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FirstAid Rapid Review 2016 - Classic Presentations, Lab Findings, Treatments, Associations, and Equations
Terms in this set (1836)
-Hepatic vein thrombosis --> Abd pain, ascites, hepatomegaly, "nutmeg" appearance of liver
-Associated with SLE (aphthous ulcers and malar rash)
Clostridium difficile infection (pseudomembraneous colitis)
Associated with what abx?
Abd pain, diarrhea, leukocytosis, recent abx use (usually clindamycin)
C. diff bacterial characteristics
Gram(+) spore-forming rod
Gram(+) spore forming rod that release a heat-labile toxin after ingestion (important cause of food poisoning)
Common sign? Cause?
-Common sign: Achilles tendon xanthoma
-Cause: Decreased LDL receptor signaling
Defects in familial hypercholesterolemia
apoB-100, or defective LDL receptor signaling
Waterhouse-Friderichsen syndrome (meningococcemia)
Adrenal hemorrhage, hypotension, DIC, diffuse purpuric skin rash w/o nuchal rigidity, Neisseria meningitidis (MC organism)
Anaphylaxis following blood transfusion
(In pts with IgA-deficiency, a percentage develop IgG antibodies against IgA, such that if they receive blood transfusions from non-IgA-deficient pts [i.e. most people...], they experience anaphylaxis)
Postive anterior drawer sign
Fibrillin defect, arachnodactyly, upward lens dislocation, aortic dissection/dilation, MVP, hyperflexible joints, pectus excavatum
Athlete presenting with polythemia
Polycythemia likely secondary to epo injection
Pott disease (vertebral TB)
Back pain, fever, night sweats
Neurofibromatosis, type 2
Bilateral acoustic schwannomas
Inheritance = AD (worse prognosis than Type 1)
Noncaseating granulomas, bilateral hilar lymphadenopathy, hypercalcemia, uveitis
"40 year-old black female"
Mucor or rhizopus fungal infection
Black eschar on face of patient with DKA
Type I collagen defect, BLUE SCLERA
Lead poisoning, bluish line on gingiva
Paget disease of bone
Increased osteoblastic and osteoclastic activity, bone pain, bone enlargement, arthritis
Bounding pulses, wide pulse pressure, diastolic murmur, head bobbing
"Butterfly" facial rash, Raynaud phenomenon in young female, type III hypersensitivity reaction
Neurofibromatosis, type 1
Cafe-au-lait spots, Lisch nodules (iris hamartoma), cutaneous neurofibromas, pheos, optic gliomas, axillary freckling
---> Inheritance = AD
Mosaic G-protein signaling mutation, UNILATERAL cafe-au-lait spots, polyostotic fibrous dysplasia, precocious puberty, multiple endrocrine abnormalities
Duchenne muscular dystrophy (DMD)
frameshift mutation of dystrophin gene, calf-pseudohypertrophy, Gower's sign (child uses arms to stand up from squat)
Cervical LAD, desquamating rash, coronary aneurysms, red conjunctivae and "strawberry tongue", hand-foot changes; treat with IVIG and aspirin
-Mental retardation, blindness, muscle weakness, hearing deficits
-Cherry-red spots on macula, ganglioside accumulation
-Onset in infancy, death in childhood
Spingomyelin accumulation in lysosomes, cherry-red spots on macula
Central retinal artery occlusion
Cherry-red spots on macula
Stable vs unstable?
Chest pain on exertion (Stable = pain on moderate exertion; Unstable = pain on little or no exertion), narrowed coronary arteries secondary to atherosclerotic plaques
-MC cause =
-O2 demand > supply --> pain
Atherosclerotic plaque formation mediated by what cell type?
Monocytes differentiating into macrophages (once monocytes leave the bloodstream)
-Autoimmune-mediated post-MI fibrinous pericarditis 2 weeks to several months after an acute episode
Chest pain, pericardial effusion/friction rub, persistent fever following MI
Unstable angina (neg troponins) or NSTEMI (pos troponins)
Chest pain with ST depressions
Erythema infectiosum/fifth disease
Parvo B19, "slapped cheek" appearance, child with fever who later develops red rash on face that spreads to body (lace-like)
Huntington's disease (Hungington's chorea)
Autosomal dominant CAG repeat expansion, chorea, dementia, caudate degeneration
Chorioretinitis, hydrocephalus, intracranial calcifications
McArdle's disease (GSD type V)
Skeletal MUSCLE glycogen phosphorylase deficiency (myophosphorylase)
--> "McArdle's" has an "M" for "Muscle"
Chornic exercise intolerance with myalgia, hypoglycemia on EXERTION
(glycogen just hanging out in muscle b/c it can't be broken down for energy, so glucose is coming from blood not muscles),
--> dead muscle cells getting pissed out in the urine
HEPATIC glycogen phosphorylase deficiency
(since liver is responsible for maintaining baseline BG level),
McArdle's vs. Hers disease
Both lack glycogen phosphorylase, but in DIFFERENT LOCATIONS in the body
Deficiency? Key ssx?
Branching enzyme deficiency
-Cirrhosis --> FATAL
Cold intolerance, myxedema, (lateral third of eyebrows lost, periobital edema, dry skin), lethargy, increased TSH
Internuclear ophthalmoplegia (INO)
Damage to MLF (unilateral or b/l), conjugate horizontal gaze palsy, horizontal diplopia
Patent ductus arteriosus (PDA)
How to keep open or close?
Continuous machine-like murmur, keep open with indomethacin, close with PGE analogs
Caused by hypothyrodism, pretibial edema in Grave's diease, cuntaneous/dermal edema due to connective tissue deposition
Increased lab value? Suggest?
-Right-sided cardiac valvular lesions, increased 5-HIAA (serotonin metabolite), cutaneous flushing, diarrhea, bronchospasm
-Suggests a NET
Associated with HHV-8, dark purple skin/mouth nodules in a patient with AIDS
Diabetic ketoacidosis (DKA)
Kussmaul respirations (deep, labored breathing/hyperventilation)
-Niacin (B3) deficiency
-Dermatitis, dementia, diarrhea
-Thiamine (B1) deficiency
-Dilated cardiomyopathy, edema, alcoholism, or malnutrition
Cellulitis at infection skin, dog or cat bite resulting in infectionlas
MC renal complication, and what can it lead to?
-Dry eyes, dry mouth, arthritis, Schirmer's test (eye strips)
-MC renal complication = distal RTA --> calcinosis in kidneys
May progress to?
Dysphagia (due to
), glossitis, iron deficiency anemia (microcytic microchromic)
--> May progress to esophageal SCC
-Type V collagen defect (type III in vascular subtype of EDS)
-Elastic skin, joint hypermobility, increased bleeding tendency
-Suggests abdominal mets
-Enlarged, hard left supraclavicular node
Episodic vertigo, tinnitus, hearing loss, earing fullness
Mycosis fungoides (Cutaneous T-cell lymphoma)
Erythroderma, LAD, HSM, atypical T-cells
Mycosis fungoides + malignant T-cells in blood
-Sign of hypocalcemia
-Facial muscle spasm on tapping
"Fat, female, forty, and fertile"
-Rapid lysis of spirochetes resulting in endotoxin release
-Fever, chills, headache, myalgia following antibiotic treatment for SYPHILIS
Fever, cough, conjunctivitis, coryza (swelling of intranasal membranes), diffuse rash
B symptoms (staging) of lymphoma
Fever, night sweats, weight loss
Connective tissue disorder resulting in fibrous plaques in soft tissue of penis with abnormal curvature
Wilson disease ("hepatolenticular degeneration") - SSx
Gold-colored Kayser-Fleischer rings around cornea (specifically, Descamet's membrane) due to COPPER accumulation
Nasal polyps in kids should raise concern of? Testing?
Concern for CF, test with chloride sweat test
Chloride sweat test
Give pilocarpine (direct muscarinic agonist), measure choride content of sweat
Wilson disease - Lab
Low serum cerruloplasmin
Wilson disease - Tx
D-penicilliamine associated with what type of renal dysfunction
-HGPRT deficiency (X-linked recessive)
-Gout, intellectual disability, self-mutilating behavior in a boy
-Inherited, benign polyposis possibly causing bowel obstruction and increased GI cancer risk
-Hamartomatous GI polyps, hyperpigmentation of mouth/feet/hands/genitalia
Deficiency? Histo findings? Tx?
-HSM, pancytopenia, osteoporosis,
aspetic necrosis of femoral head
, bone crises
-Flaring of the distal femur (a.ka., Erlenmeyer flask deformity) --> pictured
"Crumpled" or "wrinkled paper" inclusions
in cytoplasm of lipid-laden macrophages
-Tx = Recombinant glucocerebrosidase
-Collagen IV mutation
-Hereditary nephritis, sensorineural hearing loss, cataracts
-Bilateral amygdala lesion
, hyperorality, hyperdocility
UMN damage signs
Hyperreflexia, hypertonia, positive Babinski
LMN damage signs
Hyporeflexia, hypotonia, atrophy, fasciculations, denervation atrophy, negative Babinski
-Hyperplasia of mucous cells
-Hypoxemia, polycythemia, hypercapnia
Most common congenital heart defect in Down syndrome
Complete A-V septal defect
-Bartonella henselae (Gram[-] bacilli)
Erythematous vesicular lesions
-Fever, malaise weakness
Anemia blood results (table)
Increased serum transferrin in IDA because body is trying to scavenge all the additional iron it can!
E. coli features
-Gram negative rod
-Produces beta-galactosidase and beta-glucuronidase
-Can cause serious urosepsis secondary to chronic UTI infection
-Chancre (NON-painful, indurated, ulcerated genital lesion)
-Painful, indurated, ulcerated, exudative genital lesion with
Glycogen synthesis vs. glycogenolysis
Rate-limiting enzyme/step in each, and what these steps activated by?
-Rate-limiting enzyme/step in glycogen synthesis =
(activated by insulin)
-Rate-limiting enzyme/step in glycogenolysis =
(activated by glucagon, NE, cAMP)
--> whatever activates one enzyme INACTIVATES the other
Glycogen synthase creates what type of bond?
Branching enzyme in glycogen synthesis creates?
alpha-1,6 linkage (linear linkages are alpha-1,4)
-Trisomy 13 mutation
-Infant with cleft lip/palate, microcephaly, holoprosencephaly, polydactyly, cutis aplasia
von Gierke disease (Type Ib GSD)
Deficiency? What builds up? LABS?
--> build-up of glucose-6-phosphate -->
-SSx = INFANT with
hypoglycemia, hepatomegaly, hyperlipidemia
(from fat breakdown since low glucose!),
(from protein breakdown since low glucose!),
Cori disease (Type III GSD)
Deficiency? What builds up? Compared to von Gierke?
Debranching enzyme deficiency (alpha-1,6 glucosidase)
--> build-up of glucose-1-phosphate
-SAME SSx as von Gierke, except different abnormal glycogen structure (accumulated glycogen is much more BRANCHED)
von Gierke vs. Cori disease pathway
-Infant with microcephaly, rocker-bottom feet, clenched hands, structural heart defect
-Distal malignant obstruction of billiary tree
-Jaundice, palpable distended non-tender GB
-Borrelia burgdorferi (from ixodes tick)
-Erythema chronicum migrans,
large rash with bulls-eye appearance
Ixodes ticks carry what bacterial species?
B. burgdorferi, Anaplasma phagocytophilum (causes babesiosis)
Causes? Transmission? SSx?
OF SHEEP OR CATTLE
, can cause
-Fever, cough, rash, HA, myalgia, delirium
Rash = Starts on chest and spreads out, SPARES PALMS AND SOLES
Vector? Causes? SSx? RASH??
-HA, fever, RASH
Rash = Starts at wrists/ankles, spreads to trunk, palms, soles
LUCID interval after injury
-Middle meningeal artery ruputre
-Lenticular shape on CT
-Does NOT cross suture lines
Bruton disease (Bruton's agammaglobulinemia)
Inheritance/mutation? Classic picture? MUTATION?
Classic picture = Male child that is healthy until 6 mo --> maternal Abs wear off --> recurrent infection (otitis media, pneumonia, abscesses) due to no mature B-cells
Tyrosine kinase deficiency --> deficient BTK signaling in B-cell maturation pathway
--> B-cell maturation stops in pre-B-cell stage
Hyper IgM syndrome
High rates of?
Defective CD40L signaling
(T-cells have the ligand, B-cells have the receptor)
-High IgM, but no (or low) other Ig classes
-High rates of opportunistic infection
-Defect in platelet aggregation due to lack of GbIIb/IIIA --> lack of fibrinogen binding --> can't bridge platelets to each other
-MUCOSAL bleeding and prolonged bleeding time
Beck triad of cardiac tamponade
Muffled heart sounds, distended neck veins, hypotension
Gardner syndrome (subtype of FAP)
Mutiple colon polyps, osteomas/soft tissue tumors, impacted supernumerary teeth
Pompe disease (Type II GSD)
LYSOSOMAL alpha-1,4-glucosidase deficiency
(whereas cori disease is non-lysosome)
, mypopathy (infantile hypertrophic cardiomyopathy), exercise intolerance
"Pompe = Pomeii (Mount Vesuvius)...explosion! (of heart...)
"Pompe affects the pump"
Superior trunk of brachial plexus injury during birth (C5-C6)
Pitutary infarction, no lactation post-partum, absent menstruation, cold intolerance
Multiple sclerosis (MS)
Nystagmus, intention tremor, scanning speech, bilateral INO
Brain lesion in MS
Areas of oligodendrocyte loss and reactive gliosis in periventricular regions
Cirrhosis of liver
Spider angiomas, fatigue, weight loss
Cold agglutinin disease
-Autoimmune hemolytic anemia caused by mycoplasma pneumoniae, infectious mononucleosis, CLL --> IgM against RBCs
-Painful blue fingers/toes, hemolytic anemia
-Infective endocarditis, immune complex deposition
-Painful, raised red lesion on fingers/toes
, septic emboli/microabscesses
-Painless erythematous lesions on palms/soles
Cancer of pancreatic head obstructing bile duct presents as?
Henoch-Schonlein purpura (HSP)
Cause? SSx? What ssx is specific to children?
-IgA vasculitis affecting skin and kidneys
-Palpable purpura on buttocks/legs, joint pain, abd pain (child), hematuria
MEN 1 syndrome (Wermer syndrome)
SSx (3)? Associated with?
Pancreatic, pituitary, parathyroid tumors
Zollinger-Ellison Syndrome (ZES)
SSx? Centriacinar vs. panacinar?
-Pink complexion ("pink puffer") due to CO2 retention, dyspnea, hyperventilation, barrel chest, pursed-lip breathing, extertional dyspnea
-Centriacinar --> Smoking
-Panacinar --> alpha-1-antitrypsin deficiency
Protease inhibitor, made in liver
-Multiple combined dysfunction of PCT
-Polyuria, RTA type II, growth failure, electrolyte imbalances,
6 P's? Locations?
-"Pruritic, purple, polygonal, planar papules and plaques"
-Sympathetic chain lesion
-Ptosis, miosis, anhydrosis
-Argyll Robertson pupil
-Pupil ACCOMMODATES but doesn't REACT
Guillain-Barre Syndrome (GBS)
-Acute inflammatory demyelinating polyradiculopathy subtype
-Rapidly progressive ASCENDING limb weakness following GI or URI infection
What causes rash on palms and soles?
Coxsackie A, secondary syphilis, Rocky Mountain spotted fever
-"Hand, foot, and mouth disease"
-Children < 5
-Fever, painful blisters on palms, soles, mouth appearing several days after high temp and painful sore throat
Organism? SSx? Time after primary infection?
-Diffuse rash on palms and sole, condylomata lata, mucous membranes and LNs often involved
-4-10 weeks after primary infection
Rocky Mountain spotted fever
Rickettsia rickettsii from Dermacentor tick
-Fever, headache, and muscle pain, followed by development of rash (palms and soles)
Job syndrome? Cause? "FATED" SSx?
-AD form = "Job Syndrome"
-Neutrophil chemotaxis abnormality
-Coarse facies, recurrent cold (non-inflammed) abscesses, retained primary teeth, unusual eczema, high serum IgE
Klebsiella pneumoniae pneumonia
Red "currant jelly" sputum in alcoholics or diabetics
Acute mesenteric ischemia (adults), intussuception (kids)
Red "currant jelly" stools
Paget disease of the breast
Sign of? SSx?
-Sign of underlying neoplasm
-Red, itchy, swollen rash of nipple/areola
Paroxysmal nocturnal hemoglobinuria (PNH)
Absence of? SSx?
-Absence of CD55, CD59
-Red urine in moring, fragile RBCs
von Hippel-Lindau (VHL) disease
-Dominant tumor suppression gene mutation
-Bilateral renal cell carcinoma (RCC), cerebellar hemangioblastomas, retinal angiomata, pheochromocytoma
-Loss of dopaminergic neuron in substantia nigra pars compacta (a basal ganglia!)
-RESTING tremor, rigidity, akinesea, postural instability, shuffling gait
-Retinal hemorrhages with pale centers
Roth spots, Janeway lesions, Osler nodes, splinter hemorrhages on fingernails
Cause? SSx? Type I vs. Type II?
-Congenital unconjugated hyperbilirubinemia cause by
COMPLETELY ABSENT UGT ACTIVITY
-Severe jaundice in neonate
-Type I is early, severe and does NOT respond to phenobarbital
-Type II is later-onset and DOES respond to phenobarbital
Severe RLQ pain with palpation of LLQ --> suggests appendicits
Severe RLQ pain with deep palpation --> suggests appendicitis
Cause? Often progresses to? SSx?
-Genetic loss of DNA cross-link repair; often progresses to AML
-Short stature, cafe-au-lait spots, thumb/radial defects, increased incidence of tumors/leukemia, aplastic anemia
-Single palmar crease
2nd trimester screening (quad) panel results for Down syndrome
Mnemonic? US finding?
"HIgh dEFict" = increased "Hcg" and "Inhibin", decreased "Estriol" and "aFp"
--> Nuchal transluceny on US
-Dynein arm defect affecting cilia
-Situs inversus, chronic sinusitis, bronchiectasis, infertility
-Primary adrenocortical insufficiency --> increased alpha-MSH and ACTH production
-Skin hyperpigmentation, hypotension, fatigue
Becker muscular dystrophy
-X-linked missense mutation in dystrophin gene
-Less severe than Duchenne (DMD)
-Slow, progressive muscle weakness in boys
-Measles [rubeola] virus
-Small, irregular red spots on buccal/lingual mucosa with blue-white centers
Smooth, moist, painless, wart-like white lesions on genitals seen in secondary syphilis
"Strawberry tongue" caused by?
Kawasaki diseae, scarlet fever
Hemolytic disease of the newborn
Rh-negative mom exposed to her Rh-positive baby --> mom develops anti-Rh abs --> if 2nd baby is Rh-positive, anti-Rh abs will cross placenta and attack fetal RBCs
--> Prevent with rhogam
-Streak ovaries, congenital heart disease, horseshoe kidney, cystic hygroma at birth, webbed neck, lymphedema
-Associated with pyloric stenosis
Key CT scan finding of Turner's syndrome
-Sudden, swollen big toe joint, tophi
-Vitamin C deficiency --> can't hydroxylate proline/lysine for collagen synthesis
-Swollen gums, mucosal bleeding, poor wound healing, petechiae
-Osteophytes on PIP (Bouchard nodes) and DIP (Heberden nodes)
Crescendo-decrescendo systolic ejection murmur
-Telangiectasia, recurrent epistaxis, skin discoloration, AV malformations, GI bleeding, hematuria
-Inheritance = AD
MEN 2A syndrome (Sipple syndrome)
Mutation? SSx (3)?
-AD mutation in RET gene
Medullary thyroid and parathyroid tumors, pheo
MEN 2B syndrome (Wagenmann-Frobese syndrome)
Mutation? SSx (3)?
-AD mutation in RET gene
Medullary thyroid tumors, pheo, ganglioneuromatosis (mucosal neuromas)
Mechanism of hypermagnesemia in MEN syndromes
Hypercalcemia activates calcium-sensing receptor (CaSR) --> inhibits magensium reabsorption
UMN lesion --> toe extension/fanning on plantar scrape
Unilateral facing drooping
UMN vs. LMN lesions?
-UMN lesions (e.g., stroke) SPARE the forehead
-LMN lesion (e.g., Bell's/CN-VII palsy) do NOT SPARE the forehead
Reactive arthritis associated with HLA-B27
Urethritis, conjunctivits, arthritis in male
-Associated with Sturge-Weber syndrome (vascular birthmark of face, aka port wine stain)
-Alcoholic abd bulimic patients
-Vomiting blood following gastroesophageal lesions
Organism? SSx? Stain? Many of what cell type?
-Weight loss, AWFUL FOUL diarrhea, endocarditis, migratory arthritis, fever, adenopathy, steatorrhea, malabsoprtion (advanced disease)
-Stain = PAS
Subarchnoid hemorrhage often described as?
"Worse headache of my life"
Dating error, anecephaly, spina bifida (NTDs) - Lab
Increased AFP in amniotic fluid/maternal serum
Calcinosis, Reynauds, Esophageal dysmotility, Sclerodactyly, Telangiectasias
Scleroderma (CREST) - Lab
Pemphigus vulgaris (blistering) - Lab
Anti-desmoglein (anti-desmosome) antibodes
Drug-induced SLE - Lab
Drugs --> hydralazine, isoniazid, phenytoin, procainamide
Goodpasture syndrome - SSX (2)
Involement = Glomerulonephritis, hemoptysis
(RENAL + PULMONARY)
Pathogenesis: Auto-antibodies to alpha-3 chain of type IV collagen
Goodpasture syndrome - Lab
How different from Wegener's?
Linear appearance of anti-glomerular basement membrane IgG antibodies in glomeruli (glomerulonephritis) and alveoli (hemoptysis)
--> Unlike Wegener's which is pauci-immune
Rheumatoid arthritis (RA)
Systemic inflammation, joint pannus, boutonniere deformity of thumb, ulncar deviation of MCPs, swan neck deformity of fingers
RA - Labs
Primary biliary cirrhosis
Female, cholestasis, portal hypertension, granulomatous destruction of medium-sized bile ducts
Primary biliary cirrhosis - Lab
Anti-mitochondrial antibodies (AMAs)
Guyon canal syndrome
-Ulnar nerve deficits that resolve
-4th/5th digits affected
Papal sign/Hand of benediction
-PROXIMAL median nerve palsy (passes thru carpal tunnel)
-DISTAL median nerve palsy
-MCP extension with PIP/DIP flexion
Iron vs. B12 resorption locations in gut
What kind of anemias?
