🌍 MRCS Part A · subject

MRCS Part A Pathology Syllabus

The Pathology syllabus for MRCS Part A in full: 19 chapters, 72 topics and 173 sub-topics, every one listed below, plus 51 Pathology flashcards with answers.

19Chapters

72Topics

173Sub-topics

51Flashcards

Pathology syllabus: all 19 chapters

Expand any chapter to see its topics and sub-topics.

Cell Injury and Adaptation
4 topics
- Cell Injury
  - Types of Cell Injury
  - Mechanisms of Cell Injury
  - Reversible and Irreversible Injury
  - Cell Death: Necrosis and Apoptosis
- Cellular Adaptations
  - Hypertrophy
  - Hyperplasia
  - Atrophy
  - Metaplasia
- Intracellular Accumulations
  - Lipids
  - Proteins
  - Glycogen
  - Pigments
- Pathologic Calcification
  - Dystrophic Calcification
  - Metastatic Calcification
Inflammation and Repair
3 topics
- Acute Inflammation
  - Vascular Changes
  - Cellular Events
  - Chemical Mediators
- Chronic Inflammation
  - Causes
  - Cellular Components
  - Granulomatous Inflammation
- Tissue Repair
  - Regeneration
  - Healing by Connective Tissue
  - Factors Affecting Healing
Hemodynamic Disorders
5 topics
- Edema
  - Pathophysiology
  - Types of Edema
- Hemorrhage
  - Causes
  - Clinical Significance
- Thrombosis
  - Pathogenesis
  - Fate of Thrombus
- Embolism
  - Types of Emboli
  - Clinical Consequences
- Shock
  - Types of Shock
  - Pathophysiology
  - Clinical Features
Genetic Disorders
4 topics
- Mendelian Disorders
  - Autosomal Dominant Disorders
  - Autosomal Recessive Disorders
  - X-linked Disorders
- Chromosomal Disorders
  - Numerical Abnormalities
  - Structural Abnormalities
- Multifactorial Disorders
  - Examples and Mechanisms
- Molecular Basis of Genetic Diseases
  - Mutations
  - Epigenetics
Neoplasia
6 topics
- Fundamentals of Neoplasia
  - Definitions and Nomenclature
  - Benign vs Malignant Tumors
- Molecular Basis of Cancer
  - Genetic Changes in Cancer
  - Oncogenes and Tumor Suppressor Genes
- Tumor-Host Interactions
  - Local and Systemic Effects
  - Paraneoplastic Syndromes
- Carcinogenesis
  - Chemical Carcinogenesis
  - Radiation Carcinogenesis
  - Microbial Carcinogenesis
- Tumor Progression and Metastasis
  - Invasion and Metastasis
  - Angiogenesis
- Clinical Aspects of Neoplasia
  - Diagnosis
  - Grading and Staging
  - Treatment
Environmental and Nutritional Pathology
2 topics
- Environmental Diseases
  - Toxicology
  - Chemical Injuries
  - Physical Injuries
- Nutritional Diseases
  - Malnutrition
  - Vitamin Deficiencies
  - Obesity
Infectious Diseases
5 topics
- General Principles of Microbial Pathogenesis
  - Host-Pathogen Interactions
  - Mechanisms of Microbial Injury
- Bacterial Infections
  - Pathogenesis and Examples
- Viral Infections
  - Pathogenesis and Examples
- Fungal Infections
  - Pathogenesis and Examples
- Parasitic Infections
  - Pathogenesis and Examples
Immunopathology
5 topics
- Basics of the Immune System
  - Innate Immunity
  - Adaptive Immunity
- Hypersensitivity Reactions
  - Type I Hypersensitivity
  - Type II Hypersensitivity
  - Type III Hypersensitivity
  - Type IV Hypersensitivity
- Autoimmune Diseases
  - Mechanisms
