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NSAIDs Flashcards

(45 cards)

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1
Q

In general the 4 therapeutic uses of NSAIDs are…

A

Analgesia, Antipyretic effect, Anti-inflammatory effect, and Antithrombogenesis

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2
Q

Common side effects of NSAIDs

A

GI side effects: Ulceration, bleeding, nausea. Increased incidence of bleeding problems. Renal side effects: Acute renal failure and interstitial nephritis. Uterine side effects: Interference with uterine contractions in late-term pregnancy. Increased thrombotic events: Potential for increased cardiovascular events, including myocardial infarction and strokes

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3
Q

How are the 4 main groups of NSAIDs distinguished?

A

Distinguished by selectivity for COX-1 vs COX-2 and reversible vs irreversible inhibition of COX.

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4
Q

Defining characteristics of traditional NSAIDs

A

Reversible inhibition of COX-1 and COX-2

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5
Q

Therapeutic uses of traditional NSAIDs

A

Analgesia, Antipyretic effect, Anti-inflammatory effect. Because they inhibit COX-1 and COX-2 reversibly.

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6
Q

Name 3 traditional NSAIDs (that we need to know). Generic and brand name.

A

Ibuprofen [Advil, Motrin], Naproxen [Aleve, Naprosyn], Ketorolac [Toradol]

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7
Q

How is Acetaminophen [Tylenol] different from other NSAIDs?

A

No inhibition of either COX-1 or COX-2 in periphery, it reversibly inhibits CNS COX-2. For this reason there is no anti-inflammatory effect and less GI side effects. It has analgesic and antipyretic effects.

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8
Q

Selective CNS COX-2 inhibitor

A

Acetaminophen [Tylenol]

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9
Q

Name a COX-2 selective inhibitor

A

Celecoxib [Celebrex]

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10
Q

How does celecoxib [Celebrex] differ from other NSAIDs?

A

Selective reversible inhibition of COX-2 only. Analgesic, antipyretic, anti-inflammatory activities. Less GI side effects.

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11
Q

Irreversible inhibitor of COX-1 and COX-2

A

acetylsalicylic acid aka Aspirin

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12
Q

How does acetylsalicylic acid [Aspirin] differ from other NSAIDs?

A

Irreversible inhibition of COX-1 and COX-2]: Analgesic, antipyretic, anti-inflammatory, antithrombotic activities.

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13
Q

Pharmacokinetics of traditional NSAIDs

A

Rapid, complete absorption; >90% protein-bound; renal excretion or liver metabolism

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14
Q

How does ketorolac differ from ibuprofen and naproxen?

A

Ketorolac [Toradol] is given IM/IV while ibuprofen and naproxen are given orally. Ketorolac [Toradol] is available for treatment of post-surgical pain.

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15
Q

Overdose with traditional NSAIDs vs aspirin

A

generally better tolerated and safer in overdose than aspirin

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16
Q

Side effects of traditional NSAIDs on GI Tract

A

Interfere with gastric cytoprotection by inhibition of COX-1 PGE synthesis, leads to dyspepsia and gastric ulceration. Lowest risk with ibuprofen – highest with naproxen.

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17
Q

Side effects of traditional NSAIDs on Platelets

A

Interfere with platelet aggregation by inhibition of COX-1 thromboxane A2 synthesis, leads to promotion of bleeding. Aspirin effect lasts 4-7 days (lifetime of a platelet, b/c irreversible inhibitor), whereas effect of other NSAIDs last about 2 days (dependent on half-life)

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18
Q

Side effects of traditional NSAIDs on Kidneys

A

Cause renal vasoconstriction by inhibition of COX-1 and COX-2 PGE synthesis and loss of vasodilator actions, leads to reversible renal insufficiency. NSAIDs can cause fluid retention – caution advised for use in patients with risk of / or CVD.

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19
Q

Compare cardiovascular risk of ibuprofen, celecoxib, and naproxen

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A

Lowest cardiovascular risk with naproxen – highest with ibuprofen and celecoxib.

