and dilated pupils . He has no risk for MI and is only 27.\n\n
...
Coccidiomycosis
Is endemic in California Arizona and new mexico and texas. Primary Pulmonary
infection has non-specific features life fever, fatigue, dry cough weight loss.
Cutaneous Erythem multiform and erythema nodosum anf arthralgias might be.
Blastomycosis cutaneous dis is verrucous or ulcerative.\n\n
Colon Cancer
FOBT is the mc used screening test for colon cancer. Pts should be followed with
colonoscopy.\n\n
Colorectal Cancer
MC presenting symptom is bleeding!\n\n
Communicable diS.
If pt's dis could harm others he should be tx against his will. Senario is a man with
Meningitidis and fever 104 for 2 days who wants to be tx at home. Answer is treat
him in hospital agains his will since he will be harmful to others at home.\n\n
Compartment Synd
Dx is made clinically with pallor, pain, pulselesness, paralysis and paresthesia. PAIN
on passive extension of fingers is the most sensitive marker of CS. Pain is
persistant,progressive, unrelieved with imobilization and out of proportion to initial
injury. CS is cused by increased pressure w/i an anatomical space. \n\n
Complex Patial Seizure
Breif episodes of impared consiousness, failure to respond to varius stimuli, staring
spells, AUTOMATISM( Lip smacking, swollowing), and post-ictal confusion. EEG
is usually normal. DDX1,Typical Absence seizure might have lip smalcking but they
have n post-ictal confusion.\n\n
Conduct disorder
Charcterized by disruptive behavior that violate basic social norms for at least one
year in pt <18 yo. Like stealing, setting fire, fighting, animla abuse. DDX is
Antisocial disorder is when these boys become adults.\n\n
Congenital Adrenal Hyperplasia- 2
Hyponatremia, HyperKalemia, Hypoglycemia, and metabolic acidosis. Its due to 21-
Hydroxylase deficiency. Its auto recessive. Deficiency of both glucocorticoids and
mineralocorticoids. \n\n
*** IF Male infants
will NOT have ambigous external genitalia unlike
female infants, thats why male infants go on un-noticed until 2-4 weeks when they
present with salt wasting. Treatment of 21-hydroxylase deficiency is with
glucocorticoid replacement. \n\n
*****Adolescent onset of hirsutism and virilism with normal mensturationand elevated 17-OH Progesterone.\n\n
...
Congenital Diaphragmetic Hernia:
In all emergency cases remember TX supercedes Diagnosis. The 1st step if oyu
suspect CDH is to place orogastric tube and connecting it to a continues suction in
order to prevent bowel distension and further lung compression. Bag-and-mask is to
be avoided because this can cuase the stomach and intestine to become distended
with air, further compromising lung funx.\n\n
Congenital heart defects
1-TOF: VSD. 2-Down: Endocardial cushing defect. Also ASD ( L to R shunt). 3-
Turner synd:Coasrcation of aorta. 4-Congenital rubella: PDA. \n\n
Congenital Hypothyroidism:
The mcc is thyroid dysgenesis, 85% of cases. Infant has apathy, , weakness,
hypotonia, constipated, sleeps a lot, large tongue, umbilical hernia. Screening is by
T4 and TSH levels, Tx is Levothyroxine\n\n
Congenital Rubella
Triad of sensorineural deafness + Cardiac malformation (PDA & ASD) + Cataracts.
There could also be thrombocytopenia and purpule skin lesions ( Blueberry muffin
spots). \n\n
*** If transmission
occurs in first 4 week of pregnancy the risk of developing CR
is 50%, it drops to 1% in third trimester. The child might show symptoms when he
is 2 years old.\n\n
Congenital Toxoplasmosis:
Triad of Chrioretintis + Hydrocephalus + Intracranial calcification. Look for pet in
the picture somewhere.\n\n
Conjunctivitis, Neonatal - 2
Hay 3 causes for NC in US. 1-Chemical is the mc of the red eye presents at 1st 24hr
of life. About 80% who receive prophylaxis w silver nitrate (to prevent gonococcal)
experience mild conjuncitivis and tearing that resolves w/I 24 hrs.
***2-Gonococcal
is acquired through contact with infected vaginal secretions, it occurs 2-5 days after birth, it presents as Copious purulent eye discharge with swellen eyelids & Chemosis(conjunctival edema), dx is by obtaining a smear and culture of the
discharge, tx is a single intramuscular dose of ceftriaxone. \n\n
***3- Chlamydia:Trachoma,
presents with mild hyperemia and scant mucoid eye
discharge and pannus (neovascularization) formation, it occurs b/w 5-14 after birth.
TX is Systemic Erythromycin to decrease risk for Chlamydial pneumonia.\n\n
Constrictive Pericarditis. - 2
Asso with TB in immigrants.****Etiology could be early TB in life. The early third
hear sound, called Pericardial knock and the respiratory increase in JVD (Kussmal
sign) are important findings. Kusmaul is also present in right side hear failure, sever
tricuspic regurgitation ,RV infarction and cardiac temponade. \n\n
******CP will lead to
inability of ventricles to fill during diastole and would furthur cause the signs of decreased cardiac output (fatigue) and signs of venous overload like JVD, dyspnea, ascites, Kussmaul, pedal edema tender hepatomegaly. \n\n
*** Examination
Sharp 'x' and 'y' descent oncentral venous tracing is the sign of CP as is Pericardial Knock (early sound after S2).\n\n
Contraception
Lactation is a contraceptive methid in itself because prolactin inhibits GnRH thus
preventing ovulation. However, it is not a reliable methis. If a woman wants
contraception right after giving birth, give her Minipill (Progestin only pills), Don't
give her Combined OCP because Estrogen may cause decrease in milk production. \n\n
Conversion disorder - 2
Tx is psychotherapy. Pt looses eye site in stressful situation. *** If pt comes with
bilateral leg paresis, give him Sodium Amytal and he will dramatically improves.\n\n
COPD - 8
If pt is not crashing, the first line of tx is non-invasive positive pressure ventilation
before intubation. All pt with PaO2<55 and SaO2<88 are candidates for long term
home oxygen therapy. \n\n
** Pt
with pulmonary hypertension and hemoatocrit >55 should
be started with home therapy if PaO2 falls <60mmhg. Smoking cessation and home
oxygen therapy are two modalities that can reduce mortality in pt. \n\n
****Acute exacerbation of COPD is tx with
combination of inhaled /nebulized
bronchodialators and systemic steriod (Methyprednisone).
*****In a pt with multifocal atrail tachycardia
due to exacerbated CODP Theophyline and Beta Agonist (Albuterol)(remember beta agonists decrease potasium and worsen
arrythmia) will WORSEN tachycardia. Give Oxygen to stop the
arrythmia. \n\n
****COPD comprises lung OBSTRUCTIVE diseses
which includes
Chronic Bronchitis and Emphysema. The airflow obstruction is irreversible. A
chronic smoker with a productive cough and dyspnea on excertion, with decreased
FEV1/FVC is suggestive of COPD. \n\n
****Chronic Bronchitis is characterized by
chronic cough for at least 3 months for two consequetive years.The presence of chronic productive cough, prominant bronchovascular marking, mild flatening of diaphragm, and normal DLCO is suggestive of CB rather than Emphysema. \n\n
**** These are called Blue Bloaters
(for Bronchitis) they have heart failure sings and profound oxygen desaturation. Emphysema is destruction of alveolar wall, \n\n
***Pink Puffer (emPhysema) ,
hyperinflation of the chest, Decreased vascular marings, Decreased DLCO(due to destruction of alveoli) and moderate oxygen saturation. Now
remember Sarcoidosis, Silicosis, Asbestosis, Scleroderma and rheumatoid lung are
all RESTRICTIVE lung dis characterized by NORMAL Fev1/FVC. \n\n
****The most impact on COPD pt
is by Oxygen home tx. The guidline is PaO2<55 and O2 saturation <90%. \n\n
*** chronic pt comes in with severe sypnea
and confusion and
profuse sweating. Cxr shows complete collpase of L lung, possibly by a mucus plug
(atelectasis is the same after surgery). Tx is emergency Bronchopscopt to remove the
plug. And that will improve PaO2. \n\n
*****Non Invasive Positive Pressure Ventillation
is the best option for pts with COPD exacerbation. It should be tried before
intubation and mechanical ventilation in COPD pts with CO2 retention.\n\n
Core Pulmonale
Combination of Elevated JVP, Hepatomegaly,ascites, and lower extremity edema
w/o evidence of pulmonary congestion is suggestive of isolated right heart failure. \n\n
*** If there are no RALES
it means there is no pulmonary congestion. The mcc of Right
side heart failure is Pulmonary disease, and its known as Core Pulmonale. CP is
most likely caused by COPD(Smoker) , lees common causes are pneumoconiosis,
pulmonary fibrosis.\n\n
Court order
T9Q38\n\n
Craniopharyngioma - 2
Althought mc in children, they are bimodal and could happen in adults too. In
children retarded growth is the mc presentation. In adults hyposexuality.
Bitemporal blindness is a classic sign. Dx is MRI or CT. Tx is surgery or
radiothreapy. \n\n
**** h/p
A young boy with symptoms of increased ICP (HA,Vomit) ,
Bitemporal anopsia and a calcified lesion above sella has Craniopharygioma until
proven otherwise. Presense of a Cystic Calcified parasellar lesion on MRI is almost
Dx. \n\n
** DDX is Pituitary Adenoma
where its more frequent in women and
Prolactinoma is an important part of it, and there is no CALCIFICATION of the
gland.\n\n
CREST Synd - 2
Anticentromere antibody is Dx.*****Calcinosis, Reynauds, Esophageal dysfunction,
Sclerodactyly and Telangiectasia. It has a better prognosis than diffused
Scleroderma.\n\n
Creutzfeldt-Jacob - 2
Pt is b/w 50-70, with rapidly progresive dementia, myoclonic and periodic
synchronous bi or triphasic sharp wave complex on EEG.Brain biopsy shows
cortical spongiform changes. CSF is normal, Death w/I 12 months, NO TX.
Spongiform encephalopathy is caused by prion.\n\n
Crohn's disease - 2
DDX with UC is non-caseating granulomas.\n\n
Croup
Also known as Laryngotrachiatis or LaryngoTrachioBronchitis, is characterized by
laryngeal inflammation that results in hoarseness, a barking cough and respiratory
distress. Typical pt is <3 and the mcc is Parainfluenza virus. \n\n
Dx
is clinical and lateral xray shows subglotial narrowing. Always give Epinephrine before any invasive tx like intubation. This is ONLY for croup not Epigolitis. Tx is 1st O2, 2nd Epi, 3rd intubate in ER.\n\n
Cushing's Syndrme - 3
Due to ectopic ACTH.***Pt with lung cancer and ectopic ACTH production can
have Cushing's. ****Dx procedure.\n\n
Cutaneous Larava Migrans
Is a cc of dermatological disease in tropical travelers. Its caused while "Sand box
handling" and its characterized by serpiginous lesion in the skin. Tx is Applying
thiabendazole or mebendazole\n\n
CVA
Occurs in middle and late years of life. Could be either Ishcemic (85%) or
Hemorrhagic (15%). Ischemic CVA orignates from aortic arch, carotid bifurcation,
and obstruct arteries. Clinically atherothrombotic stroke occurs at rest and have a
gradual onset. \n\n
*** h/p
Pt experiecne successive strokes. Babinsky indicates UMN due to
major cerebral artery obstruction. Ischemic CVA could also be caused by thrombi
from left heartIts asso with sudden onset and preexisting cardiac disease. \n\n
** EKG is characteristic.
The mc site is lateral striate artries which are branches of MCA, they supply internal capsule,putamen. So if a pt has normal EKG and cardiac enzyme, this kind of stroke is unlikely.\n\n
Cyclical vomitting
recurrent self-limiting episodes of vomitting and nausea in children. Tx is antiemetics
and reassurance.\n\n
Cyclosporine side effects
1-Nephrotoxicity:the mc and serious side effect. It manifest as acute azothemia or irreversible progressive renal disease.
2-Hypertension:due to vasoconstriction and sodium retension. Ca chanel blokers are doc.
3-Neurotoxicity:Often reversible.
4-Tremor, headache, nasea, seizure, visual problems. \n\n
** more se
4-Glucose intolerance.
5-Infection: 40% of pt get infection chronically.
6-Malignany: Risk of squamous cellcarcinoma.
7- Gingival hypertrophy and hirsutism.
8-GI, mild.
Tacrolimus has the same se ex hirsutism and gum hypertrophy. \n\n
***tx
Azothioprine
se is dose related diarrhea, leukopenia,hepatotoxicity.
Mycophenolate se is Marrow suppression.\n\n
Cyclphosphamide SE
Bladder carcinoma is a SE. Also alopecia, sterlity, amenorrhea, acute hemorrhagic
cystitis.\n\n
Cystic Fibrosis - 8
Bronchiectasis due to pseudomonas asso. infertility and recurrent respiratory infections.
Cxr showing "Tram Track pattern" and opacities is dx for
Bronchiectasis. \n\n
CF
is due to abnormal chloride transportation
Sweat chloride concentration >60 is DX. Since there is fat malabsorbtion. So vit K is a cofactor for the enzyme g-glutamil carboxylase which adds carboxyl group to glutamate residue of factor II,VII,IX & X, and protein C & S, those will be also deficient. \n\n
*****A routine influenza vaccine
is indicated in all CF pts, not Pneumococcal vaccine.
There is asso b/w Pseudomonas pneumonia and CF.
tx Gentamycin+Pipercilline. \n\n
*****Tx in acute sever exacerbation of cf
is IV Pen/Cephalo+Gentamycin. \n\n
*****Aut rececive
we need to know both parents
DNA status to determine child's possibility of having CF. \n\n
*****The mc mutation
is
a DELETION of a three base pair coding for Phenylalanine (DjO8) in the CFTR
gene in CH7. \n\n
****Pts with CF present
with Meconium Ileus characterized by bilious
vomiting, failure to pass meconium at birth, and ground glass apperance on abdominal xray. \n\n
*****Suspect
in a pt with Bronchiectasis cough productive of
sputum for 3 months and Malabsorption , foul smelling stool due to pancreatic insufficeny. \n\n
*** One clue if
the pt starts to show in his 20s is a hx of Meconium Ilueus
(intestinal obstruction) as a neonate. Whenever hay acute exacerbation of pulmonary infection in a pt with CF,
think Pseudomonas;
tx with Pipercillin+ Gentamycin.\n\n
Cystinuria:
An inherited disease causing recurrent renal stone formation.
Look for positive family history and stones since childhood.
Stones are radiopaque and Hexagonal.
The urinary cyanide nitropruside test is a screening procedure.\n\n
Cystitis - 2
Most commonly caused by Ascending infection. h/p suprapubic tenderness.
* Uncomplicated Cystitis, where pt presents with suprapubic discomfort and signs of UTI, then there is NO need to do culture.
Just give Oral Trimeta-Sulfa. If resistant> Cipro or Nitrofurantoin.\n\n
Dacryocyctitis
Inflamatory in medial canthal region. mcc Staph & Strep.
Acute dacryocystitis is treated by frequent application of hot compresses;
cephalexin or cefazolin; and incision and drainage if an abscess has formed.
Chronic dacryocystitis may be treated by dilating the nasolacrimal duct.\n\n
De Quervains Tendonitis
abductor or extensor tendons of the thumb. Dx localized
tenderness .Sharp pain is elicited when the ipsilateral thumb is flexed across the palm, enclosed by the fingers, and the wrist is deviated ulnarly to stretch the tendons and surrounding sheath Finkelstein's sign. \n\n
***tx
Symptomatic relief is provided by rest or immobilization (splint or cast) of the tendon, application of heat for chronic inflammation or cold for acute inflammation (whichever benefits the patient should be used),and NSAIDs.Surgery for release of fibro-osseous tunnels.\n\n
Dehydration - 2
Mainstay of tx is IV sodium containing crystaloids (0.9% Saline)
*Elderly pts are sensitive to dehydraion and even mild Hypovolemia can
lead to orthostatic syncope, especially upon getting up in the morning.
INCREASED BUN/Creatinin is a good indicator of dehydration.\n\n
Delirium Tremors
Tx is Chlordiazepoxide.\n\n
Delirium vs Dementia
Delirium has:Acutenes, impaired conciousness, fluctuating course, reversible symptoms and global memory impairment.
In the absence of focal neurological signs, even if there is evidence of carotic bruit (Vascular Dementia) Delirium is the most like Dx.\n\n
Delusional Grandiosity
Pt thinks she has special powers, extraordinary accomplishments, or special relationship with God.
There are three types of Delusion:
1-Grandiose (religious in nature)
2-Paranoid
3-Somatic.\n\n
Dependant personality
When ot is so agreeing and depends on whatever the doctor suggests.\n\n
Dermatitis Herpetiformis-3. Dermo. 6/3
Pruritic papules, vesicles over the knee, elbow, buttocks. Immunofloresence shows
granular IgA desposits along dermal papillae. Asso w Celiac sprue. Tx is Dapsone. \n\n
***Suspect DH
in a pt with Malabsorption and pruritic papules and vesicels over the extensor surfaces. Anti-Endomysial antibodies are charcteristic. Pt also suffers from Gluten sensitive enteropathy or Celiac Sprue. \n\n
***Tx
Strict adherence to a gluten-free diet for prolonged periods (eg, 6 to 12 mo) may control the disease in some patients, or Dapsone.\n\n
Dermatomyocytis:
Is an autoimmune disorder involving muscles and the skin. Skin eruption is dusty
red in color. Edema around the eye and the helitrope rash of the eyelid are more
specific. \n\n
***Gottron's sign
is highly suggestive of this disorder in which skin over the
back of knuckles show non-scaly violacious erythomatous eruption.\n\n
DES toxicity
If given to pregnant women causesClear cell ADENOCARCINOMA of vagina in
their duaghters. In the old days it was the best tx for threatened abortion. With erly
dx and tx survival is 80%.\n\n
Development Dysplasia of Hip
DDH is characterized by subluxatable and dislocatable proximal femur and acetabulum. Early dx and tx is important because failure will result in sigificant morbidity. On inspection uneven gloteal fold are seen. \n\n
*** Its mc
in femlae cockasian females. Dx is confirmed by USG in infants <6mo. Positive Barlow and ortolani are highly suggestive. Tx is surgical reduction.\n\n
Developmental Milstones
1-LANGUAGE:Social smile=2mo, Bables=6mo, 2words and obey one step
command=12mo, 2-3Phrase& 2 step command=2yr. \n\n
*** 2-GROSS MOTOR
: Hold head=3mo, Rolls back to front=4mo, sits unsuported=6mo, walks alone=12mo, walks staris=2y. \n\n
*** 3-FINE MOTOR:
Raking Grasp=6mo, Throw objest=12mo, Build
tower of 2 block=15mo, build 6 blocks=2yr. 4-SOCIAL: Recognize parents=2mo.
Recognize strangers=6mo, Imitates/comes when called=12mo, play with other
kids=18mo, Pararel play=2yr.\n\n
Dextrometorphan- Poisenining 6/3
A cough medicine. has drung toxicity with MAO inhibiors, causes hyperthermia\n\n
Diagnostic Peritoneal Lavage
Is the best dx procedure for intraperitoneal organ laceration. Like a guy being hit in
the stomach. Angiography is never done.\n\n
Diabetes Incipidus - 3
Presents with polyuria and polydypsia, due to ADH def or resistance. Pt prefer cold
beverages and their urine osmolarity is < serum osmolarity. Pts pass excessive
amounts of diluted urine. Normal saline is the initial fluid of choice in hypotensive
pt and later on Hypotonic fluids. \n\n
***DDX1:
Primary hyperaldosteronism
(aldosterone=saves sodium and loses K), Hypernatremia is rarely symptomatic,
other features are hypertension & hypoKalemia. \n\n
*** DDX2:
Osmotic Diuresis(increase
renal excretion of water relative to sodium), occurs in cases of hyperglycemia and
manitol intake. Urine osmolarity is > serum osm. \n\n
DDX3:
SIADH, results in
hyponatremia, low serum osmolarity and inapropriately high urine osmolarity.
sually seen in pt with lung cancer and abnormal brain pathology like trauma or
stroke. \n\n
***DDX4:
Primary polydypsia, is a disorder where pt drinks fluid in excess of
5L/day and both plasma and urine osmolarity are low (diluted). \n\n
****Administration
of DDAVP (desmopressin) ddx b/w CDI and NDI. Pt with CDI will have increase of urine osmolarity following admin of AVP (arginin Vaso Pressin, or DDAVP), but NDI pt wont have that increase. Tx for CDI is intranasal Desmopresin.\n\n
Diabetis Melitus - 34
1-Normal anion gap metabolic acidosis in a diabetic pt with Gastroenteritis could be
either due to loss of bicarbonate due to diarrhea, or defective NH4 sunthesis due to
nephropathy. So next we need to calculate urine anion gap. [Urinary (Na+K) -
Urinary Cl]. If its positive value problem is Nephropahy, if its a negative value its
due to Gastroenteritis. \n\n
***2-Diabetic Osteomyelitis
(due to arterial insufficiency) that
involves bone adjasent to the foot ulcers is explained by contigous spread of
infection. \n\n
***3-Acanthosis nigrans
is a complication of DM. Although its associated
with both DM and Addison's disease insulin resistance is the mcc in young
population, and its asso with malignany in older individuals. \n\n
4-Somogi effect
. 5-Diabetic neuropathy tx is Gabapentin and TCA (imipramine). 6-Diabetic Cystpathy tx is Bethanechol. 7-Diabetic retinopathy. 8-Infection in diabetes. 9- Diabetic Nephropathy, detection of microalbunemia is the best detection.\n\n
*** Fasting blood glucose
is now test of choice for screening high risk individual for DM. When fasting
G is 126 or greater, repeat it, and if its still elevated the Dx is made. \n\n
***Dx
could also be made if pt is SYMPTOMATIC and G after 75gr tolerance test its 200 or greater. Ketones responsible for DKA are Acetone, acetoacetate and beta hydroxy butyrate.\n\n
**Diabetic Neuropathy
leads to denervation of bladder resulting in urinary retention,
Overflow incontinence day and night, aside from strict glucose control tx includes
intermittent cathaterizarion and Bethanechol, avoiding alcohol maybe helpful.\n\n
**** note
Antibiotics dont cure ulcers, do a debriment of the wound. ****Glomerular
Hyperfiltration is the earliest renal abnormality seen, as early as several days w/i dx
of DM. Its the major pathophysiologic mechanism of glomerular injury in these pts.\n\n
**** note
Thickening of the glomerular basement membrane is the first change that can be quantified. Effectiveness of ACE inhibitors is related to their ability to reduce
intraglomerular hypertension and decrease glomerular damage. \n\n
**** In pt with
Diabetic Nephropathy add ACE inhiitor even if BP is under control, it slows
progression of nephropathy and keeps glomerualar bp reduced. \n\n
****Glycosylated Hemoglobin (HbA 1-c) is the best way to monitor DM control.
HbA1c is fomred by non-enzymatic glycation of Hb. Its reflective of the average glucose blood levels w/i the precedding 2-3 months, which corresponds tothe life of RBC. Every 1% increase in HbA1c correspodes to 35mg increase in glucose. \n\n
Remember measurement of Cpeptide
is done to determine if the insulin use is internal or external. \n\n
DIABETIC KETOACIDOSIS:
Anion Gap Metabolic Acidosis observed during DK is
accompanied by HyperKalemia, its called paradoxial because body K reserves are
actually depleted. \n\n
** Hay hyperKalemia for 2 reasons
1-extracellular shift of K in
exchange for H with resultant intracellular K depletion. 2-Impaired insulindependant
K entry. \n\n
So in Tx for DKA,
after insulin and diuresis administer K.
****Suspect it if pt presents with rapid breathing, hx of weight loss, polydipsia nd
polyuria.END OF KA.\n\n
****Fasting bloog glucose measurement
is now the screening
of choice. A FBG of 126 or more on two occasiona is Dx. FBG b/w 100-125 is
categorized as impaired FBG or pre-DM.\n\n
If pt has symptoms, poluuria, polydyspsia,and obesity FBG of >200
may confirm the dx but its not appropriate for screening.
The 50gr glocose tolerance test is used for screening gestational DM, while 100gr is
used to confirm it.\n\n
***DM Neuropathy
seen in 50% of pts. Pt manifest with
poplyneuopathy,mononeuropathy or Autonomic Neuropathy. AN is related to the
duration of disease and glycemic control. Any part of GIT can be affected.\n\n
**Involvement of small intestine
causes diarrhea, and Colon causes constipation, and
stomach causes gastroparesis which presents as nausea, vomit, bloating, anorexia,
and early satiety. Due to delayes gastric emptying, glucose control is difficult to
achieve. Pt have post meal hypoglycemia after insulin injection. \n\n
Nuclear Medicine Scintigraphy
after ingestion of radio-labeled food is the best method to document
Delayed gastric Emptying. Management includes:1-improved glycemic control, 2-
small,frequent meals, 3-Dopamine agonist(Metachlopromide,domperidone) before
meals, 4-Bthanechol, 5-Erythromycin (reaction with Motilin promotes emptying), 6-
Cisapride. \n\n
*****The most beneficial therapy
to reduce progrssion of DN in presence
of renal insufficiency is to control HT. \n\n
*****Nonketotic Hyperosmolar synd occurs
in DM2 pt because level of insulin in these pt is enough to prevent ketoacidosis but
not hyperglycemia. Hyperglycemia occurs, with hyperglycosurea and dehydration.
