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Rheumatoid Arthritis Drug Therapy Part 4
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Rheumatoid Arthritis Drug Therapy Part 4

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Questions and Answers

What is the mechanism by which methotrexate exerts its effects in rheumatoid arthritis?

  • Inhibition of T cell apoptosis
  • Inhibition of multiple intracellular enzymes (correct)
  • Inhibition of DNA synthesis exclusively
  • Inhibition of lysosomal stability

    • What is the primary characteristic of rheumatoid arthritis?

  • Symmetric small joint inflammation (correct)
  • Local muscle atrophy
  • Rapid joint regeneration
  • Asymmetric joint inflammation

    • Which of the following describes the mechanism of action of hydroxychloroquine?

  • Decreased IgA and IgM production
  • Stabilization of lysosomal membranes (correct)
  • Activation of T cell response to antigens
  • Inhibition of cytokine release from macrophages

    • Which immune cells are primarily involved in the pathophysiology of rheumatoid arthritis?

    <p>Activated T cells and B cells</p> Signup and view all the answers

    Which drug requires administration of folic acid to prevent deficiency after its use?

    <p>Methotrexate</p> Signup and view all the answers

    What types of joints are mainly affected in rheumatoid arthritis?

    <p>Symmetrical small joints of the hands and toes</p> Signup and view all the answers

    What is the main adverse effect of methotrexate that requires patient monitoring?

    <p>Hepatotoxicity</p> Signup and view all the answers

    How does cyclosporine specifically affect T cells?

    <p>Inhibition of calcineurin phosphorylation</p> Signup and view all the answers

    Which of the following statements about symptoms of rheumatoid arthritis is true?

    <p>Morning symptoms include swelling and pain</p> Signup and view all the answers

    What is a known but not fully understood aspect of the etiology of rheumatoid arthritis?

    <p>The exact role of genetic factors</p> Signup and view all the answers

    What kind of joint deformities can occur in late cases of rheumatoid arthritis?

    <p>Characteristic joint deformities</p> Signup and view all the answers

    Which soluble mediators are mentioned as causes of joint inflammation in rheumatoid arthritis?

    <p>Cytokines, including TNF-α and IL-1</p> Signup and view all the answers

    What role does the immune system play in rheumatoid arthritis pathology?

    <p>It attacks joint structures as foreign antigens</p> Signup and view all the answers

    What is the significance of detecting Cyclic Citrullinated Peptide antibodies in patients?

    <p>They can be detected up to 10 years before RA develops.</p> Signup and view all the answers

    Which of the following statements about Disease-Modifying Antirheumatoid Drugs (DMARDs) is true?

    <p>Combining multiple DMARDs can enhance their effectiveness.</p> Signup and view all the answers

    Why are TNF-α inhibitors not recommended until after trying nonbiologic DMARDs?

    <p>They have significant costs and potential side effects.</p> Signup and view all the answers

    Which of the following manifestations is least likely to be an extra-articular manifestation of rheumatoid arthritis?

    <p>Chronic skin rash</p> Signup and view all the answers

    What role do NSAIDs play in the management of rheumatoid arthritis?

    <p>They provide symptomatic relief but do not prevent joint damage.</p> Signup and view all the answers

    Which of the following statements about the use of corticosteroids in RA management is incorrect?

    <p>Corticosteroids are used for long-term management.</p> Signup and view all the answers

    Which TNF-α inhibitor is described as a recombinant protein?

    <p>Etanercept</p> Signup and view all the answers

    What is a potential risk associated with the use of TNF-α inhibitors?

    <p>Increased risk of acute infections</p> Signup and view all the answers

    Methotrexate must be taken daily to maintain its effectiveness.

    <p>False</p> Signup and view all the answers

    The primary mechanism of action of sulfasalazine involves the inhibition of IgA and IgM production.

    <p>True</p> Signup and view all the answers

    Anakinra has a long half-life and can be given orally once a week.

    <p>False</p> Signup and view all the answers

    Gold salts primarily inhibit the functions of human macrophages.

    <p>True</p> Signup and view all the answers

    Cyclophosphamide works by enhancing DNA synthesis in immune cells.

    <p>False</p> Signup and view all the answers

    Rheumatoid arthritis primarily affects large joints in a symmetrical manner.

    <p>False</p> Signup and view all the answers

    The exact etiology of rheumatoid arthritis is well understood and solely attributed to genetic factors.

    <p>False</p> Signup and view all the answers

    Inflammation in rheumatoid arthritis is caused by activated T cells, B cells, and other immune cells.

    <p>True</p> Signup and view all the answers

    Joint deformity in late cases of rheumatoid arthritis is characterized by the absence of symptoms.

