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UWORLD first pass- week 1 > 2/3 UWORLD test #5 > Flashcards

2/3 UWORLD test #5 Flashcards

1
Q

Q 1. In what medical condition is Polyethylene glycol (PEG) used?

A

Constipation

PEG is thick non-absorbable sugar that works as osmotic laxative

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2
Q

Q 1. What is lactase deficiency and its effect on GI?

A

Impaired lactose digestion -> effect similar to osmotic laxative (non-digested chunky sugar driving water into GI) -> diarrhea

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3
Q

Q 2. Medication options for BPH? (3)

A
  1. finasteride
  2. terazosin
  3. tadalafil
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4
Q

Q 2. What is tadalafil? mechanism of action? side effects?

A

PDE-5 (phospho diesterase type 5) inhibitor
increased NO-> vasodilation
hypotension, flushing, syncope

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5
Q

Q 3. Differential diagnosis of infectious vaginitis? (3)

Diagnostic test? treatment?

A
  • bacterial: gardenella vaginalis, gray discharge, clue cell, KOH whiff test, pH >4.5 clindamycin or metronidazole
  • protozoa: Trichomonas vaginalis, green/yellow discharge, pH >4.5 saline microscope, metronidazole
  • fungal: Candida, thick white /cottage cheese discharge, normal pH (4-4.5), -azoles
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6
Q

Q 4. What is rett syndrome? hereditary pattern?

A

Developmental delay, intellectual disability, hand-wringing

X linked dominant

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7
Q

Q 4. In general, enzyme deficiency results in what type of hereditary pattern?

A

autosomal recessive

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8
Q

Q 4. In general, defective non-catalytic protein results in what type of hereditary pattern?

A

autosomal dominant

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9
Q

Q 4. What is classic galacotosemia? hereditary pattern?

Symptoms? tx?

A
  • Galactose 1-P Uridyltransferase deficiency
  • Autosomal recessive (all carbohydrate metabolism disease are AR)
  • Juvenile cataracts, Liver failure, jaundice
    : due to accumulation of galactitol, osmotically active
  • limit galactose & lactose (metabolized to glucose and galactose) on diet: diary
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10
Q

Q 4. What is Leber hereditary optic neuropathy? hereditary pattern?

A
  • degeneration of retinal ganglion cells (RGCs) and their axons that leads to an acute or subacute loss of central vision
  • mitochondrial inheritance
    : all kids from affected mother
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11
Q

Q 6. What is duration/etiology of transplant rejections:

Hyperacute, Acute, Chronic

A
  • Hyperacute; within minutes, preformed antibodies from receipient
  • Actue: months ( < 6 mo), humoral/cell mediated response, mostly CD8+ T cells
  • Chronic:, years, weak immune response, mostly CD4+T cells
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12
Q

Q 7. What maternal condition can cause NRDS (Neonatal respiratory distress syndrome)? Another cause of NRDS associated with delivery procedure?

A

Diabetic - hyperglycemia/insulin inhibits surfactant synthesis

C section- stressed induced cortisol triggers surfactant synthesis

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13
Q

Q 7. What medication can be used for infant survival in NRDS? What is the mechanism?

A

Dexamethasone

: cortisol helps surfactant synthesis

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14
Q

Q 7. When (gestation time) does surfactant synthesis start and by when fetus produces enough surfactant? How early premature gestation can cause NRDS?

A

begins at 26 weeks, normally mature in 35 weeks

less than 32 weeks of gestation is considered early, high chance to develop NRDS

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15
Q

Q 8. 1 week of focal deficits (hemiplegia, dysphagia) with evidence of brain ischemic injury. what do you expect to see in histology?

A

Reactive gliosis + microglial cells eating up necrotic cellular debris

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16
Q

Q 8. explain how ischemic brain injury proceeds

(time line: 12-48 hrs, 1-3days, 3-5 days, 1-2 wks, more than 2 weeks

A 
12-48 hrs: red neuron
1-3 days: necrosis &amp; neutrophils
3-5 days: microglia (macrophage of CNS)
1-2 wks: microgliosis
>2 wks: fibrosis
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17
Q

Q 9. Is alpha-helix or beta-sheet secondary structure? or tertiary structure? what is the strongest chemical bond that determines its structure?

A

secondary structure

Hydrogen bond

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18
Q

Q 10. What are symptoms of acute intermittent porphyria? (5Ps?)

A 
Painful abdomen
Port-wine urine color 
Precipitated by drug (P450 inducers), alcohol
Polyneuropathy
Psychiatric symptoms
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19
Q

Q 10. what are two treatments for acute intermittent porphyria?

A

Heme, Glucose

Both inhibit ALAS

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20
Q

Q 12. Crohn’s can cause what type of kidney stone? what is mechanism?

A

Calcium Oxalate
Fat malabsorption -> Calcium binds to fat in the gut -> oxalate not bound to Calcium is not fecally excreted via calcium oxalate form -> more oxalate reabsorption into blood and enter to kidney

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21
Q

Q 15. What are features of secretory phase of endometrium during menstrual cycle?

