Rheumatoid Arthritis Treatments Quiz

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Questions and Answers

What is a primary effect of leflunomide in treating rheumatoid arthritis?

Inhibits GI function

Inhibits the action of collagenase

Decreases release of antibodies

Blocks replication of lymphocytes by interfering with pyrimidine synthesis (correct)

Which of the following is a common adverse effect associated with sulfasalazine?

Nausea

Photosensitivity (correct)

Fetal toxicity

Nephrotoxicity

How do biological response modifiers function?

They reduce the production of lymphocytes.

They promote the release of inflammatory substances.

They increase cytokine activity in the body.

They inhibit or modify the immune response. (correct)

What is a significant warning associated with leflunomide?

Box warning for liver toxicity Signup and view all the answers

Which of the following drugs is associated with metallic taste and skin rash as adverse effects?

Gold compounds Signup and view all the answers

What is the primary mechanism of action for NSAIDs in the treatment of arthritis?

Inhibition of cyclooxygenase enzymes Signup and view all the answers

Which of the following is NOT classified as a Disease-Modifying Antirheumatic Drug (DMARD)?

Indomethacin Signup and view all the answers

Which types of immunosuppressives are commonly used to manage rheumatoid arthritis?

Corticosteroids and synthetic DMARDs Signup and view all the answers

Biological response modifiers primarily target which aspect of the inflammatory process in rheumatoid arthritis?

Specific inflammatory cytokines Signup and view all the answers

What common effect do biological response modifiers have when treating rheumatoid arthritis?

Suppress the immune response Signup and view all the answers

What is the primary mechanism of action for nonsteroidal anti-inflammatory drugs (NSAIDs)?

Inhibit synthesis and release of prostaglandins Signup and view all the answers

Which of the following is an example of a Disease-Modifying Antirheumatic Drug (DMARD)?

Methotrexate Signup and view all the answers

What effect does Azathioprine primarily have on the immune system?

Blocks purine synthesis and causes DNA damage Signup and view all the answers

What is a possible adverse reaction associated with Tumor Necrosis Factor-α inhibitors?

Opportunistic infections Signup and view all the answers

Which category of drugs is primarily aimed at modifying the immune response in autoimmune diseases?

Immunosuppressives Signup and view all the answers

Which of the following is a characteristic of glucocorticosteroids?

Restores blood-brain barrier effectiveness Signup and view all the answers

Which type of DMARD directly influences T-cell activity?

Cyclophosphamide Signup and view all the answers

What common feature is associated with the mechanism of action for NSAIDs?

Inhibiting cyclooxygenase enzymes Signup and view all the answers

What is one of the major risks associated with glucocorticosteroids?

Decreased bone density Signup and view all the answers

Which of the following DMARDs is known to be an antimalarial?

Chloroquine Signup and view all the answers

Which statement best describes the role of monoclonal antibodies in treatment?

They block the inflammatory process. Signup and view all the answers

What is a significant side effect of nonsteroidal anti-inflammatory drugs?

Increased bleeding risk Signup and view all the answers

What action does Methotrexate have on B-cells?

Inhibits B-cell antibody production Signup and view all the answers

What is the primary purpose of using Tumor Necrosis Factor-α inhibitors in treatment?

Block pathways leading to inflammation Signup and view all the answers

Study Notes

Pharmacology for Pharmacy Technicians, 4th Edition

Authored by Kathy Moscou PhD RPh MPH and Karen Snipe CPhT AS BA MEd
Copyright 2025 Elsevier Inc.

Chapter 13: Treatment of Gout, Osteoarthritis, and Rheumatoid Arthritis

Lesson 13.1: Treatment of Gout, Osteoarthritis, and Rheumatoid Arthritis
- Covers terminology, signs/symptoms, medication classification, mechanism of action, warning labels, and precautions for gout, osteoarthritis, and rheumatoid arthritis treatments.

Key Terms

Arthritis: Inflammation of the joints
Autoantibody: Antibody produced against the body's own tissues
Autoimmune disease: Body's immune system attacks its own tissues
Gout: A type of inflammatory arthritis caused by high levels of uric acid in the blood
Hyperuricemia: High levels of uric acid in the blood
Rheumatoid Arthritis: Chronic inflammatory autoimmune disease affecting the joints
Rheumatoid Factor: Antibody found in some individuals with rheumatoid arthritis
Synovium: Tissue lining the joints
Tumor necrosis factor: Protein involved in inflammation
Urates: Salts of uric acid
Uricosuric: Agent that increases the excretion of uric acid

Overview

Hyperuricemia: Urate levels build up in the blood serum.
Urates: Product of purine metabolism.

