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Immunity, Infection and Disease > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

The four main effects seen in NSAIDs

A

Anti-platelet, analgesic, anti-pyretic, anti-inflammatory

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2
Q

Salicylic acid

A

Topical keratolytic agent. Not an NSAID

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3
Q

Methyl salicylate

A

Topical for muscle aches (Ben Gay, Icy Hot, etc). Toxic if taken internally

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4
Q

Aspirin

A

Acetyl-salicylic acid (ASA). Prototype NSAID, organic acid salicylate derivative

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5
Q

What is the pKa of ASA?

A

3.5

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6
Q

Does ASA affect COX-1 or COX-2 and reversibly or irreversibly?

A

Inhibits both irreversibly by acetylating them

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7
Q

What are non-acetylated salicylates used for?

A

Anti-inflammatory effects used for osteoarthritis and rheumatoid arthritis

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8
Q

Name four non-acetylated salicylates

A

Sodium salicylate, choline magnesium trisalicylate, salsalate, diflunisal

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9
Q

Do the antiplatelet effects of ASA occur at low or high doses?

A

Quite low doses (60-80 mg daily)

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10
Q

What is the mechanism for the antiplatelet effects of ASA?

A

Inhibiting Thromboxane A2 synthesis in platelets by inhibiting platelet COXs (persists for life of platelet, 8-12 days)

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11
Q

How does ASA achieve analgesia in the periphery?

A

Inhibiting PG synthesis (PGI2 and PGE2 synergize with bradykinin and histamine to produce inflammation)

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12
Q

How does ASA achieve analgesia in the CNS?

A

Inhibiting PG synthesis (PGE2 causes Ca influx resulting in release of pain NTs (sub P, aspartate, glutamate, CGRP))

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13
Q

In what patients will ASA not lower body temperature?

A

Those that do not have a fever

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14
Q

How does ASA achieve antipyresis?

A

Cytokines produce PGE2 in preoptic hypothalamic area which increases cAMP to increase set point. ASA inhibits PGE2 synthesis

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15
Q

Do the anti-inflammatory effects of ASA occur at low or high doses?

A

High doses (3250 to 3900 mg)

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16
Q

ASA has anti-inflammatory effects mainly through inhibition of PG synthesis. What non PG-dependent mechanisms does ASA use to fight inflammation?

A

Inhibit neutrophil chemotaxis, stabilize lysosomes, and prevent vascular permeability. These inhibit PMN and monocyte migration to site of inflammation

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17
Q

Aspirin has a pKa of 3.5 Does the stomach absorb it when gastric pH is above or below 3.5?

A

Below 3.5

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18
Q

How does ASA damage gastric mucosa?

A

It gets trapped their due to intracellular pH being above its pKa (while gastric pH is below). Then acidic properties of ASA damage cell

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19
Q

What is ASA first metabolized to and by what?

A

To salicylate ion by tissue and plasma esterases

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20
Q

Why is sustained release not a good option for ASA?

A

Because it is subject to high levels of first pass metabolism

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21
Q

Salicylate is the first metabolite of ASA. To what is salicylate normally bound in blood?

A

Albumin

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22
Q

Salicylate is the first metabolite of ASA. Does salicylate have any pharmacologic action?

A

Yes it is a reversible inhibitor of COX (ASA is an irreversible inhibitor of COX)

23
Q

What property of distribution may increase the gastric effects of an NSAID?

A

Enterohepatic recirculation

24
Q

Symptoms of NSAID hypersensitivity

A

Vasomotor rhinitis, angioedema, generalized urticaria (hives), bronchial asthma, layngeal edema, bronchoconstriction, flushing, hypotension, shock

25
Q

Are individuals with ASA intolerance more likely to have hypersensitivity to other NSAIDs?

A

Yes. ASA intolerance is a contraindication for other NSAIDs

26
Q

What plasma level of salicylate poisoning is consistent with overdose and what are the symptoms?

A

30 to over 160 mg/dL, hyperventilation, metabolic acidosis, hyperpyrexia, coma, renal vasomotor and respiratory failure

27
Q

What can cause Reyes syndrome?

