MRCOG Part 1 · Pathology · General Pathology

General Concepts: MRCOG Part 1 questions and key facts

General pathology questions in the MRCOG Part 1 examination represent a broad survey of fundamental mechanisms rather than a single unified clinical topic. Candidates encounter vascular pathology covering Virchow's triad in post-surgical thrombosis, fat embolism, and antenatal low-molecular-weight heparin thromboprophylaxis. Tumour biology features prominently, including tumour suppressors such as p53 and BRCA1, anaplasia, psammoma bodies, metastatic pathways, Epstein-Barr virus in Burkitt lymphoma, and multiple endocrine neoplasia type 2. Questions also address fluid and sodium homeostasis, specifically dilutional hyponatraemia from 5% dextrose infusion and paraneoplastic inappropriate antidiuretic hormone secretion. Finally, several standalone items assess high-yield recall across vitamin B12 malabsorption following ileal resection, WHO body mass index categories, the urothelium (transitional epithelium) lining the bladder, and semen analysis terminology.

The Uterio bank has 31 questions on this topic. 3 arebelow in full; the syllabus detail is in the Pathology study guide.

How the exam tests General Concepts

  • Identifying Virchow's triad components, matching immobilisation to stasis in post-surgical thrombosis, and selecting antenatal low-molecular-weight heparin rather than teratogenic warfarin.
  • Distinguishing tumour suppressors like p53 and BRCA1, recognising anaplasia and psammoma bodies, and identifying lymphatic versus haematogenous routes of metastasis.
  • Differentiating mechanisms of dilutional hyponatraemia from metabolised 5% dextrose infusions versus paraneoplastic antidiuretic hormone secretion in lung carcinoma.
  • Recognising characteristic clinical triads, including fat embolism syndrome following long-bone fracture and Horner syndrome from interruption of the oculosympathetic pathway.

High-yield facts

  1. Virchow's triad comprises endothelial injury, abnormal blood flow, and hypercoagulability; post-surgical prolonged immobilisation contributes to deep vein thrombosis predominantly via stasis of flow.
  2. Following long-bone fractures, fat embolism presents after 24 to 72 hours with the classic clinical triad of respiratory distress, neurological impairment, and a petechial rash.
  3. Women with a previous pregnancy-associated deep vein thrombosis are offered antenatal low-molecular-weight heparin from early pregnancy, continued for about six weeks postnatally; it does not cross the placenta.
  4. Tumour suppressor genes include p53, which arrests the cell cycle at G1/S, triggers apoptosis and upregulates thrombospondin-1 to inhibit angiogenesis, and BRCA1, which repairs DNA double-strand breaks by homologous recombination.
  5. Benign tumours are typically slow-growing, well differentiated, non-invasive and often encapsulated; malignancy is marked by invasion, metastasis and anaplasia (pleomorphism, large hyperchromatic nuclei and loss of resemblance to the tissue of origin).
  6. Psammoma bodies are laminated, concentric calcium deposits classically seen in serous papillary ovarian cystadenocarcinoma, papillary thyroid carcinoma, meningioma, and mesothelioma.
  7. Carcinomas typically spread initially via lymphatic vessels to regional lymph nodes, whereas sarcomas characteristically disseminate haematogenously via blood vessels.
  8. Syndrome of inappropriate antidiuretic hormone secretion causes water retention with euvolaemic (dilutional) hyponatraemia; a sodium of about 120 mmol/L commonly causes confusion, and small cell lung cancer is the classic paraneoplastic cause.
  9. Epstein-Barr virus infection cooperates with MYC translocations, typically t(8;14), to drive the pathogenesis of endemic Burkitt lymphoma.
  10. Horner syndrome results from interruption of the oculosympathetic pathway (central, preganglionic or postganglionic), producing ipsilateral partial ptosis and miosis, with facial anhidrosis when the lesion is central or preganglionic.
  11. Extensive resection of the terminal ileum impairs intrinsic factor-mediated absorption of vitamin B12, causing megaloblastic anaemia and neurological complications like paraesthesia.
  12. In semen analysis, oligozoospermia denotes low sperm concentration, azoospermia denotes absent sperm, asthenozoospermia denotes poor motility, and teratozoospermia denotes abnormal sperm morphology.

Common pitfalls

  • Treating 5% dextrose as an isotonic replacement fluid: once glucose is metabolised, it acts as free water and can cause dilutional hyponatraemia.
  • Confusing teratozoospermia, which defines abnormal sperm morphology, with asthenozoospermia, which specifically describes defective sperm motility in semen analysis.
  • Prescribing warfarin for routine antenatal thromboprophylaxis; warfarin is teratogenic, making low-molecular-weight heparin the safe and recommended agent throughout pregnancy.

Practice questions: General Concepts

Single best answer, exactly as the exam asks. Commit to an option before opening the explanation.

