Pathology
MBBS Pathology — high-yield long questions and short notes from Robbins & Cotran and Harsh Mohan, covering general pathology (cell injury, inflammation, haemodynamics, immunopathology, neoplasia), haematology, and systemic pathology of the cardiovascular, respiratory, GI, hepatobiliary, renal, endocrine and other systems, written to the marks with definitions, mechanisms, morphology, classification, clinical correlation and pearls.
12chapters144questions99High-Yield
Definition
Oedema is the abnormal accumulation of fluid in the interstitial tissue spaces or body cavities.
Mechanisms
- ↑ Hydrostatic pressure — cardiac failure, venous obstruction
- ↓ Plasma oncotic pressure — nephrotic syndrome, cirrhosis, malnutrition
- ↑ Vascular permeability — inflammation, burns
- Lymphatic obstruction — filariasis, surgery, tumour
- Sodium and water retention — renal disease, ↑ aldosterone
Types
- Localised — inflammatory, lymphoedema, venous thrombosis
- Generalised (anasarca) — cardiac, renal, hepatic
- Pulmonary oedema, cerebral oedema, ascites, hydrothorax
- Pitting (fluid) vs non-pitting (lymphoedema, myxoedema)
Oedema results whenever Starling forces favour filtration over reabsorption. Cause Mechanism Cardiac failure ↑ Hydrostatic Nephrotic syndrome ↓ Oncotic Filariasis Lymphatic block Applied
- Cardiac oedema is dependent; renal oedema starts periorbitally
- Pulmonary oedema is a medical emergency
🔑KEY POINTS TO REMEMBER- Oedema = excess interstitial fluid from disturbed Starling forces.
- Mechanisms: ↑ hydrostatic, ↓ oncotic, ↑ permeability, lymphatic block, sodium retention.
- Cardiac oedema is dependent; renal oedema is periorbital.
📚SOURCES: Robbins & Cotran Pathologic Basis of Disease; Textbook of Pathology (Harsh Mohan); Robbins Basic Pathology.Definition
Thrombosis is the formation of a solid mass from blood constituents within the intact vascular system during life.
Virchow’s Triad
- Endothelial injury — atherosclerosis, trauma, inflammation
- Abnormal blood flow — stasis (immobility, atrial fibrillation) or turbulence
- Hypercoagulability — malignancy, pregnancy, oral contraceptives, factor V Leiden
Morphology & Fate
- Lines of Zahn — alternating pale platelet/fibrin and dark red-cell layers (arterial)
- Arterial thrombi — pale, occlusive; venous — red, propagating
- Fate: propagation, embolisation, dissolution, organisation and recanalisation
The three arms of Virchow’s triad together generate a thrombus. Feature Arterial Venous Colour Pale (white) Red Cause Endothelial injury Stasis Result Infarction Embolism Applied
- Deep vein thrombosis → pulmonary embolism
- Prevented by early mobilisation and anticoagulant prophylaxis
🔑KEY POINTS TO REMEMBER- Thrombosis = intravascular clot in life; Virchow’s triad explains it.
- Lines of Zahn indicate a thrombus formed in flowing blood.
- Fates: propagation, embolisation, dissolution, organisation, recanalisation.
📚SOURCES: Robbins & Cotran Pathologic Basis of Disease; Textbook of Pathology (Harsh Mohan); Robbins Basic Pathology.Definition
An embolus is a detached intravascular solid, liquid or gaseous mass carried by the blood to a site distant from its origin.
Types
- Thromboembolism — commonest (>99%): pulmonary or systemic
- Fat embolism — long-bone fracture
- Air embolism — surgery, decompression sickness (caisson disease)
- Amniotic fluid embolism — obstetric emergency with DIC
- Tumour, septic, atheromatous, foreign body, parasite
Consequences
- Pulmonary embolism — from deep leg veins; sudden death if massive (saddle embolus)
- Systemic embolism — from left heart (mural thrombus, atrial fibrillation, vegetations) → brain, spleen, kidney, limbs
- Paradoxical embolism — venous embolus crossing a septal defect
The embolus travels until the vessel becomes too narrow to pass. Source Destination Leg veins Lungs Left atrium Brain, limbs Long-bone fracture Lung, brain Applied
- Pulmonary embolism: sudden dyspnoea, chest pain, hypoxia; diagnosed by CT pulmonary angiography
- Prophylactic heparin in immobile patients
🔑KEY POINTS TO REMEMBER- Embolus = detached mass carried in blood; over 99% are thromboemboli.