  - Examples
- Immunodeficiency Diseases
  - Primary Immunodeficiencies
  - Secondary Immunodeficiencies
- Amyloidosis
  - Pathogenesis
  - Classification
  - Clinical Features
Blood Vessels
1 topic
- Vascular Disorders
  - Atherosclerosis
  - Hypertension
  - Aneurysms
  - Vasculitis
Heart
4 topics
- Ischemic Heart Disease
  - Pathogenesis
  - Clinical Syndromes
- Hypertensive Heart Disease
  - Left-sided Hypertensive Heart Disease
  - Right-sided Hypertensive Heart Disease
- Valvular Heart Disease
  - Rheumatic Heart Disease
  - Infective Endocarditis
  - Non-infective Endocarditis
- Myocardial Diseases
  - Cardiomyopathies
  - Myocarditis
Respiratory System
4 topics
- Obstructive Lung Diseases
  - Chronic Obstructive Pulmonary Disease (COPD)
  - Asthma
  - Bronchiectasis
- Restrictive Lung Diseases
  - Interstitial Lung Diseases
  - Pneumoconiosis
- Pulmonary Infections
  - Pneumonia
  - Tuberculosis
  - Fungal Infections
- Lung Tumors
  - Primary Lung Cancer
  - Metastatic Tumors
Gastrointestinal Tract
6 topics
- Esophagus
  - Esophagitis
  - Barrett's Esophagus
  - Esophageal Cancer
- Stomach
  - Gastritis
  - Peptic Ulcer Disease
  - Gastric Cancer
- Intestines
  - Inflammatory Bowel Disease
  - Infectious Enterocolitis
  - Colorectal Cancer
- Liver
  - Hepatitis
  - Cirrhosis
  - Hepatocellular Carcinoma
- Gallbladder and Biliary Tract
  - Cholelithiasis
  - Cholecystitis
  - Gallbladder Cancer
- Pancreas
  - Pancreatitis
  - Pancreatic Cancer
Urinary Tract
2 topics
- Kidneys
  - Glomerular Diseases
  - Tubulointerstitial Diseases
  - Renal Tumors
- Ureters and Bladder
  - Urolithiasis
  - Bladder Cancer
Reproductive System
3 topics
- Male Reproductive System
  - Prostate Diseases
  - Testicular Tumors
- Female Reproductive System
  - Cervical Diseases
  - Endometrial Diseases
  - Ovarian Tumors
- Breast
  - Benign Breast Diseases
  - Breast Cancer
Endocrine System
5 topics
- Pituitary Gland
  - Hyperpituitarism
  - Hypopituitarism
- Thyroid Gland
  - Hyperthyroidism
  - Hypothyroidism
  - Thyroid Tumors
- Parathyroid Gland
  - Hyperparathyroidism
  - Hypoparathyroidism
- Adrenal Gland
  - Adrenocortical Hyperfunction
  - Adrenocortical Hypofunction
  - Adrenal Tumors
- Pancreatic Endocrine Tumors
  - Insulinomas
  - Gastrinomas
Nervous System
4 topics
- Cerebrovascular Diseases
  - Stroke
  - Aneurysms
- Infections of the CNS
  - Meningitis
  - Encephalitis
- Neurodegenerative Diseases
  - Alzheimer's Disease
  - Parkinson's Disease
  - Amyotrophic Lateral Sclerosis
- CNS Tumors
  - Gliomas
  - Meningiomas
Musculoskeletal System
3 topics
- Bone Diseases
  - Osteoporosis
  - Osteomyelitis
  - Bone Tumors
- Joint Diseases
  - Osteoarthritis
  - Rheumatoid Arthritis
  - Gout
- Muscle Diseases
  - Muscular Dystrophies
  - Myopathies
Skin
3 topics
- Inflammatory Skin Diseases
  - Eczema
  - Psoriasis
  - Acne
- Blistering Diseases
  - Pemphigus
  - Bullous Pemphigoid
- Skin Tumors
  - Benign Tumors
  - Malignant Tumors
Pediatric Diseases
3 topics
- Congenital Anomalies
  - Types and Examples
- Perinatal Infections
  - TORCH Infections
- Pediatric Tumors
  - Neuroblastoma
  - Wilms Tumor

