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Pharmacology Winter Exam 2 > L13-15 NSAIDS Lecture > Flashcards

L13-15 NSAIDS Lecture Flashcards

1
Q

3 phases of inflammation

A

Three phases:
1. Acute inflammation
2. Immune response
3. Chronic inflammation

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2
Q

Clinical signs of inflammation:

A
  1. Erythema
  2. Edema
  3. Tenderness (hyperalgesia)
  4. Pain
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3
Q

What are the mediators of acute inflammation?

A
  1. Histamine
  2. Serotonin
  3. Bradykinin
  4. Prostaglandins
  5. Leukotrienes

*prostaglandins: vasodilation, vascular permeability, chemotaxis and pain

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4
Q

What is the most abundant and important precursor of prostaglandins?

A

Arachidonic acid

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5
Q

What is mobilized from membrane phospholipids by phospholipase A2?

A

Arachidonic acid

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6
Q

What are the 4 separate oxygenated routes of arachidonic acid?

A
  1. Cyclooxygenases
  2. Lipoxygenases
  3. Epoxygenases
  4. Free radicals
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7
Q

What does cyclooxygenases pathway produce?

A

COX-1 and COX-2, to form the prostaglandins:
1. Prostacyclin
2. Thromboxane (TXA)

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8
Q

What does lipoxygenases form?

A

Leukotrienes

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9
Q

[COX-1 or COX-2] is mainly responsible for synthesis of prostacyclin in endothelial cells

A

COX-2

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10
Q

What is the general function of COX-1

A

Widely distributed and has “housekeeping” functions
-constitutively expressed

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11
Q

COX-2 expression is induced by what?

A
  • COX-2 is an immediate early response gene product
  • expression is stimulated by growth factors, tumor products and cytokines
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12
Q

Gs receptor (increases/decreases) intracellular Ca++

A
  • decrease intracellular Ca++
    -causing relaxation

Mechanism: increase cAMP —> increase PK —> phosphorylation of outward Ca++ pumps

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13
Q

Gq: (increase or decrease) free intracellular Ca++

A

increase free intracellular Ca++

Mechanism: increase inositol triphosphate (IP3)
- smooth muscle contraction

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14
Q

What does PGE2 and PGI2 cause by decreasing intracellular Ca++?

A

Vasodilation

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15
Q

What is the vascular effect of thromboxane (TXA2)?

A

Vasoconstriction

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16
Q

What contracts bronchial muscles?

A

Thromboxane (TXA2) and PGF2a

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17
Q

What relaxes bronchial muscles?

A

PGE1, PGE2, and PGI2

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18
Q

What are the primary categories of Non-Steroidal Anti-Inflammatory Agents (NSAIDs)?

A

NSAIDs are categorized into:
* Specific COX-2 inhibitors
* Nonspecific COX inhibitors

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19
Q

List some examples of nonspecific COX inhibitors.

A
  • Indomethacin
  • Diclofenac
  • Ketorolac
  • Ibuprofen
  • Naproxen
  • Piroxicam
  • Nabumetone
  • Phenylbutazone
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20
Q

What is the role of arachidonic acid in prostaglandin synthesis?

A

Arachidonic acid is the most abundant and important precursor mobilized from membrane phospholipids by phospholipase A2.

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21
Q

What are the four separate routes that arachidonic acid is oxygenated?

A
  • Cyclooxygenases (COX-1 and COX-2)
  • Lipoxygenases
  • Epoxygenases
  • Free radicals
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22
Q

True or False: COX-1 is constitutively expressed and has ‘housekeeping functions’.

A

True

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23
Q

What triggers the expression of COX-2?

A

COX-2 expression is induced by growth factors, tumor promoters, and cytokines.

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24
Q

What are the effects of prostaglandins and thromboxanes on smooth muscles?

A
  • Vascular effects may be mitogenic, constrictor, or dilator
  • Bronchial muscles may be relaxed or contracted
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25
Q

Fill in the blank: Clinical signs of inflammation include ______, edema, tenderness, and pain.

A

erythema

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26
Q

What are the common adverse effects associated with NSAIDs?

A
  • Vomiting
  • Diarrhea
  • Fever
  • Bronchoconstriction
  • Hypotension or hypertension
  • Syncope
  • Flushing
  • Dizziness
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27
Q

What is the mechanism of action for acetylsalicylic acid (Aspirin)?

A

Aspirin is a nonselective, irreversible inhibitor of COX-1 and COX-2.