- Venous emboli lodge in lungs; left-heart emboli travel systemically.
- Other types: fat, air, amniotic fluid, septic, tumour.
📚SOURCES: Robbins & Cotran Pathologic Basis of Disease; Textbook of Pathology (Harsh Mohan); Robbins Basic Pathology.Definition
Infarction is an area of ischaemic necrosis caused by occlusion of the arterial supply or venous drainage of a tissue.
Types
- Pale (white, anaemic) — solid organs with end-arterial supply: heart, kidney, spleen
- Red (haemorrhagic) — loose tissue, dual blood supply or venous occlusion: lung, intestine, testis
- Septic — infected infarct (from vegetations)
- Shape: usually wedge-shaped with the apex towards the occlusion
Factors Determining Severity
- Nature of blood supply — dual supply is protective
- Rate of occlusion — slow occlusion allows collaterals
- Tissue vulnerability to hypoxia — neurons 3–4 min, myocardium 20–30 min
- Oxygen content of blood (anaemia, hypoxaemia worsen it)
Occlusion causes necrosis whose extent depends on collateral supply. Type Organ Reason Pale Heart, kidney End arteries Red Lung, bowel Dual supply / venous Applied
- Brain infarcts show liquefactive necrosis (exception)
- Infarcts heal by scar formation, not regeneration
🔑KEY POINTS TO REMEMBER- Infarction = ischaemic necrosis, usually wedge-shaped and coagulative.
- Pale infarcts in end-arterial organs; red infarcts in lung and bowel.
- Severity depends on collaterals, rate of occlusion and tissue vulnerability.
📚SOURCES: Robbins & Cotran Pathologic Basis of Disease; Textbook of Pathology (Harsh Mohan); Robbins Basic Pathology.Definition
Shock is a state of circulatory failure causing inadequate tissue perfusion, leading to cellular hypoxia and organ dysfunction.
Types
- Hypovolaemic — haemorrhage, burns, vomiting, diarrhoea
- Cardiogenic — myocardial infarction, arrhythmia, tamponade
- Septic — endotoxin-mediated vasodilatation (commonly Gram-negative)
- Neurogenic — spinal injury, anaesthesia
- Anaphylactic — IgE-mediated massive vasodilatation
Stages
- Non-progressive (compensated) — tachycardia, vasoconstriction maintain perfusion
- Progressive — tissue hypoperfusion, metabolic acidosis, oliguria
- Irreversible — cell and organ damage; death despite correction
Persistent hypoperfusion converts a reversible state into an irreversible one. Type Skin Cardiac output Hypovolaemic Cold, clammy Low Septic (early) Warm, flushed High Cardiogenic Cold Low Applied
- Complications: acute tubular necrosis, ARDS, DIC, ischaemic bowel
- Management: restore volume, treat cause, support organs
🔑KEY POINTS TO REMEMBER- Shock = inadequate tissue perfusion; five main types.
- Stages: non-progressive, progressive, irreversible.
- Early septic shock is warm; hypovolaemic and cardiogenic shock are cold.
📚SOURCES: Robbins & Cotran Pathologic Basis of Disease; Textbook of Pathology (Harsh Mohan); Robbins Basic Pathology.Definition
Virchow’s triad describes the three factors that predispose to thrombosis.
The Three Components
- Endothelial injury — the most important in arterial and cardiac thrombosis: atherosclerosis, hypertension, trauma, vasculitis, smoking
- Abnormal blood flow — stasis (immobility, atrial fibrillation, varicose veins) or turbulence (aneurysm, atheroma)
- Hypercoagulability — primary: factor V Leiden, antithrombin III/protein C deficiency; secondary: malignancy, pregnancy, oral contraceptives, prolonged bed rest, nephrotic syndrome
Any one factor may suffice, but together the risk multiplies. Factor Dominant in Endothelial injury Arterial thrombosis Stasis Venous thrombosis Hypercoagulability Malignancy, pregnancy Applied
- Stasis is the leading factor in deep vein thrombosis after surgery
- Prevention: early mobilisation, compression stockings, heparin prophylaxis
🔑KEY POINTS TO REMEMBER- Virchow’s triad: endothelial injury, abnormal flow, hypercoagulability.
- Endothelial injury dominates arterial thrombosis; stasis dominates venous.
- Guides prophylaxis with mobilisation and anticoagulation.
