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Pharmacology: Exam 3 > Nonopioid Analgesics: NSAIDs and Acetaminophen > Flashcards

Nonopioid Analgesics: NSAIDs and Acetaminophen Flashcards

1
Q

Pain source

A
  • Somatic (nociceptive): prostaglandin mediated, typically responds to NSAIDs
  • Visceral (nociceptive): responds to opioid analgesics
  • Neuropathic (deafferentiated): poor response to analgesics- better response to adjuvant Tx
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2
Q

Prostaglandin’s role in pain and inflammation

A
  • Prostaglandins act at prostaglandin (G-protein coupled) receptors on cell membranes to cause pain and inflammation
  • Dorsal Horns: PGs increase sensitivity of adenylate cyclase to stimulation by pain mediators
  • PGs enhance neurotransmitter release and act post synaptically
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3
Q

NSAIDs: MOA

A
  • Inhibit both peripheral and central cyclooxygenase (COX)
  • COX-1: Constitutive, Physiologic (increases TXA, PGE, PGI)
  • COX-2: Inducible, Inflammatory (increases PGI & PGE)
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4
Q

NSAIDs: Indications

A
  • Inflammation (surgery, arthritis- symptomatic relief)
  • Pain in multiple disease states (cancer, muscle, bone pain, menstrual pain)
  • doses for inflammation are higher than those for pain
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5
Q

NSAIDs: Effectiveness

A

-All NSAIDs have a ceiling effect on analgesia (increasing the dose will not increase analgesic efficacy, but will increase incidence of side effects)

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6
Q

NSAIDs: Non Analgesic uses

A
  • Antipyretic
  • Antiplatelet/Cardioprotection
  • Gout, cancer chemoprevention, systemic mastocytosis, Alzheimer’s
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7
Q

NSAIDs ADRs

A 
Gastrointestinal (GI bleeds)
Renal
Cardiovascular
Bleeding
Hepatic
CNS
Impairment of Joint Healing?
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8
Q

NSAIDs: ADE with GI

A
  • Mediated through both COX inhibition and local irritation
  • Increased risk: age, concurrent GI problems, smoking, alcohol use, steroid use
  • Reduced by proton pump inhibitors, misoprostol (replenishes PG), and possibly high dose histamine 2 blockers
  • Increases Ketorolac (increases risk of GI bleed)
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9
Q

NSAIDs: ADE with Renal

A
  • Renal toxicity may only be important in patients with reduced renal function, CHF, hepatic cirrhosis
  • NSAIDs can cause salt retention, hyperkalemia, and edema
  • Reduce GFR and can precipitate renal failure of: repeated or long term dosing, concomitant nephrotic therapy, dehydration, CHF, diabetes, hypertension, elderly
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10
Q

NSAIDs: Drug interactions

A
  • ACEI inhibitors
  • Corticosteroids
  • Warfarin
  • Sulfonylureas
  • Methotrexate
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11
Q

Acetaminophen: MOA

A
  • Peripherally blocks pain impulse generation
  • Inhibition of hypothalamic heat regulating center
  • Selective COX 2 inhibitor
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12
Q

Acetaminophen: Indications

A
  • Analgesic for mild to moderate pain, headache
  • Minimal anti-inflammatory activity
  • Antipyretic
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13
Q

Acetaminophen: ADE

A
  • Hepatotoxicity

- Overdose: stores of GDH depleted, NAPQI binds covalently to cell macromolecules, leads to dysfunction and apoptosis

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14
Q

Acetaminophen: Precautions

A
  • Liver Disease
  • Alcoholics
  • Max dose: 4g/day
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15
Q

Aspirin

A
  • Analgesic, anti inflammatory and antipyretic

- Antiplatelet effect: irreversible inhibition of platelet aggregation (thromboxane)

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16
Q

Traditional NSAIDs: PK and PD

A
  • Well absorbed orally
  • Peak concentrations with 1-4 hrs
  • Accumulate at sites of inflammation
  • Metabolized in liver
  • Excreted in kidneys by glomerular filtration and tubular secretion
  • Extensively protein bound
17
Q

COX 2 Inhibitors (Coxibs) MOA

A
  • COX 2 selective inhibitors (coxibs) designed to preserve COX 1 activity
  • Beneficial anti inflammatory, analgesic, and antipyretic effects without the GI and platelet effects mediated through COX 1 inhibition
18
Q

Pros and Cons of Coxibs

A

Coxibs may reduce GI complications, but increase cardiovascular events versus traditional NSAIDs

19
Q

Thromboxane activities

A
  • Exclusive COX 1 product in platelets
  • Promotes platelet aggregation
  • Vasoconstriction
  • Vascular proliferation
20
Q

Prostacyclin (PGI2)

A
  • Predominant COX 2 product in endothelium
  • inhibits platelet activation
  • vasodilation
  • prevents proliferation of vascular smooth muscle cells
21
Q

COXIBs Place in Therapy

A
  • Perioperative or acute setting

- chronic pain

22
Q

Celecoxib

A
  • Half life: 11 hours
  • contraindicated for sulfa allergy
  • metabolized by cytochrome P450 enzyme 2C9
  • African Americans and elderly often deficiency in 2C9, which could lead to elevated levels of drug
23
Q

Prostaglandin “Housekeeping” activities

A
  • Gastrointestinal Cytoprotection (PGE)
  • Renal Vasodilation (PGE2, PGI2)
  • Fever (PGE2)
  • Uterine Contraction (PGE2)
24
Q

Thromboxane

A
  • Exclusive COX-1 product in platelets
  • Promotes platelet aggregation
  • Vasoconstriction
  • Vascular proliferation
25
Q

Prostacyclin (PGI2)

A
  • Predominant COX-2 product in endothelium
  • Inhibits platelet aggregation
  • Vasodilation
  • Prevents proliferation of vascular smooth muscle cells

Pharmacology: Exam 3 (5 decks)

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