Part Four: Inflammatory DX - Rheumatoid Arthritis RA Flashcards by Divya Adukuzhiyil

Rheumatoid Arthritis (RA): What kind of disease is this considered?

Autoimmune & inflammatory

Chronic, systemic

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Rheumatoid Arthritis (RA):

Is Chronic, systemic:

What symptoms exist?

Fever, malaise, rash, lymph node or spleen enlargement

Joint swelling, tenderness

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Rheumatoid Arthritis (RA):

What is there destruction of?

Destruction of synovial joints

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Rheumatoid Arthritis (RA):

Destruction of synovial joints:

What does it line?

Why does destruction occur?

What else does it lead to?

lines the joint cavity

Immune system targets the synovium

Synovitis

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Rheumatoid Arthritis (RA):

Destruction of synovial joints:

Synovitis- What does this lead to?

Membrane thickened/swollen

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Rheumatoid Arthritis (RA):

What forms?

Pannus forms

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Rheumatoid Arthritis (RA):

Pannus forms: What is this?

Abnormal tissue growth in synovium

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Rheumatoid Arthritis (RA):

Pannus forms: What does this consist of?

Consists of inflamed synovial cells, immune cells, and blood vessels

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Rheumatoid Arthritis (RA):

Pannus forms: What does it contribute to and how?

Invades & damages nearby cartilage and bone, contributing to joint erosion and deformity

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Rheumatoid Arthritis (RA)

Predisposing Factors

Age (Young & middle aged)

Environmental factors

Females

Postpartum

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Patho of RA:

How does it start (What gets activated?)

Synovial fibroblasts (SF) that line joint cavity get activated

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Patho of RA

When synovial fibroblasts (SF) that line joint cavity get activated, what happens?

Immune system mounts an attack

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Patho of RA

What happens to synovial fibroblasts (SF)?

Synovial fibroblasts (SF) proliferate & produce inflammatory cytokines & PGs

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Patho of RA

Synovial fibroblasts (SF) proliferate & produce inflammatory cytokines & PGs

What do the cytokines do?

Cytokines: Pro-inflammatory (TNF-α, IL-1, and IL-6) drive the inflammatory process.

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Patho of RA:

What does the enflamed synovium (pannus) do?

The inflamed synovium (pannus) grows over the cartilage and bone, releasing enzymes that degrade cartilage and bone.

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Patho of RA:

What does the SFs do?

SFs attack articular cartilage –> more release of inflamm enzymes –> spreads to joint capsule, ligaments, tendons

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Patho of RA

What do activated T-cells do?

Activated T cells produce pro-inflammatory cytokines

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Patho of RA

What do B-cells do?

B cells produce autoantibodies which form immune complexes that further drive inflammation.

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Pannus formation (thickened synovium)

Granulation tissue from the synovium spreads over the articular cartilage, releasing enzymes and inflammatory mediators that destroy the cartilage.

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Slide 5: I don’t understand

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Clinical Manifestations:

How are joints?

Red, swollen, warm and painful joint

Symmetrical
Insidious onset

Multiple joints (small joints in hands, wrists, feet, larger joints like knees, shoulders, hips)

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Clinical Manifestations:

Red, swollen, warm and painful joint

Symmetrical
Insidious onset

Multiple joints (small joints in hands, wrists, feet, larger joints like knees, shoulders, hips)

What leads to this?

Abnormal immune response, causing inflammation of the synovial membrane with vasodilation, increased permeability

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Clinical Manifestations:

Red, swollen, warm and painful joint

Symmetrical
Insidious onset

Multiple joints (small joints in hands, wrists, feet, larger joints like knees, shoulders, hips)

What time of day is this most common?

Sx most intense in the AM

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Clinical manifestations:

How are muscles?

Atrophy of muscles

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Clinical manifestations: Atrophy of muscles: Why does this occur?

Disuse of muscles and stretching of tendons and ligaments related to acute inflammation

Clinical manifestations: What happens to bones? why?

Misalignment of bones Due to eroded cartilage and muscle imbalance

Clinical manifestations: Other than muscle atrophy, what happens to muscles? Why does this occur?

Muscle spasm Inflammation and pain

Clinical manifestations: What happens to mobility? What else? Why does this occur?

Deformity and impaired mobility Contractures and deformity

Clinical manifestations: What other symptoms occur? Why?

Fatigue, anorexia, mild fever, generalized lymphadenopathy, and generalized aching (systemic) From the immune factors

Clinical manifestations: Rheumatoid nodules – What are they?

Rheumatoid nodules – inflammatory tissue, consisting mainly of immune cells (macrophages, lymphocytes, fibroblasts). They may also contain deposits of fibrin.

Eval & Management How to diagnose?

Assessment Labs: Synovial fluid analysis Joint X-rays, MRI, ultrasounds

Eval & Management Diagnose: What kind of labs are needed?

Serum rheumatoid factor test Serum anticyclic citrullinated peptide antibodies test (ACPA) – specific marker ESR – erythrocyte sedimentation rate Serum C-reactive protein Serum antinuclear antibody

Eval & Management: What is treatment?

Early aggressive pharmacotherapy Surgical repair Non-pharm

Eval & Management: Early aggressive pharmacotherapy: Is there a cure?

