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UWORLD first pass- week 5 > 3/5 UWORLD test #33 > Flashcards

3/5 UWORLD test #33 Flashcards

1
Q

Q 1. How does inflammatory acne form?

A

overproduction of keratin & sebum

  • > blocks follicles (forming comedones)
  • > propionibacterium acnes infection
  • > bacteria produces lipase that breaks down TG in sebum
  • > acne
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2
Q

Q 1. Definition and example of each

  • apocrine
  • merocrine
  • holocrine
A
  • aporcine: vesicle mediated release
    ex) mammary gland (remember apocrine metaplasia that does not progress to cancer?)
  • merocrine: exocytosis mediated release
    ex) eccrine/apocrine sweat gland, salivary gland
  • holocrine: lysis and release of cytoplasmic contents
    ex) sebaccus gland (thus acne is example of holocrine)
  • all of these are exocrine system: release via duct
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3
Q

Q 2. common infection source of osteomyleitis

  • children
  • sickle cell (2)
  • pott disease
A
  • children: S. aureus
  • sickle cell: S.aureus, Salmonella
  • pott disease: Mycobacteria
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4
Q

Q 2. Moraxella catarrhalis: associated disease? (3)

* This bug is not covered in sketchy/FA

A

otitis media
sinusitis
exacerbation of COPD

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5
Q

Q 3. How to calculate median?

A

sum two middle values/2
data set should be in even number

ex: 1,2,3,4,5,6
- > median: (3+4)/2=3.5

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6
Q

Q 4. Which viral encoded protein is the major determinant for viral tropism on specific host tissue?

A

surface glycoprotein

viral surface glycoprotein attaches to corresponding receptors on host cell membrane: the very initial step.

This makes sense as orthomyxovirus major antigenic variation is on hemagluttin (surface gylcoprotein)- shift/drift

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7
Q

Q 6. epigenetics: histone acetylation vs. histone deacetylation? What each does for txn?

A
  • acetylation: txn activation

- deacetylation: txn deactivation

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8
Q

Q 6. Huntington disease

  • which gene is mutated? what chromosome? how?
  • nature of mutation: gain of function or loss of function?
A
  • huntingtin protein, chromosome 4, multiple CAG repeats
  • gain of function, mutated hungtingtin protein promotes histone deacetylation, causing transcriptional repression of many other genes
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9
Q

Q 7. histologic finding in glioblastoma multiforme? what about macroscopic finding?

A
  • mcroscopic finding: butterfly lesion that crosses corpus callosum
  • histologic finding: pseudopallisading necrosis ( cells lining up around necrosis) & angiogensis
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10
Q

Q 7. glioblastoma multiforme is tumor of what neuronal cell origin? what is kid’s brain tumor that has equivalent cell origin? What stain can be used for this cell origin?

A
  • astrocyte
  • kids: pilocytic astrocytoma
  • both are GFAP positive
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11
Q

Q 7. What is prognosis for glioblastoma multiforme?

A

very bad. it progresses rapidly. Pt usually die within 2 years after diagnosis

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12
Q

Q 8. Tetanus vaccine

  • what is it?
  • what immune response is triggered?
A
  • tetanus toxoid: formaldehyde inactivated tetanus toxin

- humoral response: antibody

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13
Q

Q 9. Lactase degrades lactose to what two sugars?

A
  • glucose

- galactose

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14
Q

Q 9. galactose metabolism disorder: galactose kinase deficiency vs. classic galactosemia
- compare phenotypes

A

Galactose kinase deficiency

  • cataracts
  • failure to track objects/ social smile

Classic Galactosemia

  • hepatomegaly
  • jaundice
  • intellectual instability
  • also cataracts

*LIVER manifestations are only for CLASSIC GALATOSEMIA

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15
Q

Q 10. Ethics: What are four exceptions for protecting patient’s confidentiality?

A
  • harming oneself/ another that may happen in the future again
  • child or elder abuse
  • knife or gunshot wounds
  • reportable communicable disease ( transmittable infectious disease such as ebola)
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16
Q

Q 12. Describe the location of AV node. Radiofrequency ablation of AV node is indicated in what heart condition?

A
  • endocardial surface near atrial septum & coronary sinus
  • Atrial fib
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17
Q

Q 12. Describe the location of SA node.

A
  • upper anterior atrium near opening of SVC
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18
Q

Q 12. Radiofrequency ablation of which part of heart is indicated for atrial flutter?

A
  • isthmus between IVC & tricuspid annulus
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19
Q

Q 13. What is the most effective approach to enhance adherence to medication for adolescent patient?

A

Finding support and role models within PEER group

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20
Q

Q 14. What determines coronary dominance? What is the most common dominance type?

