NBME Form 31 Incorrects Flashcards
2wk history of pain in R leg just below the knee of 14yr old boy. XR shows large, semi-Ca mass that erodes the medullary canal of the tibia, infiltrates the cortex, and extends into the nearby soft tissues.
osteosarcoma.
predominately affects the LONG bones: tibia, femur
erodes thru cortex givin “sunburst” periosoteal rxn, elevation of periosteum> Codman tri
histology: lesion w/ primitive cells in lace-like meshwork of bone with mitoses; osteoblast-like mesencyhmal cells that make osteoid.
aggressive, poor prognosis.
what is the most common primary bone tumor to affect the vertebrae?
osteoblastoma, benign; no response to aspirin.
vertebrae are common MET sites for breast & prostate cancer> look for pain worse in the night/sclerotic lesions
MOA of ketoconazole?
inhibition of lanosterol->ergosterol in the fungal cell wall by 14ademethylase.
what is the common cause of tinea cruris?
trichophyton rubrum
tinea cruris> “jock itch”, crotch and peritoneum.
what is the typical treatment for tinea cruris?
topical azole antifungal> clotrimazole
chronic hep C pt, 2wk hx weakness/rash on legs. 2+ edema, pupuric rash over the extremities. C3/C4 decreased. UA dysmorphic RBC, no casts. creatinine inc.
essential mixed cryoglobulinemia> cryoglobulins are IGs that precipitate out of the serum. triad: weakness, arthralgias, palpable purpura.
risk factors: chronic Hep C/B, HIV, malaria, EBV; chronic inflame- SLE, Sjogren; lymphoproliferative multiple myeloma.
causes deposition of immune complexes (HS3) in BV> leukocytoclastic vasculitis> can manifest as purpura, end organ dysfunction= renal failure/nephritic/nephrotic syndromes.
49yr old with poorly controlled HTN in ER with SOB. Ran out of meds 5 days ago. BP 240/120, pulse 98, r 32, 86% O2. Loud S4. b/l crackles on lung fields. CXR pulm edema. Diagnosis?
congestive heart failure> presenting as decompensated heart failure.
pathophyis> long-standing, uncontrolled HTN> ventricular hypertrophy> dec compliance, dec filling>diastolic dysfxn.
with a loud S4 (gallop in late diastole), most likely diastolic dysfunction HF. inc atrial P, ventricular hypertrophy, as the LA attempts to overcome stiff/noncompliant LV.
echocardiography shows thick LV muscle tissue. what is the underlying condition?
HTN> LV hypertrophy as a result of constant work against the incr afterload> impaired LV relaxation, inc diastolic P> LA enlargement> heart failure over time.
mitral stenosis findings on ECG
LA hypertrophy, reduced LV SV
opening snap with diastolic rumble murmur
23yr F w/ chronic sinusitis. Needs to drain L maxillary sinus–what is the placement of the cannula?
at middle meatus, at the hiatus semilunaris.
pt has bacterial sinusitis 2/2 viral URI; dull pain aggravated by leaning forward.
complications: orbital cellulitis, cavernous sinus thrombosis, meningitis.
the anterior portion of the piriform aperture is commonly opened during what procedure?
functional septoplasty–enhances airflow thru nose
// ant portion of aperture opens into the cartilaginous anterior nasal vestibule> lateral to maxillary bones, nasal septum medial.
sphenoethmoidal recess is found at?
the superior aspect of the nasal cavity– superior and posterior to the superior nasal concha» opens into the sphenoid sinus– common pathway for the trasnsphenoidal approach to pit gland
what is immediately anterior to the torus tubarius?
opening of the eustachian tube into the nasopharynx» connects posterior nasopharynx to the middle ear» causing acute otitis media.
what is immediately inferior to the anterior margin of the superior conchae?
superior nasal meatus–which communicates with the posterior ethmoid cells.