⍉ cure

Eval & Management: Early aggressive pharmacotherapy: What does this do?

Slowed progression, delayed joint destruction Symptomatic relief

Eval & Management: Early aggressive pharmacotherapy: RA is treated with three classes of drugs: What are they?

1. NSAIDs for pain, 2. glucocorticoids (may delay disease progression), 3. disease-modifying antirheumatic drugs (DMARDs)

Eval & Management: Early aggressive pharmacotherapy: Glucocorticoids: What do they do?

(may delay disease progression),

Eval & Management: Early aggressive pharmacotherapy: NSAIDs: What are they for?

NSAIDs for pain

Eval & Management: Non-pharm treatment? ARTHUR

Assistive devices Rest & pacing activities Therapeutic activities – Heat/cold application Use splints, braces for support & alignment to prevent deformities Relaxation techniques

Eval & Management: Non-pharm treatment? ARTHUR A = Assistive devices ~

walkers, rails

Eval & Management: Non-pharm treatment? ARTHUR Therapeutic activities –

balanced exercise & rest PT & OT ~ massage, warm baths

Eval & Management: Non-pharm treatment? ARTHUR Heat/cold application: What is heat for? What does it do What is cold for? What does it do?

Heat=vasodilation=decrease pain Cold=vasoconstriction=dec pain, swelling

Eval & Management: Non-pharm treatment? ARTHUR Use splints, braces for what?

for support & alignment to prevent deformities

DMARDs: Disease-Modifying Antirheumatic Drugs What is the aim of these drugs?

Aim: reduce joint destruction & slow disease progression

DMARDs: Disease-Modifying Antirheumatic Drugs What are the two groups? What are they based on?

Nonbiologic (traditional) vs Biological (recombinant DNA) based on molecular size & how produced

What is the most rapid acting and first choice DMARD?

Methotrexate

RA DMARDs: Methotrexate- MOA How does it treat disease progression?

Slows disease progression (not just sx relief!!!) Interferes with rapid growth/cell division

RA DMARDs: Methotrexate- MOA What does it do with B and T lymphocyte activity?

Immunosuppression of B&T lymphocyte activity

RA DMARDs: Methotrexate- MOA What does it interfere with?

Interferes with rapid growth/cell division

RA DMARDs: Methotrexate How long does it take therapeutic effects to occur?

Therapeutic effect: 3 to 6 weeks

RA DMARDs: Methotrexate What are adverse effects?

Hepatic fibrosis Bone marrow suppression GI ulceration pneumonitis CVD, infection, lymphomas

RA DMARDs: Methotrexate What are fatal toxicities that can occur?

Fatal toxicities of bone marrow, liver, lungs, kidneys, skin reactions, hemorrhagic enteritis, GI perforation

RA DMARDs: Methotrexate What is necessary when taking this med?

Supplemental folic acid necessary

RA DMARDs: Methotrexate What tests are needed when taking this med?

Periodic liver, kidney function tests, CBC, Platelet

RA DMARDs: Methotrexate How is life expectancy effected?

Reduced life expectancy: CVD, cancers

DMARDs II: Major Biologic DMARDs What are they?

Tumor necrosis factor (TNF) inhibitors

DMARDs II: Major Biologic DMARDs Tumor necrosis factor (TNF) inhibitors: What are TNF ?

TNF is an inflammatory response mediator & responsible for joint injury

DMARDs II: Major Biologic DMARDs In RA, what does TNF bind to?

In RA – TNF binds with synovial cells –

DMARDs II: Major Biologic DMARDs In RA – TNF binds with synovial cells – what does this lead to? (What is stimulated)

stimulates inflammatory mediators, promotes infiltration of neutrophils & macrophages --> inflammation & joint destruction

DMARDs II: Major Biologic DMARDs TNF inhibitors- What do they do?

Binds tightly to TNF & makes it inactive, preventing it from interacting with natural receptors on human cells in the synovium

DMARDs II: Major Biologic DMARDs TNF: Some interfere with B&T lymphocytes What does this put someone at increased risk of?

Increased risk of serious infection

DMARDs II: Major Biologic DMARDs TNF- What do some of them interfere with?

Some interfere with B&T lymphocytes

DMARDs II: Major Biologic DMARDs TNF inhibitors: How is it administered? What can it be combined with?

Weekly subQ injections Can be combined with methotrexate

DMARDs II: Major Biologic DMARDs TNF inhibitors: Work by neutralizing TNF Drugs include?

Etanercept [Enbrel]** Adalimumab [Humira] Certolizumab pegol [Cimzia] Golimumab [Simponi] Infliximab [Remicade] - end in 'mab'

Adverse effects of Etanercept

Injection site reactions Serious infections Severe allergic reactions Heart failure Cancer/Hematologic disorders Liver injury CNS demyelinating disorders

Adverse effects of Etanercept Serious infections include? What may need to be done if infection occurs?

Fungal, TB, opportunistic Reactivation of HBV Increased risk with DM, HIV, immunosuppressant drugs May need to d/c if infection develops

Adverse effects of Etanercept Serious infections include: Fungal, TB, opportunistic

TNF plays crucial role in immune response to infection, especially TB

Part Four: Inflammatory DX - Rheumatoid Arthritis RA Flashcards

Exam 4 (Final)