2/26 UWORLD test # 25 Flashcards

1
Q

Q 2. Duodenal atresia

  • pathphysiology
  • presentation
  • x-ray finding
  • other associated medical condition
A
  • failure of recanulation (makes duodenum lumen hollow during 9 weeks of gestation)
  • bilious or non-bilious vomiting
  • double bubble on x-ray (due to dilation of stomach and duodenum), polyhydramnios
  • Associated with Down syndrome
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2
Q

Q 2. Jejunum/ ileum atresia

  • pathophysiology
  • presentation
  • clinical finding
A
  • vasocclusion leading to ischemia
  • bilious vomiting
  • spiral configuration of distal ileum around blood vessel- apple peeling
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3
Q

Q 2. Pathophysiology of tracheoesophageal fistula?

A
  • Failure of tracheoesophageal septum to PARTITION the forgut into esophagus and trachea
    partition: devision
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4
Q

Q 4. Somatic mosaicism vs. Germline mosaicism

A

somatic mosaicism: somatic mutation from parents can not pass affected gene (mosaicism needs to be in germ cells to pass next generation)

germline mosaicism: multiple siblings with variable disease manifestation from NORMAL parents. Germline mutation from normal parents can pass mutant.

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5
Q

Q 5. What is H. influenzae B vaccine made of? when should it be given?

A
  • polysacchride capsule antigen conjugated to diptheria toxoid (inactivated toxin)
  • 2-18 months
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6
Q

Q 5. Describe immune response to encapsulated bacteria vaccines

A

exogenous antigen presented to CD4 T cells

  • > Th cell activation
  • > B cell activation/ plasma cell
  • > antibody production

It is antibody mediated immune response

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7
Q

Q 6. Describe the timeline regarding HBV serologic markers. Which one peaks disappears first? which one appears next? How can this time line explains window period?

  • HBsAg
  • HBeAg
  • anti-HBsAg
  • anti-HBeAg
  • Anti-HBc IgG
  • Anti-HBc IgM
A
  • Both HBsAg and HBeAg arises, but HBeAg disappears first, followed by Anti-HBeAg productin
  • HBsAg then disappear later, follwed by Anti-HBsAg production
  • These processes above are still considered as acute infection, thus Anti-HBc IgM
  • In window period, only Anti-HBeAg is positive (because it is synthesized earlier). Anti-HBc IgM will be detected
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8
Q

Q 8. Describe pathophysiology of secondary hyperparathyroidism/ renal osteodystrophy in CKD

A

CKD -> impaired 1-alpha hydroxylase

  • > impaired (1.25)-OH vitamin D production
  • > impaired gut Ca2+ absorption -> increased PTH
  • > increased bone resorption, osteodystrophy
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9
Q

Q 9. Explain the mechanism in which opioid cause RUQ abdominal pain

A

opioid constricts oddi sphincter of bile duct, causing increased bile duct pressure
-> biliary colic like symptom

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10
Q

Q 10. Which cancer is associated with chronic postmastectomy lymphedema?

A

Angiosarcoma

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11
Q

Q 11. Which cell releases cholecystokinin? How does total parenteral nutrition (say after bowel surgery) results in gallstone?

A

I cells in duodenum and jejunum

parenteral nutrition will deplete enteral stimulation, causing less cholecystokinin release

  • > less gallbladder emptying
  • > stasis -> gall stone
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12
Q

Amitryptiline

  • drug class, mechanism of action
  • side effects (what is special about this drug compared to to other drugs in same class)
A
  • TCA, block reuptake of serotonin and NE
  • tertiary amine: more anti-muscarinic effect than secondary amine, like nortriptyline
  • also QT prolongation, and cardiotoxicity by Na+ channel blocker. Cardiotoxicity can be reversed by NaHCO3
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13
Q

Q 13. Which complex mediates mRNA intron splicing? where in the cell does it occur?

A

snRNP

intron splicing occurs in nucleus

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14
Q

Q 13. What is P bodies? where is it located?