44yr M with 2 month history of dry mouth, constipation, inability to have erection, progressive fatigue. neuro exam shows weakness of alot muscles, absence of all stretch reflexes; normal sensation. CXR shows R lung mass. Labs show antibodies directed against PQ calcium channels. Why neuro findings?
impaired Ach release at NMJ, limiting cell depol, proximal muscle weakness» not dec excitation contraction coupling. pt has Lambert-Eaton paraneoplastic syndrome 2/2 small cell lung cancer.
LE= extended use makes better, gradual accumulation of Ach in synapse= better depol. PRESYNAPTIC NMJ. (MG is postsynpatic Ach NMJ)
male newborn has multiple features suggestive of Downs syndrome. Chromosomal analysis is ordered. What do you tell the parents?
The newborn has features of Downs, a chromosomal test is ordered» NOT the newborn has some unusual features on exam, and a test has been ordered to help determine diagnosis.
Doc should address objective findings by explaining diff diagnosis and the next steps in simple language in small pieces> honor autonomy w/ relevant information–do not protect patient from distressing news, allow them to process info in small pieces.
what are the symptoms of cavernous sinus thrombosis?
i/l orbit pain, sinusitis, proptosis, periorbital edema, impaired eye movement/pupil reactivity.
» CN 3,4,5a,5b,6 transverse the sinus
what patients are at risk for developing ophthalmic artery embolism?
carotid/cardiac valvular disease pt> central retinal artery occlusion» acute, painless vision loss and diminished visual acuity, pale fundus (preserved foveal color), afferent pupillary defect.
*****admit to stroke center for emergent eval
48yr man w/ 30yr PMH DM1 w/ sudden onset double vision. L eye weakness abduction. What is the development of double vision ?
diabetic mononeuropathy.
microvascular damage commonly affects the abducens n> presents as esotropia, u/l abduction defect, diplopia in horizontal gase, hypotropia. most pts have resolution of symptoms with tx of underlying cause.
**important to rule out stroke, ICP, vasculitis, optic neuropathy,
24yr woman with increased ROM in her joints. 6ft tall, 130lb, BMI 18. Pectus excavatum. Cardio exam reveals new diastolic murmur. What is the most likely cause?
aortic insufficiency» pt has Marfan syndrome, impaired collagen synthesis.
subsequently leads to an incr LV EDV» eccentric hypertrophy of the LV, progressive LV systolic dysfxn
when would you see a systolic murmur in a Marfan pt?
myxomatous degeneration of mitral value» mitral insufficiency (mitral valve prolapse)» presents with holosystolic murmur.
24yr F w/ 3day history of vaginal discharge w/ itching. Currently tx with ciprofloxacin for cystitis. Vaginal area now presents with thick, white discharge. What is the most likely caused organism?
candida albicans> pt has vaginal pruritis, thick white discharge with antibiotic tx> vulvovaginitis from Candida. “cottage cheese” appearance
neg KOH testing, normal vaginal pH, no trichomonads on wet mount
risk factors: those on antibiotics, contraceptives (oral & intrauterine), immunocompromised, DM
tx: antifungals (topical clotimazole, oral fluconazole)
N. gonorrhea is gram neg that can present with cervicitis, PID, Fitz-Hugh-Curtis, urethritis, vaginitis. How can you tell diff btw gonorrhea vs. candida?
the discharge»gonorrhea will present with mucopurulent discharge, pruritis, and be generally asymptomatic vs candida is thicker, white discharge.
76yr M in ER with inability to urinate. Markedly enlarged prostate, u/s shows large kidneys with dilated calyces. PO2 is 90mmHg. What is the suspected ABG?
pt has BPH> leading to hydronephrosis, obstructive uropathy> leading to volume expansion +RAAS> HTN» metabolic acidosis, non-anion gap via urinary acidification (generally unless uremia or another concomitant anion gap issue). will be compensated w/ resp alk, tachypnea» near normal pH.
