UWorld wrong questions part 4 (4th 200 q's) Flashcards
how to Dx H.I.T.? Tx?
Dx: ELISA for platelets; serotonin release assay (gold standard) heparin-induced platelet aggregation assay. Tx: stop heparin and give direct Thrombin inhibitor like argatroban.
ITP - how to treat?
adults: steroids, IVIG, plasmapheresis.
deficiency of metalloprotease leading to excessive platelet aggregation; hemolysis, renal failure, thrombocytopenia, neuro sz, fever; what Dz is this? Tx?
TTP-HUS. If TTP it includes the neuro sx and fever. Tx: steroids, plasmaphersis, FFP.
anti-phospholipid syndrome – what problems does this lead to?
hypercoaguability b/c cell membranes are made of PLs. See this in preg, lupus, etc and leads to DVTs.
what are the 3 major lab findings of Von Willebrand Disease and why?
Labs: increased PTT (b/c factor 8), increased bleeding time, but normal platelet COUNT; decreased ristocetin cofactor assay. / b/c vWF functions are to help Pts adhere to vessel wall and stabilize factor 8.
How to treat von Willebrand Dz? Avoid what?
Desmopressin (b/c DDAVP increased vWF), cryoprecipitate or factor 8. Avoid ASA.
what is the problem where pathologic excess clotting uses up all platelets, leading to hypocoaguability? What disease have this?
DIC. / “STOP Making Thrombi”: Sepsis, Trauma, Obstetrics, Pancreatitis, Malignancy, Transfusions
what are main labs in DIC?
decreased Pts, increased bleeding time, increased PT, increased PTT, decreased fibrinogen, increased fibrin split products, increased D-dimer, schistocytes (EVERYTHING MESSED UP)
Tx for DIX?
correct whatever is low: if decreased Pts, give Pts. if increased PT/PTT, give FFP or cryoprecipitate. Also, heparin.
most common hypercoaguable inherited diseases? When would you screen for this?
Factor V Leiden > antithrombin def, protein C and S deficiency. Screen if pt has DVT of unknown etiology.
how much PPx treatment for needlestick injury with HIV+ patient?
triple therapy (tenofovir, emtricitibine, & raltegravir for 4 weeks)
HIV patient with CD4 less than 100, non-infection problem with weight loss. Tx?
Wasting syndrome. give megestrol for appetite stimulant.
HIV: CXR showing a) B/L central infiltrates in what disease? b) B/L reticulonodular infiltrates in what disease?
a) PCP b) Coccoides
Dx of PCP? Tx?
Dx: sputum gram stain or bronchoscopy (also, see icreased LDH)……… Tx: TMP-SMX, or IV pentamidine if allergic.
HIV patient with CD4 less than 200, lung fungal infecrion
Histoplasmosis. Dx: urine/serum antigen test. Tx: amphotericin B/itraconazole
How to Dx, treat Toxoplasmosis? What should CD4 be below?
Dx: Toxoplasma IgG Ab…….. Tx: pyrimethamine + sulfadiazine, leucovorin. CD4 less than 200
Cryptococcal meningitis under what CD4 count? Dx? Tx?
CD4 less than 100. Tx: amphotericin B + flucytosine
If HIV+ patient has esophagitis that doesn’t respond to Nystatin, what is likely cause? Tx?
CMV (can cause esophagitis or colitis with painful ulcers). Tx: gancyclovir, valganciclovir, or foscarnet
MAC complex intracellulare, Dx, Tx?
Dx: blood cultires. Tx: clarithro or azithromycin (MACrolides to treat MAC)
main s.e. of NRTIs(abacavir, emtricitabine, zidovudine, tenofvir)? Specific to ZD and ABA?
lactic acidosis, lipodystrophy. ——ZD: bone marrow suppression&megaloblastic anemia. ACA: hypersensitivity rxn.
main s.e. of NNRTIs (efavirenz)?
rash, teratogenic, neuropsych (nightmares, depression)
main s.e. of Protease inhibitors (-navir)?
metabolic: hyperglycemia, hypertriglyceridemia, GI discomfort, hyperbilirubinemia/jaundice
HIV drug maraviroc - MoA? Enfuvirtide MoA, use?
Maraviroc: CCR5 antagonist. / Enfuvirtide: binds to glycoprotein 41 preventing fusion to CD4 (expensive but for if resistant to everything else)
what reasons do you use to detect viral load?
for drug therapy monitoring, infant screening(because babies born to HIV+ mom will always have HIV+ Ab even if they don’t have the disease), adults with acute HIV infection Sx (haven’t developed Ab’s yet)
Treatment of tropical sprue?
folate + tetracycline for 3-6 months
50-60 yr old patient with thrombosis (stroke, MI, DVT, etc), visual disturbances, burning pain in hands and feet, with erythema/pallor/cyanosis, red face(plethora), pruritus, hepatomegaly = ?
polycythemia vera. Tx: phlebotomy; if thrombosis risk, ihydroxyurea and ASA
elderly patient with back pain, radicular pain, weakness, weight loss, fractures, constipation, anemia, decreased WBCs, renal failure, hypercalcemia, what is this? What do you order next?