-Iron: Duodenum --> IDA
-B12: Ileum --> Macrocytic anemia
Organism? SSx? How differentiated from staph infection?
-Group A strep
-Dermarcated, raised, erythematous, painful rash PLUS systemic signs (fever, chills, malaise) --> differentiates from staph infection
Non-rapidly-conducting heart rhythm (ST depression, bradycardia, PVCs, afib), nausea, vomiting, lethargy, weakness, color vision changes (esp. objects appearing
) --> tx w/
-ER+ breast cancer
-Good in post-menopausal women
-No risk of uterine cancer (unlike tamoxifen [a SERM that AGONIZES ER's in uterus])
Microscopic polyangiitis and eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome) - Lab
No granulomas or nasopharyneal involvement (unlike Churg-Strauss), necrotizing vasculitis of lung, kidneys, skin w/ pauci-immune glomerulonephritis
Microscopic polyangiitis - Tx
Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
Asthma, rhinosinusitis, granulomatosis w/ EOSINOPHILIA, peripheral neuropathy (foot drop), pauci-immune glomerulonephritis
Granulomatosis with polyangiitis (Wegener's) - Lab
Granulomatosis with polyangiitis (Wegener's) - Tx
Granulomatosis with polyangiitis (Wegener's)
Focal necrotizing fasciitis, necrotizing granulomas in lung and upper airway, necrotizing glomerulonephritis, rbc casts,
perforated nasal septum
SLE - Lab
ANAs (anti-smith and anti-dsDNA)
Idiopathic thrombocytopenic purpura/ITP - Lab
Purpura, petichiae, low platelets, epistaxis/bleeding
Thrombotic thrombocytopenic purpura/TTP - Pathogenesis
Auto-abs to or mutation in ADAMTS13 (protease that degrades vWF) --> massive clotting
Thrombotic thrombocytopenic purpura/TTP - SSx (Pentad)
2) Confusion/mental status changes
3) Renal failure (high BUN, Cr)
4) Thrombocytopenia (low platelets)
5) Hemolysis (causing purpura)
Schistocyte (helmet cells) associated with? (4)
TTP, HUS, DIC, aortic stenosis
Diffuse systemic scleroderma
Widespread skin involement, rapid progression, early visceral involvement
Diffuse systemic scleroderma - Lab
Anti-Scl-70 antibodies (Anti-topoisomerase I antibodies)
MC cause of death in scleroderma patients
Celiac disease - Lab
---> Diarrhea, weight loss
Celiac disease associated with what skin lesion?
Colorectal cancer sign on imaging
"Apple core" lesion
on barium enema XR (usually left-sided)
Cells in EBV infection
(esp. promyelocytic/M3 type)
Azurophilic peroxidase positive granular inclusions
in granulocytes and myeloblasts
Bacitracin response in strep species
Sensitive = GAS (S. pyogenes)
Resistant = GBS (S. agalactiae, "neonatal sepsis")
Anklosing spondylitis - Imaging
"Bamboo" spine on XR
Anklosing spondylitis - Lab
Basophilic nuclear remnants in RBCs due to non-functional spleen or splenectomy (hereditary spherocytosis, SCA, HA, MDS)
Lead poisoning or sideroblastic anemia on PBS
Subarachnoid hemorrhage - CSF appearance
Bloody or yellow tap on LP
Boot-shaped heart on XR suggests?
Tetralogy of Fallot (due to RVH)
Branching Gram(-) rods with sulfur granules
-Painful abscesses in mouth, lungs, breast, or GI tract
-Characteristic sulfur granules filled with progeny bacteria (Actinomyces israelii)
-Recent dental work, poor oral hygeine, radiation therapy
Location? What can it cause?
-Bronchogenic APICAL lung tumor on imaging
-Can compress cervical sympathetic chain --> Horner syndrome
Cardiomegaly with apical trophic, T. cruzi, Latin America, mud and brick houses
Endometriosis (often b/l)
-Circular grouping of dark tumor cells surrounding pale neurofibrils ("small, round blue cells")
Bacteria in lungs? Mutation/inheritance? Associated with what at birth?
-Colonies of mucoid pseudomonas in lungs (pseudomonas is MC)
--> fat-soluble vit deficiency and
at birth which has a
"ground-glass" or "soap-bubble"
appearance on XR
Wolff-Parkinson-White (WPW) syndrome
-Bundle of Kent bypasses AV node
-Delta wave on EKG, short PR interval, supraventricular tachycardia
Improper lateral fold closure leads to?
Gastroschisis or omphalocele (protruding and exposed abdominal contents)
Improper caudal fold closure leads to?
Improper dorsal fold closure leads to?
Improper rostral fold closure leads to?
-Desquamated epithelial casts in sputum
-Sign of bronchial asthma, can result in whorled mucous plugs
-Disarrayed granulosa cells around around collections of eosinophilic fluid
cell of the ovary
-Dysplastic squamous cervical cells with "raisinoid" nuclei and hyperchromasia (of nucleus)
-Sign of HPV, which predisoses to cervical cancer!
Pericardial tamponade EKG
"Owl's eye" intranuclear inclusion bodies
CMV (a.k.a. Cowdry A bodies)
Orphan Annie eyes
-Enlarged thyroid cells w/ ground-glass nuclei and CENTRAL CLEARING
-Sign of PAPILLARY carcinoma of thyroid
Eosinophilic cytoplasmic inclusion in HEPATOCYE
-Sign of alcoholic liver disease
-Eosinophilic cytoplasmic inclusions of
-Suggests Parkinson's and Lewy body dementia
Lewy body dementia (a.k.a., Dementia with Lewy bodies/DLB)
-Usually attention/spatial deficits
Disordered REM sleep, depression
-Eosinophilic globule in liver --> represents
hepatocyte undergoing APOPTOSIS
-Sign of viral hepatitic, yellow fever
-Eosinophilic inclusion bodies in cytoplasm of
hippocampal and cerebellar neurons
beta amyloid deposition
in gray matter of brain
-Sign of Alzheimer's
Reed Sternberg cells
-"Owl eye nuclei"
-Giant B cells with with BI-LOBED nuclei with prominent intranuclear inclusions
-Sign of Hodgkin's Lymphoma (HL)
-Glomerulus-like structure surrouding vessels in germ cells
Associated with YOLK SAC TUMORS
"Crew-cut" appearance on XR suggests?
Beta-thalassemia, sickle cell disease
Coding of Hb genes
1 adult beta-subunit gene + beta-like genes (delta, epislon, gamma)
, Locus-control region/LCR ("master switch")
2 adult alpha-subunit genes + 1 alpha-like gene (zeta)
, HS40 (erythroid-specific enhancer element)
Fetal Hb (HbF)
2 alpha, 2 gamma subunits in 2nd and 3rd trimesters --> greater O2 affinty than HbA (2,3-BPG binds LESS TIGHTLY to HbF --> left shift)
symptomatic carrier state
May have mild anemia (hypochromic, microcytic anemia --> MCV =70-80)
HbH disease (alpha-thalassemia)
Forms beta-homotetramers with greatly increased O2 affinity (similar to Hb Barts) and greatly decreased solubility
Chronic, moderate to severe hemolysis (hypochromic, microcytic anemia --> MCV=60-70)
Hydrops fetalis (alpha-thalassemia)
No useful Hb produced beyond embryonic stage --> gamma-homotetramers ("Hb Barts") with VASTLY INCREASED O2 affinity --> no O2 to fetal tissues --> death in 2nd or 3rd trimester
Hb constant spring (HbCS)
-Structural variant of an alpha-thalassemia
Mutation in UAA stop codon
of an alpha-globin gene --> product is functional/stable, but only produced at
1-5% of normal
β vs β⁺ vs β⁰
β = Normal beta gene
β⁺ = Mutations that DIMINISH beta-globin synthesis
β⁰ = Mutations that COMPLETELY ABOLISH beta-globin synthesis
ββ⁺ or ββ⁰
May present with mild anemia
β⁺β⁺ or β⁰β⁺
Variable severity (including into "beta-thalassemia MAJOR range!), generally survivable without transfusion
β⁰β⁰, β⁰β⁺, or β⁺β⁺
transfusion-dependent, hypochromic, microcytic (<70) anemia
, IRON OVERLOAD is common
---> Marrow expansion --> "crew-cut" appearance of skull on XR
Solubility of alpha-globin vs. beta-globin
Alpha-globin is much less soluble, therefore much more likely to aggregate (as in the beta-thalassemias
HbA1 vs. HbA2
-HbA1 = 2 alpha, 2 beta globin chains, >90% of adult Hb
-HbA1 = 2 alpha, 2 delta globin chains, ~2.5% of adult Hb
(>3.5% is diagnostic for beta-thalassemia carrier state)
-Rest is HbF, Gower I/II, and Hb Portland I/II
Sickle cell mutation
Point mutation (Glu --> Val) in beta-chain of Hb
Massively elevated hCG suggests?
Hydatiform mole, choriocarcinoma
-Granulomatous bodies in heart muscle
-Sign of rheumatic fever
Valvular sequelae of rheumatic fever
Infectious mononucleosis - Virus
Infectious mononucleosis - Lab
-Hexagonal, eosinophilic, double-pointed, needle-like crystals in bronchial secretions
-Sign of bronchial asthma (also maybe ascariasis, schistosoma, Toxoplasma gondii infections)
High D-dimer level suggests?
DVT, PE, or DIC
Sign of (and organism)?
-Hilar LAD, peripheral granulomatous lesion in middle or lower lung lobes that can calcify
-Sign of primary TB (Mycobacterium bacilli)
XR or CT sign of interstitial pulmonary fibrosis
Underlying cause? SSx?
Adenocarcinoma of pancreas or lung --> hypercoaguability --> migrating DVTs and vasculitis
B12 deficiency - Signs on PBS (2)? Sx?
-PBS = Megablastic anemia, hypersegmented neutrophils
-Neuro ssx (e.g., parathesias)
Folate deficiency - Signs on PBS (2)?
SSx? Often due to?
-PBS = Megablastic anemia, hypersegmented neutrophils
Weight loss, sore tongue
, diminished appetite, behavioral changes
-Often due to
small bowel resection
-NO NEURO ssx
Vitamin C deficiency
-Poor wound healing and immunological response
Swollen gums, hemarthrosis, petechiae, multiple skin bruises
Primary hyperaldosteronism (Conn syndrome)
-HTN, hypokalemia, metabolic alkalosis
-Dx = Aldosterone/renin ratio > 20 (excessive aldosterone inhibits renin release)
Causes of hypochromic, microcytic anemia
IDA, lead poisoning, thalassemia (HbF sometimes present)
Cowdry A bodies
-CMV, ZVZ, HSV
-"Owls eye" inclusions (intranuclear droplets)
Classic sign of squamous cell carcinoma
(on skin biopsy)
-Iron-containing bodies in alveolar septum
-Sign of asbestos exposure --> increased risk of mesothelioma
Sign of ulcerative colitis on abd imaging
"Lead-pipe" colon (due to loss of haustra)
Pathogenesis? SSx? Histo?
Congenital failure of phagolysosome formation due to DEFECTIVE MICROTUBULE FUNCTION
--> decrease in phagocytosis --> immunodeficiency -->
recurrent pyogenic infections, albinism, peripheral neuropathy
-Histo: Large granules in phagocytes
Proteinuria < 3.5 g/day
-Bleeding/hematuria, RBC casts
-Azotemia (nitrogenous compounds)
Nephritic syndrome - Diseases
-MPGN (types I and II)
Poststreptococcal glomerulonephritis (GN)
What is deposited? Hisopathological apperance? SSx?
-Deposition of IgG, IgM, C3 in glomeruli
~2-3 weeks after strep throat
-"Lumpy bumpy" glomeruli (LM), "starry sky" (IF), subEPIthelial humps (EM)
-Periperhal, periorbital edema, tea-colored urine, HTN
-Tx: Furosemide to reduce edema, supportive care (no specific therapy exists, CS don't help)
Rapidly progressive (crescenteric) glomerulonephritis
Cells? May result from?
-Monocyte invasion --> cellular crescents in Bowman's capsule
-May result from Goodpasture, Wegener's, microscopic polyangiitis
RPGN - Tx
Diffuse proliferative GN
Often associated with death from what underlying disease? Hisopathological apperance?
"Wire-looping" of capillaries
(LM), subENDothelial deposits of IgG and C3 (EM)
-Often associated with death in
(think "wire LUpus")
IgA nephropathy (Berger Disease)
Hisopathological apperance? SSx? SSx occur concurrently with what other infections, and why?
deposits (like HSP!)
Episodic gross hematuria
that OFTEN (but not always!) occurs with
respiratory or GI tract infections
(IgA is secreted by mucosal linings!)
TIMELINE: Several DAYS after URI, while in PSGN the onset is 2-3 WEEKS after strep infection
Tx: ACEi or ARB (e.g., Losartan)
Mutation/inheritance? Histopathological appearance? SSx?
-Type IV collagen mutation (X-linked dominant) --> splitting of glomerular basement membranes
-"Basket-weave" appearance (EM)
-Retinopathy/lens dislocation, GN, sensorineural deafness ("Can't see, can't pee, can't hear a bee")
Membranoproliferative GN - Type I
-SubENDOthelial IC deposits --> "Tram-track" apperance on PAS stain (GBM splitting from mesangial ingrowth)
-Often co-presents with nephrotic syndrome
-May be idiopathic or secondary to HBV, HCV infection
Membranoproliferative GN - Type II (a.k.a., dense deposit disease)
Associated with? Serum lab value?
Associated with C3 nephritic factor (stabilizes C3 convertase --> decreased serum C3)
Associated with? What is disrupted?
Proteinuria > 3.5 g/day
Hypoalbuminemia --> edema (peripheral/periorbital), hypercholesterolemia
-Due to podocyte damage -->
disrupts CHARGE BARRIER
(due to antithrombin III loss) and increased
(loss of Ig in urine and soft tissue compromise from edema)
Minimal change disease (lipid nephrosis)
MC in what pop? Histopathological appearance? Tx?
-Normal glomeruli (maybe some lipid)
Effacement of foot processes/podocytes
-MC nephrotic syndrome in
-Often idiopathic, or secondary to infection, immunization, or immune stimulus; rarely due to lymphoma
Focal segmental glomerulosclerosis (FSGS)
Histopathological appearance? MC affected pop?
-Effacement of foot processes/podocytes (EM) --> similar to minimal change disease
-Hyalinosis, sclerosis (Type IV collagen)
-May be idiopathic or secondary to HIV, massive obesity, infection, SCA, heroin abuse, IFN tx, CKD
-Inconsistent response to steroids
CONGO RED STAIN SHOWING APPLE-GREEN BIREFRINGENCE UNDER POLARIZED LIGHT
(amyloid in mesangium)
-Kidney is MC involved organism
AL amyloid (primary), AA amyloid (secondary)
Membraneous nephropathy (membranous GN)
Histopathological appearance? MC affected pop? Causes (DRUGS?)?
-Diffuse capillary and GBM thickening (LM),
"spike-and-dome" appearance w/ subEPIthelial deposits (EM)
Abs to PLA2 receptor
, secondary to drugs (
, NSAIDs), infections
, SLE, or solid tumors
-Many progress to CKD
MC cause of? Key histopathological feature? What structures are glycosylated and what is the pathological outcome of this glycosylation?
(esosinophilic nodular glomerulosclerosis
-Non-enzymatic glycosylation of GBM --> increased permeability, thickening
-Non-enzymatic glycosylation of efferent arterioles --> increased GFR --> mesangial expansion
-MC cause of ESRD in the US
Electron microscopy (EM) is essential for diagnosing what renal diseases?
Calcium oxalate stones
Shape? Causes? Excessive intake of what vitamina can cause them? Tx?
, LOW urinary pH, ethylene glycol ingestion, Crohn's (malabsorption)
-Can occur due to
excess Vitamin C
-Tx = thiazides, citrate, low sodium diet
Calcium phosphate stones
Shape? Causes? Tx?
-HIGH urinary pH
-Tx = thiazides
Struvite stones (ammoniun magnesium phosphate)
Shape? Causes? Tx? What do they commonly form?
Coffin lid shape
-Urease+ bacteria --> HIGH urinary pH
-Tx = Remove underlying infection and/or stone itself
Struvite stones, urease+ bacteria
Urease positive bacteria (3)
P. mirabilis, Staph saprophyticus, Klebsiella
Uric acid stone
Shape? Causes? Tx?
Rhomboid or rosettes
-LOW urinary pH, oliguria, arid climates,
-Tx = Alkalinize urine, allopurinol
Shape? Cause (hereditary...)? Diagnostic test?
("SIXtine stones have SIX sides")
-LOW urinary pH
-Cause: AR condition in which cystine-resorbing PCT transporter loses function --> (poorly-soluble) cystine forms stones in urine --> staghorn calculi
sodium cyanide nitroprusside test
-Tx = Low sodium diet, alkalinize urine, chelating agents (if refractory)
Lytic "punched out" lesion on XR
Fibrocystic change of breast
Mammary gland ("blue domed") cyst
Monoclonal antibody spike
-MM (usually IgG or IgA)
-Waldenstrom (IgM) macrogloblulinemia
-Primary amyloidosis (AL)
-Asymptomatic precursor to multiple myeloma
-M-spike < 3, plasma cells < 10%
-Monoclonal expansion of plasma cells WITHOUT "CRAB" findings of MM
-1-2%/yr develop MM
-M-spike > 3, plasma cells > 10%
-Basically between MGUS and MM
Multiple myeloma (MM)
"CRAB" findings? What do the plasma cells look like and what do they "do"? M-spike represents? Urinary protein What do RBCs look like on PBS?
CRAB findings = hyperCalcemia, Renal involement, Anemia, Bone lytic lesions
"Fried egg apperance" of monoclonal plasma cells that produce LARGE amounts of IgG (55%) or IgA (25%) and have a "clock-face" nucleus
-M-spike = IgM or IgA
-Bence Jones protein (Ig light chains) in urine
-Rouleaux formation (stacked RBCs)
M-spike represents (compared to MM)? SSx (compared to MM)?
M-spike = IgM
-Hyperviscosity syndrome (Reynauds, blurred vision), NO "CRAB" findings
-Mucin-filled cell with peripheral nucleus
-Sign of gastric carcinoma
-Narrowed bowel lumen on barium XR
-Sign of Crohn disease
Gout crystals (monosodium urate)
Needle-shaped, NEGATIVELY-birefringent crystals under polarized light
Response of staph species to novobiocin
Sensitive = S. epidermidis
Resistant = S. saprophyticus
"Nutmeg" appearance of liver due to? (2)
Budd-Chiari (hepatic vein thrombosis), right-heart failure
XR appearance? Population? Location? Mutation?
XR = "Onion-skin"
appearnce (a periosteal rxn)
-Malignant small blue cell tumor
-Boys < 15
Diaphysis of long bones
, pelvis, scapula, ribs
-Mutation = t(11;22) --> "11+22=33 (Patrick Ewing's jersey number!)"
Ewing sarcoma - Tx
Dactinomycin (actinomycin D) --> Intercalates DNA; AE=myelosuppresion
Response of strep species to optochin
Sensitive = S. pneumoniae
Resistant = Viridans strep (S. mutans, S. sanguis)
What do neurofibrillary tangles (Alzheimers) and Pick bodies (Pick disease) have in common?
Both are formed from hyperphosphorylation of tau protein
Pick's disease (Frontotemporal dementia/FTD)
Characteristic feature of Pick's?
Efforts to dissociate from family
, behavioral changes, unwarranted anxiety, irrational fears, compulsive buying -->
It is a characteristic of Pick's that dysfunctional, argumentative, or hostile social conduct is initially exhibited towards family members and not initially exhibited in a workplace or neutral environment
(also, BEHAVIORAL changes occur first in Pick's, whereas in Alzheimer's MEMORY loss occurs first)
Angle of Louis (sternal angle) also marks what other anatomical structures?
-T4/T5 vertebral level
-2nd costal cartilage
-Loop of recurrent laryngeal nerve around arch
Hyperphosphorylated tau protein deposition associated with?
Beta-amyloid deposition in extracellular compartment associated with?
SILVER-staining SPHERICAL aggregation
of tau proteins in neurons
Tau protein in Alzheimers
-Forms neurofibrillary tangles --> ab stain w/ basic fibroblast growth factor, amyloid P, and heparan sulfate glycosaminoglycan
-All 6 isoforms present (Unlike Pick's)
GRAM STAIN? Family? AGAR? What can it cause in newborn?
Does NOT Gram stain
-Branched, pleomorphic bacteria
-Mycoplasma family --> thus no cell wall, no Gram stain!
-Can be passed to infant during birth if it is colonizing mom's genital tract (as an STI) -->
can cause bronchopulmonary dysplasia in newborn
-Polished, "ivory-like" appearance of bone at cartilage erosion site
-Sign of OA resulting in bony sclerosis
Key sign of glioblastoma multiforme
Pseudopalisading tumor cells (on brain biopsy)
Psammoma bodies appear in what diseases?
Meningiomas, papillary thyroid carcinoma, mesothelioma, papillary serous carcinoma of endometrium and ovary
Meningioma on CT
-Whiter and denser than an epidural hematoma
-Created by raised periosteum
-Sign of an aggressive bone lesion (As seen in esteosarcoma, Ewing sarcoma, osteomyelitis)
RBC casts in urine suggest?
-Rectangular, crystal-like, cytoplasmic inclusions in LEYDID CELLS
-Sign of Leydig cell tumor
SSx (triad)? Mutation/pathogenesis? Most "severe" lab value?
TRIAD: Thrombocytonpenic purpura, eczema, recurrent infections
-X-linked recessive mutation in
WAS gene --> T-cells unable to reorganize their actin cytoskeletons
--> increased risk of autoimmune dz, malignancy (decreased IgG,
IgM (MOST SEVERE)
; increased IgE, IgA;
Renal epithelial casts in urine suggests?
Intrinsic renal failure (i.e., ischemia or toxic injury)
Pseudogout crystals (calcium pyrophosphate dihydrate)
POSITIVELY-birefringent rhomboid-shaped crystals under polarized light
"Pseudo is Positive" (P-->P)
Rib notching on XR (inferior rib surface)
Coarctation of aorta (resulting in colateral blood flow through intercostal arteries --> "notching")
Ring enhancing brain lesion on CT/MRI in AIDS patient
Toxoplasma gondii, CNS lymphoma
Ring enhancing brain lesion on CT/MRI in immno-COMPETENT patient
Features? Commonly seen in?
