fri jul 31 Flashcards

(31 cards)

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?

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
why can naltrexone be used as an alcohol abstinence promoting drug?
blocking the mu opioid receptors inhibits the reinforcing and rewarding effects of alcohol, helping to reduce craving and improving motivation to quit
26
what is acamprosate?
an alcohol abstinence promoting drug that works by modulating glutamate transmission at NMDA receptors
27
how does demylination effect conductence of nerves?
reduces saltatory conductance
28
where does hemotogenous osteomyelitis commonly effect?
the metaphysis of long bones
29
MOA of amantatoxins?
absorbed in GI tract, go to liver, bind to DNA dependent RNA synthase - halt mRNA synthesis
30
how does one ingest amantatoxins?
eating the death cap mushroom or other poisonous mushrooms
31
presentation of amantatoxin poisoning?
abdominal pain, vomiting, severe choleria-like diarrhea | May lead to hepatic and renal failure