Anti-Inflammatory Treatments Overview

Learning Objectives

  • Identify targets of anti-inflammatory treatments and explain predicted outcomes, risks, and side effects.
  • Appropriate vs. inappropriate treatments for specific inflammatory conditions.
  • Outline alternative treatment approaches considering Quality Use of Medicines (QUM) based on patient history and reactions.

Key Concepts in Anti-Inflammatory Treatments

  • Current Edition Reference: Lehne’s Pharmacology for Nursing Care, 2019, pages 852-867 (Cyclooxygenase Inhibitors), 879-888 (Treatment of RA).
Anti-Inflammatory Drug Classification
  1. Non-steroidal Anti-Inflammatory Drugs (NSAIDs):
    • First Generation: Traditional NSAIDs like aspirin and ibuprofen.
    • Second Generation: Selective COX-2 inhibitors, e.g., celecoxib.
  2. Paracetamol (Acetaminophen): Analgesic/antipyretic effects, less effective as an anti-inflammatory.
  3. Glucocorticoid Steroids: Mimic cortisol; used in various inflammatory conditions.
  4. Disease-Modifying Anti-Rheumatic Drugs (DMARDs): Target immune system, modify disease course in autoimmune conditions.
    • Biological DMARDs: Target specific components of the immune system (e.g., TNFα antagonists).
    • Non-biological DMARDs: Traditional immunosuppressive therapies (e.g., Methotrexate).

Glucocorticoids

  • Mechanism of Action: Mimic endogenous steroid hormones (e.g., cortisol) to reduce inflammation.
  • Usage:
    • Low Doses: Treat adrenal insufficiency.
    • High Doses: Manage chronic inflammatory diseases, suppress immune response in cancer treatments.
Physiological Effects of Cortisol
  • Metabolic:
    • Increases blood glucose levels (BGL).
    • Stimulates lipolysis and gluconeogenesis; decreases protein synthesis.
  • Immune:
    • Suppresses inflammation by decreasing inflammatory cells and cytokines.
  • Renal:
    • Maintains blood pressure (BP) by increasing sodium and water retention.
Pathological Effects of Cortisol
  • Sustained high levels of cortisol may lead to Cushing’s syndrome, characterized by:
    • Polycythemia
    • Increased appetite and fat deposition
    • Osteoporosis and growth suppression.
Pharmacokinetics of Glucocorticoids
  • Absorption: Non-linear; topical effectiveness varies with location.
  • Distribution: High protein binding.
  • Metabolism: Occurs primarily in the liver.
  • Elimination: Via renal pathways.
Adverse Effects of Glucocorticoids
  • Long-term use can result in:
    • Immune suppression (increased infection risk)
    • Osteoarthritis
    • Growth retardation in children
    • Glaucoma and cataracts.
    • Drug interactions with NSAIDs and anticoagulants.

Inflammatory Pathway

  • After trauma or injury, phospholipids in cell membranes are converted into arachidonic acid by phospholipase, leading to:
    • Prostaglandins: Associated with inflammation and pain.
    • Leukotrienes: Contribute to allergic responses and asthma.
Therapeutic Uses of Glucocorticoids
  • Indicated in conditions like:
    • Addison disease (adrenal insufficiency)
    • Inflammatory disorders (e.g., arthritis, asthma)
    • Autoimmune diseases and dermatological disorders.

DMARDs Overview

  • Classification:
    • Non-biological (Traditional DMARDs):
      • Methotrexate
      • Sulfasalazine
    • Biological DMARDs: Target specific immune pathways, often more expensive.
Non-Biological DMARDs
  • Methotrexate: Low-dose immunosuppressant, suppresses cytokines; not suitable in pregnancy.
  • Sulfasalazine: Fewer adverse effects; safer during pregnancy.
  • Hydroxychloroquine: Changes intracellular pH; least toxic but doesn’t slow disease progression.
Biological DMARDs
  • Target immune response specifically (e.g., TNFα antagonists).
  • High cost and require monitoring for adverse effects (e.g., infections, hepatotoxicity).

Rheumatoid Arthritis (RA)

  • Description: Chronic systemic inflammation causing damage to synovial joints.
  • Treatment Goals: Disease control, achieving remission, and preventing progression of symptoms.
Treatment Protocols for RA
  1. 1st Line: NSAIDs (e.g., aspirin, ibuprofen, celecoxib).
    • Considerations: Gastrointestinal upset directs next choices.
  2. 2nd Line: DMARDs when NSAIDs are inadequate or poorly tolerated.
  3. 3rd Line: Short courses of glucocorticoids for flare-ups and to reduce inflammation.