56yr M w/ 2 month hx bloody cough. CT shows 4cm mass in RUL that’s obstructing SVC. Blood returns to heart via?
internal mammaries & intercostal veins.
when SVC obstructed, can drain into the IVC via internal mammary v with sup/inf epigastric v.
the azygos/hemiazygous v drain posterior intercostal/bronchial v> via lumbar venous system to IVC
long thoracic venous communicates with femoral & verterbral v> to IVC.
pt will develop venous congestion head/neck/upper extremities= SVC syndrome regardless of collaterals tho
what veins are the main venous drainage of the head?
jugular & subclavian v.
external jugular v> subclavian>internal jugular>brachiocephalic> L & R merge to make SVC.
43yr F w/ 2 mon history of intermittent abdominal pain, esp after fatty meals, localized to RUQ. u/s shows cholelithiasis. MOA of ursodiol?
decreased cholesterol secretion into bile by 40-60%, dec absorb into the gut; ursodiol=ursodeoxycholic acid (generally second line to surgery)
pt has all characteristics of cholelithiasis: middle-aged female, RUQ pain after fatty meals. risk factors: obesity, advanced age, estrogen tx, rapid weight loss, Crohn’s, 4F’s
**statins generally have lower gallstone risk; fibrates (inhibit chol 7a hydroxylase) have most risk–> end up having supersaturated cholesterol with inhibited bile acid synthesis.
32yr F with intermittent chest pain “not severe, just kinda annoying”. Mother died of sudden MI ~50s. Midsystolic click at 5th intercostal space on L midclavicular line. What cardio thing is happening?
mitral valve prolapse> generally asympt, but have palpitations, chest pain, dyspnea.
midsystolic click +- late systolic murmur of mitral regurg.
more common in females, most common cause is myxomatous degeneration, chorda tendinea rupture, mitral annular disjunction> where the mitral annulus becomes partially detached.
***degeneration results in thickened mitral valve leaflets with accumulation of fibrous & mucoid material» commonly associated w/ Marfan, PKD, SLE, polyarteritis nodosa.
ASD murmur
fixed, split S2 with low grade physiological ejection murmur
L>R shunt with abnormal flow of blood from LA to RA> volume overload R heart
Bicuspid aortic valve murmur
bicuspid aortic valve> aortic stenosis> crescendo-decrescendo systolic murmur @ R upper sternal border
Tricuspid regurg murmur
holosystolic murmur best heard in L lower sternal border» esp common with severe pulm HTN/infective endocarditis of IV user
what is the most common skin cancer?
basal cell carcinoma> originating from basal layer of epidermis, low met potential
typically: pink, pearly papules/nodules with rolled borders & central ulceration in sun exposed areas of head/neck.
tx: surgical excision removal, Mohs surgery
associated w/ mutations in hedgehog pathway of p53…primary risk factor is UV exposure.
63yr M with long history of sun exposure develops skin lesion. Lesion is 1cm, dark colored
malignant melanoma, commonly develops from pre-existing nevus or de novo; prognosis is dependent on depth of invasion
Asymmetry
Borders: irregular
Color: varied colors (pic shows brown, light parts)
Diameter: >6mm
Evolution: rapid evolution> melanoma.
what are the subtypes of malignant melanoma?
superficial spreading
nodular melanoma
lentigo maligna
acral lentiginous melanoma
what does actinic keratosis look like?
chronic rough, scaly patches. commonly treated with liquid nitrogen, topical 5FU
22yr M ER 30mins s/p tonic-clonic seizure began in L leg. 3yr PMH intermittent L arm stiffening, spasms of L thigh. No PMH or FHX of seizures. MRI of brain most likely to show lesion where?
R frontal cortex> pt presenting with L sided focal seizure (those originating from frontal lobe are generally partial/focal seizures).
primary motor cortex is in frontal lobe.
tx: begin with antiepileptic meds, then surgery as needed.
***frontal cortex also likely to have partial seizures that exhibit secondary generalization (pt here)
what lobe is most commonly affected by focal seizure activity?
temporal lobe> typically presenting with complex partial seizures– aura, motor symptoms (lip-smacking, fidgeting), autonomic dysfxn, confusion.
seizures presenting from the parietal lobe commonly present as?
somatosensory seizures> numbness, tingling, warmth, pain. receptive aphasia, dyslexia, lang comprehensive disturbances– Wernicke at jnct of parietal/temporal lobes.