They will present with semicomatose state. So first thing you do is to check blood
glucose.\n\n
*****Diabetes screening
in pregnant women is performed b/2 24-28 weeks
of gestation. If urine dipstick reveals glycosuria then the next step is Fasting Urine
samples if its positive then do a 1hr-50g oral glucose tolerant test. If its <140, DM is
rules out. If its >140, 3hr-100gr OGTT is used for confimation.\n\n
****Diabetic Neuropathy
can present with ulcer in the foot. Risk factors for development of diabetic foot ulcer are: Diabetic Neuropathy, peripheral vascular dis, poor glycemic control, bony abnormalities of the foot, male sex, smoking, chronic DM (>10ys), and a hx of previous ulcer or amputation.\n\n
** Neuropathy
is found in 80% of diabetics with foot ulcer.****Symetrical distal sensorimotor polyneuropathy is the mc type of diabetic neuropathy. Characterized by "stocking glove" pattern or sensory loss.\n\n
****DM
is a risk factor for Non alcoholic fatty stetosis \n\n
*****Hyperglycemic, hyperosmolar, non-ketioc coma
is characterized by very high blood glucose, plasma hyperosmolarity, normal aion gap and negative serum ketones.\n\n
*** DDX:
DKA is
sugested by 1-blood glucose >250, 2-pH<7.3, 3-Bicarbonate<15-20,4-Plasma
ketones.\n\n
***DDX2
Alcoholic Ketoacidosis is ketoacidosis with increased anion gap BUT
near normal glucose levels. \n\n
****Always consider candida albicans
as a casue of
infection in a pt with uncontrolled DM.\n\n
****Diabetic mothers babies
are often born
with clavicle fracture that heals spontaneouly w/o any tx.***The Dx procedure of
choice for Diabetic Polyneuropathy is Electromyography and conduction studies.\n\n
****Poorly controled pt with low grade fever,
bloody nasal discharge,nasal congestion,involvement of the eye and chemosis ,proptosis and diplopia is more likely suffering from Mucor Mycosis and maxillary sinus due to Rhizopus. \n\n
**Involved turbinates
usually become necrotic. DDX is Pseudomona which causes Malignant Otitis Externa, it my also cause black necrotic lesions. \n\n
***DDX
also H.inf and Moraxella are the mcc of bacteria sinusitis, they dont cause NECROTIC infections\n\n
*****Non-ketoic Hyperosmolar coma
presents with gllucose 1000, and
normal pH. Tx is normal saline initially and then replaces with 0.45% saline. Once
glucose is down to 250, then we give 5% dextrose that prevents cerebral edema.\n\n
**** Diabetic Cystopathy
usually secondary to diabetic autonomic neuropathy. It
begins with inability to sense s full bladder & failure to void completely. With time
bladder size increase leading to signs of BPH & recurrent UTI. \n\n
***Dx
is made with
Cystometry and Urodynamic studies. Initial mgmnt is strict voluntary urinary
scheduling couplded with Bethanechol. If there is no response intermittent
catheterization is recommended. \n\n
****Emphysematous Pyelonephritis
: is a life
threatening condition caused by E. Coli. Dx is confirmed by CT. TX is IV antibiotics
and possible Emergency Nephrectomy.\n\n
Diamond Blackfan Anemia:
Also called "congenital hypoplastic anemia". Suspect it in a child with macrocytic
anemia, low reticulocyte count and congenital anomalies. Primary path is an
intrinsic defect of erythroid progenitor cells which results in increased apaptosis.\n\n
** Over 90% are dx
w/I the first year of life. Macrocytic anemia is distinct from
megaloblastic anemia because hay no hypersegmentation of the nucleus in
neutrophils. Pt presents with anemia, short stature, webbed neck, shielded chest,
triphalangial thumbs. Tx is mainly corticosteriods, if unresponsive then transfusion
therapy.\n\n
Diaphragmatic Herniation
Occurs in accidents and Cxr sign of elevated left diaphragm could be the only
sign.*****One dx often missed in er is traumatic rupture of the diaphragm. Usually
on the left side. Pt comes back months later with breathing difficulty. \n\n
***Dx
Cxr shows
deviated mediastinum with a mass in the left lower chest. Barium Swallow is dx. In
acute cases surgery is done via abdomen and in chronic cases via chest.\n\n
Diarhhea - 6
Campylobacer Jejuni is the mcc of bloody diarrhea in US. Its from undercoocked
pultery****Vibria Parahemolyticus:by ingestion of sea food. \n\n
*** Bloody diarrhea,
abdomnal cramps,nasea and feve. Incubation 12-24hrs. Shigela diarrhea occurs in day care and institutional settings. Yersinia diarrhea is by eating
undercooked pork.\n\n
Campylobacter is the mcc
of diarrhea in US due to uncooked
infected poultry. could be watery or hemorrhagic. \n\n
***Staph causes toxin induced
gastroenteritis mostly emetic type that starts w/i 6 hours.Salad,meat and
egg.\n\n
***Travelers diarrhea,
due to E Coli, is the cause of diarrhea w/i
blood,mucus,explosive,rice watery diarrhea even in Mexico travelers. \n\n
DDX
Giardia
is endemic in Nepal. \n\n
***MCC of diarrhea in children is
Roto virus that causes acute
gastroenteritis.Most causes are self limiting but maintain hydration Ther is now a
vacine for it but it was withdrawn due to risk of Intussusseption \n\n
*****Types of
diarrhea are:
1-Inflamatory, where ESR is elevated and there is anemia and blood
positive stool. 2-Osmotic, caused by meds or hormonal disturbance. 3-Motor,
exemplified by Hyperthyroidism. 4-Factitial, is psychologic.\n\n
DIC:
Tx is FFP if pt is bleeding only. If pt is not bleeding and has sepsis (high T and low
BP) first step is IV antibiotics plus Activated Protein C.\n\n
Diffuse Esophageal Spasm - 2
Manifest with chest pain and dysphagia. Etiology in unknown but its related to
emotional stress. Unlike Achalasia LES has a normal relaxation response.
Esophagogram might show Corkscrew. \n\n
*** Tx
is with antispasmic drugs, dietry
modulation and psychiatric counselling. for USMLE know 1-pathophys, 2-present
or absence of perstalsis, 3-LES tone. \n\n
***MERCK:
A generalized neurogenic disorder of
esophageal motility in which phasic nonpropulsive contractions replace normal
peristalsis and, in some cases, lower esophageal sphincter malfunctions occur.\n\n
***Esophageal manometry shows
contractions are usually simultaneous, prolonged or
multiphasic, and possibly of very high amplitude.\n\n
*****Esophagography may not
show the corkscrew, so do Manumetry, if revealed "repetitive,nonpeistoltis,high
amplitude contraction either spontaneoud or after Ergonovin stimulation then its
Dx.\n\n
Di-George synd:
Infants have cyanotic heart dis, cranofacial anomalies, thymic dysplasia, cognitive
impairment and hypoparathyroidism. Asso with Ch 22/11 deletion. In Surgery keep
an eye on Ca levels.\n\n
Digitalis Toxicity - 2
Some of the toxicities occur in therapeutic range (AV block, ST depression, T
inversion) and there is no need to discountinue the drug. Some occur in Toxic serum
levels (Atrial Tachycardia and AV heart block) and we need to discountinue the
drug. Digoxin also causes Nasea and Anorexia.\n\n
Diphenhydramine Toxicity
Prduces seizure as well as anti-cholinergic effects.\n\n
Dipyridamole
used during myocardial perfusion scaning to reveal areas of restricted myocardial
perfussion. It shows "Coronary steal phenom"\n\n
Disk Herniation
Once you know its DH and straight leg is positive, then NSAID and early
mobilization s the tx of choice.\n\n
Displacement - 2
An immature defense mechanism, in which individual displaces negative feelings
asso with unacceptable situation onto a safer one.\n\n
Disseminated GonoCoc infx
Persents in menturating women with tampon, many partners, occasional condom,
presents with high fever, rash, tenosynovitis and migratory arthralgia. DDX with
TSS which presents with Fever, macular erythema of palms and soles,, vomit and
diarrhea nad hypotension.\n\n
Dissociative Fugue
Pt get lost in another city.\n\n
Diverticulitis - 2
the dx test to evaluate the abdomen during an acute episode of diverticulitis is a CT
scan. Colonoscopy and Sigmoidoscopy can cause perforation.\n\n
*****Acute
diverticulitis complication
may be bowel perforation where xray shows air under
diaphragm and rigidity and guarding. Next step is Laparotomy with surgical
resection of perforated bowel and proximal colostomy.\n\n
Diverticulosis.
Pseudodiverticulum can erod a penetratinf atrery. This leads to perfuse arterial
bleeding of bright red blood. Diverticulosis is the mcc of bleeding in elderly pt.\n\n
** Chronic constipation
is the single most predisposing factor to develop Diverticulosis. Normal xray does not rule out diverticulosis if its negative. You need xray with contrast ( Barium ) to be able ro see it. \n\n
***DDX1:
Colon Cancer, presetns with
chronic,occult bleeding NOT BRIGHT RED. DDX2:Ischemic Colitis, Asso with
Abdominla pain, feverand vomit and atherosclerosis, xray shows thickening of colon
wall. DDX3:Mesenteric Thrombosis, Pain out of proportion is a classical symptom,
Bloddy diarrhea rather than bright red blood is charcteristic, Bowel sounds are
diminished.\n\n
Down Synd in Pregnancy
T14Q12 explains how to test for DS in older women. Decreased MSAFP and Estriol
and Increased B-HCG is the best test. SEE FIRASR AID.. Know heart defect, and
also that they have Duedenal atresia. Learn this.\n\n
***** Hay ASD
and endocardial
cushin defects.\n\n

*****Duodenal Atresia ?? is the mc anomaly asso with Down, in xray
you see a double bubble sign. Other anomalies are Hirshsprung, Esophageal atresia,
Pyloric stenosis, malrotation. \n\n
***Congenital heart disease is
the mcc of death in
childhood, like endocardial cushin defect, VSD, PDA.\n\n
Dressler Syndrome:
It's a post MI Pericarditis. Non specific ST elevation. NSAID is tx of choice.\n\n
Drug induced Pancreatitis
1-Diuretics, furesamide and thiazide. 2-IBD, Sulphasalazine and 5-ASA. 3-
Immunosupresants, azathioprine. 4-Seizures, Valprioc acid. 5-AIDS, Didanosine,
Pentamidine. 6-Antibiotics, Metronidaole, tetracycline. CT is dx with inflamed
pancrease. Tx supportive.\n\n
Drug induces Interest Nephritis - 2
Caused by Cephalosporins, Penicillins, Sulfa drugs, NSAID, Rifampin, Phenytoin
and Allopurinole. Pt presents with Acute renal failure+Arthralgia+rash.\n\n

*** 70% of
cases are induced by drugs ?? , discountinue the drug and it will be OK. Pt present with
fever, and urine analysis shows RBC, WBC and white cell casts, eosinophelia and
proteinuria.\n\n
Drugs CI
1-Beta blockers: peripheral vascular dis (pt presents with worsening intermittant
claudication), asthma, copd, Raynaus. 2-ACE inhibitors: Hyperkalemia, pregnancy.
3-Calcium channel blockers:Second&thrid degree heart block and CHF.\n\n
Dubin-Johnson
A familial disorder of hepatic bile secretion. Leads to conjugated
Hyperbilirubinemia. May be aggrevated by women taking OCP. Liver biopsy
reveals cells with DARK granular pigments. DDX1:Rotor, like DJ but no DARK
granule pigments.\n\n
Duchenes MD
Muscle biopsy will reveal dx.\n\n
Dumping Synd
Is a common post-gasterectomy complication. Pt with recent Gasterectomy presents
with postprandial abdominal cramps, lightheadedness, diaphoresis. \n\n
First thing to do
is to Modify diet, small frequent meals and avoid simple CHO. Dx is made clinically
but occasionaly Contrast xray (barium swallow) is used.\n\n
Duedenal Atresia:
Bilous vomiyying few hous after the FIRST eating, usually asso with congenital
anomalites and Down's Synd.\n\n
Duodenal Hematoma, isolated
If pt is hemodynamically stable, she needs nasogastric succion and parenteral
nutrition (food ) not IV fluid.\n\n
Duedenal Injury:
Isolated duodenal injury is easily missed. They occurin accidents due to the belt or
steering wheel. Present with epigastric or RUQ pain. Retroperitoneal air or
obliteration of right psoas margin on xray is very suggestive. \n\n
***Best dx
with CT scan
of the abdomen with oral contrast or an upper GI study with gastrograffin, followed
by barium if necessary.\n\n
DVT - 3
OCP is a well known risk factor for DVT. TX steps:Anticoag therapy has serious
Ses so accurate dx must be made before anticoag is started. Test of choice for DVT
is Compression US. Impedence Plethysmography is for recurrent DVT. Venography
is the Gold standard for dx of DVT, but it causes discomfort so its not the initial test
for suspected DVT. Its only done when other tests are impossible or
inclusive.\n\n
***Surgical pts can be categorized
according to their risk of DVT. 1-Low
risk, Minor surgery in a pt <40 with no additional risk factors. w/o prophylaxis risk
for DVT is <2%. 2-Moderate risk, Pt>40, one or more addiiotnal risk, minor/nonminor
surgery, risk is 2-10%. 3-Hihg risk, pt is >40, additional risk factors, major
operation, risk of DVT is 10-20%.\n\n
**In Low risk pt,
prophylaxis other than early
mobilization is not recommended. In Moderate risk pt, LMWHeparin or
Unfractionted Heparin is recommended. Pts in whom bleeding risk are
unacceptable (intracranial.spinal cord injury) should receive intermittant
pneumatic compression. \n\n
***In High risk pt,
undergoing general surgery can be given
LMWH, those pts going under Orthopedic surgery of lower extremity (knee
replacemnt) LMWH or Oral Warfarin.\n\n
***INR (International Normalized ratio)
is
used to monitor tx response to Warfarin. Therapeutic Range of INR for most pts is
2-3, which is for venous thromboembolism, valvular heart dis. 3-4.5 is for Proshtetic
valves.\n\n
*****The best DVT
prophylaxis for high risk surgery ptgoing under
orthopedic surgery includes either warfarin or LMWH.\n\n
Dysfuncx Uterine Bleeding- 2
Heavy unremiting endometrial hemorhage throught menarche and perimenopause
requires Estrogen (conjugated) to supress the bleeding to ensure CV stability. Once
that is achieved D&C should be performed. \n\n
***The MCC
of DUB in adulescent is anovulation. Therefore endometrial biopsy is not required in these pts. Once bleeding is stopped , advise pt to take the following: conjugated estrogen for 25 days
, then add methoxyprogestrone for the last 10-15 days and then allow 5-7 days for
withdrawl bleeding to mimic menstural cycle.\n\n
****In which pts
with CUB do you
perform endometrail biopsy to rule out endometrial carcinoma? When a pt is >35,
obese, DM or has chronic HT.\n\n
Dysthymia
Depressed mode for more than twoyears.\n\n
Dystonia
from antipsychotics, tx is Benztopine or Diphenhydramine.\n\n
Eaten Lambert
Is asso with small cell carcinoma. And antibodies against the voltage gated calcium
channels in presynaptic motor nerve terminal. It is presynaptic, resulting from
impaired release of acetylcholine from nerve terminals.\n\n
***The diagnosis is confirmed
by finding an incremental response to repetitive nerve stimulation: Amplitude of the
compound muscle action potential increases > 200% at rates > 10 Hz. \n\n
**Treatment
is
first directed at the underlying malignancy and sometimes induces remission.
Guanidine facilitates acetylcholine release.\n\n
Eating disorder not otherwise sp
If the senario shares features of both bulemia and anorexia, its this disorder.\n\n
Echinococcus
Due to close cntct with SHEEP. Pt presents with hepatomegally, forms hydatid cyst
in liver after US. Hydatid cyst has an inner germinal layer and an outer acellular
laminated membrane. DDX is Neurocysticercosis, due to PIG farming. With cysts in
Brain, kills fast.\n\n
Eczema Herpeticum
T9Q23. A form of Herpes simplex that is asso with atopic dermatitis. Numeric
umbilicated vesicles around The healing area is typical. In infants tis could be life
threating, start acyclovir asap.\n\n
Edward synd - 2
Microcephaly, prominent occiput, micrognathia, closed fists, index finger overlaping
3-4-5 bilaterllay, rocker bottom feet. 95% die by first year.*** Pts have hear mumur
due to VSD. This is trisomy-18 (E-lection age)\n\n
EKG abnormalities
1-T wave inversion, in ischemia of myocardium. 2-ST depression, subendocardial
infarcts and unstable angina. 3-Ptoonged PR, first degree heart block. 4-Delta
waves, WPW. 5-New RBBB, seen in PE. 6-Electrical Alterns, seen in pericardial
Temponade.\n\n
Embolus, limb
If pt presents with cold hand due to embolus, immediate antocoag with heparin and
surgcal intervention is indicated.\n\n
Emphysema
In a non smoker should raise the suspicion to Alpha-1 anti trypsin def. Its also asso
with Neonatal Jaundice in the hx of the pt. Dx is made by estimating alpha-1 trypsin
levels.\n\n
Emphysematous Cholecystitis:
Is a common form of acute Cholecystitis in elderly diabetic males. It arises due to
infection of the gallbladder wall with gas forming bacteria. Dx is confirmed with
abdominal xray showing air-fluid level in the gall bladder or US showing gas line.\n\n
**Lab
shows moderate unconjugated hyperbillirubinemia or small elevation of
aminotransferases. Tx includes early fluid resuscitation, early cholecystectomy, and
parenteral antibiotic therapy effective aginast gram positive Anaerobic Clostridium
sp. (Ampicillin- Sulbactam, or combination of aminoglycoside or quinolone with
clindamycin or metronidazole.\n\n
Empyema
Can occur from parapneumonic effusions(In parapneumonic effusions, the visceral
pleura overlying a pneumonia becomes inflamed; often, an outpouring of serous
exudative fluid accompanies acute pleurisy. \n\n
**The fluid contains many neutrophils
and may contain bacteria. Parapneumonic effusions are usually caused by bacteria.
If the body's defenses do not control infection in a patient with pneumonia and
parapneumonic effusion, the number of neutrophils and bacteria increases, and the
fluid takes on the gross appearance of pus. \n\n
***The result is empyema of the thorax
(purulent exudate in the pleural space). Fluids with > 100,000 neutrophils/μL,
bacteria seen on Gram stain, and pH < 7.2 may be presumed to be empyema). \n\n
**H/P
Pt presents with low gade fever, dyspnea and chest pain. Dx with CT. When its
localized, complex and has a thick rim best tx is surgery to remove the clotted blood.
Endometria hyperplasia. \n\n
Endometriosis - 4
Pt presnts with painful periods. Bimanual exam shown a few firm nodularities in
pouch of douglas.The first line of tx is OCP. They cause a state of pseudopregnancy
and causing an "exhaustion atrohpy" of the endometriomas. \n\n
**If OCP fails
or not
tolerated then we give Danazole, its an androgen deivative that causes
Pseudomenopause state. SE are acne,hirsutism deep voice.\n\n
***GnRh agonists
have an
inhibitory action of LH & FSHwhen given continuslywhich produces temporary
castration. Its also a 2nd line of choice. \n\n
****Typically pt prestns with
Dysmenorrhea, Dysparunea(when endometriomas is in cule-de-sac), Dyschezia(Pain
on defecation), hematochezia, hematuira, and pre post menstrual spotting.
Laparoscopy is GOLD standard which shows powder burns. The hemorrhage of
endometriomas into the ovaries results in formation of cystic cavity filled with blood
with dark color, hence the name 'Chocolate cyst'.\n\n
...
****The '3Ds'
are Dyspareunia,
Dysmenorrhea and Dyschezia (defecation pain).\n\n
** Tx
is OCP. DDX1:Vaginismus, use Vaginal dialators. DDX2:Pain disorder, pain in one or more anatomical sitetxis pain managment training.\n\n
**DDX3:
Somatization disorder, tx is follow up visitsregularly
scheduled. *****Endometriosis is the location of tissue outside uterine cavity so
hysterosalpingogram cant see it.\n\n
Endometritis:
It usually occurs on 2nd-3rd day postpartum. Predisposing risk factors are
prolonged labor, prolonged and premature rupture of the membrane, manual
removal of placenta, and repeated pelvic exam. \n\n
***H/p
Clinically it presents with fever,
uterine tenderness and foul smelling luchia. Antibiotic start asap to conver both
aerobic and anaerobic. Clindamycin with aminoglycoside or ampicillin. MC
pathogen is anaerobics.\n\n
End stage lung dis:
PFT is the best test to to determine if the pt can benefit from lung resection surgery.
Predicted postoperative FEV1 is very useful for this. Blood tests don't reveal any
good info in this regard, they're more useful in determining the level of respiratory
compromise and appropriate ventilator settings for pts undergoing lung resection
surgery. \n\n
*** Results
of split function quantitative lung scans and exercise testing are
useful in pts in whom the potential benefit is doubtful even after determining the
results of the predicted postoperative FEV1.\n\n
Enterobius Vermicularis.
Or Pin worm is the MC helminthic infection in US. Most commonly seeb in school
children 5-10. Larva goes to perineal area to lay eggs, which gives characteristic
Nocturnal perianal pruritis. Dx is made by "Scotch tape test". Albendazole or
Mebendazol is the first line of tx. Pyrantel Palmate is an alternative.\n\n
Enuresis - 2
Tx is low doses of Imipraimne or desmopressin.***It should go away begore school
age. The first step is reassurance. Then wet alarms and walking the child to bath
room is tried. If persiss, then Desmopressin (ADH) is first line, Imipramine is the
2ns line tx. ****Its important to rule out treatable causes like UTI. The initial
evaluation is urine analysis.\n\n
Epididymitis, Acute
Wat\n\n
Epidemiology:
Mean is average, Mode is the number repeated mostly, Median is the number in the
middle given by vigniette, don't put them in order treat it as is. Reliable test is one
that gives similar results repeatedly. Accurate is when the results are on the
target.**** Sensitivity curve movements and its effect on PPV.\n\n
Epiglotitis - 3
MC by H. inf and 2nd mc by Strep. Tx is antibiotics, antipyretic, racemic
epinephrine, steriods and immediate intubation. Dx is by Fiberoptic Laryngoscopy
in the operating room, once its made then nasotracheal intubation secures the
airway. If intubation is CI then Emergency Tracheostomy is performd.. *****you
dont need epinephine before intubation, intubation is the first thing to do here.\n\n
Erectile Dysfunction
Types are 1-Neurogenic:A pelvic fracture with an urethral injury is usually
accompanied with ED. The cause is nerve injury and altered blood supply. 2-
Venogenic:After penile fracture and disruption of tunica albuginea. 3-
Endocrinologic:Prolactinoma. 4-Systemic:DM can cause Ed through many systems
(neuro, vascular). 5-Situational:Psychogenic, where night and morning eection is
preserved.****If pt is taking Nitrate drugs, Sildenafil is CI so the next step is Penile
prosthesis devices or Vaccum devices.\n\n
Erysipelas
Is a specific type of cellulitis in which there is superficial inflamation of epidermis
producing prominent swelling. The characteristic finding is a sharply demarcaded ,
erythomatous, edematous tender skin lesion with raised borders. Onset is abrupt
with systemic signs. Group A strep is the mcc. Penicillin V or erythromycin 500 mg
po qid should be given for >= 2 wk. See pic on desktop.\n\n
Erythema Multiform. Dermo. 6/3
Onset is usually sudden, with erythematous macules, papules, wheals, vesicles, and
sometimes bullae appearing mainly on the distal portion of the extremities (palms,
soles) and on the face. The skin lesions (target or iris lesions) are symmetric in
distribution and often annular. Stevens-Johnson syndrome is a severe form.\n\n
*** EM
Usually folows infection with Herpes Simplex. Erythema multiforme associated with
mycoplasmal pneumonia should be treated with tetracycline. If frequent or severe
erythema multiforme is preceded by herpes simplex, acyclovir. \n\n
Erythema Nodosum
Pink to redish painful subcuataneous nodules that usually develop in pretibial
region. Most often in woman 15-40. Lesion resolve w/o scaring w/I 2-6 weeks.
Histologically there is paniculitis involving inflamation of septa in the subcutaneous
fat tissue. There are other conditions that could cause EN, like TB and Sarcoidosis.\n\n
*** So the initial work up
is include Antistreptolysin O (ASO) titer, a TB test and chest
CXr. Its also asso with IBD. Sarcoidosis pt often presents with EN as an initial
symptom, cxr will show bilateral hilar adenopathy.\n\n
*** An inflammatory disease
of the
deep dermis and subcutaneous fat (panniculitis) characterized by tender red
nodules, predominantly in the pretibial region but occasionally involving the arms
or other areas. Bed rest helps to relieve painful nodules. If an underlying
streptococcal infection is suspected, antibiotic therapy is beneficial (eg, penicillin for
>= 1 yr). \n\n
Erythema Toxicum
Is a benign self imited condition in newbors characterized by rash with red haloes,
and eosinophils in sin lesions. Neonate presents with No fever, no infectious risk
factoe, looks healthy, with erythematous papules and vesicles surrounded by pathes
of erythema.\n\n
Esophageal Atresia:
It's the mc esophageal anomaly w esophagotracheal fistula. It leads to gastric
distention. It results in drooling and regurgitation due to incomplete esophagus. In
addition food gets into trachea and lungs and cuses aspiration pneumonia. Inability
to pass tube is suggestive.\n\n
Esophageal cancer - 2
It mimics Achalasia. Short hx , rapid weight loss, and inability to pass
esophaguscope isindicative of cancer. The next step is biopsy. Ofcourse BS followed
by endoscopy should be done first.\n\n
Esophageal Varices, Acute - 2
Variceal bleeding is a life threatning emergency. FIRST step is fluid replacement
with two large bore IV needles followed by fluid resucitation. SECOND step is
control of bleeding medically with vasoconstrictors (Octreotide, somatostatin).\n\n
***THIRd step
is Endoscopic Sclerotherapy or Band Ligation (which is better due to
less SE). If endoscopic therapy is not available then Baloon temponade with S-B
tube is done. If all this fails then surgery is indicated (TIPS). \n\n
****In case of EV,
need for 5 or more units os blood transfusion in a period of 24 hours is considered
an indication for surgery and Transjugular Intrahepatic Portosystemic Shunt.\n\n
** Remember both ligation
andmeso-caval shunt have high mortality rate in ER
setting, TIPS has less mortality rate.*****Varices are submucosal veins dilated due
to portal HT.\n\n
Estrogen Replacement Therapy:
Affects metabolism of thyroid hormones. The requirement for L-Thyroxine
increases, although the exact mechanism not known it could be due to induction of
liver enzymes, increased level of TBG. In pregnancy also thyroid hormon
requirement will be increased and the pt should be monitored for dose adjustment.\n\n
Essential Tremors - 3
DOC is Beta blockers.***Another drug is Primidone, Its SE is Acute Intermittent
Porphyria (Abdominal pain, neurologic and psychologic abnormalities, it can be dx
by urine prophobillinogen. ****Propranalol is the DOC for pts with benign
essential tremors + HT.****Its famililal, its worse with action and resolved at rest.
Rule out Thyroid problem before starting therapy.\n\n
Ethyline alcohol poisoning
Presents with anion gap metabolic acidosis with Rectangular envlope shaped
crystals (calcium oxalat).\n\n
Eustachian tube dysfunction
Is a common cause of conducting hearing loss in children. Aurul fulness, pop when
swallow, hearing loss, intermittant ear pain. Usually following URT infection or
allergic rhinitis. Retraction and decreased mobility of tympanic membrane.
Hallmark is a middle ear effusion. \n\n
***"Acute Otitis media":
Otalgia, hearing loss, fever
and dysequilibrium, bulging membrane. "Serous otitis media": Due to prolonged
blockage of auditory tube, common in children, membrane is hypomobile and dull,
air bubbles in the middle ear. \n\n
**"Otitis externa":
Purulent dischatge, common in
swimmers, pain with tenderness is the hallmark. "Foreign body in children": Foulsmelling
discharge and signs of infection.\n\n
Ewing sarcoma
Highly malignant tumor of lower exremities in children. With early metastasis.