Irregular, broad, non-septate hyphae
(elevated glucose, anion-gap metabolic acidosis)
-Fungus feeds on excess glucoses and ketones --> can spread to brain
Fungi- Common bread mold; black mold
Relationship of uterine artery to ureter
Ureter passes BELOW uterine a.
Key histopathological appearance? Translocation? Activation? Associated with what infection?
on histo (Sheets of medium-sized lymphoid cells w/ scattered pale, tingible body-laden macrophages)
-More common in
Giant cell tumor of bone
"Soap bubble" in femur or tibia on XR (usually benign)
Rouleaux formation ("stacks")
MM, high ESR
"Steeple" sign on CXR
Croup (parainfluenza virus)
Streptococcus bovis bacteremia associated with?
Colon cancer, foul-smelling stools
-"Tennis racket-shaped" cytoplasmic organelles in Langerhans cells on EM
-Sign of Langerhans histiocytosis
MC site of ectopic pregnancy
Ampula of Fallopian tube
-Proliferative disorder of Langerhans (dendritic) cells
-Lytic bone lesions in
+ skin rash or as recurrent otitis media w/ mass involving mastoid bone
Familial adenomatous polyposis
-AD inheritance of mutation in APC gene
-Thousands of polyps on colonoscopy
-Start CRC screening EARLY
Lines of Zahn
Thrombi made of white/red layers (representing platelets/RBCs)
"Thumb sign" on lateral XR suggests?
Epigottitis (H. flu)
H. flu characteristics
Gram(-) coccobacillus, required factors V and X, chocolate agar
Multisegmented neutrophils associated with?
B12 or folate deficiency
Thyroid-like appearance of kidney
Chronic pyelonephritis due to VUR vs. urinary tract obstruction
-VUR --> POLAR scarring/atrophy
-Obstruction --> dilated ureter, DIFFUSE scarring/atrophy
Triglyceride accumulation in liver cell vacuoles suggests?
Fatty liver disease (alcoholic or metabolic syndrome)
Increased uric acid suggests?
Gout, Lesch-Nyhan syndrome, tumor lysis syndrome, loop and thiazide diuretics
Tumor lysis syndrome
Metabolic disturbances? Pathogenesis? MC in treatment of what cancers?
--> Complication during chemo where large amounts of tumor cells are lysed at the same time, releasing their contents into the bloodstream
(MC in ALL, lymphomas)
Tumor lysis syndrome treatment
MOA of this med?
Rasburicase (Recombinant enzyme that catalyses conversion of uric acid to allantoin)
Waxy casts with very low urine flow suggests?
WBC casts in urine suggest?
"Smudged" WBCs suggest?
CLL (almost always B cell)
-Due to subarchanoid hemorrhage
Tx = Ethosuximide
-Vacant stare, lack of response, eyes roll upward,
3 second spike-and-wave pattern on EEG
2L for absence seizures
Acute gout attack - Tx
NSAIDs, colchicine (if can't tolerate NSAIDs), glucocorticoids
Absolute C/I of colchicine
Key AE of cochicine
Neuromyopathy/peripheral neuropathy (due to toxic accumulation)
, uric acid kidney stones, or hyperuricemia due to chemo
-Xanthine oxidase inhibitor
Key drug-drug interactions with allopurinol
6-mercaptopurine, azathioprine (xanthine oxidase metabolizes these drugs!)
Allopurinol - Key AEs
-Toxic epidermal necrolysis
ATRA usually combined with?
Daunorubicin or idarubicin (anthracyclines), or cytarabine (ara-c)
Acute promyelocytic leukomia (M3 type) - Tx
ATRA (all-trans retinoic acid), aka Tretinoin
Alcoholism - Tx
Disulfram, acamprostate, naltrexone, supportive care
Anorexia - Tx
Nutrition, psychotherapy, mirtazapine (atypical antidepressant)
Arrhythmia in damaged cardiac tissue - Tx
Class IB antiarrhythmic (lidocaine, mexiltene)
Good drug for rapid BP reduction in hypertensive emergencies
(mixed alpha-1 and beta-1/2 blocker, with some intrinsic beta-2 agonist activity)
Class I antiarrhythmics - MOA
Sodium-channel blockers --> increase in refractory period, increase in QT intervals
Class IA antiarrhythmics
Drugs? Effect on AP? Use? AEs? Quinidine-specifc AE? Procainamide-specific AE? Disopyramide-specific AE?
-Quinidine, procainamide, disopyramide ("The Queen Proclaims Diso's pyramid")
-Increased AP duration, effective refractory period (ERP)
-Atrial AND ventricular arrhythmias (esp.
re-entrant and ectopic SVT, VT
Cinchonism (quinidine), reversible lupus-like syndrome (procainamide), HF (disopryramide), thrombocytopenia, torsade de pointes (increased QT interval)
Blurred vision, tinnutis, HA, psychosis --> ASSOCIATE THIS COMBO WITH QUINIDINE TOXICITY!
Class IB antiarrhythmics
Drugs? Effect on AP? Use? AEs?
-Lidocaine, mexiletine ("I'd buy Liddy's Mexican tacos")
Decreased AP duration
preferentially affecting ischemic or depolarized Purkinje cells
Digitalis-induced VENTRICULAR arrhythmias, post-MI (best use!)
-AEs: CNS stimulation/depression
Class IC antiarrhythmics
Drugs? Effect on AP? Use? AEs? CONTRAINDICATION?
-Flecainide, propafenone ("Can I have Fries, Please?")
-No effect on AP duration;
Prolongs ERP in AV node and accessory tracts, but NOT elsehwere
arrythmias (SVTs, inc. a-fib), last resort in VT
-Proarrhythmic, so it is
Class II antiarrhythmics - MOA and drugs
What part of AP?
Beta-blockers (metoprolol, propanolol, esmolol, atenolol, timolol, carvedilol) --> decreased SA and AV nodal activity by decreasing cAMP --> decreased Ca++ currents -->
DECREASES SLOPE OF PHASE IV --> decreased activity of abnormal pacemakers
--> AV node is especially sensitive (increased PR interval)
Effect of beta-blockers
Decreases cardiac RATE and CONTRACTILITY
AEs of beta blockers
-Mask signs of hypoglycemia
Beta-blocker overdose treatment
Phases of depolarization
Class II antiarrhythmics - Shortest-acting drug
Class II antiarrhythmics - Use
SVT, ventricular rate control in settings of a-fib or a-flutter
Class II antiarrhythmics - AEs
Impotence, exacerbation of COPD/asthma, CV effects, CNS effects (sedation, sleep alterations), hypoglycemia
Metoprolol - AE
What beta-blockers also have alpha-antagonistic activity?
Propranolol can exacerbate?
Vasospasm in Prinzmetal angina
Class III antiarrhythmics - MOA and drugs
Potassium-channel blockers ("AIDS" = Amiodarone, Ibutilide, Dofetilide, Sotalol) --> Increased AP, ERP, QT interval
Treatment of beta-blocker overdose
Class III antiarrhythmics - Uses
A-fib, a-flutter, V tach (amiodarone, sotalol)
Sotalol - AEs
TDP, excessive beta-blockade (is a beta-blocker with some class III function)
Ibutilide - AEs
Amiodarone - AEs
Always check what before giving?
Pulmonary fibrosis, hepatoxicity, hypo/hyperthyroidism (amiodarone is 40% iodine by weight!)
, corneal depositis, blue/gray skin depositis lead to photodermatitis, CNS effects, constipation, CV effects (brady, HF, heart block)
Always check "PFTs, LFTs, TFTs"
up to 100 days --> can cause serious drug interaction issues (e.g., inhibits warfarin, coumadin metabolism)
Class IV antiarrhythmics - MOA and drugs
Calcium-channel blockers (Verapamil, diltiazem) --> decreased conduction velocity --> increased ERP, PR interval
Class IV antiarrhythmics - Use
Prevention of NODAL arrhythmias (e.g., SVT), rate control in a-fib
Class IV antiarrhythmics - AEs
Constipation, flushing, edema, CV effects (HF, AV block, sinus node depression)
Class IV antiarrhythmics - Contraindication
Wolf-Parkinson-White, CHF (due to negative inotrope effect)
Adenosine - MOA
Increased K+ efflux --> hyperpolarizes cell and decreases intracellular Ca++
Adenosine - Use
DRUG OF CHOICE in SVT
Adenosine - AEs
Flushing, hypotension, chest pain, sense of impending doom, bronchospasm
Unique effect of adenosine
BRIEF asystole --> HA, flushing, chest pain
Effects of adenosine diminished by?
Theophylline, caffeine (adenosine receptor antagonists)
Digoxin/digitalis - MOA (2 effects)
1) Blocks Na+/K+ ATPase --> increased contractility
2) Increased vagal tone --> decreased heart rate
Digoxin - Uses (2)
Digoxin - AEs
yellow blurry vision
(Van Gogh's "Starry Night"), heart block, bradycardia
Narrow therapeutic window
--> monitor drug levels
Digoxin - Drug interactions
Quinidine, verapamil, diuretics (since resultant hypokalemia can cause digoxin toxicity)
Treatment of digoxin overdose
Antibody-binding fragments, normalize K+ (hyperkalemia)
MOA? Use? AEs?
--> increase SA/AV nodal conduction velocity (seen in crash cart)
(dry mouth, blurry vision, constipation, urinary retention)
ACEi - MOA
Block conversion of Ang-I to Ang-II by blocking ACE
ACEi - Uses
-Reduces proteinuria in diabetic or non-diabetic nephropathy
ACEi - AEs
-Cough and angioedema (esp of face) --> due to bradykinin accumulation
-Acute renal failure
Major contraindication of ACEi's
PREGNANCY (cat. x)
ARBs (-sartans) - MOA
Prevent Ang-II from binding to its receptor
ARBs - Uses
Same as ACEi, except
ARBs - AEs
-RARELY causes cough
Acute renal failure
Major contraindication of ARBs
Pregnancy (cat. X)
-1 drug = Aliskrenin
-Binds directly to renin and inactivates it
-Not really supperior to ACEi or ARBs
-Don't use with ACEi or ARBs
Alpha-1 blockers - Drugs
Doxazosin, prazosin, terazosin
Alpha-1 blockers - MOA
Competitive inhibition of POST-SYNAPTIC alpha-1 adrenergic receptors --> vasodilation of veins AND arterioles --> decreased TPR
Alpha-1 blockers - Uses
Alpha-1 blockers - AEs
UNIQUE = Orthostatic hypotension
Syncope with first dose
Central alpha-adrenergic agonists - drugs
Clonidine, gaunfacine, methyldopa
Central alpha-adrenergic agonists - MOA
Activates alpha-2 receptors in CNS --> activates and inhibitory neuron --> decrease in sympathetic outflow --> decreased TRP
Central alpha-adrenergic agonists - Uses
-Htn in pregnancy (methyldopa)
---> Dosed several times per day
Central alpha-adrenergic agonists - AEs
Major AE = Rebound HTN
(if stopped suddently or missed doses)
-Sedation, depression, fatigue, bradycardia
Drugs? Uses? AEs? Hydralizine-specific AE? BiDil use?
-Drugs: Hydralazine, minoxidil
-Uses: Htn, hypertensive emergency (hydralazine)
LUPUS-LIKE SYNDRONE (hydralazine)
, reflex tachy, fluid retention
-Hydralzine + isosorbide dinitrate (BiDil) good for African American patients who can't take ACEi or ARB or have Class III or IV heart failure
Drugs with a MORTALITY BENEFIT in heart failure
-Spironolactone (Class IV only)
-Digoxin has a MORBIDITY benefit only
DIURETICS DO HAVE HAVE A MORTALITY BENEFIT HERE!! (symptomatic improvement only)
Drug? MOA? Use? AEs?
-MOA: Inhibits PDE --> increased cAMP --> increased intracellular Ca++ --> increased cardiac contractility
-Use: Refractory HF (it's a positive ionotrope)
-AEs: Bone marrow suppression, hepatotoxicity
MOA? Use? AE?
Beta-1 selective agonist
(positive inotrope, NO effect on contractility)
-Use: Refractory HF
-AE = Tachy
Arterial vs. venous thrombi
-Arterial: Due to atherosclerosis, PLATELET-rich, causes MI
-Venous: Due to blood stasis or innappropriate activation of clotting cascade, FIBRIN-rich
SVT treatment progression
Vagal maneuvers --> adenosine
A-fib treatment progression
-Rate control: Beta-blocker, CB
-Rhythm control: Amiodarone
-Add long-term anticoagulation: Warfarin w/ heparin bridge (INR 2-3)
V-tach/V-fib treatment progression
DC cardioversion --> amiodarone (lidocaine as 2L)
Mg++ as antiarrhythmic
Effective in TPD and digoxin toxicity
Depressed ST segment
Prominent U wave
Short ST segment
Long QT interval
Long ST segment
Long PR interval
Long QT interval
Wide QRS complex
Short PR interval
Narrow QRS complex
1st degree AV block
Consistently long PR interval (>200 ms)
2nd degree AV block
Mobitz type I (Wenkebach) vs. Mobitz type II?
-Mobitz type I (Wenkebach) = PROGRESSIVELY longer PR intervals, then dropped QRS ("longer, longer, longer, DROP")
-Mobitz type II = CONSISTENTLY long PR intervals, then dropped QRS
3rd degree AV block
ATRIA AND VENTRICLES ARE CONTRACTING CONSISTENTLY
--> Constant P-P and Q-Q intervals (no dropped beats!)
--> P-waves are "divorced" from QRS, and may be buried in QRS
BPH - Tx
Alpha-1 antagonists (doxazosin), 5-alpha-reductase inhibitors (finasteride), PDE5 inhibitors (sildenafil, tadalifil)
Thiazides - MOA
Inhibits Na+/Cl- contransporter in DCT
Thiazides - AEs
Hypokalemia, hyponatremia, hyperurecemia (GOUT), hyperglycemia, hypercholesterolemia
Loop diuretics - MOA
Inhibit Na+/K+/Cl- co-transporter in TAL of Loop of Henle
Loop diuretics - AEs
Potassium-sparing diuretics - Drugs
Potassium-sparing diuretics - MOA
Block absorption of Na+ and secretion of K+ in collecting duct
Potassium-sparing diuretics - AEs
Potassium-sparing diuretics - Use
Usually used in combo with HCTZ (they're pretty weak...)
Mineralcorticoid receptor antagonists - Drugs
Mineralcorticoid receptor antagonists - MOA
Reduces amount of Na+ channels in collecting ducts (inhibits apical ENaC channel insertion)
Mineralcorticoid receptor antagonists - AEs
Hyperkalemia, hyperchloremic metabolic acidosis,
gynecomastia (UNIQUE) --> less with eplerenone than spironolactone
Carbonic anhydrase inhibitors/CAIs - MOA
Reduces bicarb absorption and sodium uptake
CAIs - Use
Glaucoma, altitude sickness, htn
CAIs - AEs
Metabolic acidosis, potassium wasting
Mannitol - Use
Mannitol - Key AE
Statins - MOA
Competitive inhibition of Hmg-CoA reducation (rate-limiting step of cholesterol synthesis) --> increase LDL receptor numbers (dietary cholesterol is taken up by cells sign de novo synthesis is being inhibited)
--> Decreases mortality!
Statins - AEs
-Hepatoxicity --> check LFTs
--> increased risk if co-treatments with niacin, fibrates
Fibrates - Drugs
Fibrates - MOA
Increased lipoprotein lipase activity, decreased hepatic TG synthesis
Fibrates - Use
Fibrates - AEs
Gallstones, myopathy (esp. w/ concurrent statin use)
-Use: LDL and TG reduction, increasing HDL
/itching/burning (take ASA 30 mins prior), hyperuricemia, hyperglycemia
-MOA: Inhibits cholesterol ABSORPTION
-NO decrease in mortality, per studies
Bile acid resins
, colestipol, colesevelam
-Prevents bile acid resoprtion
-AEs: Decreased fat-solube vitamin absorption (ADEK vitamins)
Nitrates - Drugs
Nitroglycerin, isosorbide dinitrate, isosorbide, mononitrate
Nitrates - MOA
Venous vs. arterial vasodilation?
Vasodilation via increased nitric oxide and cGMP activity --> smooth muscle relaxation
More venous vasodilation than arterial vasodilation --> PREFERNETIAL decrease in PRELOAD
Nitrates - Use
Angina, acute coronary syndrome, pulmonary edema
Nitrates - AEs
HA, flushing, reflex tachy (give a beta-blocker), hypotension, tolerance (within 24 hrs)
Why give nitrates sublingually instead of orally?
Large first-pass effect
Calcium channel blockers (CCBs) - 2 types
1) Dihydropyridines (DHPs): Amlodipine, clevidipine, nicarpidine, nifedipine, nimopidine
2) Non-dihydropyridines (NDHPs): Verapamil, diltiazem
CCBs - MOA
Specificity of DHPs vs. NDHPs?
Blocks slow, voltage-dependent L-type Ca++ channels in heart --> vascular smooth muscle relaxation, decreased cardiac contractility
--> DHPs more specific for vascular smooth muscle, NDHPs more specific for cardiac contracility
CCBs - Uses
DHPs vs. NDHPs?
-DHPs: HTN, angina, Reynauds
-NDHPs: Heart rate control (a-fibs, tachy)
CCBs - AEs
DHPs vs. NDHPs?
, flushing, gingivial hyperplasia, peripheral edema, dizziness
Bradycardia, AV block
Use of nimodipine
Subarchoinoid hemorrhage to reduce cerebral vasospasm
Good CCB for hypertensive emergencies
Why do nitrates work for angina?
Due to reduction in myocardial O2 demand
Bipolar disorder - Tx
Chemo drug class that crosses BBB
Nitrosureas (-mustine drugs, septozocin) --> good for glioblastoma multiforme
Triad off ssx? Secondary to?
Triad: Conjunctivitis/uveitis, urethritis, arthritis (usually knee, SIJ, or ankles, but can be others) --> "Can't see, can't pee, can't climb a tree"
-Secondary to infection that has usually resolved by time of reactive arthritis presentation
Disseminated gonococcal infection
Acute MIGRATORY tenosynovitis
in young adults (especially WOMEN)
-Test for c6-c9 complement deficiency
Angular stomatitis (angular cheilitis)
Sores in corner of mouth, vitamin/iron deficiencies, elderly or children in poor health
Lateral medullary syndrome (Wallenburg's)
PICA occlusion --> Crossed spinothalamic dysfunction, ipsilateral Horners, ipsilateral ataxia
Medial medullary syndrome
Anterior spinal artery occlusion --> Ipsilateral tongue deviation (hypoglossal nerve) contralateral limb weakness (medullary pyramid), contralateral loss of touch and proprioception
Hirsutism, prominent gums, compression fractures
Creutzfeldt-Jakob Disease (CJD)
Cortical ribboning on MRI, elevated 14-3-3 protein in CSF, triphasic spikes on EEG, memory loss, intention tremor
Good 2L for pseudomonas (beta-lactamase resistant drug, good Gram(-) coverage)
, prosthetic limbs/joints, novobiocin-sensitive
Idiopathic intracranial hypertension (Pseudotumor cerebri)
Women of child-bearing age presenting with bilateral papilledema
, headache that is worse in moring and exacerbated by coughing/sneezing/straining, "fullness in the ears",
6th nerve palsy (diplopia upon abduction of eyes)
--> "Fat, female, and forty"*
Basal cell carcinoma
Areas of max sun exposure (e.g., under nose), stratum basale, palisading nuclei, MC skin cancer
Autoimmune diseae w/ large, fluid-filled, superficial, cutaneous vesicles, suprabasal epidermal acantholysis, clefting, blistering
Pemphigus vulgaris - Lab
Squamous cell carcinoma
, sun-exposed area, 2nd MC type of skin cancer (after BCC)
SCC precursor w/ smaller, SCALY patches in sun-exposed skin, atypical keratinocytes with w/ hyperpigmented or pleomorphic nuclei extending to basal layer
CHILDREN, WT1 gene on 11p13, painless palpable abdominal mass, loss of appetite, abd pain, fever, nausea and vomiting, hematuria, developmental delays
Autosomal dominant PKD (ADPKD)
kidney cysts, 50% require transplants, 1:1000 people
Mutations in PKD1 (chr. 16) and PKD2 (chr. 8)
Autosomal recessive PKD (ARPKD)
cysts that destroy kidney, early/PROFOUND HTN, ESRD by age 15, 1:20,000 people, early kidney transplant, can also show upi in liver
Mutations in PKHD1 (chr. 6)
Benign renal neoplasm with fat, vascular, neoplasm, >4 cm risk of bleeding
Renal cell carcinoma (RCC)
Classic triad: Flank pain, gross hematuria, palpable abd mass
->50% are incidental findings
-20% have paraneoplastic syndrome
Risk factors for RCC
, obesity, htn?
Elevated ESR, HTN, hypercalcemia, Stauffer syndrome (hepatic dysfunction)
MC extension location of RCC
--> can extend to heart
Often presents with?
MC primary malignant renal tumor in children
(avg. age = 3-4)
-RARELY crosses midline
OFTEN (1/3) presents with ANIRIDIA
SSx (and nature of fever?)? Hx of?
-Flank pain, dysuria, CYCLICAL low-grade fever (like once a day, usually at night)
IV drug use
, UTIs, kidney stones
Pyelonephritis - Imaging finding
Pocket of infection in renal parenchyma, more ill than pyelo, associated with DM, IVDA, UTIs, dx on CT
-Gas in COLLECTING system
E. coli is MC cause
-Risk factors = DM, immunocompromised, UTI
-Tx = IV abx, stenting to ensure kidney drains
-Gas in renal PARENCHYMA (meat)
-Severe infection, 80% mortality
-Risk factors = DM, immunocompromised, UTI
-Tx = IV abx, stenting to ensure kidney drains, nephrectomy
Xanthogranulomatous pyelonephritis (XGP)
MC cause? CT appearance? Tx?
-Chronically infected kidney leading to renal obstruction
-*MC cause = Proteus spp (urease-splitting) causing staghorn calculi
appearance on CT
-Tx = GET THE KIDNEY OUT! --> very difficult surgery...
Breast cancer treatment in POSTMENOPAUSAL women
Aromatase inhibitor (anastrozole)
Inflammation and thrombosis
in small and medium-sized blood vessels, typically in the legs and leading to
--> associated with
Buerger's disease - Tx
Bulimia nervosa - Tx
Candida albicans - Tx
Vaginitis vs. oral/esophageal vs. systemic?
-Vaginitis: Topical azoles
-Oral/esophageal: Nystatin, fluconazole, caspofungin
-Systemic: Fluconazole, caspofugin, Amphotericin B
Amphotericin B - MOA
Binds egosterol --> forms pores that allow electrolyte leakage ("amphoTEARicin TEARS holes in fungal membrane")
Amphotericin B - AEs
, fever/chills ("shake n' bake"), hypotension, nephrotoxicity
Supplement what with Amphotericin B?