A
  • Blood that supplies PDA (posterior descending artery)

- Right dominance is about 85%

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21
Q

Q 14. SA node and AV node are supplied by what coronary artery?

A

Dominant artery. Either by RCA (for right dominance) or LCA (for left dominance)

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22
Q

Q 15. Nitroprusside

  • MOA
  • indication
  • side effect
A
  • increase cGMP by direct release of NO => balanced vasodilation of BOTH artery and vein. Very SHORT acting
  • hypertensive crisis
  • cyanide toxicity (also releases cyanide)
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23
Q

Q 17. pancreatic head is derived from what pancreatic bud?

A
  • inferior/posterior head: ventral pancreatic bud
  • rest of head: dorsal pancreatic bud
  • Remember: ventral pancreatic bud does give rise to uncinate process, but NOT all parts of head
24
Q

Q 17. main pancreatic duct vs. accessory pancreatic duct each is derived from what pancreatic bud?

A
  • main pancreatic duct: ventral pancreadic bud

- accessory pancreatic duct: dorsal pancreatic bud

25
Q

Q 19. What urine pH condition will precipitate kidney stones

  • Ca oxalate
  • Ca phosphate
  • MAP (what is this?)
  • Uric acid
  • Cystine
A
  • Ca oxalate: - (neutral)
  • Ca phosphate: basic
  • MAP (magnesium ammonium phosphate): basic
  • uric acid: acidic
  • cystine: acidic
26
Q

Q 19. Pathophysiology of cystine kidney stone? What other amino acids will be accumulated

A
  • mutation on transporter-> impaired reabsorption in kidney and reabsorption at gut as well
- COLA
C- cysteine
O- ornithine
L- Lysine
A- Arginine

These all share same transporter

27
Q

Q 20. What mutation on what gene is implicated in melanoma? What does this mutation do?

A

BRAF V600E

increase signaling pathway in melanocyte proliferation/metastasis/survival

28
Q

Q 22. What is co-infection mechanism of HDV? (Why HepD virus needs HepB virus to infect hepatocyte? )

A

HepD virus (delta virus) must be COATED by HepB surface antigen to infect hepatocytes

29
Q

Q 21. Diazepam

  • What class of drug is this?
  • MOA
  • indications (6)
  • side effects (3)
  • should be avoided with what drugs?
A
  • BDZ
  • increase frequency (vs. phenobabitol- duration) of GABA-A
  • status epilepticus (1st line), alcohol withdrawal, insomnia, anxiety, analgesia, muscle relaxant ( to stop spasticity in stroke)
  • sedation, mental status change-confusion/disorientation (elderly), dependence/tolerance
  • Any drugs that cause same side effects
    ex: Anti-histamines (first generation, sedation is less significant in second gen.)
30
Q

Q 21. Chlorpheniramine: what class of drug is this? What other drugs (2) are in this class?

A

first generation anti-histamine

  • Diphenhydramine, dimenhydrinate
31
Q

Q 21. Loratadine: what class of drug is this? What other drugs (3) are in this class?

A

second generation anti-histamine

  • fexofenadine, cetirizine, desloratadine
32
Q

Q 22. Ranitidine

  • MOA
  • indication
  • side effect (1)
A
  • H2 receptor blocker -> less gastric acid secretion
  • peptic ulcer disease, GERD, gastritis
  • decrease renal excretion of creatinine
33
Q

Cimetidine

  • MOA
  • indication
  • side effects (3)
A
  • H2 receptor blocker -> less gastric acid secretion
  • peptic ulcer disease, GERD, gastiritis
  • side effects
    1. potent CYP450 inhibitor (DDI)
    2. decrease renal excretion of creatinine (so does ranitidine)
    3. anti-androgen effects (gynecomastia, impotence, decreased libido, prolactinemia)
34
Q

Q 23. Cheyne- stroke breathing
- Describe breathing pattern?

  • explain physiology
  • under what medical conditions? explain physiology
A
  • apnea followed by gradual increase then decrease tidal volume
  • apnea induced hypercapnea -> hyperventilation to compensate and then hypoventilation to reduce hypocapnea
  • CHF, brain trauma, stroke

w/ CHF: lack of effective ventilation (due to pulmonary conjestion) -> unbalanced hyper/hypo ventilation

w/ brain trauma/stroke: delayed pCO2 sensation in central chemoreceptor-> unbalanced hyper/hypo ventilation

35
Q

Q 24. What are diagnostic criteria for diabetes

  • Hb1AC
  • fasting glucose level
  • 2hr glucose tolerance
A
  • Hb1AC >6.5
  • fasting glucose >126
  • 2hr glucose tolerance >200
36
Q

Q 24. elevated free serum fatty acid vs. elevated C-peptide: which one contributes to progress of T2DM?