Multiple Myeloma. Order serum protein electrophoresis (M protein) and Urine protein electrophoresis (Bence-Jones protein). Skeletal survey to look for punched out lesions. DEFINITIVE DX: Bone Marrow Bx: increased plasma cells (clock formation).
Hodgkin lymphoma - what types? Main Sx? Lab?
always B cell, usually nodular sclerosis type (fibrosis of lymph nodes). —-Main Sx: painless cervical lymphadenopathy, fever, weight loss, night sweats, pruritus.—— Lab: Reed-Sternberg cells (Owl eyes: bilobed nuclei with clearing around them)
NHL - most common type? Main Sx? Lab?
diffuse large B cell. Main Sx: painless GENERALIZED lymphadenopathy, fever, weight loss, night sweats. Lab: NO RS cells, but follicular type will have cleaved cells.
t(14,18) =? t(8,14) = ?
t(14,18) = follicular. t(8.14) = Burkitt (EBV)
what leukemia has a) Auer Rods b) smudge cells? c) t(9,22) aka Philly chromosome d) treatment for CML e)progresses to blast crisis? f) PAS(+)
a) AML b) CLL c) CML>ALL d) imatinib e) CML (–> AML) f) ALL
child with short stature, abnormal skin pigmentation, hypoplastic thumb, horseshoe kidney, pancytopenia, think what disease? What interesting lab finding?
Fanconi anemia. Will have increased AFP.
child with anemia, craniofacial abnormalities, hypoplastic thumb, heart murmur, intellectual disability, hypogonadism - what disease? What interesting lab finding?
Diamond-Blackfan anemia (“make diamond over heart with hand, top points to brain/face, using thumb, points down to hypogonads”). increased EPO.
how to tell apart adrenal neuroblastoma and Wilms tumor (both have abd mass, HTN in child)
Wilms tumor has hematuria / adrenal neuroblastoma can have Horner syndrome sometimes and increased VMA, HVA.
How to treat a) Strongyloides? b) Isospora? c) Cryptosporidium
a) Ivermectin. b) TMP/SMX. c) nitazoxonide
patient with fever and low neutrophils, what do you do?
admit, culture, then broad Abx
what type of hypersensitivity is? a) hemolytic disease of the newborn b) Arthrus c) acute rheumatic fever d) immune/drug induced hemolytic anemia e) Goodpasture, Graves, myasthenia gravis, pemphiguses?
a) type II. b) type III c) type II d) type II e) type II
MoA of abciximab, tirofiban, eptifibatide? Uses?
Gly IIb/IIIa inhibitors to inhibit platelet aggregation. For unstable angina, coronary vessel intervension
MoA of dipyridamole? Use? s.e.?
adenosine re-uptake inhibitor. For recent stroke, artificial heart valve replacement (with Warfarin). S.e.=headache.
MoA of argatroban, bivalirudin? use? MoA of rivaroxaban, apixaban?
direct thrombin inhibitors. Anticoag in patients with H.I.T. 2nd ones are direct favtor Xa inhibitors b/c they have X in them.
What blood hypocoaguable state should you think about with the following: a) decreased Pts, increased bleeding time, normal PT/PTT. b) increased PTT only c)increased bleeding time, increased PTT, normal Pts and PT d) increased PT/PTT e) increased bleeding time only
a) HUS/TTP b) Hemophilia c) von Will disease d) ESRD or reg warfarin use. e) ASA use
what is next step in management of an intrauterine demise of fetus (dead >20 wks gestation)?
autopsy of fetus and placenta
a) sinusoidal pattern on heart tracings indicates what besides anemia? b) variable decelerations on fetal heart tracing indicate what besides cord compression, esp when with change in fetal station?
a) vasa previa b) uterine rupture
when would one do immediate C-section over elective C section or tocolysis/induction of labor?
when fetal heart tracing isn’t 110-160, variability isn’t >2cycles/min with beat-to-beat variability 6-20/min. Also do it if things are getting bad/labory in
treatment of choice for placental abruption?
emergency C section (esp if unstable fetal or maternal signs)
trastizumab - main s.e.; do what?
cardiotoxicity, so do echo
how to treat post-partum endometritis?
broad spectrum Abx (b/c polymicrobial): clindamycin for (+) and anaerobes, gentamicin (aminoglyc) for (-)
how to tell diff between CAH and PCOS?
CAH has increased progesterone levels along with LH, testosterine, etc. PCOS doesn’t.
how to diagnose endometriosis?
direct visualization on laparoscopy.
STI with painless ulcers that have red, beery base and no adenopathy?
Granuloma inguinale (whereas syphillis has nonexudative base and resolves w/ Abx)
Patient with no DTRs who is on MgSO4, what is 1st step in management?
Stop MgSO4 (this is magnesium toxicity) and give Ca-gluconate
in post-partum fever, what differentiates normalcy from suspected endometritis?
normal to have some fever, increased WBCs, and lochia with blood clots. Abnormal when foul-smelling lochia.