Cryptococcal meningitis - Tx
Ampho B +/- flucytosine
-MOA: Same as Amphotericin B
-Uses: "Swish and swallow" for oral candidiasis, topical for vaginal candidiasis or diaper rash
Flucytosine - MOA
Conversion to 5-FU by cytosine deaminase --> inhibits DNA/RNA synthesis
Flucytosine - AE
Bone marrow suppression
Azoles - MOA
Inhibits P-450 enzymes --> Inhibits fungal ergosterol synthesis (since P-450 converts lanosterol to ergosterol)
Azoles - Uses
-Fluconazole: Chronic suppression of cryptococcal meningitis in AIDS pts, all candida infections
-Itraconazole: Blastomyces, Coccidioides, Histoplasma
-Clotrimazole and miconazole: Topical fungal infections
Azoles - AEs
(esp. ketoconazle, due to testosterone synthesis inhibition)
MOA? Use? AEs?
-MOA: Inhibits squalene epoxidase
-Use: Athlete's foot (dermatophytoses)
-AEs: GI upset, HA, hepatotoxicity,
MOA? Use? AEs?
-MOA: Inhibit cell walls synthesis by inhibiting beta-glucan
-Use: Invasive aspergillosis, Candida
-AEs: GI upset,
MOA? Use? AEs? Deposits where?
-MOA: Interferes with MICROTUBULE function --> disrupts mitosis
-Use: PO tx of superficial infections, tinea, ringworm
-AEs: Teratogenic, carcinogenic, confusion, HA, induces CYP-450 enzymes (which requires vitamin B6 as a cofactor) + warfarin metabolism
-Deposits in keratin-containing tissues such as fingernails ("greasy fingernails")
Suramin and melarsoprol treat?
T. cruzi (Chagas) treatment
"Treat PML (pesty mites and lice) with
(permethrin, malathion, lindane), because they
you (Na, AChE, GABA blockade)"
Permethrin = blocks Na+ channels
Malathion = AchE inhibitor
Lindane = Blocks GABA channels (can lead to neurotoxicity)
Chloroquine - MOA
Blocks detoxification of heme into hemozoin --> heme accumulates --> toxic to plasmodia
Chloroquine - Uses
What spp is it NOT used for?
Treatment of plasmodial (malarial) spp
other than P. falciparum
(resistance too high, and is due to membrane pump that pumps the drug out!)
Chloroquine - AEs
, pruritis (esp. in dark-skinned people)
P. falciparum treatment
Artemether/lumefantrine or atovaquone/proguanil
Treatment of life-threatening malaria
-US: Quinidine or artesunate
-Elsewhere: Quinine or artesunate
Treatment of carcinoid syndrome
Chlamydia trachomatis - Tx
Eye infection prophylaxis?
(+ ceftriaxone for gonorrheal infection),
(for prophylaxis in infants)
Reticulate body vs. elementary body
-Reticulate body = Non-infectious, replicating, intracytoplasmic form
-Elementary body = Infectious, non-replicating form
Chronic gout - Tx
-Xanthine oxidase inhibitors (
(inhibits reabsorption of uric acid in kidney by inhibiting organic acid transporters/OAT)
MC cause of congential adrenal hyperplasia (CAH)
Chronic HBV, HCV infection - Tx
IFN-alpha (HBV, HCV); ribavirin, simeprevir, sofosbuvir (HCV)
-Langerhans cell histiocytosis
-Children < 3
-Scaly skin lesions, ear drainage, LAD, osteolytic lesions, HSM
Bacteria causing it? SSx?
-Bacteria = Malassezia furfur
Pale, velvety, hypopigmented macule usually on chest, back, shoulder
Leydig vs. Sertoli cells
-Leydig cells = Secrete testosterone
-Sertoli cells = Make sperm
alopecia WITH SCALY SCALP SKIN
(unlike alopecia areata)
-Species = Trichophyton
-Ab against melanocytes --> areas of depigmentation
-Associated with autoimmune conditions, such as hyperparathyroidism
MOA of Warfarin
Vitamin K epoxide reductase inhibitor (VKOR)
--> reduce production of multiple clotting factors and regulatory proteins
MOA of heparin
Binds and activates antithrombin III --> inactivation of Factors Xa, factor II (thrombin) --> thrombin CAN'T convert fibrongin to fibrin to cross-link platelets
PE, DVT prevention in hospitalized pts
-Prevent a-fib or mechanical heart valve clots
Unfractionated vs. LMWH?
-Unfractionated heparin --> measure
-LMWH --> anti-Xa levels (esp. obese, renal impairment, impairment)
MOA? Use? Advantages?
-MOA: Binds anti-thrombin III --> inhibits factor Xa (like heparin!)
-Use: PE, DVT prevention in hospitalized pts
Advantages: Injection only, can be used in HIT pts, no monitoring required
C/I: Renal insufficiency
Switch to what if HIT develops?
Direct thrombin inhibitor
Direct thrombin inhibitors
Drugs? MOA? Which one is available PO?
-Lepirudin, bivalrudin, argatroban, dabigatran (available PO)
-MOA: Bind directly to thrombin --> inhibition
CAN USE WITH HIT!
Which direct thrombin inhibit is ok to use in renal impairment
Heparin reversal drug
Only direct thrombin inhibitor that does NOT need monitoring
Direct Xa inhibitors
Drugs? Contraindication? ADVANTAGES?
-C/I = Renal impairment
ADVANTAGES: Rapid onset/offset so no need for heparin bridge, no monitoring, available PO, fewer drug interactions than warfarin has
Warfarin - MOA
Inhibition of Vitamin K --> Inhibition of factors II, VII, IX, X, protein C, protein S
Delayed (~5 days), since it involves synthesis of NEW clotting factors
Warfarin - Use
Warfarin - AEs
Bleeding, skin necrosis (due to protein C, protein S inhibition), teratogenicity
Warfarin - Antidote
Phytonadione (vitamin K), or FFP if need reversal IMMEDIATELY
--> recominant factor VIIa can also be used for immediate reversal, but it is $$$
Warfarin - Monitoring
Warfarin - Drug interactions
Key: BACTRIM --> inhibits warfarin metabolism
-And many others
Anticoagulation in pregnancy
-Abciximab, eptifibatide, tirofiban
MOA: Blocks platelets from adhering to fibrinogen
Acute coronary syndromes
*MOA? Reversibility? AEs? Drug interaction?
MOA: IRREVERISBLE COX-1 inhibitor --> Thromboxane A2 synthesis inhibition --> prevents platelet aggregation
Lasts for 7-10 days
(since brand new platelets need to be made)
-Uses: MI/stroke prophylaxis, inflammation control
-AEs: Hemorrhage stroke,
-Interactions: Ibuprofen (decreases ASA efficacy)
ADP receptor inhibitors
Drugs? MOA? AEs?
-Clopidigrel (Plavix), prasugrel, ticagrelor
MOA: Prevent platelet aggregation by blocking ADP receptor
-Use: Prevent stent thromboses, CV events
-Drug interactions = Omeprazole, esomeprazole (2C19)
-NOT a prodrug
-MOA: PDE inhibitor --> increases cAMP and cGMP to block platelet aggregation (cAMP) and causes vasodilation (cGMP)
-Use: In combo with ASA for
-MOA: PDE type 3 inhibitor --> increased cAMP, cGMP
-Use: Intermittent claudication
Fibrinolytics ("clot busters")
MOA? KEY AE?? ANTIDOTE? Uses?
, reteplase (tPA), tenecteplase (tPA)
MOA: Activates plasminogen to plasmin --> breaks down clots
Antidote = Aminocaproic acid (breaks down plasmin)
, PE, MI
-Alteplase is fibrin-selective (i.e., has low affinity for free plasminogen in blood)
Thrombin cleaves fibrinogen to fibrin, which cross-links plateletes and forms clot
Intrinsic coagulation pathway
Best drug for preventing recurrence of TIA or stroke
Extrinsic coagulation pathway
Common coagulation pathway
: Crunching sound on lung auscultation (air in mediastinum)
FULL THICKNESS esophageal rupture
-Intense wretching and vomiting, chest pain
Mallory weiss syndrome
who vomit a lot
"Patchy or diffuse infiltrates on CXR", anti-erythrocyte antibodies (agglutination!), many PMNs
Mycoplasma pneumoniae - Treatment
Erythromycin or azithyromycin (macrolides are good for atypical pneumonia)
MC causative species of bacterial sinusitis and otitis media in children (3)
Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis
Moraxella catarrhalis vs. Neisseria meningitidis
N. meningitidis grows on Thayer-Martin agar, M. catarrhalis does NOT
CML - Tx
Imatinib ("Gleevec") --> Inhibitor of the constitutively-active tyrosine kinase in CML (Philadelphia chromosome)
CML translocation, fusion gene
t(9;22) --> BCR-ABL ("Philadelphia chromosome")
Clostridium botulinum - Tx
MOA of C. botulinum (botulism) toxin
Blocks Ach release from pre-synaptic terminals at NMJ by cleaving T and V snare proteins
What type of toxin is botulism?
C. diff - Tx
-Mild: Metronidazole (DNA synthesis inhibitor via free radical formation)
-Severe or refractory: Vanco (cell wall synthesis inhibitor/d-ala-d-ala inhibitor)
Definitive dx of botulism - Adults vs. infants
Mouse bioassay in serum for adult, stool culture for infants
Clostridium tetani - Tx
MOA of C. tetani toxin
Binds to the presynaptic membrane at NMJ --> internalized and transported retroaxonally to the spinal cord --> spastic paralysis induced by the toxin is due to the blockade of neurotransmitter release from spinal inhibitory interneurons
Clostridium bacteria characteristics
Tennis racket or drumstick-shaped Gram(+)
Where are Clostridium spp. found?
Spores in SOIL
CMV - Tx
Gangciclovir, foscarnet, cidofovir
Encapsulated yeast, BIRD DROPPINGS, immunocomprosed (esp. as secondary meningitis infection in AIDS pts)
Cryptococcus neoformans - Stain
Cryptococcus neoformans - Tx
What MUST you provide prophylaxis for when an HIV patient's CD4 drops below 50? Drug?
Mycobacterium avium complex (MAC) --> Use a macrolide (e.g., azithromycin)
BRANCHING? What does it have a tendency to do? SSx?
SEPTATE fungus that branches at ACUTE angles
-Affects immunocompromised (e.g., HIV < 200 CD4 count)
ANGIOINVASIVE TENDENCIES --> hemopysis, pleuritic chest pain
Shape? Causes? Stain? Prophylaxis?
-Affects immunocompromised (e.g., HIV < 200 CD4 count)
PNEUMONIA IN HIV+ PATIENTS!
-Ground glass appearance of lungs
-Prophylaxis = TMP/SMX (CD4<200)
-Stain = Methanamine silver
BRANCHING? What patients does it affect? Where can it spread to, and what can it cause once there?
-Affects neutropenic and diabetic pts in DKA
-Can spread from nasal sinuses to brain --> rhinocerebral mucormycosis -->
frontal lobe abscess, cavnernous sinus thrombosis
Crohn Disease - Tx
CS, infliximab, azothioprine
-"Valley fever", deserts of southwest US,
-Triad: fever, joint pains, and erythema nodosum
Cyclophosphamide-induced hemorrhagic cystitis - Tx
Depression - 1L tx
Diabetics insipidus - Tx
Central vs. nephrogenic?
-Central = Desmopressin
-Nephrogenic: HCTZ, indomethacin, amiloride
T1DM - Tx
Dietary intervention + insulin replacement
T2DM - Tx
Dietary intervention (low carb) + oral hypoglycemics or insulin if needed
Diabetic ketoacidosis - Tx
Fluids, insulin, K+
Drug of choice for anticoagulation during pregnancy
Enterococci - Tx
Erectile dysfunction - Tx
Sildenafil, tadalifil, vardenafil
ER+ breat cancer - Tx
Ethylene glyclol (antifreeze) or methanol ingestion - Tx
Fomepizole (alcohol dehydrogenase inhibitor)
H. flu B - Tx for prophylaxis
Generalized anxiety disorder - Tx
1L vs. 2L?
-1L: SSRIs, SNRIs
Granulomatosis w/ polyangiitis (Wegener's) - Tx
Key AE of one of these drugs?
Cyclophosphamide (beware hemorrhagic cystitis!), CS
HER/neu+ breast cancer - Tx
Hyperaldosteronism - Tx
Hypercholesterolemia - Tx
Hypertriglyceridemia - Tx
Immediate coagulation drug
Infertility - Tx
Leuprolide, PULSATILE GnRH agonist, clomiphene
Influenza (virus) - Tx
Oseltamivir ("Tamiflu"), zanamivir
Legionella pneumophilia - Tx
Macrolides (e.g., azithromycin)
Legionella pneumophilia associated with?
AIR-CONDITIONING SYSTEMS, HYPONATREMIA
Warfarin, dabigatran, rivaroxaban, apixaban
Neonatal respiratory distress syndrome
-*Low L/S ratio (due to low lethicin production)
-Increased surface tension due to decreased surfactant
-Atelectasis in very young infant
Strepococcus pneumoniae resistance mechanism to beta-lactam abx
Alterations in the target of beta-lactams....THE PENICILLIN-BINDING PROTEIN (PBP)!
Fc portion binds to MAST CELLS at Fce receptor, allergen binds to variable region of IgE
MC salivary gland tumor
Pleomorphic adenoma (chondromyxoid stroma and epithelium)
Well-circumscribed, painless, mobile mass near angle of jaw (parapharyngeal), frequently recurr, may become malignant
Pain becomes WORSE when eating or even thinking about food (e.g., drooling) --> "mealtime syndrome
LWMH vs. unfractionated heparin
LMWH: Monitor with anti-factor Xa assay, NOT completely antagonized by protamine sulfate, longer half-life, more predictable half-life, better bioavailability
-Unfractionated heparin: Monitor with aPTT/PT/INR, COMPETELY antagonized by protamine sulfate, shorter half-life
Only abnormal ABG finding in CO poisoning
Low SaO2 (O2 saturation of Hb) --> CO has bound to Hb forming carboxyHb, so O2 can't bind nearly as well!
1L treatment for Pseudomonas
Piperacillin-Tazobactam (e.g., in setting of otits externa, burn infections)
Acute intermittent porphytia (AIP)
-Mutation in gene for
-Triad: Port-wine urine, abdominal pain, polyneuropathy (esp. tingling)
Wernicke's encephalopathy triad
Ophthalmoplegia, ataxia, altered mental status
--> Tx =
Korsakoff's syndrome triad
Amnesia, confabulation, dementia
--> Tx = Thiamine (B1), F&E
Malaria - Tx
For blood schizont? For Liver hypnozyte?
Chloroquine, mefloquine, atovaquone/proguanil (for blood schizont), primaquine (for liver hypnozyte)
Malaria life cycle
-Ryanodine receptor mutation
-Tachy, rigidity, unexplained rise in ETco2, increase in minute ventilation
-Halothane, sevoflurane, desflurane, isoflurane, enflurane (volatile anesthetics)
Malignant hyperthermia - Tx
Dantrolene (RyR blocker)
Medical abortion - Tx
Migraine - Tx
Abortive vs. prophylaxis?
-Abortive therapies =
-Prophylaxis = Propranolol, topiramate, CCBs, amitriptyline
Multiple sclerosis - Tx
Disease-modifying vs. acute flares?
-Disease-modifying: Beta-interferon, natalizumab
-Acute flares: IV steroids
Add what to cover likely concurrent C. trachomatis?
Ceftriaxone (add doxy to cover like concurrent C. trachomatis)
-Gram(-) diplococci (kidney bean-shaped), non-motile, fastidious
-Chocolate or Thayer-Martin agar
Mycobacterium tuberlosis - Tx
RIPE (rifampin, isoniazid, pyrazinamide, ethambutol)
Neural tube defect prevention
Osteomalacia/rickets - Tx
Vitamin D supplementation
Osteoporosis - Tx
-Prophylaxis: Ca++/Vit D supplementation
-Treatment: Bisphosphonates, SERMs, calcitonin, denosumab
Patient ductus arteriosus - Tx
Close with indomethacin, keep open with PGE analogs
Pheochromocytoma - Dx
What do you NOT do?
-Plasma free metanephrines
-24-hr urine VMA
---> Do NOT do a biopsy (can precipitate a hypertensive crisis)
Pheochromocytoma - Tx
--> *DO NOT GIVE BETA-BLOCKER FIRST ("follow your ABCs")
Pneumocystis jirovecii - Tx
TMP/SMX (prophlaxis AND treatment in immunosuppressed pts)
Prolactinoma - Tx
Capergoline/bromocriptine (dopamine agonists)
Silicosis lung disease ("Potter's rot")
Key signs of CXR?
What can result in long-term?
-Exposure to silica (e.g., ceramics)
Key signs on CXR = NUMEROUS small opacities/densities in UPPER LUNG FIELDS + hilar LAD
-Pulmonary fibrosis results over the LONG-TERM
Key signs on CXR = ROUNDED nodules in upper lung fields + lower zone emphysema
Prostate adenocarcinoma/uterine fibroids - Tx
Leuprolide, GnRH (continuous)
Prostate adenocarcinoma tx
Pseudomonas aeruginosa - Tx
Antipseudomonal PCNs (pip-taz), aminoglycosides, carbapenems
Cephalosporins with good anti-pseudomonal activity (3)
-Cefepime (4th gen)
-Ceftazidime (3rd gen)
-Cefoperazone (3rd gen)
Pseudomonas aeruginosa characteristics
-Gram(-) rod, catalase(+), oxidase(+), citrate (+)
(inactivates eukaryotic elongation factor 2 via ADP-ribosylation in the host cell)
Pseudomonas produces what on blood agar?
Pulmonary arterial hypertension (PAH) - Tx
Sildenafil, bosentan, epoprostenol
Non-selective blocker of endothelin receptors
Rickettsia rickettsii - Tx
Schizophrenia (negative symptoms) - Tx
Schizophrenia (positive symptoms) - Tx
Typical and atypical antipsychotics
SIADH - Tx
Fluid restriction, IV hypertonic saline, conivaptan/tolvaptan, demeclocycline
MOA? Route? AEs?
-MOA: Non-selective AVP receptor antagonist
, infusion site reactions, cardiac effects
MOA? Route? AEs?
-MOA: V2-specific AVP receptor antagonist
Demeclocycline - MOA
-Tetracycline (inhibits 30S ribosome)
-Interferes with intracellular second messenger cascade (specifically, inhibiting adenylyl cyclase activation) after ADH binds to vasopressin V2 receptors in kidney
Sickle cell disease - Tx
Hydroxyurea --> increases fetal Hb
MOA? Key AE?
-MOA: Decreases the SYNTHESIS (S-phase) of DNA (via inhibition of the enzyme ribonucleotide reductase)
-AE: Severe myelosuppression
Sporothrix schenckii - Tx
Itraconazole, oral potassium bromide
Stable angina - Tx
Staph aureus - Tx
-MSSA: Nafcillin, oxacilin, dicloxacillin (anti-staph PCNs)
, daptomycin, linezolid, ceftaroline
Strep bovis (gallolyticus)
-Catalase(-), oxidase(-), nonmotile, non-sporulating, Gram-positive lactic acid bacterium cocci in chains
Associated with endocarditis and colorectal cancer
-Alimentary tract of cattle, sheep, and other ruminants
Strep bovis (gallolyticus) - Tx
PCN prophylaxis, evalution for colon cancer if linked to endocarditis
Strep pneumo - Tx
Systemic infection/pneumonia vs. meningitis?
PCN/cephalosporin (systemic infection, pneumonia), vancomycin (meningitis)
Strep pyogenes - Tx
Temporal arteritis - Tx
Levetiracetam, phenytoin, valproate, carbamazepine
-MOA: Mostly unknown, inhibits NT release by binding SV2A
-AE: CNS effects,
MOA (kinetics)? AEs? Uses?
-MOA: Blocks Na+ channels (zero-order kinetics)
, hirsutism DRESS syndrome, SJS, megaloblastic anemia, nystagmus, diplopia, ataxia, sedation, peripheral neuropathy
Tonic-clonic (1L), status epilepticus prophylaxis (1L)
, simple and complex focal seizure
Valproic acid (valproate)
MOA? AEs? Uses?
-MOA: Increased Na+ channel inactivation, increased GABA concentration by inhibiting GABA transaminase
-AEs: GI distress, fatal hepatoxicity (MEASURE LFTs!), neural tube defects, tremor, C/I in pregnancy!
, abscence, simple and complex focal seizures
MOA? AEs? Uses?
-MOA: Blocks Na+ channels
-AEs: Diploplia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver tox, teratogenesis, SIADH, SJS
Toxoplasma gondii - Tx
Sulfadiazine + pyrimethamine
Treponema pallidum - Tx
Trichomonas vaginalis - Tx
Metronidazole (pt and partner!)
Trigeminal neuralgia (tic douloureux) - Tx
Ulcerative colitis - Tx
-5-ASA preparations (e.g., mesalamine), 6-MCP, infliximab, colectomy
Acute vs. non-acute?
-Acute: Fresh frozen plasma/FFP
-Non-acute: Vitamin K (takes longer!)
Actinic (solar) keratosis
Precursor lesion to squamous cell carcinoma
Acute gastric ulcer associated with CNS injury
Cushing ulcer (increased ICP pressure stimulates vagal gastric H+ secretion)
Acute gastric ulcer associated with severe burns
Curling ulcer (greatly reduce plasma volume result in sloughing of gastric mucosa)
Age ranges for patient with ALL, CML, AML, CML
-CML: Adults 45-85
-AML: Adult ~65
-CLL: Adult >60
Alternating areas of transmural inflammation and normal colon
Skip lesions (Crohn disease)
Aortic aneurysm in abdomen (AAA) usually due to?
Aortic aneurysm in ascending aorta or aortic arch usually due to?
Tertiary syphilis ("syphilitic aortitis"), vasa vasorum destruction
Aortic aneurysm in thoracic cavity usually due to?
Marfan syndrome (idiopathic cystic medial degeneration)
Aortic dissection usually due to?
Atrophy of mamillary bodies
Wernicke encephalopathy (thiamine deficiency causing ataxia, opthalmoplegia, confusion)
Autosplenectomy (fibrosis and shrinkage) usually due to?
Sickle cell disease (HbS)
Bacteria associated with gastritis, PUD, and gastric malignancies (e.g, adenocarcinoma, MALToma)
What allows H. pylori to withstand extreme acidic environment of stomach?
