Unit 14 Question Bank
The five tabs are the five sections of the real paper. Items tagged
Past Paper 2019 or 2020 are the genuine questions, reproduced verbatim.
Items tagged Slide come from the TMU lecture; items tagged Janeway's are built
from the textbook to cover examinable ground. Nothing is invented. Janeway's 10e is a reflowed
edition with no printed page numbers, so it is cited by numbered section (§1-14), not by page.
0 / 27 answered
1In the following diseases, which one has target cell damage?
Answer: B
Type II is defined by antibody binding a specific target cell and destroying it. In asthma (type I) the mast cell degranulates but is not itself destroyed; in contact dermatitis (type IV) T cells damage tissue diffusely; in rheumatoid arthritis (type III) immune complexes deposit in synovium with no single target cell marked. ⚠️ The original paper misprints this question, labelling two options “B”; reproduced here with corrected lettering.Past Papers 2019 & 2020, Section III Q19 — verbatim, both years
2Which antibodies mediate type II hypersensitivity?
Answer: C
IgG and IgM binding antigen already present on a cell surface. IgE mediates type I, where the antibody sits on a mast cell rather than on the target.TMU Type II Hypersensitivity deck (Yu Chunyan) Slide 8
3Which effector mechanisms destroy the target cell in type II hypersensitivity?
Answer: D
All three are normal antibody effector functions from Unit 3 working perfectly — the pathology lies entirely in the target, not in the machinery. The other options describe types I, III and IV.TMU Type II Hypersensitivity deck (Yu Chunyan) Slides 11, 14
4Which cell performs ADCC in type II hypersensitivity?
Answer: A
The NK cell, binding the IgG coating the target through FcγRIII (CD16). This is why True/False Q10 — NK cells, macrophages and complement act in type II — is true, while MCQ Q17 has the NK cell as the answer to “not involved in type I”.Past Papers 2019 & 2020, Section IV Q10 · TMU Type II Hypersensitivity deck (Yu Chunyan) Slide 13
5Which is NOT a source of the cell-surface antigen in type II hypersensitivity?
Answer: B
Type II requires the antigen to be on a cell surface. Soluble antigen forming circulating complexes is type III — and that single difference is what separates the two.TMU Type II Hypersensitivity deck (Yu Chunyan) Slides 8–10
6An ABO-incompatible transfusion reaction is mediated by:
Answer: C
Anti-A and anti-B are natural IgM antibodies — present without prior transfusion, and IgM because they arise against carbohydrate (TI) antigens with no class switching. Being IgM they are outstanding complement activators, which is why the haemolysis is immediate and intravascular.TMU Type II Hypersensitivity deck (Yu Chunyan) Slide 17
7Which is a recognised feature of an acute transfusion reaction?
Answer: D
Haemolysis releases free haemoglobin, which appears in the urine. Other features are fever, chills, nausea, intravascular clotting and lower back pain. The distractors belong to types I, IV and III.TMU Type II Hypersensitivity deck (Yu Chunyan) Slide 17
8Therapy for a transfusion reaction includes:
Answer: A
Stop the cause, then protect the kidney from the free haemoglobin load by maintaining urine flow. Adrenaline and antihistamines treat type I anaphylaxis; intrauterine exchange transfusion is a treatment for HDN.TMU Type II Hypersensitivity deck (Yu Chunyan) Slide 17
9Haemolytic disease of the newborn is caused by:
Answer: B
Only IgG crosses the placenta (Unit 3). Maternal IgM produced in the primary response cannot cross — which is precisely why the first baby is spared and the second is not.TMU Type II Hypersensitivity deck (Yu Chunyan) Slide 18
10Why is the first Rh⁺ baby of an Rh⁻ mother usually unaffected?
Answer: C
Sensitisation usually happens at delivery, when the baby is already out, and the primary response makes IgM — a 900 kD pentamer that cannot cross. But memory cells form, and it is those that endanger the next pregnancy.TMU Type II Hypersensitivity deck (Yu Chunyan) Slides 19–20
11How does Rhogam (anti-Rh antibody) prevent haemolytic disease of the newborn?
Answer: D
The target is the mother's memory. Clearing fetal Rh⁺ cells before she can respond means no memory forms, so there is no secondary response and no IgG in the next pregnancy. It is the one place in the course where antibody is given to prevent an immune response rather than to provide one.Past Papers 2019 & 2020, Section IV Q7 · TMU Type II Hypersensitivity deck (Yu Chunyan) Slide 22
12Within what period after the first delivery must Rhogam be given?
Answer: A
72 hours — it must act before sensitisation is established. Once memory cells have formed, clearing the fetal cells no longer helps.Past Papers 2019 & 2020, Section IV Q7
13Brain damage in haemolytic disease of the newborn occurs because:
Answer: B
The bilirubin released from destroyed red cells is lipid-soluble and therefore able to enter brain tissue. This is why phototherapy — breaking down bilirubin — is a treatment, and why exchange transfusion is done primarily to remove bilirubin.TMU Type II Hypersensitivity deck (Yu Chunyan) Slide 22
14Which treatment for HDN is used primarily to remove bilirubin?