MRCS Part A Pathology flashcards — 51 questions with answers

What are the two principal patterns of cell death, and how do they differ in energy requirement and inflammation?
Necrosis: passive, ATP-independent, causes membrane rupture with leakage of contents and an inflammatory reaction. Apoptosis: active, ATP-dependent, programmed self-destruction with intact membranes, apoptotic bodies, and no inflammation.
List the common biochemical mechanisms of cell injury.
ATP depletion, mitochondrial damage, increased intracellular calcium, accumulation of reactive oxygen species (oxidative stress), defects in membrane permeability, and damage to DNA/proteins.
What is the point of irreversibility in reversible vs irreversible cell injury?
Irreversibility is marked by severe mitochondrial dysfunction (inability to regenerate ATP) and profound disturbance of membrane function (plasma membrane rupture), leading to death. Reversible injury shows cell swelling and fatty change but intact membranes.
Name the six morphologic types of necrosis.
Coagulative, liquefactive, caseous, fat, fibrinoid, and gangrenous necrosis.
Which type of necrosis is characteristic of ischemic infarction of solid organs, and which is characteristic of brain infarction?
Solid organs (e.g. heart, kidney): coagulative necrosis. Brain (CNS): liquefactive necrosis.
What are the three main free radicals (reactive oxygen species) involved in cell injury, and name antioxidant defenses.
Superoxide anion ($\ce{O2^{.-}}$), hydrogen peroxide ($\ce{H2O2}$), and hydroxyl radical ($\ce{^{.}OH}$). Defenses: superoxide dismutase (SOD), catalase, glutathione peroxidase, and antioxidants such as vitamins E, A, C.
Define the four main cellular adaptations to stress.
Hypertrophy (increased cell size), hyperplasia (increased cell number), atrophy (decreased size/number), and metaplasia (reversible change of one differentiated cell type to another).
What is metaplasia and give the classic example seen in Barrett esophagus?
Metaplasia is the reversible replacement of one differentiated cell type by another. In Barrett esophagus, stratified squamous epithelium is replaced by columnar (glandular) epithelium due to chronic acid reflux.
Distinguish physiologic from pathologic hyperplasia with examples.
Physiologic: hormonal (e.g. pregnant uterus, breast at puberty) or compensatory (liver regeneration). Pathologic: excessive hormonal/growth-factor stimulation, e.g. endometrial hyperplasia, benign prostatic hyperplasia.
List the main intracellular accumulations and a disease example for each.
Lipid (fatty change in liver, atherosclerosis), protein (Mallory bodies, Russell bodies), glycogen (diabetes, glycogen storage diseases), and pigments (lipofuscin, melanin, hemosiderin).
What is lipofuscin and what does its presence signify?
Lipofuscin is an insoluble brown-yellow 'wear-and-tear' pigment composed of lipid-protein complexes from lipid peroxidation. It signifies aging or cellular atrophy (brown atrophy of heart/liver) and is not injurious.
Differentiate hemosiderin from hemosiderosis and hemochromatosis.
Hemosiderin is an iron-storage pigment (aggregated ferritin). Hemosiderosis is localized/systemic iron accumulation without organ damage. Hemochromatosis is iron overload causing tissue injury (cirrhosis, diabetes, cardiac failure, skin pigmentation).
Contrast dystrophic and metastatic calcification.
Dystrophic: calcium deposition in dead/damaged tissue with NORMAL serum calcium (e.g. atheromas, damaged heart valves, caseous foci). Metastatic: deposition in normal tissue due to HYPERCALCEMIA (e.g. hyperparathyroidism, vitamin D excess, bone destruction, renal failure).
Name four major causes of hypercalcemia leading to metastatic calcification.
Increased PTH (primary or ectopic hyperparathyroidism), destruction of bone (tumors, immobilization, Paget disease), vitamin D disorders (intoxication, sarcoidosis), and renal failure (secondary hyperparathyroidism).
What are the five cardinal signs of acute inflammation and their Latin names?
Redness (rubor), heat (calor), swelling (tumor), pain (dolor), and loss of function (functio laesa).
Describe the vascular changes in acute inflammation.
Transient vasoconstriction, then vasodilation (increased blood flow = heat and redness), followed by increased vascular permeability causing exudation of protein-rich fluid, stasis, and margination of leukocytes.
List the sequential steps of leukocyte extravasation in acute inflammation.
Margination and rolling (selectins), adhesion (integrins–ICAM/VCAM), transmigration/diapedesis (PECAM-1/CD31), and chemotaxis toward the injury.
Name the key selectins and their ligands in leukocyte rolling.
E-selectin (endothelium) and P-selectin (endothelium/platelets) bind sialyl-Lewis X on leukocytes; L-selectin (leukocytes) binds GlyCAM-1/CD34 on endothelium.
What is the difference between transudate and exudate (including specific gravity and protein)?
Transudate: low protein, few cells, specific gravity $< 1.012$, due to hydrostatic/osmotic imbalance (ultrafiltrate). Exudate: high protein, many cells, specific gravity $> 1.020$, due to increased vascular permeability in inflammation.
List the major chemical mediators of acute inflammation grouped by source.
Cell-derived: histamine, serotonin, prostaglandins, leukotrienes, PAF, cytokines (TNF, IL-1), nitric oxide, ROS. Plasma-derived: complement (C3a, C5a, MAC), kinins (bradykinin), and coagulation/fibrinolytic factors.