Presentation is pain and swelling for weeks. Oftern confused with Osteomyelitis due
to intermittent fever, leukocytosis, anemia, elevated ESR. \n\n
**CXr
shows "ONION SKINING" peroosteal retraction. Lesion is Lytic and central. Onion skin is followedby 'moth eaten' appearance. Tx includes surgery , radiation, and multiple
drug chemo. \n\n
** DDX
is Osteomyelitis:Pt presnts with feve, malaise, local pain in joints
and swelling. Xray in chronic osteomyelitis shows Lytic bone defect with surounding
sclerosis termed as "Brodie's Abscess".\n\n
ExtraPyramidal Synd (EPS)
Is seen as SE of antipsychotics (Risperidone). 1-Tardive dyskinesia, lip smacking,
tongue protrusions, chewing,biting. It occurs b/w 4mo-4ys.\n\n
*** Tx
is discontinue Risperidone and give Clozapine. 2-Akathesia is the feeling of restlessness, beta blocker gives some releif. 3-Dystonia, occurs b/w 4h-4d, there is muscle spasm, stiffness, twisting, opisthotonus. Antihistamine (diphenhydramine) or
Anticholinergic (Benztropine) releif.\n\n
Factitious diarrhea
Laxative abuse, profuse diarrhea. 10-20 times a day. DDX with IBS diarrhea is that
IBS does not happen nocturnaly but factitious does. \n\n
**FD
is usually done by women of
high socioeconomic status and Nurses. There is also characteristic dark brown
discoloration of the colon with lymph folicles shining through as pale patches that
confirms the dx.\n\n
False Labor
Characterized by painless and irregular contractions for 5hrs or more. In the last
month these contractino may become rhythmic occuring every 10-20 minutes
mimicking contraction of real labor. The main characteristic is however they are
not accompanied with progressive cervical changes, so cervix is closed shut. All the
pt needs is reassurance.\n\n
Familial Colonic Polyposis
Pt hace 100% risk of colon caner, so when they are dx (colonoscopy reveals 100s
polyps), then then next step is elective proctocolectomy.\n\n
Fanconi's Anemia:
An auto recessive dis, progressive pancytopenia and macrocytosis. Deformities
include, café au lait spots, microcephaly, micropthalmia, short staure, horseshoe
kidneys and ABSENT thumb. Dx agerage age is 8 YO\n\n
Fantacy Defense Mechanism
An immature defense mechanism, that does not exist in the real world, like an angel
telling you things are gonna be OK.\n\n
Fat embolism
Dyspnea, confusion and petechia in the upper part of the body, After multiple
fractures of long bones. Tx should include prompt respiratory support. Use of
heparin, steriods is controversial.\n\n
Fat Necrosis
Biopsy shows foamy macrophages and fat globules. Coarse calcification is indicative
of benign, and microcalcification indication of malignant tumors. FN is asso with hx
of surgery or trauma and it mimics breast cancer.Exisional biopsy is dx and no tx is
needed and standard follow up and mamogram is sufficient.\n\n
Febrile Neuropenia - 2
A neutropenic pt with sustained fever of >100.4 for one hour. Its an emergency,
admit to hospital and obtain blood cultures and IV Cefepime, or Ceftazidime, or
Imipenem. Vancomycin is added IF pt is hypotensive, evidence of skin or line
infection, Hx of resistant to S. Aureus or pneumococcus, or recent prophylaxis with
flouroquinolones.\n\n
Femor Shaft fractures
Most can be managed with closed intra medulary fixation of the shaft. This allows
for early mobilization improved hip and knee function and less hospital cost. I this
technique, closed reduction of fracture segment is followed by inrta medullary nail
insertion through small skin insertion over the greater trochaner.Closed nailing is
preferedover OPEN nailing due to reduce risk of infection. Internal fixation with
plates and screws are used in NECK fractures of femur.\n\n
*****Interochanteric fracture of the femur is mostly
an extracapsular fracture in elderly. Occurs along the line b/w greater and lesser trochanter, Extremity is shortended and internally or externally rotated. \n\n
**Dx
is xray. Operative tx is indicared asa pt is stabilized. Do
internal fixation with sliding screw with plate and early mobilization.\n\n
Femoral Neck Fractures
They are seen in Elderly. The limb is shortended and rotated and painful with
limited motion. Unstable fractures (complete neck fractures), need Open reductionb
and internal fxation or Primary Athroplasty(surgical reconstruction of the joint) as
soon as pt is stabalized. If surgery is CI the pt should be mobilized asap and
eventual malunion can be dealt with later.\n\n
Fetal Alcohol Synd - 2
Irritability, mild to moderate mental retardation, hpoplastic maxilla, lng philtrum,
thin upper lip border and microcephaly, and epicanthal folds.\n\n
Fetal Demise - 6/24/06
if pt comes to you due to not feeling any mvemnt and you cant hear any beats with
Doppler, then the first thing to do is to do a Real Time Sonogram.. It's the most
appropriate test to confirm fetal demise. BhCG might be lower but it doesn't make
it a dx tool.\n\n
Fetal Distress Repetative Late Decelerations
Is an indication for C-section. Remember Tocolysis means not delivering.\n\n
Fetal Hydantoin Synd. - 2
Caused by using Phenytoin in pregnancy due to seizure. Infants presents with small
size, microcephaly, hypoplasia of distal phalanx of fingers and toes, nail hypoplasia,
low nasal bridge, cleft rib and rib abnormality and cardiac mmurmur. Its also asso
with Neuroblastoma. Karytype and TORCH should be measured.\n\n
***Diphenylhydantoin (phenytoin)
is metabolized to Epoxide Metabolite,
which is eliminated inturn by enzyme Epoxide Hydroxylase. The genetic expression
of EH is different from one subject to other and its substrate EMis the agent
incriminated in the syndrome.\n\n
Fever, Post operative:
Fever after the first day is due to Atelectasis. Pt might have pain at the incision and
not take deep breaths causing atelectasis. Fever 3-5 days post surgery is due to UTI.
Fever 3-7 days post surgery may be due to Pulmonary Embolism. \n\n
*** H/P
Pt is Tachypnea,tachycardia and Hypoxia. Dx requires Duplex US to look for clots in extremities. Eventhough pt are given anticoags, 200,000/y die of PE. Fever one to two months post durgery is due to post spleenectomy sepsis. All pt are given
Pneumococcal vaccine after surgery to prevent this. \n\n
*** H/P
Fever due to Pneumonia can
occur 3-6 days post surgery. Pts are most likely, smokers,obese, elderly and fail to
ambulate. Pt will have sputum and leukocytosis. Fever due to wound infection is 4-7
days post surgery. Redness, pain and induration.\n\n
Fibroadenoma:
1x1 cm firm rubbery freely mobile round mass in a 35 yo women w/o axillary nodes
palpable. Best initial step is Mamogram.\n\n
Fibrocystic Dis of Breast
A 4x5x6 cm moveable rubbery mass that will go away after poking the needle and
secretion of clear discharges. The best approach after aspiration of fuid is to wait 4-
6 weks . In FCD the mass goes away and doesn't come back. It it recure or doesn't
go away, then a biopsy is indicated. If the fluid (initially) was bloody or foul
smelling, cytology is needed at that stage.\n\n
Fibroid uterus
Presents with Dysmenorrhea, heavy menses, and enlarge uterus is almost dx of
either Adenomyosis or FU. Submucosal fibroids often imterefre with rmbryonal
implantation and infertility. Fibroids are the mc benign uterin tmors in women and
the mc indication for hysterectmy. \n\n
*** note
Tey are estrogen-dependent tumors, therefore
they increase in csize with OCP and pregnancy. and often regress after menopause.
DDX is Endometriosis which presents with Amenorrhea. Make sure you can DDx
the above conditions with Adenomyosis.\n\n
Fibromuscular Dysplasia - 2
Is the mcc of 2ary HT in childern. It responsible for 20% of the cases of renal HT.
Its also seen in premenopausal women. PE shows a hum or bruit (soft to-and-fro
bruit) in the right costovertebral angle due to well developed collaterals. The right
renal artery is more affected than the left. Angiography shows 'string of beads '
pattern in the renal artery \n\n
****Pt presents with Occipital HA, HT and renal bruit,
suggestive of renovasculat HT due to Renal Artery Stenosis. The usual cause in
youner pt (30) is FMD. In older pt its atheroslcerotic plaques. Goal of tx is decrease
BP and restore perfusion to kidneys. Interventanl therapy is better than medical
mgmnt alone, so Angioplasty with stent replacemnt is best tx. \n\n
...
***If it fails
then Surgery
is indicated. Ace inhibitors are reserved for Elderly pts who are not good candidate
for surgery. Remmber Ace inbitors are CI in bilateral renal stenosis.\n\n
Fibromyalgia- 4. Rheumo 6/3
Occurs mainly in females and may be induced or intensified by physical or mental
stress, poor sleep, trauma, or exposure to dampness or cold .Pt presents with diffuse
musculoskeletal pain, multiple tender points, with no joint swelling/pain. Initial
work up is 1-CBC, 2-ESR, 3-TFT, and 4-CK enzyme. \n\n
***Normal spine movement
makes "Ankylosing Spodylitis" unlikely. Normal ESR with pain rather than
stiffness makes "Polymyalgia Rheumatica" unlikely. "Polymyocytis", usually
presents with weakness rather than diffuse pain and increased CK.\n\n
***Characterized by muskuloskeletal PAIN and presents of 11-18 tender points. Pt prsents with recurrent HA, IBS, Reynauds, The most importnat ddx of this diseases is masked depression and somatoform disorder. \n\n
...
Tx
is excercise & Antidepresssants.****DDX1:Chronic Fatigue Synd: pt prestns with extreme fatigue and not body aches. It must be there for 6mo.
\n\n
***DDX2
:Polymyalgia
Rehumatica:Pain and stiffness of shoulder and pelvic. Very unlikely in pt <50yo.
ESR is elevated. Complain of stiffness rather than weakness or pain. Asso with
fever,weight loss and HA.\n\n
** DD3:
Polymyositis:Proximal weakness of muscle in upper
and lower extremity. Pt complains of difficulty raising from chair position or
climbing stairs. No pain just weakness\n\n
***** Fibromyalgia
is not an inflmatory
disease so NSAISs like Naproxen & steroids are not helpful. Tricyclic antidepressant
like Amitriptine are tx at bedtime. For daytime pain use acetaminophen. You can
also use Cyclobenzaprine.\n\n
*** So the initial tx
is either Amitriptalin or cyclobenzaprine.
If refractory to the above medicine then SSRI are added. When pt feels better then
exercise is initialed. Other refractory tx is trigger point injections.\n\n
First degree heart block
wat \n\n
Fluphenazine SE:
Hypothermia by causing vasodialation and inhibition of shivering.\n\n
Focal segmental GN
Asso with HIV.\n\n
Fragil X syndrome - 2
Pt can be tought to take care of himself with and perfor simple task with close
observation, like down's. *** Low to normal IQ, with learning disability. , general
language disability, short attention span, autism, Mutation of FMR-1 gene caused
by increased number of CGG trinucleotide repearts. Large head, prominent jaw
and large low set ears.\n\n
Friedrisk Ataxia
Auto rec. excessive number of trinucleotide repeats resulting in abnormalilty of
topopheral transfer protein. Poor ptognosis. Tell the parent to seek genetic
counseling for future pergnancy. MRI of the brain and spinal cord shows marked
atrophy of cervical spinal cord and minimal cereberal atrophy. \n\n
*****Auto rec dis.
Begins before 22 years of age. Neurological manifesration gait ataxia, falling,
dysarthria) result from degeneration of spinal tracts (spinocerebellar, posterior
tract, pyramidal tracts). Non neuro symptoms include concentric HCM, DM and
skeletal abnormality (scoliosis annd Hammer toes). Median survivial is 20 years.
Mcc of death is CV, 90%. \n\n
Frost bite injury
Warm up the body with warm water is the tx.\n\n
Frozen Shoulder
There is stiffnes and limited motion due to glenohumeral joint stifness. In PE range
of motion in all directions is limited whether passive or active movement. This is as a
result of Pericapsulitis. Majority are idiopathic. \n\n
***Arthroscopy
establishes the dx by
showing decreased joint space volume and loss of normal axillary pouch. Tx
involves NSAIDa, steriods injection in the joint and physical therapy. Rotator Cuff
Tear or Rotator Cuff Tendinitis presents with severe pain and weakness of shoulder
abduction. \n\n
** Positionng arm
above shoulder aggrevates the pain. Range of motion is
only limited in active movement but is normal in passive flextion. A positive drop
arm sign, with inability to actively maintain 90 degree of passive abduction maybe
present in large tears. Tendinitis can be ddx from Tear by injecting Lidocain that
would result in improvment in motion in Tendinitis but not in Tear.\n\n
Furosemide Tox:
Causes oto-toxicity. Aminoglycosides, vancomycin, quinine, and chloroquin also
cause oto-tox. Aspirin causes Tinnitus.\n\n
Galactosemia
In a newborn or young infant with failure to thrive, bilateral cataracts, jaundice and
hypoglycemia. Early dx and tx by removing galactose from diet are mandatory. It's
a metabolic disrorder causd by Galactose-1Phosphate Uridyl Transferace def. That
leads to increse level of Galactose. DDX: galactokinase def, only have cataratct and
otherwise asymptomatic.\n\n
Gallblader Carcinoma
It's a rare tumor, found in pts with chronic Choledocholithiasis usually diagnosed
intra or post operatively after cholecystectomy.*****Chronic Cholecystitis
predisposes to carcinoma, in xray we can see Porceline gall bladder, due to calcium
deposition in gall bladder.\n\n
Gastric Carcinoma
Pt might present with blood vomiting and Acanthosis Nigrans. Don't be fooled into
thinking that its Aspirin tox, becaseu aspirin tox doesn't cause AN. AN is a diease
that causes dark,thick areas on the skin.\n\n
** MC
in arm pits and other folds. Its
associated with being over weight and other tumors like GASTRIC carcinoma. so pt
needs complete work up like endoscopy and bioposy.\n\n
Gastric MALT
H. Pylori has an important role in parhogenesis of Gastric Mucosa-Asso Lymphoid
Tissue Lymphoma. These Lymphomas may regress after eradication of H. Pylori, IF
THERE IS NO METASTASIS.\n\n
** If Pylori eradication fails
then Chemotherapy is the
choice (CHOP). In the old days they used to do radical gasterectomy. Tx Pylori with
Omeprazole+Clarithromycin+Amoxicilline.\n\n
Gastroschisis:
Bowel protrudes through a defect. Bowel not covered with protective membrane.
First thing is to cover the exposed bowel with sterile wrapping, then iv access for
nutrition and then iv antibiotics, then surgery to fix the defect.\n\n
** Omphalocele:
Bowel
protrudes through unbilicla ring. Bowel covered with amnioperitoneal membrane.
Asso with other congenital abnormalities. Management is first wrapping, then
orogastric tube to decompress stomach. If <2cm repair with primary closure if
bigger Silastic Silo.\n\n
Gaucher's Dis:
Sphingolipidosis due to deficiency of glucocerebosidase. Characterized by
Hepatomegaly, anemia, leukopenia, and thrombocytopenia, but NOT chery red
macula.\n\n
General Anxiety Disorder
First line of tx is Buspirone, because it does not show the dependence and withdrawl
symptoms asso with Benzodiazepines. If sexual performance is a problem use
Nefazodone.\n\n
Gentamycin
causes nephrotoc and Ototoxicity, vestibular toxicity that causes the pt to feel dizzy
w/I a couple of weeks of use.\n\n
GERD - 6
In neonates is regurgitation after eating and failure to thrive. The child assumes the
position of tilted head and arched back. Dx is 24hr pH monitoring of esophagus.\n\n
*****When its unclear
whether the pt has nocturnal asthma or GERD, a trial of
proton pump inhibitor (Omeprazole) before breakfast is both Dx and therpeutic.
***** Esophagoscopy is indicated when a pt fails to respond to antibiotics and or
theye are signs of implications (weight loss in cancer).\n\n
****Dx Process:
once pt
presents with cough, and the vigniette says esophagoscopy is normal, the next thing
is 24 hour pH monitoring. Then Manometry will confirm dx.\n\n
****GERD can happen
due to hiatal hernia. Chronic GERD can lead to metaplastic change in lower
esophagus called Barret esophagus and is a risk for Adenocarcinoma of
esophagus.\n\n
****When pt comes in with symptoms of GERD
you need to differenciate
b.w Barrets,PUD,Gastritis, or tumor. Endoscopy is the most informative procedure
for all these. Now if the vingette says "he has no Dysphagia" then you can skip the
normal Barium test that precedes endoscopy and go straight to
endoscopy.\n\n
*****Indications to endoscopy are
1-Nausea/vomiting, 2-weight loss,
anemia or melena, 3-Long duration of symptoms (>1-2 yr), 4-Failre to responde to
PPI. So here is the order, if there if Dysphagia first do BS, then EC then
Manometry. If no dysphagia, first EC and then Manometry, you can skip BS.\n\n
Giant cell arteritis - 3
Don't wait for biposy start high dose Prednisone right away.***Lab may show
elevated ESR and normochromic normocytic anemia. Thoracic aortic aneurysm is a
complication of this dis, maybe due to disruption of collagen and elastin.\n\n
Giardiasis
Adheres to mucosal surfaces by adhesive disk and cause malabsorption, may lead to
weight loss. The MC symptom is foul smelling sttol, fatty stool, bloating and
flatulence, nausea, malaise, abdominla cramps. Empiric tx should be given w a
course of Metronidazole.\n\n
Gilbert synd
Partial absecnce of enzyme leads to : 1-mild uncongugated hyperbilirubinemia, 2-
More elevated values happen with stress, fasting, alcohol abuse. 3-normal cbc, 4-
normal liver enzyme, 5-complete reversal of hyperbilirubinemia.\n\n
** DDX1
Crigler-
Najar-I: cgaracterized by 1-Unconj.Hyperbilirubinmeia 8-30, 2-Normal liver
enzymes, 3-High rates od Kernicterus, 4-No response to Phenobarbital.\n\n
** DDX2
: characterized by 1-Unconj HyperB, 2-Normal liver enz, 3-No Kernicterus, 4-25% decrease of Bilirubin with Phenobarbital. DDX3:Rotor synd: Conjugated
Hyperbilirubinemia.\n\n
Glascow coma scale - 2
EYE opening:Spontanous 4, to verbal command 3, to pain 2, none 1. VERBAL
response:Oriented 5, confused 4, Inappropriate 3, Incomprehensive 2, non 1.
MOTOR respopnse:Obeys 6, localization 5, Flexion 4, abnormal felxtion 3,
extenstion 2, none 1. Total 15. \n\n
** Minor injury
is GCS of >14. Moderate <13 and >9.
Severe <8. ****Pt with GCS of 7 in an accident is having a severe head injury. All
pts with sever head injury should be intubated, with mechanical ventilation,and
admin of IV fluids,analgesics and sedatives.\n\n
Glaucoma
it's the leading cause of blindness in North America. Its characterized by elevated
ICP. Symptoms are sudden onset of photophonia., eye pain, HA nasea. Eye is hard
to touch.\n\n

** A non reactive mid dialated pupil ?? suggest Acute Glaucoma.The best Dx is
Tonometry. OPEN angle glaucoma: has incidious onsert with gradual loss of
peripheral vision and consequence tunnel vision. Intraoclar pressures are high.
Opthalmoscopic exam shows cupping of the optic disk.\n\n
*****once you suspect
it do
MAPPING VISUAL FIELDS to find out defects.\n\n
Glaucoma, Acute closure angle 2
Age 55-70, Acute onset of severe pain and blurred vision, nausea and vomiting.
Anterior chamber is shallow with inflammatory changes. Tonometry reveals
increased IOP. IV Acetozolamide, Manitol, Pilocarpin with subseq oral. Permanent
cure is laser peripheral iridotomy. Avoid Atropine.\n\n
Glaucoma, Acute Open angle:
Its more common in blacks. Gradual loss of peripheral vision, tunnel vision. IOP is
high. There is cupping of the optic disk with loss of peripheral vision. Beta blockers,
Timilol are effective in initial mngmnt. Later on Trabeculoplasty. Its asso with
Diabetes.\n\n
Glioblastoma Multiform
GBM or HIGH grade astrocytoma. CT shows butterfly appearnce in the frontal
lobe of alesion (surrounded by white calcification, looks like cyst membrane but not
round).\n\n
** DDX
is Brain Metastasis, pt will have a duration of symptoms of <2months,
the site is grey-white juunction or watershed zones, they are multifocal and round.
DDX2:Lowgrade astrocytoma, prestns with seisure and longer duration os
symptoms.\n\n
Glucagonoma
Triad of Hyperglycemia, necrotizing Dermatitis, and weight loss. It's a tumor of
islet cells in Pancrease . The excess glucagon causes symptoms like glucose
intolerance, and hyperglycemia. It also causes a distint skin lesion called 'Necrolytic
migratory erythema'. \n\n
**Dx
is confirmed by fasting glucose elevation, elevated
glucagon, and pancreatic tumor by CT. Surgery is the prefered tx. It doesnt respond
to Chemotherapy.\n\n
Glucose 6 Phosphatase deficiency:
Also glycogen storage type 1 or Von Gierke Dis. Presents with hypoglycemia, lacic
acidosis, hyperuricemia, & hyperlipidemia. Hypoglycemic seizure occurs. Hay
hepato and renal megally. Doll face, fat cheeks, thin legs, and a protuberant
abdomen.\n\n
Glucocorticoud SE
Long term use in asthmatic pt can lead to Neutrophilia by increasing BM release
and mobilization of marginated neutrophil pool. Eosinophils and lymphocytes are
decreased.\n\n
Glycogen storage diseases
1-Von Gierke, 2-Pompe, type 3 and type 4. Read on them.
Gonococcal arthritis
Urethral cultures have the highest yeled than synovial or blood or urine cultures in
cases of suspected purulent gonococcal arhtritis.\n\n
Gonorrhea - 2
Commonly causes cervisitis, urethral discharge. It also causes Pharyngitis. *It also
causes GA(arthritis), which is asymetric migratory polyarthralgia, followed by
monoarticular arthritis and rash, palms and soles have multiple necrotic pustules.\n\n
Goodpasteur's synd - 3
Involves lung and kidney. There is lower respiratory problems (hemoptosis) and
proteinuria (renal failure), there is antibodies against glomerular basement
membrane. Sputum shows iron in form of hemosiderin . There is anemia and RBC
cast in urine.\n\n
** DDX1
:Idiopathic pulmonary Hemosiderosis: Like GP, but there is
more copious hemoptasis and its for children. DDX2: Wegner's, involves Upper
(rhinorrhea) and Lower (hemoptasis) and Kidney problems. And Granular
granulomatosis. Cresent formation.\n\n
******Caused by circulating antiglomerular
basement membrane antibodies. Early removal is imperative in order to minimize
the damage tokidney. Emergency Plasmaphoresis is indicated. \n\n
***Pt presents
with
massive hemoptosis, weightloss, hematuria and proteinuria. To confirm measure
anti glumerulat basement membrane antibodies.\n\n
Goughers Dis
Is due to deficient activity of the lysosomal enz, acid beta glucosidase. The typical pt
is Ashkani Jew adulescent with chronic fatigue, easy bruisability, bone pain and
pathological fractures. The dx is conformed with radiologic (Erlenmeyer flask
deformity of the distal femur) and bone marrow studies (Gaucher cells with
wrinkled paper appearance).\n\n
GOUT- 2
Fluid joint aspiration for dx.*****In pt with frequent attacksof gout not controlled
by Colchicine, a 24hr uric acid level in urine is determined. This evaluates whether
hyperuricemia id due to over production or under secretion. A value of <800
indicates under secretion, so use a Uricosuric agent (Probenecid) is needed. If its
>800 indicates over production, so add a xanthin oxidase inhibitor (Allopurinol).\n\n
Gouty arthritis - 2
Very painful, mostly in toe but sometimes hands.
Alcohol is metabolized to Lactate which competes with Urate for renal excretion leading to acc. of urate
Cessation of alcohol is important.
Acute attack give oral indomethacin, colchicine or steriods.
Chronic Cholcicine.\n\n
Graft Vs Host Disease
By activated donor T lymphocytes.
Targeted at Skin
maculopapular rash in palm,sole and face
Intestine ; bloody diarrhea, Liver.\n\n
Granuloma Inguinale
Is an STD caused by Donovane granulomatis. Its uncommon in US and is mc in
Balck population. It starts with a papule that rapidly develops into a painless ulcer
characterized by irregular border and red beefy granular base. Inguinal
lymphadenopathy occurs w/o Buboes. \n\n
**Advnced stage
has scaring, depigmentation and keloids.
Fibrosis may lead to vaginitis and elephantitis.
Dx is by identifying Donovan bodies, visulized by giemsa or wright stain of tissue smears, and appear reddish, encapsulated bipolar bacteria found within Monocytes.\n\n
** Tx
is tetracycline,
500mg, every 6hr, 10-21 days. \n\n
** DDX1
:Ulcer of primary syphlis has roled edges and
punched out base. \n\n
**DDX2:
Ulcer in Chancroid is very painful and foul smelling,
buboes form and are painful. \n\n
DDX3:
in Genital herpes many vesicles appear before
they turn into ulcers. \n\n
** DDx4
Ulcer in Lymphogranuloma Veneruem is also painless
but its shallow and asso w non-specific systemic symptoms, also lymphadenopathy is inflamatory and does not appear at the same time as ulcers.\n\n
*****The first thing
to do is stop Heparin. However, most pt need anticoag so two options are offered: - Danaparoid and a direct thrombin inhibitor such as Lepirudin or Argatruban.\n\n
Granulosa Cell Tumor
Are SOLID tumors. Bimodal distribution. If occur before puberty ,
Precociouspuberty is presented. It produces excess estrogen and causes pubic hair,
hpertrophy of brest and hyperplasia of uterus. \n\n
** Usually removal of tumor
reverses
the problem. If its in postmenopausal women it causes bleedingand uterus shows
myohyperplasia. \n\n
**DDX1
:Dysgerminoma, in young women and children, unilateral
and go under torsion. It doesnt produce any hormones. \n\n
** DDX2:
Sertoli- Leydig,produces androgen and DEFEMINIZATION, followed by masculinization in childbearing years.\n\n
** DDX3:
Mature teratoma or Dermoid cysts, benign and dont produce any hormones. \n\n
** DDX4
;Serous cystadenomas, are the mc CYSTIC ovarian neoplasm. 25% are malignant,half cases are bilateral. They dont produce any
hormones. Ovarian mass and abdominla pain are presenting features.\n\n
Grave's Disease - 3
Tx is radioactive iodine. Might cause hypothyroidism *** Sudden onset of Atrial
Fibrilation (irregularly irregulat rhythm with tachycardia) in pregnant women
should alert the doctor to look for Hyperthyroidism, GRAVES is the MCC of
hyperthyroidism in pregnancy.\n\n
** Remember Dx
is made by TSH, T3 & T4, BUT the
best SCREENING is just TSH. So next step is ordering TSH. Now the vigniette may
not even indicate other signs of Graves, but you must recognize it as well. DDX is
Hydatiform Mole, but sonogram will easily show it.\n\n
Green stick fracture
Commonly seen in children because the bone is less brittle. Also see torus fracture
and plastic deformation.\n\n
Growing Pain
Common in children from 2-12. Mostly at night, awakens the pt, responds to
massage and NSAIDs. Obs/Reasur.\n\n
Guillain Barre - 4
The best way to monitor respiratory function is to measure serial bedside vital
capacity, to make sure it stays above 15ml/kg.\n\n
***DDX
is Tick borne paralysis
charcterized by rapidly progresive ascending paralysis, absence of feve , absence of
sensory abnormality and normal CSF. \n\n
****Campylobacter Jejuni
is the most
frequent precipitant in GB. \n\n
***GB is characterized
by Ascending paralysis ,
previous hx of infection, CSF shows albumino-cytologic dissociation(Elevated
protein despite normal cell count). \n\n
**Tx
is IVIG and plasmophoresis. DDX is Botulism
which presents with desceing paralysis, tx is antitoxin.\n\n
Gun Shot wound:
If its below 4thrib, level of nipples, then exploratory laparatomy is done.\n\n
Hairy Cell Leukemia - 2
It's a type of B-lymphocytic derived chronic leukemia. Tartrate resistant acid
phosphatase stain is Dx.****Picture looks like hairy projections of large cells. BM
may become fibrotic so BM aspirate are frequently unsuccessful (Dry Tap). \n\n
** Tx
DOC is a purine analog, Cladribine.Its toxic to BM, it causes neurological and
kidney damage. Remember CHOP is for Nonhodgkins, Chlorambucil+Prednisone
are for CLL.\n\n
Hashimoto Thyroiditis - 2
Transient thyrotoxicosis can occur in initial stages due to thyroid-stimulating
antibodies. Positive anti-thyroperoxidase antibodies with an enlarged rubbery goiter
are virtually diagnostic. \n\n
**The risk of thyroid Lymphoma
60 x greater in these pts.
