1) Rheumatoid Arthritis – Definition
Define rheumatoid arthritis (RA).chronic
Chronic, systemic, autoimmune inflammatory arthritis.
Symmetric polyarthritis involving small joints (MCP, PIP).
Persistent synovitis → pannus → cartilage + bone erosion.
Associated with extra-articular features.
2) RA – Pathogenesis
Key immunologic mechanisms in RA.
HLA-DR4, HLA-DR1 association.
Autoantibodies: RF (IgM anti-IgG), anti-CCP (specific).
Cytokines: TNF-α, IL-6, IL-1.
Synovial hyperplasia → pannus formation.
3) RA – Clinical Features
Core clinical manifestations of RA.
-Morning stiffness > 60 min.
-Symmetric small-joint arthritis.
-Swan-neck + Boutonnière deformities.
-Rheumatoid nodules.
-Extra-articular: ILD, scleritis, pleuritis, anemia of chronic disease.
4) RA – Diagnosis
Diagnostic criteria for RA (high-yield).
-Anti-CCP positive (most specific).
-RF positive (70–80%).
-↑ ESR/CRP.
-Ultrasound/MRI: synovitis, erosions.
-X-ray: joint space narrowing, marginal erosions.
5) RA – Treatment Overview
Outline RA treatment per Harrison.
-First-line: Methotrexate.
-Add folic acid supplementation.
-If inadequate → add biologic DMARD (TNF inhibitors).
-NSAIDs for symptoms only.
-Steroids for bridging therapy.
6) SLE – Definition
Define systemic lupus erythematosus.
-Multisystem autoimmune disease.
-Autoantibodies against nuclear antigens.
-Immune-complex deposition → tissue inflammation.
-Relapsing–remitting course.
7) SLE – Autoantibodies
Important antibodies in SLE.
ANA: screening.
Anti-dsDNA: disease activity, renal involvement.
Anti-Smith: highly specific.
Antiphospholipid: thrombosis + pregnancy loss.
8) SLE – Clinical Features
Common clinical manifestations of SLE.
-Malar rash.
-Photosensitivity.
-Oral ulcers.
-Arthritis (non-erosive).
-Nephritis (proteinuria, RBC casts).
-CNS: seizures, psychosis.
-Serositis (pleuritis/pericarditis).
9) SLE – Treatment
Treatment of SLE based on organ involvement.
-Mild: Hydroxychloroquine + NSAIDs.
-Moderate: steroids + azathioprine/mycophenolate.
-Severe nephritis/CNS: high-dose steroids + cyclophosphamide/rituximab.
-Sun protection mandatory.
10) Sjögren Syndrome
Key features and antibodies in Sjögren syndrome.
-Dry eyes (keratoconjunctivitis sicca).
-Dry mouth (xerostomia).
-Anti-SSA (Ro), anti-SSB (La).
-↑ risk of MALT lymphoma.
11) Systemic Sclerosis (Scleroderma)
Types and autoantibodies of systemic sclerosis.
-Limited (CREST): anti-centromere.
-Diffuse: anti-Scl-70 (anti–topoisomerase I).
-RNA polymerase III: renal crisis risk.
12) Polymyalgia Rheumatica
Features + treatment of PMR.
-Pain & stiffness in shoulders/hips.
-Age > 50.
-Markedly ↑ ESR.
-Rapid response to low-dose prednisone.
13) Giant Cell Arteritis
Key clinical features of GCA.
-New headache (scalp tenderness).
-Jaw claudication.
-Visual loss risk. tummpural vin
-↑ ESR.
-Treat immediately with high-dose steroids.
14) Ankylosing Spondylitis
Classic features of AS.
-Young male with inflammatory back pain.
-Morning stiffness, improves with exercise.
-HLA-B27.
-Bamboo spine (syndesmophytes).
-Uveitis + enthesitis.
17) Gout – Pathogenesis
Why does gout occur?
-Hyperuricemia → MSU crystal deposition in joints.
-Triggers inflammation via NLRP3 inflammasome.
-Major causes: ↓ renal excretion, ↑ production, alcohol.
18) Gout – Acute Attack Treatment
First-line therapy for acute gout.
-NSAIDs (indomethacin).
-Colchicine.
-Steroids for contraindications.
19) Gout – Chronic Management
Chronic therapy of gout.
-Allopurinol (xanthine oxidase inhibitor).
-Febuxostat.
-Probenecid (uricosuric).
-Lifestyle: ↓ alcohol, ↓ red meat, weight loss.
20) Pseudogout (CPPD)
How does pseudogout differ from gout?
-Calcium pyrophosphate crystals.
-Rhomboid, positively birefringent.
-Knee most affected.
-Treat with NSAIDs, colchicine, steroids.
21) Vasculitis – Classification
Classify vasculitides by vessel size.
-Large: GCA, Takayasu
-Medium: PAN, Kawasaki
-Small: GPA, MPA, EGPA, HSP
22) Granulomatosis with Polyangiitis (GPA)
Key features of GPA.
-Necrotizing granulomas in ENT + lungs.
-Glomerulonephritis.
-c-ANCA (PR3) positive.
-Treat with steroids + cyclophosphamide/rituximab.
23) Microscopic Polyangiitis (MPA)
How does MPA differ from GPA?
No granulomas, no ENT disease.
p-ANCA (MPO) positive.
24) Henoch–Schönlein Purpura
Classic tetrad.
-Palpable purpura.
-Arthralgia.
-Abdominal pain.
-IgA nephropathy.
25) Takayasu Arteritis
Key signs.
-Young Asian female.
-Limb claudication.
-Decreased pulses (“pulseless disease”).
-Aortic arch involvement.
27) Dermatomyositis
Skin findings of dermatomyositis.
-Heliotrope rash.
-Gottron papules.
-Shawl sign.
-Perimysial inflammation.
-change the colour of the skin
