Pathology & Disease Progression studies

Syllabus Unit: Pre & Para Clinical Subjects

Why it matters

Chapter overview

Pathology links cellular-level mechanism to bedside pattern recognition — how reversible cell injury becomes irreversible necrosis, how a normal cell acquires the hallmarks of cancer, how a CBC and coagulation panel localise a blood disorder, and how a single pathognomonic lesion (Ghon complex, Aschoff body, Reed-Sternberg cell) identifies an entire disease — and AIIMS PG tests this pattern-recognition skill relentlessly through classic named findings.

Postgraduate Medical Exam Syllabus Pre & Para Clinical Subjects 50% weightage

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1VasodilationIncreased blood flow to the injured area

2Increased Vascular PermeabilityFluid and proteins exit into tissue, causing oedema

3Neutrophil Margination & AdhesionNeutrophils roll and stick to the endothelium

4Transmigration & PhagocytosisNeutrophils exit vessels and clear debris/bacteria

1Cell Injury, Inflammation & Repair

Reversible cell injury, the cardinal signs of acute inflammation, and the phases of wound repair form pathology's foundational cause-and-effect chain from insult to outcome.

Learning Objectives

Distinguish reversible cell injury from irreversible injury (necrosis) and their key markers.
Name the patterns of necrosis with a classic example of each.
Sequence the vascular and cellular events of acute inflammation.
Differentiate the chemical mediators of inflammation by their principal effect.

Key Terms

Coagulative NecrosisPreserved cellular/tissue outline with loss of nuclear detail due to protein denaturation outlasting enzymatic digestion; classic in ischaemic infarcts of solid organs (heart, kidney, spleen) except the brain.

Liquefactive NecrosisTissue converted to a liquid, viscous mass by enzymatic digestion; classic in brain infarcts (high lipid content, microglial action) and bacterial abscesses (neutrophilic enzymes).

Caseous NecrosisA cheese-like, structureless combination of coagulative and liquefactive necrosis, pathognomonic for tuberculosis (and some fungal infections).

Chemical Mediators of InflammationHistamine (immediate vasodilation/permeability), prostaglandins (vasodilation, pain, fever, targeted by NSAIDs), leukotrienes (neutrophil chemotaxis, bronchoconstriction), and complement (C3a/C5a anaphylatoxins, C5a chemotaxis, C3b opsonisation).

Cell injury and inflammation questions test pattern matching: given a described necrosis pattern or inflammatory event, identify the exact named process and the clinical scenario it points to.

Patterns of necrosis

Coagulative — ischaemic infarcts of solid organs (except brain); architecture preserved.
Liquefactive — brain infarcts, bacterial abscesses; tissue liquefies.
Caseous — tuberculosis; cheese-like, combines both patterns.
Fat necrosis — acute pancreatitis (enzymatic) or trauma to fatty tissue.
Fibrinoid necrosis — immune-mediated vessel wall damage (vasculitis, malignant hypertension).
Gangrenous necrosis — ischaemic limb necrosis, may be dry (coagulative) or wet (with superimposed infection, liquefactive).

Exam TipCaseous necrosis on histology means tuberculosis until proven otherwise.

Acute inflammation

Injury → Vasodilation → Increased Vascular Permeability → Neutrophil Margination & Adhesion → Transmigration → Chemotaxis → Phagocytosis

Chemical mediators

Histamine (from mast cells) causes immediate vasodilation and permeability; prostaglandins (via the COX pathway, the target of NSAIDs) cause vasodilation, pain and fever; leukotrienes (LTB4 for chemotaxis, LTC4/D4/E4 for bronchoconstriction) are targeted by drugs like montelukast; complement (C3a/C5a, C5a chemotaxis, C3b opsonisation) links innate and adaptive immunity.