fri jul 31 Flashcards

1
Q

clopidogrel MOA

A

irreversibly blocks the PY12 component of ADP receptors- prevents aggregation

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2
Q

what alternate antiplatelet agent do you give someone with aspirin sensitivity?

A

clopidegrel

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3
Q

cilostazol MOA

A

PDE inhibitor

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4
Q

eptifibatide MOA

A

platelet glycoprotein IIb/IIIa inhibitor-blocks platelet aggregation

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5
Q

during an acid fast stain, what does carbofuscin bind to?

A

mycolic acid -holds onto the colour in the following steps of hydrocloric acid and alcohol

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6
Q

naproxen MOA

A

reversibly inhibits COX1 and COX2

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7
Q

pathogenesis of bloom syndrome?

A

mutation in BLM - dysfunctional helicase - chromosomal instability and breakage

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8
Q

presentation of bloom syndrome?

A

growth retardation, face anomalies, photosensitive rash and immunodeficiency

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9
Q

what are the three stages of acute tubular necrosis? (and timelines)

A
  • Initiation (24-36 hours)
  • Maintenance (1-3 weeks)
  • Recovery phase (months)
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10
Q

what is the initiation stage of acute tubular necrosis?

A

Injury from ischemia or cytotoxins

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11
Q

what are the findings in the maintenance phase of acute tubular necrosis?

A
  • oliguric renal failure (decreased GFR, decreased urine output, fluid overload)
  • increased creatine/BUN, increased potassium and metabolic acidosis
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12
Q

what are the findings in the recovery phase of acute tubular necrosis?

A
  • gradual increase in urine output, leading to high volume diuresis
  • continued impairment of renal tubular function, resolving in electrolyte wasting (decreased potassium magnesium, phosphorous, calcium)
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13
Q

what is the most common viral oppurtunistic infection of the GI tract in AIDs patients?

A

CMV

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14
Q

Presentation of CMV colitis

A

fever, aorexia, weight loss, abdominal pain.

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15
Q

colonoscopy findings of CMV colitis?

A

mucosal erythemia, erosions, ulcerations

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16
Q

histological findings of CMV colitis?

A

acute and chronic inflammation. Vasculitis, giant cells with larve, ovoid nuclei with basophilic cytoplasmic inclusions

17
Q

cryptosporium effects which part of the GI tract?

A

small intestine

18
Q

brain findings of normal pressure hydrocephalus?

A

enlarged ventricles

19
Q

what is diltiazem and verapamil?

A

non-dihydropyridine Ca blockers

20
Q

GI side effect of non-dihydropyridine Ca blockers?

A

constipation

21
Q

what is an incidactor that erectile dysfunction is psychogenic?

A

normal erections at night time or during masturbation

22
Q

lisdexamfetamine use?

A

Binge-eating disorders (overeating - not bulimia

23
Q

what is acute dystonia?

A

sudden, involutnarly contraction of a muscle or muscle group (ex. cocked head)

24
Q

naltrexone MOA

A

blocks mu opioid receptor

25
Q

why can naltrexone be used as an alcohol abstinence promoting drug?

A

blocking the mu opioid receptors inhibits the reinforcing and rewarding effects of alcohol, helping to reduce craving and improving motivation to quit

26
Q

what is acamprosate?

A

an alcohol abstinence promoting drug that works by modulating glutamate transmission at NMDA receptors

27
Q

how does demylination effect conductence of nerves?

A

reduces saltatory conductance

28
Q

where does hemotogenous osteomyelitis commonly effect?

A

the metaphysis of long bones

29
Q

MOA of amantatoxins?

A

absorbed in GI tract, go to liver, bind to DNA dependent RNA synthase - halt mRNA synthesis

30
Q

how does one ingest amantatoxins?

A

eating the death cap mushroom or other poisonous mushrooms

31
Q

presentation of amantatoxin poisoning?

A

abdominal pain, vomiting, severe choleria-like diarrhea

May lead to hepatic and renal failure