20
Q

Compare risk associated with aspirin, acetaminophen, ibuprofen, naproxen, ketorolac, celecoxib in pregnancy

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A

Traditional NSAID (ibuprofen, naproxen, ketorolac) use during pregnancy not recommended (especially 3rd trimester), “safety not established”. Celecoxib: category C, but category D in 3rd trimester due to inhibitory effect on uterine prostaglandins necessary for labor contractions. Acetaminophen: considered safe in all stages of pregnancy (at therapeutic doses for short-term use). Aspirin: generally avoid use during pregnancy, especially 3rd trimester (can delay onset of labor).

21
Q

Therapeutic effect of Celecoxib and Pharmacodynamics

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A

analgesic, antipyretic, and anti-inflammatory actions; Selectivity for reversible inhibition of COX-2 over COX-1 is 5-7 fold

22
Q

Selective COX-2 inhibitor is used for what diseases/conditions? Why?

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A

Indicated for rheumatoid arthritis; osteoarthritis, dysmenorrhea, acute pain in adults. Better in long-term use because of less GI side effects.

23
Q

What is the advantage and disadvantage of COX-2 selective inhibitors with regards to platelets?

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A

No inhibition of COX-1 mediated TXA2 synthesis in platelets, so no bleeding risk. But, Inhibition of endothelial COX-2 could reduce antithrombotic PGI2 activity relative to prothrombotic TXA2, so increases risk of ischemic CVD and HF.

24
Q

What patients may be allergic to Celecoxib?

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A

Celecoxib [Celebrex] is sulfonamide i.e. patients with sulfa allergy.

