Pathology for MRCS Part A

What the paper tends to test

• Questions typically test the phases of wound healing and the factors that delay it — infection, ischaemia, diabetes, steroids, malnutrition, smoking and radiotherapy.
• Expect the vocabulary of adaptation applied to a clinical example: hyperplasia, hypertrophy, metaplasia and dysplasia, and the point at which neoplasia begins, with Barrett’s oesophagus as the usual illustration.
• Thrombosis and embolism questions use Virchow’s triad, the fate of a thrombus and the types of embolus — fat, air, tumour and amniotic as well as thrombotic.
• Neoplasia is examined through tumour markers, grading against staging, the routes of spread of carcinoma and sarcoma, and the paraneoplastic syndromes.
• Immunology lines ask about the hypersensitivity types, transplant rejection and the consequences of splenectomy.
• Haematology and clinical chemistry questions test transfusion reactions, the causes of a raised calcium or a low sodium, and the interpretation of a clotting screen.
• System pathology questions are usually a short histological or clinical description to match to a diagnosis — a thyroid nodule, a breast lump, a bone tumour, a skin lesion.

Classic traps and discriminators

• Wound tensile strength is about 10% of normal at 1 week and about 20% at 3 weeks, and reaches roughly 80% of unwounded skin only after months, which is why an abdominal wound can dehisce after the sutures come out and why the skin is never as strong as before.
• Hypertrophy is an increase in cell size and hyperplasia an increase in cell number; metaplasia is a reversible change of one mature cell type to another and dysplasia a disordered growth that may progress; only invasion through the basement membrane makes a carcinoma.
• Coagulative necrosis is the pattern of infarction in most solid organs; the brain liquefies, tuberculosis caseates and the pancreas and breast undergo fat necrosis. Apoptosis is energy-dependent, affects single cells and does not provoke inflammation.
• Fat embolism presents 24–72 hours after a long-bone or pelvic fracture with hypoxia, confusion and a petechial rash over the upper trunk, axillae and conjunctivae — a triad that separates it from pulmonary thromboembolism, which comes later and without the rash.
• Hypersensitivity: type I is IgE-mediated (anaphylaxis), type II antibody against a cell surface (ABO-incompatible transfusion, Goodpasture’s), type III immune-complex (serum sickness, post-streptococcal glomerulonephritis) and type IV cell-mediated and delayed (contact dermatitis, the tuberculin test, acute cellular rejection).
• The commonest cause of hypercalcaemia in an outpatient is primary hyperparathyroidism; in a hospital inpatient it is malignancy — through parathyroid hormone-related peptide from squamous cancers, lytic bone metastases and myeloma.

Free revision notes

Pathology questions, answered