30yr F 18wk gestation. U/s shows intracranial anomalies: single ventricle, small cerebrum, fused thalamus, corpus callosum agenesis. Where did failure originate?
prosencephalon> should’ve separated into telencephalon (cortial hemi & lateral ventricles) diencephalon (thalamus, hypothalamus).
pt has holoprosencephaly.
pros- forebrain
mes- midbrain
rhomb- hindbrain
failure of the rhombencephalon leads to what abnormalities?
rhombencephalon> metencephalon & myelencephalon–> brainstem, cerebellum, 4th V> Dandy-Walker is associated here.
58yr M with progressive hair loss in past few weeks. Father & grandfather had similar hair. Scalp shows loss of hair in M pattern over frontal hairline. What is the mechanism?
dihydrotestosterone binding to androgen receptors at terminal hair follicles> “male patterned baldness”= androgenic alopecia.
testosterone->dihyrotestosterone (more potent) via 5a reductase. hairs transition to finer fairs “miniaturization”
2 month M newborn ER with noisy/difficult breathing for 6 hr. Pt has multiple, slender, finger-like excrescences on both vocal cords. What was the maternal infection?
HPV (6/11)> laryngeal papillomatosis, commonly affecting the vocal cords as nodules/growths
Manifestations of fetal infection with HSV
tender vesicles that ulcerate & crust, generally at skin, eyes, mouth. systemic manifestations of meningoencephalitis.
transmission via placenta or birth canal.
***can also present as more aggressive laryngeal papillomatosis, but stick with HPV 6/11
Hepatocytes don’t grow in culture well (dedifferentiated), but do grow effectively with coculturing w/ biliary epithelial cells. Compared to when alone, the cocultured cells most likely produce increase amt of what?
urea> heptaocyctes have urea cycle, removing ammonia to urea for kidney excretion. Failure of this process leads to hepatic encephalopathy.
**dedifferentiated cells will maintain core metabolic pathways common to most cells–glycolysis, mito resp, but loose metabolic fxn: urea cycle, AA de/transamination, gluconeo, synthesis of proteins/coagulation factors
Coculturing hepatocytes would be expected to have increased metabolism/consumption of?
alanine> more coversion of alanine to glutamate for gluconeo
fructose> absorb via GLUT2, metabolize more fructose via fructolysis, only happening in liver
54yr w/ severe HTN suddenly collapses and LOC while having telephone argument. Pt has pinpoint pupils and decorticate posturing. CT shows what most likely hemorrhage?
intraparenchymal> most commonly with uncontrolled HTN, occurring in putamen/thalamus/pons/cerebellum.
**pinpoint pupils, decorticate posture (lesion above red nucleus= disinhibition, flexor posturing) localizes to thalamic hemorrhage.
epidural hematoma presents
CT lens shaped, bi-convex, hyperdense collections abutting the inner table of the calvarium= trauma to MMA.
initial LOC, lucid interval, progressive decline to death
subarachnoid hemmorhage presents
CT hyperdense blood products in cerebral sulci and basal cisterns> aneurysmal rupture of artery in subarach space/traumatic injury
acute, severe headache, photophobia, stupor/coma “worst headache of life”
subdural hemmorhage presents
CT crescent shaped collection abutting the internal surface of the calvarium, not bound by suture lines= bridging veins problems
headache, vomiting, meningism, UMN findings
30yr F w/ 2 day hx of double vision and eye deviation. 24hrs s/p MVA. L ptosis, L eye “down & out”. What happens when light shined into R eye?
R pupil constriction, L pupil no change> deficit in CN 3 (oculomotor)
CN3 holds efferent branch of light response (interneurons at Edinger-Westphal nucleus); susceptible to injury while crossing the post comm artery to ciliary ganglion>, controlling iris sphincter.
