Pathology
Inflammation
Inflammation for MBBS and NEET-PG: cardinal signs, vascular and cellular events, chemical mediators, patterns of acute inflammation, and granulomatous inflammation, mapped to NMC codes PA4.1 to PA4.4.
MedNext Academy | 3 min read
Inflammation
Inflammation for MBBS and NEET-PG: cardinal signs, vascular and cellular events, chemical mediators, patterns of acute inflammation, and granulomatous inflammation, mapped to NMC codes PA4.1 to PA4.4.
Inflammation is the protective response of vascularised tissue to injury. This chapter covers the vascular and cellular events of acute inflammation, its chemical mediators, the morphological patterns, and the features of chronic and granulomatous inflammation that examiners test through recognition and comparison.
High-yield: Inflammation
- The five cardinal signs of inflammation are redness, heat, swelling, pain and loss of function.
- Acute inflammation has vascular changes and a neutrophil-rich cellular response; chronic inflammation is dominated by macrophages, lymphocytes and plasma cells.
- The vascular events are transient vasoconstriction, then vasodilatation and increased vascular permeability causing exudation.
- Increased vascular permeability in acute inflammation is chiefly due to endothelial contraction mediated by histamine.
- Leucocyte recruitment proceeds through margination, rolling, adhesion, transmigration and chemotaxis.
- Selectins mediate rolling, while integrins binding to ICAM mediate firm adhesion of leucocytes.
- Histamine, released from mast cells, causes early vasodilatation and increased permeability.
- Arachidonic acid gives rise to prostaglandins and leukotrienes; the cyclooxygenase pathway makes prostaglandins and the lipoxygenase pathway makes leukotrienes.
- Prostaglandins mediate pain, fever and vasodilatation, which is why NSAIDs that block cyclooxygenase relieve these features.
- Neutrophils predominate in the first 24 hours of acute inflammation and are then replaced by macrophages.
- A granuloma is a focal collection of activated epithelioid macrophages, often with a rim of lymphocytes and giant cells.
- Caseating granulomas are typical of tuberculosis; non-caseating granulomas are seen in sarcoidosis and Crohn disease.
- Langhans giant cells have peripherally arranged horseshoe nuclei and are seen in tuberculosis.
- Serous, fibrinous, suppurative and ulcerative are the morphological patterns of acute inflammation.
- Chronic inflammation is characterised by simultaneous tissue destruction, ongoing inflammation and attempts at repair.
Acute versus chronic inflammation
- **Onset and duration:** Acute is rapid and short-lived; chronic is insidious and prolonged.
- **Dominant cell:** Acute: neutrophils. Chronic: macrophages, lymphocytes and plasma cells.
- **Vascular change:** Prominent in acute inflammation; less prominent in chronic inflammation.
- **Tissue effect:** Chronic inflammation combines destruction, inflammation and repair together.
NMC competencies in this chapter
- **PA4.1:** General features of acute and chronic inflammation: stimuli, vascular and cellular events
- **PA4.2:** Mediators of acute inflammation
- **PA4.3:** Chronic inflammation: causes, non-specific and granulomatous types
- **PA4.4:** Identify acute and chronic inflammation in gross and microscopic specimens
Frequently Asked Questions
What are the cardinal signs of inflammation?
Redness, heat, swelling, pain and loss of function, which reflect the underlying vasodilatation, exudation and cellular response.
Which cell predominates in acute inflammation?
The neutrophil dominates the first 24 hours of acute inflammation, after which macrophages take over.
What is a granuloma?
A granuloma is a focal collection of activated epithelioid macrophages, often with giant cells and a lymphocyte rim, seen in tuberculosis, sarcoidosis and other chronic conditions.
How do NSAIDs reduce inflammation?
They block cyclooxygenase and reduce prostaglandin synthesis, which lessens the pain, fever and vasodilatation of inflammation.
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