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ANALGESICS - GOUT AND ARTHRITIS

Q: What are the specific and non-specific anti-inflammatory drugs used to reduce inflammation during acute gout attacks?

Colchicine : specific anti-inflammatory in gout Indomethacin : non-specific anti-inflammatory

Q: What are the indications for Colchicine?

Acute Gouty Arthritis: 1mg then 0.5mg/2hrs until pain is relieved or nausea and diarrhea occur. Mediterranean fever

Q: What enzyme converts hypoxanthine to xanthine in the pathophysiology of gout?

Xanthine oxidase converts hypoxanthine to xanthine in the pathophysiology of gout. This process is a key step in the formation of uric acid, which can lead to gout.

49 important questions on ANALGESICS - GOUT AND ARTHRITIS

What is the value of Allopurinol or Uricosuric agents in acute Gout?

Allopurinol or Uricosuric agents are of no value in acute Gout and may precipitate an acute attack. Lowering of serum uric acid causes its withdrawal from tissues initiating an inflammatory reaction.

What is the mechanism of action for uricosuric agents like Probenecid?

Uricosuric agents compete with uric acid in the renal tubule for reabsorption by the weak acid carrier mechanism, resulting in increased uric acid excretion.

What is the recommended dose for Probenecid?

The recommended dose for Probenecid is 0.5 – 1mg/day.

What is the mechanism of action for Allopurinol?

Inhibits Xanthine oxidase enzyme.
Converts hypoxanthine to xanthine and xanthine to uric acid.
Decreases uric acid synthesis.
Decreases urate pools in the body.

What is the recommended dose of Allopurinol?

100 - 300mg/day orally.

What is the mechanism of action of Colchicine?

It is a selective inhibitor of microtubule assembly reducing leukocyte migration and phagocytosis.
It may also reduce production of leukotriene-B4 (chemotactic for neutrophils).

What are the specific and non-specific anti-inflammatory drugs used to reduce inflammation during acute gout attacks?

Colchicine: specific anti-inflammatory in gout
Indomethacin: non-specific anti-inflammatory

What are the indications for Colchicine?

Acute Gouty Arthritis: 1mg then 0.5mg/2hrs until pain is relieved or nausea and diarrhea occur.
Mediterranean fever

What is the role of uricosuric drugs in gout treatment?

Uricosuric drugs like Probenecid and Sulphinpyrazone increase renal excretion of uric acid.

What are the toxicities associated with Colchicine?

GIT disturbances especially diarrhea
Alopecia
Liver and kidney damage

What enzyme converts hypoxanthine to xanthine in the pathophysiology of gout?

Xanthine oxidase converts hypoxanthine to xanthine in the pathophysiology of gout. This process is a key step in the formation of uric acid, which can lead to gout.

How does Allopurinol function in the treatment of gout?

Allopurinol inhibits the synthesis of uric acid by Xanthine oxidase inhibitors.

What characterizes gout as a metabolic disorder?

Gout is a metabolic disorder characterized by increased body stores of uric acid. Hyperuricemia results in deposition of urate crystals in tissues (kidney and joints) causing pain and inflammation.

What role does allopurinol play in the treatment of gout?

Allopurinol inhibits xanthine oxidase, reducing the conversion of hypoxanthine to xanthine and xanthine to uric acid, thus lowering uric acid levels in the body.

Which drugs are recommended for acute gout?

Acute gout is treated with Indomethacin or Colchicine.

What is Penicillamine and what are its adverse effects?

Penicillamine is a copper-chelating agent. The Penicillamine-copper complex acts as superoxide dismutase inhibiting formation of toxic oxygen metabolites. Adverse effects include renal damage and aplastic anemia.

What does the inflammatory reaction in gout involve?

The inflammatory reaction involves migration of leucocytes that phagocytose the urate crystals. This results in production of inflammatory mediators (PGs and Chemotactic LTB4 that attracts neutrophils) and oxygen metabolites that induce tissue damage.

How do uricosuric agents like sulfinpyrazone and probenecid affect uric acid levels?

Uricosuric agents such as sulfinpyrazone and probenecid increase renal excretion of uric acid, helping to lower uric acid levels and manage gout.

What treatments are suggested for chronic gout?

Chronic gout is treated with Allopurinol or Uricosurics (Probenecid, Sulphinpyrazone).

What are the effects of antimalarial drugs like Chloroquine and Hydroxychloroquine on T-lymphocyte activity?

Antimalarial drugs such as Chloroquine and Hydroxychloroquine interfere with T-lymphocyte activity. They also decrease leukocyte chemotaxis, stabilize lysosomal membranes, and interfere with DNA and RNA synthesis.

What is Sulphasalazine and what are its adverse effects?

Sulphasalazine is a scavenger of toxic oxygen metabolites produced by neutrophils. Adverse effects include GIT upset, headache, and neutropenia.

What is the role of indomethacin in the treatment of gout?