    <p>False</p> Signup and view all the answers

    Symptoms of rheumatoid arthritis are often more severe in the evening.

    <p>False</p> Signup and view all the answers

    Cytokines such as TNF-α and IL-1 are type of soluble mediators that contribute to joint inflammation in rheumatoid arthritis.

    <p>True</p> Signup and view all the answers

    Rheumatoid arthritis can lead to cartilage destruction and bone erosion due to an abnormal immune response.

    <p>True</p> Signup and view all the answers

    Extra-articular manifestations of rheumatoid arthritis are rare and seldom observed.

    <p>False</p> Signup and view all the answers

    Cyclic Citrullinated Peptide antibodies can be detected up to 5 years before the development of rheumatoid arthritis.

    <p>False</p> Signup and view all the answers

    Disease-Modifying Antirheumatoid Drugs (DMARDs) begin to show their effects within hours of administration.

    <p>False</p> Signup and view all the answers

    Adalimumab and infliximab are examples of nonbiologic DMARDs.

    <p>False</p> Signup and view all the answers

    Joint X-rays can show symptoms specific to rheumatoid arthritis such as joint swelling and bony erosions.

    <p>True</p> Signup and view all the answers

    Corticosteroids are intended for long-term therapy in the management of rheumatoid arthritis.

    <p>False</p> Signup and view all the answers

    Combinations of two DMARDs are generally less effective than using a single DMARD.

    <p>False</p> Signup and view all the answers

    NSAIDs are effective in preventing joint destruction due to rheumatoid arthritis.

    <p>False</p> Signup and view all the answers

    Live virus vaccination is a contraindication for the use of TNF-α inhibitors.

    <p>True</p> Signup and view all the answers

    What must be administered 24 hours after a dose of methotrexate to counteract possible deficiency?

    <p>Folic acid 5mg must be administered.</p> Signup and view all the answers

    How does leflunomide compare to methotrexate in terms of effectiveness for bone damage?

    <p>Leflunomide is as effective as methotrexate in inhibiting bone damage.</p> Signup and view all the answers

    What is the main mechanism by which gold salts function in the treatment of rheumatoid arthritis?

    <p>Gold salts inhibit the functions of human macrophages.</p> Signup and view all the answers

    Identify the key mechanism by which cyclosporine exerts its effects on T cells.

    <p>Cyclosporine inhibits the phosphorylation of calcineurin.</p> Signup and view all the answers

    Which drug is a competitive IL-1 receptor antagonist and requires daily subcutaneous administration?

    <p>Anakinra is the drug that fits this description.</p> Signup and view all the answers

    What role do activated immune cells play in the pathophysiology of rheumatoid arthritis?

    <p>Activated immune cells, including T cells and B cells, produce soluble mediators that lead to joint inflammation and damage.</p> Signup and view all the answers

    Describe a common clinical manifestation of rheumatoid arthritis in small joints.

    <p>Affected small joints are often swollen and painful, with limited mobility, particularly worsening in the morning.</p> Signup and view all the answers

    What is a significant, yet unclear factor, contributing to the development of rheumatoid arthritis?

    <p>Genetic factors are significant but their exact role in the etiology of rheumatoid arthritis remains unclear.</p> Signup and view all the answers

    What is the impact of cytokines like TNF-α and IL-1 in rheumatoid arthritis?

    <p>Cytokines such as TNF-α and IL-1 exacerbate joint inflammation and contribute to tissue destruction.</p> Signup and view all the answers

    In severe cases of rheumatoid arthritis, which additional joints may become affected?

    <p>In severe cases, larger joints such as the knees and elbows may also become involved.</p> Signup and view all the answers

    What distinguishes the joint symptoms of rheumatoid arthritis from other types of arthritis?

    <p>Rheumatoid arthritis typically causes symmetric joint inflammation and deformities, particularly in small joints.</p> Signup and view all the answers

    Explain the significance of the term 'extra-articular manifestations' in rheumatoid arthritis.

    <p>Extra-articular manifestations refer to symptoms outside the joints, such as fatigue and organ involvement, which are common in RA.</p> Signup and view all the answers

    What does the immune system's misidentification of joint structures as 'foreign' indicate in rheumatoid arthritis?

    <p>It indicates an autoimmune response where the immune system mistakenly targets joint tissues, leading to inflammation.</p> Signup and view all the answers

    What role do DMARDs play in the management of rheumatoid arthritis?

    <p>DMARDs prevent disease progression and slow joint destruction by modifying immune reactions.</p> Signup and view all the answers

    What are the implications of detecting anti-CCP antibodies in a patient?

    <p>The presence of anti-CCP antibodies indicates a higher specificity for rheumatoid arthritis and can be detected years before the disease manifests.</p> Signup and view all the answers

    Why are large doses of NSAIDs typically required in the management of rheumatoid arthritis?

