Membership of the Royal College of Surgeons (MRCS) Pathology, Microbiology and Pharmacology Syllabus

Pathology, Microbiology and Pharmacology syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Pathology, Microbiology and Pharmacology in Membership of the Royal College of Surgeons (MRCS), not a summary of it.

1. 1

   General Pathology

   4 topics

   • Cell injury and death
     • Reversible and irreversible injury
     • Apoptosis versus necrosis
   • Inflammation and repair
     • Acute and chronic inflammation
     • Wound healing and granulation tissue
   • Disorders of growth
     • Hyperplasia, metaplasia and dysplasia
     • Atrophy and hypertrophy
   • Thrombosis, embolism and infarction
     • Virchow's triad
     • Ischaemia-reperfusion injury
2. 2

   Surgical Oncology and Neoplasia

   4 topics

   • Carcinogenesis
     • Oncogenes and tumour suppressor genes
     • Carcinogens and hereditary cancer syndromes
   • Tumour classification and grading
     • Benign versus malignant features
     • TNM staging principles
   • Metastasis and tumour markers
     • Routes of spread
     • Common tumour markers
   • Principles of cancer treatment
     • Surgery, radiotherapy and chemotherapy roles
     • Multidisciplinary team management
3. 3

   Microbiology and Surgical Infection

   4 topics

   • Surgically important organisms
     • Gram-positive and Gram-negative bacteria
     • Anaerobes, fungi and viruses
   • Surgical site and healthcare-associated infection
     • MRSA, C. difficile and gas gangrene
     • Asepsis, sterilisation and decontamination
   • Sepsis and antimicrobial therapy
     • Recognition and management of sepsis
     • Antibiotic prophylaxis and stewardship
   • Blood-borne viruses and infection control
     • Hepatitis B/C and HIV in surgery
     • Needlestick and exposure management
4. 4

   Systemic and Surgical Pathology

   4 topics

   • Vascular and cardiac pathology
     • Atherosclerosis and aneurysms
     • Ischaemic disease
   • Gastrointestinal and hepatobiliary pathology
     • Inflammatory bowel disease and polyps
     • Cirrhosis and gallstone disease
   • Breast and endocrine pathology
     • Benign and malignant breast disease
     • Thyroid and adrenal lesions
   • Skin and soft tissue pathology
     • Melanoma and non-melanoma skin cancer
     • Sarcomas and benign lesions
5. 5

   Clinical Pharmacology for Surgeons

   4 topics

   • Pharmacokinetics and pharmacodynamics
     • Absorption, distribution, metabolism and excretion
     • Drug interactions and the perioperative period
   • Analgesia and anaesthetic agents
     • Opioids, NSAIDs and the analgesic ladder
     • Local and general anaesthetics
   • Anticoagulants and antiplatelets
     • Heparin, warfarin and DOACs
     • Perioperative bridging and reversal
   • Cardiovascular and antimicrobial drugs
     • Inotropes and vasopressors
     • Antibiotic classes and resistance

Pathology, Microbiology and Pharmacology flashcards for Membership of the Royal College of Surgeons (MRCS)

21 of 60 cards from the Pathology, Microbiology and Pharmacology deck — real questions with worked answers.

1. Define reversible vs irreversible cell injury, and name the key morphological hallmark that signals the transition.

   Reversible injury: cellular swelling and fatty change with intact membranes, restorable if the stimulus is removed. Irreversible injury: severe membrane damage, mitochondrial dysfunction and lysosomal rupture. The key hallmark of irreversibility is severe membrane damage with massive calcium influx; histologically the point of no return is marked by nuclear changes (pyknosis, karyorrhexis, karyolysis).

2. List the morphological types of necrosis and give a classic example of each.

   Coagulative (MI/solid organ infarcts), liquefactive (brain infarcts, abscesses), caseous (TB), fat (acute pancreatitis), fibrinoid (vasculitis/malignant hypertension), and gangrenous (limb ischaemia, a clinical term).

3. Contrast necrosis and apoptosis in terms of energy, membrane integrity and inflammation.

   Necrosis is passive (ATP-independent), causes membrane rupture, leaks cell contents and provokes inflammation. Apoptosis is active, ATP-dependent, energy-requiring, keeps membranes intact (forms apoptotic bodies), affects single cells and does NOT provoke inflammation.

4. Name the two main apoptotic pathways and their key triggering molecules.

   Intrinsic (mitochondrial) pathway: triggered by cellular stress/DNA damage, regulated by Bcl-2 family, releases cytochrome c, activates caspase-9. Extrinsic (death receptor) pathway: Fas/FasL and TNF receptor engagement activates caspase-8. Both converge on executioner caspases-3, -6, -7.

5. What are the five cardinal signs of acute inflammation and their Latin terms?

   Redness (rubor), heat (calor), swelling (tumor), pain (dolor), and loss of function (functio laesa).