CT shows elragemnt of thyroid around trachea, "Doughnut sign".
US shows"psudocycst pattern".
RAIU is decreased. Since FNA might miss dx, Core biopsy is
prefered. * Anti Thyroid Peroxidase Antibodies are present in >90% of pts.\n\n
HCV
If pt is + but no sign and symptoms, just follow up w yearly tests. No Tx.\n\n
Head trauma - 2
always do spine xray in pt with falls or accidents leading to head trauma.
Pt with increased ICP should be treated with hyperventilation , head elevation, and IV
Manitol and diuretics.
Hyperventilation works by VC and decreasing the ICP by decreasing cerebral blood flow volume.\n\n
Heart Block - 2
1-First Degree: prolonged but constant PR >0.2s . No tx is neede. 2-Mobitz Type-1:
or Wenkeback, narrow QRS and progressive increase in PR until a ventricular beat
is dropped. It may occur with Digoxin, or Inferior MI. \n\n
**If pt is symptomatic Atropine
\n\n
is gven. 3-Mobitz Type-2: Fixed PR with occasional drop . QRS is wide. Its seen
after MI. Its dangerous and all pts have to be monitored in ICU. It can progress to
complete heart block and needs Pace maker. Atropine must be by bed side at all
times until a permanant pacemaker is inserted.\n\n
*****Third degree heart block,
no atrail impulses will travel to ventricles. , Atrail rate is 80 and Vent is 30. Pts are at risk of suden cardiac death and they should be transmitted to ICU and PERMANENT pacemaker should be placed. Always have Atropine by bed side. Bblocker WILL KILL HIM IMMEDIATELY.\n\n
Heat Exhaustion
Characterized by volume depletion under the conditions of heat stress. DDX:Heat
Stroke, has CNS symptoms and T>40. DDX2:Heat Syncope:breif syncope after
exposire to heat. DDX3:Heat cramps: painful muscle cramps due to depletion of salt
in muscles.\n\n
Heat stroke
Characterized by body T of >40.5, due to filaure of thermoregulatory center. Rapid
Evaporation cooling is the tx of choice. Immersion in ice water is also useful but
makes it difficult to monitor the pt.\n\n
HELLP Syndrome
Hemolysis & Hypertension (preeclampsia), Elevated Liver enzyme, Low
platele(thrombocytopenia). DDX are DIC, Preeclampsia, TTp, HUS, and Acute
Fatty Liver of Pregnancy. \n\n
** In AFLP tx
is supportive with early dx and rapiddelivery,
there is incresed PT & PTT. In HUS, thrombosis of the glomerular arteries,
happens in children. Often preceeded by infection. . \n\n
**TTP
is wide spread of HUS and
it occurs in Adults and Asso with NEUROlogical symptoms. Tx is exchange
transfusion or plasmaphoresis with FFP \n\n
****Delivery
is definitive tx for HELLP in
women beyond 34 weeks, give Mg SO4 to reduce BP & VAGINAL deliver.\n\n
Hematochezia, scant
Pt see fresh blood on toilet paper. Most common causes are hemorhhoids, fistulas or
even cancer. If pt is <50 chance for cancer very low. Do Anoscopy first and then if
still nnot clea do sigmoidoscopy or colonoscopy is done.\n\n
Hemi Neglect Synd
Involves the Right (Non dominant ) parietal lobe.\n\n
Hemochromatosis - 3
Genetic disorder of iron absorption, increased aborption from intestine . Liver,
pancrease, heart and joints are mc affected. Pt prsents with weakness, loss ob libido,
skin pigmentation, weight loss, abdominal pain and symptoms of DM (polyuria&
polydypsia). \n\n
**Trensferin saturation
(>=50%) and Ferritin (>1000) is a simple reliable sreen test.
Hepatoma(Hepatocellular Carcinoma) is the most serious complications.
Hay increased Fe and Feritin. Its Auto Recessive causing increased iron absorp
and deposition in skin (pigmentation), Testes(decreased libido), pancrease
(Diabetes), Joints (Arthralgia), and liver (cirrhosis).\n\n
*** Pts are at increased risk
for
Listeria Monocytogenes, maybe due to impaired phagocytosis. Iron overload is also
a risk for Yersenia Enterocolitica and sepsis from Vibria Vulnificus which are iron
loving bacteria. \n\n
*** IF pt presents
with Joint pain and Hepatomegally and no other
sysmptoms suspect it and FIRST thing you do is CBC to check Fe level. It presents
with hepatomegaly,hyperpigmentation,diabetes (BRONZE diabetes), arthropathy,
heart failure and hypogonadism.\n\n
Hemolytic Uremic Synd - 4
When you get Thrombocytopenia (decreased platelet 56000), a MicroAngiopathic
Hemolytic Anemia(MAHA) (Increasesd bilirubin, and schitzocytes and RBC
fragments and abnormal renal function) in a pregnant woman \n\n
**DDX
include
HEELP(Hemolysis, Elevated Liver enzymes, Low platelet count), HUS, TTP, DIC,
preecclampsia and Acute Fatty Liver of Pregnancy (AFLP). \n\n
**Oliguric renal
failure+MAHA+Thrombocytopenia points
to HUS. Its characterized by thrombosis
of the glomerular arterioles and capilaries. It occurs more frequesntly in childhood
and presents with fever, thrombocytopenia, MAHA, HT and renal failure. Usually
preceded with viral infection and asso with E. Coli. \n\n
TTP is a variant of HUS
the thrombosis is systemic and it obstructs microvascular of several organs. It presents
with fever, altred level of consciousness, focal neurologic signs, renal failure, MAHA
and thrombocytopenia. \n\n
**tx
is exchange transfusion, or plasmophoresis with FFP.
HELLP is a variant of preeclampsia, in women older than 25, multipara, before 36
weks gestation. \n\n
DIC
is a comsumptive coagulopathy, Presents with elevated PT,
PTT, fibrin degradation product and decreased fibrin.\n\n
****Occurs in young
children. Preceeded by a diarrheal disease. Hallmark is Microcangiopathic
hemolytic anemia.\n\n

**Other features ?? are renal filure, fever, oliguria,
thrombocytopenia. GI bleeing is common. Purpura and HT. Schizocytes, which
represent frabmented RBC. Also Giant Platelets. \n\n
**Intravasculat hemolysis
results in
elevated LDH, indirect bilirubin and reticulocyte count. BUN andCrt are markedly
elevated. . Urine contains, Hb, Hemosiderin, albumin, RBC,WBC and casts.\n\n
****Its caused by
E.coli released toxin, it injures kidney epithelium. Pt prsents with
abdomnal pain, young pt, decreased Hb,Hct and Platelets. , bloody diarhea and
swollen face. When kidney is damaged mortality is 5-10%. \n\n
*****Its caused by
toxin released by E.Coli, it destroys epithelial lining and causes bloody diarrhea. Subsequesnt activation of coagulation system and red cell hemolysis causes Jaundice. \n\n
**Its mc
in children adn initial presentation is abdomnal pain and diarrhea.
The classis TRIAD is Uremia(Renal Failure), Thrombocytopenia, and Hemolytic
Anemia.\n\n
** Tx
is generally suportive and involves Plasmaphoresis and Dialysis if
necessary and steriods. DDX it with Campylobacter jejuni, althought it causes
bloody diarrhea, there is no Thrombocytopenia.\n\n
Hemophilia
Bruising since child hood, excessive bleeding in a tooth extration procedure and
uncle having the same problem. In these pts recurrent Hemarterosis ma lead to
injury called 'hemophilic arthropathy'. \n\n
**Iron
(HEMOSIDERINE) deposition and
synovial thickening with fibrosis is characteristic. ***** Its X-linked. PTT is
elevated and PT & BT are normal.\n\n
Hemothorax
Collectin of blood in pleural cavity. Tachypnea,tahcycardia,hypotention, deviated
trachea , dullness to percusion, elevated JVP, fluic in pleural cavity(seen in Cxr) and
collapsed lung. \n\n
** Lung is the usual bleeding source
2ary to rib fracture. Its very
important to evacuate the blood in order to stop bleeding, which stops on its own.
Best initial interventon is to insert a low anterior chest tube to remove blood.
Surgical Thoracotomy is indicated when more than 1500ml blood recovered when
tube is inserted, or if more than 600ml blood loss after 6 hour post tube insertion.\n\n
Henoch-Schonlein Purpura
A common vasculitic of childhood, its commonly seed after URT infection and is
more common in males. \n\n
**Classis findings
are palpable Purpura in buttucks and
lower extrmity. Peripheral edema nd scrotal swelling. Renal finding are Hematuria
dn proteinuria. Tx includes steriod and monitoring renal function. \n\n
**When pt prestns
with Abdominla pain two pathologies should be rules out emergently, GI bleeding
and Intussuseption. Intus is characerized by sudden onet of abdominlapain with
large amount of blood in stool. This is a surgical emergency and is tx with
Air/barium enema.\n\n
*****HSP
is an IgA mediated vasculitis of small vessels, which
results in rashes, arthralgias, abdominal pain and renal disease. Immuno
florescence microscopy reveals IgA deposition in the kidney.\n\n
HepA
Acute disease asso w travelling. If travel <4 weeks, give Ig. If >4 weeks give vaccine.\n\n
Heparin induced thrombocytopenia - 3
Its seen in 5-15% of of pt taking Heparin with onseet b/t 3-15 days and resolution in
4-5 days of discontinuation. While PTT is a therapeutic effect of heparin, the
thrombocytopenia is an adverse effect. So PTT is increased and Platelets are
decreased.\n\n
****Hospitalized pt
who develop DVT after a period of bed rest are
standardly treated with Heparin. An adverse effect is Thrombocytopenia, along
with thrombosis (causes stroke sysmptoms). \n\n
**The combination os Arterial/Vnous
thrombosis and thrombocytopenia in pts receiving Heparin is suggestive of HIT.
Antibodies against Heparin-Platelet factor 4 complex are responsible for this. The
antibodies activete platelets which will cause their removal form circulation.\n\n
Hepatic Adenoma
Is a benign tumor seen in middle age females taking OCP . Intra tumor hemorhhage is a major comlication.
Dx is by biopsy, atypical hepatocytes withglycogen deposits. Tx Superficial and large adenomas are resected.
But smaller and asymptomatic onces are under surveilance with imaging.\n\n
Hepatic Encephalopathy - 3. Hepatology. 6/3
Characterized by reversal of sleep cycle, asterixis, porgreive coma, and Delta waves
in EEG. It's a CNS complication of liver failure secondary to accumulation of
ammonia in blood becuase of inability of live to detoxify ammonia (that comes from
intestine) into urea.\n\n
** Eliminating toxic enteric products
is the other main therapy: (1)
The bowels should be cleared with enemas. (2) Dietary protein should be eliminated,
and oral or IV carbohydrate should be given. (3) Oral lactulose should be given. (4)
Oral neomycin.\n\n
****Pt with hepatic failure
should be given vit K to correct PT and
if they are bleeding in this setting, or he needs immediate surgey, then FFP is
indicated.Platelet transfusion is only indicated if it falls below 20,000-30,000.\n\n
**Cryoprecipitate
is requied for coag factor def like factor VIII. Packed RBC is
indicated when RBC is <8 in asymptomatic pt or <10 in symptomatic pt.\n\n
Hepatitis B -8. GIT. 6/3
Hepatitis B virus Ig + Lamivudine is used to prevent recurrent HBV after liver
transplant.For HepB Interferon+Lamuvidine. \n\n
**Vaccination criteria:i
f someone is
exposed and has Documented response there is no need for furthur action. If
vaccined but no response to vaccine must be vaccined again. If vaccined many times
and still no response, give HBIG on exposure.\n\n
** If exposed to virus
and never been
vaccinated before, give HBIG w/i 24 hrs and start HBV vaccination. Best screening
test to dx acute HepB is AntiHBcAg and HBsAg. \n\n
**** HepB vaccine is
a
recombinant vaccine containing HBsAg, which stimulated Anti HBsAg, person who
receives it will have immunity and thus be positive for Anti HBsAg and negative for
HBsAg.\n\n
** Person with ACUTE HBV
will have HBsAg, HBeAg and IgM Anti HBcAg.
Chronic HBV will have HBsAg only, for >6months. Person with recovery phase
HBV will have AntiHBsAg, HBsAg, Anti HBeAg and ABSENT HBeAg. \n\n
****If seroogy
shows HBsAg, HBeAg positive and high titers of HBV DNA, he has Chronic HEpB. \n\n
The 2 drugs approved
are Inerferone and Lamuvidine. Either one is
indicated for pt with positive HBsAg,HBeAg,HBV DNA and persistantly elevated
ALT. \n\n
**Degree os elevation of ALT
is important in deciding the Tx. Serum ALT of
mor than two times the upper limit requires need for Lamuvidinr or alpha
interferone. \n\n
** If less than that its not useful. Generally Lamuvidine has less SE and
easier to administer (ORAL). Inteferone is not successful in young children and
immunocompromised pts. NOW, if the pt has just been exposed to virus,
POSTEXPOSURE and has never had response to vaccine, we give vaccine+Ig, and
if did have response and has antibodies then we just give Ig.\n\n
...
****Of all acute Hep B
cases 90% recover, minority go to chronic, out of those 1% goes to Fulminant
hepatic failure, defined as hepatic encephalopathy that develops w/I 8 weeks of the
onset of acute liver failure and evidence by marked increase in ALT. and signs of
Hepatic encephalopathy. Liver transplantation is the only effective method for tx, so
initial step in tx at this point is to put her name on the list. \n\n
****Newborn of mothers
with active HebB should be passivly at birth with HepB immunoglobin followed by
Vaccination. \n\n
*****Transmission from mother
w chronic dis & +HBs antigen and
Hbe antigen to the fetus is 90%.****If given choice b/w Interferon and Lamuvidine
in a depressed pt, pick Lamuvidine cause interferone is CI in Psych pts..\n\n
Hepatitis C - 4
Risk factors for rapid progression of liver fibrosis in chronic HepC are: 1-Male sex,
2-Acquire infection after age of 40, 3-Co-infection with HepB or HIV, 4-Alcohol
intake.\n\n
** Complications
of Chronic HepC: 1-Cryoglobulinemia (causes Membraneous
glomerulonephritis), 2-B-cell Lymphomas, 3-Plasmocytosis, 4-Autoimmune dis like
Sjogren and thyroiditis, 5-Lichen Planus, 6-Porphyrea cutanea tarda, 7-ITP. \n\n
***Management:
All pt with mild Hep C(alevated ALT,HCVRNA, moderate
bridgenecrosis) should get Interferone+Ribavirin. Liver transplantation is the last
step and its done when Pt and Albumin levels are very affected. \n\n
**** HCV RNA
is
the single most sensitive serological marker to screen HepC, HCV RNA antibody
takes months to show up dont do that one. \n\n
**** All pts with chronic HepC
including Pregnant women, should be tested for HepA and HepB and if not
immuned should be vaccinated which is safe for pregnancy.\n\n
** Ribavirin & Interferone
are teratogenic.****Transmission risk could be a steady sex partner but the chances
are low.\n\n
Hepatitis E
Asso with pregnant women.Ocurs in India,Asia, Africa and central USA.Ther is no
vaccin or Ig avaible for HepE.\n\n
Hepatocellular carcinoma- 2
Most are palpable mass. It accts for 80-90% of liver cancers. Occurs more often in
men. Cause is unknown but contributing factors are Chronic liver disease, HepB &
HepC, hemochromatosis. Dx is by abdominal CT.\n\n
***High serum AFP >500)
in an
adult with liver disw/o an obvious GI malignany is HCC. Pt has a hx ox Chronic
HepC. Dx is confirmed by biopsy, Tx is surgical resection.\n\n
Hepato-Renal Synd
Hypotension, Hyponatremia, Azothemia and oliguria with normal urine analysis
with sever liver disease. No tx is available. Pathogenesis is not clear. Initial mgmt is
careful volume loading and withholding of Spironolactone and Furesamide.\n\n
Hereditary Spherocytosis - 3
Osmotic fragility test is dx.***An auto RECESSIVE dis. Folic acid is encouraged in
ALL pts. MCV is normal or Elevated. They rarely require transfusion unless they
have Aplastic crisis. Splenectomy is usually curative.\n\n
****The tx
for most pt involves
Folic acid oral and blood transfusion. during periods of extrmem anemia.
Splenectomy is considered if htey are refractory to medication. \n\n
**The most feared
long term complication is overwhelming sepsis with encapsulated bacteria Strep
Pneumonia. The risk is present for up to 30 years and even longer after
splencetomy.\n\n
** Current recommendations
state that pt shuld receive antipenumococcal,
Haemophilus and Meningococci Vaccinces several weeks before the
operation and daily oral Penicilline prophylaxis for 3-5 years following splenectomy.\n\n
Herion Withdrawl
Signs are muscle spasm, abdominla pain, rhinorrhea , lacriation, sweating. Dilated
pupils. These are oppsit signs when pt is toxicated, pin point pupil, constipated,
depressed respiration and bp. DDX is Cocain withdrawl:irritable, fatigue,
HUNGRY(opped to anorexic when toxicated).\n\n
Hernia
Respiration and hemodynamics are altered after repair of large hernias. Because
large hernia content is displaced inside the peritoneal cavity, the pressure inside the
cavity increases. \n\n
**The diaphram is pushed upwards
and this impaires respiration,
causing hypoventillation. At least a week is needed for the pt to accomudate to its
new state. Early physiotherapy and respiratory excercises (blowing against
resistance) are mandatory to prevent , Atelectasis, mucus pluggung and possible
subsequent penumonia development.\n\n
Herpes Simplex Encephalitis -2
Mainly affects the Temporal lobe, bizare behavior and gustatory hallucination. CSF
show Lymphocytosis, low glucose, and elevated proteins. HSV PCR is the gold
standard. Tx Acyclovir.\n\n
Herpes Simplex Keratitis
or Herpetic Keratitis due to HSV-1
Simplex More common in young pt. Zoster is mc in old pt. DX is with Slit lamp.
Common in health workers.\n\n
Herpes Zoster Ophthalmicus
DDX with Herpes simplex keratitis is addition of vesicular rash in Varicella-Zoster.
"Bacterial keratitis" occurs w contact lenses.\n\n
Herpetic Whitlow
Is the mc viral infection of the hand. The appearance of vesicles on the volar or
dorsal distal phalanx is diagnostic. Caused by type I or II herpes simplex and its self
limiting. Dentist are at increased risk.\n\n
Hirshsprung dis - 2
Pts with Down, are more likely to present with Duedenal atresia, Hirshsprung,
endocardial cushin defect and acute leukimia. double buble
sign" is seen.*This is an emerrgency, so if the infant has
it and mother refuses tx, then go ahead and treat the infant because court order will
take a while.\n\n
Hirsutism
Women produce androgens. DHEA-s and Testosterone in adrenals and ovaries.
DHEA-S is only in adrenals by adrenal tumors. ACTH increase in pts
w hirsutism is seen with ectopic or pituitary dependant Cushings dis. ACTH
increases the production of cortisol as well as androgens from the adrenal glands,which show diffuse hyperplasia rather than a discrete adenoma
Histoplasmosis - 3
Is a common and asymptomatic infection in endemic areas of Mississippi & Ohio.
Found in bird or bat dropings. ***** It's the mf endemic fungal infectinin USA.
Disseminated histoplasmosis occurs in immuncompromised pts. Presnece of mucous
membrane ulcers, hepatospleenomegally and pancytopenia are clues to Dx. **** Tx
is IV amphotericine followed by lifelong Itraconazole. Histoplasmosis happens to
HIV pt in OHIO.\n\n
HIV- 30
TB occurs in the course of HIV when the CD4 counts are >200. Uper lobe consolidation and cavitation is typical Xray fiding. Asso with Hairy Leukoplakia, white painless lesion that appears hairy, found on the tounge, caused by EBV). \n\n
**All HIV pt should have the following done:
1-Hx & PE, 2-routine chemistry and
hematology, 3-two plasma hivRNA levels, 4-CD4 count. 5-VDRL for syphlis. 6-PPD
test. 7-Anti Toxoplasma antibody titer. 8-MMSE. 9-Pneumococcal vaccine, unles
CD4 is <200. 10-HepA&B serology & vaccine, if seronegative. 12-
Counselling. \n\n
CMV Colitis
is suspected in pt with CD4<50, bloody diarrhea and abdominal pain multiple ulcers
and biopsy shows basophilic intracytoplasmic inclusions or owel eye effect, Tx is
Gancyclovir or if intolerance Foscarnet. \n\n
MAC (Micobacterium Avium Complex)
presents with unexplpained fever and cough, Azithromycin is used for prophylaxis
against MAC when CD4 falls below 50, now Clarithromycin with Ethambutol is
used for tx of MAC. **** Breast feeding is CI in HIV.\n\n
**** Prophylaxis for PCP
in HIV pt w CD4<50 doc are Azithromycin or Clarithromycin. Prophylaxis for
Histoplasmosis in CD<100 is Itraconazole, in endemic areas. Prophylaxis for CMV
in CD<50 is Gancyclovir. \n\n
***HIV pt
are at risk of 3 types of Esophagitis when their
CD falls below 50. MC is Candida, so first we give Oral Fluconazole. If pt didt
responde w/i 3-4 days, then we do esophagoscopy to check for Herpes or CMV
causes. \n\n
**** Once PPD is >5mm in HIV pt
then Prophylactic theapy with Isoniazide + Pyridoxine is indicated for 9months. **** in a pt with bilateral interestitial pneumoni, the agent is PCP.\n\n
** Tx
is Trimeta-Sulfa, in pt with moderate to severe infection adding corticosteriods has reduced mortlity. Indication for steriod is 1- PaO2<70 and 2-A-a gradient >35. *** Best screening test is Eliza, then confirmatory with Western bloting.\n\n
*** Multiple ring enhancing lesionson on CT in aids pt
is tx w Sulfadiazine and Pyrimethamine which is both diagnostic and therapeutic.
Remember trimeta-sulfa is for prophylaxis.\n\n
**** If health worker is infected,
right
away get blood for serology and start him on 3 drug therapy while waiting for
results. Blood serology should be repeated in 6 weeks, 3 and 6 moths.\n\n
***** HIV pts
are at increased risk of TB which may cause collapse of vertebral bodies and
intervertbral disk.\n\n
*** DDX of Diarrhea in HIV pt with CD4=80.
1-Cryptosporidium :Modified Acid fast stain shows Oocytes in stool. It becomes
persistent in CD<180, its self limited. 2-Isospora is dx like Cryptosporidiosis but its
not as common. 3-Microsporidia organisms are asso with severe malabsorption and
persistent diarrhea in pt with HIV(immunocompetent).\n\n
**In stool they are SPORES \n\n
not Oocytes. So Cryptosporidium is the majot cause of persistant diarrhea in HIV
pts with CD<180cells/mm3.****HIV pt with fever,ha, csf india ink shows
encapsulated yeast, dx is Cryptococcus Meningitis, Tx is IV Fluconazole + IV
flucytosin.\n\n
...
***** PCP tx is IV Trimeta-Sulfa.
Inhaled Pentamidine is for prophylaxis. Prednisone is used in combo with Trim-Sulfa when PaO2 is <70mm/hg.\n\n
*** Role of BCG
is not proven in HIV pts so dont give it to them. But Pneumococcal vaccine is recomended in pts with CD4>200.\n\n

******* PML (by JC virus) presents in HIV pt with CD4<100??
CT shows multiple NON-ENHANCING lesions with no mass effect. DDX1:Toxoplasmosis, the mc RING enhancing mass lesion in HIV. MRI shows multiple spherical lesions in basal ganglia. Just because antibody is positive doesnt mean pt has it. \n\n
DDX2:
CNS Lymphoma,is the 2ns mcc of mass lesion in HIV pt. It also presnts with ring enhancing lesion in MRI but its usulaly SOLITARY and periventricular. Presnece of EBV DNA in CSF is Dx.\n\n
*****Kaposi sarcoma
is elliptical, arranged linearaly on legs arms, face, oral cavity and
genitalia. Initilay papules and later develop into plaques or nodules, and their color
changes from brown to violet. No necrosis of the skin.\n\n
DDX:
Bacillary Angiomatosis
is caused by G- rod Bartonella and is cured with antibiotics. they are red papules r
nodulesasso with fever, chills, malaise, HA and anorexia. They are highly vascular,
initialy and smooth. Later on eroded and encrusted. \n\n
**** BAL
(Bronch Alveolar Lavage) is >90% effective in dignosinfg PCP in HIV pt, especially when
CD<200.**** DDX of cough in HIV pt:1-Pneumococcus Penumonia, presents with
acute, high grade fever, and plrutal effusion, Its still the mcc of penumoniain HIV
pt. \n\n
2-TB,
presents with Chronic coug, night sweat and weight loss. 3-
Coccidiomycosis, presents with milliary pattern or nodular infiltrate on cxr, in
southwest USA. 4-PCP, Presents with DRY cough, and dyspnea, NO
EFFUSIONS.\n\n
*** HIV pt with cavitation:
posibilites are TB, NOCARDIA. Nocardia is partialy acid fast So if pt prestns with night sweat,feve and cough and has PPD of 3mm, and partial acid fast filmaents branching rods, its Nocardia. TX is trmeta-Sulfa.\n\n
***Since diarrhea in HIV pt
could be caused by a number of organisms, the first step is Stool exam and not Empiric anbibiotics.\n\n
**** When HIV IV drug user
comes with dry cough, regardless of having, diarrhea, iv drug user and other things,
the MCC is PCP. If he is alergic to sulfa, then Pentamdine is DOC. \n\n
***Lymphoma
in HIV pt presents
with EBV DNA, SOLITARY ring enhancing mass in
periventricular with MRI.\n\n
DDX1:
Toxoplasmosis, MRI shows MULTIPLE ring
enhaned leiosn in basal ganglia. A positive toxoplasma serolog is common in US so
its not specific. Also if pt is taking Trimeta-sulfa, this etiology in unlikely.\n\n
DDX2:
Progg Multifocal Leukoecephalopathy lesions are NON enhancing and dont
produce mass effect.\n\n
****Condylomata acuminata
(anogenital warts) are skin colored or pink, verrucous or papiliform skin lesions present around the anus andPodophyline(antimitotic agent) is a tx option. Its CI in pregnancy. \n\n
**DDX
isCondylmata Lata, due to 2ary Syphlis, tx is Pecnicilline, are flat or velvety. \n\n
**** HIV EYE problems
1-CMV Retinitis, occurs in HIV pt w CD4<50, presents with
yellowish-white patches of retinal opacification & retinal hemorrhages. Tx is
Ganciclovir or Foscarnet. 2-Ocular Toxoplasmosis, severe retinal choroiditis, >50%
have encephalitis. Necrosis of inner retina as white flyffy lesions.\n\n
DD 3
3-Herpes Simples
Keratitis, pain, photophobia and decreased vision. Dendritic ulcer is the mc
presentation. 4-Herpes Zoster Ophtalmicus, mostly in elderly, or HIV pt. Presents
with fever, malaise, itching and burning around the eye. Vesicular rash following
trigeminal nerve. If eye is involved hay conjunctivitis and dendriform corneal
ulcers. \n\n
DD5-
HIV Retinopathy, presents as benign cotton wool spots in retina which
remits spontaneously. ****Tx for Condylomata Acuminata is Podophyline.