    <p>Large doses of NSAIDs are needed to provide symptomatic relief of pain and inflammation, as they do not prevent joint destruction.</p> Signup and view all the answers

    What is a significant reason for the contraindications associated with TNF-α inhibitors?

    <p>TNF-α inhibitors are contraindicated due to the increased risk of serious infections and complications in certain health conditions.</p> Signup and view all the answers

    How do biologic DMARDs, such as Adalimumab and Infliximab, function in treating rheumatoid arthritis?

    <p>Biologic DMARDs inhibit the action of TNF-α, which is involved in the pathogenesis of rheumatoid arthritis, preventing its interaction with immune cells.</p> Signup and view all the answers

    What key advantage do combinations of DMARDs offer over single DMARD therapy?

    <p>Combinations of DMARDs are more effective than single drugs in preventing disease progression and managing rheumatoid arthritis symptoms.</p> Signup and view all the answers

    What is the rationale behind using corticosteroids as a short-term therapy in rheumatoid arthritis management?

    <p>Corticosteroids provide prompt relief of inflammation and symptoms while waiting for DMARDs to take effect.</p> Signup and view all the answers

    Why should the administration of TNF inhibitors be delayed until after the use of a nonbiologic DMARD?

    <p>Delaying TNF inhibitors until after a nonbiologic DMARD reduces unnecessary exposure to expensive treatments and potential side effects.</p> Signup and view all the answers

    Methotrexate is a folic acid antagonist with cytotoxic and immunosuppressant properties and is used in more than 60% of RA cases, inhibiting multiple intracellular ______.

    <p>enzymes</p> Signup and view all the answers

    Cyclophosphamide and azathioprine suppress immune function through their cytotoxic action by inhibiting ______ synthesis.

    <p>DNA</p> Signup and view all the answers

    Hydroxychloroquine decreases synthesis of ______ and RNA in inflammatory cells and also stabilizes lysosomal membranes.

    <p>DNA</p> Signup and view all the answers

    Leflunomide suppresses pyrimidine synthesis and the functions of ______ cells.

    <p>T and B</p> Signup and view all the answers

    Anakinra is a competitive ______ receptor antagonist and must be administered subcutaneously daily.

    <p>IL-1</p> Signup and view all the answers

    Rheumatoid arthritis (RA) is characterized by symmetric small joint ______, swelling, and deformity.

    <p>inflammation</p> Signup and view all the answers

    The immune system mistakenly attacks joint structures as if they were ______ antigens.

    <p>foreign</p> Signup and view all the answers

    In RA, the involvement of small joints most often includes the hands and ______.

    <p>toes</p> Signup and view all the answers

    The exact ______ of rheumatoid arthritis remains unclear, although genetic factors play an important role.

    <p>etiology</p> Signup and view all the answers

    Clinical manifestations of RA include swollen, painful joints with limited ______.

    <p>mobility</p> Signup and view all the answers

    In rheumatoid arthritis, affected joints tend to be especially worse in the ______.

    <p>morning</p> Signup and view all the answers

    The pathophysiology of rheumatoid arthritis involves activated immune cells including T cells and ______.

    <p>B cells</p> Signup and view all the answers

    Chronic inflammation in RA can lead to cartilage destruction, bone erosion, and ______.

    <p>deformity</p> Signup and view all the answers

    Detection of Cyclic Citrullinated Peptide antibodies is more specific than ______ and can be detected up to 10 years before the development of RA.

    <p>rheumatoid factor</p> Signup and view all the answers

    They prevent progression of the disease and slow joint destruction by modifying the immune ______.

    <p>reactions</p> Signup and view all the answers

    Adalimumab and infliximab are monoclonal antibodies that complex with ______ and prevent its interaction with T cells.

    <p>TNF-α</p> Signup and view all the answers

    NSAIDs offer symptomatic relief of pain and inflammation but don't prevent joint ______.

    <p>destruction</p> Signup and view all the answers

    Combinations of two or more DMARDs are generally more ______ than a single drug.

    <p>effective</p> Signup and view all the answers

    Acute and chronic infections are contraindications to the use of ______ inhibitors.

    <p>TNF-α</p> Signup and view all the answers

    Corticosteroids are given as short-term therapy till ______ give their effect.

    <p>DMARDs</p> Signup and view all the answers

    Joint X-ray can show joint swelling and bony ______ typical of RA.

