USMLE facts 7

ang93's version from 2017-05-02 17:31


Question Answer
Marcus Gunn pupilafferent pupillary defect e.g. due to optic nerve damage(MS), retinal detachment; diagnosis made by swinging light between eyes when light shines in affected eye both eyes do not constrict fully swing light to normal eye and both eyes constrict swing light back to affected eye and both eyes dilate
Argyll Robertson pupilpupils constrict with accommodation but do not react to light; see in neurosyphilis; prostitute's pupil (they accommodate but do not react) also seen in diabetes
Horner syndromeloss of sympathetic input to pupil, results in constricted and, unreactive pupil, also present with ipsilateral ptosis
Adie pupilslowly reacting pupil that is dilated, response better to accommodation than to reaction, common in young females who lack knee jerk reflexes
Transtentorial (uncal) herniationblown-pupil, fixed and dilated pupil, due to ↑ in intracerebral pressure and compression of CN III
inflam vasculature sheathing and assocd hemorrhage, full thickness retinal necrosis and edemaCMV induced retinitis, eventually it will be replaced by scar tissue ; AIDS pts CD4 <50
MC complication of CMV retinitisretinal detachment due to tearing thin, atrophic scar
open angle glaucomainc production or dec secretion aqueous humor, progressive loss of periph visual fields
HTN retinopathyretinal hemorrhage, thickened arteriolar walls (copper or silver wiring), compression of assocd vein (arteriovenous nicking), small white foci retinal ischemia (cottonwool spots)
cherry red spotdiffuse retinal ischemia, central retinal artery occlusion (athlerosclerosis, cardioembolic dz, vasculitis (giant cell arteritis)
smokin and hyperlipidemia retinal issuesinc risk retinal ISCHEMIA, and OPTIC VASC DZ but NOT HEMORRHAGE




Question Answer
hydralazine is often used in combo wisosorbide dinitrate to tx HF


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asthma histosm hypoertrophy, goblet hyperplasia, thickening bm, inc eosinophil recruitment


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acute phase h pylori gastritisprimarly neutrophil infiltrate
chronic phase h pylori gastritislymphocytes, lymphoid follicles, macrophages, and plasma
involvmt of the gastric body in longstanding H pylori infxn inc risk ofgastric adenoma and MALT lymphoma
common complication of acute pancreatitispancreatic pseudocyst - collection of fluid rich in enzymes and inflam debris, usu borderd by stomach, duodenum, traverse colon - walls consist of granulation tissue and fibrosis (take 4-6w) (true cyst would be lined by epith)
Gardners syndromeFAP + osseous and soft tissue tumors, cong hypertrophy of retinal pigments epith, impacted/supernumerary teeth
FAP/Lynch + malignant CNS tumorTurcot syndrome (think turban)
AD, numerous hamartomas thru-out GI, hyperpigmtd mouth, lips, hands and genitalia, inc risk breast and GI cancersPeutz Jeghers syndrome


Question Answer
CKD/osteodystrophyglom and tub failure -> hyperP O4 + hypoCa -> hyperPTH; pt can even develop PTH resistance and have low bone turnover -> osteomalacia
CKD/uremiadec preph conversion T4 to T3 - fxnal HYPOthyroidism
imperm to H2O no matter the level of vasopressinTAL LOH
PAHfiltered by glom and nearly completely secreted by PTs wo resorption - RPF
most signif risk factor for UTIduration of catheterization
CKD/fatigue, weakness, itchingaccumn of uremia toxins
hypovolemia RPF & GFRdec RPF, dec GFR, inc FF


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leaking w cough, sneezing, liftingSTRESS - DEC urethral spincter tone
sudden overwhelming urge to urinateURGE - detrustor overactivity
incompletely emptying & persistent involt dribblingOVERFLOW - impaired detrusor contractility OR OUTLET OBSTRUCTION
internal uretheral sphincterANS (s - contraction, p - relax)
ext urethral sphincterpelvic floor skel muscle, voluntary control
bladder emptyingdetrusor


Question Answer
glomisotonic to bowmans cap
PCTelectrolytes, glucose, aa, water (passive) ISOTONIC
dLOHpermeable to H2O (moves into intersitium), ions retained in lumen; HYPERTONIC
TAL LOHimperm to H2O, absorbtion of NaCl (thin limb) and Na/K/2Cl (thick); OSMOLARITY DEC
DCTelectolytes reabsorbed more than water (early) perm to H2O becomes regulated by vasopressin (late)
coritcal and medullary CDH2O perm depends on water deprivation level
V2vasopressin and desmopressin - inc in H2O and urea perm at the inner medullary CD - rise in urea reab enhances gradient - allowing max concentrated urine


Question Answer
CN3 palsysomatic (all others + LEVATOR PALPEBRAE); parasym (iris sphincter and ciliary muscle - fixed dilated pupil & accomodation loss)
Dandy Walkerdilation of 4th v, absence of cerebellar vermin, small cerebellar hemis, posterior fossa cysts, enlarged posterior fossa, assocd w hydrocephlus and spina bifida - progressice skull enlargment
Dandy Walker presentationdevelopmtal delay and progressive skull enlargement - unsteadiness, impaired muscle coordination
MSloss of myelin sheaths, depletions of oligodendrocytes within plaques; oligoclonal bands of IgG (oligo depletion also in PML)
Cushing triadHTN, bradycardia, bradypnea. - inc ICP due to hemorrhagic intracranial mets! (left temporal lobe)
central herniationdwnward displacement of brainstem (can lead to abducens palsy)
hornersmiosis, ptosis, anhidrosis
UMN lesionINITIALLY flaccid paralysis w hyporeflexia (SPINAL SHOCK) then SPASTICITY/HYPERREFLEXIA
damage causing pinpoint pupilslarge bilateral, pontine lesions - damage to descending sympathetic tracts
kluver bucyhyperorality, hyperphagia, hypersex - bilat amygdala


