USMLE step 2 UWORLD NOTES

2000 terms by khaled_omar 

Ready to study?
Start with Flashcards

Create a new folder

Advertisement Upgrade to remove ads

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