Question 1

Pathology

Which tumour suppressor gene, when activated by cellular stress or damage, can arrest the cell cycle and inhibit angiogenesis?

  1. ABRCA1
  2. BRB1
  3. CAPC
  4. Dp53
  5. EHER2
Show answer and explanation

Correct answer: D. p53

Key takeaway

When activated by cellular stress, the tumour suppressor p53 arrests the cell cycle and inhibits angiogenesis, for example by upregulating thrombospondin-1, thereby restricting tumour growth.

The p53 gene, often called the 'guardian of the genome', plays a crucial role in preventing cancer formation. When activated by cellular stressors like DNA damage, hypoxia, or oncogene activation, the p53 protein halts the cell cycle (typically at the G1/S checkpoint) to allow for DNA repair. If the damage is irreparable, p53 can trigger apoptosis (programmed cell death). It also inhibits angiogenesis (the formation of new blood vessels) by upregulating anti-angiogenic factors like thrombospondin-1, thereby restricting tumour growth and spread.

RB1 (Retinoblastoma protein) is another tumour suppressor involved in cell cycle control, primarily acting as a brake at the G1/S checkpoint. BRCA1 is involved in DNA repair, particularly double-strand breaks. APC (Adenomatous Polyposis Coli) is a tumour suppressor involved in the Wnt signalling pathway, frequently mutated in colorectal cancer. HER2 (Human Epidermal growth factor Receptor 2) is not a tumour suppressor but a proto-oncogene; its amplification or overexpression drives cell proliferation and is implicated in certain breast and gastric cancers.

Question 2

Pathology

Which of the following is commonly found within psammoma bodies?

  1. ACollagen fibres
  2. BCalcium deposits
  3. CNecrotic debris
  4. DHaemosiderin
  5. ECholesterol crystals
Show answer and explanation

Correct answer: B. Calcium deposits

Key takeaway

Psammoma bodies are microscopic, concentrically laminated calcium deposits (a form of dystrophic calcification) laid down around a nidus of degenerating cells, most often within tumours with a papillary architecture.

Psammoma bodies are microscopic, laminated, calcified structures often found in certain types of tumours. They are formed by the progressive deposition of calcium deposits, often in concentric layers, around a small nidus which may consist of necrotic cells or degenerated papillae. This process leads to the formation of small, round, acellular structures resembling grains of sand (psammoma means 'sand-like'). They are classically associated with papillary thyroid carcinoma, serous papillary cystadenocarcinoma of the ovary, meningioma, and mesothelioma.

The other options are incorrect components of psammoma bodies. While necrotic debris might form the initial nidus, the defining feature is the subsequent calcification. Collagen fibres form part of the surrounding stroma. Haemosiderin is an iron-containing pigment associated with haemorrhage. Cholesterol crystals are typically seen in atheromas or areas of chronic inflammation with lipid breakdown.

Question 3

Pathology

A patient develops deep vein thrombosis following prolonged immobilisation after surgery. According to Virchow's triad, which factor contributes most directly to thrombosis in this scenario?

  1. AIntravascular vessel wall damage
  2. BHypercoagulable state
  3. CStasis of flow
  4. DIncreased vascular permeability
  5. EInflammation
Show answer and explanation

Correct answer: C. Stasis of flow

Key takeaway

According to Virchow's triad, prolonged immobilisation primarily causes stasis of flow in the deep veins, which is the main factor promoting deep vein thrombosis in this scenario.

Virchow's triad identifies three primary factors contributing to thrombosis: endothelial injury, abnormal blood flow (stasis or turbulence), and hypercoagulability. In the case of deep vein thrombosis (DVT) following prolonged immobilisation (e.g., post-surgery bed rest), the most direct contributing factor is stasis of flow. Reduced muscle pump activity in the legs leads to slowed venous blood flow, particularly in the deep calf veins. This stasis allows platelets and activated coagulation factors to accumulate, increases the likelihood of endothelial contact, and prevents dilution by fresh flowing blood or clearance by inhibitors, thereby promoting thrombus formation.

While surgery itself can cause some endothelial injury and induce a systemic hypercoagulable state (due to tissue factor release, inflammation, and decreased anticoagulant activity), the prolonged immobility specifically leads to stasis, which is the key mechanism directly linked to the lack of movement. Increased vascular permeability and inflammation are generally related to inflammatory processes rather than being primary factors in immobilisation-induced DVT, although inflammation can contribute secondarily to endothelial dysfunction or hypercoagulability.

28 more general concepts questions in the bank

Every question carries a full explanation and a key takeaway like the ones above. Pay once for 1, 3, 6 or 12 months; no subscription.

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What the syllabus covers under general concepts

  • Thrombosis and Embolism
  • Infarction
  • Shock
  • Electrolyte Disturbances
  • Tumour Markers
  • Increased Uric Acid Production
  • Caseous Necrosis of Endometrium

Read the full section in the Pathology guide, or check the next exam dates.