📚SOURCES: Robbins & Cotran Pathologic Basis of Disease; Textbook of Pathology (Harsh Mohan); Robbins Basic Pathology.Definition
Hyperaemia and congestion both mean increased blood volume in tissue, but differ in mechanism and appearance.
Hyperaemia (active)
- Active process — arteriolar dilatation
- ↑ Inflow of oxygenated blood
- Tissue appears red (erythema) and warm
- Examples: inflammation, exercise, blushing
Congestion (passive)
- Passive process — impaired venous outflow
- Accumulation of deoxygenated blood
- Tissue appears blue-red (cyanotic) and cool
- Examples: cardiac failure, venous obstruction, deep vein thrombosis
- Long-standing congestion → hypoxia, haemorrhage, fibrosis
Increased inflow reddens tissue; blocked outflow makes it cyanotic. Feature Hyperaemia Congestion Process Active Passive Blood Oxygenated Deoxygenated Colour Red Blue-red Applied
- Chronic congestion causes nutmeg liver and brown induration of lung
- Congestion may lead to stasis and thrombosis
🔑KEY POINTS TO REMEMBER- Hyperaemia is active arteriolar dilatation with oxygenated blood (red).
- Congestion is passive venous outflow obstruction with deoxygenated blood (cyanotic).
- Chronic congestion causes hypoxia and fibrosis.
📚SOURCES: Robbins & Cotran Pathologic Basis of Disease; Textbook of Pathology (Harsh Mohan); Robbins Basic Pathology.Definition
Chronic venous congestion (CVC) is long-standing passive engorgement of tissue due to impaired venous drainage, most often from cardiac failure.
CVC Lung (left heart failure)
- Pulmonary veins engorged → alveolar transudate and haemorrhage
- Heart failure cells — haemosiderin-laden macrophages in alveoli
- Fibrosis + haemosiderin → brown induration of the lung
- Clinically: dyspnoea, orthopnoea, rusty sputum
CVC Liver (right heart failure)
- Centrilobular congestion and necrosis with peripheral fatty change
- Cut surface shows alternating red and pale areas → ‘nutmeg liver’
- Long-standing → cardiac cirrhosis
- Also CVC spleen — congestive splenomegaly with Gamna-Gandy bodies
Sustained back-pressure produces the characteristic organ changes. Organ Appearance Lung Brown induration Liver Nutmeg liver Spleen Gamna-Gandy bodies Applied
- Nutmeg liver indicates right heart failure
- Heart failure cells in sputum support pulmonary congestion
🔑KEY POINTS TO REMEMBER- CVC lung: heart failure cells and brown induration (left heart failure).
- CVC liver: nutmeg appearance, may progress to cardiac cirrhosis.
- CVC spleen shows Gamna-Gandy bodies.
📚SOURCES: Robbins & Cotran Pathologic Basis of Disease; Textbook of Pathology (Harsh Mohan); Robbins Basic Pathology.Definition
Fat embolism is the presence of fat globules in the circulation, typically after long-bone fractures or major trauma.
Causes & Mechanism
- Fracture of long bones (femur, tibia) and pelvis — commonest
- Orthopaedic surgery, severe soft-tissue trauma, burns, acute pancreatitis
- Mechanical — marrow fat enters torn venules
- Biochemical — free fatty acids injure endothelium and cause platelet aggregation
Fat Embolism Syndrome
- Onset 24–72 hours after injury (a symptom-free interval)
- Classic triad: respiratory distress, neurological symptoms (confusion, coma), petechial rash (upper trunk, axilla, conjunctiva)
- Thrombocytopenia, anaemia; fat globules in urine and sputum
- Treatment is supportive — oxygen, ventilation; prevention by early fracture fixation
Fat globules obstruct capillaries and release damaging fatty acids. Feature Detail Onset 24–72 hours Triad Lung, brain, petechiae Treatment Supportive Applied
- Petechial rash is the most specific sign
- Most cases are subclinical; only ~10% develop the syndrome
🔑KEY POINTS TO REMEMBER- Fat embolism usually follows long-bone fractures.
- Syndrome appears 24–72 hours later with dyspnoea, confusion and petechiae.
- Treatment is supportive; early fixation prevents it.
📚SOURCES: Robbins & Cotran Pathologic Basis of Disease; Textbook of Pathology (Harsh Mohan); Robbins Basic Pathology.Definition
Infarcts are classified as red (haemorrhagic) or pale (anaemic) depending on the blood supply of the affected tissue.
