252 Pharmacology - NSAIDS and Antigout Flashcards

1
Q

Done nomogram

A

A standard plot of graphic data, originally published in 1960 in the journal Pediatrics, for rating the severity of aspirin toxicity following overdose; serum salicylate levels are plotted against time elapsed since ingestion.

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2
Q

Gout

A

Hyperuricemia (elevated blood uric acid level); the arthritis caused by tissue buildup of uric acid crystals.

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3
Q

Inflammation

A

A localized protective response stimulated by injury to tissues that serves to destroy, dilute, or wall off (sequester) both the injurious agent and the injured tissue.

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4
Q

Salicylism

A

The syndrome of salicylate toxicity, including symptoms such as tinnitus, nausea, and vomiting.

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5
Q

Define NSAID.

A
  • A large and chemically diverse group of drugs that have:
    • Analgesic activities
    • Anti-inflammatory activities
    • Antipyretic activities
    • aspirin-platelet inhibition
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6
Q

What are the main uses of NSAIDs?

A
  • Relief of mild to moderate headaches
  • Relief of myalgia
  • Relief of neuralgia
  • Relief of arthralgia
  • Relief of postoperative pain
  • Relief of pain associated with arthritic disorders such as rheumatoid arthritis, juvenile arthritis, ankylosing spondylitis, and osteoarthritis
  • Treatment of gout and hyperuricemia
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7
Q

What three properties do all NSAIDs share?

A
  • Antipyretic properties
  • Analgesic properties
  • Anti-inflammatory properties
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8
Q

What are 3 acetic acid derivatives?

A
  • diclofenac sodium (Voltaren®)
  • indomethacin sulindac
  • ketorolac (Toradol®)
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9
Q

What are 2 propionic acid derivatives?

A

ibuprofen

naproxen

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10
Q

Indications re: MI for aspirin.

A
  • Shown to reduce cardiac death after myocardial infarction (MI)
  • Should be administered at the first sign of MI
  • If aspirin is not given before the patient arrives at the emergency department, it is one of the first drugs given if there are no contraindications.
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11
Q

Mechanisms of action associated with NSAIDs

A
  • Inhibition of the leukotriene pathway, the prostaglandin pathway, or both
  • Blocking the chemical activity of the enzyme COX
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12
Q

What are contraindications of NSAIDS?

A
  • Conditions that place the patient at risk for bleeding
    • Rhinitis
    • Vitamin K deficiency
    • Peptic ulcer disease
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13
Q

What are the main adverse effects of NSAIDS?

A
  • Heartburn to severe GI bleeding
  • Acute kidney injury
  • Noncardiogenic pulmonary edema
  • Altered hemostasis
  • Hepatotoxicity
  • Skin eruption, sensitivity reaction
  • Tinnitus, hearing loss
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14
Q

Why is misoprostol used with NSAIDs?

A
  • Many of the adverse effects of NSAIDs are secondary to their inactivation of protective prostaglandins that help maintain the normal integrity of the stomach lining.
  • Prevents GI bleed
  • A synthetic prostaglandin E1 analogue: inhibits gastric acid secretion and has a cytoprotective component
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15
Q

What effect can NSAIDS have on kidneys?

A
  • Kidney function depends partly on prostaglandins.
  • Disruption of prostaglandin function by NSAIDs is sometimes strong enough to precipitate acute or chronic kidney injury or failure.
  • Use of NSAIDs can compromise existing kidney function.
  • Kidney toxicity can occur in patients with dehydration, heart failure, or liver dysfunction, or with the use of diuretics or angiotensin-converting enzyme inhibitors.
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16
Q

What is the Health Canada warning regarding NSAIDs?

A
  • All NSAIDs (except aspirin) share a Health Canada warning regarding an increased risk of adverse cardiovascular thrombotic events, including fatal MI and stroke.
  • NSAIDs cause an increased risk of serious GI adverse events
  • Older adults are at greater risk.
17
Q

Uses for aspirin

A
  • Inhibits platelet aggregation
  • Antithrombotic effect: used in the treatment of MI and other thromboembolic disorders
  • Headache, neuralgia, myalgia, and arthralgia
  • Pain syndromes resulting from inflammation: arthritis, pleurisy, and pericarditis
  • Systemic lupus erythematosus: antirheumatic effects
  • Antipyretic action
18
Q

What is salicylate intoxication?

