2/3 UWORLD test #5 Flashcards

(52 cards)

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?

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 17. What medications (2) are useful for BOTH acute symptomatic relief and mortality rate in congestive HF?
- nitrate | - hydralazine
26
Q 17. Is digoxin useful for HF? For symptomatic relief? mortality rate? or both?
Digoxin is only useful for symptomatic relief
27
Q 17. What is Flecainide?
class 1C anti-arrythmetics (Fries please)
28
Q 18. What is anatomical location of esophagus relative to heart, trachea, and aortic arch
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 23. Define dystonia
sustained contraction
30
Q 23. Define hemiballism
unilateral arm and leg movement
31
Q 23. Define myoclonus
sudden rapid contraction
32
Q 24. medication for Plasmodium infection?
Chloroquine | For chloroquine resistant strain, mefloquine
33
Q 25. What disease is associated with anti-smooth muscle antibody?
autoimmune hepatitis type 1
34
Q 25. What disease is associated with anti-mitochondrial antibody?
primary biliary cirrhosis
35
Q 25. Describe histologic finding of hepatocytes in Reye sydrome
panlobular microvascular steatosis
36
Q 25. Describe histologic finding of hepatocytes in Acetoaminophen overdose
centrilobular necrosis
37
Q 25. Describe histologic finding of hepatocytes in primary biliary cirrhosis
non-caseating granuloma
38
Q 25. Describe histologic finding of hepatocytes in primary sclerosing cholangitis
onion-skin appearance
39
Q 26. What is the major immune defense mechanism against Giardia lamblia?
secretory IgA and CD4 T cell | Although Giardia is parasite, it is NOT mediated by eosinophils
40
Q 31. What nerve damage results in dorsiflexed/everted foot?
tibial nerve
41
Q 31. What nerve innervates anterior thigh?
femoral nerve
42
Q 32. What are osmolarity values for each segment of nephron? - PCT - most medullary portion of loop of Henle - DCT
- PCT: 300 - most medullary portion of loop of Henle: 1200 - DCT: 100 DCT is the most diluted segment
43
Q 33. What is Bacteroides?
gram negative anerobe rod
44
Q 34. What is Cholesteatoma?
conductive hearing loss due to overgrowth of desquamated keratin in middle ear may perforate tympanic membrane
45
Q 35. What is Chlordiazepoxide?
benzodiazepine | first line for alcohol withdrawal
46
Q 37. How abetalipoproteinemia causes fat malabsorption?
apoB-48 is required for chylomicron synthesis | apoB is absent in abetalipoproteinemia
47
Q 37. What is histologic findings of enterocyte in abetalipoproteinemia
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 37. What are lab findings for abetalipoproteinemia
- 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 37. What gene is associated with abetalipoproteinemia? Hereditary pattern?
MTP, autosomal recessive
50
Q 37. What abnormality is seen on blood smear in abetalipoproteinemia? why?
Acanthocyte (spur cell) abnormal lipid composition-> irregular spiny RBC
51
Q 38. What vessel is most vulnerable to developing atherosclerotic plaque? why?
abdominal aorta Lack of vasa vasorum, limited blood supply of artery wall leading to atrophy of media
52
Q 40. What is T3 & T4 level in Hashimoto? why?
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