*****Cryptococ Meningitis infection in AIDS pts, tx is iv. Amphotericin+Flucytosine. \n\n
Hodgkin's :
Tx is ABVD. Adriamycin SE is cardiomyopathy. Bleomycin SE is pulmonary.
Dacabrazine is Ematogenic. Vinblastin SE is Neuropathy leading to constipation. \n\n
Homocystinuria
Marfan features+mental retardation+thromboembolic events+downward
dislocation of the lens is suggestive. Tx is high dose Vit B6.\n\n
Hordeolum ( Stye)
a common staph abscess of the eyelid. Tx is warm compresses. Incision and drainage
is performed if resolution does not begin in the next 48 hours.\n\n
Hormone Replacement Therapy:
According to 2005 studies HRP increases the risk for Cerebrovascular accident, CV
disease, Breast Cancer and DVT. It Decreases the risk of Hip fracture, Colorectal
cancer and vulvovaginal atrophy.\n\n
Human Bites
Tx of choice is Amoxicilline/Clavulanic.\n\n
Humeral Fractures
Tx of choice is closed reduction and hanging cast. In cases of Segmented fragtures,
or open fracture in trauma, pathologic fracture and vascular structures, open
reduction and internal fixation is done.\n\n
Huntington - 2
Atrophy of caudate nucleous is characteristic. Mood disturbance, Dementia, Chorea
and family history.\n\n
Hyaline membrane dis
should be suspected in preerm infacnts. With respirtory distress and hypoxia, NOT
responding to oxygen therapy. The characterisric cxy shows fine reticuar
granularity of the lung parenchyma. Tx includes early ventillation and surfactant.\n\n
Hydatid Cyst of Liver
Is due to infection with Echinococcus ganulosis. Can be contacted from dogs. It can
cause Cyst in lung,muscle,bone,liver. In most pts its asymptomatic. "Eggshel
calcification" of a hepatic cyst on CT is highly suggestive. Aspiration is NOT
indicated due to chance of anaphylactic shock. Tx is surgical resection under the
cover of Albendazole.\n\n
Hydrocele
1-Non Communicating Hydrocele is refered to a fluid containing sac which is a
remnant of processus vaginalis. The upper limits of the mass is easily identified.
Most cases of NCHC will dispear spontanously by the age of 12 months. 2-
Communicating Hydrocele, the upper limit cant be reached and it treated with
surgery.\n\n
Hydrocephalus
Happens in infants. CT scan , dialation of entire ventricular system with distinct
enlargment of subarachnoid space ofer the cerebral cortex), is very suggestive of
non-communicating or commuicating hydrocephalus.\n\n
*** Accumulation of blood in
subarachoid space
may destry Arachnoid villi and whose job is to absorb CSF and
lead to hydrocephalus. SAH is the mcc od communicating hydrocephalus. Its very
common in PREMATURE infants. \n\n
***Non-Communicating hydrocephalus examples
are Dandy-Walker and Arnorld-Chiari. DW shows a cyctic exapansion of fourth
ventricle, and AC will rreveal posterior protrusion of posterior fossa through
foramen magnun.\n\n
Hydroxychloroquine
is the safest drug for SLE but rarely it may cause serious eye dis including Macular
degeneration, so eye exam at 6mo to 1yr intervals should be performed. Remember
the mc SE is Alegic skin reaction. Also CI is G6PD Def.\n\n
Hyperandrogenism
A female prsetns with virilization, balding and clitonegaly. What to do next?
Rapidly developing hyperandrogenism with virilization is indicative of androgensecreting
neoplasm of OVARY or ADRENAL. So next measure serum Testosterone
and DHEAS to determine the site of tumor. \n\n
***Elevated Testosteone level with noraml
DHEAS indicate ovarian source, but Elevated DHEAS with normal Testtosterone
indicate Adrenal source. Now dont try to measure 17-HO, because that is for
Congenital Adrenal Hyperplasia and happen very early inlife.\n\n
Hypercalcemia - 8
Hypercalcemia due to metastatic tumor (Breast) cancer. In all womem w metastaic
breast cancer and radiographic lytic bone disease who are receiving either hormone
therapy or chemotherapy (Tamoxifen), IV Pamidronate (Biphosphonate) is
recommended. \n\n
* In acute severe hypercalcemia
, its importnant to FIRST give IV
0.9% Saline before giving Furesamide. Its complicated read MERCKs. \n\n
***MCC H/P in hypercalcemic pt
Constipation is the mc GI presentation in hypercalcemic pt. The important renal manifestation is neprolithiasis. \n\n
Chronic therapy with vitD
is a major cause for Hypercalcemia. Tx is stopping vitD tx and low calcium diet, keeping urin acidic and give corticosteriods.\n\n
****Hypercalcemia
is the mc Paraneoplastic syndrom that is asso with Squamous
CC lung cancer. Hypercalcemia production is due to ectopic PTH related petide
(PTHrP) production.\n\n
*****Immobilization can lead to HyperCa.
Prolonged bed rest
can lead to accelerated bone resorption, OsteoClastic activation in increased bone
turn over is established. Biphosphonate therapy is helpful. \n\n
**DDX:
Rhabdomyolysis,
HypOcalcemia (not HyperCa) is seen, normaly du eto increased binding of Ca to
Phosphorous that was released by muscle.\n\n
** DDX2
Hypercalcemia due to
Malignancy, Causes include local osteolytic metastasis, secretion of PTHrPand
increased 1-25VitD. \n\n
** DDX3
Hypoalbuminemia, Any change in albumin levels will
affect total serum Ca levels w/o affecting the ionized fraction. In pt with decreased
albumin total serum ca is decreased.\n\n
****Malignancy is a frequent casue
like Breast cancer. There are various mechanism by which cancer causes hypercalcemia.
1-Procuction of Cytokins:Tumors that are metastatic to bones cause local osteolysis
by production of Cytokins like IL-1 and TNF. The mf tumors that produce
hyperalcemic by this method are lung and breast cancer. \n\n
2-PTHrH
(related
hormones):Themcc of Hypercalcemia in pt with non-metastatic solid tumors is
production of PTHrH. in these pt PTH is low. \n\n
3-Calcitriol
Hypercalcemia in case of
Hodgkins is due to Calcitrol 4-Ectopic PTH:Its very rare and has been reported in
ovarian cancer, lung cancer and neuroectodermal tumurs.\n\n
***Hypercalcemia 2ary to malignancy is dueto multiple reasons
including osteolytic metastasis, secretion os PTHrP, increased formation of 1,25-dihydroxyVitD, increased interleukins-6.Generaly, hypercalcemia due to malignancy(2ary HCa) is higher than primary HCa.\n\n
*****Pt with Squamous cell carcinoma
will have Hypercalcemia, now if he
vomits, he will be at risk for Acute Hypercalcemic Crisis. \n\n
**Tx
is first normal saline for hydration and 2nd Furesamide to maintian urine output at 200cc/hr. Biphosphonate Pamidronate would work too, but by givng saline you both take careof hypercalcemia and hydrate to prevent Azothemia (renal failure) in the pt.\n\n
Hyperemesis Gravidarum:
In a pregnant female in her first trimester, who presents with severe and persistant
vomiting think of HG. It is severe enough that requires admission.\n\n
** Cause
is unknown but related to elevated HCG, which maybe indicative of Hydatiform mole. Order HCG to confirm that levels are consistant with the stage of pregnancy.\n\n
HyperKalemia - 4
MC due to Rhabdomyolysis. Ekg shows Tall T waves. Calcium Gluconate is given
first and then Insulin, glucose and Kayexalate. Insulin drives K in to the cell, \n\n
** its given with glucose to prevent hypoglycemia,
and Kayexalate exchanges Na for K in GI and excretes K. \n\n
* Caused by either Medication
K sparing diuretis, ACE inhibitors, NSAID or Pseudo hyperKalemia if the lab sample is hemolysed , decreased renal K excretion, transcellular shift, increased K intake. \n\n
**The most serious SE is cardiac toxicity
so do an EKG in ALL pts. It shows peaked T waves, prolong PR and QRS, progressive widening of QRS leads to Ventricular Fibrillation
or Asystole. \n\n
The approach to Tx hyperkalemia
depends on EKG and degree of HyperKalemia.Immediate tx is needed if there is cardiac toxicity, muscular paralysis, or K>6.5. For these pts 10ml of 10% calcium gloconate stabalizes cardiac membrane.\n\n
** To lower K level
, insulin or B2 agonist is used since they drive K into cells. Sodium Bicarbonate can also drive K into cells. Slower acting tx is loop or thiazide diuretics which excrete K. \n\n
**Dialysis
is reseved for pts with renal failure and those with lilfe threating hyperlalemia wich wont respond to medication. So...If the pt is Asymptomatic and just non malignant hyperkalemia, just discontinue Amiloride ( to get rid of K ) for a weak and recheck.\n\n
** If the pt has evidence of cardiac tox
or K is >6.5, then give Calcium Gloconate and IV Dextrose plus Insulin.
* best drug to excrete K from body is Kayaxelate.\n\n
Hyperparathyroidism - 3
Increaed Calcium, decreased phosphate, increased PTH. Could be Asymptomatic.
While all pt with symptomatic HPTshould have parathyroidectomy, not all
Asymptomatic pt need this surgery. \n\n
***Criteria is as follows
1-Serum Ca level at least 1mg/dl above upper normal limit
2-24hr urinary Ca above 400mg
3-Young age<50
4-Bone Mineral Density < T-2.5 at any site
5-difficulty in follow up of the pt.\n\n
*****Hyperparathyroidism is asso with Pseudogout,
Joint fluid aspiration reveals rhomboid shape calcium pyrophosphate crystals with positive bifringent. \n\n
**Tx
is Colchicine, Indomethacin often stops acute attacks promptly.\n\n
****Primary HPT is the mcc
of hypercalcemia in ambulatory pts. Its asso with elevated PTH and decreased phsphorous. Now CRF can lead to SECONDARY HPT,\n\n
** PTH levels
are higher in 2ary than Primary HPT, Ca levels are normal to low in 2ary HPT because cause of elevated PTH level is hypocalcemia. \n\n
**Now
in Sarcoidosis there is increased conversion of 25-hydroxy VitD to 1,25 hydroxy VitD. thereby increased absorption of calcium from GIT and hypercalcemia, PTH is supressed.\n\n
*****Asympomatic Primary Hyperpara
HyperCa, HypoPO4, Elevated PTH. Its common in female
>60, identified during routin lab work. While Parathyroidectomy is needed for all
symptomatic pts, not all Asymptomatic pts need surgery. \n\n
**Criteria includes:
1-Serum
Ca level at least 1mg/dL above the upper limit of normal. 2- 24hr urinary Ca level
>400mg. 3-Young age <50. 4-Bone Mineral Density lower than T-2.5 . 5-Difficulty to
follow up pt.\n\n
Hypertension - 7
In elderly HT leads to Benign Nephrosclerosis.
HT is the 2nd mcc of renal dis in US.
The process of kidney damage evolves from Nephrosclerosis to Glomerulosclerosis.\n\n
**Nephrosclerosis is characterized by
hypertrophy & intimal medial fibrosis of renal arteries,
whereas, GlomeruloSclerosis is progressive loss of glomerular capilary surface area and glomerular and peritubular fibrosis.
**Microscopic Hematuria and
proteinuria
occurs due to glomerular lesions. So pt presents with Anemia (decreased Hb)
**DDX:
Diabetic Nephropathy, is the leading cause of end stage renal disease in US.
Increased extracellular matrix, , basement membrane thickening, mesangial expansion and fibrosis characterize DN.\n\n
***Isolated SYSTOLIC HT,
is an importnat cause of HT in Elderly.Pathophys is decreased elasticity of arterial wall,
leading to increased SYSTOLIC bp, w/o diastolic bp leading to wide pulse pressure.Hydrochlorothiazide is the DOC. \n\n
**DDX:
Aortic Insufficiency can cause the
same systems, Echo will differentiate. \n\n
****Tx
of choice for Pt with Intermittant
claudication due to atherosclerosis and HT is Ca chanle blocker.\n\n
****OCPs
are
common causes of 2ary HT caused by Estrogen mediated increase in in teh synthesis
of Angiotensinogen in the liver.\n\n
** So stop taking the OCP
and HT should go back to
normal. If it didnt then its Essential HT and life style modification can be tried. If
that didnt work either, then the next step is Thiazides.\n\n
****Alcohol is a risk factor
for HT, Smoking is not.****The tx of choice for Isolated Systolic HT (150/70,160/78)
is Thiazides low dose.\n\n
****Lifestyle modification
should ALWAYS be a part of
mngmnt. All pts should be encouraged to lose WEIGHT , reduce SALT, avoid
excess ALCOHOL (3bottle a week is excess). and stop SMOKING. This is more
important than DRUG MODIFICATION. REMEMBER.\n\n
Hypertensive Retinopathy -2
Don't show any symptoms assos with visual loss. Initially hay focal spasm of
arteriols followed by progressive sclerosis and narrowing. Fundoscopy may reveal
AV nicking, coper or silver wiring, exudates and hemorrhages\n\n
.*****Grade
1=slight
AV nicking. Grade2=Copper wiring, AV depression with humping heads.
Grade3=Silver wiring, flame shaped hemorrhages, exudates. Grade4=Flame shape
hemorrhages, exudates and papil edema.\n\n
Hyperthyroidism - 5
Hyperchlosterolemia (increased LDL) is the most frequent lipid abnormality in pts.\n\n
*****High estrogen levels in pregnancy
result in increase TIBG production by\n\n
liver. So production of T4 nd T3 is increased (but not Free ones) . \n\n
**This increase however
does not result in clinical symptoms because excess T3&T4 are bound to excess TIBG. And since Free T3&T4 are the same TSH will be normal.\n\n
*****Atrial Fibrilation is a common complication
in hyperthyroidism, Graves disease. In pts
with Hyperthyroidism related tachysystolic Atrial Fibrilation a beta
blocker,propranolol, is the doc.\n\n
**** Antithyroid drugs, PropylThioUracil and
Methimazole are asso
with Agranulocytosis. Immune destruction of granulocytes
starts w/i 90 days post therapy. Fever and sore throat are indicative of
Agranulocytosis. Monitering in ineffetive. Stop othe drug
immediately.\n\n
****Palpitation should make you think of it.
The the 1st test is TSH, almost all pt have low TSH (only exception is TSH secreting pituitary Adenoma). If TSH is low then measure Free T4, if its elevated Dx is established. \n\n
**Then do 24-hr
thyroid radioiodine uptake
to ddx Graves form the rest. Propranolol is initially used
for symptoms until definitive cause is known. Radioactive iodine is tx of choice for
ALL Grave's pts, \n\n
** however,
Propranalol is STILL best initial choice. PTU can be
used but hyperthyroidism can recur w/i 6 months. So PTU is only used when Iodine
tx is CI, like in Pregnancy. Subtotal Thyroidectomy is also curative but its not the
INITIAL tx of choice.\n\n
Hypertrophic Osteoarthropathy
Characterized by chronic proliferative periostitis of long bones , clubing of fingers
and synovitis, Its asso with Squamou cell carcnimoa and Adenocarcinoma of the
lung.\n\n
HypoCalcemia
Plasma calcium exists in three forms: ionized calium (45%), ALBUMIN-BOUND
(40%), and calcium bound to organic and inorganic anions. Homeostasis of these
forms is significantly influenced by the extracellularpH level. \n\n
** An increased pH level
causes an increase in the affinity of serum albumin to calcium, thereby increasing
the level of albumin-bound calicium, and consequently decreasing the levels of
ionized calcium. Ionic calcium is the only physio logically active form, which means
the decreased levels of this form can result in clinical manifestations of hypocalemia
(crampy pain, paresthesias and carpopedal spasm). \n\n
**Increased extracellular pH
levels (Respiratory Alkolosis) can cause an increase in the affinity of serum albumin
to calcium, thereby increasing the levels of albumin-bound calcium, and
consequently decreasing the levels of ionized calcium leading to hypocalcemia. Hay increased DTR.\n\n
*****Hypocalcemia can occur during or right after
SURGEY, especially if transfusion is involves. First manifestation is increased DTR.
HypoMg manifest with Decreased DTR.\n\n
...
Hypochondiasis
Symptoms occur durng periods of stress (med student worried about intracranial
hemorrhage), pt shoudlbe asked about current emotional stresses and then referd
for a breif psychotherpay.\n\n
Hypogonadism
T9Q4. Re-read Merck highlights.\n\n
HypoKalemia - 2
A35. All Beta-2 agonist reduce serum K by driving it in to cells. In occasional pt they
cause HypoKalemia. So any pt taking B2 and complaining of muscle weakness
Hypokalemia must be rules out.\n\n
** PEFR
(peek expiratory flow rate) and Cxr are not
of any use. We need to do Serum Electrolyte panel. and EKG to see "U" waves.
Beta-2 also produces a more common SE of Fine resting tremor of fingers and
peripherla edema.\n\n
Hyponatremia
Is a bad prognostic factor for pt with heart disease.\n\n
Hypothermia
Fluphenazine causes hypothermia by causing vasodialation and inhibition of
shivering. Hyperthermia is common in drug abusers.\n\n
Hypothyroidism - 5
Generalized resistance to thyroid hormones.***Its asso with wide spectrum of musle
involvement ranging from astmptomatic elevation of CK to Myalgia, muscle
hypertrophy, myopathy. So suspect it if hay elevated CK and Myopathy.\n\n
*It's the most common SE
of radiation therapy for Graves. * Asso with Hyperlipidemia. So unexplained hyponatremia, hyperlipidemia ane elevated serum muscle enzymes are indication for thyroid function tests.\n\n
****Always rule out
Hypothyroidims in a pt with Major Deppresive Disorder.If this option, "ordering blood test" for TSH was offered pick it over other options. ***** Thyroid dysgenesis is the mcc of congenital hypothyroidism in US.\n\n
Iatrogenic Esophag perforax
Pt comes back w/I hours with problems. Do contrast study of esophagus, if
perforation is present , priary closureof esophagus, , and drainge of mediastinum
must be done w/I 6 hours to prevent development of Mediastiitis.\n\n
Ichthyosis Vulgaris(Lizard Skin)
Dry and rough skin with horny plates over the surfaces of the limb. Tx is
minimizing bathing, Oral retinoids (CI in pregnant women).\n\n
Idiopathic Pulmonary Fibrosis
Presents in 4-5 decade of life, fatigue,anorexia,weightloss, rthralgia, cyanosis and
clubbing. Xr shows bilateral interstitial involvement. Biopsy is done to rule out
sarcoid. Tx is Steriods. \n\n
**Mean survival is
2-5 yr after dx. Pleurodesis (where visceral
and parietal pleura are fused, is used to treat recurrent pneunomothorax and
effusion) is not used here.\n\n
Iga Deficiency, Misc 6/2
Recurrent sinopulmonary and GI infections (diarrhea), and anaphylactic
transfusion reaction. Dx is made if IgA serum concentration is <7mg/dl with normal
IgG and IgM levels. \n\n
**Tx
targets prophylaxis and prevention. Initialy a six month
course of daily prophylactic Trimeta-Sulfa or Amoxicilline , if fails needs IVIG with
least amount of IgA. Don't confuse sinupilmonary recurrent infection with CF, CF
doesn't cause anaphylactic reaction.\n\n
IgA Nephropathy
Is the mcc of glomerulonephritis in adults. Pt have recurrent episodes of gross
hematurea, beginning 1-3 days after upper respiratory infection. Serum
complement levels are normal.\n\n
Immune Thrombocytopenia
Occurs in children 2/6 yo. Pathogenesis involves antibodies that bind to platelets and
subsequent destruction of these complexes in spleen. Its preceded with viral
infection, and presents with petechia,purpura,hematuroa,or GI bleeding. No
adenopathy.\n\n
** Lab
shows no abnormality ecept thrmbocytopenia (60000). The course
is felf limited. It requires no TX. If thrombocytopenia is <30000corticosteriods are
DOC.\n\n
Impetigo Bullous - 2 . Dermo. 6/3
Tx: Mupirocin ointment is choice for local impetigo. If no respose then treat
systmicallly. Because most cases are caused by penicillinase-producing
staphylococci, Cloxacillin or a 1st-generation cephalosporin is the drug of choice in
severe cases. Penicillin-allergic patients should receive cefadroxil or cephalexin
rather than erythromyc.\n\n
Incontinence - 4
1-STRESS incintinence: Occurs when there is a sudden increase in abdominla
muscle. Pelvic muscle exercise (Kegel exercise) Urethropexy are rcommended tx.
It's a CC of incontinence in older women, HIGH PARITY is a major risk factor. \n\n
**A high number of vaginal deliveries
may lead to pelvic floor weakness over a period of time. Urethra relapses outside the pelvic so whenrver there is increase
intraabdominal pressure (cough,sneez,laugh) urine ensues.\n\n
** Aggrevating factors are
Obesity, pregnancy, COPD and Smoking. Postvoid cystometry is normal. Tx include
Kegel excercise, esterogen in post menopasusal women. Surgical tx is Burch and
Sling procedures. \n\n
2-URGE Incontinence:
Detruser instability, blader irritation form
neoplasm, and interestitial cyctitis result in UI, which causes sudden and frequesnt
loss of moderate to large amount of urine. Often accomodated with Nocturia.\n\n
3- OVERFLOW:
Diabetic Nephropathy causes OI. Characterized by loss of small
amount of urine from an over extended bladder and a markedly increased residual
volume. There is hx of DM which is not controlled. \n\n
****CC are certain medications
(Ibuprofen), Diabetic nephropathy, MS and spinal cord injury. NSAIDs have an
inhibitory action on the detruser, so the first step is to stop NSAID. Then cholinergic
drug (Bethanechol) should be added afterwards to improve detruser action .
Intermittent self catheterization can be used.\n\n
****One of effects of epidural
anesthesia is urinary retension due to denervation of bladder. When bladder
presure is > sphingter pt urianates until balace is achieved again. This incontinence
is transient. \n\n
...
**PE may show distended blader. Postvoidal vol is high. Tx is by
Intermittant cathaterization until control is regained. Oxybutyrin is used for Urge
incontinence. Urethroplexy is for stress incontinence.\n\n
...
Infantile SAH:
CT scan shows dilation of entire ventricular system with distinct enlargment of
subarachnoid space over the cerebral cortex, is suggestive of nonobstructive or
communicating hydrocephalus secondary to SAH. \n\n
** SAH is the mcc
of communicating hydrocephalus. Accumulation of blood in subarachnoid space may lead to destruction of arachnoid villi and cisterns (that absorb CSF), \n\n
**SAH is caused by
intracranial hemorrhage common in premies. DDX Arnord Chiari, noncommunicating, protrusion of structures through foramen magnum. DDX Dandy -
Walker, NC, cystic expantion of 4th ventricle.\n\n
Infectious Diarrhea
Classified into 2 types, bloody or non bloodt. Bloody is caused by E.coli O157:H7
most commonly, also by Shigella, salmonella, Campylobacter, E. Histolytica and
Yersinia and C. difficile.\n\n
Infectious Mononucleosis - 7
Heterophil antibody test is sensitive and specif. If its negative and you're still
suspitious, do EBV specific antibody test. Splenic rupture is a serious complication.
So pts with splenomegally are advised bed rest and avoidance of contact sports until
no more spleenomegally.\n\n
** Glucocorticoids are indicated
if IM is complicated by
upper airway obstruction, autoimmune hemolytic anemia, and thrombocytopenia(
and resultant petechia).\n\n
IM is caused by Ebstein Bar virus.
Sometimes it is detected
only after pt develops a characteristic polymorphic rash after taking Ampicilline for
an apparant upper respiratory track infection.\n\n
**** Is asso
with Autoimmune Hemolytic Anemia.*****Blood smear with Atypical Lymphocytes ( Large basophilic Lymphocytes) should make oyu tink of it. It might also be in
Toxoplasmosis by CMV is the mc organism.\n\n
*****A negative Heterophile antibodies
dont exclude IM, because sometimes they appear later in the course.\n\n\n\n
Infective Endocarditis - 14, Infx 6/2
Generally if the procedure involves bleeding, prophylaxis is recommended. For
procedures that is low risk like, GI endoscopy, there is no need for prophylaxis. \n\n
Tx
inclludes: 1-For IV drug user is IV Vancomycin+ IV gentamycin, since the incidence
of MRSA is increased in IV users Vancomycin is better than Nafcilline). 2-For non
IV users IV Nafcilline+ IV gentamycin. \n\n
If IE
is due to Strep Bovis, he is at risk for
Colon cancer, colocoscopy is recommended. Chordinae tendinea rupture occurs as a
complication if IE. \n\n
**** Pathophysiological consequesnces
and clinical manisfestation od IE can be explained by:1-Cytokine production, responsible for fever. 2-Embolization of veg fragments that leads to Pulm and Spleen infarction. 3- Hematogenous infection of sites. 4-Tissue injury due to Immune complex and immune responses to the deposited bacterial antigens. \n\n
H/P
ROTH spots, are due to
immune vasculitis. They are oval retinal hemorrhages with pale centers, they have
been noticed in pts with collagen vasculat dis and hemorrhagic disorders. OLSER
NODES, violacious nodules founf at the pulp of the fingers and toes, due to immune
complex deposition. \n\n
H/P
Immune complex is also responsible for GN and Rehumatolic
manifestation of IE. JANEWAY LESIONS, macular,blanching, non painful
erythomatous lesions on the palms and soles, they are due to SEPTIC EMBOLI,
revealing subcutanous abcesses.\n\n
****Tricuspid Endocarditis
is asso with IV drug abusers. S.aureus is the mc organism. Tricuspid murmurs are accentuated by inspiration and neck vein distention. Echo is the dx choice. Cxr shows peripheral Welll circumsribed lesion with cavitation, Surgery is required in majority of pts. Valve repair or replacement is therapeutic. \n\n
*****Pt with IE who goes inder GU
instrumentation for evaluation of microscopic hematuria could have an
exacerbation post procedure with murmur and other symptoms of IE.\n\n
****Subacute bacterial infective endocarditis
(SABIE) is seen n pts with damaged valves. Strep Viridens is the mcc. Acute BIE is caused by S.Aureus in IV drug users.
