Membership of the Royal College of Physicians (MRCP UK) Infectious Diseases, Rheumatology and Immunology Flashcards

24 sample cards from the Infectious Diseases, Rheumatology and Immunology deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. Compare the antibodies and muscle features of polymyositis vs dermatomyositis.

   Both: proximal symmetrical muscle weakness, raised creatine kinase, anti-Jo-1 (antisynthetase, linked to ILD). Dermatomyositis adds skin signs (heliotrope rash, Gottron's papules, shawl sign) and anti-Mi-2; in adults it carries a strong association with underlying malignancy.

2. Classify the vasculitides by predominant vessel size with key examples.

   Large vessel: giant cell arteritis, Takayasu. Medium vessel: polyarteritis nodosa, Kawasaki. Small vessel ANCA-associated: granulomatosis with polyangiitis, eosinophilic GPA, microscopic polyangiitis. Small vessel immune-complex: IgA vasculitis (HSP), cryoglobulinaemic.

3. What is the ANCA pattern and target antigen for granulomatosis with polyangiitis vs microscopic polyangiitis?

   GPA: cANCA / anti-PR3 (proteinase 3). Microscopic polyangiitis and eosinophilic GPA: pANCA / anti-MPO (myeloperoxidase). GPA classically affects upper airway (saddle nose), lungs and kidneys.

4. What are the diagnostic features and management of giant cell (temporal) arteritis?

   Age > 50, new headache, scalp tenderness, jaw claudication, visual loss, raised ESR/CRP; temporal artery biopsy shows granulomatous inflammation with skip lesions. Treat immediately with high-dose glucocorticoids (IV if visual symptoms) — do not delay for biopsy.

5. List the key autoantibodies in rheumatoid arthritis and their significance.

   Rheumatoid factor (IgM anti-IgG-Fc): sensitive, not specific. Anti-CCP (anti-cyclic citrullinated peptide): highly specific, predicts erosive/severe disease and may precede symptoms.

6. Describe the typical joint involvement and characteristic hand deformities of rheumatoid arthritis.

   Symmetrical polyarthritis of small joints — MCP and PIP joints, sparing DIP. Deformities: ulnar deviation, swan-neck, boutonnière, Z-thumb. Early morning stiffness > 30-60 min. Atlanto-axial subluxation is a key cervical complication.

7. What is the first-line DMARD for rheumatoid arthritis and what monitoring/co-prescription is required?

   Methotrexate (weekly) is first-line, usually with bridging steroids. Co-prescribe folic acid; monitor FBC, U&E and LFTs for myelosuppression and hepatotoxicity; teratogenic (avoid in pregnancy).

8. Name the seronegative spondyloarthropathies and their unifying associations.

   Ankylosing spondylitis, psoriatic arthritis, reactive arthritis, enteropathic arthritis. Unifying features: HLA-B27 association, rheumatoid-factor negative, axial/sacroiliac involvement, enthesitis, dactylitis, and extra-articular features (uveitis, etc.).

9. What are the classic clinical and radiological features of ankylosing spondylitis?

   Young male, inflammatory back pain improving with exercise, reduced lumbar flexion (Schober's test), sacroiliitis; X-ray shows bamboo spine, syndesmophytes, squaring of vertebrae. Extra-articular: anterior uveitis, apical lung fibrosis, aortic regurgitation, AV block.

10. What is the classic triad of reactive arthritis and its common triggers?

    "Can't see, can't pee, can't climb a tree": conjunctivitis/uveitis, urethritis, and arthritis. Triggered after GI infection (Salmonella, Shigella, Campylobacter, Yersinia) or genital Chlamydia trachomatis; HLA-B27 associated.

11. Compare the synovial fluid crystal findings in gout vs pseudogout.

    Gout: monosodium urate crystals — needle-shaped, negatively birefringent (yellow when parallel to compensator). Pseudogout: calcium pyrophosphate crystals — rhomboid, weakly positively birefringent (blue when parallel).