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cholesteatomascollections of squamous cell debris - form round pearly mass behind TM in middle ear
1' cholesteatomaresult of chronic negative pressure in middle ear causing retracting pockets in TM that become cystic - sq cell debris accum
2' cholesteatomawhen sq epith migrates to or is implanted in middl ear (skin in wrong place)
MC cause of painless otorrheacholestomas - can produce lytic Es that erode ossicles (conductive hearing loss), if large enough can erode into vestibular app or facial nerve - vertigo or facial palsies
MC malignant tumor of ear canalsq cell carcinoma - ulcerated plaque or nodule
Meniere's dzdisorder of inner ear characterized by inc volume and pressure of endolymph (endolymphatic hydrops) - due to defective resorption of endolymph - destension of endolymphatic sys - damage to vestibular and cochlear components of inner ear
meniere triadlow fq tinnitus (w feeling of fullness), vertigo (spinning or motion), sensorineural hearing loss (worsens over time)
acute onset vertigo, n/v, single episode viral syndromelabrynitis (inflam vestibular nerve)
otosclerosisbony overgrwth foot plate of stapes - conductive hearing loss - persistent
rapid tachyphylaxis, allergic rhinitisalpha adrenergic agonist (decongestant - phenylephrine, xylometazoline, oxymetazoline) - vasoconstriction - rapid decline in effect - dec prodn of endogenous NE from nerve terminals due to negative feedback mech - results in relative vasoDILATION -> edema and congestion ; use for >3 days ***NG also causes tachyphylaxis *** NEED DRUG FREE INTERVALS
kiesselbach plexusanterior nasal septum - anastomose of anterior ethmoidal, sphenopalatine, superior labial arteries - EPISTAXIS
high freq hearing losschronic noise exposure - trauma to stereocilitated hair cells
auditorystaples -> oval -> scala vestibuli -> helicotrema -> scala tympani -> round window
malignant otitis externapseudomonas aeruginosa, elderly diabetes, exquisite ear pain and drainage (granulation tissue see within ear canal, TM intact -> progression of infxn can lead to osteomyelitis of the skull base and cranial nerve damage - USE CIPROFLOXACIN
inflamed, red, bulging, immobile TMacute otitis media (immobile infected fluid in middle ear)




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livedo reticularismottled reticulated vasc pattern - caused by swelling of venules owing to cap obstruction by small blood clots


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T2DM/high FFAsinsulin resistance in adipose hinders the antilipolytic effects of insulin -> inc lipolysis and FFAs
chronic FFA inc in T2DMinc resistance by impairing insulin dependent glucose uptake & inc gluconeogenesis
metabolic syndromeinc TGs, low HDL, central obesity, HTN, elevated glucose
sudden cessation of glucocorticoids after prolonged useadrenal insuff/ CRISIS
cortisol prodcing adrenocoritcal adenomaunilate atrophy of contralat adrenal gland - ACTH supression


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Potter Sequenceflat facies, pulm hypoplasia, limb deformities - ARPKD
cerebral aneurysms PKDassoc w autosomal DOMINANT type


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alporttype 4 collagen -> thinning splitting glomerular bm; eye , glomnepphritis, sensorineural deafness (CANT SEE, PEE, HEAR A BEE)


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JOB SYNDROMEhyper IgE, def in Th17 due to STAT3 mutn -> impaired recruitment of neutrophils to infected site
fx of hyperIgE syndromecoarse facies, cold (noninflamed) staph abscesses, retained primary teeth, inc IgE, eczema, bone fx from minor trauma


Pharm – General

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wet AMD txsmoking cessation and VEGF inhibitors (ranibizumab, bevacizamab) "bevers by the VEG patch so I ran
TNFa inhibitorsused in inflam autoimmune conditions (RA, IBD, seroneg spond)
AntiIL2immunosuppression for organ transplant, graft vs host
improve trabecular outflowmuscarinic agonists
improve uveoscleral outflowprostaglandin agonists
aqueous humor inflowBB, a2 agonists, CAIs
MOA ca glaucomadec HCO3 in ciliary body -> dec Na and fluid transport & subsequently dec production of aqueous humor
MOA a agonist (brimonidine)inhib aqueous production via ciliary body vasoconstriction
MOA BB glaucoma (timolol)dec prodn aqeous humor - act on ciliary EPITH
PG glaucomaDONT dec prodn aq humor
aq outflow dec'ercholinergic agonsist (pilocarpine, carbachol), postaglandin F2a

Pharm – Adverse Effects

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digoxin toxvisual changes and gi disturbance - adjust dose in elderly bc age related renal insuff



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MM/renalbence jones precip w tamm-horsfall -> obstruct tubular lumen - amorphous hyaline material in tubular lumen