USMLE facts 5

ang93's version from 2017-04-30 20:13


Question Answer
systemic mastocytosisabnl prolifn of mast cells and inc histamine, histamine -> hyper acid secretion of gastric acid from parietal cells
sys mastocytosis mutationKIT - tyrosine kinase
sx sys mastocytosissyncope, flushing, hypotension, pruritis, urticaria - excess acid causes inactivation of pancreatic and intestinal enzymes -> diarrhea


Question Answer
HBV histocytoplasm filled w HBV surface antigen, finely granular, pale eosinophilic ground glass appearance
hepatocyte necrosisbalooning degeneration, apoptosis, steatosis, and portal inflammation w mononuclear inclusions (lymphocytes and macrophages)
coucilman bodiesdeeply eosinophilic globules that rep shrunken apoptotic, variety of liver dz
accumn of large and small vesicles of fat wi hepatocyteshepatic steatosis (alcoholic - >15 drinks men, >10 drinks women, and non - like obesity )
clumped, amorphous eosinophilic intracytoplasmic inclusions made up of tangled intermed filamentmallory bodies
area of macrovesicular steatosis, lymphoid aggreg in portal tractsHCV infxn
CNS necrosisliquifative - dead tissue is digested and removed by autolytic mechs
liquifactive necrosisCNS infarct and suppurative bacterial infxns


Question Answer
inactivate Rho reg proteinsc diff
intraNUCLEAR acidophilic inclusionsHSV
intraNUCLEAR basophilic inclusionsCMV
e coli LPSmacrophage activation - widespread IL1,6 and TNFa, bacteremia & septic shock
e coli K1 capsular polysaccprevents phago & complement med lysis - neonatal mening
e coli verotoxinshiga like toxin, inact 60S ribosomal component, halt protein synth ans cause cell death - gastroenteritis (bloody)
e coli heat stable/labile enterotoxfluid and electrolyte secretion from intestinal epithelium - gastroenteritis (watery)
e coli p fimbraeallows adhesion to uroepith - UTIs
MC neonate meningGBS then e coli and l. monocytogenes


Question Answer
fibrinoid necrosisinflamm and necrosis of arterial walls in vasculitis, immune complex, complement and plasma proteins form fibrin like eosinophillic deposits


Question Answer
clincial cystic fibrosis (Resp)OLD (bronchiectasis), recurrent pneumonia, chronic rhinosinusitis
clinical CF (GI)obstruction - meconium ileus, distal intestinal obstruction syndrome, pancreatic dz - exocrine pancreatic insuff, CF-related diabetes, biliary cirhosis
clinical CF (repro)infertility - mainly men
clinical CF (MSK)osteopenia (fx), kyphoscoliosis, digital clubbing


Question Answer
progression from normal colon to adenocarcinomanL -> APC inactivation, B catenin accumn -> hyperprolifn -> KRAS ACTIVN -> adenoma -> p53 INactivation -> carcinoma
what type of diet prediposed to colon adenocarcinomahigh fat and carbs low fiber
APC location and mutation repercussionschromosome 5, Bcatenin accumn and uncontrolled cell prolifn
KRAS and colon adenocarcinomastims unregulated cell grwth
malignant transformation adenocarcinomaTP53
internal hemoroid venous drainagemiddle and superior rectal veins -> internal illiac and inf mesensteric respectively
external hemorrhoidsinf rectal v -> internal pudenal vein -> internal iliac vein -> common iliac vein -> IVC
why does pregnancy inc risk GERDprogesterone dec motility
painful hemorrhoidsexternal - somatic innervn - inf pudendal
nonpainful hemorrhoidsinternal, visceral innervn
lymphatic drainage above pectinate line internal iliac LNs
lymphatic drainage below pectinate linesuperficial inguinal LNs
secretory diarrhea that persists w fasting and flushingVIPoma
chronic diarrhea malasbsorption campergiardia
migratory polyarthritis, abdominal pain, malabsorptive diarrhea, neuro and cardiac sxwhipple dz
reye syndrome findingshepatic failure and encephalopathy, microvesicular steatosis wo inflammatin and cerebral edema
dont give aspirin to children <16 except...kawasaki dz - main tx
enteropeptidaseduodenal BB enzyme activation of trypsin (from trypsinogen)
enteropeptidase deficiencyprotein and fat malabsorption - dairrhea, FTT, edema(hypoproteinemia)
amino acids involved in bile salt formationbile acid conjd to glycine and taurine
pepsin activationmade by chief cell -> stomach acid activates -> inital protein digestion
secretinstim secretion of bicarb from pancreas and inhibs gastric acid from stomach
diarrhea, cholelithiasis, hyperglycemiasomatostatin pancreatic tumor
somatostatin/insulin/glucagoninhibts both
layers of the stomachmucosa-muscularis mucosa-submucosa-muscularispropria-serosa
erosionsdont fully extend through muscularis mucosa
ulcersextend into submucosal layers
muscularis propria layersinner circum and outer long
NOD2 mutationcrohns dz - encodes intracell microbial receptor resulting in dec activity of NFkB (proinflamm) -> dec cytokine production -> impairs innate barrier fxn -> intest microbes allowed to indice exagg adaptive immune response -> chronic gast inflamm