    <p>erosions</p> Signup and view all the answers

    Match the following types of joint manifestations in rheumatoid arthritis with their descriptions:

    <p>Small joint manifestations = Affects hands and toes symmetrically Large joint manifestations = May be affected in severe cases Joint swelling = Indicates inflammation of the joint Joint deformity = Characteristic in late stages of the disease</p> Signup and view all the answers

    Match the following soluble mediators with their roles in rheumatoid arthritis pathophysiology:

    <p>TNF-α = Causes joint inflammation IL-1 = Promotes cartilage destruction Lysosomes = Involved in immune cell response Cytokines = Act as signaling molecules in inflammation</p> Signup and view all the answers

    Match the following components of the immune system with their involvement in rheumatoid arthritis:

    <p>T cells = Actively participate in joint inflammation B cells = Produce antibodies against joint antigens Macrophages = Contribute to cartilage destruction Polymorphonuclear leukocytes = Involved in response to inflammation</p> Signup and view all the answers

    Match the following characteristics of rheumatoid arthritis with their correct descriptions:

    <p>Chronic inflammatory disease = Characterized by persistent joint issues Symmetrical joint inflammation = Occurs in a bilateral manner Morning stiffness = Symptoms often worse upon waking Extra-articular manifestations = Involves symptoms beyond joints</p> Signup and view all the answers

    Match the following phases of rheumatoid arthritis with their features:

    <p>Early phase = Joint inflammation and swelling Advanced phase = Presence of joint deformities Chronic phase = Ongoing damage and erosion Acute phase = Severe pain and mobility issues</p> Signup and view all the answers

    Match the following risk factors with their relevance to rheumatoid arthritis:

    <p>Genetic factors = Play a significant role in disease susceptibility Environmental triggers = May exacerbate or induce symptoms Hormonal influences = Can affect disease progression Age = Increases likelihood of development</p> Signup and view all the answers

    Match the following terms related to immune response in rheumatoid arthritis with their definitions:

    <p>Autoimmunity = Immune system attacking body tissues Inflammation = Response leading to joint swelling and pain Cytokine storm = Excessive release of immune signaling molecules Joint erosion = Destruction of bone due to chronic inflammation</p> Signup and view all the answers

    Match the following symptoms of rheumatoid arthritis with their typical characteristics:

    <p>Pain = Worsens during morning hours Swelling = Indicates ongoing inflammation Deformity = Occurs in late-stage disease Stiffness = Often experienced after periods of inactivity</p> Signup and view all the answers

    Match the following management strategies with their descriptions for rheumatoid arthritis (RA):

    <p>NSAIDs = Provide symptomatic relief of pain and inflammation Corticosteroids = Short-term therapy until DMARDs take effect DMARDs = Prevent progression of the disease and joint destruction Biologic DMARDs = Target TNF-α to reduce inflammatory response</p> Signup and view all the answers

    Match the following conditions with their corresponding extra-articular manifestations in rheumatoid arthritis:

    <p>Pleural effusion = Involves fluid accumulation in the pleural space Vasculitis = Inflammation of blood vessels Pericarditis = Inflammation of the heart's outer layer Anemia = A common systemic manifestation in RA patients</p> Signup and view all the answers

    Match the following serological tests with their relevance in diagnosing rheumatoid arthritis:

    <p>Rheumatoid Factor (RF) = Found in 80% of RA patients Cyclic Citrullinated Peptide antibodies = Can be detected 10 years before RA develops Joint X-ray = Shows joint swelling and bony erosions Anti-CCP = More specific than RF for rheumatoid arthritis</p> Signup and view all the answers

    Match the following biologic DMARDs with their mechanism of action:

    <p>Adalimumab = Monoclonal antibody that complexes with TNF-α Infliximab = Prevents TNF-α interaction with immune cells Etanercept = Recombinant protein that inhibits TNF-α binding TNF-α inhibitors = Reduce inflammatory cell activation</p> Signup and view all the answers

    Match the following contraindications with their relevance to TNF-α inhibitors:

    <p>Acute infections = Increased risk of complications from immunosuppression Live virus vaccination = Avoid due to potential severe reactions Demyelinating disorders = Risk of exacerbating neurological conditions Recent malignancies = Potentially dangerous in immunocompromised patients</p> Signup and view all the answers

    Match the following characteristics with their corresponding types of DMARDs:

    <p>Nonbiologic DMARDs = Use methotrexate initially in treatment Biologic DMARDs = More expensive and used second-line Traditional DMARDs = Include sulfasalazine and leflunomide Combination therapy = More effective than single DMARD therapy</p> Signup and view all the answers

    Match the following statements with their implications for RA management:

    <p>DMARDs = Should be started as early as possible NSAIDs = Do not prevent joint destruction Corticosteroids = Utilized for short-term relief Biologics = Prescribed after insufficient response to nonbiologics</p> Signup and view all the answers

    Match the following symptoms with their characteristics related to rheumatoid arthritis:

