Q 11. what movement disorders in the lesion at - superficial peroneal nerve - deep peroneal nerve

- superficial peroneal n.: eversion - deep peroneal n.: dorsiflexion

2/12 UWORLD test # 13 Flashcards by harry park

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

BMPR2

inhibit proliferation of endothelial cells

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Q 5. How urea reabsorption is mediated by ADH?

ADH activates urea transporters in medullary collecting duct

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

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

blackheads and whiteheads, subtype of acne

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

it can exacerbate acne, but not cause acne

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

pallor of cholinergic nuclei
seizure
intellectual disability
musty body odor

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

phenylalanine hydroxylase

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

microcephaly
congenital heart defect
intellectual disability
growth retardation

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Q 11. what movement disorders in the lesion at

superficial peroneal nerve
deep peroneal nerve

superficial peroneal n.: eversion

- deep peroneal n.: dorsiflexion

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Q 12. Define/example passive aggression

indirect expression of emotion

: coming in late to express negative thought to boss

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Q 12. Define/example displacement

transferring emotion to another weaker person

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Q 12. Define/example projection

attributing unacceptable internal impulse to another person

: husband who wants to cheat accusing of his wife

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Q 12. Define/example Reaction formation

doing (or reacting) opposite

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

strep. pneumo, Neisseria, H infulenza B

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

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

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

2GSH+ H2O2 —> GS-SG+ 2H2O

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

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

oxygen radical
inflammation
complement

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

plasma membrane damage -> leakage of intracellular CK

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Q 16. What is thoracic outlet syndrome? symptoms?

What is the most common anatomical site?

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

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

binge- eating disorder: obese- no compensatory behaviors

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

Q 18. Which strain of H. influenzae causes meningitis

H. influenza B

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

$ 2.18 in sketchy

2 months- 18 months

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

basically empty marrow

aplastic anemia
myelofibrosis
hairy cell leukemia

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

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

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

chorioretinitis

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

- purulent vaginal discharge | - abdominal pain with vaginal bleeding

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

- infertility | - ectopic pregnancy

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

reactive arthritis

Q 27. What is olanzapine? adverse effects?

- atypical antipsychotic | - dyslipidemia, weight gain

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

risperidone

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

- clozapine | - myocarditis or cadrdiomyopathy

Q 28. What is plasma renin activity?

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

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

- AngII receptor blocker - valsartan increases renin activity - thiazide increases renin activity

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

decreased GFR -> increase renin activity

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

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

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

- decreased left ventricular size with collagen deposition within wall - dilated aortic root - enlarged left atrium - sigmoid shaped septum

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

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

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

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

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

- Ionotropic receptors: ligand mediated ion channel ex) Nicotinic receptor - metabotropic receptors: G protein coupled second messenger system ex) Muscarinic receptor

Q 34. Drug resistance mechanism for each drug? - penicillin (3) - aminoglycoside (3)

- 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

Q 35. What is predisposing factor for infectious endocarditis?

valvular abnormality - easier to destruct it if there is pre-existing condition

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

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

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

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

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

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

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

IRREVERSIBLE damage | red neuron normally happens 12-24 hours after ischemic stress

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

- 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.

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

type 1: HLA- DR3 and DR 4 anti-GAD65 (Glutamic acid decarboxylase) type 2: no association with autoimmune