Answer: C
Blood-exchange transfusion removes bilirubin; intrauterine transfusion replaces fetal Rh⁺ cells with Rh⁻ ones; plasmapheresis discards maternal plasma containing anti-Rh antibody; Rhogam is prevention, not treatment.TMU Type II Hypersensitivity deck (Yu Chunyan) Slide 24
15Streptococcal antigens cross-reacting with cardiac valve tissue illustrate which source of type II antigen?
Answer: D
This is Unit 2's cross-reaction and molecular mimicry returning as a disease mechanism: antibody raised legitimately against a streptococcus binds a cardiac valve because the two share an epitope.TMU Type II Hypersensitivity deck (Yu Chunyan) Slide 9
16Drug-induced haemolytic anaemia illustrates which source of type II antigen?
Answer: A
A drug too small to be immunogenic alone adsorbs to the red cell surface, making that cell a target — Unit 2's hapten principle, with the red cell membrane serving as carrier.TMU Type II Hypersensitivity deck (Yu Chunyan) Slide 10
1 Type II hypersensitivity — 3 marks+
Antibody-mediated cytotoxic or cytolytic hypersensitivity. IgG and IgM bind antigen present on a cell surface; complement, macrophages and NK cells then destroy the target — typically a blood cell or self tissue cell. Its defining feature is damage to a specific target cell.TMU Type II Hypersensitivity deck (Yu Chunyan) Slides 7–8
2 Mechanisms of type II damage — 3 marks+
① Complement-mediated lysis — IgG/IgM activates the classical pathway and the MAC (C5b–C9) lyses the cell. ② Opsonised phagocytosis — via FcγR binding antibody and C3b binding complement receptors on macrophages and neutrophils. ③ ADCC — NK cells bind the coating IgG via FcγRIII (CD16) and kill the target.TMU Type II Hypersensitivity deck (Yu Chunyan) Slides 11, 14
3 Haemolytic disease of the newborn (HDN) — 3 marks+
Disease caused by Rh or ABO blood-group incompatibility between mother and fetus, developing when maternal IgG against fetal blood-group antigen crosses the placenta and destroys fetal red blood cells. Consequences: fetal anaemia, jaundice and bilirubin deposition, with brain damage from lipid-soluble bilirubin. Prevented by anti-Rh antibody (Rhogam) within 72 hours of the first delivery.TMU Type II Hypersensitivity deck (Yu Chunyan) Slides 18, 22
4 Sources of cell-surface antigen in type II — 3 marks+
① Constitutive components of the cell membrane — ABO, Rh and HLA antigens. ② Common antigens shared by host cells with exogenous antigens — e.g. streptococcal cell wall and cardiac valve. ③ Modified self antigens — altered by chemicals, infections or drugs. ④ Antigens or haptens adsorbed to the cell surface.TMU Type II Hypersensitivity deck (Yu Chunyan) Slides 8–10
1Type II hypersensitivity is mediated by antibodies ? and ? against antigen located on the ? .3 mark(s)
The antigen's location on a cell is what makes the damage target-specific — the basis of MCQ Q19.
TMU Type II Hypersensitivity deck (Yu Chunyan) Slides 7–82The three mechanisms of target-cell destruction in type II are ? , ? and ? .3 mark(s)
All three are ordinary antibody effector functions — the pathology is in the target, not the mechanism.
TMU Type II Hypersensitivity deck (Yu Chunyan) Slide 143The effector components of type II hypersensitivity are ? , ? and ? .3 mark(s)
This is True/False Q10, and it is true. Contrast type I, where the NK cell plays no part.
Past Papers 2019 & 2020, Section IV Q104Haemolytic disease of the newborn develops when maternal ? against fetal blood-group antigen crosses the ? and destroys fetal ? .3 mark(s)
Only IgG crosses the placenta — the same mechanism that gives newborns passive immunity destroys their red cells here.
TMU Type II Hypersensitivity deck (Yu Chunyan) Slide 185HDN is prevented by giving ? to the mother within ? hours of the first delivery, which prevents ? activation and ? generation.4 mark(s)
No memory means no secondary response, so no IgG in the next pregnancy.
Past Papers 2019 & 2020, Section IV Q71NK cells, macrophages and complements are involved in type II hypersensitivity.
TRUE
TRUE. All three effector routes: complement-mediated lysis, opsonised phagocytosis by macrophages, and ADCC by NK cells. Contrast MCQ Q17, where NK cells are the answer to “not involved in type I” — because ADCC needs IgG on a target cell, which type I does not have.Past Papers 2019 & 2020, Section IV Q10 — verbatim, both years
2Haemolytic disease of newborn caused by Rh antigen incompatibility can be prevented by administrating Anti-Rh antibody (Rhogam) in mother within 72 hours after the first delivery.
TRUE
TRUE. Rhogam binds fetal Rh antigen and clears those cells before the mother's immune system can respond, preventing B-cell activation and memory-cell generation. No memory, no secondary IgG response, no disease in the next pregnancy.Past Papers 2019 & 2020, Section IV Q7 — verbatim, both years
3Maternal IgM crosses the placenta and causes haemolytic disease of the newborn.
