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Bloc F - Defense > Mar22 M2-Antipyretics > Flashcards

Mar22 M2-Antipyretics Flashcards

1
Q

3 drugs discussed in fever

A
  • NSAIDs
  • aspirin
  • acetaminophen
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2
Q

cytokines of fever and end result

A

IL-1B, IL-6, TNF-a, INF. regulate secretion of PGs

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3
Q

initial fever response

A

ceramide release from the anterior hypothalamus neurons

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4
Q

late fever response

A

induction of COX-2 and microsomal PGE synthase-1 in endothelium of blood vessels in preoptic hypothalamic area to form PGE2

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5
Q

What’s the effect of PGE2 (from blood vessels of preoptic area)?

A
  • binds EP3 and EP1 Rs on thermosensitive neurons of hypoth.
  • more heat gen and less heat loss
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6
Q

steps to PGE2 synthesis

A
  1. phospholipase A2 cleaves phospholipid membrane of the cell to make AA
  2. AA made into PGH2 by COX1 and COX2
  3. PGH2 can become diff things depending on tissue specific enzymes (one of these is PGE2)
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7
Q

how NSAIDs work

A

block reversibly COX enzymes. so inhibit PG synthesis

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8
Q

3 major NSAIDs (and anti-pyretics) actions

A
  • analgesia
  • anti-pyretic
  • anti-inflammatory (exept acetaminophen)
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9
Q

how aspirin has an anti-pyretic action

A

blocks COX1 and COX2 irreversibly (NSAIDs and acetaminophen DON’T DO THAT) so blocks PG synthesis

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10
Q

other thing aspirin can do

A
  • anti-platelet, anti-thrombotic effect

- decreases platelet prod of TXA2 bc blocks COX-1 (this is with low dose aspirin).

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11
Q

main worries with aspirin and NSAIDs (adverse effects)

A
  • pregnancy
  • GI bleeding
  • renal problem (will block EA of nephron and reduce water, NA, K excretion but not bad in healthy kidney. bad in HF, dehydration, older people)
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12
Q

anti-pyretics that can cause sensitivity reactions

A
  • aspirin (ASA, salicylate)
  • NSAID
  • acetaminophen doesn’t*
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13
Q

charact. of anti-pyretic sensitivity rx

A
  • because of histamine release (not immuno mediated)

- rhinitis, asthma, urticaria (hives), laryngeal edema, bronchospasm

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14
Q

why anti-pyretics (NSAIDs and aspirin) can cause hypersensitivity rx

A

inhibit COX so more AA shunted to leukotriene pathway. leukotrienes cause these symptoms

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15
Q

tx of febrile pt with anti-pyretic hypersensitivity

A

acetaminophen for the fever

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16
Q

3 effects that antipyretics can have (each is better at some things)

A
  • analgesia
  • anti-pyretic
  • anti-inflammatory (exept acetaminophen)
17
Q

naproxene best thing it does

A

anti-inflammatory (less for fever or pain relief)

18
Q

risk factors for GI effects (bleeding) of aspirin and NSAIDs

A
  • age over 65
  • multiple NSAID use
  • peptic ulcer or bleeding hx
  • high dose
  • alcohol
  • anticoagulant use
19
Q

how NSAID effect on PGs affects GIT (bleeding)

A

loss of protection from PGs in stomach

  • less inhibition of acid secretion
  • less protective mucus
  • less mucosal blood flow
20
Q

how NSAID anti-platelet effect affects GIT (bleeding)

A

lose TXA2 actions

  • harder to coagulate (platelet aggreg inhibited)
  • loss of vasoconstriction
21
Q

people in whom you can’t use an anti-pyretic with anti-coag effect

A

people that don’t have CV (healthy people with normal coag and CV health)
*bc will disturb coagulation

22
Q

one thing aspirin doesn’t do well

A

pain relief

23
Q

active ingredient in aspirin

A

salicylate (ASA becomes salicylate)

24
Q

half life of ASA before it becomes salicylate (the active ingredient)

A

15 min

25
Q

half life of low-dose vs high-dose salicylate

A

low dose = 2-3 hrs

high dose = 12-15 hrs

26
Q

consequences of aspirin overdose

A
  • metabolic acidosis and respiratory alkalosis (S in MUDPILES)
  • tinnitus (constant whistling in the ear)
27
Q

ibuprofen good at what and bad at what

A
  • used as anti-pyretic and analgesic
  • ok to reduce inflam but not the best (use naproxen instead)
  • NOT used as anti-coagulant
28
Q

acetaminophen good at what and bad for what

A 
good = anti-pyretic and analgesic
bad = anti-inflam and anti-platelet
29
Q

acetaminophen mechanism of action and why no anti-inflam or anti-coag effect

A
  • inhibition of neuronal and vascular PGE2 (PGE2 INHIBITION ONLY IN THE BRAIN)
  • doesn’t inhibit inflammatory PGE2
  • doesn’t inhibit TXA2
30
Q

main worry when using acetaminophen

A
  • hepatoxicity over 4g a day or below if binge drink before
  • hepatic centrilobular necrosis
  • AST over ALT > 1000
31
Q

treatment of acetaminophen toxicity

A

n-acetylcysteine orally

Bloc F - Defense (57 decks)

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