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UWORLD first pass- week2 > 2/12 UWORLD test # 13 > Flashcards

2/12 UWORLD test # 13 Flashcards

1
Q

Q 3. What gene is associated with hereditary pulmonary HTN? What is role of this gene?

A

BMPR2

inhibit proliferation of endothelial cells

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2
Q

Q 5. How urea reabsorption is mediated by ADH?

A

ADH activates urea transporters in medullary collecting duct

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3
Q

Q 7. Explain pathophysiology of acne formation. What hormone is specifically involved with this? Is UV involved?

A

DHT causes excess sebacum production and keratin synthesis (hyperproliferation of epidermis)

UV is not specifically involved, rather it causes skin cancer

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4
Q

Q 7. What is comedone? (pathoma p. 201)

A

blackheads and whiteheads, subtype of acne

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5
Q

Q 7. What does excessive perspiration (sweating) do for acne?

A

it can exacerbate acne, but not cause acne

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6
Q

Q 10. What are 4 clinical presentations of phenylketonuira (PKU)?

A
  • pallor of cholinergic nuclei
  • seizure
  • intellectual disability
  • musty body odor
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7
Q

Q 10. What enzyme is missing in PKU? What about in malignant PKU?

A

phenylalanine hydroxylase

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8
Q

Q 10. What are 4 clinical presentations of infant of maternal PKU?

A
  • microcephaly
  • congenital heart defect
  • intellectual disability
  • growth retardation
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9
Q

Q 11. what movement disorders in the lesion at

  • superficial peroneal nerve
  • deep peroneal nerve
A
  • superficial peroneal n.: eversion

- deep peroneal n.: dorsiflexion

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10
Q

Q 12. Define/example passive aggression

A

indirect expression of emotion

: coming in late to express negative thought to boss

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11
Q

Q 12. Define/example displacement

A

transferring emotion to another weaker person

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12
Q

Q 12. Define/example projection

A

attributing unacceptable internal impulse to another person

: husband who wants to cheat accusing of his wife

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13
Q

Q 12. Define/example Reaction formation

A

doing (or reacting) opposite

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14
Q

Q 13. 3 bacteria that produce IgA protease? What does this virulence factor facilitate (what is normal protection mechanism of IgA against bacteria) ?

A
  • strep. pneumo, Neisseria, H infulenza B

- breaksdown IgA to facilitate colonization in mucosa: IgA inhibits mucosal adherence

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15
Q

Q 14. What is the active form of thyroid hormone? How is it predominantly released? Is it also directly released from thyroid?

A
  • T3 is active form
  • predominantly released form is T4
  • Although small amount, T3 also directly released from thyroid (5’-deiodinase is also present in thyroid)
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16
Q

Q 15. What does glutathione peroxidase do? What is specific reaction that this enzyme is involved?

A

2GSH+ H2O2 —> GS-SG+ 2H2O

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17
Q

Q 15. Hallmarks of reversible cell injury (4) vs. irreversible cell injury . (4)

A

Reversible cell injury

  • membrane blebbing
  • ribosome detachment from ER
  • cellular swelling
  • chromatin clumping

Irreversible cell injury

  • mitochondrial leakage (mitochondrial vacuolization)
  • pyknosis: nuclear condensation
  • karyorrhexis: fragmented chromosome
  • karyolysis: fading
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18
Q

Q 15. Explain pathophysiology of reperfusion injury (3 possible explanations)

A
  • oxygen radical
  • inflammation
  • complement
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19
Q

Q 15. Explain the mechanism how irreversible injury in reperfusion injury leads to increased serum CK

A

plasma membrane damage -> leakage of intracellular CK

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20
Q

Q 16. What is thoracic outlet syndrome? symptoms?

What is the most common anatomical site?

A
  • compression of lower trunk of brachial plexus
  • claw hand: ulnar innervates lumbricals/interossei
  • scalene triangle: anterior/ middle scalene + FIRST rib
21
Q

Q 17. Difference between binge-eating disorder and bulimia nervosa?

A
  • binge- eating disorder: obese- no compensatory behaviors

- bulimia nervosa: normal shape due to excessive exercise or emesis to compensate

22
Q

Q 18. Which strain of H. influenzae causes meningitis

A

H. influenza B

23
Q

Q 18. When is the H.influenzae b vaccine given to child?

A

$ 2.18 in sketchy

2 months- 18 months

24
Q

Q 19. What is dry tap bone marrow aspiration? Name three diseases that can result dry tap

A

basically empty marrow

  • aplastic anemia
  • myelofibrosis
  • hairy cell leukemia
25
Q

Q 21. What do you see on ultra sound for ectopic pregnancy? what about histology from uterine curettage?

A
  • ultrasound: adnexal mass
  • histology: decidulazied endometrium (normal pregnancy- dilated coiled endometrial glands & vascularized edematous stroma)
26
Q

Q 22. What eye condition can be seen congenital CMV?

