Pathology: MRCEM Primary questions with answers
Pathology carries 9 of the 180 questions in MRCEM Primary, so this topic is compact but wide. It covers innate and acquired immunity, lymphocytes, the complement cascade, antibodies and hypersensitivity reactions, blood groups, inflammation, autoantibodies, cell death, anaemia, sickle cell disease and wound healing. Anaphylaxis, transfusion reactions, sickle cell crises and wound care are everyday emergency problems that rest on these mechanisms.
5 free questions below, each with the answer and the full explanation · 169 in the full bank · Last updated after the 27 October 2026 MRCEM Primary sitting.
Question 1 · Pathology
At journal club you present a paper about using a biomarker to predict the presence of clinically important infection.
What is the most useful statistical attribute when assessing applicability to facilitate safe discharge?
- ANegative predictive value
- BPositive likelihood ratio
- CSensitivity
- DPositive predictive value
- ESpecificity
Show answer and explanation
Answer: A. A high negative predictive value means a negative result reliably excludes infection, supporting safe discharge.
- B: Positive LR helps rule in disease.
- C: Sensitivity alone does not give post-test probability.
- D: PPV helps rule in, not exclude.
- E: Specificity helps rule in disease.
Full explanation
- The negative predictive value (NPV) describes the probability of not having the disease. If the test result is negative, the chances of the patient to have the disease is low and can be safely discharge.
Question 2 · Antibodies and Hypersensitivity Reactions
Type-III hypersensitivity is initiated by?
- ANk cells and IgG
- BDeposition of antigen antibody complexes
- CT-cells
- DMast cells and IgE
- EIgM
Show answer and explanation
Answer: B. Type III is mediated by deposition of antigen-antibody (immune) complexes.
- A: Describes antibody-dependent cytotoxicity, type II.
- C: T-cells mediate type IV.
- D: Mast cells and IgE mediate type I.
- E: IgM on cell surface antigens mediates type II.
Full explanation: Antibodies and Hypersensitivity Reactions
Antibodies:
Hypersensitivity reaction:
Type1 Type2 Type3 Type4 IGE mediated IgG OR IGM IgG (Recall) T Cells mediated Urticaria
Angioedema
Allergic rhinitis
Hay fever
AnaphylaxisRed blood cell destruction after transfusion with mismatched blood (Recall) or during hemolytic disease of the newborn. Post-streptococcal glomerulonephritis (Recall)
Rheumatoid arthritis (Recall)
systemic lupus erythematosusMostly T
Contact (Touch) dermatitis (Recall)
Tuberculin skin test
Type 1 diabetes
Transplant rejectionQuestion 3 · Wound Healing
A male aged 40 presents to the ED with an infected surgical wound that is not healing and the suture line has separated. Which one of the following is the most likely reason for delayed wound healing?
- AFibrin degradation
- BIncreased angiogenesis
- CDecreased oxidative stress
- DExtra cellular matrix shortage
- EOngoing inflammation
Show answer and explanation
Answer: E. Persistent inflammation is the hallmark of chronic, non-healing wounds, particularly when infected.
- A: Excess degradation is not the key mechanism.
- B: Angiogenesis would aid healing.
- C: Oxidative stress is increased, not decreased.
- D: Matrix is degraded by proteases, but ongoing inflammation is the root cause.
Full explanation: Wound Healing
Wound healing
Healing is the process of replacing dead and damaging tissue with healthy tissue; this may occur through regeneration or repair.
The regenerative capacity of cells can be categorized in three main ways:
- Labile cells are constantly dividing and have a good capacity for regeneration, this allows the replacement of ageing tissue such as the surface epithelia of the skin, gastrointestinal tract and uterus; blood cells are derived from labile cells of the bone marrow.
- Stable cells slowly replicate e.g., cells of liver, renal tubular epithelium, endocrine glands.
- Permanent tissues: incapable of division and cannot be regenerated e.g., brain cells, myocardial cells, skeletal muscle cells.
Healing by primary intention:
- Healing of a clean, uninfected surgical incision approximated by surgical sutures.
- Day-1: Neutrophilic infiltration + fibrin clot
- Day-2: Epithelial cells from both edges have begun to migrate and proliferate along the dermis, yielding a thin but continuous epithelial layer.
- Day-3: Macrophages replace neutrophils Appearance of granulation tissue. Type III collagen deposition begins but do not bridge the incision.
- Day 5: Abundant granulation tissue Collagen fibrils bridge the incision.
- Neovascularization is maximum.
- Week-2: Dense scar tissue produced from granulation tissue contains type III collagen (weak collagen) that must be remodeled. Remodeling increases the tensile strength of scar tissue.
- 1 month: Replacement of collagen type III with collagen type I (has greater tensile strength) due to action of collagenase enzyme.
- The predominant collagen in adult skin is type I, whereas in early granulation tissue, it is type III.
Healing by secondary intention
Occurs in large wounds abscess formation and ulceration.