25
Possible side effects of COX-2 inhibitor on Kidneys
Similar to non-selective NSAIDs and can precipitate acute renal failure. Avoid use in at-risk patients.
26
Pharmacodynamics of Acetaminophen [Tylenol]
Equivalent to aspirin as analgesic or antipyretic agent, but less anti-inflammatory properties (no inhibition of COX-1 or COX-2 at peripheral sites of inflammation, but possibly selective for inhibition of CNS prostaglandin synthesis [COX-2])
27
Pharmacokinetics of Acetaminophen [Tylenol]
Absorption related to gastric emptying, peak levels in 30-60 min. Metabolized to inactive sulfate and glucuronide (phase II conjugation); in large doses metabolized to product toxic to liver. In overdose, glutathione stores are depleted and are no longer able to inactivate the toxic metabolite, leading to liver damage.
28
Advantage of Acetaminophen [Tylenol] over other NSAIDs. Why does it have this advantage?
Little risk of GI dyspepsia-ulceration, bleeding, or renal dysfunction because no inhibition of COX-1 or COX-2 in the periphery--only in the CNS.
29
Adverse effects of acetaminophen [Tylenol]
Hepatotoxicity. Most common cause of acute liver failure in US. Liver damage seen with as little as single 6 gm dose; also 5-8 g/day for several weeks or 3-4 g/day for 1 year (children appear less susceptible to liver toxicity). Alcohol induces the enzyme (CYP2E1) that produces hepatotoxic metabolite, thus liver damage may occur at lower doses with concomitant alcohol consumption
30
Dose limits of Acetaminophen for safe use
Max dose at 4000 mg / 24 hrs - OTC recommended max dose of 3250 mg
31
What is the maximal efficacious dose of acetaminophen [Tylenol]?
650 mg. 1000 mg dose does NOT provide more analgesic efficacy than 650 mg but it does increase risk of hepatotoxicity.
32
Pharmacodynamics of acetylsalicylic acid [Aspirin]
Irreversible inhibition of cyclooxygenase (COX) 1 and 2
33
What kind of pain is aspirin best for? Which is it worst for?
Best: Pain of inflammatory origin (pain of muscular / vascular origin, postpartum states, arthritis, bursitis, dental pain). Worst: Less effective for visceral pain (acute abdomen, renal colic, pericarditis, MI), i.e., pain that is caused by direct stimulation of sensory nerves (Aδ)
34
What are the 2 mechanisms that allow for aspirin's inhibition of platelet aggregation?
Low-dose aspirin is essentially platelet COX-1 selective. (1) Platelets cannot synthesize new COX-1 enzyme, thus TXA2 synthesis is inhibited for life of platelet (\> 8 days). (2) Largest concentration of acetylsalicylic acid is presystemic in portal vein (prior to hepatic metabolism by esterases), thus greater effect on circulating platelet COX-1 (TXA2 synthesis) relative to tissue endothelial cell COX-2 (prostacyclin synthesis) resulting in a decreased tendency for clotting.
35
Side effects of Aspirin
Gastric irritation, increased bleeding time, renal dysfunction, avoid in pregnancy (can delay onset of labor--like other peripherally-acting NSAIDs), Reye’s syndrome
36
What is Reye's syndrome? What are its signs and symptoms? How do you prevent it?
Occurs in salicylate use only. Liver damage encephalopathy unexpected vomiting, sleepiness. Avoid use if flu or other viral infections present (esp., Varicella/chicken pox).
37
What are the signs and symptoms of Aspirin poisoning--mild and acute? What is a lethal dose?
Mild intoxication: Headache, dizziness, tinnitus, visual disturbances, mental confusion, drowsiness, sweating, thirst, hyperventilation, n/v, diarrhea. Acute intoxication (lethal dose: 10-30 grams): Vomiting, fever, and sweating (uncouples oxidative phosphorylation) leading to respiratory alkalosis followed by respiratory and metabolic acidosis. Death usually due to severe acidosis / electrolyte imbalance.
38
What are the 2 most important/common drug-drug interactions of Acetylsalicylic acid [Aspirin]?
Warfarin, heparin. Inhibit platelet function hemorrhage. Avoid concomitant use. Alcohol. Additive gastric irritation internal bleeding. Avoid concomitant use.
39
What reaction does Cyclooxygenase catalyze? What is the product of the reaction converted to?
Arachidonic acid to PGH2, which in turn is converted to either PGD2, PGE2, PGF2, PGI2 (prostacyclin), or TXA2.
40
What are the main locations of the constitutively expressed COX-1? What are the effects at these sites?
GI tract: [PGE2/PGI2/PGF2]: Secretions: acid/pepsin secretion, mucous/bicarbonate production (cytoprotective effects); Smooth muscle [PGE2/PGF2]: contractions; Platelets [TXA2]: Pro-aggregatory effect; Kidneys [PGE2/PGI2]: Renal blood flow, promotion of diuresis; Vascular smooth muscle: PGI2/PGE2: vasodilation; TXA2: vasoconstriction; Bone [PGE2]: Stimulates bone formation and resorption.
41
Where is the inducible COX-2 expressed? What are its effects at these sites?
Areas of pain/inflammation [PGE2 / PGI2]: Enhance edema formation and leukocyte infiltration via vasodilation; potentiation of bradykinin pain-producing activity; Hypothalamus/Fever [PGE2]: Increase in heat generation and decrease in heat loss; Kidneys [PGE2/PGI2]: Renal adaptation to stresses via maintenance of renal blood flow, most critical in elderly and when renal function deteriorates; Endothelial cells [PGI2]: Vasodilation and anti-aggregatory platelet effects; Uterine smooth muscle [PGE2/PGF2]: Contributes to labor contractions near parturition; Ductus arteriosus [PGE2]: Maintenance of patent ductus arteriosus via vasodilatory effects
42
What reaction does 5-Lipoxygenase catalyze? What is the product converted to and where?
Arachidonic acid to Leukotriene A4, which is converted to leukotriene B4 (LTB4) in neutrophils, LTB4 diffuses into mast cells, eosinophils, basophils, and macrophages for conversion into the cysteinyl leukotrienes (CysLTs) LTC4, LTD4, and LTE4.
43
What are the biologic effects of LTB4, LTC4, LTD4, and LTE4?
LTB4: Neutrophil chemotaxis, aggregation, and transmigration through endothelium. LTC4 / LTD4 / LTE4: Increased vascular permeability, bronchoconstriction, vasoconstriction. Important role in pathophysiology of asthma, psoriasis, and various arthritic/allergic/hypersensitivity processes.
44
Can you draw the pathways that arachidonic acid is involved in and the effects of its products?
45
Can you draw the pathways that COX-1 and COX-2 are involved in?

Pharmacology (2 decks)

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