Medical Conditions Associated with Hyperuricemia

Gout
Cardiovascular disease
Chronic kidney disease
Hyperlipidemia
Insulin resistance
Obesity

Pathophysiology of Gout (1 of 3)

Urate crystals deposited in joints.
Crystals produce inflammation and pain.
Tophi: Lumps under skin around joints and at rim of ear.

Pathophysiology of Gout (2 of 3)

Flare-ups produced by foods high in purine.
Affected joints: Big toe, Foot, Ankle, Knee, Wrist, Finger, Elbow.

Pathophysiology of Gout (3 of 3)

Sharp, needlelike pain.
Possibly no symptoms.
Resolves spontaneously in 7 to 10 days.

Drugs Used to Treat Gout

Analgesics
Antiinflammatories
Uricosurics
Inhibitors of uric acid synthesis

Antiinflammatory Drugs Used in the Treatment of Gout

Colchicine
NSAIDs: indomethacin
Glucocorticosteroids: Oral prednisone, Glucocorticosteroid injections

Uricosurics Used in the Treatment of Gout

Probenecid
Probenecid + colchicine

Inhibitors of Uric Acid Synthesis

Xanthine oxidase inhibitors: Allopurinol, Febuxostat
- Allopurinol: easily absorbed and eliminated.
- Febuxostat: more selective than allopurinol.
- Both for hyperuricemia due to gout, malignancy, or other drugs, or chronic cases.

Drugs Used to Treat Gout: MOA (1 of 2)

Colchicine: Penetrates inflammatory cells, inhibits ability to respond to site of irritation, inhibits histamine release, and blocks cell division.

Drugs Used to Treat Gout: MOA (2 of 2)

Recombinant urate oxidase enzymes: Metabolize uric acid to water-soluble allantoin. Pegloticase: Chronic gout. Rasburicase: hyperuricemia induced by chemotherapy, Increased clearance of uric acid, Inhibit uric acid reabsorption in renal tubules, Promote elimination of urates.

Nonpharmacological Therapy

Weight loss.
Diet low in purines to prevent gout attacks.
Rest and ice packs for acute attacks.

Warning Labels

Antiinflammatories: Avoid alcohol, take with lots of water.
Uricosurics: Take with food, and lots of water, avoid aspirin.

Osteoarthritis

Inflammation of the synovial fluid contributes to pain.
Symptoms: Joint pain, stiffness, swelling, crepitus, pain may occur after activity or at rest.
Risk Factors: Previous joint injury or surgery, obesity, increasing age, muscle weakness, occupational overuse.

Pain Control for Osteoarthritis

Acetaminophen
Aspirin
Nonsteroidal anti-inflammatory drugs (NSAIDs)

Rheumatoid Arthritis (1 of 2)

Inflammation of the joint lining.
Signs/symptoms: Pain, joint damage, disability, elevated levels of rheumatoid factor. Other symptoms include fatigue, weakness, flu-like symptoms, nodules under skin, muscle pain, decreased appetite, depression, and dry mouth.

Rheumatoid Arthritis (2 of 2)

Phase 1: Synovial membrane inflamed, swelling, pain, stiffness.
Phase 2: Rapid cell growth causes synovium to thicken.
Phase 3: Inflamed cells in synovium release enzymes, enzymes digest bone and cartilage.

Treatment of Rheumatoid Arthritis

Suppress inflammation and reduce swelling and pain: Glucocorticosteroids, NSAIDs, Salicylates
Slow progression of disease: Disease-modifying antirheumatic drugs (DMARDs), Biological response modifiers

Tumor Necrosis Factor-a Inhibitors (1 of 2)

Genetically engineered drugs.
Block inflammatory process triggered by high TNF concentrations.
Prevent cell lysis, release of substances causing inflammation.
Monoclonal antibodies, Fusion protein (etanercept)

Tumor Necrosis Factor-a Inhibitors (2 of 2)

Can produce allergic reaction and anaphylactic shock.
Opportunistic infections (tuberculosis, fungal).
Can cause onset of MS.
Associated with development of secondary cancers.