S.Epidermitis is seen in pt with Prosthetic valves.\n\n
***Strep Viridans
(S. Mutans) are the mc responsible for endocarditis after dental work.\n\n
****Decision to giveprophylactic antibiotis
depends on risk due to condition of the pt and also depends
on the procedure being done. \n\n
Risk classication
are:1-HIGH risk pt are Prosthertic
valves, previous hx of IE, Cyanotic pts. 2-MODERATE risk pt are congenial cadiac
abonormmalies Acquired valve dis, MVP and regurgitation, and HCM.\n\n
** Now conditions that DONT REQUIRE prophylaxis
are MVP w/o regorgitation, innocent murmurs, Pacemakers and defibrilators.\n\n
****IE in IV drug users is
in right heart and caused by staph aureus with involvemtn of Tricuspid valve. The holosystolic mumur that intensifies with inspiration is Tricuspid Regurgitation. Vegetations can emboli to remote organs, so if pt have fever and hemoptysis this would be SEPTIC EMBOLI. \n\n
****DDX
with Bronchiectasis is that there s a hx of CHRONIC productive
cough. DDX of Abscess is foul smell and cavity in Cxr.\n\n
****Prophylaxis medication
guides: 1-Amoxicilline is the DOC in Dental, and Respiratory procedures. In pt with
penicilline allergy, Cefazolin, Clindamycin or Clarithromycin is used. 2-In
Genitourinary and GI procedures, other than esophageal, the doc is Ampicillin plus
Gentamycin.\n\n
If pt is allergic
to penicillin Vancomycin Plus Gentamycin is
used****Once you suspect it the next step is to give IV biotics after you draw blood.
TEE comes afterwards. Positive blood cultures and vegetatin on the valve seen in
TEE confirms dx.\n\n
****Always suspect IE
when a pt is febrile , hx of Rheumatic fever
and hematuria. Hematuria in Bacterial Endocarditis is due to glomerlar injury
caused by deposition of immune complex. *****If pt has FUNGAL endocarditis
then the next step is surgery because they are very aggressive in the valves.\n\n
Infertility - 4, OBGYN, 6/2
The first step in WOMEN is to check Basal Body Temperature and mid luteal
PROGESTERONE. The ovulatory factor involves defects in the hypo-thalamic
pituitary ovarian axis, and related infertility maybe due to impairment of follicular
maturation ovulation or endometrial development. \n\n
***BBT
assess the DURATION
luteal finction and MLP asseses LEVEL of lutal function. Endometrial biposy is
done to confirm luteal phase defect. rather than initial evaluation. \n\n
****MALES
Male coital factor is responsible for 40% of all cases infertility, common conditions
include varicocele, genital tract trauma or surgerydisruption of hypothalamic-pic
axis, or Iatrogenic causes like smoking and occupational exposure. The first step in
MALE evaluation is sperm count.\n\n
** if its normal
then an endocrine hormonal
evaluation is carried out. It includes: 1-TFT (since increaed TSH inhibits GnRH and
then decrease FSH. 2-Testosterone levels to indicate the presene or not of Gonadism.
3-Gonadotropin to determine whether hypogonadism is central or testicular and 4-
Prolactin lelevs.\n\n
****Causes of infertility in femlaes
falls in 4 factors: 1-Peritoneal factor. 2-Ovulatory. 3-Cervical. 4-tubo-uterine. Peritoneal is the mc type and includes Endometriosis and peritoneal adhesions. Laparoscopy is the procedure of choice. for dx and tx.\n\n
** Mild forms of endometriosis usually respond to meds like
GnRH agonists, Danazol and Medroxyprogesterone. 2-Ovulatory factor involves
hypothalamus-pit-ovary axis. and infertility might be due to impairment of
follicular maturation, ovulation,or endometrial development. ovulatory abnormality
may initially be screened by Basal body temp and midluteal phase level of
progesterone, the former asseses DURAtion and later LEVEL of luteal function. \n\n
...
If luteal phase shows low progesterone,
hence infertility, then tx is suppository
progesterone deposition. 3-Tubo0uterine is seldom a cause. It onvolves Fibroids,
endometrial polyps, tubal occlusion(2ary to IUD or endometriosis). Investigation is
ainlt hysterosalpingography or laparoscopy. 4-Cervial involves cervial structure
abnormalities and abnormal mucus production. In 5-10% infertility remains
unidentified. Intrauterine insemination is the tx.\n\n
*****Clomiphene Citrate
is an antiesterogen that acts by competitively inhibiting esterogen receptors at hypothalamus, thus inhibiting the negative feed back esterogen has on GnRH production
and consequesntly increasing LH & FSH secretion and improving ovulation. Along
with HCG and HMC its indicated for chronic anovulaation.\n\n
Side effects include
large ovaries, hot flashes, abdominal bloating, breast discomfort and abnormal
uterine bleeding. Major complications include Ovarian Hyperstimulation Synd and
multiple gestations.\n\n
** Danazol is
an androgen derivative having a gonadotropin
inhibitory effect, indicated in endometriosis, fibroids and fibrocystic breast disease.\n\n
Inflamatory Bowel Disease - 2
Erythema nodosum, arthralgias, diarrhea, and positive PANCA ( 60-80% in UC
and 10-25% in Crohn) in a young pt are highly suggestive of IBD. ***Any young pt
with with bloody diarrhea should make you think of IBD\n\n
DDX
would be infectious
diarrhea, mostly Campylobacter. If pt presents with rectal tenderness and mucus
and distended abdomen he might have UC with a fulminant course and Toxic
megacolon. Fulminant colitis is a serious comlication, xray shows it.
Proctosigmoidoscopy with biopsy establishes Dx.\n\n
Influenza
Presnts with, cough,coryza,fever,chills,malaise,sorethroat, muscle pain. Dx is made
clinicaly, however a rapid lab test for Influenza antigens srom nasal swap is
available. The infection is self limiting b/w 1-7 days. Treat with bed rest and
acetaminophen. Two calsses of drugs for prvention and tx are 1-Amantidine (influ-
A), 2-Oseltamivir for both A & B.\n\n
Influenza Vaccine:
Is recommended in annual basis for all adults over 65 and adults of any age at risk
of developing influenza (1-Chronic dis like CV or COPD. 2-Immunocompromised.
3-Nersing home residents. 4-Pregos in 2nd trimeseter in influenza season). This is
NOT Influenza B vaccine.\n\n
Insulinoma - 2
Pancreatic B-cell tumor. Whipple's triad of attack occurs in fasting, there is
hypoglycemia and ingestion of CHO releives the symptom. Tx is surgery. 80-90%
are single benign tumor. !0% is malignant.DDX with Sulfunyluria(The
sulfonylureas lower plasma glucose primarily by stimulating insulin secretion. SE is
hypoglycemia and increased Cpeptide and increased plasma sulfunyluria) and
DDX2 is Exogenous insulin admin (normal Cpeptide).\n\n
Intellectualization
Helps the pt to be emotinaly detached from the wrong doing (murder) or
unacceptable fact (cancer). DDX:Rationalization is a logical reasoning for an
upsetting event rather than the true reason (students says they failed me).\n\n
Interestitial Lung Diseases
1-Extrinsic Allergic Alveolitis or Hypersensitivity Pneumonitis, due to exposure to
organic dust like fungal sporres or actinomyces, Farmer's Lung and Bird Breeders
are two examples. Features are fever, sypnea and non productive cough. Cxr shows
interstitial infiltrates. \n\n
**PFT
shows restrictive pattern (Reduces total lung volume).
The best tx is aviodance. 2-Alveolar Proteinosis, accumulation of phospholipid rich
material in alveoli. It presents with dyspnea and cough. \n\n
**Cxr
shows Bilateral alveolar
infiltrate and PFT shows restrictive pattern. Dx is lung bipsy and PAS positive
material. Tx is total lung Bronchoalveolar lavage. 3-Acute Interestitial Pneumonia,
an acute fatal disorder that rapidly progress to pulmonary fibrosis. \n\n
It presents in
>40 people, fever, breathlessness and cough. Pt has hypoxia and requires
ventilation. Cxr shows diffused bilateral alveolar infiltrate. 4-Asbestosis, Its initial
presentation may be Obstructive. Presents with Pleural Fibrosis. Its exposed to IN
organic dusts.\n\n
Intermittant explosive disorde
Is an impulse control disorder. Characterized by multiple episodes of assault
resulting from aggressive impulses, out of proportion to any stressor. \n\n
Its asso
with abnormality in serotonergic pathway of limbic system.
Internal carotid a. occlusion most commonly manifest in ocular disturbances and ischemia in middle cerebral artery territory.\n\n
Interossseous access
whenever pediatric iv line cant be found, this is the best place for it.\n\n
Intestinal Obstruction:
If hay simple mechanical obstruction then both Barium enema and Naslgastric
tube+IV fluids+NPO would be appropriate. \n\n
But
if hay obstruction with metabolic
acidosis and shock, then laparotomy is the only way to go and Laparoscopy is CI
due to shock & acidosis.\n\n
Intestinal perforation:
Best test is standing abdominal xray. Used for PUD rupture. If negative then US,
Ctand DPL is indicated.\n\n
Intra abdominal bleeding
Once you know the pt is bleeding into the abdomen the next thing to do is either US
or Diagnostic Peritoneal Lavage to find out the location of bleeding and then
exploratory laparotomy.\n\n
Intracranial Pressure:
Increased ICP is indicated by 1-Bilat dilated pupils. 2-Anisocoria, pupils are non
reactive to light. 3-Flacidity or decerbrate motor posturing. 4-Papiledema. Glascow
is not anindication for increased ICP.\n\n
Intraductal Papiloma:
A benign tumor of lactiferous ducts. Clinically manifest as serous bloody discharge.
Mamo wont show it, too small. Resection has to be done to relief pain guided by
galactogram.\n\n
Intra parebchymal hemorhage -2
Due to hypertension, think of Straie arteries that cause bleed in parenchymal in
Basal Ganglia.***** HT is the most important risk factor. 1-Cerebellar hemorhage:
acts for 16% of cases. \n\n
** Pt presents with Ataxia,vomit,occipital HA, gaze palsy. NO
HEMIPARESIS. Emegent decompresion may be life saving. 2-The mc site of
hypertensive hemorhage is Putamen, 35%. \n\n
...
** Internal capsule is always
affected
thereby leading to HEMIPARESIS. Other signs are hemi-sensory loss, homonomous
hemianopsia. stupor and coma. \n\n
**The eyes
are deviated form paralytic side. 3-Pontine
is accounted for 5-12%. Pt presents with DEEP COMA, and paraplegia that
developed w/i minutes. Pupils are pinpoint and reactive to light. No horizontal eye
movement.\n\n
Intrahepatic cholestasis of Preg
Jaundice in the third trimester of pregnancy should be evaluated for hepatic
disorders specific for pregnancy. Marked pruiritis and elevation of bile acids should
make you think of ICP. \n\n
Tx
includes Cholestyramine with or w/o Phenobarbital or
Ursodeoxycholate. Fetal monitoing is mandatory. DDX is Primary Billiary Cirhosis,
intense pruiritis, makredly elevated Alk phosphatase and cholestrol levels. DDX
primary Sclerosing Cholangitis is asso with UC, presents with RUQ pain,Jaundice
and pruritis.\n\n
Intratrochanteric Fracture
Of the femur is mostly seen in elderly fall. The extremity is shortened and rotated.
Xray is Dx. Tx is internal fixation with sliding screw and plate and EARLY
mobilization.\n\n
Intrauterine fetal demise
It's the death of the fetus in utero that occurs after 20 weeks gestation and before
the onset of labor. Its suspected when mother reports the disappearance of fetal
movements, decrease or stagnation in the uterus size and no heart tones. \n\n
The most
appropriate to confirm is
Real Time US, which will demonstarate the lack of
movement and absence of fetal heart activity. After dx is established coagulation
profile has to be determined to to detect an eventual DIC, which is a serious
complication of IUFD early in the course.\n\n
Intra Ventricular Hemorrhage of the new born:
Occurs in low birth weight infants. Its most commonly seen in premature infants. Pt
presnts with palor, cyonosis, hypotension, seizures, focal neurologic signs, bulging or
tense fontanels. So transfuntanel US is mandatory for all infants with risk factors.\n\n
Intussusception
2-yr old child with abrupt onser of abdominal pain,nasea,vomit, red current jelly
stool containing blood and mucus. 75% of pts are yonger than 1-yr old, the mc is in
Ileiocolic. Sausage like abdominal mass and draws knees towards chest.\n\n
Iron Def Anemia - 8. Hemo. 6/3
Fe normal is b/w 50-170. Decreased Fe, increased TIBC (460), MCV=68 and
hypochromic microcytic anemia. Infants are at increased risk of this disease due to
lack of Fe in milk. \n\n
DDX1
is Sideroblastic Anemia, is apart of utilization anemia
which is caused by inadequate or abnormal utilization of intracellular Iron for Hb
sysnthesis despite increased amount of Iron, sometimes it help to give Pyridoxone
(B6)]. \n\n
**IDA
is the mcc of anemia, suspect it when a person is not eating well and lab
shows microcytic hypochromic anemia.\n\n
**** In elderly, blood loss
from GI will lead to Fe def anemia. Since fecal blood test is NOT sufficient we need to do Colonoscopy because in elderly pt w/o GI complain, the cause is probabely cancer. \n\n
****Its the mcc of anemia in children
The early intruduction of Cow milk to infants diet
clearly asso with iron def anemia, the larger the amount of milk consumed the
higher the risk. \n\n
Typical lab shows,
low MCV, low Hb, Low hematocrit, low
reticulocyte count, microcytosis, hypochromia, low serum Iron, elevated TIBC. Low
serum feritin is diagnostic for IDA. Infants should receive breast milk for the first
year or iron fortified formulas. iron fortified cereal should be added the first 4-6
months. \n\n
DDX1:
Thalasemia, High Ferittin and signs of extramedulary hemopoises
(hepato/spleno megaly and widened bones.).\n\n
*****Microcytic hypochromic anemia
due to chronic blood loss (Iron def anemia) results in decresed serum Fe, Ferittin,
Transferin Saturation, and increased TIBC. DDX:Sideroblastic naemia has,
Increased Fe, noraml Ferritin, Increased TIBC, normal to incresaed Transferin
saturation. \n\n
DDX2
Anemia of Chronic DISEASE will show decreased Fe, increased
Feritin, low TIBC and low Transferin saturation.\n\n
***The mc type
of anema in
elderly pts. This pt presents with Fatigue and palor. Another cause of IDA is
cheronic diseases like infections, inflamatory dis, neoplasm. \n\n
****BM Iron stain
is
most definite way to dx IDA. Low feritin, increased TIBC, Low Iron are not as
specific.\n\n
Iron Poisoning
Presents with N&V and Diarrhea and abdominal pain, GI bleeding and Metabolic
acidosis. Fe accumulates in mitchochondria and resulting in cellular damage.
Hypotensio nthen occurs due to increased vascular permeability and venodialation.
\n\n
Since Iron tablets are radiopaque
they will be seen on Xray. Dx is confirmed by
serum Fe levels. IV Defroxamine is tx. DDX is Aspirin Tox, presents with
lethargy,fever,hyperpnea,vomit, tinnitus and metabolic acidosis. Abdomen Xray is
unremarkable.\n\n
Ischemic Colitis
MC site is Splenic flexure because its supplied by end arteries, It's a 'watershed'
area b/w superior and inferior mesenteric A.\n\n
*****Ischemic colitis is due to
onstruction of IMA. After AAA repair, diarrhea and blood in stool should raise
suspicion. If CT is inconclusive a sigmoidoscopy is recommended. Angiogram is not
recommended. Barium enema could cause perforation in case of IC. It's a good
technique for detection of colonic masses.\n\n
Isolated Proteinuria
IP (w/o pyuria or Hematuira) can happen due to stress or any febrile illness.
Evaluation of pt should begin by testing the urine on at least three occasions
(dipstick testing).\n\n
Isoniazide Tox
It might cause elevation of AST ALT in the beginning, do nothing it will decline.\n\n
ITP - 2
Idiopathic thrombocytopenic Purpura is an autoimmnue disorder characterized by
isolated thrombocytopenia absecence of splenomegally, absence of fever or other
systemic signs normal BM with normal or incresed Megakaryocytes.. \n\n
ITP is acute
and self limiting in children, but becomes chronic in adults. It presents with skin or
mucosal bleeding. Coagulation studes are normal. Autoimmnue destruction of
platelets maybe primary or it may be 2ary to SLE or infection with
CMV,Toxoplasma, HIV.\n\n
Whnever pt is having Chronic ITP
BM must be exam must
be performed to rule out primary hematological disorder. Pt must also be screned
for SLE by anti niclear antibody testing, as isolated Thrombocytopenia may be a
presenting feature of SLE, especially in a young female.\n\n
Now, if a pt shows
hepatomegaly,
lymphadenopathy,or atypical lymphocytes , 2ary causes of
autoimmune thrombocytopenia like CMV, HIV, Hepatitis and toxoplasma should
be cinsidred. \n\n
***The mc acquired bleeding disorder in childen
It follows after viral infection, with easy bruisability,and petechia. Thrombocytopenia and normal PT&PTT. DDX:HUS, combination of Thrombocytopenia,Microangiopatic
hemolytic anemia and Acute renal failure.\n\n
IUGR - 2
IUGR is defined as birth weight below the 10% for a given gestational age, and
refers to fetuses and neonates whose growth potential has been restricted by
pathologic processes in utero. \n\n
** These fetusus are particulary prone
to problems such
as meconium aspirarion, asphyxia, polycythemia, hypoglycemia and mental
retardation. IUGR maybe of maternal, , fetal or placental origin. \n\n
Common maternal causes include poor nutrition
, cigarette smoking, drug abuse, alcoholism, cyanotic heart disease, pulmonary insufficiency, and antiphospholipid syndrome. Placentall causes include conditions that result in a lack of decidualization of myoetrial arteries resulting in deficient perfusion of the fetus.\n\n
** Such conditions include
Hyper Tension, DM, CRF, and Preeclampsia. Feal causes are TORCH and congenital abnormalies. IUGR maybe symmetrical, the insult to the fetus before 28 week leads
to damage to both Head and Body. \n\n
Its caused by fetal factors.
Asymmetrical IUGR
is a result of insult after 28 week, only abdominal circumference is small. Its usually
caused by maternal factors like DM, Hypertention, Preeclampsia & CRF and it has
a better prognosis. \n\n
****The most effective parameter
for estimation of fetal weight in
cases of suspected IUGR is Abdominal circumference.\n\n
****Is defined
as birth weight
below 10% for a given age. These fetuses are prone to Meconium aspiration,
hypoglycemia, and mwntal retardation. Once IUGR is dx fetal well being has to be
monitored, with NST and BPP twice weekly. \n\n
**Mother can contribute to this
monitoring by assesment
of the kick count. Delivery is usually indicated at 34 weeks
or when lung is matured. If there is Oligohydramnios, AFI of 4, DELIVERY
SHOULD BE STRONGLY CONSIDERED. \n\n
***At birth , neonates with IUGR are
prone
to hypothermia and hypoglycemia. RDS also frequently occurs. So bottomn
line is that eventhogh gestational week is 28, go ahead and deliver vaginally.\n\n
Jaundice Dx Procedure
Once the pt has jaundice (bilirubin>1, then the next step is to determine if its mostly
conjugated or unconjugated. Conjugated hyperbilirubinemia is present when direct
bilirubin cinstitues >50% of total bilirubin. \n\n
***Unconjugated Hyperbilirubinemia is
present
when in-direct bilirubin constitutes >90% of the total bilirubin. Normaly
direct bilirubin constitutes <10% of bilirubin.\n\n
**** Conjugated HBR occurs in
a)Intrahepatic causes:1-intrahepatic obstruction(occurs in viral or autoimmune
hepatitis, alcoholic hepatitis, drug reaction, third trimester pregnancy) or 2-
Congenital defects in biliary excretion (Dubin Johnson and Rotor). b)Extrahepatic
billiary obstruction.\n\n
*** Now the next step in pt with Conjugated HBL is
to study liver
enzymes. Pts with dominant aminotransferase elevation have hepatocelllular dis,
whereeas pts wth dominant Alkaline Phosphatase elevation have intra or extra
hepatic obstruction.\n\n
*** In the second group,
its important to rule out extrahepatic
obstruction with US or CT of abdomen. If these fail to show extra hepatic billiary
dialation then the next step would be ERCP or PTC.\n\n
Jervel-Lang-Neilson
Or Congenital 'Q' synd. Syncopal episode w/o following disorientation, hearing
impairent, normal PE, and familt hx os sudden cardicac death is characterictic of
this syndrome. Tx is Beta blockers.\n\n
Juvenile RA or Still's Dis.
Child presents with systemic features, high fever, fleeting maculopapular rash
(central clearing), hepatospleenomegaly, lymphadenopahty, pleuropericarditis, and
myocarditis. Rheumatic factor is rarely positive. Tx is NSAID and monitoring of
liver enzymes. Cortcosteriods are used if pt does not responde to NSAID or if hayt
myocarditis.\n\n
Kallman Synd
Consists of congenital absence of GnRH secretion asso with Anosmia (cant smell)
and a normal 46XX. Also amenorrhea and absent 2ndary sexual characteristics.\n\n
Kartagener
Baby with recurrent sinusitis, bronchiectasis, destrocardia due to sydmotile cillia
(dynine aberannt).\n\n
Kawazaki Disease - 2
Fever >5 days. Mucous membrane changes (fissured lips) extremity changes
(edema, erythema) , at least one cervical node >1.5cm and polymorphus rash.
Coronary artery aneurysm or ectasia(widened) develps in 15-25% of children.
\n\n
***MERCK:
A syndrome occurring usually in infants and children < 5 yr,
characterized by prolonged fever, exanthem, conjunctivitis, mucous membrane
inflammation, cervical lymphadenopathy, and polyarteritis of variable severity.
Therapy is started ASAP, optimally within the first 10 days of illness, with a
combination of high-dose IGIV and oral high-dose aspirin. MERCK
END.\n\n
***Criteria are
1-Fever>5 days. 2-4 of the following, Bulbar conjunctival
injection, Desquamation of finger ans toe tips, Erythema fissuring and crusting of
the lips and strawbery tongue, Morbiliform truncal exanthem, Cervical
lymphadenopathy. \n\n
**Kawasaki or Mucocutanous Lymph node Syns is
one of the mcc
of generalized vasculitis in children. Its self limited It can be fatal due to thrombos
leading to MI. A 2D Echo is done to asses cardiac function. \n\n
**A baseline Echo is done
w/i 7 days then repeared 6-8 weeks later. Fever does not respond to Acetaminophen.
All pts with Kawasaki should be hospitalized and treated with IV IG and High dose
Aspirin. If untreated 25% will develop coronary artery aneurysm. \n\n
**DDX1:
Scarlet
fever, which have poitive strep test and no LIP fissures. Latex Agglutination test id a
rapid Dx test. Tx is 10 day Penicline course, or Erythromycin for Pen allergy.\n\n
Klumpke Paralysis
Is a brachial palsy that occurs in newborns following excessive traction of arms. It
consist of hand paralysis, and ipsilateral Horner syndrome (ptosis & myosis) and its
secondary to injury to seventh and eight cranial nerves and first thoracic nerve.\n\n
Knee Injury:
MCL injury is Dx with MRI. As MCL resists valgus angulations at the knee, injury
to this ligament leads to increased angulation of the affected knee in vlgus
maneuver. If MRI in inconclusive then we do Arthroscopy. Surgery is rarely
necessary for MCL tear.\n\n
*****ACL prevents
leg from gliding anteriorly, it is
damaged when knee is hyperextended. Its asoo with MCL and medial meniscus.
Lachman is the most sensitive test for Dx. \n\n
**Anterior drawer sign is
also used for
testing but its not as sensitive. Mc Murray is for meniscus testing. Valgus is used for
MCL (Medial Colateral Ligamnet) testing.\n\n
****Meniscal injury
result from twisting
injury with the foot fixed. Bucket handle tear is mc. Tenderness along medial side. It
results in LOCKING of the knee joint during the terminal extension. Initial tx is
conservative with immobilization and bracing.\n\n
Krabb's Dis:
Sphingolipidoses due to def in galactocerebrosidase. Characterized by hyperacusis,
seizure and irritability.\n\n
Labor - 2
Labor is defined as progressive cervical effacement, dilatation, or both resulting
from uterine contractions, which occur at least every five minutes and last 30 to 60
seconds. \n\n
Labor progress through four stages:
The first stage from the onsert of labor until full dilation of the cervix, and includes
two phases: a latent phase, during which dilation progresses in a slow rate until
reachins 2-3 cm, followed by an active phase, during which the dialation is more
rapid.\n\n
** The length of the latent phase is highly variable
but its considered prolonged
when it exeecds 20 hours in the primiparous and 14 hours in multiparous. The
progression of active phase is measured by the rate cervical dilation. At this phase,
the cervix is dilated with a ate of at least 1cm/ hr. in the primiparous and 1.2cm/hr
in a multiparouse.\n\n
***The second stage of labor extends
from complete dialation of the cervix to delivery
of the baby. It usually last 30 min to 3 hours in primiparous and 5 to 30 minutes in
multi.\n\n
***The third stage
starts with delivery of the baby, and ends with the delivery of
placenta.