If pregnant patient has comorbidity like HTN, a) what test should you do? What to do if it’s b) normal aka reactive(>2 accelerations)? c) abnormal(
a) nonstress test. b) repreat nonstress test in 1 wks . c) biophysical profile (rthis will show oligohydramnios if abnormal)
what nerves are injured and what does it look like clinically: a) Klumpke palsy b) Erb-Duchenne palsy
a) claw hand, Horner syndrome; C8-T1. b) waiter’s tip, C5-6
a)what kind of shoulder dislocation is externally rotated with slight abduction, with prominent acromion and loss of shoulder roundness, and axillary nerve compromise? b) What shoulder dislocation is internally rotated and adducted with inabilitiy to externally rotated with flat anterior shoulder, and can be caused by electrocution?
a) anterior b) posterior
what nerve is affected in the following: a) unable to wipe bottom b) can’t pronate arm c) can’t supinate arm d)can’t initiate abduction of arm e) can’t abduct arm past 10 degrees f) can’t raise arm above horizontal
a) Thoracodorsal nerve b) median nerve c) MC nerve d) suprascapular e) axillary f) LTN, spinal accessory
supracondylar fracture in the arm affects what nerve?
median n.
what is a) proximal ulnar fracture with radial dislocation called, and how does it happen? b) distal radial fracture with ulnar deviation?
a)Monteggia (“MU”) fracture caused by FOOSH with forearm in excessive pronation (defensive injuries common) b) Galeazzi (“GR”)
how to definitively diagnose compartment syndrome?
manometry needle
if patient has back pain a) relieved by flexing knees and hips, what is this? b) worse with exertion c) worse with standing d) better with activity/worse with rest e) worse with straight leg raise/Valsalva and sensorimotor deficits
a) spondylolisthesis b) disc herniation c) spinal stenosis d) ankylosing spongylitis e) Degenerative disc disease
a) how to treat degenerative disc disease? b) how to treat cauda equina?
a) gabapentin, pregabalin; if comorbid depression can use duloxetine b) surgical decompression, IV steroids
how to diagnose osteomyelitis?
MRI: bone edema (NOT x-ray); increased uptake after 72 hrs on bone scan; tagged WBC scan
How to diagnose Lyme disease?
ELISA, Western blot
how to treat R.A.?
refer to rhematologist early, use DMARDs early (hydroxychloroquine, sufasalazine, methotrexate, TNFalpha inhibitors i.e infliximab)
what kind of casts in a) acute tubular necrosis b) tubulointerstitial nephritis? c) chronic renal failure
a) muddy brown grandular casts b) WBC casts (usually this is caused by analgesic nephropathy) , eosinophils c) broad and waxy casts
Child with proteinuria on U/S, what is next step in management? after that?
repeat dipstick twice. Then referral to nephrologist with 24 hr urine collection, renal U/S, renal Bx
patient who took IV acyclovir/sulfonamides/MTX/ethylene glycol/protease inhibitors, increased Cr 1-7 days later, hematuria, pyuria and crystals, in person with CKD or volume depletion? Tx?
crystal induced AKI causing renal tubular obstruction and direct tubular toxicity. Tx with D/C drug and volume replete, or give acyclovir WITH IVF
what drug can help a small renal stone pass (that doesn’t need Sx)?
alpha-1 receptor blockers, i.e. tamsulosin (decrease muscle tone in ureters)
a) blood at beginning or urination points to what? b) at end of urination, with clots? Next step? c) throughout all of urination, no clots?
a) urethral damage b) bladder disease. Do cystoscopy c) renal/ureter damage
after giving calcium gluconate to stabilize hyperkalemia, what is a) fastest next step? b) other options? c) last step?
a) insulin + glucose to shift K+ intracellularly (takes 15-30 min) b) furosemide or beta agonist i.e albuterol c) kayexalate aka sodium polystyrene sulfonate, or hemodialysis, both of which decrease total body K+
in acute oliguria, what is a) 1st step in management? b) next step?
a) bedside bladder scan b) if urinary retention present, put catheter in to decompress. If no urine retention, do serum/urine studies + imaging.
posterior urethral valves in fetus cause what problems?
Potter sequence (hydronephrosis –> oliguria -> oligohydramnios –> pulm hypoplasia, flat facies, limb deformities)
correcting hypernatremia too fast leads to what problem?
cerebral edema (correcting HYPOnatremia, however, leads to central potnine myelinolysis)
what is first step in correcting SEVERE hypernatremia?
0.9% normal saline bolus, THEN other things (b/c don’t want to correct too rapidly)
what main other-system problem does constipation cause in toddlers?
recurrent cystitis *b/c fecal retention causes rectal distension which compresses the bladder and causes urinary statis and incomplete voiding). Might also get anal fissures & hemorrhoids
first lab to check in patient with suspected BPH? Then what?
U/A to look for hematuria & serum Cr, plus PSA if man has life expectancy >10 yrs. If Cr is increased then suspect other obstruction causes and do renal U/S
What is the 1st then 2nd treatment step of hypercalcemia?
IVF + calcitonin, then bisphosphonates (long term)