    <p>Joint swelling = Indicates active inflammation in RA Bony erosions = Visible on joint X-rays Systemic fatigue = Commonly reported in RA patients Morning stiffness = A hallmark symptom of rheumatoid arthritis</p> Signup and view all the answers

    Match the following drugs with their primary mechanism of action:

    <p>Methotrexate = Inhibition of multiple intracellular enzymes needed for activation of immune cells Hydroxychloroquine = Decreases synthesis of DNA and RNA in inflammatory cells Sulfasalazine = Inhibition of IgA and IgM production Cyclosporine = Inhibition of phosphorylation of calcineurin in T cells</p> Signup and view all the answers

    Match the following drugs with their administration route:

    <p>Methotrexate = Orally once weekly Anakinra = Subcutaneously daily Gold salts = Intramuscularly or orally Cyclophosphamide = Intravenously or orally</p> Signup and view all the answers

    Match the following medications with their common adverse effects:

    <p>Methotrexate = Hepatotoxicity and myelosuppression Anakinra = Increased risk of infections Cyclosporine = Nephrotoxicity Leflunomide = Diarrhea and rash</p> Signup and view all the answers

    Match the following drugs with their classification:

    <p>Methotrexate = First line DMARD Hydroxychloroquine = Antimalarial drug Azathioprine = Immunosuppressant Leflunomide = Pyrimidine synthesis inhibitor</p> Signup and view all the answers

    Match the following drugs with their specific effects on immune functions:

    <p>Methotrexate = Inhibits activation of T cells and macrophages Sulfasalazine = Suppresses B cell functions Cyclophosphamide = Inhibits DNA synthesis Gold salts = Decreases release of inflammatory cytokines</p> Signup and view all the answers

    Study Notes

    Definition of Rheumatoid Arthritis (RA)

    • Chronic inflammatory disease characterized by symmetrical small joint inflammation, swelling, and deformity.
    • Extra-articular manifestations are common and can affect systemic organs.

    Pathophysiology

    • Exact etiology is unclear; genetic factors significantly influence RA development.
    • Immune system involvement includes activated T cells, B cells, polymorphonuclear leukocytes, macrophages, and the complement system.
    • Production of soluble mediators (lysozymes, cytokines such as TNF-α and IL-1) leads to joint inflammation, cartilage destruction, bone erosion, and deformity.

    Clinical Manifestations

    Articular Manifestations

    • Primarily affects small joints of hands and toes symmetrically; larger joints can be affected in severe cases.
    • Symptoms include swelling, pain, limited mobility, and worsened symptoms in the morning.
    • Late-stage complications lead to characteristic joint deformities.

    Extra-Articular Manifestations

    • RA can manifest in systemic organs, potentially causing pleural effusion, pericarditis, vasculitis, and anemia.

    Diagnosis

    • Serological tests detect abnormal "rheumatoid factor" antibodies in 80% of RA patients.
    • Cyclic Citrullinated Peptide (anti-CCP) antibodies are more specific and can be identified up to 10 years before RA onset.
    • Joint X-rays reveal characteristic joint swelling and bony erosions.

    Management of RA

    Symptomatic Treatment

    • NSAIDs provide relief for pain and inflammation but do not prevent joint destruction.
    • Corticosteroids are used short-term until DMARDs take effect.

    Disease-Modifying Antirheumatoid Drugs (DMARDs)

    • DMARDs are crucial and should be initiated early; effects may take 3 weeks to 3 months.
    • They prevent disease progression and joint damage by altering immune reactions.
    • Combination therapy with multiple DMARDs is more effective than single-drug treatment.

    Biologic DMARDs: TNF-α Inhibitors

    • These are key DMARDs due to TNF-α's role in RA pathogenesis.
    • Drugs include Adalimumab and Infliximab (monoclonal antibodies), and Etanercept (recombinant protein).
    • Contraindications include acute/chronic infections, live virus vaccinations, demyelinating disorders, severe heart failure, and recent malignancies.
    • Guidelines recommend using these after one nonbiologic DMARD, typically methotrexate, has failed.

    Specific DMARDs

    • Methotrexate: First-line treatment in over 60% of RA cases; folic acid antagonist with cytotoxic properties. Weekly dosing with needed folic acid supplementation due to adverse effects including hepatotoxicity and myelosuppression.

    • Hydroxychloroquine: Antimalarial drug that reduces DNA/RNA synthesis in inflammatory cells and stabilizes lysosomal membranes.

    • Sulfasalazine: Metabolizes into sulfapyridine and 5-aminosalicylic acid, inhibiting IgA/IgM production and suppressing T and B cell functions.

    • Immunosuppressants: Cyclophosphamide and azathioprine inhibit immune function through cytotoxicity. Cyclosporine specifically targets T cell function.