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28
Q

What are the primary effects of Aspirin?

A
  • Analgesic effect
  • Antipyretic effects
  • Anti-inflammatory effects
  • Platelet effects (ASA only)
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29
Q

What is the significance of PGE1 (alprostadil) in medical treatments?

A

PGE1 is used to enhance penile erection and keep ductus arteriosus patent in neonates.

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30
Q

What role does PGE2 and PGF2α play in female reproductive health?

A

PGE2 and PGF2α have potent oxytocic actions and are used to promote uterine contractions.

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31
Q

What is the effect of low-dose aspirin on myocardial infarction?

A

Low-dose aspirin inhibits thromboxane synthesis for primary prophylaxis of myocardial infarction.

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32
Q

What is the primary use of zileuton?

A

Zileuton is a lipoxygenase inhibitor effective against asthma.

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33
Q

True or False: Acetaminophen is classified as a non-steroidal anti-inflammatory drug.

A

False

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34
Q

What is the role of Lubiprostone in gastrointestinal treatment?

A

Lubiprostone is a unique gastrointestinal agent that increases intestinal fluid secretion by activating specific ClC-2 chloride channels.

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35
Q

What are the primary mediators of acute inflammation?

A
  • Histamine
  • Serotonin
  • Bradykinin
  • Prostaglandins
  • Leukotrienes
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36
Q

Fill in the blank: The clinical pharmacology of PGE2 (dinoprostone) includes its use for ______, facilitating labor, and treatment of dysmenorrhea.

A

abortion

37
Q

What is the significance of the term ‘prostaglandin’?

A

The term arose from the mistaken belief that prostaglandins in semen came from the prostate.

38
Q

What type of pain does aspirin primarily relieve?

A

Pain arising from integumental structures rather than from hollow viscera.

39
Q

What is the mechanism of action of aspirin in pain relief?

A

Inhibiting prostaglandin synthesis, which is responsible for pain and local inflammation.

40
Q

How does aspirin affect pain receptors?

A

Prevents the sensitization of pain receptors to mechanical and chemical stimuli.

41
Q

Where does aspirin act centrally to reduce fever?

A

At the hypothalamic area.

42
Q

Is aspirin effective as an analgesic in non-inflamed painful conditions?

A

No, aspirin is generally not very effective in non-inflamed painful conditions.

43
Q

In what conditions does aspirin lower body temperature?

A

In febrile patients, such as those with infection, tissue damage, and inflammation.

44
Q

What happens to the body temperature in hyperthermia?

A

It may be elevated by exercise, heat stroke, drugs, or metabolic disorders.

45
Q

How does aspirin reduce fever?

A

By ‘resetting’ the hypothalamic ‘thermostat’ to normal body temperature.

46
Q

What is the initial response in acute inflammation?

A

The initial response to cell injury.

47
Q

What type of agents are effective beyond analgesia in inflammation?

A

Antiinflammatory agents.

48
Q

What do NSAIDs inhibit?

A

Prostaglandin synthesis.

49
Q

What is the pKa of aspirin?

A

3.5.

50
Q

What is the absorption profile of aspirin?

A

Good and fast oral absorption.

51
Q

How does aspirin distribute throughout the body?

A

Distribution occurs throughout body tissues and extracellular compartments.

52
Q

Does aspirin cross the placental barrier?

A

Yes, it readily crosses the placental barrier.

53
Q

What is the binding rate of aspirin to plasma proteins?

A

50-90%.

54
Q

What type of kinetics does aspirin exhibit at low doses?

A

First order kinetics.

55
Q

What type of kinetics does aspirin exhibit at high doses?

A

Zero order kinetics (above 600 mg).

56
Q

What promotes renal excretion of aspirin?

A

Alkalinization of the urine.

57
Q

What are the pharmacodynamic effects of aspirin?

A
  • Anti-inflammatory effect
  • Analgesic effect
  • Antipyretic effect
  • Platelet effects
58
Q

What is the duration of aspirin’s effect on platelet COX enzymes?

A

Lasts for 8-10 days.

59
Q

What are the primary uses of aspirin?

A
  • Mild and moderate pain
  • Antipyresis
  • Anti-inflammatory agent (NSAID)
  • MI and thrombosis prophylaxis
60
Q

What are common adverse effects of aspirin?

A

Respiratory alkalosis, then metabolic and respiratory acidosis.

61
Q

What is the normal arterial pH range?

A

7.40.