Question Answer
meningitis AIDS ptcryptococcal
aspergillosis and AIDSsingle ring enhancing lesion - abscess often accompanied by pulmonary and orbital manifestations
lack of clinical response to toxoplasmosis tx when tx multiple ring enhancing lesions in the brainprimary CNS lymphoma
PCNSLdiffuse large nonHog lymphoma of B cell origin - late HIV complication (EBV)
mech of malignany hyperthermiaABNL ryanodine receptors release large amounts of Ca after exposure to anesthetic - excess free Ca in cytoplasm stim ATP dependent reuptake by SR -> excess ATP consumption -> generates heat -> ATP loss lead to muscle damage -> rhabdomyolysis -> K, myoglobin, and CK release into cien
sx malignant hyperthermiatachy HTN hyperK myoglobinemia muscle rigidity and hyperthermia
MC movement disorderessential tremor
tremor worsens w particular posture, improves w alcoholessential tremor
MGautoimmune Ab agst nicotinic Rs on postsynap membrane
myasthenic crisis undertreated pt (suboptimal dosage), positive tensilon test - need to inc pt dose
cholinergic crisisinapprop high dose AChEi - excess Ach at cleft - muscle becomes refractory to future impulses, negative tensilon test - temporarily discont AChEis
lateral cerebellum hemimotor planning
medial cerebellum hemimotor execution
intermed cerebellum hemimotor execution
inf vermis and floculonodular lobevestibular nuclei- balance and eye movement
truncal ataxiawide based unsteady gait
cerebellar hemorrhageusu from HTN vasculopathy, if hx lung adenocarcinoma - may be hemrrhagic mets
limb dysmetriaover shoot and undershoot during targeted mvmts (lesions to cerebellar hemis involving lateral descending motor)
oropharyngeal dysphagiaCN 9,10,12 and or their nuclei lesions
MC cause of cavernous sinus thrombosiscontiguous spread of infxn from medial third of face, sinuses or teeth - communicates via venous sys - superior or inferior ophthalmic veins - STAPH AND STREP
headache, fever, diploplia, ptosis, mydriasis, loss of upper facial sensation and afferent limb corneal reflex, proptosis and chemosis (conjunctival swelling)cavernous sinus thrombosis - CN3,4,5,6, impaired venous drainage thru opthalmic veins
frontal lobe pathologydisinhibition, issures plannign and organizing, personality changes - NO CN deficits
ipsilat dysphagia, hoarseness, loss of gag reflex, deviation of uvula twd nL sidejugular foramen lesion - CN 9,10,11
tabes dorsalis and argyll robertson pupils, neurogenic bladder w overflow incontinencemanifestations of tertiary neurosyphillis
argyll robertson pupilslight near dissocn and caused by damage to the midbrain tectum
tabes dorsalisloss of p/v sense and severe lancinating pains
when does neurosyphilis normaling appear5-20 y post primary infxn w traponema pallidum
acute encephalitis which primarily infects TEMPORAL LOBEHSV1
headache, confusion, personality changes, HIVHSV1 encephalitis
CN at the level of MCPtrigem - mid pons
pathogenesis huntingtonsgain of fxn mutation in huntingtin protein - pathological interaction w TFs -> transcriptional repression (silencing) -> inc histone deacetylation -> silence genes needed for neuronal survival
optimal location for needle insertion for lumbar punctureL3/4 or L4/5
highest points of liliac crestL4 body - lumbar puncture landmark
interscalenenerve block anesthesizes brachial plexus (anesth for upper arm and shoulder) risk for paralysis of ...diaphragm (C3-C5)
platysma innrvnfacial nerve
HIV dementiamicroglial nodules, groups od activated macrophages/microglial cells formed around small areas of necrosis that may fuse to form multinucleated giant cells
low 5-HIAA CNSimpulsive, destructive behaviors, parrticularly aggressive, suicide and violence
elevated 14-3-3CJD
progressively decreasing level of melatoninAlz dz
LATE onset alz dzmutations in ApoE - impaired synthesis and clearance of AB amyloid from brain
EARLY onsetdown syndrome - APP found on chromosome 21 - extra copy - accelerate accumn
TTR mutationmisfold extracell depo of thranstheryin (prealbumin) - familial amyloid polyneuropathy or cardiomyopathy
Ach/Alz dzdecreased - dec in choline acetyl transferase
hypoxic encephalopathydec oxygenation of blood - usu CARDIAC ARREST; presents w decreased consciousness
lobar/cortical hemorrhagecerebral amyloid angiopathy
hypertensive encephalopathyPRGRESSIVE HEADACHE, n/v, nonlocalized neuro sx
dysdiadochokinesiaimparied alternatin movments
inf vermis lesionvertigo and nystagmus
lesion to ipsilat lateral hypothalamus or sympathtic tracts in brainstemHorners
headache worsens w valsavainc ICP
lower facial droopUMN
full sided facial droopLMN