The forth stage starts with delivery of placenta to 6 hours postpartum.The mother
should be closely observed because of high risk of postpartum hemorrhage.\n\n
****Prolonged latent phase
can be caused by hypertrophic uterine contractions,
hypotonic contractions, or premature or excessive use of anesthesia or seduction,
Hypertonic contractions, although intense are ineffective. \n\n
**They are more painful
and asso with increased uterine tone. Hypertonic activity of the uterus usually
responds to therapeutic rest with Morphine Sulphate. Hypotonic contractions are
less painful and are characterized by easily indentable uterus during the
contraction.\n\n
** Sometimes pts diagnosed with prolonged latent phase
may actually still
be in false labor. Contractions of false labor are painless and sporadic, but can be
rhythmic, occurring every 10-20 minutes.\n\n
** Their main characteristic however is
that
they are not accompanied by cervical changes. Pts with hypocontractile dysfunction
are best treated with a diluted infusion of oxytocin.\n\n
*****Fetal head compression
is asso with early deceleration, Uteroplacental insuff presens with late deceleration
and Fetal cord comprerssion is asso with late deceleration (decrease in fetal HR of
20 for a duration of 35 sec with absence of contraction).\n\n
** 1st step in Tx for FCC
is O2
admin and change in maternal position and elevating the presenting part .\n\n
Lactation suppression:
Tight fitting bra and ice packs. Bromocriptine is no longer used.\n\n
Lactic Acidosis, posticteric
T9Q45. Its transient and it resolves in 60-90 minutes.\n\n
Lactose Intolerance
Chatacteized by a positive hydrogen breath test, positive Clinitest of stool for
REDUCING substances and increased osmotic gap.\n\n
Lacunar Infarction
The principal cause is HYPERTENTION. There are 4 types, MEMORIZE THEM:
1-Pure motor Hemiparesis:
Lacunar infarction in post Genu of Internal Capsule,
presents with unilateral motor deficit (face, arm and some leg);mild
dysarthria(poorly articulated speech);NO sensory or visual dysfunction. \n\n
**2-Pure
Sensory stroke:
in VPL nucleous of thalamus, presents with Unilateral numbness,
paresthesias, hemisensory deficit involving face,arm and leg and trunk. \n\n
**3-Ataxic
Hemiparesis:
Lacunar infarction in post limb of IC, presents with weakness more
prominent in lower extremity, and ispilateral arm and leg incoordination.\n\n
** 4-Dysarthria-Clumsy hand synd:
Lacunar stroke of basis of pontic, presents with
Hand weakness, mild motor aphasia, NO sensory abnormality.\n\n
Laryngomalacia:
Is the mcc of chronic inspiratory noise in infants. Laryngoscopy shows flaccidity of
the larynx, and collapses during inspiration. It's a self limiting condition mostly.
Mother needs to hold the baby in upright position for half an hour after feeding and
never to feed the child while lying down.\n\n
Latex Allergy
can manifest as an anaphylactic reaction during exposure to gloves or condoms. Pt
is anaphylactic during surgery and sex.\n\n
Lead Poisening
Microcytic Hypochromic anemia and basohilic stippling, not normocytic
normochromic.\n\n
Leg nerves
1-Femoral: thigh ext, hip flex. Sensory ant thigh and medial leg through saphanus.
2-Tibial: Flextion of knee and sigits. Plantar flexion of foot . Sensation ro leg (except
medial) and plantar foot. \n\n
3-Obturator:
adduction of thigh. Sensation of medial
thigh. 4-Common Peroneal: muscles of ant and laterla leg. sensation of anterolateral
leg and dorsum of the foot.\n\n
Legg-Calve-Perthes - 3
B/t 2-12 yo. Pain is absent or mild. Gait is antalgic and range of motion is lilmited to
internal rotation,flextion and abduction. AP and lateral view show widening of the
joint spaceand collapse of the femoral head. \n\n
*** DDX:
Osgood-Shlatter involves tibial tuberosity resulting in tendernes over it. Ages 10-16. Xray shows irregularity of tubercle contour. DDX SCFE occurs in obese kids, with painful limb, xray shows displacement of femoral epiphysis.\n\n
****A serious but self limiting dis of children 4- 10yo,
characterized by avasculat necrosis of th ehead of feur. MC in boys and
usually unilateral.Pt prestns with painless limp or mild pain. There is sever
limitation of internal rotation and abduction at the hip joint.\n\n
***MRI and bone scan
show findings of necrosis of the headof femur. Children <5 no tx. Children >5 need
abduction bracing or surgicacl corrrection. \n\n
***DDX1:
Slipped Capitis Femoral
Epiphysis, seen in adulescent obese boyswith a gait. DDx2:Septic Arthritis presents
with systemic signs and leukocytosis. \n\n
DDX3:
Osteomyelitis, of the hip also systemic
signs nad leukocytosis. DDX4:Developmetnal Dysplasia of the Hip, a congenital
disorder. \n\n
DDX5:
Osgood-Schaltter( 2 Qs) or Osteochondrosisof tibial tubercle, its an
apophysitis of tibial tubercle, caused by overuse commonly seen in teenagers. \n\n
**Chief complain is
pain and swelling around tibial tubercle. Pain increases on contraction of quadricept muscles. Xray shows characteristc fragmentationon laterla view. Tx is symptomatic with rest, NSAIDs and breif casting.\n\n
Legionella
T9Q39. Remember PhD (Pneumonia, Hyponatremia and Diarrhea) is almost always
indicative of Legionella. Tx is Erythromycine.\n\n
Leprosy
A chronic granulomatous disease that primary affects peripheral nervers and skin.
Dx is by acid fast bacilli in the skin biopsy. Pt is from Asia, lesion on arm, dry
cough. \n\n
**Lesion has
no sensory feeling and muscle atrophy. Next step is to do skin
biopsy for acid fast.\n\n
Lesch-Nyham synd
Def of HGPRT. Self mutilation and neulogic features, gouty arthritis (gout is for
men over 50, so if you see a BOY with gout suspect this syndrome). Tx is
Allopurinol.\n\n
Leukemia
1-Acute Monocytic (FAB M5) Leukemia. The onset is dramatic HA and fever are
chief complains. , Also fatigue, weight loss, bleeding from mmouth and nose,
Gingyval hyperplasia.\n\n
** labs
There is leukocytosis with high proportions of blast cells.
Chemically they are 'Alpha-Naphtyl Esterase' positive. \n\n
**DDX:
Acute Myeloblastic
Leuk with Maturation (M2) Myeloblasts predominant.\n\n
** DDX2:
Acute Promyelocytic
Leuk( M3) has lots of Promyelocytes. DIC is sometimes seen with ths type.\n\n
**DDX 3
Acute Lymphoblastic Leuk, predomiant cells are Lymphoblasts. They are
mostly PAS positive. DDX4:Acute Erythro Leuk (m6) characerized by
erythroblasts.\n\n
Leukemoid reaction
is a marked increase in leukocytes by a severe infection or inflamation. CML and
LR are indistinguishable. Leukocyte Alkaline Phosphotase increase establishes ddx
b/w CML and LR (increased LAK). In CML , ALK is decreased and there is
Philadelphia chrom.\n\n
Lewy Body Demntia
Characterized by fluctuating cognitive imparment and bizzare , visual
hallucination. Parkinsonism is aldo seen. The central feature required for dx is
progressive , cognitive decline tht interfers with normal social functions.\n\n
Lichen Sclerosis:
Is epithelial lining inflammation and dry skin . Usually occurs in postmenopausal
women. Thr mc presentation is a severe itch and vaginal soreness. It might progress
to vaginal cancer. Once diagnosed start superpotent steroid cream while awaiting
biopsy results.\n\n
Lithium Toxicity - 4
Presents with tremulousness, headache, confusion, GI disturbances, fatigue, seizure,
coma, hyperreflexia and opisthotonus. Lithium exacerbate or precipitate
Psoriasis.\n\n
***Lithium exposure in the 1st trimester of pregnancy causes
a 20 fold
increase in the risk of Ebstein anomaly, a CARDIAC malformation. Its
characterized by a malformed and inferiorly attahced tricuspid valve that causes
decrease in size of right ventricle.\n\n
****SE are
Nephrogenic DI, Hypothyroidism,
Ebstein anomalyin fetus. So test the pt for TFT, Creatinine and pregnancy before
perscribing.\n\n
*****if a pt presents with refractory mania despite therapy
with a mood
stablizer, a urine toxicology screen and mood stablizer drug levels should be
obtained in initial evaluation.\n\n
Liver Cirhosis: Liver functions can be divided into the following categories
1-
Synthetic:Synthesis of clotting factors, cholesterol, proteins. 2-Metabolic:
metabolismof drugs and steriods including detoxification.\n\n
** 3-Excretion of biles.
So pts manifestations could include: A-Gynecomastia in cirrhotic pt is due to liver not metabolizing estrogen. Other manifestations of hyperestronism are testicular atrophy, decreased body hair in males, palmer erythema and Spider nevi (angioma).
** B-Caput medusa is due to
portal HT, along with that hay hematemesis and
hemmorhoids. C-Ascites is a result of 1-Underfilling theory:
Sequestration(accumulation) of fluid in splanchnic circulation due to portal HT.\n\n
** 2- Overflow theory:
Primary abnormality is inappropriate retention of salt and water
by kidney. D-Asterixis is 2ary to hyperammonemia leading to hepatoencephalopathy. E-Pedal edema is due to hypoalbuminemia.\n\n
Liver disease criteria
Lab tests used to evaluate liver dis is cllasified into two claases: A-Tests to asses the
function of liver which includes 1-PT, 2-Albumin, 3-Cholesterol, 4-Billirubin. \n\n
**BTests that assess structural integrity and cellular damage, 1-Transaminases, 2-
Gamma glutamyl transferase, 3-Alkaline phosphatase. Now PT is considered the
most important tst to asses function of liver, since liver makes all clotting factors
(except VIII).\n\n
...
** Elevated TransAminase
are indictive of liver cell damages since this
intracellular enzyme leaks out of damaged cells. A marked increase in TA is an
indication of an ongoing tissue destruction. \n\n
A progressive decrease in TA could mean either
recovery from liver injury or that there is little tissue is left (as in Fullminant hepatitis), so this interpretation is dependant on functional test like PT.\n\n
**If PT is OK then
TA decrease means recovery, if PT is increased, TA decrease
means fulminant hepatitis.\n\n
Liver failure coagulopahy
FFP is the tx of choice. Liver makes all clothing factors, except VIII. Among these
are vitK dependant factors, II, VII, IX and X. FFP has all cloting factors. \n\n
VitK can reverse the bleeding problem if
vitK def is the cause but if the cause is liver fialure it is of no use to hepatocytes, also vitK takes a while to work.\n\n
Liver failure, Acute
When PT is 20s it means hepatic failure. 1-ACUTE liver failure means development
of lilver failure w/I 8 weeks of onset of hepatocellualr injury. 2-FULLMINANT
hepatic failure means AHF+Encephalopathy.\n\n
** Acetaminophen toxicity is the mcc
for
both. AST will be very high ( >3000), ans hay 20% mortality rate. FHF has the most
favoable prognosis. \n\n
*****In the evaluation of Asymptomatic elevation of aminotransferases
, FIRST step is to rule out Alcohol and drug abuse. and risk factors for viral hepatitis by taking detailed hx. \n\n
**The NEXT step is LFT
. If only AST is elevated then ALT should be checked to rule out extrahepatic causes of AST elevation, because ALT is more specific for liver injury than AST.\n\n
Liver metastasis
Metastasis are the mc neoplasm in the adult liver and are 20 times more common
than primary tumors. It's the 2nd mc organ after lymph node that gets metastasis
due to its big size and dual blood supply. Dx is by US, CT, MRI, however biopsy is
confirmatory.\n\n
Liver pathology
1-Ballon degeneration w polymorphic cellular infiltrates:Acute Alcoholic Hepatitis.
2-Panlobular mononuclear infiltration w hepatic cell necrosis:Acute Viral Hepatitis.\n\n
**3-Portal necrosis including
piecmeal necrosis and/or bridging fibrosis: Chronic
Hepatitis. 4-Inflamatory destruction of small intrahepatic billiary ducts: Primary
Billiary Cirrhosis. 5-Extensive fatty vaculorization of the liver: Rey'e Synd (aspitin
toxicity in children).\n\n
Lower extremity edema
The two important causes are 1-Liver disease (HepB favors it. Lower ext edema,
ascites, hepato and spleenomegally. ) 2-Cardiac diease (Constrictive Pericarditis: TB
favors it. Lower ext edema, ascites, hepatomegaly,splenomegaly. Hepato-Jugular
reflex is a useful tool is the ddx).\n\n
Lower extremity nerves:
1-Tibial
2-Obturator
3-Common peroneal
4-Femoral. \n\n
Ludwig Angina
is infection of sumaxillary and sublingual glands and souorce of infection is an
infected tooth. Pt presents with inflamed mouth, drooling and fever and dysphagia.
Tx is IV penicillin with coverage of anaerobics.\n\n
Lukemia
1-ALL: 2-CML:Leukocytosis, Anemia, increased granular cells like segmented
neurophils and bands. Its mostly seen after 50 and presnets with fatigue, malaise,
low grade fever, anorexia, weight loss, and bone pains. \n\n
** Night sweats and fever asso
with increased metabolism due to granulacytic cell turn over . Examination of the
bone reveals hypecellularity with prominant granulocytic hyperplasia. The
Leukocyte Alkaline Phosphate is low, the only other diseaes that this may happen is
Hypophosphatemia and PNH. \n\n
**Elevated Leukocyte Alkaline Phosphatase is
characeristic of Leukemoid reaction. Presence of Philladelphia chromosome and
LOW Leukocyte Alkaline Phosphatase makes CML more likely than Leukemoid
reaction.\n\n
Lumbosacral strain
The mcc of back pain. Paravertebral tendernesspain after physical excertion,
negative staight led sign.Tx is NSAID and early mobilization.\n\n
Lung Adenocarcinoma
t9q29. Least asso with smoking.
Luteal phase defect. - 2
A15.
***LPD is suggested by short cycles
, hx of spontanous abortion, abnormal
Basal Body Temperature, or low levels of mid-leuteal Progesterone. The Dx is
confirmed by Endometrial biopsy which demonstrates a lag in endometrial
maturation of 2 days or more. \n\n
**LPD is tx
with progesterone vaginal supository
FIRST, if that didnt work then Clomiphene citrate or hcG (Human Menopausal
Gonadotropin) is tried. They both increase serum FSH.\n\n
Lyme dis - 7 , 6/2
Tx for Pregnant women is Oral Amoxicilline, EVEN if there is no reaction give
prophylaxis for anxierty. *Facial nerve palsy and classical Eryhtema migrnas
indicate Lyme. \n\n
**DDX:
Bells palsy, is the term used to refer to idiopathic facial nerve
palsy. *Lyme dis prophylaxis (Oral Amoxicilline) is given to pregnant women who
have been exposed to the tick and are asymptomatic or have anxiety about getting
the diease.\n\n
****Lyme arthritis
is a late manifestation of Lyme infection , suspect it
with a hx of travel to endemic areas, Rhode island, NY, conneticut, jersey,wisconsin.
\n\n
**DDX:
Septc arthritis, sudden onset of acute MONOarticular arhtritis in previously
damaged joint, asso with Chills and fever. DDX2:Reactive arthritis, occurs 2-4
weeks after genitourinary or GI infection. Onset is acute, with malaise and fever.
Symetrical joint involvement.\n\n
***** organism
By Ixodes tick. Antibosy crossreacts with T.
Pallidium.****Remember that dx of early dis is Clinical and there is no need for
serology. So the first thing to do is to give Doxycyline for 28 days.\n\n
**** Remember
in children <9 yo, dont give Doxy, give Amoxicilline.\n\n
Lymphoganuloma Venereum
It's a STD caused by C.Trochomatis. Serotype L1L2L3. Initially there is headache
and fever, then a papul apears that turns in to an ulcer typicaly in vulvovaginal
region. Ulcer is painless and disease may go un noticed unti inguinal adenitis
develops a month after. \n\n
**If untreated
at this stage LGV becomes chronic causing
ulceration, PROCTATITIS, rectal stricture rectovaginal fistulas and elephantiasis.
Tx is Doxycycline or erythromycin .\n\n
** DDX1:
Granuloma Inguinale is caused by
Donovania granulomatis, Unlike LGV the ulcer and lymphadenopahty present
simultaneously. Also the ulcer here has irregular borders and beefy red granular
base. Recommended Tx include azithromycin, doxycycline, erythromycin.\n\n
Lynch synd
or HNPCC(Hereditary Non Polyposis Colorectal Cancer). Criteria includes 1-
atleast 3 relatives with CC, 2-involvmnet of 2 or more generations, 3-At least one
case dx before 50, 4-FAP is rules out.Its also asso with extra colonic tumors, the mc
is Endometrial carcinoma\n\n.
Macular Degeneration
Age related. Progressive loss of bilateral CENTRAL vision. Due to degeneration and
atrophy of the outer retina, retinal pgment epithelium. Laser photo-coagulation is
tx. DDX with Open Angle Glaucoma in which PERIPHERAL vision is lost.\n\n
Malabsorption Syndrome
One cause is bacterial over growth could be assosiated with stomach surgery (peptic
ulcer or spcially after billroth II surgery). There could be A(night blindness)
D(tetany due to hypocalcemia) Neuropathy (due to B12 def) , dematitis, arthritis
and hepatic injury.\n\n
Malaria
People travelling to India or Pakistan should get chemoprophylaxis against malaria.
DOC is Chloroquine, but in case of chloroquine resistance P.Falciparum,
Mefloquine is doc. Tx with Primaquine is for Plasmodium Vivax and Ovale.
****The most sensitive test for DX is Giemsa stain thick smear.\n\n
Malignant HT
BP > 200/140. The most consistant sign is Papilledema. The pathological change
responsible for end organ damage is Fibrinoid Necrosis of the small arteries.\n\n
Malignant Melanoma - 7
Always suspect it in a changing mole. DDX is Keratoacanthoma which is the family
of Squamous Cell carcinoma.\n\n
** Best protection
is wearing protective clothing, because
sunscreen with SPF 15-30 protects ONLY against non-malignant melanoma (Basal
and Squamous) skin cancers. \n\n
**Excision biopsy
with narrow margins is the preffered
study for dx. If the depth is <.76mm the melanoma can be excised with a 1cm tumor
free margin and they have 99% 5year survival rate. \n\n
**The MC subtype is
"Superficial spreading melanoma, 70%), the least common is "Acral Lentiginous". \n\n
***Still the best way to protect fair skin
individulas is avoidance of the sun in the middle of the day (10am-4pm). Better than lotion or clothing or what have you.***The strongest risk factor for MM is recent change (color, size).***It metastasizes YEARS later to the BRAIN.\n\n
Malingering
Intentional production of false symptoms to get secondary gain (money or
morphine.) Factitious is production of false symptoms to get the sick role, no
secondary gain. \n\n
Malory-Weiss tears
increased intragastric pressure during vomiting could cause tear in the mucosa of
the cardia and distal esophagus.\n\n
Mania - 5
Manic episodes are characterized by DIGFAST. Distractability,Insomnia,Flight of
ideas, Activity inrease,Speech(extreme talkative),Thoughtlessness(excessive
gambling).\n\n
**** Initial tx of choice
is antipsychotic, Haloperidol****For general
population risk Bipolar dis is 1%, but for first degree relatives its 10%. ****If pt
shows signs of Mania, Bipolar is a good dx. For CHRONIN tx Lithium is first line
but not for a pt with renal problems.\n\n
****tx
Valproate or Carbamazepine is bette for those pts. Also remember that Haloperidol is the doc for ACUTE mngmnt of iniital agitation and agresiveness.\n\n
****Lithium and Valproate first line,
2nd line cabamazepine.****If pt has renal problem don't give him Lithium, give him valproate for long term treatment, \n\n
Marfan Sybd
Asso with Fobrillin -1 gene defect. Its auto Dominnat. Aortic root dilatation. Lens
dislocation.\n\n
Marijuana tox - 2
Impaired concentration and conjunctival injection are important features.*** A
cannabis group, causes dry mouth, tachycardia, increased appetite, and
conjunctival injection.\n\n
March fracture of Stress fracture:
Is common amongs young active adults (female dancer) involved in vigorous and
excessive exercise. Tibia is common.\n\n
Marjoli's Ulcer:
Years after burn surgery pt presents with an ulcer that still hasn't healed. Biopsy
will dx it. Its asso w SCC of the skin. \n\n
Massive Hemoptosis
Is greater than 600ml of blood per 24hrs. Its an Emergency. The Initial intervention
of choice is RIGID bronchoscopy, cause it gives better faster vision and has laser for
control of bleeding. FLEXIBLE is not good for ER but its good for diagnosis.\n\n
Mastitis
Infection of breast with S. Aureus. It must be ddx with Breast Engorgement
(heavy,tender,firm and warm breasts bilaterallyin women who not nursing. Its
manged with tight fiting bras, anagesics and ice pack, breast feeding should be
resumed).\n\n
*** Mastitis is tx
with oral Dicloxacillin. Breast feeding should be suspended
but milk has to be pumped until infection clears. If it onvolves abscess, incision and
drainge is required.\n\n
Mastoiditis, ENT 6/2
Its very rare. It's a complication of AOM. Pt presents with fever, otalgia and tneder
mastitis. CT confirms fluid filled middle ear & demineralization of mastoid. Tx is IV
antibiotics immediately.\n\n
Maternal Hyperthyroidism:
Seen in 2/1000 pregnancies. MCC is Graves disease. Pt may present with sudden
onset of Atrial Fibrilation ( irregularly irregular rythem and tachycardia. Dx is best
made with serum TSH and free T4. However the best screening test would be TSH
only.\n\n
Maternal substance abuse
1-Herion abuse: Newborn will show tremors, increasd weakness, frequent loose
stool, high pich cry, fist sucking, poor feeding and tachypnea, Hyperirritability.
Symptoms manifest w/I 24/48 after birth, Exclude hypocalcemia and hypoglycemia.
\n\n
2-Mthadone withdrawl:
presents at the 2nd to6th wek of life with seizure. 3-Cocaine:
asso w IUGR, intracranial hemorrhages, and premature labor or abrupta placenta.
Its not common. 4-Alcohol withdrawl: presents with tremors, agitation, lethargy
and seizures .Its rare.\n\n
McCune-Albright Syndrome
Rare, characterized by precocious puberty, café au lait spots (large and irregular
borders DDX w Von Reklinnghausen) & multiple bone deffects (Polyostotic fibrous
dysplasia). Its responsible for 5% of female precocious puberty. \n\n
** PATH
Its been related to defect in the G-protein cAMP-kinase in the affected tissue. \n\n
**Remember three P's :
Precocious puberty, Pigmentation (cafe), Polyostitic fibrous dysplasia. \n\n
**Tx
for Precocious puberty: a GnRH agonist (an analog of GnRH)--such as Hist-relin
acetate, sc; or Nafa-relin acetate, intranasally; or Leuprolide acetate.Remember the
three Ps, Precicious Puberty, Pigmentation, Polycystic fibros dysplasia.\n\n
Measles:
Vitamin A is known to reduce mobidy and mortality in pts with
measles.*****Includes koplik spots. It should be reported. \n\n
**DDX
Fifth disease or
erythema infectiousum, by Parvo virus B19, rash is slapped cheek appearance.
Fever is not present or is very mild. DDX2 Scarlet fever, pharyngitis, fever and
sandpaper like erythomatous rash . Strawberry tongue may be present.\n\n
Meconium Ileus:
Asso w CF. presents with failure to pass stool w/I the 1st 24 hour of life.\n\n
Meckel's Diverticulum - 2.
Painless Melena (dark stool) in a 2-3 y child is most likely MD. It results from the
failure of viteline duct to obliterate during fetal development .\n\n
*** Dx
is best made with Technitium 99m pertechnetate ( is uptaken with heterotropic gastric mucosa) . MD is the mc anomaly in GIT. Heterotropic gastric tissue may be present in the diverticulum,which resutls in ulcerating and bleding.\n\n
****In a pt with only
abdominal pain and pale and hx of childhood meckle, do Pertechnetate scintigraphy to dx it. Angiography can document bleeding at a rate of 0.5ml/min so its not helpful
for this situation.\n\n
Mediastinitis
Hemorrhage and large pericardial effusionmay accnt for widening of mediastinum.
Antibiotic alone is not sufficient for this SERIOUS dis. Mediastinitis needs,
\n\n
*** tx
Thoracotomy for debridement, drainge, and antibiotic therapy. Remember
widening of mediastinum is not because of that little pericarial fluid shows in Echo,
that will resolve spontaneously, its because of effusion.\n\n
Medulabelastoma
It's the second mc posterior fossa tumor in children after Cerebellal Astrocytoma.
90% occur in Vermis of cerebellum.\n\n
Medullary cystic dis
Its not asso with renal failure or Hypertension. Pt presents with stone formation or
is found incidentaly. IVP shows typical radial arrangment of contrast filled cyst.
Adult form is Auto Dominant. \n\n
*** tx
There is no therapy to prevent progression of cysts.
Stones are treated like regular stones, increase intake of water and salt. So suspect
MCD in adults with recurent UTI or renal stones and contrast filled cyst shown in
IVP.\n\n
Megaloblastic Anemia - 3
Alcohol abuse is the mcc of Folate deficiency in chronic alcoholics in US. \n\n
Memberoproliferative GN
Dense inttramembraneous deposits that stain for C3(only, no Ig) is a characteristic
finding for MPGN type 2 (also called dense deposit diseae). Its unique because cause
its caused by IgG antibodies directed against C3 convertase of alternative
complement pathway.\n\n
Membraneous GN
is the most likely dx in pt with both HepB and Nephrotic syndrome. HepC is asso
with MPGN. MCD is asso with Hodgkins. FSGN is asso with HIV. Diffuse
proliferative GN I sht esevere form of GN seen in pt with SLE.\n\n
MEN I - 2
Type-I:Tumors od Parathyroid (hypercalcemia), Pituitary and Pancrease
(Hypergastrinemia leads to recurrent peptic ulcers).\n\n
MEN IIA - 2
Total thyroidectomy is recommended. Hyperparathyroidism+Thyroid medulary
carcinoma+Pheochromocytma. ***Thyroid C cell hyperplasia becomes Thyroid
medullary carcinoma.\n\n
** Following helps to Dx:
Increased Ca, Increased Calcitonin,
decreased Phosphorus, elevated urine metanephrine, increased Alk Phosphatase,
elevated catecholamine, normal thyroid hormones, \n\n
**MRI of abdomen
shows mass,
Thyroid biopsy shows medulary carcinoma, Adrenal bipsy shows
Pheochromocytoma, , Parathyroid biopsy shows tumor, PTH is increased.\n\n
MEN IIB
Pheochromocytoma, Thyroid medulary cancer, Neuroma.
Meniere's Disease Recurrect episodes of rotational vertigo, sensorineural hearing loss and tinnitus.\n\n
*** Dx
is clinically. Tx is not necessary or impiric. DDX is Acoustic Neuroma where Vertigo is CONTINUES, and may be asso w ataxia.\n\n
Meningitis
1-Meningococcemia:Suspect it in a neonate with signs of meningitis and petechial
rash. Rash appears w/I 24 of sickness. 2-H. InfCauses meniggitis w/o rash.
Epigolitis, rihnoehea. 3-Listeria causes meningitis w/o rash.\n\n
** mcc
4-Strep group B is the
mcc of meningitis in infants. acuired from mother during childbirth. No rash.