Bacterial meningitis cause - Adults and elderly
Bacterial meningitis cause - Newborns and kids
GBS (newborns), S. pneumoniae/N. meningitidis (kids/teens/college)
Bilateral ovarian mets from gastric carcinoma
Krukenberg tumor (mucin-secreting signet cells)
CSF profile in bacterial meningitis (protein, glucose, white cells)
-Protein = HIGH
-Glucose = LOW
-WBCs = Neutrophils
CSF profile in fungal or TB meningitis (protein, glucose, white cells)
-Protein = HIGH
-Glucose = LOW
-WBCs = Monocytes; more lymphocytes in TB vs. fungal etiologies
-Mets from gut to ovary
Bleeding disorder with Gp1b deficiency
Bernard-Soulier syndrome (defect in platelet adhesion to vWF)
Median nerve sensory innervation
Radial nerve sensory innervation
Ulnar nerve sensory innervation
Treatment of Klebsiella pneumonia infection
Carbapenems, PCN+beta-lactamase inhibitor, aminoglycosides, 3rd generation cephalosporins
Chronic benezene exposure can lead to?
MC brain tumor types - adults
Usually supratentorial: Mets, astrocytoma (inc. GBM), meningioma, schwannoma
MC brain tumor types - kids
-Infratentorial: Medulloblastoma (cerebellum)
MC breast tumor type
Invasive ductal carcinoma (often w/ fibrosis)
Bloody or serous nipple discharge
in women aged 35-55
-Non-painful, under aereola, do not change w/ menstrual cycle
Lobular carcinoma of breast
-Row of cells due to
reduced E-cadherin expression
Medullary carcinoma of breast
Bulky palpable mass and AXILLARY LAD
Papillary carcinoma of breast
-Well-defined border, finger-like projections
Breast mass usually means?
Fibrocystic change or carcinoma (in post-menopausal women)
A benign breast tumor in a young woman is usually?
Leaf-like (from "phyllodes") lobulations
-Women in 50's
Primary cardiac tumor in kids
Often seen in what concurrent disease?
Rhabdomyoma (often seen in tuberous sclerosis)
Cerebellar tonsilar herniation
Chiari II malformation
Direct inguinal hernia
Borders? Defect? Passes through?
-Medial border = rectus abdominis
-Inferior border = Inguinal ligament
-Lateral border = Inferior epigastric vessels
--> Hesselbach's triangle
--> Due to defect in abdominal wall (passes through here!)
Indirect inguinal hernia
Borders? Defect? Passes through?
-Medial border = Inferior epigastric vessels
-Inferior border = Inguinal ligament
MC type, due to CONGENITAL defect in processus vaginalis (incomplete obliteration), pass through deep inguinal ring
MC chronic arrhythmia
a-fib (high risk of emboli!)
Chronic atropicgastritis (usually autoimmune) can predispose to?
Gastric carcinoma (also can cause pernicious anemia)
-a.k.a., Vitamin B12 deficiency
Anti-partietal cell antibodies
-Fatigue, glossitis, paresthesias
Clear cell adenocarcinoma of vagina associated with?
DES (synthetic estrogen) exposure in utero
Congenital adrenal hyperplasia + hypotension suggests?
21-alpha hydroxylase deficiency
Common congenital cardiac anomaly
Defect? Key sign?
-Congenital conjugated hyperbilirubinemia/
(KEY SIGN, inability of hepatocytes to secrete conjugated bilirubin into bile)
-*Defect in EXRETION of conjugated bilirubin into bile ducts --> conjugated hyperbilirubinemia
Compared to Dubin-Johnson syndrome?
Very similar to Dubin-Johnson syndrome, except it is
milder and is NOT associated with a black liver
Etiologies of constrictive pericarditis
Developing vs. developed world?
-Developing world = TB
-Developed world =Idiopathic, viral illness
MC coronary arteries involved in thrombosis
LAD > RCA > circumflex
-Iodine deficiency/congenital hypothyroidism
-Profound mental retardation, coarse hair, protuberant abdomen, delayed closure of epiphyses, short stature
Cushing syndrome causes (4)
1) Iatrogenic (from corticosteroid/prednisone therapy)
2) Adrenocortical adenoma (excess cortisol)
3) ACTH-secreting pituitary adenoma
4) Paraneoplastic (ACTH secretion by tumors)
Causes of neonatal cyanosis
Tetralogy of Fallot, transposition of great vessels truncus arteriosus
Tetralogy of Fallot
-Pulmonary valve stenosis
Death in CML often results from?
Death in SLE often results from?
MC causes of dementia
Alzheimer's, vascular dementia (multiple infarcts)
Demyelinating disease in young women
Severe sepsis, obstetric complications, cancer, burns, trauma, major surgery, acute pancreatitis, APL
Ejection click suggests?
Diverticulum in pharynx
Dx with? SSx?
(dx with barium swallow)
-SSx = Persistant halitosis, regurgitation of UNDIGESTED food, esophageal dysmotility
Cause = LES denervation
-Dx = Barium swallow
-Progressive dysphagia to solids and liquids
Where does an aortic stenosis murmur radiate to?
MC types of esophageal cancer - Worldwide vs. US
-Squamous cell carcinoma (worldwide)
Location? Arises from? Risk factors?
-Arises from Barrett esophagus
-Risk factors =
Esophageal squamous cell carcinoma
Location? Risk factors?
-ANYWHERE in esophagua
-Risk factors =
, caustic injury
Food poisoning (exotoxin-mediated) - 2 common bacterial species
Signs of mets (2)? SSx?
Ominous metastatic signs: Virchow's node (Left supraclavicular LAD), Sister Mary Joseph nodule (umbilicus)
Dyspepsia/GERD, weight loss
, post-prandial vomiting, DVT, acanthosis nigricans
Glomerulonephritis in adults
IgA nephropathy (Berger disease)
MC gynecologic malignancies - Worldwide vs. US
-Worldwide: Cervical carcinoma
-US: Endometrial carcinoma
MC congenital heart murmur
Heart valves involved in endocarditis
Rheumatic fever? IV drug use?
-Rheumatic fever: Mitral > aortic
-IV drug use: Tricuspid
Common helminth infections in US (2)
Enterobius vermicularis, Ascaris lumbricoides
NEMATODE: Enterobius vermicularis (pinworm)
Key ssx? Dx? Transmission? Tx?
-Dx w/ scotch tape test
-Transmission = Fecal-oral
-Tx = Albendazole (b/c worms are "bendy"!)
NEMATODE: Ascaris lumbricoides (giant roundworm)
SSx? Dx? Transmission? Tx?
-Intestinal infection w/ possible obstruction at ileocecal valve
-Dx = Eggs visible under microscope
-Transmission = Fecal-oral
-Tx = Albendazole
NEMATODE: Strongyloides stercoralis (threadworm)
SSx? May mimic? Transmission? Tx?
-Intestinal infection --> vomiting, diarrhea, epigastric pain (may mimic peptic ulcer)
-Transmission = Larvae in soil penetrate skin
-Tx = Albendazole or ivermectin
NEMATODE: Ancyclostoma duodenale, Necator americanus (hookworms)
SSx? Transmission? Tx?
-Intestinal infection causing ANEMIA by sucking blood from intestinal wall
Cutaneous larva migrans
= Pruritic, serpingous rash from walking barefoot on contaminated beach
-Transmission = Larvae penetrate skin
-Tx = Albendazole or pyrantel pamoate
NEMATODE: Trichinella spiralis
SSx? Transmission? Tx?
-Larve enter bloodstream and
ENCYST IN MUSCLE
-Trichinosis = Fever, vomiting, nausea, periorbital edema
-Transmission = Fecal-oral, eating undercooked meat (esp.
-Tx = Albendazole
-Crosses suture lines
Can result in? Tx?
-Mutiple blood transfusions or hereditary HFE mutation
-Can result in heart failure, "bronzing" of skin, increased risk of hepatocellular carcinoma
-Tx = Phlebotomy, iron chelators
Hereditary hemochromatosis inheritance pattern
Associated with? Dx/therapeutic response monitoring?
-Associated with HBV, HCV, alcoholism
-Dx = Increased AFP (good way to monitor therapeutic response)
Hereditary bleeding disorder
von Willebrand disease
von Willebrand disease
What does vwf bind to?
Binds to Gp1b and collagen
Activity of what is reduced?
Mildly reduced UGT activity
--> Problem with bilirubin UPTAKE from hepatic sinusoids
-May present with mild jaundice, unconjugated hyperbilirubinemia when stressed or fasting
-Benign congenital hyperbilirubinemia
Psoriatic arthritis, ankylosing spondylitis, IBD-associated arthritis, reactive arthritis (formerly Reiter syndrome)
DM-Type I, SLE, Graves disease, Hashimoto thyroiditis, Addison disease
DM-Type I, RA, Addison disease
Holosystolic murmur suggests?
VSD, tricuspid regurgitation, mitral regurgitation
Suggests increased risk of?
Hypercoagulability, endothelial damage, blood stasis
--> Suggests increased risk of THROMBOSIS
Circulating Abs bind to TSH receptors
-SMOOTH, NON-PAINFUL gland enlargement
-Increased T3, T4 --> decreased TSH
Goiter due to plasma cell and lymphocyte infiltration
-Women aged 60-70
-High auto-ab levels
-Euthyroid or hypothyroid
-May be initial period of hyperthyroidism
FIBROTIC TISSUES replaces thyroid parenchyma --> FIXED, STONY THYROID
-Euthyroid or hypothyroid
MC causes of secondary HTN
Renal artery stenosis, chronic kidney disease, (e.g., polycystic CKD, diabetic nephropathy), hyperaldosteronism
MC cause of hypoparathyroidism
Accidental excision during thyroidectomy
MC cause hypopituitarism
Pitiutary adenoma (usually benign)
MC infections in granulomatous disease
S. aureus, E. coli, Aspergillus (catalase-positive)
Common infection secondary to blood transfusion
Hepatitis C (flavivirus)
Hepatitis associated with IVDA
HBV (hepadnavirus), HCV (flavivirus)
Hepatitis A viral family
Intellectual disability suggests?
Down, Fragile X syndrome
Fragile X syndrome
Autism, large jaw, facial elongation, everted ears, MVP
Fragile X syndrome - Inheritance
X-linked dominant (MC XLD disorder)
-Onset later in life
-Late cynatotic shunt in which a pre-existing left-to-right heart defect/shunt (e.g., ASD, VSD, PDA) BECOMES a right-to-left shunt due to long-standing RVH and pulmonary hypertension/diminished lung elasticity --> less venous return to lungs --> cyanosis
Left renal vein passes under
SMA --> if SMA dilated, LRV is compressed
--> backs up into left testicular vein -->
Malignant associated with non-infectious fever
Common malignancies in kids
ALL, medulloblastoma (cerebellum)
MC tumor in what pop? SSx? Key mets location, and what is the term for this?
MC BRAIN TUMOR IN KIDS
granular layer of cerebellar vermis
-SSx: Cerebellar signs (poor rapid alternating movements of hands) due to hydrocephalus or mass effect
Key mets location = Cauda equina (a.k.a. "drop metastasis") via CSF
MC in what ptients? Arises from? SSx? MC location?
-MC in infants in young kids
-Arises from NEURAL CREST DERIVATIVES*
-Firm, irregular abdominal mass
-Homer-Wright rosettes (since it arises from neuroectoderm)
-MC location = Adrenals
Key differentiating factor from medulloblastoma? MC location?
-1st 2 decades
Key differentiating factor from medulloblastoma = Perivascular pseudorosette
(medulloblastoma = Home-Wrigh rosettes)
-MC location =
--> obstructive hydrocephalus
Glioblastoma multiforme (GBM)
Age? Tumor of what cell type? KEY IMAGING SIGN? Cells?
Ring-enhancing "butterfly lesion" that crosses the midline
Age? KEY CELLULAR CHARACTERISTIC?
KEY CHARACTERISTIC OF CELLS = "Fried-egg appearnce"
-Tumor of oligodendrocytes
Mets to bone
Prostate, breast > lung > thyroid
Mets to brain
Lung > breast > genitourinary > melanoma > GI
Mets to liver
Colon >> stomach, pancreas
Disease occurs in both males and females, inherited through FEMALES ONLY
Rheumatic heart disease heart valve abnormality
Mitral valve stenosis
Mixed (UMN and LMN) motor neuron disease
Infectious agent causing myocarditis
Nephrotic syndrome in adults
Nephrotic syndrome in kids
Minimal change disease
-Cause: Neuron migration failure
-Hypogonadotropic hypogonadism and anosmia
Nosocomial pneumonia causes
S. aureus, Pseudomonas, other enteric GNRs
Nosocomial pneumonia occurs approximately how long after admission?
Obstruction of male urinary tract
Opportunistic infection in AIDS
Pneumocystis jirovecii pneumonia
Osteomyelitis - Infectious agent
S. aureus (MC overall)
Osteomyelitis in sickle cell disease - Infectious agent
Osteomyelitis with IV drug use - Infectious agent
Pseudomonas, candida, S. aureus
Benign, bilateral ovarian tumor
Malignant ovarian tumor
Causes of acute pancreatitis
Causes of chronic pancreatitis
ETOH (adults), cystic fibrosis (kids)
PID - Infectious agents
C. trachomatis, N. gonorrhoeae
Pathophysiology? Bacterial spp? SSx?
-Seeding of throat infection/abscess to internal jugular vein
Associated w/ Fusobacterium spp.
Cervical LAD, neck pain
, HA, memory loss, muscle pain,
decreased ability to open jaw, crepitations over lungs
Translocation? Associated with?
-t(9;22) --> BRC-ABL translocation
(sometime also associated with ALL/AML)
Pituitary tumors - MC causes
Prolactinoma, somatotrophic adenoma
Primary amenorrhea suggests?
Turners (45,XO or 45,XO/46,XX mosaic)
Primary bone tumor in adults suggests?
Primary hyperaldosteronism suggests?
Adenoma of adrenal cortex
Primary hyperparathyroidism suggests?
Adenomas, hyperplasia, carcinoma
Hepatocellular carcinoma causes
Chronic hepatitis, cirrhosis, hemochromatosis, alpha-1-antitrypsin deficiency, Wilson disease
Idiopathic, heritable, left heart disease (e.g., HF), lung disease (e.g., COPD), hyperemic vasoconstriction (e.g., OSA), thromboembolic (e.g., PE)
Buerger disease (thromboangiitis obliterans)
Strongly associated with??
-STRONGLY associated with
-Recurrent inflammation, thrombosis of small and medium vessels in extremities (esp. HANDS)
Associated with what syndrome? Signs?
-Gastrinoma of duodenum or pancreas
MEN 1 syndrome
Signs: Refractory peptic ulcers and high serum gastrin levels, diarrhea, steatorrhea (malabsorption)
Renal cell carcinoma associated with?
von Hippel-Lindau and cigarette smoking
von Hippel-Lindau (a.k.a., Familial cerebello retinal angiomatosis)
Retinal angiomas, cerebellar hemangioblastoma, pheos, RCC
, bilateral papillary cystadenomas of the epididymis (men) or broad ligament of the uterus (women)
-Mutation: VHL gene on chr. 3p
Renal cell carcinoma paraneoplastic syndrome
EPO, renin, PTHrP, ACTH
Right heart failure due to pulmonary cause
S3 heart sound
↑ventricular filling pressure (e.g., mitral regurgitation, HF), common in dilated ventricles
S4 heart sound
Stiff/hypertrophic ventricle (aortic stenosis, restrictive cardiomyopathy)
Secondary hyperparathyroidism usually due to?
Hypocalcemia of chronic kidney disease
C. trachomatis usually co-infected with?
SIADH often due to?
Small cell carcinoma of lung
Site of diverticula
Cause? Rule of 2's?
-Incomplete fusion of
Rule of 2's:
2% (of the population)
2 feet (proximal to the ileocecal valve)
2 inches (in length)
2 types of common ectopic tissue (gastric and pancreatic)
2 years is the most common age at clinical presentation
2:1 male:female ratio
Sites of atherosclerosis
Abdominal aorta > coronary artery > popliteal artery > carotid
--> BCL-2 activation, anti-apoptotic oncogene
Burkitt lymphoma --> c-myc fusion, transcription factor oncogene
Philadelphia chromosome, CML --> BCR-ABL activation, tyrosine kinase oncogene
SSx? Dx? Tx?
-Risk of ipsilateral blindness due occlusion of ophthalmic artery, painful chewing
-Dx = Biopsy
-Tx = Steroids ASAP
-Associated with increased placental ALP
Prognosis? Histo features? Associated with?
-Histo: "Orphan Annie" eyes (ground glass appearance), Psammoma bodies
-MC, best prognosis
-Associated with radiation exposure in childhood, RET mutation
Prognosis? Associated with?
-Associated with iodine-deficient areas, RAS mutation
Secretes? Associated with?
-Secretes calcitonin but pt is eucalcemic
-Associated with MEN 2A and 2B syndromes; RET mutation
-MC in older patients
Leiomyoma (uterine fibroids)
-Common tumor in women
Grows RAPIDLY but regresses spontaneously by childhood
-Adrenal medulla tumor in adults, usually benign
-Sweating, pallor, HA, severe HTN, tacky
-Malignant tumor of adrenal medulla in KIDS
-Key feature: Homer-wright rosettes
Common type of Hodgkin lymphoma
Nodular sclerosing (vs. mixed cellularity, lymphocytic predominance, lymphocytic depletion)
Common type of Non-Hodgkin lymphoma
Diffuse large B-cell
UTI - MC causative organisms
E. coli (MC), Staphylococcus saprophyticus (young women)
Vertebral compression fracture a sign of?
Type I vs. Type II?
Osteoporosis (Type I = Post-menopausal women, Type II = elderly man or woman)
Viral encephalitis affecting temporal lobe
Common vitamin deficiency in US
Folate (pregnant women at high risk, body only stores 3-4 month supply, prevents neural tube defects)
Sensitivity vs. specificity tells you?
Sensitivity = A/(A+C)
Specificity = D/(B+D)
Positive predictive value (PPV)
PPV = A/(A+B)
Negative predictive value (NPV)
NPV = C/(C+D)
Odds ratio/OR (for case-control studies)
OR = (A/C)/(B/D) = ad/bc
Relative risk (RR)
RR = (A/[A+B])/(C/[C+D])
Attributable risk (AR)
AR = a/(a+b) - c/(c+d)
Relative risk reduction (RRR)
RRR = 1 - RR
Absolute risk reduction (ARR)
ARR = c/(c+d) - a/(a+b)
Number needed to treat (NNT)
NNT = 1/ARR
Number needed to harm (NNH)
NNH = 1/AR
p² + 2pq + q² = 1
Answer = C
Volume of distribution
Vd = Amount of drug in body/Plasma drug concentration
Units = Volume (e.g., L)
t1/2 = (0.693 x Vd)/CL
CL = drug clearance rate
CL = rate of elimination of drug/ plasma drug concentration = Vd x Ke (elimination constant)
LD = (Cp x Vd)/F
Cp = plasma concentration
F = Bioavailability
D = (Cp x CL x tau)/F
Km = Concentration of substrate [S] at which the reaction velocity is 1/2 of Vmax
Effects of enzyme inhibition - Competitive vs. non-competitive
Competitive = Km increases
Non-competitive = Vmax decreases, Km remains the same
Lineweaver-Burk plot - Competitive vs. non-competitive
Competitive = Increased slope
Non-competitive = Curve shifts to left
Cardiac output (CO) equations (2)
CO = Rate of O₂ consumption/(Arterial O₂ content - venous O₂ content)
CO = stroke volume x HR
Mean arterial pressure (MAP) equation
MAP = CO x Total peripheral resistance (TPR)
MAP = 1/3 systolic BP + 2/3 diastolic BP
Stroke volume (SV)
SV = EDV - ESV
Ejection fraction (EF)
EF = SV/EDV = (EDV-ESV)/EDV
Resistance = driving pressure ("∆P")/Flow (Q) = (8η["viscosity"]) x length)/πr⁴
Capillary fluid exchange
Net fluid flow = Flow out - Flow in = (Capillary hydrostatic pressure + interstitial oncotic pressure) - (interstitial hydrostatic pressure + capillary oncotic pressure)
Renal clearance equation
Cx = UxV/Px
Ux = Urine concentration of substance "X" (e.g., mg/mL)
V = Urine flow rate (mL/min)
Px = Plasma concentration of substance "X" (e.g., mg/mL)
Glomerular filtration rate (GFR) equation
GFR = Uinulin x V/Pinulin = Cinulin
Creatinine slightly _____________ GFR because _______
overestimates; it is moderately secreted by renal tubules
Effective renal plasma flow (RPF)
eRPF = Upah x V/Ppah = Cpah
PAH = para-aminohippuric acid --> Good estimator of RPF because it is basically 100% of PAH that enters the kidney is freely filtered at the glomeruli or secreted, and is NOT resorbed (thus PAH that enters kidney = 100% of excretion)
----> This method slightly underestimates true PRF
Effect of angiotensin II on renal arterioles
Preferentially constricts EFFERENT arteriole --> decreased RPF, increased GFR, increased FF
--> ACEi block these effects!
Best anti-hypertensive med for patients w/ diabetes, and why
ACEi, because they preferentially dilate efferent renal arterioles, thereby reducing GFR --> reduced proteinuria --> less exacerbation of any pre-existing diabetic nephropathy
Effect of prostaglandins on renal arterioles
Preferentially constrict AFFERENT arteriole --> decreased RPF and GFR, no change in FF
--> NSAIDs block these effects!
Filtration fraction (FF)
FF = GFR/RPF
GFP x Px
Px = Plasma concentration of substance "X"
Henderson-Hasselbach equation (for extracellular pH)
pH = 6.1 + log([HCO3⁻]/0.03 Pco₂)
Pco₂ = 1.5[HCO3⁻] + 8 ± 2
---> Estimates if there is sufficient respiratory compensation (i.e., Pco₂) in the setting of a metabolic acidosis
-If MEASURED Pco₂ (i.e., from ABG lab) is > than the value predicted by the Winter's formula --> suggests overlying respiratory ACIDOSIS
-If MEASURED Pco₂ (i.e., from ABG lab) is < than the value predicted by the Winter's formula --> suggests overlying respiratory ALKALOSIS
Normal arterial blood gas values
Physiologic dead space equation
Volume of dead space = Vt x [(PaCO₂ - PeCO²)/PaCO₂]
Na⁺ - (Cl⁻ + HCO3⁻)
Normal = 8-12 mEq/L
Causes of INCREASED anion gap in setting of acidemia
"MUDPILES" (see pic)
Causes of NORMAL anion gap in setting of acidemia
Anion gap in RTAs?