Neuro - Nerve Roots

Question Answer
L2upper AM thigh, hip flexion (iliopoas)
L3lower AM thigh, hip flexion and adduction, knee extension(quads)
L4lower AM thigh, knee, medial calf & foot, hip adduction, knee extension (quad), patellar reflex
L5buttocks, PL thigh, AL leg, dorsal foot, foot dorsiflex & inversion (tibialis ant), foot eversion (peroneus), toe extension (extensor hallucis, digitorum)
S1buttocks, P thigh & calf, Lat foot, hip extension (glutmax), knee flexion (hamstrings), foot plantarflexion (gastrocnemius), achilles reflex
sciaticaback pain that radiates down the leg - mc compression of L5 or S1

Neuro - Injury

Question Answer
transient severe injury that leads to cell deathacute neuronal injury
cell body shrinkacute neuronal injury
pyknosis nucleus, loss of nissl, eosinophillic neuron, cell body shrinkacute neuronal injury
loss of axonaxonal rxn
cell body enlargementloss of axon, axonal rxn
eccentric nucleus, enlarged nucleolus, nissl dispersion, enlarged cell bodyaxonal rxn
progressive degen dzneuronal atrophy
loss of neurons and fxnal grps of neurons, reactive gliosisneuronal atrophy
acute irrev damage causeshypoglycemia, toxicity, ischemia, hypoxia
metabolic encephalopathyhypoglycemia, hyperglycemia, hepatic encephalopathy
wallerian degenaxonal degen and myelin brkdwn DISTAL to injury
regen capacity of CNSDOES NOT REGEN - persistent myelin debris, secrete neuronal inhib factors and develop dense glial scqar
cytotoxic edemaintracell edema caused by impaired ATP-dep Na/K pumps on neuronal cell membranes
vasogenic edemaextracell edema caused by inc'd vasc perm due to proinflam cytokines
risk duration for embolic stroke hemorrhagic transformationwi first 7 days!


Question Answer
acute stress disorder vs PTSDASD - 3d-1m, PTSD >=1m


Question Answer
susceptible to injury at the lateral neck of fibula by compression fxcommon peroneal n
common peroneal n injuryweakness on dorsiflexion (foot drop), and eversion as well as toe extension, SENSORY loss over lateral leg and dorsolat foot
obturator nthigh adduction and distal medial thigh sensation - commonly compressed due to pelvic trauma
muscles that close the jaw3 - temporalis, MEDIAL pterygoid, masseter
muscles that open the jaw: 1 - LATERAL pterygoid
unilat injury to V3: deviation of mandible towards paralyzed side




Question Answer
nodular lymphoid hyperplasia of intestinescommon variable immunodef syndrome
common variable immunodef syndromelow Ig and B lymphocytes that presidpose to recurrent sinopulm and GI infxn
IgAinhib attachmt to intestinal epith cells


Question Answer
ARP eqnRR-1/RR
ARP repsexcess risk in exposed population that is explained by the risk factor
risk# affected in exposure group /total exposure group
RR(a/a+b)/(c/c+d) (tx rate/control rate)
contingency tabledz + & dz - X risk factor + & risk factor -
ARRcontrol rate - Tx rate
low NNTmore beneficial tx

Pharm – General

Question Answer
toxoplasmosis w sulfa allergychange pyrimethamine and sulfadiazine to pyrimethamine and clindamycin
aspergillosis brain txvoriconazole
RLS txdopamine agonist (pramipexole)
which def is assoc with RLSiron def - linked to dopamine
cataplexy txmuscarinic antagonists
essential tremor txpropanolol - nonselective BB
parkinsons tremor txbenztropine
counteract EPS of neuroleptic medicationsbenztropine
postivie sx psychosis txhaloperidol
atypical antipsychotic that blocks D2 and 5HT2 receptors in CNSclozapine
selegiline/parkinsonsinhib of MAOB - MPTP-assocs park metabolite formed from this - induce damage to DA neurons; selegilline delays progression
sequence of park txcombo selegiline, anticholinergics, amantidine until they non longer control sx then levodopa/carbidopa
anticholinestase that cant cross BBBneostigmine and edrophonium- quatenary ammonium structure
why does physostigmine inhib AChE cnetrally and peripherallytertiatry structure capable of crossing BBB

Pharm – Adverse Effects


Question Answer
organophosphate actionAChEi - tx with atropine and pralidoxime