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Pharmacology Winter Exam 2 > L13-15: Learning Objectives > Flashcards

L13-15: Learning Objectives Flashcards

1
Q
A
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2
Q

What triggers acute inflammation?

A

Cell injury leading to the release of various mediators.

Key mediators include histamine, serotonin, bradykinin, prostaglandins, and leukotrienes.

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3
Q

What are the effects of mediators released during acute inflammation?

A

Vasodilation, increased vascular permeability, chemotaxis, and pain.

Chemotaxis attracts immune cells to the site of injury.

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4
Q

What characterizes chronic inflammation?

A

Prolonged response when the acute inflammatory response fails to eliminate the cause of injury.

Involves cytokines, growth factors, and immune cells like macrophages and lymphocytes.

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5
Q

What are the effects of chronic inflammation?

A

Tissue damage and fibrosis due to continuous presence of inflammatory cells and mediators.

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6
Q

What is the first line of defense in the immune response?

A

Innate Immunity.

It involves physical barriers, phagocytic cells, and release of inflammatory mediators.

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7
Q

What is the role of adaptive immunity?

A

Activation of lymphocytes (B cells and T cells) that recognize specific antigens.

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8
Q

What do B cells produce in the immune response?

A

Antibodies.

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9
Q

What is the role of T cells in the immune response?

A

T cells can directly kill infected cells or help other immune cells.

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10
Q

What enzyme mobilizes arachidonic acid from membrane phospholipids?

A

Phospholipase A2 (PLA2).

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11
Q

What is the cyclooxygenase pathway responsible for?

A

Converting arachidonic acid into prostaglandins, thromboxane, and prostacyclin.

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12
Q

What differentiates COX-1 from COX-2?

A

COX-1 is constitutively expressed for ‘housekeeping’ functions; COX-2 is inducible and involved in inflammation.

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13
Q

What are the therapeutic effects of aspirin?

A

Analgesic, antipyretic, anti-inflammatory, and antiplatelet.

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14
Q

What is the mechanism of action of aspirin?

A

Irreversible inhibition of COX enzymes, preventing synthesis of prostaglandins and thromboxanes.

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15
Q

What are common adverse effects of aspirin?

A

Gastrointestinal distress, respiratory effects, renal issues, hypersensitivity, and Reye’s syndrome.

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16
Q

Fill in the blank: Aspirin is contraindicated in children with viral infections due to the risk of _______.

A

Reye’s syndrome.

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17
Q

What is the pharmacokinetic characteristic of aspirin regarding absorption?

A

Rapidly and completely absorbed from the stomach and upper small intestine.

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18
Q

What does celecoxib selectively inhibit?

A

COX-2 enzyme.

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19
Q

What are the major therapeutic uses of celecoxib?

A

Osteoarthritis, rheumatoid arthritis, acute pain, and dysmenorrhea.

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20
Q

How does celecoxib differ from aspirin in terms of gastrointestinal effects?

A

Celecoxib has a lower risk of gastrointestinal ulceration and bleeding.

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21
Q

What is a significant cardiovascular risk associated with celecoxib?

A

Increased risk of cardiovascular events due to imbalance between prostacyclin and thromboxane.

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22
Q

What is the mechanism of action for nonspecific COX inhibitors?

A

Inhibition of both COX-1 and COX-2 enzymes.

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23
Q

What are common side effects of nonspecific COX inhibitors?

A

Gastrointestinal irritation, renal toxicity, cardiovascular risks, and hypersensitivity reactions.

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24
Q

What is indomethacin known for?

A

Very potent anti-inflammatory and analgesic agent.

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25
Q

What is the pharmacokinetic profile of ibuprofen?

A

Rapid oral absorption with peak plasma levels in 1-2 hours and a half-life of 1.6-2.5 hours.

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26
Q

What is the primary use of ketorolac?

A

Analgesic for postsurgical pain.

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27
Q

What differentiates naproxen’s pharmacokinetics from ibuprofen?

A

Naproxen has a long half-life of 13 hours.

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28
Q

What effect does piroxicam have on PMN migration?

A

Inhibits PMN migration.

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29
Q

What is nabumetone’s characteristic as a prodrug?

A

Converted to an active metabolite with a long half-life.

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30
Q

What are the main properties of indomethacin?