NORMAL! (hyperchloremic metabolic acidosis)
Type I (distal) RTA
Urine pH? Pathogenesis? Associated with? Causes?
-Urine pH > 5.5
-Pathogenesis = inability of
to secrete H⁺ in setting of decreased serum pH --> no new HCO3⁻ generated --> metabolic acidosis
-Associated w/ HYPOKALEMIA (since lumen is made more negative by decreased H⁺ in lumen of CD), increased risk of calcium phosphate stones (due to increased urinary pH and bone turnover)
-Causes = Ampho B toxicity, analgesic nephropathy, congenital obstruction of urinary tract
Type II (proximal) RTA
Urine pH? Pathogenesis? Associated with? Causes?
-Urine pH < 5.5 (acidified by the PROPERLY FUNCTIONING alpha-intercalated cells)
-Pathogenesis = Defect in HCO₃⁻ resorption in PCT --> increased bicarb excretion --> metabolic acidosis
-Associated with hypokalemia (secondary to hyperaldosteronism that results from Na⁺ combining with excess HCO₃⁻ molecules --> increased Na⁺ excretion in form of NaHCO₃), increased risk of hypophosphatemic rickets
-Causes = Falconi syndrome, CAIs
Type IV (hyperkalemic, distal) RTA
Urine pH? Pathogenesis? Causes?
-Urine pH < 5.5
-Pathogenesis = Hypoaldosteronism/aldosterone insensitivity --> hyperkalemia --> decreased NH₃ synthesis in PCT --> decreased NH4⁺ excretion (i.e., decreased ability to bind free H⁺, hence urinary pH < 5.5)
-Causes = Decreased aldosterone production (e.g., diabetic hyporeninism, ACEi, ARBs, NSAIDs, heparin, cyclosporine, adrenal insufficiency) or aldosterone resistance (e.g., K⁺-sparing diuretics, nephropathy due to obstruction, TMP/SMX)
RBC casts suggest?
Glomerulonephritis, malignant hypertension
WBC casts suggest?
Tubulointerstitial inflammation, acute PN, transplant rejection
Fatty casts ("oval fat bodies") suggest? Associated with?
Nephrotic syndrome (associated with "maltese cross" sign)
Associated with nephrotic syndrome and babesia infection
Granular ("muddy brown" casts) suggest?
Acute tubular necrosis
Waxy casts suggest?
ESRD or chronic renal failure
Hyaline casts suggest?
Non-specific...can be a normal finding, or are often seen in concentrated urine samples
Pulmonary vascular resistance (PVR)
PVR = [P(pulm artery) - P(left atrium)]/CO
Alveolar gas equation
PAO₂ = PIO₂ - (PaCO₂/R)
-V/Q at apex = 3
-V/Q at base = 0.6
-If blocked airway (e.g., foreign body), V/Q = 0 (100% FiO2 does NOT improve PaO2 [arterial O2])
-If blood flow obstruction (e.g., PE), V/Q = ∞ (100% FiO2 improves PaO2)
Anti-ACH receptor abs
Abs? SSx? Associated with? Dx? Tx? Effect of AChE inhibitor?
-MC NMJ disorder
-Abs to POST-SYNAPTIC ACh receptor
-SSx = Ptosis, diploplia, weakness, WORSENS with muscle use/exercise (i.e., weaker at end of day)
-Associated with thymoma, thymic hyperplasia
-Dx = Edrophonium
-Tx = Pyridostigmine
-AchE inhibitor REVERSE symptoms
Abs? SSx? Associated with? Effect of AchE inhibitor?
-Abs to presynaptic Ca++ channel --> decreased ACh release
-Proximal muscle weakness, autonomic ssx (dry mouth, impotence), IMPROVES with muscle use/exercise (i.e., better at end of day)
-Associated with small cell lung cancer
-AChE inhibitor has no effect
-Increased CK, +ANA, anti-Jo-1, anti-SRP, anti-Mi-2 abs
-Tx = Steroids followed by long-term immunosuppressive therapy (e.g., MTX)
Associated with? Inflammation?
-Progressive symmetrical proximal muscle weakness, esp.
Endomysial inflammation from CD8+ T-cells
Associated with? Inflammatory location and cells?
-Similar to polymyositis
Associated with malar rash (like SLE), Grotton papules, heliotrope (erythematous periorbital) rash, "shawl and face" rash (V-sign), "mechanic's hands", increased risk of occult malignancy
Perimysial inflammation with atrophy and CD4+ T-cells
Anticardiolipin ab, lupus anticoagulant
SLE, antiphospholipid syndrome
Limited scleroderma (CREST syndrome)
Anti-desmoglein (anti-desmosome) abs
Anti-dsDNA, anti-Smith abs
What test correlates best with SLE disease ACTIVITY?
Anti-glutamic acid decarboxylase (GAD-65) abs
Drug-induced SLE (lupus)
Anti-Jo-1, anti-SRP, anti-Mi-2 abs
Anti-microsomial, anti-thyroglobulin abs
Primary billiard cirrhosis
Anti-nuclear abs (ANA)
SLE (however, this is non-specific)
Anti-parietal cell abs
Anti-phospholipase A2 receptor abs
Primary membraneous nephropathy
Anti-Scl-70 (anti-DNA topoisomerase I) abs
Anti-smooth muscle abs
Autoimmune hepatitis type I
Anti-SSA, anti-SSB (anti-Ro, anti-La) abs
Anti-TSH receptor abs suggest?
Anti-U1 RNP (ribonucleoprotein) abs suggest? What does this test help distinguish from?
Mixed connective tissue disease
--> Helps to distinguish from SLE, dermatomyositis, SSc
Voltage-gated Ca++ channel abs
IgA anti-endomysial, IgA, anti-tissue transglutaminase abs
p-ANCA (MPO-ANCA) abs
Microscopic polyangiitis, eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
c-ANCA (PR3-ANCA) abs
Granulomatosis with polyangiitis (Wegener's)
Rheumatoid factor (IgM ab that targets IgG Fc region), anti-CCP (more specific) suggests?
Excessive bleeding during childhood tonsillectomy suggests what bleeding disorder?
von Willebrand disease
Chemo drug causing dilated cardiomyopathy
Key AE of cyclophosphamide (DNA alkylating agent)
Key AE of 5-FU (antimetabolite)
Bone marrow suppression
Key AEs of MTX (dihydrofolate reductase inhibitor)
-Bone marrow suppression
-Drug-induced pulmonary fibrosis (rare)
Key AE of vincristine (microtubule-depolymerizing agent)
Key AE of vinblastine
Bone marrow suppression
Key AE of bleomycin
Pulmonary toxicity (ILD; "honeycomb" lung on CT)
MC causes of CULTURE-NEGATIVE endocarditis
Who is at increased risk?
Coxiella burnetti --> farmers at increased risk (transmitted via aersolized amniotic fluid from sheept or cattle)
Natural killer (NK) cells
CD16+, CD56+, CD3-, CD5-
-Target and kill cells that downregulate their MHC molecules
Chromosomal anomaly? SSx? Abnormal development of?
-Tetralogy of Fallot, abnormal facies, thymic aplasia, hypoparathyroidism (leading to hypocalcemia)
Abnormal development of 3rd and 4th pharyngeal pouches
-Undevelopment of T-cells housed in paracortex (due to thymic aplasia)
"CATCH-22 = Cardiac Abnormalities, Abnormal facies, Thymic aplasia, Cleft palate, Hypocalcemia/hypoparathyroidism associated with chromosome 22"
If range of confidence interval in odd ratio INCLUDES 1, then what?
Then the odds ratio is NOT statistically significant
Diffuse alveolar hemorrhage (DAH)
-Rare complication of SLE
Destruction of very long chain fatty acids
-Demyelination of periventricular white matter (MRI)
-Cognitive impairment, gait ataxia, diffuse UMN signs, adrenal insufficiency
SSx? Associated with? Metabolic derangement?
Olive-shaped mass in abdomen
Projectile, NON-BILOUS vomiting
-Associated with Turner's (e.g., webbed neck)
-Hypochloremic, hypokalemic metabolic alkalosis
-Associated with Down's syndrome
-"Double-bubble" sign on XR
Testicular cancer treatment
"BEP" (bleomycin, etoposide, and cisplatin [platinum analog])
"Eradicate ball cancer"
Hemisection --> contralateral loss of pain and temp below lesion + ipsilateral loss of touch and proprioception below lesion
Spinal tract responsible for upper limb flexor tone
(inhibited by CST) --> damage to CST results in
Spinal tract responsible for upper and lower limb extensor tone
Potine reticulospinal tract
--> damage results in
(all 4 limbs extended)
Coordinates head and eye movements
Damage results in? Test?
Coordinates upright posture and head stabilization
--> Damage results in postural instability, ataxis (Positive Rhomberg --> falls toward injured side)
Corticospinal tract damage
UMN signs with paresis and exagerated DTRs
(NO decerebrate, decorticate posturing!)
Downregulation of what gene often seen in melanoma and prostate cancers?
Subacute sclerosing panencephalitis (SSPE)
Associated with NOT BEING VACCINATED AGAINST MEASLES (Rubella)
MANY YEARS after initial infection
, degenerative, usually lethal
-Intracellular inclusion in brain cells
-Involunary spasm of UE at rest
Acute disseminated encephalomyelitis (ADEM)
Much faster time course than SSPE
-SSx resemble MS
Treatment of idiopathic pulmonary hypertension (i.e., NOT due to heart failure)
Bosentan (endothelin-1 receptor blocker --> ET-1 normally constricts PULMONARY vasculature)
ASSOCIATED WITH? LOCATION?
-Waterways with snails
calcification and fibrosis of bladder walls, SCC of bladder, hematuria
-Negative for nitrates, leukocyte esterase, bacteria, casts
Risk of? Transmission?
-Associated with sheep (intermediate host),
-Transmission = Tapeworm from dog feces
-RENAL CYSTS --> risk of anaphylaxis if cysts rupture --> be careful!
Use (as an oral/systemic abx, NOT as "neosporin")?
-Inhibits 30S ribosome
Use: Kills gut bacterial species that produce NH3, thereby reducing its absorption and its contribution to hepatic encephalopathy
-Basically sounds like TB, but on XR the infiltrates are more diffuse (rather than apical)
Increased eos on WBC!
Tx = Steroids
Burr cell (echinocyte)
Uremia/ERSD (or missed dialysis)
, pyruvate kinase deficiency, liver dz
Bite cell (degmacyte)
Teardrop cell (Dacrocyte)
Severe bone marrow infiltration (e.g., myelofibrosis) --> RBCs mechanically "squeezed" out of marrow
-Bile acid sequestrant
-Indications: Hypercholesteromia (not really used for this anymore), diarrhea related to Crohn's (if terminal ileum removed, bile acids aren't resorbed and can cause diarrhea)
Key AE: Raises triglycerides!
AEs of niacin
Irritates gastric mucosa, precipitates gout, can cause GERD
Herpes zoster ophthalmicus
-Unilateral vesiculopapular lesions on forehead that do NOT cross the midline
-Painful eye/corneal lesions
-Reactivation of opthalmic branch of trigeminal nerve
Appendicitis Chapman point
Anterior vs. posterior?
-Tenderness over tip of right 12th rib (anterior)
-Tip of right T11 transverse process (posterior)
Prostate Chapman point
Posterior margin of IT band
Splitting defense mechanism
Seeing people as all bad or all good (can't reconcile good and bad behaviors in a person)
Therapeutic pulse in counterstrain treatment
PATIENT'S HEART RATE
, and appears at approximately 90 seconds
Starts where? Spreads how?
Starts in aleveoli --> spreads throughs pores of Kohn
-D I F F U S E
-Starts in bronchus and bronchioles
Clamping of anterior border of lesser omentum (hepatoduodenal ligament) through epiploic foramen during sugery --> clamps of
common bile duct, hepatic portal vein, hepatic artery proper
MC in what pops?
-Grows BEYOND the original boundaries of the wound, does NOT regress over time (unlike hypertrophic scar)
Herpesviridae viral characteristics
Key AE of bisphosphonates (e.g., alendronate)
Osteonecrosis of the jaw
NO (or minimal) ssx
-Villous atrophy and lymphocyte infiltration
-Tropical countries in Africa and Asia, esp. in indigenous pops and long-term travellers
Diarrhea and malabsorption usually affecting non-native travellers to tropical areas, may occurs months after visit,
ALL PARTS OF INTESTINE INVOLVED
Past exposure to breast cancer irradiation increases risk of?
Angiosarcoma (painless, firm mass)
-Head, neck, or breast
JAK-2 mutation associated with (2)?
-Left gastric vein (drains to portal vein) anastamoses with azygous vein (drains systemic circulation)
Treatment of esophageal varices
ACUTE vs. PREVENTION?
-Acute = Octreotide (somatostatin analog)
-Prevention of new episodes = Propranolol or nadolol (non-selective beta-blockers)
-Superior rectal veins --> middle and inferior rectal veins --> internal pudendal vein
-Left gastric vein --> esophageal veins --> azygous vein
Bacterial etiology associated with seborrheic dermatitis (dandruff)
---> Tx = Selenium disufide shampoo
---> Often affects ADOLESCENTS
Key virulence mechanism of E. coli
Cytolethal distending toxin --> damages target cell DNA
Key virulence mechanism of S. aureus
Fibronectin-binding Protein A (Binds Fc-IgG --> inhibits phagocytosis)
Bacteria secreting IgA protease
S. pneumoniae, HiB, Neisseria
Key virulence mechanism of Group A strep (GAS)
"Mash on the GAS"
Key virulence mechanism of strep pyogenes
Diagnostic test for rheumatic fever
ASO (Abs to streptolysin O)
Narcolepsy treatment (and MOA)
Methylphenidate (MOA = Inhibits NE and DA reuptake)
TRAP positivity suggests?
Hairy cell leukemia
Treatment for hairy cell leukemia
Hairy cell leukemia - Histo
literally looks hairy
Cladribine - MOA
Purine analog --> inhibitis DNA polymerase, causes double-stranded breaks
AEs of cladribine (3)
Myelosuppression, nephrotoxicity, neurotoxicity
Solid tumors, leukemia, lymphoma
Cyclophosphamide - MOA
Cross-links DNA, requires liver activation
Anti-CD20 ab --> NHL, CLL, ITP, rheumatoid arthritis
Treatment of advanced NSC lung cancer
Erlotinib (RTK inhibitor of EGFR)
Treatment of stage IV colorectal cancer w/ wild-type KRAS mutation
Cetuximab (MAB against EGFR)
Treatment of relapsed multiple myeloma and mantle cell lymphoma
Bortezomib (proteasome inhibitor)
Key characteristic of abnormal B-cells in CLL
(4 key ssx)
-Sensorineural hearing loss
Congenital herpes simplex virus
-Diffuse VESICULAR RASH
Timing of tissue changes following infarction
-0-4 hours: No change
-4-12 hours: Coagulative necrosis and wavy fibers (surrounding viable myocardium continues to contract)
-1-4 days: Neurophilic infiltrate
-1 week: Granulation tissue
-1 month: Acellular fibrosis:
GCPR subtypes by receptor type
Gi: = D2, alpha, 2
Gs = D1, beta-type
Supraspinatus and infraspinatus innervated by? Nerve roots?
Suprascapular nerve (C5-C6)
-Supraspinatus covers shoulder abduction from 0-15 degrees
-Infraspinatus covers shoulder external rotation
Deltoid innervated by? Nerve roots?
Axillary nerve (C5-C6)
Radial nerve course
Brachial plexus --> spiral groove --> underneath midshaft of humerus --> lateral epidcondyle
"My sexy lingerie" --> midshaft, spiral groove, lateral epicondyle
Radial nerve distribution
Median nerve course
Brachial plexus --> supracondyar process
Median nerve distribution
Paramesonephric ducts form?
The uterus and associated structures
--> failure of fusion can be a cause of spontaneous abortions in women (b/c they have an incompletely fused uterus, or "heart-shaped" uterus)
Mesonephric ducts form?
Trigone (regresses completely in females)
Urogenital sinus forms?
Bladder, urethra, lower vagina (female)
Guides descent of ovaries and testes in utero
--> persists as round ligament of ovary and round ligament of uterus (female)
Genital tubercle forms?
Penis male, clitoris in female
Methenamine silver stain
Fungi (e.g., pneunocystis jirovecii)
Stains GLYCOGEN and MUCOPOLYSACCHARIDES
Malaria, trichomonas vaginalis, and other parasites
Acid-fast bacili (e.g., TB)
Reservoir? KEY CHARACTERISTICS?? Tx?
-Aerobic, Gram(+), rod-shaped,
BRANCHING, PARTIALLY ACID-FAST (key!)
--> not a fungus though
-Opportuninstic pathogen in
-Tx = TMP/SMX
Growth hormone receptor pathway
RTK --> JAK/STAT
--> Same as PDGF, insulin prolactin, IGF-1, FGF
Anti-phospholipid antibody syndrome
-Lupus anticoagulant ab or anti-cardiolipin ab
10% of SLE pts
Dental abscess EMPIRICAL treatment
1L? PCN allergy?
1L empiric = Amoxicillin
2L empiric = TMP/SMX
(e.g., in setting of PCN allergy)
Lab results? SSx?
-High PTH, low Ca++, high phosphorus
-Scaly, red, dry, itchy skin
-Shortened 4th and 5th metacarpals, round face, short stature, calcified basal ganglia, low IQ
Similar to pseudohypoparathyroidism, except with
What stage of sleep does bruxism (teeth grinding) occur in?
N2 (sleep spindles and K complexes on EEG)
Mnemonic? When does bruxism occur? When do night terrors occur? When does dreaming/nightmares/penile tumescence occur?
-Awake (eyes open) = Beta waves (highest freq. lowest amplitude)
-Awake (eyes closed) = Alpha waves
-N1 (5%) = Theta waves (lighest sleep)
-N2 (45%) = Sleep spindles, K complexes (deeper sleep, when bruxism occurs)
-N3 (25%) = Delta waves (lowest frequency, highest amplitude; night terrors, sleep-walking bed-wetting)
-REM sleep (25%) = Beta waves (loss of motor tone, increased brain O2 use, variable pulse/BP, dreaming, nightmares, penile/clitoral tumescence, memory processing)
"BATS Drink Blood" = Beta, alpha, theta, sleep spindles/K-complexes, delta, beta
Bedwetting (sleep enuresis) treatment
Desmospressin (ADH analog)
Night terrors, sleepwalking treatment
NEUTRAL AMINO ACID absorption from SMALL INTESTINE and PROXIMAL TUBULES of KIDNEY
-Pellagra-like ssx (diarrhea, dementia, dermatitis)
Pathogenesis of Hartnup disease
Decreased neutral AA absorption from gut and kidneys (e.g., tryptophan) --> decreased tryptophan conversion to niacin --> pellagra-like ssx
Pellagra results from?
Niacin deficiency (B3)
3 D's of pellegra-like ssx
-Dementia (also hallucinations)
-Dermatitis (C3/C4 dermatome "broad collar" rash/casal necklase; hyperpigmentation of sun-exposed skin)
Drugs for HTN in pregnancy
"Hypertensive moms love nifedipine"
Pt needs an NSAID (COX-1 inhibitor), but they have gastric ulcers - what can you give?
Celecoxib (COX-2 inhibitor)
Treatment for heparin-induced thrombocytopenia (HIT)
STOP HEPARIN --> then give direct thrombin inhibitor (argatroban)
Diuretic for patient with sulfa allergy
Timeframe for HIT
5-10 after heparin is started
Two main drugs that cause gynecomastia
-Spironolactone (can switch to eplerenone)
Key AEs of diuretics
-Hypocalcemia (loops --> "loops lose)
-Worsened gout/hyperuricemia (thiazides)
Drugs causing ototoxicty (4)
Drugs causing nephrotoxicty (2)
1) Aminoglycosides (amiNOglycosides, where "NO means "Nephrotoxic" and "Ototoxic")
2) Ampho B
Drugs causes dilated cardiomyopathy (2)
1) ETOH (tx = stop drinking!)
2) Doxorubicin/danorubicin (tx = Dexrazoxane)
Orange body secretions drug cause (harmless)
Red man syndrome drug cause
Grey baby syndrome drug cause
Key drug causing agranulocytosis
What must be monitored for?
Clozapine (atypical antipsychotic)
--> Must monitor CBCs ("monitor your CBC Clozly")
Drugs causing drug-induced lupus (5)
---> Ab = anti-histone abs
Drug class causing cough and angioedema
What drug can you switch to if these AEs become problematic? Mechanism?
ACEi (can switch to ARB/-sartans)
--> mechanism = bradykinin build-up
Drug causing hemorrhagic cystitis
Cyclophosphamide (Tx = mensa)
Drug class causing cartilage damage or long tendo rupture in young peope
Drug class causing bone/tooth damage
--> they chelate bone/tooth matrix
Mechanism of resistance in tetracycline drugs
Drug efflux pumps
Drug classes causing long QT
1) Azithromycin (macrolide)
2) Class 1a, Class Ic, and Class III anti-dysrhythmics --> affect K+ in cardiac AP --> prolongs QT
Drugs causing hemolysis in G6PD
TB drugs, and associated key AEs
1) Rifampin = Orange secretions
2) Isoniazid = Neuropathy, B6 deficiency, drug-SLE, hemolysis
3) Pyrazinamide = Gout
4) Ethambutol = Optic neuritis
Pancoast tumor causes?
Causes Horner's (Partial ipsilateral ptosis, ipsilateral miosis, anhydrosis), hoarseness, lower brachial plexus trunk lesions (i.e., radial and ulnar nerve)
Left atrium location
"Left atrium lies low, lessens larynx":
-Most posterior chamber
-Impedes ability to swallow
Seen in garnerella vaginosis
Erythema multiforme rash viral cause
Type IV hypersensitivty
reaction, often to HSV
-Acute and usually self-limiting
-Often appears on palms and soles before spreading to trunk and face/neck
Most important prognostic factor melanema
Depth of lesion
Phyllodes tumor (a breast cancer)
Hand signs of RA
Ulnar deviation, MCP involvement
Hands signs of OA
Situs inversus associated with?
Lead pipe sign
Associated with ulcerative colitis
Apical lung cavitation suggests?
Location? Key XR sign? SSx? Lesions?
"lead pipe colon" on XR
-SSx = Fever, weight loss, bloody diarrhea, abd pain
crypt abscesses WITHOUT skip lesions or fistula formation
Location? SSx? LESIONS?? Complication?