Pale (White) Infarct
- Occurs in solid organs with end-arterial supply
- Sites: heart, kidney, spleen
- Arterial occlusion; dense tissue limits haemorrhage
- Wedge-shaped, pale, firm; coagulative necrosis
Red (Haemorrhagic) Infarct
- Occurs with dual blood supply (lung, liver), loose tissue (lung), venous occlusion (testis, ovary, bowel volvulus)
- Also after reperfusion of a previously infarcted area
- Sites: lung, intestine, testis, ovary, brain (haemorrhagic transformation)
- Blood seeps into the necrotic loose tissue
Whether blood can seep into the dead area decides the colour. Type Organs Cause Pale Heart, kidney, spleen End artery Red Lung, bowel, testis Dual/venous Applied
- All infarcts eventually heal by fibrous scarring
- Brain is exceptional — liquefactive necrosis
🔑KEY POINTS TO REMEMBER- Pale infarcts occur in end-arterial solid organs (heart, kidney, spleen).
- Red infarcts occur with dual supply, loose tissue or venous occlusion.
- Both heal by scarring; brain infarcts are liquefactive.
📚SOURCES: Robbins & Cotran Pathologic Basis of Disease; Textbook of Pathology (Harsh Mohan); Robbins Basic Pathology.Definition
Disseminated intravascular coagulation (DIC) is widespread activation of coagulation causing microthrombi, consumption of clotting factors and bleeding.
Causes
- Obstetric — abruptio placentae, amniotic fluid embolism, retained dead fetus, eclampsia
- Infections — Gram-negative sepsis, malaria
- Malignancy — acute promyelocytic leukaemia, adenocarcinoma
- Massive trauma, burns, severe shock, incompatible transfusion
Pathogenesis & Findings
- Release of tissue factor or endothelial injury → widespread thrombin generation
- Microthrombi → ischaemia and organ failure
- Consumption of platelets and factors + secondary fibrinolysis → bleeding
- Labs: ↓ platelets, ↑ PT and aPTT, ↓ fibrinogen, ↑↑ D-dimer/FDP
- Blood film: schistocytes (microangiopathic haemolysis)
Paradoxically, excessive clotting exhausts the clotting system and causes bleeding. Test Result Platelets Low PT / aPTT Prolonged D-dimer Markedly raised Applied
- Treat the underlying cause first
- Support with platelets, fresh frozen plasma and cryoprecipitate
🔑KEY POINTS TO REMEMBER- DIC = widespread clotting with consumption of factors → bleeding.
- Causes: sepsis, obstetric emergencies, malignancy, trauma.
- Labs: ↓ platelets, ↑ PT/aPTT, ↓ fibrinogen, ↑↑ D-dimer, schistocytes.
📚SOURCES: Robbins & Cotran Pathologic Basis of Disease; Textbook of Pathology (Harsh Mohan); Robbins Basic Pathology.Definition
Shock is classified by the underlying haemodynamic mechanism causing inadequate tissue perfusion.
Main Types
- Hypovolaemic — ↓ blood volume: haemorrhage, burns, severe vomiting/diarrhoea
- Cardiogenic — pump failure: myocardial infarction, arrhythmia, tamponade, pulmonary embolism
- Distributive — vasodilatation: septic, anaphylactic, neurogenic
- Obstructive — tension pneumothorax, massive pulmonary embolism
Distinguishing Features
- Septic shock — early warm phase (high output, low resistance), later cold; endotoxin-driven
- Anaphylactic — IgE-mediated; urticaria, bronchospasm; treat with adrenaline
- Neurogenic — loss of sympathetic tone; bradycardia with hypotension, warm skin
- Hypovolaemic and cardiogenic — cold, clammy skin, tachycardia, low output
Cardiac output and vascular resistance define the clinical picture. Type Output Skin Hypovolaemic Low Cold Cardiogenic Low Cold Septic (early) High Warm Applied
- Anaphylaxis → immediate intramuscular adrenaline
- All types converge on multiorgan failure if uncorrected
🔑KEY POINTS TO REMEMBER- Types: hypovolaemic, cardiogenic, distributive (septic, anaphylactic, neurogenic), obstructive.
- Hypovolaemic and cardiogenic shock are cold; early septic shock is warm.
- Neurogenic shock shows hypotension with bradycardia.
📚SOURCES: Robbins & Cotran Pathologic Basis of Disease; Textbook of Pathology (Harsh Mohan); Robbins Basic Pathology.