    • Gold salts: Administered IM or orally; inhibit macrophage function and decrease inflammatory cytokines.

    • Leflunomide: Suppresses pyrimidine synthesis, inhibiting T and B cell functions; comparable to methotrexate in preventing bone damage.

    • Anakinra: Competitive IL-1 receptor antagonist, requiring daily subcutaneous administration due to a short half-life.

    Definition of Rheumatoid Arthritis (RA)

    • Chronic inflammatory disease characterized by symmetrical small joint inflammation, swelling, and deformity.
    • Extra-articular manifestations are common and can affect systemic organs.

    Pathophysiology

    • Exact etiology is unclear; genetic factors significantly influence RA development.
    • Immune system involvement includes activated T cells, B cells, polymorphonuclear leukocytes, macrophages, and the complement system.
    • Production of soluble mediators (lysozymes, cytokines such as TNF-α and IL-1) leads to joint inflammation, cartilage destruction, bone erosion, and deformity.

    Clinical Manifestations

    Articular Manifestations

    • Primarily affects small joints of hands and toes symmetrically; larger joints can be affected in severe cases.
    • Symptoms include swelling, pain, limited mobility, and worsened symptoms in the morning.
    • Late-stage complications lead to characteristic joint deformities.

    Extra-Articular Manifestations

    • RA can manifest in systemic organs, potentially causing pleural effusion, pericarditis, vasculitis, and anemia.

    Diagnosis

    • Serological tests detect abnormal "rheumatoid factor" antibodies in 80% of RA patients.
    • Cyclic Citrullinated Peptide (anti-CCP) antibodies are more specific and can be identified up to 10 years before RA onset.
    • Joint X-rays reveal characteristic joint swelling and bony erosions.

    Management of RA

    Symptomatic Treatment

    • NSAIDs provide relief for pain and inflammation but do not prevent joint destruction.
    • Corticosteroids are used short-term until DMARDs take effect.

    Disease-Modifying Antirheumatoid Drugs (DMARDs)

    • DMARDs are crucial and should be initiated early; effects may take 3 weeks to 3 months.
    • They prevent disease progression and joint damage by altering immune reactions.
    • Combination therapy with multiple DMARDs is more effective than single-drug treatment.

    Biologic DMARDs: TNF-α Inhibitors

    • These are key DMARDs due to TNF-α's role in RA pathogenesis.
    • Drugs include Adalimumab and Infliximab (monoclonal antibodies), and Etanercept (recombinant protein).
    • Contraindications include acute/chronic infections, live virus vaccinations, demyelinating disorders, severe heart failure, and recent malignancies.
    • Guidelines recommend using these after one nonbiologic DMARD, typically methotrexate, has failed.

    Specific DMARDs

    • Methotrexate: First-line treatment in over 60% of RA cases; folic acid antagonist with cytotoxic properties. Weekly dosing with needed folic acid supplementation due to adverse effects including hepatotoxicity and myelosuppression.

    • Hydroxychloroquine: Antimalarial drug that reduces DNA/RNA synthesis in inflammatory cells and stabilizes lysosomal membranes.

    • Sulfasalazine: Metabolizes into sulfapyridine and 5-aminosalicylic acid, inhibiting IgA/IgM production and suppressing T and B cell functions.

    • Immunosuppressants: Cyclophosphamide and azathioprine inhibit immune function through cytotoxicity. Cyclosporine specifically targets T cell function.

    • Gold salts: Administered IM or orally; inhibit macrophage function and decrease inflammatory cytokines.

    • Leflunomide: Suppresses pyrimidine synthesis, inhibiting T and B cell functions; comparable to methotrexate in preventing bone damage.

    • Anakinra: Competitive IL-1 receptor antagonist, requiring daily subcutaneous administration due to a short half-life.

    Definition of Rheumatoid Arthritis (RA)

    • Chronic inflammatory disease characterized by symmetrical small joint inflammation, swelling, and deformity.
    • Extra-articular manifestations are common and can affect systemic organs.

    Pathophysiology

    • Exact etiology is unclear; genetic factors significantly influence RA development.
    • Immune system involvement includes activated T cells, B cells, polymorphonuclear leukocytes, macrophages, and the complement system.
    • Production of soluble mediators (lysozymes, cytokines such as TNF-α and IL-1) leads to joint inflammation, cartilage destruction, bone erosion, and deformity.

    Clinical Manifestations

    Articular Manifestations

    • Primarily affects small joints of hands and toes symmetrically; larger joints can be affected in severe cases.
    • Symptoms include swelling, pain, limited mobility, and worsened symptoms in the morning.
    • Late-stage complications lead to characteristic joint deformities.

    Extra-Articular Manifestations

    • RA can manifest in systemic organs, potentially causing pleural effusion, pericarditis, vasculitis, and anemia.