Main features:
- A larger clot or scab
- Inflammation: more intense Granulation tissue: much larger amount
- Scar tissue: greater mass
- Wound contraction: by myofibroblast e.g. Within 6 weeks, large skin defects may be reduced to 5% to 10% of their original size, largely by contraction.
Healing by tertiary intention
- Contaminated wound is initially treated with debridement and antibiotics followed by surgical wound closure (suture, skin graft replacement, flap)
- Note: Regarding the neat surgical scar after 2 months of surgery fibroblasts have predominant role
- Most important for delayed wound healing is due to infection.
Factors affecting wound healing:
Local factors affecting wound healing
- Mechanical injury / Frequent trauma
- Infection
- Edema
- Ischemia/necrotic tissue
- Topical agents
- lionizing radiation
- Low oxygen tension
- Foreign bodies
Systemic factors affecting wound healing
- Diabetes mellitus
- Anaemia
- Malnutrition
- Immunodeficiency
- Immunosuppressive medications
- Age
- Obesity
- Smoking
- Vit A, C and Zinc deficiency
Complications of Healing
- Hypertrophic scar
- Keloid formation
- Failure to heal (abscess or empyema formation)
- Failure to unite (skin, muscle or fascia wound breakdown)
- Fracture complications
Stages of bone/fracture healing:
- Hematoma formation (Immediately in Day 1)
- Inflammation and proliferation (8 hours to 1-2 weeks) predominant cells neutrophils and macrophages
- Callus formation (2-3 weeks)
- Consolidation (2 to 3 months)
- Re-modelling (2 months to years) Osteoclasts are responsible.
Factors that prevent efficient healing:
- Malnutrition
- Infection
- Corticosteroids therapy
- Poor blood supply
Question 4 · Inflammation
Which one of the following cytokines mediates fever in inflammation?
- AInterleukin-10 (IL-10)
- BInterleukin-6 (IL-6)
- CInterferon-gamma (IFN-γ)
- DInterleukin-1 (IL-1)
- ETumor Necrosis Factor-alpha (TNF-α)
Show answer and explanation
Answer: D. IL-1 is the classic pyrogenic cytokine causing fever.
- A: IL-10 is anti-inflammatory.
- B: IL-6 stimulates acute phase protein production.
- C: IFN-gamma activates macrophages.
- E: TNF-alpha also contributes, but the mnemonic key answer is IL-1.
Full explanation: Inflammation
Inflammation
Acute Inflammation Chronic Inflammation - Immediate reaction of tissue to injury
- Persistent reaction of tissue to injury
- Rapid Onset
- Slow Onset
- Innate Immunity
- Adaptive Immunity
- Neutrophil Predominant
- Lymphocytes, plasma cells, macrophages Predominant
- Duration: Hours to weeks
- Duration: Weeks, months or years
Note: Chronic nonspecific inflammation: Nonspecific inflammatory cell infiltration seen in chronic osteomyelitis, lung abscess
Chronic specific inflammation: Formation of granuloma e.g., in T.B, Leprosy, syphilis and sarcoidosis
Note: TNF-Alpha and IL-1 are key cytokines in acute inflammation
- Neutrophils and macrophages produce IL-1 which act on the hypothalamus and induce fever in inflammation.
- Blood changes in inflammation include Increased ESR, Leukocytosis and increased CRP.
Inflammation inducing substances:
- Histamine
- Serotonin
- Bradykinin
- Prostaglandin
Interleukin functions:
Mnemonic: Fever Tablet Means Effective Antipyretics Action
- IL-1: Fever
- IL-2: T cell stimulator
- IL-3: Marrow stimulator
- IL-4: IgE stimulator
- IL-5: Class switching to IgA
- IL-6: Stimulates Acute Phase Protein Production
Question 5 · Blood Groups
A new blood test to screen patients for heart failure is trialled in 500 patients. The test was positive in 40 of the 50 patients shown to have heart failure by echocardiography. It was also positive in 20 patients who were shown not to have heart failure. What is the positive predictive value of the test?
- A0.8
- B0.1
- C0.33
- D0.66
- ECannot be calculated
Show answer and explanation
Answer: D. PPV = TP/(TP+FP) = 40/(40+20) = 0.66.
- A: This is the sensitivity, 40/50.
- B: Not derived from the data.
- C: Not derived from the data.
- E: It can be calculated from the figures given.
Full explanation
Positive predictive value can be calculated as: TP / (TP + FP) = 40 / (40 + 20) = 0.66
Heart failure: (Disease present)
- Test positive or True positive (TP)= 40
- Test negative or False negative (FN) 10
No heart failure (Disease absent)
- Test positive or False positive (FP)= 20
- Test negative or True negative (TN)= 430
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Subtopics in Pathology
- Innate vs Acquired Immunity · 9
- Lymphocytes · 11
- Complement Cascade · 23
- Antibodies and Hypersensitivity Reactions · 20
- Blood Groups · 8
- Inflammation · 17
- Plasma Autoantibodies · 4
- Cell Death · 6
- Anemia · 1
- Sickle Cell Disease · 5
- Wound Healing · 27