A

Very potent anti-inflammatory and analgesic agent

Indomethacin is effective for conditions such as acute gout and ankylosing spondylitis.

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31
Q

What is the mechanism of action of indomethacin?

A

Reduces PMN migration and inhibits phospholipase A

This action helps in its anti-inflammatory properties.

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32
Q

What are the common side effects of indomethacin?

A

High incidence of gastrointestinal side effects, CNS effects (headache, dizziness), renal toxicity

These side effects limit its use in some patients.

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33
Q

What is ketorolac primarily used for?

A

Short-term management of moderate to severe pain

It is frequently used for postsurgical pain management.

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34
Q

What is the mechanism of action of ketorolac?

A

Potent COX inhibitor

This allows it to provide analgesic effects.

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35
Q

What are the side effects associated with ketorolac?

A

Frequent gastrointestinal side effects after prolonged use, potential renal toxicity

36
Q

What are the properties of diclofenac?

A

Potent COX inhibitor, decreases arachidonic acid bioavailability

37
Q

What is the primary mechanism of action of diclofenac?

A

Inhibits COX enzymes and reduces prostaglandin synthesis

38
Q

List some uses of diclofenac.

A
  • Osteoarthritis
  • Rheumatoid arthritis
  • Ankylosing spondylitis
39
Q

What side effects are associated with diclofenac?

A

Mostly gastrointestinal, increased cardiovascular risk, liver enzyme elevation

40
Q

What properties make ibuprofen the first choice drug?

A

Low incidence of side effects

41
Q

What is the mechanism of action of ibuprofen?

A

Reversible inhibition of COX-1 and COX-2

42
Q

What are the uses of ibuprofen?

A
  • Mild to moderate pain
  • Fever
  • Inflammation
  • Rheumatoid arthritis
  • Osteoarthritis
43
Q

What are the side effects associated with ibuprofen?

A

Generally well-tolerated, less gastrointestinal bleeding than aspirin, potential renal toxicity

44
Q

What are the properties of naproxen?

A

Effective for rheumatoid arthritis, osteoarthritis, and ankylosing spondylitis

45
Q

What is the mechanism of action of naproxen?

A

Reversible inhibition of COX-1 and COX-2

46
Q

What are the uses of naproxen?

A

Long-acting, suitable for chronic inflammatory conditions

47
Q

What side effects are associated with naproxen?

A

Gastrointestinal disturbances, headache, dizziness, potential cardiovascular risk

48
Q

What are the properties of piroxicam?

A

Long half-life, allowing once-daily dosing

49
Q

What is the mechanism of action of piroxicam?

A

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

50
Q

What are the uses of piroxicam?

A

Effective for chronic inflammatory conditions like rheumatoid arthritis and osteoarthritis

51
Q

What side effects are associated with piroxicam?

A

High incidence of gastrointestinal side effects, potential renal toxicity

52
Q

What are the properties of nabumetone?

A

Prodrug converted to an active metabolite, long half-life

53
Q

What is the mechanism of action of nabumetone?

A

Inhibits COX enzymes after conversion to active form

54
Q

What are the uses of nabumetone?

A

Effective for osteoarthritis and rheumatoid arthritis

55
Q

What side effects are associated with nabumetone?

A

May cause fewer gastrointestinal effects than other NSAIDs, potential renal toxicity

56
Q

What are the effects of acetaminophen?

A
  • Analgesic
  • Antipyretic
  • Very weak anti-inflammatory effect
57
Q

What is the mechanism of action of acetaminophen?

A

Inhibits prostaglandin synthesis in the CNS, but not significantly in peripheral tissues

58
Q

What are the uses of acetaminophen?

A
  • Pain relief for headaches, toothaches, and non-inflammatory pain
  • Fever reduction in adults and children
  • Preferred in patients with peptic ulcer disease, anticoagulants, aspirin allergies
59
Q

What are the side effects of acetaminophen?

A

Generally well-tolerated, minimal GI irritation, risk of hepatotoxicity

60
Q

What is the mechanism of toxicity of acetaminophen?

A

Hydroxylated intermediate metabolite can cause hepatotoxicity when large quantities are ingested

61
Q

What treatment options are available for acetaminophen overdose?

A
  • Gastric emptying
  • Forced diuresis
  • Hemodialysis
  • N-acetylcysteine (Mucomyst)
62
Q

What are the effects of aspirin?