"Mouth to anus"
-SSx = Chronic diarrhea, abd, non-bloody diarrhea (usually)
TRANSMURAL SKIP LESIONS WITH FISTULA FORMATION
-CRC can occur as a complication
Irritable bowel syndrome (IBS)
Alternating constipation and diarrhea that is
relieved by defecation
Starburst appearance of bone on XR suggests?
Onion-skinning of bone on XR suggsets?
Antacid toxicity - Aluminum hydroxide
, muscle weakness
--> "aluminum is a HARD metal, thus makes your poops HARD"
Antacid toxicity - calcium carbonate
Hypercalcemia --> decreased PTH --> increased bicarb retention by kidneys --> renal vasoconstriction and reduced GFR, inhibition of Na-K-2Cl cotransporter (due to activation of Ca++ sensors in TAL), impaired ADH sensitivity --> loss of free water and Na+ --> hypovolemia
Antacid toxicity - Magnesium citrate
Diarrhea (it's a component of osmotic laxatives)
Antacid toxicity - Magnesium hydroxide
Diarrhea, cardiac arrest, hypotension, muscle weakness
The ONLY DEPOLARIZING neuromuscular blocker
hyperkalemia, rhabdo --> C/I in setting of hyperkalemia or rhabdo
(e.g., crush injury and patient continues to decompensate and needs to be intubated but is becoming hyperkalemic or developing rhabdo)
-Can also cause
-TOF = 1 (phase I) --> TOF <0.4 (phase II)
Succinylcholine metabolized by?
Attach to ulnar nerve --> watch for twitch of adductor pollicus brevis
Phase I vs. phase II block
-REVERSIBLE AchE inhibitor --> increased ACh in synapse
-NON-depolarzing neuromusclar blocker --> thus no effect on serum potassium
-Competitive, reversible inhibitor of AchR at NMJ
-Can overcome blockade at LOW doses with an AchE inhibitor, but CANNOT overcome at HIGH doses of roc
-Faster onset than vecuronium
Best paralytic for RSI
Succ (unless hyperkalemia or rhabdo)
-NON-depolarzing neuromusclar blocker
Prostaglandin analogs and their uses
-Misoprostol = E1 analog, used for abortions
-Alprostadil = E1 analog, used for keeping PDA open in Tetralogy of Falot (until surgery can be done)
-Dinoprostone = E2 analog, used for labor induction
-Latanoprost = F2 analog, used to treat IOP in glaucoma
Hyperkalemic periodic paralysis
Action potential ions
Common finding in patients with OA
Early sign of?
Early sign of RA
Radiodense deposits in cartilage suggests?
Pseudogout (linear radiodense deposits in menisci or articular cartilage, MC in elderly, calcium pyrophosphate dehydrate crystals)
MC genetic hypercoaguability disorder
Factor V Leiden
Factor V Leiden
Mutant version of factor V that is
less sensitive to Protein C
--> active for longer --> hypercoaguability
Anti-thrombin III deficiency
-Normally inactivates Factor Xa, potentiated by heparin
-Inheritance = AD
VERY POTENT, and a double-hit is lethal in utero
Protein C deficiency
Normal function? Leads to?
-Normally inactivates factors Va (cofactor for Xa) and VIIIa
constitutive factor Va and VIII activity
Protein S deficiency
Normal function? Leads to?
-Normally a cofactor for Protein C
constitutive factor Va and VIII activity
Normal function? Mutation?
-Normally accelerates production of factors VIIIa, XIa, XIIIa, and fibrin
Second MC genetic hypercoaguability disorder (mutation = prothrombin G20210A)
Sudden-onset SHOULDER and/or HIP pain, especially upon waking
-ESR often elevated (although non-specific), CPK is usually NORMAL
Biscuspid aortic valve
MC cause of aortic valvular stenosis in patients under 70
(over 70 calcific stenosis is MC)
-Presents as sudden syncope, chest pain dyspnea (whereas mitral regurg is more insidious with dysnpea, exercise intolerance, etc.)
-Murmur = late systolic ejection at RUSB, pansystolic apical murmur (due to FUNCTIONAL mitral regurg from increased LV pressure from the aortic stenosis)
--> Arnold Schwarzenerger had this!
MOA of PPD (Mantoux) test
Memory Th1 (cell-mediated, since TB bacteria are intracellular!) cells previously made against M. tuberculosis cells recognize MHC-II complexes on surface of APCs -->release of inflammatory cytokines presensitized by CD4+ lymphocyes
--> A Type IV (delayed-type) hypersensitivity reaction
-Anaphylactic/atopic = type I
-Cytotoxic (antibody-mediated) = type II
-Immune complex formation = type III
-Delayed-type (cell-mediated) = type IV
Antoni A and B patterns
Type I hypersensitivity reaction
Ig? Mediated by what cell type? Poison ivy?
IgE on pre-sensitized mast cells
CD8+ (cytotoxic) T-cells
(e.g., poison ivy)
---> "first (i.e., type I) and fast"
Type II hypersensitivity reaction
Ig? 3 mechanisms? Examples?
-Antibody-mediated (IgM, IgG) --> abs bind antigen on an "enemy" cell
-3 mechanisms: Opsonization + phagocytosis, complement + Fc-receptor mediated inflammation, antibody-mediated cellular dysfunction
-e.g., transfusion reactions, autoimmune HA, Goodpastures, Graves, GBS, ITP, MG, PV, pemphigus vulgaris, rheumatic fever
Cell type = NK cells
--> "type II is 'cy2toxic'"
Type III hypersensitivity reaction
-Antigen + antibody (IgG) + complement stick together to create an inflammatory reaction
-e.g., SLE, PAN, post-strep GN, serum sickness, arthus reaction
Type IV hypersensitivity reaction
Cells? What is NOT involved? 4 T's? Examples?
Delayed type, mediated by T cells encountering antigen and releasing cytokines, macrophages
-NO ANTIBODIES INVOLVED
-4 T's: T-cells, transplant rejection, TB tests, touching (contact dermatitis)
-e.g., GVHD, MS, contact dermatitis (e.g., poison ivy, nickel allergy)
Transfusion-related GVHD vs. acute hemolytic transfusion reaction (AHTR)
-GVHD onsets 4-30 days later, while AHTR is immediate
-NO pancytopenia, bullous skin rash, or LAD in AHTR (unlike GVHD)
---> Mechanism of both = Transfer of immunocompetent lymphocytes into immunocompromised host --> donor lymphocytes attack host tissue
Deficiency in __________ can result in meningococcal infections?
C5b-C9 (MAC complex)
Cruzan vs. Director
Landmark "right-to-die" case
Public Health Services Act
-Clearly established the federal government's quarantine authority for the first time
-Gave United States Public Health Service responsibility for preventing the introduction, transmission and spread of communicable diseases from foreign countries into the United States
Schloendorff v. Society of New York Hospital
Established principles of informed consent (1914)
Tarasoff v. Regents of the University of California
"Duty to Warn" act from 1976: Mental health professionals have a duty to protect individuals who are being threatened with bodily harm by a patient
Patient Self Determination Act
Who does it NOT apply to?
Requires hospitals, nursing homes, home health agencies, hospice providers, HMOs and other health care institutions (But NOT physicians individually) to provide information about advance health care directives to adult patients upon their admission to the healthcare facility
Res ipsa loquitor
-Latin for "the thing speaks for itself")
-Doctrine that infers negligence from the very nature of an accident or injury in the absence of direct evidence on how any defendant behaved (e.g., leaving behind a surgical sponge)
Someone is held responsible for the actions or omissions of another person (e.g., employer responsible for actions of a employee)
Volenti non fit injuria
-Latin for "to a willing person, injury is not done"
-Common law doctrine which states that if someone willingly places themselves in a position where harm might result, knowing that some degree of harm might result, they are not able to bring a claim against the other party involved
"Well, you signed up for it!"
Vs. ordinary negligence?
Conscious and voluntary disregard of the need to use reasonable care, which is likely to cause foreseeable grave injury or harm to persons, property, or both
(conduct that is extreme when compared with ordinary Negligence, which is a mere failure to exercise reasonable care)
Brings an orderly and systemic means of federal natural disaster assistance for state and local governments in carrying out their responsibilities to aid citizens
Emergency Medical Treatment and Active Labor Act (EMTALA)
Requires hospital Emergency Departments that accept payments from Medicare to provide an appropriate medical screening examination (MSE) to anyone seeking treatment for a medical condition, regardless of citizenship, legal status, or ability to pay
How can a physician LEGALLY terminate a relationship with a patient (e.g., because their insurance no longer covers their care) and thus avoid claims of abandonment by the patient?
A physician is allowed to terminate care if the patient is provided with a notice of withdrawal of service by certified mail (emergency care is guaranteed for 30 days, however)
--> referral to another provider would be ok, but it is it NOT A LEGAL OBLIGATION
Battery (against patient)
Example? Vs. assault?
-"Intentional and unauthorized touching of a patient"
-e.g., Surgeon is doing abominal surgery and notices a "suspicious" looking appendiceal cyst (which wasn't the original, consented purpose of the surgery) and removes it w/o pt's consent
-Assault = "causing someone apprehension of harm or unwanted contact" (DOESN'T necessarily imply physical CONTACT, unlike batter)
Nonmaleficence vs. beneficence
-Nonmaleficence: Duty to do NO harm
-Beneficence: Maximize good
Uniteral hearing loss and dizziness suggests damage to what artery?
lesion (lateral inferior pons)
Brainstem cranial nerve nuclei
Small, drop-like, salmon-pink nodules on trump and proximal extremities
-Childhood hip disorder initiated by a disruption of blood flow to the head of the femur --> avascular necrosis
Increased pain on hip internal rotation
MC risk factors for AVN of the hip
-Chronic steroid use (as in SLE)
-Chronic ETOH use
Marcus Gunn pupil (aka. relative afferent pupillary defect)
-Marcus Gunn pupil
Often secondary to a viral infection
-Reduced vision and color vision changes
Pain on eye movement
-May have normal fundoscopy
Best site for surgical emergency airway
(NOT 2nd, 3rd, 4th tracheal rings because thyroid isthmus is here!)
Rb/retinoblastoma chromosome mutation
VHL syndrome chromosome mutation
WT1/WT2 (Wilm's tumor) chromosome mutation
p53/Li-Fraumeni syndrome chromosome mutation
Sarcoma, breast, leukemia adrenal (SBLA) cancers
BRAC1/ovarian and breast cancer chromosome mutation
BRAC2/breast cancer mutation
APC (familial colon cancer) chromosome mutation
5 (semaphorin F, 5A; and delta catenin deficiencies)
Kras chromosome mutation
12 (implicated in colon cancer)
Cri-du-chat chromosome mutation
Neurofibromatosis type 1 chromosome mutation
Neurofibromatosis type 2 chromosome mutation
[a tumor suppressor])
Frataxin/Friedreich's ataxia chromosome mutation
DiGeorge syndrome chromosome mutation
Fibrillin (Marfan syndrome) chromosome mutation
PKD-1 chromosome mutation
PKD-2 chromosome mutation
PKHD1 chromosome mutation
Hypothalamus lesion corresponding to over-eating
Ventromedial hypothalamus (VHM)
Hypothalamus lesion corresponding to under-eating
Adenosine deaminase deficiency (ADA)
Results in severe combined immunodeficiency (SCID) of newborn
Warfarin inhibits what factors?
II, VI, IX, X, protein C, protein S
Severe combined immunodeficiency (SCID) of newborn
2 pathogenic mechanisms? MC?
-MC = Defective IL-2 receptor --> defective T-cell maturation and proliferation
-2nd MC = Adenosine deaminase deficiency (ADA) --> impaired ability of T-cell to synthesize DNA
Polycythemia vera associated with what pathway?
Renal vein passes under what structure as it joins the IVC?
Superior mesenteric artery
Herpes simplex encephalitis
Presents very similar to meningoccal meningitis, except has
extensive TEMPORAL LOBE involvement (FLAIR hyperintensities on MRI)
Paroxysmal noctural hemoglobinuria (PNH)
RBC defect? Mediated by binding of?
Phosphatidylinositol glycan A defect in RBCs
binding of COMPLEMENT
--> creates membrane defect that makes them more sensitive to lysis in
--> relative acidosis at night due to hypoventilation -->
DARK URINE IN THE MORNING
Febrile blood transfusion reaction
Ssx? Importantly, what is NOT present? Mechanism?
-Fever, chills, nausea WITHOUT hemolysis or BACK PAIN
-Mechanism: Recipient's anti-HLA abs attack donor WBCs
Hemolytic blood transfusion reaction
-Fever, chills, nasuea IN ADDITION to back pain, flank pain, back, flank, abdominal, or chest pain; nausea and vomiting; dyspnea; a sense of distress or impending doom; hemorrhage; tachycardia; hypotension and hemoglobinuria; a falling hematocrit, jaundice (delayed reactions)
-Mechanism: Usually due to ABO incompatibility (rare)
Nerves in cavernous sinus
Afferent limb of corneal (touch) reflex is carred by?
V1 (opthalmic division)
Aortic dissections often can expand into what other arterial structure?
Left renal artery
S. epidermidis often colonizes?
WHAT DOES IT FORM?
(FORMS A BIOLFILM)
Carina at what vertebtral level?
What suggests a secondary causes of adrenal insufficiency vs. primary (Addison's) cause? (2)
Secondary cause has a LACK of skin hyperpigmentation (because cause is usually hypopituitarism, and thus no MSH is produced) and relatively NORMAL electrolyte and BUN levels
What suggests an adrenal insufficiency vs. hypothyroidism?
Adrenal insufficiency will present with hypoglycemia and elevated eosinophils and lymphocytes
Increased gastrin, gastric ulcers unresponsive to conventional treatment, profuse watery diarrhea
MOA of this tx?
Octreotide (somatostatin agonist)
Drug to increase Factor VIII levels (e.g., treating a person with Hemophilia A who gets a laceration)
DES exposure in utero increases risk of?
ADENOCARCINOMA of the vagina
Biggest risk factor for SCC of the vagina
Multiple sexual partners
What phase of cardiac cycle shortens the most during exercise (i.e., during exercise/increased HR)?
DIASTOLE (TQ interval)
Used in chronic granulomatous disease (e.g., chronic infections with catalase-positive organisms such as Listeria, E. coli, staph)
--> increase in green fluorescence
Chronic granulomatous disease
-Chronic infections with catalase-positive organisms such as Listeria, E. coli, staph
-Lack of NADPH oxidase activity
Characteristics? Virulence mechanisms/proteins involved?*
Facultatively intracellular Gram(+) coccobacillus
-Virulence mechanism = Binds extracellular internalin protein --> phagocytosis --> release listeriolysin to lyse phagolysosome --> enters host cell cytoplasm --> intracellular polymerization of actin (inside host cell) by associating with WASp protein --> spreads cell-to-cell via phagocytosis
Integrin protein dsyfunction
-Neutrophils can't adhere to sites of infetion
-Elevated neutrophils, lack of pus at infection sites
-Delayed umbilical cord separation
Job's syndrome (Hyper-IgE syndrome)
Recurrent NON-INFLAMMED staph infections, scaly skin, pulmonary infections, coarse facies, dental/teeth abnormalities
L4/L5 vs. L5/S1 spinal cord herniations
MC spinal cord herniation sites:
-L4/L5: Patient can only complete toe-walking (since L4/L5 supplies tibialis anterior and allows for heel-walking), decreased dorsiflexion
-L5/S1: Patient can only complete heel-walking (since L5/S1 supplies gastrocnemius and allows for toe-walking), decreased plantarflexion
Palmar grasp reflex in adults suggests?
Anterior cerebral artery syndrome (ACA) affecting FRONT LOBE
Anterior cerebral artery (ACA) syndrome
Key sign? Lesion location?
PALMAR GRASP REFLEX
(contralateral side of lesion)
-Very specific for
FRONTAL LOBE LESION
Contralateral motor and sensory loss
-Transudative (increased hydrostatic pressure, decreased oncotic pressure in serum)
-Exudative (inflammatory process disrupts barrier, causes proteins and LDH to diffuse much more easily into pleural space, hence less disparity between pleural fluid and serum LDH and protein levels)
MC cause of transudative pleural effusion
(nephrotic syndrome is less common)
-Microsporum, trichophyton, epidermophyton on KOH krep demonstrating septate hyphae
-Gray pseudomembrane, massive cervical LAD, respiratory distress
-Toxin encoded on bacteriophage --> *affects cardiac myocytes, neurons, respiratory tract
Virulence mechanism of diphtheria toxin
A-B toxin (B toxin binds cell and is endocytosed, A toxin follows it inside --> A toxin binds to EF-2 on mRNA to inhibit mRNA translaton)
-Dark urine (esp on standing up)
-Cartilage and organ darkening
-Dark spots on sclera
-Deficiency = Homogentistic acid oxisdase (part of tyrosine degradation pathway) --> accumulation of alkapton bodes (homgentistic acid)
-Intellectual disability, growth retardation, seizures, musty body odor
-Must avoid phenylalanine in diet
-Deficiency = phenylalanine hydroxylase
Maple syrup urine disease (MSUD)
-Vomiting, poor feeding, urine that smells like maple syrup or burnt sugar
-Defiency = Branched-chain-alpha-ketoacid dehydrogenase
-Tetrad = Retinitis pigmentosa, peripheral polyneuropathy, cerebellar ataxia, elevated CSF protein WITHOUT increase in CSF cells
-Deficiency = Inability to break down branched-chain fatty acids
What NT is made in locus coerulus?
-Abrupt loss of muscle tone during times of high anxiety, excitement, LAUGHTER
-Defiency in NE (from LC)
Pathogenesis? Chromosome? Protein product affected?
-Overweight, thin/downturned upper lip, flat nasal bridge, strabismus, hyperphagia
-Pathogenesis: Paternal deletion, maternal imprinting on chr. 15 --> low SRNPN --> increased ghrelin --> OBESITY
Pathogenesis? Chromosome? Protein products affected?
-Happy mood, inappropriate laughter, hand-flapping, sleep disturbances, seizures, ataxia
-Pathogenesis: Maternal deletion, paternal imprinting on chr. 15 --> low UBE3A (a ubiquin ligase)
Gender? Age? Mutation? KEY SIGN? Other SSx?
-FEMALES, age 6-18 months of age
-Inheritance = X-linked
-Mutation = MECP2 gene
-SSx = Issues with language, coordination,
HAND-WRINGING repetitive movements (Key sign!)
Chromosome mutation location? Protein product affected?
-Chr. 17p --> defective PMP22
-Arms and legs tingle, gradually loose functioning,
high foot arches, hammer toes
, peripheral limb weakness
5-alpha reductase deficiency
-Lack of production of dihydrotestosterone/DHT (drives external male genitalia and prostate development) from testosterone
Undescended testes, hypospadias,
feminized external genitalia in a genetic boy (46,XY)
17-alpha hydroxylase deficiency
-Lack of secondary female sex characteristics, amenorrhea, HTN hyperkalemia
-Can't produce estradiol
21-alpha hydroxylase deficiency
-MC cause of CAH
-Masculinization of external genitalia in females
Androgen insensitivity syndrome (AIS)
-46-XY karyotype but strictly female external genitalia
-Normal or ELEVATED testosterone
Optic tract lesions
A lesion in occipital lobe will have MACULAR SPARING (temporal lobe will not)
Rare but life-threatening complication of metabolic acidosis
Lactic acidosis (high anion gap)
-MOA: Increased tissue sensitivity to insulin by activating PPAR-gamma
-e.g., -glitazone drugs
EDEMA (can exacerbate CHF)
Common drugs causing a disulfram-like reaction
"Colorado Cannabis Consumers Got Marijuana (legalized)":
Key virulence factor of strep pneumoniae
(also autolysin that releases its cell wall contents)
What arm muscle attaches to all 3 arm bones?
Flexor digitorum superficialis
MC bacterial causes of impetigo
Staph aureus, strep pyogenes
Honey-colored lesions/exudate on face, esp. KIDS
Tinea pedis (athlete's foot) treatment
Imidazoles (MICONAZOLE, clotrimazole, ketoconazole)
Acne vulgaris treatment
MC bacterial causes of neonatal conjunctivitis
Neisseria gonorrheae or chlamydia trachomatis
Treatment of orotic aciduria
Carbon monoxide damages what part of brain?
Globus pallidus (and basal ganglia)
Globus pallidus function
-Direct target is subtantia nigra
-Plays role in unconscious movement
Anthrax chest xray
Bacillus anthracis characteristics
EKG signs of pulmonary embolism
Still's disease (aka, systemic juvenile idiopathic arthritis)
-Undulant fevers, HSM, arthralgia, salmon-pink papules, pericarditis, pleuritis, peritonitis ("4 P's")
-Basically a systemic version of JIA
Osgood-Schlatter disease (OSD)
Inflammation of patellar tendon at tibial tuberosity
-May result in avulsion fx
knee pain during jumping/running/kneeling activities/sports
SSx (classic triad)? Enzyme deficiency? Substrate build-up? Inheritance pattern?
-SSx: Episodic peripheral neuropathy, angiokeratomas, hypohydrosis
-Enzyme deficiency = alpha-Galactosidase A
-Substrate buildup = Ceramide trihexoside
-Inheritance = X-linked recessive
"My FABrite activity is CERamics. We made a GALaXy" (X in 'galaXy' is for XR inheritance)
SSx? Enzyme deficiency? Substrate build-up? Inheritance pattern? Special histo?
-SSx: HSM, pancytopenia, osteoporosis, aseptic necrosis of femur, bone crises, Gaucher cells
-Enzyme deficiency = Glucocerebrosidase
-Substrate buildup = Glucocerebroside
-Inheritance = AR
(in a crying voice, since
on histo): "Oh my GAUCH, he's such a BRO"
SSx? Enzyme deficiency? Substrate build-up? Inheritance pattern?
CHERRY-RED SPOTS ON MACULA, NO HSM (unlike Niemann-Pick)
positive neurodegeneration, onion-skin lysosomes, developmental delay
-Enzyme deficiency = Hexoaminidase
-Substrate buildup = GM2 ganglioside
-Inheritance = AR (esp. amongst
"A GANG of 6 (from 'hex') small (NO HSM, unlike in the very similar Neiman-Pick disease) Jews"
SSx? Enzyme deficiency? Substrate build-up? Inheritance pattern?
