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Pharmacyology 3 > Aspirin > Flashcards

Aspirin Flashcards

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1
Q

Prostaglandins are major mediators of

A

pain
fever
inflammation

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2
Q

COX leads to…

A
  • Prostaglandins
  • thromboxane
  • prostacyclin
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3
Q

RLS in PG synthesis

A

COX

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4
Q

COX-1 is _____ expressed

A

constitutively

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5
Q

Where does COX1 work?

A
  • CNS: fever/pain
  • peripheral: pain
  • stomach: protect mucosal lining
  • platelets: increase platelet aggregation and blood clotting
  • regulate kidney function
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6
Q

Prototype COX-1 inhibitor

A

aspirin

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7
Q

COX2 is ____ expressed ____

A

constitutively expressed isozyme

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8
Q

Where does COX2 work?

A
  • CNS: pain
  • stomach: protect mucosal lining
  • endothelial cells: decrease platelet aggregation
  • wound healing, bone repair
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9
Q

COX1 work in platelets or endothelial cells?

A

Platelets: increase platelet aggregation

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10
Q

COX2 work in platelets or endothelial cells?

A

endothelial cells: decreases platelet aggregation

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11
Q

COX2 has a ____ isozyme that is critical for inflammation

A

inducible

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12
Q

COX1 or COX2 key target for NSAID anti-inflammatory effects?

A

COX2

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13
Q

Prototype COX2 inhibitor

A

Celecoxib

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14
Q

Most NSAIDs inhibit both COX1 and COX2, usually stronger on ______. This makes them useful for treating what?

A

COX1

  • pain (1 and constitutive 2)
  • fever (1)
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15
Q

COX1 and COX2 suppression of inflammation

A

require high doses

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16
Q

COX 2 inhibitor drugs used for

A
  • inflammation
  • sometimes pain
  • fewer unwanted COX1 adverse effects
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17
Q

Prototype of all NSAIDs and non-opioid analgesics

A

Aspirin

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18
Q

Aspirin is ____ ___

A

acetyl-salicylic acid

- rapidly hydrolyzed (de-acetylated) to salicylic acid

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19
Q

The anti-inflammatory and analgesic effects of aspirin are mediated by its ______ metabolite

A

salicylate

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20
Q

Salicylate are what type of inhibitors?

A

reversible

competitive

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21
Q

T/F salicylates are distributed throughout body

A

True

- including CNS for fever/pain

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22
Q

Aspirin is ____% protein bound in plasma

A

80%

  • slow accumulation of free drug
  • drug interactions from displacing warfarin, methotrexate, sulfonamides
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23
Q

At low to moderate doses, salicylate is metabolized where? what kinetics?

A
  • liver by conjugation
  • first order
  • saturable
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24
Q

At higher doses, salicylate is metabolized where? what kinetics?

A
  • unmetabolized by kidneys
  • zero order
  • OATs
  • half-life increases with increasing dose
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25
Lower doses of aspirin effects
analgesic anti-pyretic COX1 response
26
Higher doses of aspirin effects
- anti-inflammatory | - COX2 response
27
Low doses of aspirin how is it excreted?
glycine salts | glucuronide salts
28
Higher doses of aspirin how is it excreted?
free salicylate excretion
29
Aspirin amount for analgesia, anti=pyresis
2 tablets | 650mg
30
Aspirin amount for anti inflammation
5 tablets
31
Aspirin t1/2 for low dose
2 hour
32
Aspirin t1/2 for moderate dose
10-12 hour
33
Aspirin t1/2 for high dose
15-30 hour
34
Is aspirin good for pain of inflammation?
yes! | inhibit pain and underlying inflammation
35
Unique use of aspirin
prevent thrombus formation (blood clotting) | prolong bleeding time
36
Aspirin can _____ inactivate COXs in some tissues by _____ acetylating enzyme
irreversible | covalently
37
____ near the site of GI absorption are the main cells exposed to acetyl-salicylic acid and covalent acetylation of COXs
platelets
38
Major current use of aspirin
prevent MI and stroke
39
lifetime of platelets
7 days
40
Why is MI and stroke a unique feature of aspirin?
- covalent acetylation of COX - irreversible and prolonged action - acetyl effect! not salicylate!
41
Side effects of aspirin
- bleeding (even at low doses)
42
CI aspirin
clotting deficiency
43
To ensure adequate clotting during and after surgery aspirin is stopped ____ days prior to surgery
7-10 days
44
Other possible uses of Aspirin
reduce GI cancer risk | AD
45
Platelets use ___ to make thromboxanes
COX1 | - increase clotting and thrombosis risk
46
Endothelial cells use ____ to make prostacyclins
COX2 | - decrease clotting and thrombosis risk
47
Low aspirin dose and thrombosis
- anti-thrombosis PGIs formation from endothelial cells
48
Prolonged inhibition of platelet COX1 causes _______
sustained reduction in Txs
49
Current aspirin recommendation for thrombosis prevention
75-81 mg | - if benefit outweighs risk of GI hemorrhage
50
Enteric coating to reduce ____
GI distress
51
Cautions of aspirin
- premature closure of ductus arterioles - avoid 3rd trimester - renal and hepatic toxicities (long term use, elderly)
52
Salicylism
mild toxicity - from excess chronic use in older adults - tinnitus, dizzy, HA, confusion, deafness - drowsy, thirst, N/V
53
low dose aspirin toxicity
- increase O2 consumption, CO2 production - stimulates respiration - exces CO2 inhaled
54
high dose aspirin toxicity
- respiratory alkalosis
55
Adverse effects of aspirin
- GI irritation - GI bleeding - peptic ulcers - CV effects - induce asthma attacks
56
____ is responsible for 15,000 aspirin related deaths
GI hemorrhage
57
Reyes syndrome
- aspirin | - do not use <16
58
overdose aspirin
- children ingest large dose: >150 lethal - GI disturbance - CNS disturbance - fever, dehydration, sweating - skin eruptions - metabolic acidosis, hypokalemia - decrease blood flow
59
______ is eventual cause of death in aspirin OD
- respiratory failure | - respiratory depression: respiratory acidosis
60
Low dose aspirin acid base effect
- increased CO2 | - acidosis
61
Low dose aspirin respiratory effect
compensation for acidosis by respiration
62
low dose aspirin serum pH
normal
63
higher dose aspirin acid base effect
- compensation for alkalosis by HCO3 excretion
64
higher dose aspirin respiratory effect
direct stimulation leads to alkalosis
65
higher dose aspirin serum pH
normal
66
toxic dose aspirin acid base effect
metabolic acidosis | renal + respiratory
67
toxic dose aspirin respiratory effect
central depression produces acidosis
68
toxic dose aspirin serum pH
acidic with organ failure
69
treating OD in aspirin
- hospitalize and maintain vital signs - whole bowel irrigation - activated charcoal - hasten elimination
70
How to hasten elimination of aspirin
- volume repletion - alkalization of urine with sodium bicarb - ion trapping

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