A
  • Salicylate intoxication (when chronic, known as salicylism)
    • Increased heart rate
    • Tinnitus, hearing loss, dimness of vision, headache, dizziness, mental confusion, drowsiness
    • Nausea, vomiting, diarrhea
    • Sweating, thirst, hyperventilation, hypoglycemia or hyperglycemia
19
Q

What are the uses for the acetic acid derivative indomethacin?

A

Uses: therapy for rheumatoid arthritis (RA), osteoarthritis (OA), acute bursitis or tendonitis, ankylosing spondylitis, acute gouty arthritis

(Analgesic, anti-inflammatory, antirheumatic, and antipyretic properties)

20
Q

What are the uses for the acetic acid derivative ketorolac?

A
  • Some anti-inflammatory activity
  • Used primarily for its powerful analgesic effects, which are comparable to those of narcotic drugs such as morphine sulphate
  • Indication: short-term use (up to 5 to 7 days) to manage moderate to severe acute pain
21
Q

What is the most commonly used NSAID?

A

ibuprofen

22
Q

What is the second most commonly used NSAID?

A

naproxen

23
Q

Why might naproxen be a better choice than ibuprofen?

A
  • Somewhat better adverse effect profile than ibuprofen
  • Fewer drug interactions with angiotensin-converting enzyme inhibitors given for hypertension
24
Q

With what kind of allergy is celecoxib contraindicated?

A

sulpha allergy

25
Q

What are the adverse effects of NSAIDS?

A
  • GI
    • Dyspepsia, heartburn, epigastric distress, nausea, vomiting, anorexia, abdominal pain
    • GI bleeding* (misoprostol can help)
    • Mucosal lesions* (erosions or ulcerations) (misoprostol can help)
  • Renal
    • Reductions in creatinine clearance
    • Acute tubular necrosis with acute kidney injury
  • Cardiovascular
    • Noncardiogenic pulmonary edema
26
Q

What interactions are there with NSAIDS?

A
  • Serious interactions can occur when given with:
    • Alcohol
    • Anticoagulants
    • acetylsalicylic acid (ASA)
    • Biphosphonates
    • Corticosteroids and other ulcerogenic medications
    • Protein-bound drugs
    • Diuretics and angiotensin-converting enzyme inhibitors
27
Q

What is gout?

A
  • A condition that results from inappropriate uric acid metabolism
    • Underexcretion of uric acid
    • Overproduction of uric acid
  • Uric acid crystals are deposited in tissues and joints, resulting in pain
  • Hyperuricemia
28
Q

List 3 antigout drugs

A
  • allopurinol (Zyloprim®)
  • colchicine
  • probenecid (Benuryl®)
29
Q

How does allopurinol work?

A
  • Used to prevent uric acid production and to prevent acute tumour lysis syndrome
  • Side effects: exfoliative dermatitis, Stevens-Johnson syndrome, and toxic epidermal necrolysis
30
Q

How does probenecid work for gout?

A

ØInhibits the reabsorption of uric acid in the kidneys and thus increases the excretion of uric acid

31
Q

How does colchicine work for gout?

A
  • Oldest available therapy
  • Reduces the inflammatory response to the deposits of urate crystals in joint tissue
  • Powerful inhibitor of cell mitosis, and can cause short-term leukopenia
  • Prophylaxis of acute attacks in dosages of 0.6 mg once or twice a day
32
Q

What drug interactions are there for chondroitin and glucosamine?

A
  • Enhance the effects of warfarin
  • Glucosamine may increase insulin resistance
33
Q

What is important for the nurse to know about aspirin and children and teenagers?

A

˜Do not give salicylates to children and teenagers because of the risk of Reye’s syndrome.