Antiinflammatories and Analgesics (1 of 3)

Glucocorticosteroids: Reduce flare-ups, treat pain, restore blood-brain barrier effectiveness, may be prescribed for other conditions, eliminated in urine.

Antiinflammatories and Analgesics (2 of 3)

Inhibit synthesis of proinflammatory substances and antibodies, responsible for attacking healthy cells, Decrease accumulation of leukocytes and T cells, interfere with binding of antibodies to receptor sites on cell surfaces, Decrease synthesis of prostaglandins, leukotrienes, cytokines, arachidonic acid, macrophages.

Antiinflammatories and Analgesics (3 of 3)

Adverse Reactions and Precautions: CNS (insomnia, euphoria), Cardiovascular (edema, hypertension), Endocrine (hyperglycemia/diabetes), GI (infection, ulceration), other (nausea, weight gain, osteoporosis, acne, cataracts, poor wound healing).

Antiinflammatories and Analgesics: Look-Alike/Sound-Alike Drugs

Hydrocortisone, cortisone, hydrocodone
Medrol and Mebaral
Methylprednisolone and medroxyprogesterone
Prednisone, prednisolone, Pramosone, and primidone

Nonsteroidal Antiinflammatory Drugs (1 of 2)

Inhibit synthesis and release of prostaglandins.
Block activity of cyclooxygenase (COX-1 and COX-2) enzymes.

Nonsteroidal Antiinflammatory Drugs (2 of 2)

Black box warning: Cardiovascular toxicity, Gastrointestinal ulceration.

Disease-Modifying Antirheumatic Drugs (DMARDs)

Immunosuppressives
TNF inhibitors
Interleukin antagonists
Antimalarials
Leflunomide
Gold salts
Penicillamine
Sulfasalazine

NSAID's and DMARD's: Look-Alike/Sound-Alike Drugs

Celebrex, Celexa, Cerebyx
Naprosyn, Naprelan, Niaspan
Anaprox and Avapro

Immunosuppressives (1 of 3)

Azathioprine: Blocks purine synthesis, damages DNA, suppresses immune responses mediated by T cells.
Cyclophosphamide: Interferes with DNA synthesis, inhibits B-cell antibody production, T-cell activity, cytokine and immunoglobulin production, suppresses antigen-induced response to T cells.

Immunosuppressives (2 of 3)

Cyclosporine: Selectively interferes with T-cell proliferation and interleukin production.
Methotrexate: Inhibits folate formation for purine synthesis. Decreases cytokine and immunoglobulin production, COX-2 activity.
Mitoxantrone: Interferes with DNA repair and RNA synthesis.

Immunosuppressives (3 of 3)

Cyclosporine solution for injection: Do not refrigerate, protect from light, dilute and use immediately, stable for 6 hours in plastic IV bag or 24 hours in glass.

Antimalarials

Accumulate in cell structures.
Raise pH and interfere with immune response.
Exact mechanism not known.
Hydroxychloroquine.

Look-Alike/Sound-Alike Drugs

Cyclosporine, cycloserine, cyclophosphamide
Gengraf, Prograf
Neural, Nizoral

Additional DMARDs

Leflunomide: Blocks lymphocyte replication by interfering with pyrimidine synthesis.
Sulfasalazine: Slows progression of rheumatoid arthritis, decrease release of antibodies inhibit collagenase action.
Gold compounds: Decreases release of antibodies, inhibits collagenase action.
Penicillamine: Inhibits T-cell function, blocks collagen cross-linking.

Additional DMARDs: Adverse Effects

Leflunomide: Warning for liver toxicity, fetal toxicity, nausea, diarrhea, rash, hair loss, liver dysfunction
Sulfasalazine: GI upset, photosensitivity, allergy, crystalluria, impaired folic acid absorption, damage to white blood cells.
Gold compounds: Itching, rash, metallic taste, sore mouth, photosensitivity, cytopenias, interstitial pneumonia, proteinuria
Penicillamine: Rash, GI upset, nephrotoxicity

Biological Response Modifiers

Inhibit or modify immune responses.
Inhibit release of cells body identifies as harmful and invasive, release of substances producing inflammation.
Interfere with immune system mediators like cytokines, leukocytes, B cells, and T cells.

Questions?

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Description

Test your knowledge on the various treatments for rheumatoid arthritis, including leflunomide and sulfasalazine. This quiz covers primary effects, common adverse reactions, and the mechanism of biological response modifiers. Challenge your understanding of crucial medications used in managing this chronic condition.