Rheumatology Flashcards

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Flashcards covering Rheumatoid Arthritis, Osteoarthritis, and related topics.

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140 Terms

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Rheumatoid Arthritis (RA)

Chronic, systemic autoimmune disorder primarily affecting synovial joints, leading to bone erosion and joint deformity.

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Target Tissue (RA)

Synovium, cartilage, and underlying bone

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Osteon

Structural Unit of Bone

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Organic Matrix Components

Collagen and reticular fibers

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Inorganic Matrix Components

Hydroxyapatite (Ca & phosphate)

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Concentric Lamellae

Matrix layers around a central (Haversian) canal.

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Lacunae

Small cavities housing osteocytes.

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Osteoblasts

Build bone, secrete matrix, become osteocytes

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Osteocytes

Maintain matrix; communicate via canaliculi

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Osteoclasts

Resorb bone, secrete H⁺ and proteases

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Ruffled border

↑ surface area for resorption (osteoclasts)

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PTH Effect on Bone

↑ Osteoclast activity (indirect)

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Calcitonin Effect on Bone

↓ Osteoclast activity

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Pro-inflammatory Cytokine Effects on Bone Cells

↓ Osteoblasts, ↑ Osteoclasts

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Anti-inflammatory Cytokine Effects on Bone Cells

↑ Osteoblasts, ↓ Osteoclasts

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IGF, BMP, TGF-β

Promote osteoblast differentiation

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RANK

Found on the surface of osteoclast precursors (immature osteoclasts); stimulates osteoclast formation and activation, leading to bone resorption.

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RANKL (RANK Ligand)

Made and released by osteoblasts and stromal cells; binds to RANK on osteoclast precursors, stimulating their differentiation, activation, and survival.

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OPG (Osteoprotegerin)

Secreted by osteoblasts; acts as a “decoy receptor”, binding to RANKL and preventing it from activating RANK

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RANKL → RANK

Stimulates osteoclasts; Increased bone Resorption

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OPG → Binds RANKL

Blocks RANK activation; decreased bone resorption

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Vitamin D Effect on Bone

↑ RANKL

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Glucocorticoids Effect on Bone

↓ OPG

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Immune Activation (RA Pathogenesis)

Self-antigens (Self-antigens e.g., citrullinated proteins like fibrinogen, collagen are misidentified as foreign are taken up by antigen-presenting cells (APCs like macrophages and dendritic)→ APCs (dendritic cells, macrophages) present via MHC II; Activation of Th1 and Th17 cells → produce RANKL, ↑ osteoclastogenesis.

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Synovial Inflammation (RA Pathogenesis)

Synoviocytes + T cells produce cytokines (TNF-α, IL-1, IL-6), NF-κB (↑ COX enzymes → ↑ PGE2), MMPs (degrade cartilage/bone)

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RF (Rheumatoid Factor)

IgM antibody targets region of IgG; creates immune complexes which are very inflammatory

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Anti-CCP (ACPA)

Antibodies against citrullinated proteins; targets these altered self-proteins, thinking they’re foreign

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Clinical Presentation of RA

Symmetric joint pain, morning stiffness >1 hr, fatigue, nodules

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RF, anti-CCP Significance in diagnosing RA

Autoantibodies (Anti-CCP = early + specific)

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ESR, CRP Significance in diagnosing RA

Inflammation markers

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Imaging results - RA

Soft tissue swelling, tenosynovitis (early); Marginal erosions (esp. 2nd/3rd MCP & PIP), periarticular osteopenia (progression)

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HLA-DRB1

Strongest genetic link to RA.

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Synovitis Stage of RA

Inflamed synovial membrane

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Pannus Formation Stage of RA

Invasive granulation tissue

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Fibrous Ankylosis Stage of RA

Fibrous fusion of joint

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Bony Ankylosis Stage of RA

Bone fusion, complete immobility

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STAT4

T-cell activation, RA + lupus

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TRAF1-C5

Cytokine signaling

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Smoking Risk Factor for RA

↑ Citrullination, oxidative stress

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Silica Risk Factor for RA

Immune activation

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Oral contraceptives Risk Factor for RA

Protective against RA

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NSAIDs Purpose in Treating RA

Symptom relief, no disease modification

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Steroids Purpose in Treating RA

Short-term; suppress immune function

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Methotrexate (DMARD) Mechanism

Inhibits DHFR (reductase) → ↓ folate → ↓ T/B cell proliferation; ↑ adenosine (anti inflamm effects)

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Sulfasalazine (DMARD) Mechanism

Metabolites inhibit TNF-α, NF-κB, COX enzymes, and immune cells

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Leflunomide (DMARD) Mechanism

Inhibits DHODH enzyme → blocks DNA synthesis in immune cells

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Hydroxychloroquine (DMARD) Mechanism

↑ pH in lysosomes → interferes with antigen processing

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↑ pH in lysosomes Effect

HCQ makes these compartments less acidic.