A

chorioretinitis

27
Q

Q 24. What are clinical features (2) of Gonorrheal cervicitis?

A
  • purulent vaginal discharge

- abdominal pain with vaginal bleeding

28
Q

Q 24. If Gonorrheal cervicitis is left untreated what (2) could happen?

A
  • infertility

- ectopic pregnancy

29
Q

Q 26. Diarrheal infection and 2 weeks after, joint pain. no bacteria in joint aspiration. what is going on?

A

reactive arthritis

30
Q

Q 27. What is olanzapine? adverse effects?

A
  • atypical antipsychotic

- dyslipidemia, weight gain

31
Q

Q 27. Among second generation antipsychotics, what is the drug that may cause prolactinemia?

A

risperidone

32
Q

Q 27. Among second generation antipsychotics, what is the drug that may cause agranulocytosis? What is another common side effect of this drug?

A
  • clozapine

- myocarditis or cadrdiomyopathy

33
Q

Q 28. What is plasma renin activity?

A

activity of renin (amount of angiotensin 1 generated per unit time )

34
Q

Q 28. What is valsartan? what is its effect on plasma renin activity? what about thiazide?

A
  • AngII receptor blocker
  • valsartan increases renin activity
  • thiazide increases renin activity
35
Q

Q 28. What would be plasma renin activity in renal artery stenosis?

A

decreased GFR -> increase renin activity

36
Q

Q 29. What does brownish perinuclear cytoplasmic inclusion suggest? what cells will show this?

A

lipofuscin

aged cells that do not have regenerative potency (permanent tissues- cardiomyocytes, skeletal muscle, neuron)

37
Q

Q 29. Describe 4 characters of old heart (aging)

A
  • decreased left ventricular size with collagen deposition within wall
  • dilated aortic root
  • enlarged left atrium
  • sigmoid shaped septum
38
Q

Q 30. How are beta blockers useful for hyperthyroidism? explain mechanism of action

A

beta blockers can inhibit 5’-idodinase, thus preventing T4->T3 conversion

39
Q

Q 31. What is side effect of acyclovir? Explain the mechanism. How can it be reversed?

A
  • interstitial nephritis
  • excess acyclovir will crystalize, damage renal tubule
  • can be reversed with sufficient hydration (to solubilize acyclovir crystal)
40
Q

Q 32. Compare ionotropic receptors vs. metabotropic receptors. Example of each?

A
  • Ionotropic receptors: ligand mediated ion channel
    ex) Nicotinic receptor
  • metabotropic receptors: G protein coupled second messenger system
    ex) Muscarinic receptor
41
Q

Q 34. Drug resistance mechanism for each drug?

  • penicillin (3)
  • aminoglycoside (3)
A
  • penicillin
    1. beta-lactamase production
    2. PBP mutation
    3. mutated porin
  • aminoglycoside
    1. modification enzyme (acetylation, phosphorylation, adenylation)
    2. mutated ribosomal subunit (50S)
    3. mutated porin
42
Q

Q 35. What is predisposing factor for infectious endocarditis?

A

valvular abnormality

  • easier to destruct it if there is pre-existing condition
43
Q

Q 36. With pre-existing valvular abnormalities, what would be the first initial step of infectious endocarditis? next steps?

A

pre-existing valvular abnormality -> fibrin deposition -> infectious bacteria colonization on fibrin -> activation of coagulative necrosis -> further valvular damage

It is fibrin deposition that happens first. Almost all bacterial vegetation happens on top of fibrin deposited on valve

44
Q

Q 37. How cyanide poisoning is treated? Explain mechanism of action

A

nitrite

nitrite converts Fe2+ (ferrous) to Fe3+ (ferric) in Hb. Ferric form has much higher affinity to cyanide, sequestering it to blood from tissue, reducing its toxic effect on tissue

45
Q

Q 37. Cyanide is enriched in what? How does cyanide poisoning present? What is the pathophysiology for action of cyanide?

A
  • Chemical fumes
  • reddish skin discoloration, tacypena, tachycardia, headache
  • cyanide inhibits oxidation phosphorylation in mitochondria by inhibiting cytochrome c oxidase in ETC
46
Q

Q 38. Does red neuron indicate reversible damage or irreversible damage? When does it happen after ischemic stress?

A

IRREVERSIBLE damage

red neuron normally happens 12-24 hours after ischemic stress

47
Q

Q 40. Is defective insulin secretion also pathophysiology for type 2 diabetes? What is supportive evidence for this?

A
  • Although main pathophysiology for type 2 DBM is insulin resistance, it is also believed that impaired insulin secretion is also possible cause of type 2 DBM

The evidence for this is deposition of amylin (amyloid) on Beta islet cell in type 2 DBM.

48
Q

Q 40. What HLA & autoantibodies are associated with type 1 DBM? type 2 DBM?

A

type 1: HLA- DR3 and DR 4
anti-GAD65 (Glutamic acid decarboxylase)

type 2: no association with autoimmune

UWORLD first pass- week2 (6 decks)

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