Show the other 31 Pathology flashcards

Which arachidonic acid metabolites arise from the cyclooxygenase vs lipoxygenase pathways?
Cyclooxygenase (COX): prostaglandins ($PGE_2$, $PGD_2$, $PGF_2$), prostacyclin ($PGI_2$), thromboxane $A_2$. Lipoxygenase: leukotrienes ($LTB_4$ chemotactic; $LTC_4/D_4/E_4$ vasoconstriction and bronchospasm) and lipoxins.
What are the functions of complement fragments C3a, C5a, C3b, and the MAC?
C3a and C5a: anaphylatoxins (increase vascular permeability, mast cell degranulation); C5a is also chemotactic. C3b: opsonization. Membrane attack complex (C5b-9): cell lysis.
What are the possible outcomes of acute inflammation?
Complete resolution, healing by fibrosis (scarring), abscess formation, or progression to chronic inflammation.
What cells characterize chronic inflammation, and what defines it?
Chronic inflammation is prolonged inflammation with simultaneous tissue destruction and repair. Characterized by mononuclear cells: macrophages, lymphocytes, and plasma cells, with angiogenesis and fibrosis.
What is a granuloma and name the two types.
A granuloma is a focus of chronic inflammation with aggregated activated epithelioid macrophages, often with multinucleate giant cells. Types: foreign-body granuloma (inert material) and immune granuloma (T-cell mediated, e.g. TB, sarcoidosis).
Give examples of caseating vs non-caseating granulomatous diseases.
Caseating: tuberculosis (central caseous necrosis). Non-caseating: sarcoidosis, Crohn disease, foreign-body reactions, cat-scratch disease (though stellate necrosis), berylliosis.
Describe the roles of macrophages in chronic inflammation (M1 vs M2).
M1 (classically activated, by IFN-γ/microbes): microbicidal, produce ROS, NO, and inflammatory cytokines. M2 (alternatively activated, by IL-4/IL-13): tissue repair, fibrosis, anti-inflammatory (TGF-β, IL-10), angiogenesis.
Distinguish labile, stable, and permanent cells with examples relevant to tissue repair.
Labile: continuously dividing (surface epithelia, bone marrow). Stable: quiescent, divide when stimulated (hepatocytes, renal tubular cells, fibroblasts). Permanent: non-dividing (neurons, cardiac and skeletal muscle) — heal by scar.
What are the steps of healing by primary vs secondary intention?
Primary intention: clean, apposed wound edges (surgical incision) — minimal tissue loss, small scar. Secondary intention: large tissue defect — heals by granulation tissue, wound contraction (myofibroblasts), and larger scar.
Outline the components and sequence of granulation tissue formation.
Angiogenesis (new capillaries), proliferation of fibroblasts, deposition of loose ECM/collagen, and infiltration by inflammatory cells. It appears soft, pink, and granular, and later matures into a fibrous scar.
Which growth factor drives angiogenesis and which drives fibroblast proliferation and collagen deposition in wound healing?
Angiogenesis: VEGF (vascular endothelial growth factor). Fibroblast proliferation, collagen synthesis, and scar formation: TGF-β (also PDGF and FGF).
Which collagen predominates in early granulation tissue and which in the mature scar?
Early wound/granulation tissue: type III collagen. Mature scar: type I collagen (via remodeling by matrix metalloproteinases, MMPs).
List local and systemic factors that impair wound healing.
Local: infection, poor blood supply/ischemia, foreign bodies, mechanical stress, denervation. Systemic: diabetes, malnutrition (especially vitamin C and protein deficiency), glucocorticoids, zinc deficiency, old age, and smoking.
State Starling's forces and the equation governing fluid movement across capillaries.
Net filtration depends on hydrostatic and oncotic pressure gradients: $$J_v = K_f\left[(P_c - P_i) - \sigma(\pi_c - \pi_i)\right]$$ where $P$ is hydrostatic pressure, $\pi$ is oncotic pressure, $K_f$ is the filtration coefficient, and $\sigma$ is the reflection coefficient.
List the four main pathophysiologic causes of edema.
Increased hydrostatic pressure (venous obstruction, heart failure), reduced plasma oncotic pressure (hypoalbuminemia — nephrotic syndrome, liver disease, malnutrition), lymphatic obstruction (lymphedema), and increased vascular permeability/sodium retention (inflammation, renal disease).
Define hematoma, petechiae, purpura, and ecchymosis by size.
Hematoma: accumulation of blood within tissue. Petechiae: 1–2 mm hemorrhages. Purpura: 3–10 mm (≥3 mm). Ecchymosis: >1–2 cm subcutaneous bruise.