12. What is the acute and long-term management of gout, including the urate target?

    Acute: NSAID, colchicine, or corticosteroid. Long-term urate-lowering therapy (allopurinol, started after the acute attack settles, with colchicine cover): target serum urate $< 360\ \mu\text{mol/L}$ (or $< 300$ if tophi/recurrent).

13. What organism most commonly causes septic arthritis, and how is the diagnosis confirmed?

    Staphylococcus aureus is the most common cause (Neisseria gonorrhoeae in young sexually active adults). Diagnosis: urgent joint aspiration for Gram stain, culture and crystals before antibiotics; treat with IV antibiotics and joint drainage/washout.

14. What is the most common causative organism and key risk factors for osteomyelitis (and the exception in sickle cell disease)?

    Staphylococcus aureus most commonly. Risk: diabetes, PVD, trauma/surgery, IV drug use. In sickle cell disease, Salmonella is a characteristic cause. MRI is the most sensitive imaging.

15. List the radiographic hallmarks of osteoarthritis (LOSS).

    L — Loss of joint space, O — Osteophytes, S — Subchondral sclerosis, S — Subchondral cysts. Clinically: DIP (Heberden's) and PIP (Bouchard's) nodes, pain worse with activity, brief (<30 min) morning stiffness.

16. What are the diagnostic features and treatment of polymyalgia rheumatica?

    Age > 50, bilateral shoulder/pelvic girdle pain and morning stiffness > 45 min, raised ESR/CRP, rapid (dramatic) response to low-dose prednisolone (~15 mg). Strong association with giant cell arteritis.

17. How is fibromyalgia diagnosed and managed?

    Chronic widespread pain (> 3 months) with fatigue, non-restorative sleep, cognitive symptoms; normal inflammatory markers and imaging — a clinical diagnosis of exclusion. Management: education, graded exercise, CBT; amitriptyline, duloxetine, or pregabalin.

18. Classify primary immunodeficiencies by the affected immune component, with one example each.

    Antibody/B-cell (most common, e.g. common variable immunodeficiency, X-linked agammaglobulinaemia); T-cell/combined (e.g. SCID, DiGeorge); phagocyte (chronic granulomatous disease); complement deficiencies. Pattern of infection helps localise the defect.

19. Which infections characterise complement deficiencies, particularly of the terminal pathway?

    Terminal complement (C5-C9, membrane attack complex) deficiency predisposes to recurrent Neisseria infections (meningococcal). Early classical pathway (C1-C4) deficiency predisposes to SLE-like autoimmunity and encapsulated organisms.

20. What complement abnormality causes hereditary angioedema, and how does it present?

    C1 esterase inhibitor deficiency (low C4 between attacks). Presents with recurrent non-pruritic, non-urticarial angioedema of skin, gut (abdominal pain) and airway, without an allergic trigger. Treat acutely with C1 inhibitor concentrate/icatibant — antihistamines and adrenaline are ineffective.

21. Distinguish anaphylaxis from a milder allergic reaction by its defining features.

    Anaphylaxis is a severe, life-threatening, generalised type I hypersensitivity reaction with rapid onset of Airway (swelling/stridor), Breathing (wheeze/hypoxia) and/or Circulation (hypotension/shock) problems, usually with skin/mucosal changes.

22. State the first-line drug, dose, route and site for adult anaphylaxis.

    Intramuscular adrenaline 0.5 mg (0.5 mL of 1:1000) into the anterolateral mid-thigh, repeated every 5 minutes as needed. Plus high-flow oxygen, IV fluids, and lie patient flat with legs raised.

23. What blood test confirms anaphylaxis retrospectively and when is it taken?

    Serum mast cell tryptase — peaks 1-2 hours after onset. Take samples: as soon as feasible after resuscitation, then 1-2 hours, and a baseline at $> 24$ hours/convalescence.

24. Classify the four Gell and Coombs hypersensitivity reactions with an example of each.

    Type I — immediate IgE-mediated (anaphylaxis, atopy). Type II — antibody-mediated cytotoxic (autoimmune haemolytic anaemia, Goodpasture). Type III — immune complex (SLE, serum sickness, post-strep GN). Type IV — delayed T-cell mediated (contact dermatitis, TB granuloma, Mantoux).

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