Part 2-2 (Management of pain and inflammation) Flashcards

1
Q

Nonopioid Analgesics

A

NSAIDs

Acetaminophen

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2
Q

NSAIDs primary effects

A
Analgesic
Anti-inflammatory
Antipyretic (anti-fever)
Anticoagulant
Anticancer?
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3
Q

OTC NSAIDs

A

Aspirin
Ibuprofen
Naproxen
Ketoprofen

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4
Q

Prescription NSAIDs

A
Etodolac
Fenoprofen
Ketorolac
Meclofenamate
Piroxicam
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5
Q

NSAIDs mechanism of action

A

Inhibit synthesis of prostaglandins

Decrease prostaglandins by inhibiting cyclooxygenase

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6
Q

Prostaglandins

A

Lipid compounds produced in cells that cause pain, fever, inflammation, and coagulation

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7
Q

COX-1

A

Normal
Synthesize PGs to protect cells, maintain function
Stomach, kidneys, platelets

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8
Q

COX-2

A

Induced when cell is injured
Synthesizes PGs that mediate pain, inflammation
RA, other pathologies

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9
Q

COX-2 selective drugs

A

Inhibit synthesis of PGs in pain, inflammation
Spare production of beneficial PGs in organs
May decrease pain and inflammation w/ less toxicity
Example: Celecoxib

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10
Q

Cox-2 inhibition CV problems

A

Evidence that COX-2 inhibitors promote infarction
Some drugs recalled
Some NSAIDs more selective for COX-2

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11
Q

COX-2 selective NSAIDs

A

Diclofenac
Etodolac
Meloxicam

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12
Q

Why does COX-2 inhibition promote infarction

A

Drugs inhibit dilating PGs; allow PGs that increase platelet activity & promote constriction to dominate

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13
Q

Acetaminophen

A

Analgesic and antipyretic effects
No gastric irritation
No anti-inflammatory or anticoagulant effects
Liver toxicity high doses

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14
Q

Nonopioids adverse effects

A
Gastric irritation
Hepatic renal toxicity
CV problems
Impaired bone & cartilage
Aspirin toxication
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15
Q

Anti inflammatory steroids

A

Glucocorticoids
Act on inflammatory cells (macrophages, leukocytes)
Drug-receptor travels to nucleus

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16
Q

Anti Inflammatory steroid method

A

Drug receptor travels to nucleus
Decreased expression of inflammatory proteins
Increased expression of antiinflammatory proteins

17
Q

Steroid adverse effects

A

Catabolic effect on bone, mm, ll, tendon, skin

Salt/water retention, increased infection, gastric ulcers, adrenal suppresion

18
Q

Adrenocortical shock

A

Vascular collapse, severe hypotension

Can occur when GCs are suddenly discontinued