**KEY: all injuries to efferent are i/l, so pt damages L CN3 injury= L efferent injury= L pupil arc unable to respond to direct & consensual light response (no ability to constrict at all)
Explain Marcus Gunn pupillary phenomenon
relative AFFERENT pupillary defect (rAPD) “swinging flashlight”, u/l or asymmetric response to light stimulation> generally with optic neuropathy, glaucoma, or retinal pathology.
dilation of one pupil as light moves quickly=abnormal response
what is the most common setting for b/l non-reactive pupils?
elderly patients with pupillary scarring via uveitis, or patients on opioid analgesics.
what muscles does CN3 innervate
levator palpebrae superioris
superior/medial/inf rectus
inferior oblique
*also the efferent arc of pupil light response
Clinical study of sickle cell allele, frequency of AA is 1/20, in Hispanics 1/200. Which genetic mechanism originally produced this stratification of allele frequency?
heterozygote advantage> continuous presence of the allele at high freq, in two genetically separate populations suggests heterozyg provides advantage that allows recess allel to persist.
what is assortative mating
non-random type mating where individuals select partners based on phenotypes that are similar/dissimilar to own» skews population toward more homozygous than would happen purely by chance
what is balanced polymorphism
presence of multiple phenotypes vartations of trait w/in population
heterozygous advantage is the specific mechanism by which the balanced polymorph of sickle cell trait is maintained
what is founder effect
type of genetic drift that reduces genetic diversity when a subgroup of pop becomes genetically separated from rest of population; significantly alters freq of alleles
what is gene flow
introduction of new alleles into the population due to migration from genetically separate population> if rate of flow is high enough, the two populations will merge into single genetic population
Drug X is given IV. Produces HR increase, AV conduction increase, no chnage in ventricular contraction. It is most similar to what class (alpha +-, beta+-, muscarinic +-)?
muscarinic antagonist (parasympathetic)> M2 works on SA/AV node> dec HR, atrial contraction
what are the differences between sympathetic vs parasympathetic effects on heart characteristics?
sympathetic– will change pressures, HR, atrial & ventricular contraction
parasympathetic– HR, atrial contractility only (SA/AV node)
6yr M fever & cellulitis on R hand. 2cm, red, macular lesion. Tx with nafcillin begins. Next 24hrs pt develops 102.2F, cultures grow MRSA. Production of what caused the resistance to methicillin?
new penicillin binding protein
Serratia, Klebsiella, Pseudomonas have demonstrated B-lactam resistance via?
mutations in genes coding for porins in cell envelope»allows for passive transport of hydrophilic molecules thru the outer membrane of gram - organisms primarily
what classic organism has resistance to antibiotics via altered antibiotic efflux pump
EColi> altered efflux pump lowers concentration of antibiotics
Increasing the production of folate causes resistance to TMX via
increased production B9 via DHF reductase increases synthesis of purines needed for cell growth/division, ultimately leading to resistance to TMX.
*TMX targets DHF reductase to decrease folate synthesis
what is the main mechanism of resistance to B lactam antibiotics (penicillin, ampicillin) in gram - bacteria
penicillinase & B lactamases> these genes encoding enzymes can be transferred on plasmids btw bacteria>inactivate B-lactam antibiotics
**commonly why we give B-lactamase inhibitors with some of those classes as well
62yr F with 25yr PMH DM2. 165cm, 79kg, BMI 29. Doc recommends influenza virus vaccine at this visit. Admin of vaccine is most likely to produce antibodies against what viral structure protein?
hemagglutinin> a membrane fusion protein binding sialic acid receptor on host cells allowing for viral entry. prevents subsequent infection of host cells
**vaccination contains multiple strains of killed virus due to random mutations in hemagglutinin protein= antigenic drift
MOA of oseltamivir
anti-influenza med, targets neuraminidase, enzyme on viral surface that enables release of influ virus from host cell by cleaving sialic acid from glycoproteins
what are M1 matrix protein, M2 ion channel, nucleoprotein
M1- influenza virus matrix protein that coats the inner viral envelope.
