Hesi NSAIDS_mod_3_updated

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Flashcards covering key concepts from Anti-Inflammatory, Anti-Arthritic, and Related Agents, including NSAIDs, salicylates, acetaminophen, gold compounds, DMARDs, TNF blockers, and their indications, mechanisms, contraindications, and adverse effects.

Last updated 8:19 PM on 9/13/25
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27 Terms

1
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What are the four main actions of salicylates (aspirin) beyond anti-inflammatory effects?

Antipyretic, analgesic, and antiplatelet (inhibits platelet aggregation).

2
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What is the typical dosing range for low-dose aspirin used for antiplatelet protection?

81 mg (often listed as 81 mg); sometimes 325 mg tab for other uses; baby aspirin is 81 mg but not for babies.

3
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What are common contraindications for salicylates?

Allergy to salicylates, NSAIDs, or tartrazine (dye); recent surgery (1 week prior); pregnancy/lactation.

4
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What are potential adverse effects and toxicity signs of salicylates?

GI effects and bleeding; salicylate toxicity can include dizziness, tinnitus, hearing loss, N/V, diarrhea, confusion, tachypnea, hemorrhage, pulmonary edema, seizures, coma.

5
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What is COX-1’s role in the body?

Present in all tissues; protects the stomach lining; maintains Na and water balance in kidneys; involved in clotting; converts arachidonic acid to prostaglandins.

6
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What is COX-2’s role in inflammation?

Active at trauma sites or sites of cellular injury; increases pain and inflammation via prostaglandins.

7
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What is a key effect of COX-2 inhibitors compared to nonselective NSAIDs?

COX-2 inhibitors reduce inflammation with lower GI risk but have higher cardiovascular risk.

8
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What is Celecoxib (Celebrex)?

A COX-2 selective NSAID used for conditions like osteoarthritis and RA; associated with cardiovascular risk; watch for GI side effects.

9
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Name the major categories of NSAIDs.

Propionic acids, Acetic acids, Fenamates, Oxicam derivatives, COX-2 inhibitors (and nonselective NSAIDs).

10
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What is the general mechanism of NSAIDs?

Block COX-1 and COX-2, reducing prostaglandin synthesis to relieve inflammation, pain, and fever.

11
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What are the effects of COX-1 inhibition?

Gastric erosion/ulceration, bleeding tendencies, renal impairment; but protection against MI and stroke in some contexts.

12
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What are the effects of COX-2 inhibition?

Reduction of inflammation, pain, and fever; potential renal impairment; possible increased risk of MI and stroke; may reduce colorectal cancer risk.

13
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List examples of nonselective, semi-selective, and COX-2 selective NSAIDs.

Nonselective: ibuprofen, naproxen, indomethacin, ketorolac, diclofenac; Semi-selective: meloxicam, diclofenac, etodolac, piroxicam, nabumetone, sulindac; COX-2 selective: celecoxib.

14
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What is a known risk associated with COX-2 selective NSAIDs?

Increased risk for cardiovascular events; relatively decreased GI side effects compared with nonselective NSAIDs.

15
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Why was rofecoxib (Vioxx) removed from the market?

Because of increased cardiovascular risk leading to market withdrawal.

16
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What are common NSAID contraindications?

Allergy to NSAIDs or salicylates; celecoxib allergy with sulfonamides; CV dysfunction or hypertension; peptic ulcers/GI bleed; pregnancy/lactation; renal or hepatic disease.

17
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What is acetaminophen (Tylenol) not considered NSAID-wise, and what are its key cautions?

Not an NSAID; analgesic and antipyretic; hepatotoxic at high doses; max daily dose 4000 mg/day; antidote is acetylcysteine; caution with liver disease/alcohol use.

18
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What are acetaminophen dosing guidelines and overdose concerns?

Typically 325–1000 mg every 4–6 hours; maximum 4000 mg/day; overdose is a major risk, especially in children; liver toxicity is the major concern.

19
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What are acetaminophen contraindications and major adverse effects?

Contraindications: hepatic dysfunction, chronic alcoholism. Adverse effects: hepatotoxicity, headache, hemolytic anemia, renal dysfunction, rash, fever.

20
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What are gold compounds used for in anti-arthritic therapy, and how do they work?

Chrysotherapy (gold salts: auranofin, aurolate); gold uptake by macrophages inhibits phagocytosis, reducing lysosomal enzyme release and tissue destruction.

21
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What is a key caution about gold compounds as DMARDs?

Reserved for patients not responding to other treatments; not a repair agent but prevents progression; contraindicated in pregnancy/lactation and several organ dysfunctions.

22
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What are DMARDs and their general purpose?

Disease-Modifying Anti-Rheumatic Drugs; slow or prevent joint damage; some classify gold as DMARD; includes TNF blockers and other agents; adverse effects can be severe.

23
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What are TNF blockers and typical uses?

Adalimumab, certolizumab, etanercept, golimumab, infliximab; used for RA, polyarticular juvenile arthritis, psoriatic arthritis, plaque psoriasis, ankylosing spondylitis.

24
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What are the major contraindications for TNF blockers?

Black box warning for serious infections and lymphoma/cancer risk; avoid in acute infection, cancer, sepsis, TB, hepatitis, myelosuppression, demyelinating disorders; pregnancy; live vaccines; animal product allergy.

25
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What are other DMARDs and their roles?

Methotrexate, cyclophosphamide, abatacept, anakinra, IL-1 receptor antagonist; used alone or in combination; adverse effects can be serious; often used with TNF blockers.

26
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What is the IL-1 receptor antagonist Anakinra’s mechanism?

Blocks IL-1, which is responsible for cartilage degradation in RA.

27
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How do DMARDs compare to NSAIDs in terms of onset and disease progression?

DMARDs have a slow onset but can arrest disease progression and prevent deformities; used in chronic disease. NSAIDs have rapid onset for symptom relief but do not stop disease progression and are used in acute cases.