CHERRY-RED SPOTS ON MACULA, HSM (unlike Tay Sachs)
, positive neurodegeneration, foam cells
-Enzyme deficiency = Sphingomyelinase
-Substrate buildup = Sphingomyelin
-Inheritance = AR (esp.
amongst Ashkenazi Jews
"PICK your big (has HSM) nose with your SPHINGer"
SSx? Enzyme deficiency? Substrate build-up? Inheritance pattern? Special histology
-SSx: Peripheral neuropathy, developmental delay, optic atrophy, globoid cells (pictured)
-Enzyme deficiency = Galactocerebrosidase
-Substrate buildup = Galactocerebroside
-Inheritance = AR
"The KRABBE is out of this world (as in 'galacto-')"
"You want a GLOB (for 'GLOBoid' cells) of KRABBE meat"
SSx? Enzyme deficiency? Substrate build-up? Inheritance pattern?
-SSx: Developmental delay, gargoylism, airway obstruction,
CORNEAL CLOUDING (unlike Hunter)
-Enzyme deficiency = Alpha-L-iduronidase
-Substrate buildup = Dermatan sulfate, heparan sulfate (same as Hunter)
-Inheritance = AR
SSx? Enzyme deficiency? Substrate build-up? Inheritance pattern?
-SSx: Mild Hurler + aggressive behavior,
NO CORNEAL CLOUDING (unlike Hurler)
-Enzyme deficiency = Iduronate sulfatase
-Substrate buildup = Dermatan sulfate, heparan sulfate (same as Hurler)
-Inheritance = X-linked recessive
"X marks the spot" (X-linked recessive, no corneal clouding and hunter's cannot have their corneas clouded to hunt!)
X-linked lysosomal storage diseases (2)
Lysosomal storage diseases with a cherry red macula (2)
Affects what part of brain? SSx? Dx? Tx?*
Affects TEMPORAL lobe
-Hallucinations, seizures, contralateral body weakness
-Dx = PCR of CSF, CSF protein should be HIGH (since it's viral)
-Tx = Acyclovir ASAP
What often fails to develop in CF patients?
Overview of branchial arches, clefts, grooves
MC cause of watery diarrhea in children in the developing world
(these kids are often immigrants to the US from developing world such as India, have no vaccine history, and present with watery diarrhea)
(segmented, Reoviridae family)
-Responsible for 40% of hospitalizations of kids under age 5 -->
IMPORTANT CAUSE OF DIARRHEA!
Characteristics? When do outbreaks tend to occur?
ssRNA, outbreaks during winter months
Characteristics? What does it cause?
-Causes pharyngitis, conjunctivitis, pneumonia
Characteristics? What does it cause? Family?
-(+) sense ssRNA, non-enveloped
-MC cause of
-Family = Picornaviridae
Pyruvate kinase deficiency
When does it present in life? Labs? SSx? Pathogenesis?*
-Presents EARLY in life (infancy)
-Labs: Reticulocytosis, hemolytic anemia, elevated indirect bilirubin
-HSM, icteric sclera, pallor
-Pathogenesis: Decrease in ATP, pyruvate --> rigid RBCs from decreased glycolysis
Pathogenesis? Inheritance? SSx?
-Pathogenesis: Can't convert orotic acid to UMP due to lack of UMP synthase --> impaired de novo pyrimidine synthesis
-Inheritance = AR
-SSx: FTT, developmental delay, megaloblastic anemia that does NOT respond to folate or B12
Pathogenesis? SSx? Hb? Anemia type?
-Pathogenesis: Congenital defect in erythryoid precursor cell synthesis in bone marrow --> rapid-onset anemia in first year of life
-Asymptomatic newborn period --> symptomatic later in life (short stature, craniofacial abnormalities, UE malformations)
-Increased HbF, but overall decreased Hb
Macrocytic, non-megaloblastic anemia
Mutation? Compared to HbSS? PBS???
Glumatic acid --> lysine mutation in beta-globin gene
-Milder dz than HbSS
PBS: Target cells and crystals inside RBCs
(epi stimulates alpha-1, alpha-2, beta-1, beta-2 --> phenoxybenzamine blocks alpha-1, alpha-2 --> epi can bind only beta-1, beta-2 --> beta-2 stimulation cause relaxation of smooth muscle --> drop in BP)
Usual cause of death in heparin overdose
Acute adrenal insufficiency
Extreme sensitivity to UV light
--> facial basal cell carcinomas, photophobia, conjunctivitis
Mutation = Genetic defect in EXCISION MISMATCH REPAIR OF DNA
-Inheritance = AR
Mutation? Genes? Increased risk of?
Mutation = Genetic defect in DNA MISMATCH REPAIR
-Genes = MLH1, MSH2
-More common in right colon
-Inheritance = AD
-Increased risk of
ovarian, skin, endometrial cancers
Postive PPD by risk factor
5mm vs. 10mm vs. 15mm?
ELDERLY are most vulnerable
(esp. splenic flexure and distal colon)
-Risk factors = Hematochezia, CHF, hypercoagulable states (e.g., SLE), cholesterol emboli
-Lab = Increased serum lactic acid
KEY SIGN = "Thumb printing" (submucosal edema) on XR
Why do type II errors occur? How to fix?
Because the study has low statistical power --> fix by increasing sample size
Low-potency typical anti-psychotics
Drugs? Advantage? Disadvantage?
-Advantage: Less EPS
-Disadvantages: Needs higher doses --> more muscarinic, alpha receptor acitation (sedation, postural hypotension, hyperprolactinemia)
High-potency typical anti-psychotics
-Disadvantages: More likely to cause EPS, hyperprolactinemia
AEs of typical vs. atypical AEs
Atypicals more likely to cause metabolic syndrome but have less EPS issues
Hallucinations and delusions due to?
Excess dopamine in mesolimbic system
Typical antipyschotics - MOA
Blocks D2 receptor
Typical antipsychotics - Use
of psychosis associated with schizophrenia or bipolar disorder
Typical antipsychotics - AEs
, sedation, postural hypotension
Haloperidol - Use
Psychosis or delerium in emergency settings
Tic suppression treatment
Atypical antipsychotics - Drugs
Olanzipine, risperidone, ziprasidone, aripiprazole, clozapine, quetiapine, lurasidone, paliperidone
Atypical antipsychotics - MOA
Blocks D2 and 5-HT2 (serotonin) receptors --> thus blocks both POSITIVE (D2) and NEGATIVE (5-HT2) symptoms
--> Aripiprazole also a partial AGONIST at D2 receptors
Atypical antipsychotics - Uses
Best drug for negative ssx of schizophrenia?
-*Postive AND negative symptoms associated with psychosis associated with schizophrenia or bipolar disorder (acute mania in bipolar disorder)
-Adjuvant tx for MDD
Clozapine best for negative ssx of SCHIZOPHRENIA (but has lots of AEs...)
Atypical antipsychotics - AEs
-EPS (less than typicals)
-Hyperprolactinemia --> galactorrhea, gynecomastia, sexual dysfunction, amenorrhea
-Anticholinergic effects (e.g., dry mouth)
-Increased mortality in elderly w/ dementia/psychosis --> BLACK BOX WARNING
-Type II DM
Antipsychotics most associated with EPS
Typicals and risperidone
Atypical antipsychotics MOST associated with weight gain (3)
Clozapine, olanzapine, quetiapine,
Atypical antipsychotics LEAST associated with weight gain (2)
Aripiprazole (Abilify), ziprasidone
Atypical antipsychotics most associated with hyperprolactinemia (3)
Clozapine, quetiapine, aripiprazole
Atypical antipsychotics most associated with anticholinergic side effects (2)
Less likely with?
Olanzapine, clozapine (less likely with risperidone)
Key AE of ziprasidone
Atypical antipsychotics most associated with Type II DM (2)
Olanzapine, clozapine (all the metabolic syndrome issues...)
Neuroleptic malignant syndrome
-Hyperthermia, mental status changes, muscle rigidity ("lead pipe rigidity"), elevated CK, bradykinesia
-Tx = Stop drug --> Dantrolene, bromocriptine
Key AE of clozapine
MUST MONITOR CBCs frequently (every 1-4 weeks)
Treatment of EPS
Acute dystonia? Akathisia? Parkinsonism? Tardive dyskinesia?
~Always start by lowering dose of causative agent~
Tx by specific EPS reaction (in order that they tend to appear in:
-Acute dystonia (e.g., torticollis) = Benztropine, diphenhydramine (benadryl)
-Akathisia (contant movement/pacing) = Propranolol
-Parkinsonism (tremor, bradykinesia, rigidity) = Benzotropine
-Tardive ('late') dyskinesia (tongue movements, lip smacking) = STOP DRUG --> TD can be permanent...
EPS due to?
Dopamine blockage in basal ganglia
SSRIs - Drugs and uses
-Citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, sertaline
-MDD, GAD, panic disorder, OCD, social anxiety, PTSD, eating disorders, chronic pain
SSRIs - Key AEs (3)
What SSRI has the most and which has the least issues with discontinuation syndrome? Black-box warning?
-Discontinuation syndrome (Nausea, HA, dizziness, chills, parathesias, insomnia, body aches (basically like the flu) --> worst with paroxetine (shortest half-life), best with fluoxetine (longest half-life)
-Suicidal ideation in kids and adolescents (black-box warning)
-Amitriptyline, clomipramine, desipramine, doxepin, imipramine, nortriptyline
NARROW therapeutic window
-MDD, GAD, chronic pain syndromes (e.g., FM), isonmia (due to sedation effects), Parkinson's, HA/migraine prophylaxis
TCAs - MOA
Blocks BOTH serotinonin and NE reuptake
TCAs - AEs
-Sedation (H1 and H2 affinity)
-Discontinuation syndrome (taper!)
-Altered mental status --> do an EKG
Cardiotoxicity of TCAs
MOA of toxicity: Inhibits Na+ channels
(also some L-type Ca++ blocking)
ECG changes (Wide QRS)
Three "C's" of TCA overdose
Coma, convulsions, cardiotoxicity
TCA overdose treatment
Activated charcoal if within 2 hours, then sodium bicarb drip
-MOA: Bicarb helps bind up TCA, sodium stabilizes arrhythmia
High body temp, hyperreflexia, CLONUS agitation, tremor, sweating, dilated pupils, diarrhea, seizures, muscle breakdown
Serotonin syndrome treatment
Cyprohepatidine (serotonin receptor antagonist)
MOA? KEY ADVANTAGE? Uses? Important C/I?
-MOA: DA and NE reuptake inhibitor
-KEY ADVANTAGE: LESS SEXUAL AEs
-Uses: MDD, smoking cessation
Seizure or anything else that lowers seizure threshold
(anorexia, bulemia, benzo withdrawal state, alcoholism)
-MOA: Blocks alpha-2 in CNS (enhances NE release), blocks 5-HT2, H1, and muscarinic receptors
-Uses: Depression, hypnotic, antiemetic, appetite stimulant, anxiolytic
AEs: Constipation, sleepiness, weight gain, dry mouth
-MOA: SNRI (mostly serotonin at lower doses, NE=serotonin at lower doses)
-Uses: MDD, GAD, panic disorder, social phobias
Key AE: HTN
Fibromylagia and neuropathic pain
, MDD, GAD
-AEs: Nausea, somnolence, insomnia, sleepiness
MAOIs - Selective vs. non-selective drugs
-Selective MAO-B inhibitors: Rasagiline, seleginine
-Non-selective MAO-A and B inhibitors
MAOIs - MOA
-MAO-A: Preferentially deaminates serotonin, melatonin, NE/Epi
-MAO-B: Preferentially deaminates phenylethylamine and other trace amines
---> Key factor: Irreversible inhibition, so need a
2-week washout period if switching from MAOI to new med
MAOIs - Uses
(depression with psychosis, catatonia, etc.) --> need to inhibit both A and B enzymes
-Parkinsons --> need to inhibit B enzymes (normally breaks down dopamine)
MAOIs - AEs
AVOID WHAT WITH MAO-A INHIBITORS?
-*MAO-A inhibitors = Hypertensive crisis w/ TYRAMINE-containing foods --> AVOID TYRAMINE (e.g., liver and fermented substances, alcohol, aged cheeses, etc.)
-MAO-B inhibitors don't have the dietary restrictions
Use? KEY AEs (3)? AVOID WHAT DRUGS (2)?
ANTI-MANIC AGENT (e.g., in bipolar, schizophrenia)
Nephrogenic DI, hypothyroidism, EBSTEIN'S ANOMALY (defective tricuspid valve leading to hypoplastic RV)
Avoid NSAIDs and DIURETICS (decreases Lithium clearance)
Drug with less abuse potential?
-NE and DA reuptake inhibition: Dextroamphetamine, methamphetamine, methylphenidate, lisdexamphetamine
-NE reuptake inhibition: Atomoxetine (LESS ABUSE POTENTIAL so no DA reuptake inhibition)
Allows passage of
--> hyperpolarization of neuron
MOA: Increases DURATION of GABAa channel opening
-Uses: Seizures, anxiety, insomnia
-AEs: Dependence, respiratory depression
Benzodiazepines (-olam, -epam, chlordiazepoxide)
MOA?? Metabolism? Uses?
MOA = Binds between alpha and gamma subunits --> increases FREQUENCY of GABAa channel opening
-Metabolized by LIVER --> active metabolites
-Uses: Anxiety, insomnia, ETOH withdrawal, seizures
Benzos for insomnia
Benzo for procedural sedation
Benzos for status epilecticus
Benzo for alcohol withdrawal
Benzo for muscle spasms
Benzo overdose treatment
Mechanism? Risk of?
(competitively blocks benzo binding [but not barb binding]; risk of withdrawal seizures)
Benzos with active metabolites (2)
Long-acting benzos (2)
Intermediate-acting benzos (3)
Alprazolam, clonazepam, lorazepam
Short-acting benzos (2)
Good for use in what patients?
Triazolam, midazolam (pre-procedure sedation so you want short-acting...) -->
thus, good for use in elderly
-MOA: Partial serotonin agonist at 5-HT1a
Doesn't really work!
-Low sedation, low risk of dependence
AEs? Overdose tx?
-Zolpidem, zaleplon, eszopiclone
Sedation, PARASOMNIAS (sleep walking, eating, driving), abuse
-Overdose tx = Flumazenil
-MOA: Melatonin receptor agonist
Low abuse potential
Compared to dementia presentation? Treatment? MUST AVOID WHAT DRUGS?????
Decline in function from baseline
Acute FLUCUATION in sleep-wake cycles, arousal; psychotic features
Fix underlying cause, haloperidol (1L drug), AVOID BENZOS!!!
Simple partial vs. simple complex?
-Simple partial = single locus, consciousness NOT altered
-Simple complex = single locus, conscious altered
Continuous contractions + rapid contraction and relaxation phases
Anti-seizure drugs that block voltage-gated Na+ channels
Phenytoin, carbamazepine, lamotrigine, topiramate (so, basically most anti-seizure drugs work this way...)
MOA of ethosuxamide
Block voltage-gated dendritic T-type Ca++ channels
MOA? Uses? METABOLISM?
MOA: Blocks Na+ channels that have already fired
, tonic-clonic seizures
--> 1st order kinetics at low doses, zero order kinetics at high dosese
-Monitor therapeutic range
Phenytoin/fosphenytoin - Key AEs (3)
Carbamazepine and oxcarbamazepine
KEY: Drug of choice for? Key AE?
-MOA: Block Na+ channel
-Uses: Many seizure types,
TRIGEMINAL NEURALGIA (drug of choice)
-Key AE: Hyponatremia
Valproic acid/val (Depakote)
Uses? 2L for? Key AE? C/I?
-MOA: Increases GABA, modifies Na+ channels
-Uses: Bipolar disorder, migraine prophylaxis, 2L for absence seizures
-Key AE: Hepatotoxicity --> watch LFTs
ABSOLUTELY DO NOT USE IN Pregnancy (known teratogen)
-Well-tolerated, few AEs -->
Major use in seizures!
Blocks dendritic T-type Ca++ channels
1L for absence seizures
-MOA: Modulation of VG-Ca++ channels? GABA analog?
KEY USE: Neuropathic pain (FM, diabetic foot pain)
KEY AEs? Dosing? Interaction with valproic acid?
-MOA: Inhibits VG-Na+ channels
-Use: Adjunct for multiple seizure types,
SJS, toxic epidermal necrolysis --> "start low and go slow"
-Be careful with starting lamotrigine if valproic acid is onboard --> TITRATE EVEN SLOWER
Uses? Key AE?
-MOA: Inhibits VG-Na+ channels
Migraine prophylaxis, weight loss
(also seizure disorders)
-MOA: Inhibits VG-Na+ channels and T-type Ca++ channels
-Used in many seizure types
Status epilepticus - Definition
>5 mins of continuous seizure, or >2 discrete seizures in which there is incomplete recovery of consciousness
Sequence of treatment in status epilecticus
Benzo (diazepam or lorazepam) --> try 2nd benzo dose --> phenytoin --> try 2nd dose phenytoin --> intubation w/ phenobarbital, propofol or midazolam drip
Teratogenicity of anti-seizure drugs
-Many are teratogenic
Increase FOLIC ACID DOSE PRIOR TO CONCEPTION
Huntington's disease - Pathophysiology
Decrease in Ach from caudate nucleus --> increase in DA transmission to putamen --> choreiform movements
Huntington's disease - Tx
Approved drug and its MOA?
-Target = DA release
Tetrabenazine (approved for Huntington's): Inhibits vesticular monoamine transporter
Huntington's disease - Inheritance
Parkinsonian tremor is what type of tremor?
Essential/intentional tremor treatment
-Reduce stress, caffeine
Lipophilic beta-blocker = propranolol, metoprolol
-Levodopa = Dopamine precursor that is converted to DA by DOPA-decarboxylase (3% crosses BBB)
-Carbidopa = Inhibits DOPA-decarboxylase OUTSIDE THE CNS, thus preventing peripheral conversion of levodopa to DA and reducing peripheral AEs (but without interfering with conversion to DA in the CNS)
Levadopa-Carbidopa - AEs
Dyskinesia, depression, insomnia, delusions, hallucinations
Levadopa-Carbidopa - C/I
Psychosis (due to increased DA), glaucoma
Dopamine agonists for Parkinson's
Drugs? KEY AE?? RLS Tx?
-Bromocriptine, pramipexole, ropinirole
-D2, D3 receptors
Key AE: Increase in gambling, drug use, sexual acitivity (due to increase in DA!)
-Pramipexole, ropinirole for restless leg syndrome/RLS
MAO-B Inhibitors for Parkinson's
-MAO-B selectively degrades DA
NO DIETARY RESTRICTIONS NEEDED!
COMT inhibitors for Parkinson's
-COMT breaks down DA
-AEs: N/V/D, dyskinesia, red/brown urine
Amantidine for Parkinson's
-Uknown AE for Parkinson's
-Key AE = Livedo reticularis*
Alzheimer's disease treatment - Acetylcholinesterase inhibitors
-Donepezil, galantamine, rivastigmine
Loss of cholinergic transmission drives memory loss...so increase Ach!
-AEs: N/V/D, bradycardia, tremor, anorexia
Alzheimer's disease treatment - Memantine
MOA: NMDA receptor antagonist --> prevents neuron apoptosis
-Use: Moderate-severe AD in conjuction w/ AchE inhibitor
Multiple sclerosis (MS) treatment - IFN-beta-1a/1b
-MOA: Prevent inflammation from demyelinated axons
Flu-like ssx, depression
(also increased LFTs)
Multiple sclerosis (MS) treatment - Glatiramer
-MOA: Resembles myelin proteins --> acts as a decoy for T-cells
-AEs: Injection site pain
Migraine prophylaxis drugs (5)
Migraine treatment drugs (4)
Which drugs actually ABORT the headache?
Tension HA treatment
MOA? AEs? C/I?
-Sumatriptan, zolmitriptan, rizatripan
MOA: Agonism of 5-HT1b and 5-HT1d receptors --> vasoconstriction, reduction of Subtance P (pain signal)
-AEs: CV effects, serotonin syndrome
-C/I: Non-selective MAOIs (can cause serotonin syndrome, hypertensive crisis)
Activity of PCNs (overall)
Gram(+) cocci (except enterococci), Treponema pallidum (syphillus)
, GPRs, anerobes (except B. fragilis), gonococci
Oxacillin, dicloxacillin, nafcillin
--> Activity = staphylococcus (except MRSA)
--> Activitiy = Staph + better Gram(-) coverage such as
H. flu, N. meningitidis, P. mirabilis, E. faecalis
--> GOOD FOR PSEUDOMONAS!
1st gen cephalosporins
Cefazolin, cephalexin, cefadroxil
--> Activity = Some Gram+ (staph), some Gram- (E. coli, Klebsiella),
Skin infections, SURGICAL PROPHYALXIS (esp. cefazolin)
2nd gen cephalosporins
Cefoxitin, cefotetan, cefaclor, cefuroxime, cefprozil
--> Activity =
Expanded coverage that includes strep, Proteus, ANAEROBES (esp. C. diff)
3rd gen cephalosporins
Cefriaxone, ceftazidime, cefdinir, cefixime, cefotaxime, ceftizoxime, cefoperazone
--> Activity = Further expanded Gram- (H. flu, N. gonorrhoeae, N. meningitides, Enterobacter, Salmonella, Proteus, Serrattia spp. E. Coli, Pseudomonas (Ceftazidine, cefoperazone)
Empiric menigitis coverage
Ceftriaxone + vanco (good CNS penetration!)
4th gen cephalosporins
--> Activity = Same Gram- as 3rd gen,
but ADDS PSEUDOMONAL COVERAGE
5th gen cephalosporins
--> Activity = Similar to 3rd gen overall...
Covers MRSA but NOT pseudomonas!
Activity? Can use in what patients?
-*GRAM(-) ONLY--> good for serious Gram(-) infections such as Pseudomonas, Enterobacter
-Can use in PCN allergy
Coverage? WHY GIVE WITH CILASTIN WITH IMIPENEM?
SERIOUS GRAM(-) INFECTIONS
-Does cover anaerobes and some Gram(+), but
Cilastin inhibits renal dihydropeptidase I
--> prolongs imipenem duration of action
Key AE of imipenem
Lowers seizure threshold
MOA? Activity? What is it given 2L PO for?
-MOA = Inhibits elongation and cross-linking of peptidolgycan
Gram(+) ONLY --> covers MRSA
Red-man syndrome (if infused too fast) nephrotoxicty
-Measure peak and troughs!
-Give PO for
-MOA = Prevents transfer of mucopeptides into cell wall
MOA? What does it cover?
KEY AE? Check what? What can it NOT be used for, and why?
-MOA = Depolarizes cell membrane
-Covers MRSA and
--> give only for
Key AE = Rhabdo (check CK!)
-Inactivated by lung surfactant --> can't use for pneumonias
-MOA = Inhibits pyruvyl transferase needed for cell wall synthesis
-Use = Uncomplicated UTIs
MOA (compared to tetracyclines)? Activity? Key AEs (2)?