A

elevated free serum acid

Elevated free serum acid -> less need of insulin dependent glucose uptake -> insulin resistance

  • elevated C-peptide is also seen in T2DM, but it is byproduct of insulin resistance (increased insulin synthesis in insulin resistance), not causation of insulin resistance
37
Q

Q 25. What is eplerenone?

A

aldosterone antagonist

just like spironolactone

38
Q

Q 27. What ECG finding is seen after beta-blocker?

A

PR prolongation

39
Q

Q 28. Varicose vein

  • What is gross appearance ?
  • etiologies (4)?
  • what is complication?
A
  • dilated & tourtuous vein
  • long standing, >50 age, multiple pregnancy, obesity
  • ischemic necrosis and skin ulceration
40
Q

Q 30. What agent decreased radioactive I uptake treatment for Graves disease? why?

A

Pertechneate or Perchlorate

These two agents also undergo uptake by Na+/I- cotransporter. Thus, it will reduce radioactive Iodine uptake

41
Q

Q 30. What is additional function of propylthiouracil that methimazole doesn’t have? What is the function that these two commonly have?

A

5’-deiodinase inhibitor

Both propylthiouracil and methimazole can block TPO (thyroid peroxidase- iodine oxidation/ organification/ coupling)

42
Q

Q 31. What is the best therapy for febrile seizure?

A

supportive care only

43
Q

Q 31. Is active cooling recommended for febrile seizure? what about antipyretics?

A
  • active cooling is not recommended. It can precipitate seizure by inducing shivering
  • antipyretics do not show efficacy in reuding seizure
44
Q

Q 32. What do leukotrines (LTC4, LTD4, LTE4) do? Which medications target leukotrines for asthma?

A
  • bronchoconstriction
  • Monteleukast/ Zafirleukast: leukotrine receptor inhibitor
  • Ziluton: Direct LOX inhibitor
45
Q

Q 33. hemoptysis, elevated DLCO, proteinuria, hematuria. what is diagnosis?

A

Goodpasture

Elevated DLCO is due to accumulation of blood within alveoli. Blood will uptake CO (hemoglobin has great affinity to it)

46
Q

Q 34. Which vitamin is precursor for NAD?

A

Niacin

47
Q

Q 35. peripheral chemoreceptor vs. central chemoreceptor

  • location
  • senses what?
A

peripheral chemoreceptor
: carotid body
=> senses pO2

central chemoreceptor
: ventral surface of medulla
=> senses pCO2, pH

48
Q

Carotid body vs. Carotid sinus

  • difference
  • similarity
A
  • difference: body is chemoreceptor, sinus is pressure receptor
  • similarity: they both fires glossopharyngeal nerve to solitary nucleus of medulla
49
Q

Q 37. Blue toes, livedo reticularis after surgery. What is happening?

A

Thromboembolism

After surgery, cholesterol gets dislodged from big size arteries, and lodged to small size arteries.

50
Q

Q 37. Histologic finding of hyperplastic arteriolor changes in kidney. What is diagnosis?

A

renal hypertension

51
Q

Q 38. Screening marker in urinalysis for early stage diabetic nephropathy? explain pathophysiology

A

albumin

In diabetes, upregulation of heparanse will result in loss of negative charge barrier in GBM

52
Q

Q 38. What is earliest morphological change in diabetic nephropathy?

A

GBM thickening & mesangial matrix expansion due to non-enzymatic glycosylation

53
Q

Q 38. Which molecule in GBM is responsible for barrier for protein filtration?

A

heparan sulfate

: it is negatively charge. so it creates charge barrier (most protein is negatively charged)

54
Q

Q 38. What medication slows progression of diabetic nephropathy? explain mechanism

A

ACEI

dilation of efferent arteriole to reduce hyperfiltration damage of glomeruli

55
Q

Q 39. lepromatous leprosy vs. tuberculoid leprosy

  • symptoms
  • immune response
A

lepromatous

  • severe presentation- diffuse/leonine face (lion face)
  • mediated by Th2

tuberculoid

  • less severe presentation- limited, skin plaques
  • mediated by Th1
  • think like this: lepromatous is more nasty one. so you need to stimulate Th2 -> antibody to handle this nasty shit
56
Q

Q 39. What is lepromin skin test? which form of leprosy is more sensitive? why?

A
  • injection of M leprae antigen (like PPD): positive result will show indurated nodule
  • lepromin skin test is more sensitive to tuberculoid as it has stronger Th1 response.
57
Q

Q 40. Cavernous hemangioma

  • what morphological change?
  • affected organs (2)
  • complication?
A
  • vascular malformation causing dilated blood vessel
  • liver and brain
  • blood vessel malformation leads to hemorrhage (intrehepatic, intracranial), stroke, and even seizure (due to mass effect)

UWORLD first pass- week 5 (8 decks)

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