Indomethacin is a non-specific anti-inflammatory used in gout. It reduces inflammation by inhibiting PGs, which are involved in the inflammatory reaction.

What is Methotrexate and its function?

Methotrexate is an immunosuppressant cytotoxic drug that acts by reducing the inflammatory response.

What are the adverse effects of antimalarial drugs like Chloroquine and Hydroxychloroquine?

Adverse effects of antimalarial drugs include dermatitis, bone marrow suppression, and retinal degeneration. These effects are important considerations when using these medications.

How does colchicine specifically help in treating gout?

Colchicine is a specific anti-inflammatory for gout. It inhibits leukocyte migration and phagocytosis of urate crystals, reducing the inflammatory response.

What are NSAIDs used for in therapeutics?

NSAIDs are first-line drugs used for their Analgesic and Anti-inflammatory properties. They are considered essential in the initial management of certain conditions due to these effects.

How do antimalarial drugs like Chloroquine and Hydroxychloroquine affect free radicals?

Antimalarial drugs trap free radicals. This action is part of their mechanism, alongside interfering with T-lymphocyte activity and stabilizing lysosomal membranes.

What is the effect of leukocyte migration in the pathophysiology of gout?

Leukocyte migration leads to phagocytosis of urate crystals, contributing to the inflammatory reaction in gout. This process can exacerbate symptoms.

What combination of medications is given after the initial diagnosis of Rheumatoid Arthritis?

After initial diagnosis, a combination of Steroids, NSAIDs, and DMARDS is given because DMARDS take several weeks before effects are felt (6-12 weeks).

How do Gold salts function in DMARDs?

They alter the activity of macrophages, inhibit lysosomal enzyme activity, and reduce Histamine release.

Why are corticosteroids considered third-line drugs?

Corticosteroids are considered third-line drugs because they are too toxic for chronic use. They should be reserved for temporary control of severe exacerbation of inflammatory joint conditions.

What is the function of LTB₄ in gout inflammation?

LTB₄ is a chemotactic factor that attracts more leukocytes, enhancing the inflammatory reaction in gout by increasing leukocyte presence at the site.

How do drugs act in therapeutics for rheumatoid arthritis?

Drugs act by suppressing the immunity and inflammatory responses by inhibiting T cells and B cells.

What is the role of NSAIDs in treating Rheumatoid Arthritis?

NSAIDs alone are not enough to treat RA. They relieve immediate symptoms such as pain and inflammation and bridge the time until treatment with DMARDS is effective.

When should corticosteroids be stopped in treatment?

Corticosteroids should be stopped when DMARDs become effective. They are used temporarily for severe exacerbation of inflammatory joint conditions as second-line treatment.

What are the adverse effects of Gold salts?

Dermatitis.
- Bone marrow suppression.
- GIT disturbances with oral Gold compounds.

What is one goal of therapy for RA related to pain?

One goal of therapy for RA is to relieve pain by suppressing muscle spasm and joint stiffness.

What is the drug of choice for rheumatoid arthritis?

DMARDs (Disease-modifying anti-rheumatic drugs) are the drug of choice for rheumatoid arthritis.

Why should corticosteroids be used cautiously in Rheumatoid Arthritis treatment?

Corticosteroids are too toxic for chronic use compared to DMARDS and should be reserved for temporary control and stopped when DMARDS become effective to prevent long-term exposure.

What are some examples of second-line drugs in therapeutics?

Second-line drugs include Disease-modifying slow acting agents such as Gold salts, Penicillamine, Sulfasalazine, Antimalarial drugs, and Methotrexate. These drugs modify disease progression.

What characterizes Rheumatoid Arthritis?

An auto-immune disease characterized by over reactive white blood cells attacking the synovium (joint tissue), resulting in inflammation and subsequent tissue damage. Progression results in deformities.

How does therapy for RA aim to preserve functional status?

Therapy aims to preserve functional status by addressing morning stiffness (45-90 minutes) and flares with severe symptoms like intense pain and stiff joints affecting daily tasks.

Name the main drugs used in DMARDs for rheumatoid arthritis.

The main drugs used are methotrexate, hydroxychloroquine, azathioprine, sulfasalazine, and leflunomide.

How is Rheumatoid Arthritis diagnosed?

Diagnosed clinically and by presence of the rheumatoid factor in the blood.

What is a goal of RA therapy concerning joint inflammation?

A goal of RA therapy is to reduce or suppress joint inflammation.

What is the purpose of DMARDs in rheumatoid arthritis treatment?

DMARDs are used for long-term maintenance in helping suppress inflammatory activity.

How does RA therapy help prevent disease progression?

RA therapy helps prevent disease progression by controlling systemic involvement.

What is the rationale for using DMARDs in rheumatoid arthritis?

The rationale is to limit long-term exposure to steroids.

What is a preventative goal of RA therapy?

A preventative goal of RA therapy is to prevent complications.

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Phamarcology

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