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Q1 > ACI - Pharm (NSAIDs, Glucocorticoids, Anticancer drugs) > Flashcards

ACI - Pharm (NSAIDs, Glucocorticoids, Anticancer drugs) Flashcards

1
Q

NSAID–albumin dissociates at what

A

low PH (of inflammatory site)

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2
Q

reasons (4) for ACETAMINOPHEN having a poor AI activity

A

weak COX inhibitor
weak base (all others are w.acids)
less than 20% bound to plasma protein (vs 99%)
no accumulation at inf site

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3
Q

PGE2 & bradykinin: have synergistic effect on what receptor

A

Nociceptive C-nerve pain fibers

released during inflammation

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4
Q

NSAIDS (vs narcotics)

A

tolerance to the analgesic effects does NOT dev w/ chronic use (don’t need to increase dose)
do NOT have addictive properties
NO dependence liability develops

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5
Q

normal tempt

A

98.6 F

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6
Q

fever: induced by which molecule

A

prostaglandin (PG): block PG -> reset tempt back to base line
IL-1, IL-6, TNF-a -> hypothalamus

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7
Q

nsaids for FEVER

A

acetominophen
aspirin
ibuprofen

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8
Q

Reye syndrome

A

def: viral infection (influenza B, chicken pox-vzv) that has been tx’d w/ aspirin

fatal childhood hepatic encephalopathy

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9
Q

dysmenhorrea: mechanism

A

abnormally elevated [PG]
pain directly related to [PG]

PG: inc uterine contraction -> STOP W/ ibuprofen

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10
Q

nsaids for DYSMENHORREA

A

INKDR

ibuprofen 
naproxen 
ketoprofen 
diflunisal 
rofecoxib
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11
Q

life span of plts

A

~ 1 wk

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12
Q

cox1/2 inhibitors vs. cox2 inhibitor on bleeding time

A

cox1/2 inhibitor: significantly inc bleeding time (by blocking cox1 in plts)
cox2 inhibitors: not that diff from normal bleeding time (since doesn’t affect TXA2)

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13
Q

stop NSAIDS if pts have these renal problems - worsened by NSAIDS which blocks PG (that is good for renal function)

A

Na+ retention, edema, hyperkalemia
acute deterioration of renal function
nephrotic syndrome w/ interstitial nephritis
papillary necrosis

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14
Q

NSAIDS hypersensitivity

A

10-20% in asthmatics
within min-hrs after ingestion
s/s like drug allergy but no immune response is involved
rxn: structurally independent

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15
Q

NSAIDS during 3rd trimester results in

A

inc risk of maternal/fetal hemorrhage during delivery (prostacyclin)
dec uterine contractions -> prolonged labor (prostaglandin)
premature closure of fetal ductus arteriosus
high dose aspirin teratogenic in rats (not in humans)

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16
Q

pharmacodynamics - interaction of nsaids w/ other drugs; avoid combination or adjust dose, recognize high risk pt population with these drugs

A 
antihypertensive drugs (b-blockers, diuretics): blunts the drug efficacy  
anticogulants: affects bleeding time
17
Q

antidote for Methotraxate overdose/toxicity

A

(high dose) leucovorin

18
Q

after gene expression analysis: prognostic

A

primary tumor -> prognostic: natural course of the disease (outcome) -> tx or not?

19
Q

after gene expression analysis: PREDICTIVE

A

compare pre vs post tx tumor samples:

prediction of drug efficacy/resistance

  • choice of tx
  • prediction of drug efficacy or drug resistant
20
Q

mechanism of drug resistance: mutational heterogeneity in a single cancer

A

have subclones w/ unique genotype or ‘driver’ mutation

21
Q

Prednisone

A

binds to intra-cytoplasmic receptor
alters gene transcription

most commonly used glucocorticoids in cancer chemo

22
Q

circadian rhythm of plasma [cortisol]

2-20ug

A

give cortisol in AM & LATE AFTERNOON (for replacement therapy)
draw blood at constant/same time (to measure cortisol)

Cushing’s Disease: no circadian changes in cortisol level

23
Q

corticosteroid nucleus SUBSTITUTION results in (3)

A
  1. change in glucocorticoid potency = AI efficacy (DIRECT)
  2. change in mineralocorticoid potency
  3. prolong plasma & biological half-life
24
Q

2 non-endocrine tx use of glucocorticoids that are not AI/immunosuppresive

A

shock

neurological diseases

25
Q

glucocorticoid AI activity: mechanism (3)

A
  1. block receptors that induce inf cytokine protein synthesis
  2. inhibit PROSTAGLANDIN, cox2 synthesis
  3. lymphocyte trafficking - move them away from their usual posts
    (move lympocytes: blood -> lymphoid tissue)
    (increase blood neut by dec adherence molecules and preventing accumulation at inf site)
26
Q

Lipocortin

A

synthesized by corticosteroids to block phospholipaseA2 (anti-inflammatory effect)

27
Q

complications of glucocorticoid tx

A

GI (due to dec PG)
CV (mineralo activity)
metabolic (inc glucose -> inc insulin)
endocrine: growth failure, secondary amenorrhea, suppress axis system
inhibit fibroplasia (impared wound healing, skin tissue atrophy)
immune suppression (breakdown of protein by gluco to make glucose, WBCs have lots of protein)

therefore, c/i in pts w: peptic ulcer, HT, infection, diabetes

Glaucoma, osteoporosis, psychosis

Q1 (7 decks)

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