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GI/Liver > Lec 13 NSAIDS/Aspirin > Flashcards

Lec 13 NSAIDS/Aspirin Flashcards

1
Q

Aspirin: mech of action

step1

A

Irreversibly inhibits cyclooxygenase (both COX-1 and COX-2) enzyme by covalent acetylation.

Platelets cannot synthesize new enzyme, so effect lasts until new platelets are produced:
decrease bleeding time, inhibit TXA2 and prostaglandins. No effect on PT [prothrombin time] or PTT [partial thromboplastin time].

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2
Q

How long does anti-platelet effect of aspirin last?

A

8-10 days —> need to be off aspirin for at least 7 days before surgery

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3
Q

Which prostaglandins increase body temp?

A

PGE2, PGF2, PGI2

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4
Q

Which prostaglandins are pro-inflammatory?

A

PGE2, PGI2

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5
Q

What is clinical use of aspirin?

A

Antipyretic, analgesic, anti-inflammatory, anti platelet aggregation.

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6
Q

Aspirin: toxicities?

A

Gastric ulceration, tinnitus (CN VIII).

Chronic use can lead to acute renal failure, interstitial nephritis, and upper GI bleeding.

Reye syndrome in children with viral infection.

Overdose causes respiratory alkalosis initially, which is then superimposed by metabolic acidos

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7
Q

What is reye syndrome?

A

childhood hepatoencephalopathy
= swelling of liver and brain

associated w/ viral infection [esp VZV and influenza B] that was treated w/ aspirin

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8
Q

What is mech of reyes?

A

aspirin metabolites decrease beta-oxidation by inhibition of mitochondrial enzyme

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9
Q

What are clinical findings of reyes?

A
  • mitochondrial abnormalities
  • fatty liver
  • hypoglycemia
  • vomitting
  • hepatomegaly
  • coma
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10
Q

What is samter’s triad sensitivity?

A
  • aspirin sensitivity
  • nasal polyps
  • asthma
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11
Q

How is ASA distributed?

A

widely distributed = 75-90% protein bound

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12
Q

How is ASA metabolized/excreted?

A

metabolized in liver; excreted renally as salicyluric acid

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13
Q

What are signs of aspirin overdose?

A 
headache
tinnitus/ hearing impairment/ dizziness due to direct effect on cochlear hair cells
decreased vision
N/V
bleeding
fever
acid base derangement
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14
Q

What kind of acid base derangement in aspirin overdose?

A
  • respiratory alkalosis initially due to stimulation of medulla resp centers
  • then superimposed metabolic acidosis: from salicylic acid and uncoupling of oxidative phosphorylation resulting in lactic acid
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15
Q

How does mech of action of aspirin differ from that of ibuprofen?

A

both are non-selective cox inhibitors

aspirin is irreversible; ibuprofen is reversible

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16
Q

Can you use dialysis to treat aspirin overdose?

A

no because it has a huge volume of distribution –> most is protein bound and will not go through dialysis membrane

17
Q

Ibuprofen: mech

A

Reversibly inhibit cyclooxygenase (both COX-1 and COX-2). Block PG synthesis.

18
Q

Ibuprofen: clinical use

A

Antipyretic, analgesic, anti-inflammatory

19
Q

Ibuprofen: toxicity

A

Interstitial nephritis, gastric ulcer (PGs protect gastric mucosa), renal ischemia (PGs vasodilate afferent arteriole).

20
Q

What are the 5 NSAIDS?

A
  • Ibuprofen
  • Naproxen
  • Indomethacin
  • Ketorolac
  • Diclofenac
21
Q

Celecoxib: mech

A

Reversibly inhibit specifically the cyclooxygenase (COX) isoform 2, which is found in inflammatory cells and vascular endothelium and mediates inflammation and pain; spares COX-1, which helps maintain the gastric mucosa.

Thus, should not have the corrosive effects of other NSAIDs on the GI lining. Spares platelet function as TXA2 production is dependent on COX-1.

22
Q

Celcoxib: clinical use

A

Rheumatoid arthritis and osteoarthritis; patients with gastritis or ulcers.

23
Q

Celcoxib: toxicity

A

increases risk of thrombosis. still have renal symtpoms

Sulfa allergy.

24
Q

Acetaminophen: mech

A

weakly reversibly inhibits cyclooxygenase, mostly in CNS. Inactivated peripherally.

25
Q

Acetaminophen: clinical use

A

Antipyretic, analgesic, but not anti-inflammatory.

Used instead of aspirin to avoid Reye syndrome in children with viral infection.

26
Q

Acetaminophen: toxicity

A

Overdose produces hepatic necrosis; acetaminophen metabolite (NAPQI) depletes glutathione and forms toxic tissue adducts in liver.

27
Q

What is treatment for acetaminophen toxicity

A

N-acetylcysteine is antidote—regenerates glutathione.

28
Q

WHat is the major metabolite of acetaminophen that leads to hepatotoxicity?

A

NAPQI

GI/Liver (36 decks)

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