State Virchow's triad for thrombosis.
Endothelial injury, abnormal blood flow (stasis or turbulence), and hypercoagulability (thrombophilia).
How do arterial and venous thrombi differ in composition and appearance?
Arterial thrombi: form under high flow, platelet-rich ('white'), grow retrograde, and show lines of Zahn. Venous thrombi: form in stasis, red/RBC-rich ('red'), grow in the direction of blood flow, and almost always occlusive.
What are the lines of Zahn and their significance?
Lines of Zahn are alternating pale layers of platelets/fibrin and darker layers of red cells in a thrombus. They indicate the thrombus formed in flowing blood ante-mortem, distinguishing it from a post-mortem clot.
List the possible fates of a thrombus.
Propagation, embolization, dissolution (fibrinolysis), and organization with recanalization.
Name the major inherited (primary) causes of hypercoagulability.
Factor V Leiden (activated protein C resistance), prothrombin G20210A mutation, antithrombin III deficiency, protein C deficiency, and protein S deficiency.
Define embolism and list the main types.
An embolus is a detached intravascular solid, liquid, or gas mass carried to a distant site. Types: thromboembolism (most common), fat, air/gas, amniotic fluid, tumor, septic, and foreign-body emboli.
Where do most pulmonary emboli originate, and what is a saddle embolus?
Most pulmonary emboli arise from deep vein thromboses of the lower extremities (especially popliteal and larger proximal veins). A saddle embolus lodges at the bifurcation of the main pulmonary artery and can cause sudden death.
What is a paradoxical embolus?
A paradoxical embolus is a venous (systemic) thrombus that passes into the arterial circulation through a right-to-left cardiac shunt (e.g. patent foramen ovale or atrial/ventricular septal defect), reaching systemic sites such as the brain.
Define shock and list its three major categories.
Shock is systemic hypoperfusion causing inadequate tissue oxygenation and cellular hypoxia. Categories: hypovolemic (blood/fluid loss), cardiogenic (pump failure), and distributive (septic, anaphylactic, neurogenic — vasodilation).
Describe the three clinical stages of shock.
Nonprogressive (compensated): reflex mechanisms (tachycardia, vasoconstriction) maintain perfusion. Progressive: tissue hypoperfusion, metabolic (lactic) acidosis, worsening circulation. Irreversible: cellular/organ injury so severe that survival is impossible even if hemodynamics are corrected.
What is the pathophysiology of septic shock?
Most often gram-negative or gram-positive bacterial infection; microbial products (e.g. LPS/endotoxin) trigger massive cytokine release (TNF, IL-1), causing systemic vasodilation, increased vascular permeability, DIC, myocardial depression, and multi-organ failure — a hyperdynamic, warm, high-cardiac-output early state.
Explain the difference between autosomal dominant and autosomal recessive inheritance patterns.
Autosomal dominant: one mutant allele suffices; affects both sexes, vertical transmission through generations, often structural proteins/receptors (e.g. Marfan, familial hypercholesterolemia). Autosomal recessive: two mutant alleles needed; often enzyme defects, may skip generations, associated with consanguinity (e.g. cystic fibrosis).
What are the karyotype and key features of Down syndrome, Klinefelter syndrome, and Turner syndrome?
Down syndrome: trisomy 21 (47,XX or XY,+21) — intellectual disability, flat facies, cardiac defects. Klinefelter: 47,XXY — male hypogonadism, tall, infertility. Turner: 45,X — short stature, webbed neck, ovarian dysgenesis, coarctation of aorta.
What is the two-hit hypothesis (Knudson) in cancer genetics?
For tumor suppressor genes, both alleles must be inactivated ('two hits') for tumorigenesis. In hereditary cancers the first hit is inherited (germline) and only one somatic hit is needed; in sporadic cancers both hits are somatic, hence later onset. Classic example: retinoblastoma (RB gene).
Define neoplasia and distinguish the essential features of benign vs malignant tumors.
Neoplasia is autonomous, uncoordinated new tissue growth persisting after the stimulus stops. Benign: well-differentiated, slow-growing, encapsulated, non-invasive, do NOT metastasize. Malignant: poorly differentiated (anaplastic), rapid growth, invasive, and metastasize.