  • what hormone is secreted?
  • what mucus is secreted?
  • spiral artery? uterine wall?
A
  • progesterone
  • glycogen rich mucus
  • tortious (more) spiral artery, edematous (thickened) uterine wall
22
Q

Q 17. What is first line treatment for symptomatic relief of acute congestive HF?

A

Diuretics

23
Q

Q 17. What are long-term medications for survival improvement in patient with congestive HF? (4)

A
  • Beta blockers
  • ACEI
  • AngII receptor blocker
  • spironolactone
24
Q

Q 17. What is Amlodipine? Mechanism of action? Indications? Can this drug be useful for congestive HF?

A
  • Dihydrophyridine CCB
  • vasodilation of peripheral vessels
  • hypertension, Raynaud phenomenon
  • No. dihydrophyridine CCBs are more like peripheral blood vessel dilation- blood pressure control. Does not really have impact on preload and afterload
25
Q

Q 17. What medications (2) are useful for BOTH acute symptomatic relief and mortality rate in congestive HF?

A
  • nitrate

- hydralazine

26
Q

Q 17. Is digoxin useful for HF? For symptomatic relief? mortality rate? or both?

A

Digoxin is only useful for symptomatic relief

27
Q

Q 17. What is Flecainide?

A

class 1C anti-arrythmetics (Fries please)

28
Q

Q 18. What is anatomical location of esophagus relative to heart, trachea, and aortic arch

A

esophagus is lateral (left) with respect to heart
esophagus is the most posterior of all

From anterior to posterior;
pulmonary trunk -> aortic arch -> trachea -> esophagus

29
Q

Q 23. Define dystonia

A

sustained contraction

30
Q

Q 23. Define hemiballism

A

unilateral arm and leg movement

31
Q

Q 23. Define myoclonus

A

sudden rapid contraction

32
Q

Q 24. medication for Plasmodium infection?

A

Chloroquine

For chloroquine resistant strain, mefloquine

33
Q

Q 25. What disease is associated with anti-smooth muscle antibody?

A

autoimmune hepatitis type 1

34
Q

Q 25. What disease is associated with anti-mitochondrial antibody?

A

primary biliary cirrhosis

35
Q

Q 25. Describe histologic finding of hepatocytes in Reye sydrome

A

panlobular microvascular steatosis

36
Q

Q 25. Describe histologic finding of hepatocytes in Acetoaminophen overdose

A

centrilobular necrosis

37
Q

Q 25. Describe histologic finding of hepatocytes in primary biliary cirrhosis

A

non-caseating granuloma

38
Q

Q 25. Describe histologic finding of hepatocytes in primary sclerosing cholangitis

A

onion-skin appearance

39
Q

Q 26. What is the major immune defense mechanism against Giardia lamblia?

A

secretory IgA and CD4 T cell

Although Giardia is parasite, it is NOT mediated by eosinophils

40
Q

Q 31. What nerve damage results in dorsiflexed/everted foot?

A

tibial nerve

41
Q

Q 31. What nerve innervates anterior thigh?

A

femoral nerve

42
Q

Q 32. What are osmolarity values for each segment of nephron?

  • PCT
  • most medullary portion of loop of Henle
  • DCT
A
  • PCT: 300
  • most medullary portion of loop of Henle: 1200
  • DCT: 100

DCT is the most diluted segment

43
Q

Q 33. What is Bacteroides?

A

gram negative anerobe rod

44
Q

Q 34. What is Cholesteatoma?

A

conductive hearing loss due to overgrowth of desquamated keratin in middle ear
may perforate tympanic membrane

45
Q

Q 35. What is Chlordiazepoxide?

A

benzodiazepine

first line for alcohol withdrawal

46
Q

Q 37. How abetalipoproteinemia causes fat malabsorption?

A

apoB-48 is required for chylomicron synthesis

apoB is absent in abetalipoproteinemia

47
Q

Q 37. What is histologic findings of enterocyte in abetalipoproteinemia

A

accumulation of fat within villi due to impaired chylomicron synthesis.
Fat is reabsorbed in vili, but can not further reabsorbed into lacteal in the chylomicron form

48
Q

Q 37. What are lab findings for abetalipoproteinemia

A
  • absence of apoB-100 (chylomicron)
  • absence of apoB-48 (VLDL, LDL)
  • very low TGA, cholesterol level
    : cholesterol is packed in cholesterol ester, carried by chylomicron, VLDL, and LDL
49
Q

Q 37. What gene is associated with abetalipoproteinemia? Hereditary pattern?

A

MTP, autosomal recessive

50
Q

Q 37. What abnormality is seen on blood smear in abetalipoproteinemia? why?

A

Acanthocyte (spur cell)

abnormal lipid composition-> irregular spiny RBC

51
Q

Q 38. What vessel is most vulnerable to developing atherosclerotic plaque? why?

A

abdominal aorta

Lack of vasa vasorum, limited blood supply of artery wall leading to atrophy of media

52
Q

Q 40. What is T3 & T4 level in Hashimoto? why?

A

T3 level is variable: T3 is active form. Either directly synthesized from thyroid or converted from T4

T4 level is low

T3/T4 measurement is less reliable than TSH

UWORLD first pass- week 1 (4 decks)

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