A

Use of NSAIDs in children with fever caused by viral illness (or given varicella virus vaccine). Reyes is very serious

28
Q

Drug interactions of ASA

A

Anticoagulants (warfarin, heparin, etc), Alcohol (GI bleeding), Methotrexate (increases methotrexate toxicity)

29
Q

For the following are they constitutive or inducible: COX-1 and COX-2

A

COX-1 is constitutive, COX-2 is inducible

30
Q

Is COX-1 more related to the TXA pathway or PGI2 pathway, and what does that mean for its effects on coagulation?

A

More related to TXA pathway. Inhibiting solely COX-1 leads to excessive bleeding

31
Q

Is COX-2 more related to the TXA pathway or PGI2 pathway, and what does that mean for its effects on coagulation?

A

More related to the PGI2 pathway (which inhibits platelet aggregation). Sole inhibition of COX-2 can lead to hypercoagulability (stupid Vioxx)

32
Q

Which COX is found everywhere, and which is found mainly at sites of inflammation?

A

COX-1 found everywhere, COX-2 found mainly at sites of inflammation (and in kidney and endothelial cells)

33
Q

Name two COXs that are variants of other COXs

A

COX-3 is variant of COX-1 and COX-2b is variant of COX-2

34
Q

Which non-selective COX inhibitors are irreversible, and which are reversible

A

ASA is irreversible, all other salicylates and organic acid NSAIDs are reversible

35
Q

What type of compounds are selective COX-2 inhibitors?

A

Organic sulfur containing compounds

36
Q

Are selective COX-2 inhibitors reversible or irreversible?

A

Slowly reversible

37
Q

Ibuprofen

A

Propionic acid derivative NSAID. 20x more potent inhibitor of COX as apirin

38
Q

Naproxen

A

Propionic acid derivative NSAID. 20x more potent inhibitor of COX as apirin

39
Q

Name some acetic acid derivative NSAIDs

A

Ketorolac (Toradol), Indomethacin, Sulindac, Nabumetone, Diclofenac, Etodolac, Tolmetin

40
Q

What is the equivalency between potency (in dose) of ketorolac (IM) and morphine (IM)

A

30 mg ketorolac IM is equivalent to 6 to 12 mg morphine IM

41
Q

What NSAID is used for patent ductus arteriosis and what are its other uses?

A

Indomethacin. Also used for arthritis (e.g. ankylosing spondylitis) and acute gout

42
Q

Which acetic acid derivative NSAID is given as a prodrug?

A

Sulindac

43
Q

Which NSAID suppresses familial intestinal polyposis?

A

Sulindac

44
Q

What characteristics are unique about Nabumetone (Relafen)?

A

Less gastric effects (non-acidic prodrug), very little antiplatelet effects, once daily dosing

45
Q

Name three selective COX-2 inhibitors

A

Celecoxib (Celebrex), Rofecoxib (no longer on market), Valdecoxib (Vioxx, no longer on market)

46
Q

What are the effects of acetaminophen?

A

Anti-pyretic, analgesic (NOT ANTI-INFLAMMATORY)

47
Q

What is the mechanism of acetaminophen?

A

Inhibition of COX-1 and COX-2 in CNS, but not in periphery. Also strong inhibition of COX-3

48
Q

When do peak blood levels of acetaminophen occur and what is its half life?

A

30 to 60 min, half life is 2 hours

49
Q

Metabolism of acetaminophen

A

95 percent goes glucuronidation and suflation, 5 percent goes CYP dependent glutathione (GSH) conjugation

50
Q

What toxic metabolite is generated by acetaminophen, is it the primary or alternate pathway, and what clears this toxic metabolite?

A

NAPQI, alternate pathway (primary overwhelmed). Cleared by hepatic GSH, which can be depleted quickly in overdose

51
Q

What treatment is given for acetaminophen overdose and why?

A

N-acetylcysteine, it increases hepatic stores of GSH. Does not reverse any liver damage that has already occurred

52
Q

What nuclear receptor does acetaminophen activate, what does it do, and why is this a problem?

A

Activates Constitutive Androstane Receptor (CAR) which induces CYP1A2, 2E1 and 3A, increasing rate of NAPQI production

53
Q

Drug interactions of acetaminophen

A

Warfarin (hypothrombinemic response with high doses of acetaminophen), Caffeine (may enhance analgesia)

54
Q

Two main adverse reactions with acetaminophen

A

Hepatic necrosis and kidney necrosis (analgesic nephrophathy)

Immunity, Infection and Disease (86 decks)

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