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PA3.4 | Inflammation Morphology — Practical — SDL Guide (Part 2)

Acute Patterns: Fibrinous and Serous

Side-by-side pathology diagram comparing fibrinous inflammation with shaggy fibrin-coated pericardial surfaces and serous inflammation with a clear fluid-filled skin blister. — **Panel A:** Fibrinous inflammation: visceral pericardium, parietal pericardium, shaggy fibrin strands, bread-and-butter appearance, eosinophilic fibrin meshwork, scattered neutrophils, trapped red cells.. **Panel B:** Serous inflammation: lifted epidermis, subepidermal blister cavity, clear serous fluid, intact dermis, pale eosinophilic fluid, sparse neutrophils.. **Central strip:** Key distinction: fibrin threads with cellular exudate versus clear protein-poor fluid with few cells..

Fibrinous inflammation occurs when the vascular leak is large enough to allow high-molecular-weight fibrinogen to escape and polymerise as fibrin.

Microscopic: eosinophilic, thread-like or meshwork material on a serosal surface or within an organ; may contain trapped neutrophils and red cells.

Classic example: fibrinous pericarditis — the friction-rub lesion. Grossly described as 'bread-and-butter' pericarditis: when the pericardial surfaces are pulled apart they look like two pieces of buttered bread being separated. Microscopically: fibrin strands coat the visceral and parietal pericardium; neutrophils scattered within.

Serous inflammation involves a more dilute, protein-poor exudate with few cells.

Microscopic: pale eosinophilic fluid in body cavities or subepidermally (skin blisters); sparse neutrophils. Example: the blister of a second-degree burn, or an early viral pleuritis.

Distinction to know: fibrinous vs. serous — fibrin threads vs. clear fluid; fibrinous is more cellular and exudative.

SELF-CHECK

A slide shows eosinophilic thread-like material coating a serosal surface with scattered neutrophils. The gross description from the post-mortem report reads 'roughened, dull surface that peeled off in strings'. What is the pattern and what classic gross description applies?

A. Fibrinous pericarditis — 'bread-and-butter' appearance

B. Serous inflammation — 'honey-coloured crust'

C. Suppurative inflammation — 'pyogenic membrane'

D. Granulomatous inflammation — 'caseous necrosis'

Reveal Answer

Answer: A. Fibrinous pericarditis — 'bread-and-butter' appearance

Eosinophilic thread-like (fibrin) material on a serosal surface with neutrophils = fibrinous inflammation. On the pericardium, the two apposing fibrinous layers produce the classic 'bread-and-butter' gross appearance when separated. This is a favourite university examination spot-diagnosis.

Acute Patterns: Ulcer and Phlegmon

Diagram comparing a chronic peptic ulcer with four microscopic layers to phlegmonous diffuse inflammation and a contained abscess. — **Panel A:** Peptic ulcer crater with absent surface epithelium, fibrinopurulent exudate, zone of necrosis, granulation tissue with new capillaries and fibroblasts, and fibrous scar tissue with collagen bands.. **Panel B:** Phlegmon/cellulitis showing neutrophils diffusely infiltrating between muscle fibers, fat lobules, and dermal collagen without capsule or central necrosis; streptococcal hyaluronidase indicated as a spreading factor.. **Panel C:** Comparison of phlegmon as diffuse non-localized neutrophilic inflammation versus abscess as localized pus with central necrosis and a containing wall..

Ulcer = a local defect (excavation) of the surface of an organ produced by the sloughing of necrotic tissue.

Microscopic layers of a peptic ulcer (prototype):
1. Superficial: fibrinopurulent exudate (fibrin + neutrophils)
2. Below: zone of necrosis (eosinophilic, no viable nuclei)
3. Below: granulation tissue (thin-walled new capillaries, fibroblasts, lymphocytes)
4. Base: fibrous scar tissue (collagen bands, often with chronic inflammatory cells)

An ulcer spanning all four zones indicates a long-standing lesion — the granulation and fibrosis confirm chronicity even though the surface is acutely inflamed.

Phlegmon (cellulitis) = diffuse spreading acute inflammation through tissue planes, without localisation.

Microscopic: neutrophils diffusely infiltrating between muscle fibres, fat lobules, or dermal collagen — no central necrosis, no capsule. Streptococci produce spreading factors (hyaluronidase) that prevent walling-off.

Distinction: phlegmon spreads; abscess is contained.

SELF-CHECK

A gastric biopsy shows, from surface to base: fibrin + neutrophils → coagulative necrosis → new capillary buds with fibroblasts → dense collagen. The surface epithelium is absent. What is the diagnosis and what does the presence of collagen at the base indicate?

A. Acute erosion — collagen indicates normal gastric mucosa

B. Peptic ulcer — collagen indicates the lesion has a chronic fibrous base

C. Phlegmon — collagen indicates diffuse tissue infiltration

D. Suppurative gastritis — collagen indicates a pyogenic membrane

Reveal Answer

Answer: B. Peptic ulcer — collagen indicates the lesion has a chronic fibrous base

The classic four-layer sequence (fibrinopurulent exudate / necrosis / granulation tissue / fibrosis) is diagnostic of a peptic ulcer. The collagen at the base confirms chronicity — this is not an acute erosion. This distinction matters clinically because scarring can cause pyloric stenosis.

The Four Inflammation Patterns — H5P Image Hotspots Activity

Study the composite panel below. Each quadrant shows one pattern at representative H&E magnification. For each panel, identify the dominant cell and name the pattern before reading the label.

IMPORTAN: Look at each quadrant in sequence. Use the low-to-high strategy: start with the predominant colour and cellular density, then identify nuclear morphology.

IMPORTAN: After completing the hotspot activity, try to sketch (from memory) the nuclear shape that distinguishes a neutrophil from a macrophage.

A four-panel H&E-style histology comparison shows acute suppurative, fibrinous, chronic, and granulomatous inflammation with labeled dominant cells and tissue features. — **Panel A:** Acute suppurative inflammation with multilobed neutrophils, central liquefactive necrosis, abscess wall, and cellular debris.. **Panel B:** Fibrinous inflammation of serosa with eosinophilic fibrin strands, serosal surface, and scattered neutrophils.. **Panel C:** Chronic inflammation with lymphocytes, plasma cells with clock-face chromatin, and macrophages with kidney-shaped nuclei.. **Panel D:** Tuberculoid granuloma with central caseation, epithelioid histiocytes, Langhans giant cell, and outer lymphocyte cuff..