FALSE
False. IgM cannot cross the placenta — it is a 900 kD pentamer. That is exactly why the first Rh⁺ baby is spared: the mother's primary response is IgM. The disease requires the IgG of a secondary response.TMU Type II Hypersensitivity deck (Yu Chunyan) Slides 18–19
4In type II hypersensitivity the antigen is soluble and circulates in plasma.
FALSE
False. In type II the antigen is on a cell surface. Soluble circulating antigen forming immune complexes defines type III — and that difference is the whole distinction between the two.TMU Type II Hypersensitivity deck (Yu Chunyan) Slide 8
5ABO-incompatible transfusion reactions are mediated by IgG.
FALSE
False — by IgM. Anti-A and anti-B are natural antibodies against carbohydrate (TI) antigens, so no class switching occurs and they remain IgM. Being IgM they activate complement extremely efficiently, causing immediate intravascular haemolysis.TMU Type II Hypersensitivity deck (Yu Chunyan) Slide 17
6Bilirubin accumulating in the brain in HDN is lipid-soluble.
TRUE
True, and that is precisely why it causes brain damage — it can enter brain tissue. Phototherapy breaks it down, and exchange transfusion is performed primarily to remove it.TMU Type II Hypersensitivity deck (Yu Chunyan) Slide 22
1
Describe the mechanism of type II hypersensitivity.
6 marks
Components. Antibodies IgG and IgM; antigen present on the cell surface; effectors complement, macrophages and NK cells. Blood cells and self tissue cells are the targets.
Sources of the surface antigen. ① Constitutive membrane components (ABO, Rh, HLA). ② Common antigens shared with exogenous antigens (e.g. streptococcal cell wall and cardiac valve). ③ Modified self antigens (chemicals, infections, drugs). ④ Antigens or haptens adsorbed to the cell surface.
Three mechanisms of destruction.
| Mechanism | How |
|---|---|
| Complement-mediated lysis | IgG/IgM activates the classical pathway; the MAC (C5b–C9) lyses the cell |
| Opsonised phagocytosis | FcγR binds antibody and complement receptors bind C3b on macrophages and neutrophils |
| ADCC | NK cells bind the coating IgG via FcγRIII (CD16) and kill the target |
Worth stating: every one of these is a normal antibody effector function working correctly — the pathology lies entirely in the target.
Marking guide: 2 marks for components, 1 for antigen sources, 3 for the three mechanisms (1 each). Naming complement, macrophage and NK cell explicitly answers True/False Q10 at the same time.
2
Explain the mechanism of haemolytic disease of the newborn caused by Rh incompatibility, and how it is prevented.
6 marks
Sensitisation. An Rh⁻ mother carries an Rh⁺ fetus. Fetal Rh⁺ red cells enter the mother — at delivery of the first baby, or through transfusion or abortion.
Primary response. The mother makes IgM, which cannot cross the placenta, so the first baby is unharmed. But memory cells are formed.
Secondary response. In a subsequent pregnancy with an Rh⁺ fetus, memory cells produce IgG at high titre. IgG crosses the placenta, binds fetal red cells and lyses them.
Consequences. Anaemia (mild to fatal); jaundice; brain damage, because haemoglobin is converted to lipid-soluble bilirubin which accumulates in the brain.
Prevention. Anti-Rh antibody (Rhogam) given to the mother within 72 hours of the first delivery. It binds Rh antigen on fetal red cells and clears them before the mother responds, thereby preventing B-cell activation and memory-cell generation.
Therapy. Intrauterine blood-exchange transfusion (replacing fetal Rh⁺ cells with Rh⁻); blood-exchange transfusion (to remove bilirubin); phototherapy (to break down bilirubin); plasmapheresis (to discard maternal anti-Rh antibody).
Marking guide: 2 marks for the sensitisation and primary/secondary sequence, 1 for the IgM/IgG placental-transfer point, 1 for consequences, 2 for prevention with the correct mechanism and the 72-hour window.
3
Compare type I and type II hypersensitivity.
6 marks
| Type I | Type II | |
|---|---|---|
| Name | Anaphylactic / immediate | Cytotoxic / cytolytic |
| Antibody | IgE | IgG and IgM |
| Antigen | Soluble allergen | On a cell surface |
| Antibody location | On the mast cell (FcεRI) | On the target cell |
| Effector cells | Mast cells, basophils, eosinophils | Complement, macrophages, NK cells |
| Complement | Not involved — IgE does not fix | Central |
| Timing | Minutes | Hours |
| Diseases | Asthma, rhinitis, urticaria, anaphylaxis | Transfusion reaction, HDN, haemolytic anaemia, hyperthyroidism |
The single most useful contrast: in type I the antibody sits on the effector cell waiting for antigen; in type II it sits on the target cell marking it for destruction.
Marking guide: 0.75 per row. The antibody class and the antibody-location rows are the two that must be right.