A

mRNA quality control (turnover)

cytoplasm

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15
Q

Q 14. sproatic colorectal cancer vs. colitis associated colorectal cancer

  • From which cell does it arise?
  • grade: which one is more aggressive?
  • molecular pathogenesis
  • distribution
A

Sporatic CRC

  • arise from polyps
  • less aggressive, lower grade
  • APC mutation -> KRAS mutation -> COX-2 overexpression -> p53 mutation
  • focal

Ulcerative colitis associated CRC

  • arise from flat lesion
  • more aggressive, higher grade
  • early p53 mutation, followed by APC mutation
  • multi-focal
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16
Q

Q 15. Where does bronchial vein drain to? How does it explain difference of pO2 between pulmonary vein and systemic artery?

A

pulmonary vein

Due to mixture of deoxygenated blood, systemic pO2 drops little bit compared to pulmonary venous pO2

17
Q

Q 16. Injury to what structure will most likely impair common peroneal nerve?

A

fibular head

18
Q

Q 18. Which nerve injury leads to wrist drop?

19
Q

Q 18. Damage to which artery should be concerned for humeral midshaft fracture?

A

deep brachial artery

it runs posteriorly with close proximity to radial nerve

20
Q

Q 19. Up to which point can lung/pleura is located?

A

lung/pleura extends above clavicle!

21
Q

Q 22. How does bordetella toxin works?

A

inhibition of Gi by Adenylylcyclase ribosylation

  • > increased cAMP
  • > edema & phagocyte dysfunction
22
Q

Q 22. What does streptolysin O from group A strep do?

23
Q

Q 23. Rotavirus

  • RNA structure
  • enveloped?
  • what medical condition? to what population?
A
  • dsRNA
  • naked
  • # 1 cause of diarrhea in kids
24
Q

Q 24. Wound contraction

  • when & what phase of wound healing does it happen?
  • mediated by which mediator?
A
  • proliferative phase, day 3 - weeks

- myofibroblast

25
Q 25. How is plasma renin activity in primary hyperaldosteronism?
decreased PRIMARY: adrenal gland, independant of renin
26
Q 25. What is aldosterone escape? How does this phenomenon explain phenotypes of primary hyperaldosteronism?
Escape from aldosterone effect - > Initial high sodium retention by aldosterone triggers ANP release -> increased natriuresis - > normalize sodium/ volume state This is why it is rare to see hypernatremia/edema in primary hyperaldosteronism
27
Q 26. Gross appearance of metastatic brain tumor (or all kind of metastatic tumor) ?
multifocal
28
Q 26. Gross appearance of oligodendrioglioma?
grey mass with calcification
29
Q 26. Gross appearance of glioblastoma?
well circumcised hemorrhagic/necrotic lesion | may cross corpus callosum (butterfly glioma)
30
Q 27. Vaginal dryness suggests deficiency of what hormone?
estrogen
31
Q 32. sublingual nitrate vs. oral nitrate for angina - indications - duration of action
- sublingual: rapid onset of action, acute symptomatic relief - oral: long acting, prevention of angina recurrence. Need higher dose than sublingual due to first-pass metabolism
32
Q 33. What reaction does lactate dehydrogenase facilitate?
pyruvate lactate
33
Q 33. What reaction does pyruvate dehydrogenase facilitate?
pyruvate -> Acetyl-coA * Dehydrogenase sounds like mismonomer, but whatever..
34
Q 36. Back-pain: what would be clinical symptoms/clues for each case? - degeneratvie (OA) - malignancy - vertebral osteomyelitis - Radiculopathy (disc herniation)
- degenerative: pain relief with postural change/ rest - malignancy: no pain relief with postural change/ rest + systemic symptoms- night sweat, weight loss - vertebral osteomyelitis: unifocal, tenderness, recent infection/ history of IV drug - radiculopathy: radiate to leg, positive straight leg test
35
Q 39. Which nuclei in brainstem is primarily responsible for serotonin release?
Raphe nuceli
36
Q 40. How hypocapnia changes cerebral perfusion? how?
Hypocapnia (low pCO2 due to hyperventilation) decreases cerebral perfusion, leading to dizziness and headache. Hypocapina is sensed by chemoreceptors and subsequently triggers cerebral vasoconstriction