    Diagnosis

    • Serological tests detect abnormal "rheumatoid factor" antibodies in 80% of RA patients.
    • Cyclic Citrullinated Peptide (anti-CCP) antibodies are more specific and can be identified up to 10 years before RA onset.
    • Joint X-rays reveal characteristic joint swelling and bony erosions.

    Management of RA

    Symptomatic Treatment

    • NSAIDs provide relief for pain and inflammation but do not prevent joint destruction.
    • Corticosteroids are used short-term until DMARDs take effect.

    Disease-Modifying Antirheumatoid Drugs (DMARDs)

    • DMARDs are crucial and should be initiated early; effects may take 3 weeks to 3 months.
    • They prevent disease progression and joint damage by altering immune reactions.
    • Combination therapy with multiple DMARDs is more effective than single-drug treatment.

    Biologic DMARDs: TNF-α Inhibitors

    • These are key DMARDs due to TNF-α's role in RA pathogenesis.
    • Drugs include Adalimumab and Infliximab (monoclonal antibodies), and Etanercept (recombinant protein).
    • Contraindications include acute/chronic infections, live virus vaccinations, demyelinating disorders, severe heart failure, and recent malignancies.
    • Guidelines recommend using these after one nonbiologic DMARD, typically methotrexate, has failed.

    Specific DMARDs

    • Methotrexate: First-line treatment in over 60% of RA cases; folic acid antagonist with cytotoxic properties. Weekly dosing with needed folic acid supplementation due to adverse effects including hepatotoxicity and myelosuppression.

    • Hydroxychloroquine: Antimalarial drug that reduces DNA/RNA synthesis in inflammatory cells and stabilizes lysosomal membranes.

    • Sulfasalazine: Metabolizes into sulfapyridine and 5-aminosalicylic acid, inhibiting IgA/IgM production and suppressing T and B cell functions.

    • Immunosuppressants: Cyclophosphamide and azathioprine inhibit immune function through cytotoxicity. Cyclosporine specifically targets T cell function.

    • Gold salts: Administered IM or orally; inhibit macrophage function and decrease inflammatory cytokines.

    • Leflunomide: Suppresses pyrimidine synthesis, inhibiting T and B cell functions; comparable to methotrexate in preventing bone damage.

    • Anakinra: Competitive IL-1 receptor antagonist, requiring daily subcutaneous administration due to a short half-life.

    Definition of Rheumatoid Arthritis (RA)

    • Chronic inflammatory disease characterized by symmetrical small joint inflammation, swelling, and deformity.
    • Extra-articular manifestations are common and can affect systemic organs.

    Pathophysiology

    • Exact etiology is unclear; genetic factors significantly influence RA development.
    • Immune system involvement includes activated T cells, B cells, polymorphonuclear leukocytes, macrophages, and the complement system.
    • Production of soluble mediators (lysozymes, cytokines such as TNF-α and IL-1) leads to joint inflammation, cartilage destruction, bone erosion, and deformity.

    Clinical Manifestations

    Articular Manifestations

    • Primarily affects small joints of hands and toes symmetrically; larger joints can be affected in severe cases.
    • Symptoms include swelling, pain, limited mobility, and worsened symptoms in the morning.
    • Late-stage complications lead to characteristic joint deformities.

    Extra-Articular Manifestations

    • RA can manifest in systemic organs, potentially causing pleural effusion, pericarditis, vasculitis, and anemia.

    Diagnosis

    • Serological tests detect abnormal "rheumatoid factor" antibodies in 80% of RA patients.
    • Cyclic Citrullinated Peptide (anti-CCP) antibodies are more specific and can be identified up to 10 years before RA onset.
    • Joint X-rays reveal characteristic joint swelling and bony erosions.

    Management of RA

    Symptomatic Treatment

    • NSAIDs provide relief for pain and inflammation but do not prevent joint destruction.
    • Corticosteroids are used short-term until DMARDs take effect.

    Disease-Modifying Antirheumatoid Drugs (DMARDs)

    • DMARDs are crucial and should be initiated early; effects may take 3 weeks to 3 months.
    • They prevent disease progression and joint damage by altering immune reactions.
    • Combination therapy with multiple DMARDs is more effective than single-drug treatment.

    Biologic DMARDs: TNF-α Inhibitors

    • These are key DMARDs due to TNF-α's role in RA pathogenesis.
    • Drugs include Adalimumab and Infliximab (monoclonal antibodies), and Etanercept (recombinant protein).
    • Contraindications include acute/chronic infections, live virus vaccinations, demyelinating disorders, severe heart failure, and recent malignancies.
    • Guidelines recommend using these after one nonbiologic DMARD, typically methotrexate, has failed.