Same Pathology syllabus in other exams

The Pathology outline above is identical in these 3 exams:

MRCS Part A Pathology FAQ

What is in the MRCS Part A Pathology syllabus?

MRCS Part A Pathology is split into 19 chapters: Cell Injury and Adaptation, Inflammation and Repair, Hemodynamic Disorders, Genetic Disorders, Neoplasia, Environmental and Nutritional Pathology, Infectious Diseases, Immunopathology, Blood Vessels, Heart, Respiratory System and Gastrointestinal Tract, and 7 more. Together they contain 72 topics and 173 sub-topics.

How many chapters are in MRCS Part A Pathology?

19 chapters, containing 72 topics and 173 sub-topics. The largest chapter is Neoplasia, with 6 topics.

Are there flashcards for MRCS Part A Pathology?

Yes — a 51-card Pathology deck, printed in full in the flashcards section of this page and available in the Examius app with spaced repetition. The free plan covers one exam of your choice, including its flashcards; Examius Pro, a one-time purchase, unlocks every other exam and deck.

MRCS Part A Pathology Syllabus

Pathology syllabus: all 19 chapters

Cell Injury and Adaptation

Inflammation and Repair

Hemodynamic Disorders

Genetic Disorders

Neoplasia

Environmental and Nutritional Pathology

Infectious Diseases

Immunopathology

Blood Vessels

Heart

Respiratory System

Gastrointestinal Tract

Urinary Tract

Reproductive System

Endocrine System

Nervous System

Musculoskeletal System

Skin

Pediatric Diseases

MRCS Part A Pathology flashcards — 51 questions with answers

Same Pathology syllabus in other exams

MRCS Part A Pathology FAQ