A
  • Analgesic
  • Antipyretic
  • Anti-inflammatory
  • Antiplatelet
63
Q

What is the mechanism of action of aspirin?

A

Irreversible inhibition of COX-1 and COX-2 enzymes

64
Q

What are the pharmacokinetics of aspirin?

A
  • Rapidly absorbed from stomach and upper small intestine
  • Peak plasma concentration in 2-4 hours
  • Primarily excreted by kidneys
65
Q

What are the uses of aspirin?

A
  • Pain relief
  • Fever reduction
  • Anti-inflammatory conditions
  • Cardiovascular protection
  • Long-term use may decrease colon cancer incidence
66
Q

What are the adverse effects of aspirin?

A
  • Gastrointestinal irritation
  • Increased bleeding time
  • Renal damage
  • Risk of Reye’s syndrome in children
67
Q

What are the contraindications for aspirin?

A
  • Gastric ulcer
  • Severe hepatic damage
  • Hypoprothrombinemia
  • Pregnancy
  • Hypersensitivity to aspirin or salicylates
68
Q

What are some drug interactions with aspirin?

A
  • Decreased effect of beta-blockers
  • Increased nephrotoxicity with aminoglycosides
  • Increased bleeding risk with anticoagulants
69
Q

What is the primary use of acetaminophen?

A

Analgesic and antipyretic

Acetaminophen has minimal anti-inflammatory effects.

70
Q

What can acetaminophen overdose lead to?

A

Severe hepatotoxicity

Overdose situations can progress to encephalopathy, coma, and death.

71
Q

What is a crucial step in the treatment of acetaminophen overdose?

A

Administration of N-acetylcysteine (Mucomyst)

Must be given within 10-12 hours after intoxication.

72
Q

What enzyme does celecoxib selectively inhibit?

A

COX-2 enzyme

This enzyme is responsible for the synthesis of prostaglandins involved in inflammation and pain.

73
Q

What are the gastrointestinal benefits of celecoxib?

A

Reduced risk of gastrointestinal ulceration and bleeding

This is due to its selective inhibition of COX-2.

74
Q

Does celecoxib significantly inhibit platelet aggregation?

A

No

This reduces the risk of bleeding complications.

75
Q

What cardiovascular risk is associated with celecoxib?

A

Increased risk of myocardial infarction and stroke

Compared to non-selective NSAIDs.

76
Q

What is the mechanism of action of indomethacin?

A

Reduces PMN migration and inhibits phospholipase A

PMN refers to polymorphonuclear leukocytes.

77
Q

What is a notable side effect of indomethacin?

A

High incidence of severe GI adverse effects

Also includes pancreatitis.

78
Q

What is the pharmacokinetic profile of ketorolac?

A

Oral, IV, IM administration; half-life of 4-8 hours

Used mostly as an analgesic in postsurgical pain.

79
Q

What is a common side effect profile of diclofenac?

A

Mostly GI side effects, increased risk of cardiovascular diseases

It is a potent COX inhibitor.

80
Q

What is the mechanism of action for ibuprofen?

A

Equipotent on COX-1 and COX-2, reversible inhibition

It is the first choice drug for anti-inflammatory, antipyretic, and analgesic effects.

81
Q

What is the side effect profile of naproxen?

A

GI disturbances, headache, dizziness, pruritus, rash

It is effective in treating rheumatoid arthritis, osteoarthritis, and ankylosing spondylitis.

82
Q

What action does piroxicam perform?

A

Inhibits PMN migration, lymphocyte function, decreases oxygen radical production

It has a high incidence of GI side effects.

83
Q

What is unique about nabumetone’s mechanism of action?

A

Requires conversion to an active metabolite

It may cause fewer adverse GI effects than other NSAIDs.

84
Q

What do NSAIDs generally inhibit to manage pain, inflammation, and fever?

A

COX enzymes

This leads to reduced prostaglandin synthesis.

85
Q

Fill in the blank: Celecoxib is a specific _______ inhibitor.

A

COX-2

86
Q

True or False: Ibuprofen has the highest incidence of side effects among NSAIDs.

A

False

Ibuprofen has the lowest incidence of side effects.

Pharmacology Winter Exam 2 (4 decks)

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