Complement in Health & Disease

20 questions β€’ 1 test β€’ tap a section to begin

Welcome! 7.5 Complement in Health & Disease β€” Test 1 — 20 questions, CSIR-NET style.

What this test covers

  • Early-component deficiency & lupus; late-component & Neisseria
  • Hereditary angioedema (C1-INH); PNH (CD55/CD59)
  • Factor H/properdin defects; complement in tissue injury
  • Therapeutic inhibition (eculizumab); CH50; regulation balance

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7.5 Complement in Health & Disease β€” Test 1
Q1. Deficiency of early classical-pathway components (C1, C2, C4) is most strongly associated with:βœ“ Systemic lupus erythematosus (immune-complex disease)
Q2. Deficiency of late (terminal) complement components (C5–C9) characteristically predisposes to:βœ“ Recurrent Neisseria (meningococcal/gonococcal) infections
Q3. Hereditary angioedema is caused by a deficiency of:βœ“ C1 inhibitor (C1-INH)
Q4. Paroxysmal nocturnal haemoglobinuria (PNH) results from a deficiency of GPI-anchored regulators, leading to loss of:βœ“ CD55 (DAF) and CD59 on red cells
Q5. The anti-C5 monoclonal antibody eculizumab treats PNH and atypical HUS by:βœ“ Blocking C5 cleavage, preventing MAC formation
Q6. C3 deficiency, affecting the central component, typically causes:βœ“ Severe, recurrent pyogenic bacterial infections
Q7. Factor H deficiency or dysfunction is associated with kidney diseases such as:βœ“ Atypical haemolytic uraemic syndrome and some membranoproliferative glomerulonephritis
Q8. Complement activation contributes to tissue injury in conditions such as:βœ“ Ischaemia–reperfusion injury and some autoimmune diseases
Q9. Why must patients on eculizumab (anti-C5) be vaccinated against meningococcus?βœ“ Blocking C5 prevents the MAC needed to kill Neisseria
Q10. In age-related macular degeneration, complement is implicated because:βœ“ Variants in complement regulators (e.g. factor H) increase risk
Q11. Complement's beneficial role in clearing apoptotic cells means its deficiency can:βœ“ Allow accumulation of self-antigens, promoting autoimmunity
Q12. Therapeutic complement inhibition is a strategy in diseases driven by:βœ“ Excessive or dysregulated complement activation
Q13. A laboratory finding of low C3 and C4 during active disease (e.g. lupus flare) usually indicates:βœ“ Consumption of complement by ongoing activation
Q14. Properdin deficiency, affecting a positive regulator, predisposes to:βœ“ Severe Neisseria (meningococcal) infections
Q15. The complement system links to adaptive immunity in health by:βœ“ Enhancing B-cell responses (C3d–CR2) and clearing complexes/apoptotic cells
Q16. Anaphylatoxin (C5a) overproduction contributes to pathology in conditions such as:βœ“ Sepsis and severe inflammatory states
Q17. A patient with recurrent Neisseria meningitidis infections should be evaluated for:βœ“ Terminal complement (C5–C9) or properdin deficiency
Q18. The CH50 assay is used clinically to:βœ“ Assess the functional integrity of the classical complement pathway
Q19. Overall, complement in health and disease illustrates that the system must be:βœ“ Tightly regulated to defend against pathogens without harming host tissue
Q20. Match each complement disorder with its key feature and select the correct option.βœ“ A-iii, B-i, C-ii, D-iv