Quick revision: every question with its correct answer. For the full explanation, open the test and tap View Solution.
7.5 Complement in Health & Disease β Test 1
Q1. Deficiency of early classical-pathway components (C1, C2, C4) is most strongly associated with:β Systemic lupus erythematosus (immune-complex disease)
Q2. Deficiency of late (terminal) complement components (C5βC9) characteristically predisposes to:β Recurrent Neisseria (meningococcal/gonococcal) infections
Q3. Hereditary angioedema is caused by a deficiency of:β C1 inhibitor (C1-INH)
Q4. Paroxysmal nocturnal haemoglobinuria (PNH) results from a deficiency of GPI-anchored regulators, leading to loss of:β CD55 (DAF) and CD59 on red cells
Q5. The anti-C5 monoclonal antibody eculizumab treats PNH and atypical HUS by:β Blocking C5 cleavage, preventing MAC formation
Q6. C3 deficiency, affecting the central component, typically causes:β Severe, recurrent pyogenic bacterial infections
Q7. Factor H deficiency or dysfunction is associated with kidney diseases such as:β Atypical haemolytic uraemic syndrome and some membranoproliferative glomerulonephritis
Q8. Complement activation contributes to tissue injury in conditions such as:β Ischaemiaβreperfusion injury and some autoimmune diseases
Q9. Why must patients on eculizumab (anti-C5) be vaccinated against meningococcus?β Blocking C5 prevents the MAC needed to kill Neisseria
Q10. In age-related macular degeneration, complement is implicated because:β Variants in complement regulators (e.g. factor H) increase risk
Q11. Complement's beneficial role in clearing apoptotic cells means its deficiency can:β Allow accumulation of self-antigens, promoting autoimmunity
Q12. Therapeutic complement inhibition is a strategy in diseases driven by:β Excessive or dysregulated complement activation
Q13. A laboratory finding of low C3 and C4 during active disease (e.g. lupus flare) usually indicates:β Consumption of complement by ongoing activation
Q14. Properdin deficiency, affecting a positive regulator, predisposes to:β Severe Neisseria (meningococcal) infections
Q15. The complement system links to adaptive immunity in health by:β Enhancing B-cell responses (C3dβCR2) and clearing complexes/apoptotic cells
Q16. Anaphylatoxin (C5a) overproduction contributes to pathology in conditions such as:β Sepsis and severe inflammatory states
Q17. A patient with recurrent Neisseria meningitidis infections should be evaluated for:β Terminal complement (C5βC9) or properdin deficiency
Q18. The CH50 assay is used clinically to:β Assess the functional integrity of the classical complement pathway
Q19. Overall, complement in health and disease illustrates that the system must be:β Tightly regulated to defend against pathogens without harming host tissue
Q20. Match each complement disorder with its key feature and select the correct option.β A-iii, B-i, C-ii, D-iv