M2- influ virus ion channel on viral envelope of influenza A.
nucleoprotein- structural protein binds to viral RNA
52yr M lives in Indiana w/ 1 month hx fever, nonproductive cough, works construction. 101.1F, crackles heard over all lung fields. CXR shows b/l interstitial infiltrates. Transbronchial biopsy shows oval yeast w/in macrophages. The most likely causal organism in the patient has a cell wall with?
glucans> pt has Histoplasma capsulatum
pulmonary histoplasmosis characterized by fever, malaise, cough, with develop calcified nodules in mediastinal/hilar lymphadenopathy.
transmission: inhalation of fungal spores
endemic to Mississippi/Ohio river valley
what is the virulence of H.capsulatum
dependent on growth inside non-activated macrophages, protecting fungal cells from detection & elimination.
risk factors: exposure to bird/bat droppings
Histoplasma on culture grows via septate mycelia–with what components in cell wall
glucans (mostly), chitin, glycoproteins
Polyglutamic acid is the organic polymer synthesized by what bacteria
Bacillus species»expressed in cell capsule as virulence factor allowing for immune system evasion
14yr M w/ small lump in L breast 2 months ago. 2.5cm, mildly tender, rubbery mass under L areola. Sexual maturity is 2 for genital/pubic hair. Remainder of exam shows no abnormalities. Most likely diagnosis?
physiologic gynecomastia> increased amt of glandular breast tissue in males, and common in puberty. Commonly present 12-14yrs w/ tender mass behind the nipple, typically self-resolving.
gynecomastia is small, rubbery, mobile, well-circumscribed.
Sebaceous cysts commonly contain squamous epithelium, located?
commonly on trunk, face> well-circumscribed lesions with central punctum, generally painless unless infected.
interventions for puberty gynecomastia
puberty gynecomastia with disruption of androgens/estrogens; increased levels of estrogen with conversion of androstenedione/T to estrone/estradiol.
tx: aromatase inhibitors, liposuction if continued annoyance
41yr M acute onset abd pain caused by calculus at R ureterovesical junction. Pain is most likely to radiate where on the R?
R groin> sensory fibers that intervate ureters enter spinal cord at T12-L2> pain referral is common to groin via dermatomes
**pain at costovertebral angle is suggestive of pyelonephritis: fever, flank pain, tenderness–> nephrolithiasis pain can refer here is stone obstructs kidney w/ hydronephrosis
32yr M w/ 6wk hx persistent pain, swelling in R arm beginning after fall on hike. 2 months ago he had hike in Andes Mountains. He splited arm w/ stick, food supply was limited to saltine crackers, PB, processed cheese. Xray today shows R arm with poorly formed callus, nonunion of fracture ends. Most likely pt had dec fxn of what protein?
prolyl-4-hydroxylase» facilitates the hydroxylation of proline & lysine in collagen synthesis/tissue repair w/ Vit C.
Vit C is essential, found in fruits/veggies–pt’s diet indicates deficiency
scurvy presents as
BV fragility (easy bruising, petechiae, perifollicular hemorrhage)
impaired wound/bone healing
disordered “kinky” hair growth
Investigator studying T-cell clone recognizes a peptide from the hemagglutinin glycoprotein of influenza virus. This clone most likely recognizes a peptide that was combined with HLA_DR2 in which cellular component?
endosomes>cytoplasmic organelles mainly composed of microtubules/vesicles that traffic/sort endocytosed material (vaccines, live virus). HLA-DR2 (MHCII) synthesized in rER trafficked to golgi, then late endosomes.
Peptides combined with MHC1 are located
ER (lmao so close)
8yr boy 6month hx of difficulty reading, impulsive behavior. IQ is 203, reading/math, 101/97. Screening shows clinicially significant levels of inattention, impulsivity, hyperactivity. Mood disorder screening is normal. The most appropriate tx for this pt is durg effecting what neurotransmitter?
norepi> ADHD w/