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↓ Antigen processing Effect

Enzymes can't break down proteins properly.

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↓ MHC-II antigen presentation Effect

T-cells are less activated

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↓ Inflammation Effect

Less immune system overactivity.

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TNF-α inhibitors (Biologic DMARDs)

Etanercept, Infliximab, Adalimumab, target TNF-α

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IL-6 inhibitors (biologic DMARDs)

Tocilizumab, Sirukumab, target IL-6

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B-cell depletion

Rituximab, target CD20 B cells

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T-cell co-stimulation block (biologic DMARDs)

Abatacept, target CTLA-4

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Synovial Fluid Function

Lubricates and nourishes cartilage.

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RA Takeaways

autoimmune → joint destruction; Central: T cells, synoviocytes, RANKL, MMPs, cytokines

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RA Diagnosis

Clinical + serological + imaging

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RA Treatment

Immune modulation with DMARDs, focus on preventing long-term joint damage

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Osteoarthritis (OA) Definition

degenerative joint disease, especially common with aging; knee joint

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Periosteum

Pain-sensitive outer covering of bones.

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Articular Cartilage

Hyaline cartilage; shock absorption and smooth movement.

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Fibrous Capsule

Encloses synovial membrane; together they form the articular capsule

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Ligaments

Provide joint stability.

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Meniscus

Fibrocartilage for stability and shock absorption (knee)

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Osteocytes Function

Mature bone cells.

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Osteoblasts Function

Build bone.

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Osteoclasts Function

Break down bone.

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Synovial Macrophages Function

Immune cells involved in inflammation.

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Key Features of OA

Articular cartilage degeneration, joint space narrowing, Osteophytes (bone spurs), Subchondral sclerosis (bone hardening below cartilage)

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Primary OA

Idiopathic, age-related

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Secondary OA

Due to trauma, congenital abnormalities, or inflammatory diseases

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Risk Factors for OA

Aging, female sex (hip OA), obesity, joint injury, deformity (genu varus/valgus), rheumatic disease, genetics

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OAPathophysiology Macrophages

Macrophages in synovium stimulated by risk factors; release cytokines (TNF-α, IL-1β, IL-6), VEGF, E-selectin

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Cartilage Breakdown Leading to Bone Changes in OA

Damaged cartilage releases IL-1β, IL-6, and TNF-α, stimulating osteoblasts to lay down new bone

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Dysregulation Process in OA

Leads to bony overgrowths (osteophytes) and subchondral sclerosis (thickening/hardening of the bone below cartilage)

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Pain Mechanism in OA

Cytokines, prostaglandins, bradykinin stimulate sensory nerves; Pain increases with activity, relieved by rest; severe OA can cause night/rest pain.

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Clinical Presentation of OA

Pain (activity-related → rest/night), stiffness, malalignment (genu valgus/varus), muscle wasting, tenderness, possible osteophytes (bone spurs), joint effusion, crepitus, reduced movement.

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first line and 2nd option for RA

Methotrexate

First-line for most patients


Hydroxychloroquine

Mild RA or add-on

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X-ray Findings (OA)

Loss of joint space Osteophytes, Subchondral sclerosis, Subchondral cysts

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Joint Aspiration (Arthrocentesis) for OA

Synovial fluid WBC ≤ 2000/uL

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ESR, CRP (Blood Work) Meaning

Rule out inflammatory disease

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RF, Anti-CCP (Blood Work) Meaning

Rule out RA

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ANA (Blood Work) Meaning

Autoimmune screen

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CBC (Blood Work) Meaning

Anemia, WBC, PLT status

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Hb/Hgb (Blood Work) Meaning

Anemia evaluation

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WBC (Blood Work) Meaning

Infection/inflammation

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PLT (Blood Work) Meaning

Thrombocytosis

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LFTs (Blood Work) Meaning

Baseline for medication use

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U&E / RFT (Blood Work) Meaning

Kidney health before NSAID use

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TSH (Blood Work) Meaning

Rule out thyroid-related symptoms

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HLA-B27 (Blood Work) Meaning

Spondyloarthropathy marker

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Serum uric acid - (Blood Work) Meaning

Elevated in gout

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Non-Pharmacological Management (OA)

Weight loss, education, physiotherapy, walking aids, knee braces, good footwear, acupuncture, heat/cold

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Pharmacological Management (OA)

paracetamol aka acetaminophen; Topical NSAIDs or capsaicin; Oral NSAIDs + PPI; Glucocorticoid injections; Viscosupplementation; Opioids; Glucosamine, chondroitin, turmeric, fish oil

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Swelling

Hallmark feature of RA

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Rheumatoid Arthritis (RA) Overview Definition

Chronic, systemic autoimmune inflammatory disease targeting joints, especially synovium.

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Clinical Presentation - RA

Symmetrical arthritis Pain, swelling, and stiffness Subcutaneous nodules

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RA Joints

MCP, PIP, wrist

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OA Joints

DIP, PIP