*****When a child presents with signs of ICP and memingitis, CT should be done
before LP, HOWEVER start Cefotaxim 1st.\n\n
Meningococcal Vaccine:
Recommended to people with Asplenia.\n\n
Menopause - 3
Peripferal FAT tissue has the enzyme aromatase that converts
Androesteodion(androgen) to Esterone (Estrogen), this process helps fat post
menopausal women not to feel many of post menopausal symptoms like hot flashes,
dryness of vagina, dyspareunia.\n\n
****Estrogen replacemtn therpy affects
metabolism
of thyroid hormones. , The requremtn for L-thyroxine increases, probabely due to
increase metabolism of hormones due to induction of P450.\n\n
** note
Rifampin,carbamazepine and phenytoin act the same way. Other causes might be increased TBG, increased vol of distribution. In pregnancy also, thyroid hormone
requiremtn would be increased and pt should be monitored every 4-6 weeks for dose
adjusmnt. \n\n
****Estrogen is responsible
for 2ary sex characteristics, emotional andphysical health. Progesterone, produced by corpus leutum at ovulation, prepared for implantation and maintaining pregnancy. MenoPause occurs b/w 40-55, average
is 51.\n\n
** Before MP there is period of transition,
it last 2-4 years before complete
cessaion of themenses. First complain is of chanfge of floe and duration. Afterwards,
menses become more irregularmarking occurance f anovulatory
cycles,hotflashes,vaginal ddyness.\n\n
** A women is considerd menopaused
when at least
one year of no menses has occured. Hor flashes there after may become more
frequent vaginal dryness more prominent and may result in dysparunia, infections
vaginal, and UTI. Psychological problems may be less concentration, sleeping
problems, mood swings.\n\n
Mesenteric Thrombosis:
It can lead to massive fluid sequestration in bowels, Hypovolemic shock ensues.
Extreme elevation of Cksuggest massive ischemia, characteristic. Abdominal pain
and diarrhea with blood further supports Dx. Pt presents with BP 60/0, CVP of 0.
DDX is MI (EKG abnormality). DDX2 is AAA, which will show in US.\n\n
Metabolic Acidosis - 3
In case of MA the first step is to calculate anion gap. Normal anion gap is
b/w 6-12. Some of the CC of AG-MA are Lactic acidosis, Ketoacidosis, Methanol
ingestion, ethylene glysol ingestion, Salicylate poisoning, Uremia (ESRD).\n\n
** A pt is said to have a normal anion gap MA when
he has decreased HCO3, but a normal anion gap. This is also called Hyperchloric metabolic acidosis. \n\n
**Some of the CC of normal anion gap MA are
1-renal loss of bicarbonate (RTA, Carbonic anhydrase inhibitors). 2-GI loss of bicarbonate ( diarrhea). Urine anion gap tells us if the loss is due GI or renal.\n\n
Metabolic Alkalosis - 10, 6/2
Hypochloric MAlk due to vomitting causes loss of water, H, K, Na and Cl. To treat
it use IV normal saline and K. Also remember that there is MA in presence of
uncompensated Cirrhosis. Also Diuretic use is one of the mcc of MA..ie Thaizides.\n\n
****NG tube placement may lead to
loss of large amount of gastric acid leading to
contraction metabolic alkolosis even in pt with preexisting metabolic acidosis. An
example of MA after three days due to vomitting is pH=7.55, PCO2=50,HCO3=42.
\n\n
**So CO2 is increased to
neutralize alcolosis and make up for acid lost, and HCO3 is
also increased because there is no acid to neuralize it. Metabolic Alkolosis can occur
in Hemodialysis pt who receive Citrate.\n\n
*****Met Alk can be divided into two broad category based on urinary chloride level
1-chloride sensitive MA (Urinary Cl <20) that is suggestive of ECF contraction. The loss of gastric hydrochloric acid by suction or vomiting produces metabolic alkalosis that is perpetuated by concomitant ECF volume contraction (NaCl loss in gastric juice) and development of K deficiency, due more to secondary aldosteronism (i.e., renal K wasting) than to K loss in gastric juice.\n\n
*** It can be corrected with
saline infusion and is called Chloride
sensitive MAlk. Some causes are thiazide or Loop, loss of gastric secretion
(Sureptitious Vomiting), acid ingestion, CF, Villus Adenoma ). 2-chloride resistant
MAlk (Urinary Cl>20. due to persistant mineralocorticoid stimulation and
HypoKalemia. Hay ECF expansion. \n\n
***They are characterized by
HT and so are not
corrected with Saline infusion. Some causes are Primary Hyperaldosteronism,
Cushings synd, also Barret's and Gittermna Syndromes (both are kidney
syndromes). When we give Kayaxelate it causes MAlk. *** MAlk is the mc acid base
abnormality in hospitalized pts.\n\n
Metatarsus Adductus
Is a congenital foot deformity. In the first born only. Thre are 3 tyes, 1-feet over
correct both passively and actively into abduction. These corrent spontaneouslt and
no tx is neede. 2-foot that corrct to neutal position with pasiv eand active movemtns.
this is corrected with orthosis or corrective shoes and sometimes plaster cast.\n\n
** 3-foot is rigid andis not corrected ,
these are manged with serila cast. Now surgical tx may be required if there is significant residual metatarsus adductus in children bythe age of 4.\n\n
Metformin
Is added to DM pt who needs a better control of glucose. Make sure pt renal
function is good, because it causes Lactic acidosis if otherwise. Also it helps to
reduce weight in borderline obese pts. ****CI in dye procedures and hospital
stays.****Most Serious but rare SE is Lactic Acidosis, Most Common SE is GI
Distress.\n\n
Methanol alcohol Tox
Blindness. Tx is Ethanol. Pt also has Anion Gap Met Acidosis. Its Asso with renal
fialure and Crystalluria (rectangular).\n\n
Methyphenidate Toxicity
Its used for ADHD. Its SE is nervousness, decreased appetite, weight loss, insomnia
and abdominal pain.\n\n
MI - 24
RV infarction: Presents with JVD, kusmmaul sign, hepatomegaly
and hypotension in presence of clear lung fields. Sometimes Tricuspid regurg is
present. \n\n
The mechanism for these findings
is that RV becomes less compliant
resulting in decreased filing ad stroke volume with a resulting elevated central
venous pressure. RV also becomes dialated and tricuspid regurgitation may develop.\n\n
** Loss of LV diastolic function gives rise
to the symptoms. Manage a pt with ST
elevation MI with immediate PTCA and angiography is sublingual thrombolytics
are CI (hemorrhagic stroke a < 1 yr ago). \n\n
**Thrombolytics therapy is indicated
when there is ST elevation >1mm AFTER nitroglycerine rules out Coronary artery spasm (by persisting after Nitro admin). Another indication is a new LBBB. Its NOT indicated for ST depression or Unstable Angina. \n\n
******Absolute CI for thrombylitic
therapy is internal bleeding, stroke w/i a year, intracranial neoplasm, BP>180/110,
or suspected Aortic Aneurysm. Thrombolytic therapy with t-PA requires co-admin
of Heparin and aspirin, for Streptokinase heparinis not needed. \n\n
**MI Complications:
LV Aneurysm, is a late complication of MI, usually occurs after anterior wall MI,
could present with either asymptomatic or with CHF. Precordial exam shows
Double apical beat, a murmur of Mitral regugitation exist due to papilary muscle
dysfunction,\n\n
CXr
shows characteristic prominence of the left border of the heart,
EKG shows persistant ST elevation. DDX1 VSD & Papilary muscel rupture, present
w/i the first week after MI, with cardiogenic shock.\n\n
** Drugs that reduce mortality in MI
are Betablockers, Aspirin, Aceinhibitors. Lidocaine is not given prophylactically to MI pts, althought it might decrease the risk for VF, it may increase the risk for Asystole. \n\n
**In post MI
hypetensive pt beta blockers and ACE inhibitors are preffered
over diuretics and calcium channel blockers. Beta blockers decrease myocardial
oxygen demand by reducing heart rate and contractility. ACE inhibitors are
indicated when EF is decreased.\n\n
*ANTERIOR wall MIs
are asso with high risk of ARTERIAL thmboembolism, so pts need full dose of Heparin when hospitalized, followed by 3 mo of Warfarin therapy. \n\n
*Ventricular wall rupture
:hypotention, pullsus paradoxus, pulsless electrical avtivity in a pt w recent MI, due to Cardiac temponade. Occurs the first week after MI. \n\n
**DDX
is Papilary muscle rupture:It also occurs first week after MI. It will lead to acute mitral regurgitation and a pansystolic murmur is audible.\n\n
****Ventricular Septal rupture:
Pt presents with 4
day post MI, low BP, JVD, harsh pansystolic murmur at the lower sternal border.
with wide radiation. \n\n
Dx
can be made if there is evidence of L-to-R shunt on Swan
Ganz cathater, when a 2-D Echo is not available.****Pain that radiates to arm
should make you think of MI, so u need to rule out MI wth Echo. \n\n
****In a pt with acute heart failure
ACUTE INFERO-LATERAL MI, Pulmonary Edema (Bilateral
crackles, edema, JVD) can set in Even though beta blockers decrease mortality in
MI they are CI in presence of Pulmonary Edema. Diuretics are DOC in this setting.
The most commonly used in Furesamide.\n\n
***Reentrant Ventricular arrythmia
Ventricular Fibrillation is the mcc of death in pt with acute MI.\n\n
**** In case of ST
elevation MI
reperfusion therapy with PTCA (PCI) with or w/o Stent should be
done asap. PTCA (PCI) is prefered over Thrombolytics(tPA).\n\n
****The earliest EKG
findng in MI is Peaked T waves, followed by ST elevation, followed by T inversion,
followed by Q waves.\n\n
****All pt who had MI sould receive what 2ary prevention
The follwoing drugs have shown to have mortality benefit:1-Aspirin, 2-Beta blocker, 3-
ACE inhibitors, 4-Lipid lowering Statis drugs. I\n\n
***in addition,
Clopidogril should be prescribed to all pt with unstable angina /non ST elevation, as well as pts who are post PCI(percutaneous Coronary Intervention). Clopidegrel is preffered over Ticlopidine due to less toxicity.\n\n
***Chest pain in an MI pt a few days after the
attack
that presents with friction rub is either Acute Pericarditis or Dressler's
Synd. Knowing the Dressler is a LATE complication of MI that occurs b/w 2-10
WEEK post MI, tells us that this is Acute pericarditis. Fever is not a must for the
Dx.\n\n
***Post MI is pt is on Heparin
an embolifrom heart can block supply to the leg
and pt can presnt with Cold pulsess leg. Pt has to go to surgery for the leg, but we
have to do an ECHO to rule out thrombus in LV.\n\n
****Drugs tht improve survival in Acute MI are
Thrombolytics, Beta blokers, Aspirin, ACE inhibs. Ca chanels
DONT.\n\n
****Pt with ST elevation in lead II,III and aVF means Inferior wall MI
Now if this pt later in ER presents with low cardiac output (cold extremity adn BP) and
low arterial pressure MI has resulted in RV infarction. \n\n
**RVI
leads to reduced filling and so reduced stroke volume of RV and then to reduced LV stroke volume and CO and reduced BP. Therefore any medication that reduces Preload, like diuretics or nitrates shold be avoided. \n\n
**Severe RV failure dould lead to
cardiogenic shock, initial therapy for acute RV infarction, who has hypotension is imediate volume expansion
with normal saline. to increase RV filling pressure. If fluid resusitation alone is
insufficient then inotropic and Chronotropic stimulation with Dobutamine should
be initiated.\n\n
*****The most important enzyme for evaluation of RE-infaction (MI)
is CK-MB.\n\n
****St elevation in lead II,III and aVF is indication of Inferior wall MI
It results from occulsion of either RCA or Left Circumflex artery. witha ratio of 5:1.
Also if pt has bradycardia and hypotension suggesting involvment of SA node and
right ventricle. \n\n
******A pt who develops a cold leg after an MI episode
should be
suspected of an emboluls. An Angiography should be done and Embolectomy
performed. \n\n
****Dressler Synd occurs 2-4 weeks post MI
with low grade fever and
malaise, and pleurtic chest pain. ECG reveals non specific ST elevation and maybe
pericardial effusion. Once oyu suspect it start pt n NSAIDs, dont need ECHO or CT
or Xray.\n\n
Migrain HA
Tx Steps: First start with NSAID, if that had a minor effect then use
Acetaminophen, if that didn't work either then give Ergotamine. Ergotamin is CI in
pregnancy. Give Ergotaimn if attack last more than 48 hours or its recurrent.
Prophylaxis: Betablocker, if pt has asthma Amitryptaline.\n\n
Migratory Thrombophlebitis - 2
Or Trousseau's Synd. Is indicative of chronic DIC, most probabely due to cancer.
Lung, pancreatic,stomach, prostate malignancies are the mcc. \n\n
**CT of the chest,
abdomen and pelvic is indicated for complete work up of malignancy along with age
appropriate cancer screening such as digital exam, mamography and
colonoscopy.\n\n
****Pt have occult tumor
which is not always detected when they come
in. The mc tumor is Adenocarcinoma . The thrombophlebitis of ATYPICAL sites
like ARMS and CHEST are good clues. Tumors are 24%Pancreatic carcinoma,
20% lung, 13% prostate. 12% stomach.\n\n
Minimal Change disease - 2
In general "membraneous nephropathy" is the mc nephropathy asso with
carcinoma, however, nephrotic synd is a well known complication of Hodgkins
lymphoma and is usualyy caused by "MCD".\n\n
*****In Children we don't do biopsy
,
once we suspect it we start Prednisone.*****Light microscopy is normal but
electron microscopy shows effacement of foot processes of podocytes.\n\n
Missed abortion - 2
Once the dx is made, surgical evacuation (dilatation & cuertagge) of the uterus has
to be performed to avoid complications such as DICand sepsis and to minimize
hemorrhage.\n\n
**** Missed abortion involves a dead fetus
that is still retained in th e
uterus. Dx is suspected when there is disappearance of the nasea and vomiting of
early pregnancy and arrest of uterine growth. Urine pregnancy test would still be
Positive.\n\n
Mittelschmerz:
It's a mid-cycle (LMP was 2 weeks ago) abdominal pain that typically presents in
young females. If there is no fever its not PID.\n\n
Mitral regurgitation - 4,
Mitral valve prolapse is the mcc of isolated MR( It sounds like soft S1 and a blowing
high pitched pan-systolic murmur, that radiates to axilla.) \n\n
Other causes of MR
are:1-RHD, acounts for 1/3 of cases, more common in males. 2-IE, by causing
damage to leaflets or chorda tendina, 3-HCM, causes MR by systolic anterior
motion of mitral valve, 4-Mitral anual calcification, due to aging in elderly, 5-
Ischemic heart dis, MI can cause it by papilary muscle.\n\n
****Papilary muscel rupture
inn the MI setting is the reason for MR a few days after MI.***Subacute IE usually
involves previously damaged heart valves. The mc predisposing factor to native
valve endocarditis is MVP. Mitral valve is mc-ly affected in endocarditis pts who are
not IV drug abusers , and MR is the mc valvular abnormality observed in these pts.\n\n
****Causes of MR:
1-MVP is hte mcc, Pt prstns with DCM, Apical impuse is
displaced. 2-Myocardial Ischemia, is the 2nd mcc, ischemia leads to papilary muscel
dysfunction or infarction. 3-Rheumatic Heart Fever. 4-IE, pt prsents with fever. 5-
Mitral Annular Calcification, usually in elderly.\n\n
Mitral Stenosis - 3
Hallmark is elevated left atrioventricular pressure gradient that ultimately leads to
left atrial enlargement. Excertional dyspnea and later pulmonary hypertension and
right heart failure. Very common Atrial fibrilation is due to atrial dilatation. S&S:
1-RHD, 2-L&R side failure, 3-MidSystlic Rumble w opening snap at apex, 4-AF,
Pulm Rales, Increase intensity of S1, RV heave, 5-TX:Diuretics, Anticoag, Digitalis,
Ballon valvuloplasty.****Tapping apex beat and malar rash are in MS.\n\n
Mitral valve prolapse - 2
Late systolic click, may or may not be followed by late systolic crescendodecrescendo
murmur. The click and murmur occur with maneuvers that decrease
LV volume such as Valsalva and standing. Both are delayed with squatting and
exercise(increase LV volume).\n\n
****Beta blockers are used to
treat chest pain,
palpitation, autonomic sysmtoms of MVP. If pt prestns with TIA then Aspirin is
given, if no response then Warfarin is given. MV repair is indicated when pt with
MVP develops symptomatic or svere MR.\n\n
Mittelschmerz
Abdominal pain in a young female in the middle of her cycle with a benign hx and
clinical exam is most likely this.\n\n
Mixed acid base disorders - 2
MA disorders are defined as independently coexisting and not merely compensatory
responses. In order to Dx them first look for pH to determine status. Second see if
the changein PCO3 or PaCO2 can explain the change in pH. \n\n
** Third step to
see the
degree of compensation possible for the disorder and if the values are not matching
with the observed values, pH=7.4, PaO2=51, PaCO2=32, HCO3=18. . Example:DM
pt with Metformin has pH=7.23, PaCO2=40, HCO3=16.\n\n
** OK first there is acidosis,
then we see decreased HCO3 so its Metabolic Acidosis (Metformin induced), then
use Winter's formula [1.5 x (16) + 8]=32, so Co2 must be 32 (compensated value) but
its 40, so there is also a respiratory acidosis. Pt with Lobar pneumonia (tachypnia
leads to Res Alk, Alk pH and low PaCO2), with N&Vomit (Met Alk, with Normal
HCO3 of 24), and DKA (AG Met Acid). This pt will have Res Alk+Met Alk+AG Res
Acidoosis).\n\n
Mixed Cryoglobulinemia - 2
80% of the cases are asso with Hepatitis C. So always do HCV RNA assay. Suspect
in a pt with palpable purpura, hematuria and proteinuria, non specific systemic
symptoms, peripheral neurapahty and hypocomplementemia.
\n\n
**MERCK:
Cryoglobulinemia is characterized by the presence of immunoglobulins
that precipitate when plasma is cooled (ie, cryoglobulins) while flowing through the
skin and subcutaneous tissues of the extremities. \n\n
Monoclonal immunoglobulins
formed in Waldenström's macroglobulinemia or in multiple myeloma (see Ch. 140)
occasionally behave as cryoglobulins, as may mixed IgM-IgG immune complexes
formed in some chronic infectious diseases, most commonly in hepatitis C.\n\n
Cryoglobulinemia can lead to
small vessel damage and resultant purpura.
Cryoglobulinemia can be recognized after clotting blood at 37° C (98.6° F),
incubating the separated serum at 4° C (39.2° F) for 24 h, and examining the serum
for a gel or precipitate.END MERCK\n\n
Mixed CT disease
Ovelaping symptoms of SLE+Scleroderma+Myositis. Asso with antibody to
RiboNuclear Protein. Occurs in much younger generation. DDX with
Dermatomyositis, Polymyositis\n\n
Mobitz-I heart block
Mobitz-I or Wenkebach
Charaterized by narrow QRS, progressive increase in PR
until a ventricular beat is dropped. It's a benign arrythmia and unless pt is
asymptomatic, no tx is needed. \n\n
If pt is symptomatic
Atropine is needed, and rarely pacemaker. Mobitz-I is seen with Digitalis tox, increased vagal tone and inferior wall MI.\n\n
Moluscum contagiusom - 2
Pic. It's a POX virus family. Its asso with AIDS when CD<100. It resovles
spontaneously in one year. Tx options are excision and cryotherapy.\n\n
Mongolian spots - 2
it found in dark skined population, presents at birth and usually disappear in
several years. No tx is neccesary. Its caused by entrapment of melanocytes. The
lesion is a bluish-grey, mostly located at lower back buttucks.\n\n
DDX
The lesion does not
fade in to surrounding skin. DDX:Salmon patch, a falt salmon colored lesion
commonly seen over the eyelids, and neck and glebella(forehead bone). Its a
vascular lesion that diappears at early childhood.\n\n
Monteggia & Galeazzi Fractures:
Monteggia is isolated proximal third Ulna fracture with anterior dislocation of
radial head. May be asso with radial nerve injury ro neurovascular exam is
mandatory. In adults its treated with open reduction and internal fixation. \n\n
**Galleazzi
is isolated radial shaft fracture asso w disruption of radial and ulna distal joint
needs open reduction and internal fixation.\n\n
Monoclonal gamopathy
MG of Undetermined Significance should DDX with Multiple Myeloma. There is
only increased IgG. Plasma cell is <10% and no anemia or other signs of Multiple
Myeloma. Tx is Asurance.\n\n
MERCK:
Low M-protein levels in serum, normal levels
of other serum immunoglobulins, and no lytic bone lesions or Bence Jones
proteinuria\n\n
Mucopurulent Cervicitis
By C. Trochomatis is asymptomatic in 50% of pts. Presents with scant vaginal
discharge, abdomen is non tender, Yellow mucopurulent discharge is seen.\n\n
Mucormycosis
Pts with DM are prone to it. Pt has fever, dull facial pain, bloddy nasal discharge,
diplopia, , nasal turbinates are necrotic. Requires aggressive surgical debridment
and early systemic chemotherapy with IV amphotericine B. \n\n
Multiinfarct Dementia:
History of heart disease and hypertension is suggesting, however, if there is no
indication of focal neurologic defects, this dx is ruled out and AD is the more
probable cause.\n\n
Multiple Myeloma - 5
A malignant proliferation of plasma cells mainly in the bone marrow. characterized
by marrow plasmacytomas (plasma cell tumors) and overproduction of an intact
monoclonal immunoglobulin (IgG, IgA, IgD, or IgE) or Bence Jones protein (free
monoclonal or light chains)..\n\n
** MC presentation
is bone pain and old age, also anemia,
renal failure and hypercalcemia. Pathologic fractures may occur and vertebral
collapse may lead to spinal cord compression. Bone lesions are osteolytic. Serum and
urine electriphoresis is used to detect monoclonal protein. \n\n
** dx
Skull xray rerveal punched out lesions. Hypercalcemia is a characteristic of MM, it manifests as Constipation, anorexia, weakness, renal tubular dysfnction and neuro sysmptoms.\n\n
***DDX
1:Osteoporosis, is reduction of bone density, Bone density scan (DEXA) is dx.
DDX2: Pagets disease, excessive resoprtion of bone mediated by osteoclast, followed
by replacement of normal marrow by vascular fibrous connective tissue.\n\n
*** Pt presents
with elevated alkaline phosphatase, bone deformity, large skull and pain. Hearing
loss and nerve palsy may occur. Sarcoma is a long term complication. \n\n
***MM is
caused by the proliferation of a single transformed plasma cell usually producing
IgG. Following are the classic findings: 1-Lytic bone lesions, 2-Marrow
Plasmacytosis, 3-Urine and serum monoclonal proteins. \n\n
***MM presens
in old age and
bone pain is the mc presentation. Complications include Renal failure,
Hypercalcemia, hyperviscosity syndrome. Complete work upincludes CBC with
differencial and morphology, serum electrolyt, kidney and liver screening, skeletal
survey and serum electrophoresis and BM biopsy which shows over production of
plasma cells. \n\n
**BM DDX1:
Essential Thrombocytopenia, increased marrow cellularity
with megakaryocytic hyperpplasia. DDX2:Aplastic Anemia, Hypoplastic fat-filled
marrow with no abnormal cells.\n\n
****Any elderly with bone pain,renal failure and
hypercalcemia
has MM until proven otherwise. Hay obstruction of distal and
collecting tubules by large laminated cast containing Paraproteins (Bence Jones).\n\n
Multiple Sclerosis - 9
For acute symptoms ONLY steriods ( IV Methylprednisolone) are indicated. For
relapsing-remitting episodes use Interferon B or Glatiramar acetate.MS is
assosiated with Trigeminal neuralgia. Asso with MLF. \n\n
***MS is asso
with
Glosophareayngeal Neuralgia, sharp pain asso with swallowing, chewing, talking
and yawning. * Dx of choice is MRI which shows white matter disease.\n\n
****Pt might
present with patchy neurological problems(right upper extremity, right lower
extremity, optic neuritis) which is characteristic of MS.\n\n
****Csf shows
Oligoclonal
bands but its not specific. However seeing Plaques in periventricular regions on T2-
Weighted MRI is Dx.\n\n
Mumps
Asso with Orchitis.
Munchausen Synd by proxy
Is when a family member recieves satisfaction by making another member sick.
Like the mother who gives her baby insulin to make her hypoglycemic.\n\n
Murmur
1-Diastolic and loud systolic murmurs should always be investigated with
Transthoracic Duppler Echo. 2-Midsystolic soft murmurs in a young pt are benign
and no further work upis needed.\n\n
Mutations
1-Silent: does not effect the structure of protein. 2-Nonsense is very severe. 3-
Missense is mild structural changes.4-Frameshift is also very severe.\n\n
Myasthenia Gravis - 8
Hallmark is decreased acetylcholine receptors due to antibodies. DDX with botulism
is that in MG pupils are spared. \n\n
There are 3 TX
options available for MG, 1-
Anticholinesterase, 2-Immunosuppresive agents, 3-Thymectomy. Anticholinesterase,
Pyridiostigmine, is the first line of tx, \n\n
SE
of abdominal cramps and fasciculations is
treated with Atropine. Immunosuppresive agents, prednisone, azothioprine and
Cyclosporine. Thymectomy is the best tx to induce remission and provide long term
benefit.\n\n
*****Once the dx is established
EMG and antibody t
acetylcholinereceptor the next step is to locate Thymoma ( CT os the chest)
especially in pt <60yo. It rakes a 3-4 years to notice the difference after
thymectomy.\n\n
****The resolution of weakness
with rest is the hallmark of MG. Pt
presents with Dysarthria(speech difficulty),dysphagia,ptosis,
diplopia.\n\n
****AB Determination
of level of antibodies to Ach receptors is Dx.
TENSILON test is not used anymore.\n\n
****Myasthenia Crisis
is a lifethreatening
situation. caracterized by weakness is respiratory and pharyngeal mscles. The tx
includes endotrachial intubation and withdrawl from anticholinesterase for a few
dadys. \n\n
The most important cause is
an infection, pt has high fever. ALL pts should
have bed side PFT done.\n\n
****DDX MG
with TRICHONOSIS which is GI complans
followed by muscle pain, swelling and weakness. Presence of subongul splinter
hemorrhages , conjunctival and retinal hemorrhages, periorbital edema and
Chemosis should make oyu think of Trichonosis. *****Level of lesion is in
Neuromuscular junction.\n\n
Myelodysplastic Syndromes
Are clonal stem cell disorders, which may progress to Acute Leukemias. They are
characterized by Pancytopenia.\n\n
Myositis, Dermato & Poly - 3
Polymyocitis and Dermatomyocitis are both inflamatory myopathies, charcterized
by proximal muscle WEAKNESS, and ultimatly wasting.\n\n
** Dermatomyocitis involves typical skin changes:
Helitrop rash around the eye asso w periorbital edema, and Gotrron's papules (red scally papules over metacarpophalangeal joints). These conditions may occur alone or with cancers: breast, ovary, lung, prostate, colon.\n\n
***Unlike Myasthenia
ocular muscle weakness is UNCOMMON. Unlike Sclreoderma
whic affects lower SMOOTH muscle, these affect STRAITED muscle of upper
pharynx. Spcefic Dx is with muscle biopsy. \n\n
**They both responde