62
Q

What are the potential effects of aspirin on platelet aggregation?

A

Inhibits platelet aggregation and increases bleeding time.

63
Q

What should aspirin be avoided in?

A
  • Gastric ulcer
  • Severe hepatic damage
  • Hypoprothrombinemia
  • Vitamin K deficiency
  • Hemophilia
64
Q

What is salicylism?

A

A form of toxicity characterized by headache, dizziness, and other symptoms after repeated large doses.

65
Q

What condition is associated with Reye’s syndrome?

A

Cerebral edema in children with viral infection.

66
Q

What is the fatal dose of aspirin?

A

Approximately 20 grams (10-30 grams).

67
Q

What are nonacetylated salicylates known for?

A

Effective anti-inflammatory drugs but less effective analgesics than aspirin.

68
Q

What are specific reversible inhibitors of COX-2 enzymes?

A
  • Celecoxib (Celebrex)
  • Valdecoxib (Bextra)
  • Rofecoxib (Vioxx)
69
Q

What are common adverse reactions of selective COX-2 inhibitors?

A

GI disturbances including ulceration and bleeding.

70
Q

What is the first choice drug among NSAIDs?

A

Ibuprofen.

71
Q

What are reversible inhibitors of COX-1 and COX-2?

A

Various chemical structures similar effects to that of aspirin, but inhibition is not irreversible.

72
Q

What is the first choice drug that has the best side effects profile?

A

Ibuprofen.

73
Q

Which drugs are considered the worst (but potent) for side effects?

A
  • Indomethacin
  • Phenylbutazone (not in the US)
74
Q

What are common toxicities associated with NSAIDs?

A
  • GI: pain, bleeding, ulcer, pancreatitis, diarrhea
  • CNS: headache, dizziness, confusion, depression
  • Lung: bronchoconstriction
  • Bone marrow: agranulocytosis, aplastic anemia
  • Nephrotoxicity: acute renal failure, interstitial nephritis, nephrotic syndrome
  • Hepatotoxicity: enzyme elevation, hepatitis
  • Hypersensitivity reactions
75
Q

What is the mechanism of action for Indomethacin?

A

Reduces PMN migration and inhibits phospholipase A.

76
Q

What is the half-life of Diclofenac?

A

1.2 - 2 hours.

77
Q

What are the primary side effects of Ketorolac?

A

Frequent GI side effects.

78
Q

What is Ibuprofen’s half-life?

A

2 - 4 hours.

79
Q

What are the effects of Naproxen?

A

Similar to aspirin, ibuprofen, etc. with a mean plasma half-life of 13 hours.

80
Q

What is the toxicity profile of Naproxen?

A

G.I. disturbances, heartburn, dyspepsia, abdominal pain, constipation, diarrhea; gastric bleeding is less severe than with aspirin.

81
Q

What is the mechanism of action for Piroxicam?

A

Inhibits PMN migration and lymphocyte function, decreases oxygen radical production.

  • long half-life
  • high incidence of GI side effects
82
Q

What factors should be balanced when choosing an NSAID?

A
  • Efficacy
  • Cost-effectiveness
  • Toxicity
  • Personal factors (e.g. other drugs, concurrent illness, compliance, medical insurance coverage)
83
Q

Why is Acetaminophen often preferred to Aspirin?

A
  • Better tolerated
  • Lacks several undesirable side effects of aspirin
  • Overdose can cause fatal hepatic necrosis
84
Q

What are the pharmacokinetics of Acetaminophen?

A
  • Oral absorption
  • Some plasma protein binding
  • Half-life: 2 - 3 hours
  • Liver metabolism, conjugation, renal excretion
85
Q

What is the primary adverse effect of Acetaminophen?

A

Dose-dependent fatal hepatic necrosis.

86
Q

What is the treatment for acetaminophen intoxication?

A
  • Gastric emptying
  • Forced diuresis
  • Hemodialysis
  • N-acetylcysteine (Mucomyst) as specific antidote
87
Q

What should be administered as soon as possible after acetaminophen intoxication?

A

N-acetylcysteine must be administered parenterally within 10-12 hours.

88
Q

Which analgesics are recommended for patients with a history of PUD?

A
  • No history of PUD: any NSAID
  • PUD in history but not active: celecoxib with or without antacids, some NSAIDs with misoprostol or ‘-prazols’
  • Active PUD: acetaminophen and/or opioids (e.g. codeine) only.

Pharmacology Winter Exam 2 (4 decks)

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