6. Describe the sequence of leucocyte extravasation in acute inflammation.

   Margination and rolling (selectins), firm adhesion (integrins binding ICAM-1/VCAM-1), transmigration/diapedesis through the endothelium (PECAM-1/CD31), and chemotaxis toward the stimulus (e.g. C5a, LTB4, IL-8, bacterial peptides).

7. Name the predominant cell of acute inflammation versus chronic inflammation.

   Acute inflammation: neutrophil (polymorph). Chronic inflammation: macrophages, lymphocytes and plasma cells.

8. Distinguish healing by primary versus secondary intention.

   Primary intention: clean, apposed wound edges (e.g. sutured incision), minimal tissue loss, little granulation tissue, fast with a fine scar. Secondary intention: wide tissue defect, edges not apposed, heals from the base up by abundant granulation tissue, wound contraction and a larger scar.

9. List the phases of wound healing with their approximate timing.

   Haemostasis (immediate), inflammation (0-3 days), proliferation/granulation (3 days-3 weeks: angiogenesis, fibroplasia, epithelialisation), and remodelling/maturation (weeks to months-years; type III collagen replaced by type I, increasing tensile strength).

10. Define hypertrophy, hyperplasia, atrophy, metaplasia and dysplasia.

    Hypertrophy: increased cell size. Hyperplasia: increased cell number. Atrophy: decreased cell size/number. Metaplasia: reversible change of one differentiated cell type to another (e.g. Barrett's). Dysplasia: disordered growth with cytological atypia, pre-malignant but still confined within the basement membrane.

11. State Virchow's triad for thrombosis.

    Endothelial injury, abnormal blood flow (stasis or turbulence), and hypercoagulability.

12. Differentiate arterial from venous thrombi by composition and appearance.

    Arterial (white) thrombi form in high flow, are platelet-rich and pale, often on atherosclerotic plaques. Venous (red) thrombi form in stasis, are fibrin- and RBC-rich (the lines of Zahn are most evident in arterial/cardiac thrombi), and tend to propagate.

13. List the main types of embolism.

    Thromboembolism (most common), fat (long-bone fractures), air/gas (decompression sickness, surgery), amniotic fluid, septic, tumour, and foreign body emboli.

14. Differentiate a red (haemorrhagic) from a white (pale/anaemic) infarct.

    Red infarcts occur in venous occlusion or in organs with dual blood supply/loose tissue or after reperfusion (e.g. lung, intestine). White infarcts occur in solid organs with end-arterial supply (e.g. heart, spleen, kidney).

15. Define carcinogenesis and name the broad categories of carcinogens.

    Carcinogenesis is the multistep accumulation of genetic/epigenetic alterations transforming normal cells into malignant ones. Categories: chemical (e.g. aromatic amines, polycyclic aromatic hydrocarbons), physical (UV, ionising radiation), biological/viral (HPV, EBV, HBV/HCV, H. pylori), and inherited mutations.

16. Contrast the function of oncogenes and tumour suppressor genes, with examples.

    Oncogenes are gain-of-function (dominant) mutations of proto-oncogenes that drive proliferation, e.g. RAS, MYC, HER2/neu. Tumour suppressor genes are loss-of-function (recessive, needing two hits per Knudson) brakes on the cycle, e.g. TP53, RB, APC, BRCA1/2.

17. List the recognised hallmarks of cancer (Hanahan & Weinberg).

    Sustaining proliferative signalling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, plus the enabling characteristics of genome instability and tumour-promoting inflammation, and emerging hallmarks of deregulated metabolism and immune evasion.

18. State the general rule for naming benign versus malignant tumours of epithelial and mesenchymal origin.

    Benign epithelial: -oma (adenoma, papilloma). Malignant epithelial: carcinoma (adenocarcinoma, squamous cell carcinoma). Benign mesenchymal: tissue + -oma (lipoma, leiomyoma). Malignant mesenchymal: tissue + -sarcoma (liposarcoma, osteosarcoma).

19. What features are assessed in tumour grading versus tumour staging?

    Grading assesses the degree of differentiation/anaplasia and mitotic activity (how the tumour LOOKS). Staging assesses the extent of spread (how far the tumour has GONE), e.g. TNM: tumour size/invasion, nodal involvement, distant metastasis. Stage is generally more prognostically important than grade.

20. Describe the steps of the metastatic cascade.

    Detachment (loss of E-cadherin), invasion of basement membrane and ECM (proteases e.g. MMPs), intravasation into vessels/lymphatics, survival in circulation (evading immune attack), arrest and extravasation at a distant site, and colonisation/growth with angiogenesis at the secondary site.

21. Match these tumour markers to their associated cancers: CEA, CA 19-9, CA 125, AFP, PSA, CA 15-3, hCG.

    CEA: colorectal (also other GI). CA 19-9: pancreatic. CA 125: ovarian. AFP: hepatocellular carcinoma and non-seminomatous germ cell tumours. PSA: prostate. CA 15-3: breast. hCG: germ cell tumours, choriocarcinoma, gestational trophoblastic disease.

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