    Specific DMARDs

    • Methotrexate: First-line treatment in over 60% of RA cases; folic acid antagonist with cytotoxic properties. Weekly dosing with needed folic acid supplementation due to adverse effects including hepatotoxicity and myelosuppression.

    • Hydroxychloroquine: Antimalarial drug that reduces DNA/RNA synthesis in inflammatory cells and stabilizes lysosomal membranes.

    • Sulfasalazine: Metabolizes into sulfapyridine and 5-aminosalicylic acid, inhibiting IgA/IgM production and suppressing T and B cell functions.

    • Immunosuppressants: Cyclophosphamide and azathioprine inhibit immune function through cytotoxicity. Cyclosporine specifically targets T cell function.

    • Gold salts: Administered IM or orally; inhibit macrophage function and decrease inflammatory cytokines.

    • Leflunomide: Suppresses pyrimidine synthesis, inhibiting T and B cell functions; comparable to methotrexate in preventing bone damage.

    • Anakinra: Competitive IL-1 receptor antagonist, requiring daily subcutaneous administration due to a short half-life.

    Definition of Rheumatoid Arthritis (RA)

    • Chronic inflammatory disease characterized by symmetrical small joint inflammation, swelling, and deformity.
    • Extra-articular manifestations are common and can affect systemic organs.

    Pathophysiology

    • Exact etiology is unclear; genetic factors significantly influence RA development.
    • Immune system involvement includes activated T cells, B cells, polymorphonuclear leukocytes, macrophages, and the complement system.
    • Production of soluble mediators (lysozymes, cytokines such as TNF-α and IL-1) leads to joint inflammation, cartilage destruction, bone erosion, and deformity.

    Clinical Manifestations

    Articular Manifestations

    • Primarily affects small joints of hands and toes symmetrically; larger joints can be affected in severe cases.
    • Symptoms include swelling, pain, limited mobility, and worsened symptoms in the morning.
    • Late-stage complications lead to characteristic joint deformities.

    Extra-Articular Manifestations

    • RA can manifest in systemic organs, potentially causing pleural effusion, pericarditis, vasculitis, and anemia.

    Diagnosis

    • Serological tests detect abnormal "rheumatoid factor" antibodies in 80% of RA patients.
    • Cyclic Citrullinated Peptide (anti-CCP) antibodies are more specific and can be identified up to 10 years before RA onset.
    • Joint X-rays reveal characteristic joint swelling and bony erosions.

    Management of RA

    Symptomatic Treatment

    • NSAIDs provide relief for pain and inflammation but do not prevent joint destruction.
    • Corticosteroids are used short-term until DMARDs take effect.

    Disease-Modifying Antirheumatoid Drugs (DMARDs)

    • DMARDs are crucial and should be initiated early; effects may take 3 weeks to 3 months.
    • They prevent disease progression and joint damage by altering immune reactions.
    • Combination therapy with multiple DMARDs is more effective than single-drug treatment.

    Biologic DMARDs: TNF-α Inhibitors

    • These are key DMARDs due to TNF-α's role in RA pathogenesis.
    • Drugs include Adalimumab and Infliximab (monoclonal antibodies), and Etanercept (recombinant protein).
    • Contraindications include acute/chronic infections, live virus vaccinations, demyelinating disorders, severe heart failure, and recent malignancies.
    • Guidelines recommend using these after one nonbiologic DMARD, typically methotrexate, has failed.

    Specific DMARDs

    • Methotrexate: First-line treatment in over 60% of RA cases; folic acid antagonist with cytotoxic properties. Weekly dosing with needed folic acid supplementation due to adverse effects including hepatotoxicity and myelosuppression.

    • Hydroxychloroquine: Antimalarial drug that reduces DNA/RNA synthesis in inflammatory cells and stabilizes lysosomal membranes.

    • Sulfasalazine: Metabolizes into sulfapyridine and 5-aminosalicylic acid, inhibiting IgA/IgM production and suppressing T and B cell functions.

    • Immunosuppressants: Cyclophosphamide and azathioprine inhibit immune function through cytotoxicity. Cyclosporine specifically targets T cell function.

    • Gold salts: Administered IM or orally; inhibit macrophage function and decrease inflammatory cytokines.

    • Leflunomide: Suppresses pyrimidine synthesis, inhibiting T and B cell functions; comparable to methotrexate in preventing bone damage.

    • Anakinra: Competitive IL-1 receptor antagonist, requiring daily subcutaneous administration due to a short half-life.

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    Description

    This quiz covers part 4 of drug therapy related to rheumatoid arthritis (RA). It includes definitions and characteristics of RA, focusing on its chronic inflammatory nature, joint inflammation, swelling, and deformities. It also touches on extra-articular manifestations associated with the disease.

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