Pathology Inflammation-2 By Prof. Dr. SALAH FAYED.

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PathologyInflammation-2

By Prof. Dr. SALAH FAYED

Inflammation-2

• Suppurative inflammation: characterized by:– Dense infiltration by neutrophils (PNLs).– Rapid liquefaction of necrotic tissue.– Pus formation.Types: • Localized (abscess). • Diffuse (cellulitis).

Inflammation-2

Abscess:• Definition: – Localized area of suppurative inflammation.

• Causative organisms: – Many bacteria, but the most common is

Staphylococcus Aureus, which produces coagulase enzyme.

• Site: any organ or tissue.

Inflammation-2

• Morphology of an abscess: – Central area of necrosis.– Pus (yellowish fluid composed of proteins and

dead cells) in the cavity.– Peripheral pyogenic membrane (the limiting layer

of the cavity of an abscess). – Granulation tissue.

Skin abscess

Diagram for gross appearance Microscopic

Inflammation-2

Furuncle:• Small abscess in a hair follicle or sebaceous

gland.• The commonest sites are:– Face.– Neck.– Axilla.

Furuncle, gross appearance

Inflammation-2

Carbuncle:• Multi-locular abscess with multiple sinuses

discharging pus.• Usually occurs in patients with diabetes

mellitus.• Site: usually the back of the neck.

Carbuncle, in the back of the neck

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• Fate of an abscess:– If evacuated, healing occurs by minimal fibrosis.– If not evacuated, complications may occur as:• Ulcer: area without covering epithelium.• Sinus: blind tract connecting the abscess cavity to the

surface.• Fistula: tract connecting between two cavities or

surface and cavity, e.g. gastro-colic fistula and peri-anal fistula.

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Cellulitis:• Diffuse suppurative inflammation.• Occurs in loose subcutaneous tissue.• The causative organisms: most commonly

group A streptococcus hemolyticus.• The organism secretes:– Fibrinolysin.– Hyaluronidase enzyme.

Cellulitis

Differences between abscess and cellulitis

Abscess Cellullitis

Cause: Staphylococcus Aureus Group A Streptococci

The organism secretes: coagulase enzyme

FibrinolysinHyaluronidase

It is localized inflammation It is diffuse

Central zone of necrosis Extensive necrosis

Pus: rapid formation, thick and yellow Slow formation, thin and contains RBCs

Inflammation-2

Non suppurative inflammation:• Catarrhal inflammation:– Mild inflammation of mucous membranes.– There is excess mucus secretion.– Examples are:

• Rhinitis.• Gastritis.• Colitis.

– If bacterial infection occurs, the secretion becomes muco-purulent.

Catarrhal inflammation, rhinitis

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• Serous inflammation:– There is serous exudate with low fibrin content.– Examples are:• Blisters of superficial burns.• Herpes simplex infection.

Herpes simplex

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• Serofibrinous inflammation:– There is serous fluid & fibrin secretion.– Occurs in serous and synovial membranes.– Examples: • Pericarditis, • Pleurisy, • Arthritis.

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• Fibrinous inflammation:– Characterized by excess fibrin secretion.– The causative organism: Pneumococci.– The best example: • Lobar pneumonia (fibrinious exudate fills the alveoli).

Lobar pneumonia

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• Hemorrhagic inflammation:– Presence of large number of RBCs in the exudate

due to vascular damage:– Examples:• Plague.• Anthrax.

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• Membranous inflammation:– There is severe damage to the mucosa.– Examples:• Diphtheria.• Bacillary dysentery.

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• Necrotizing inflammation:– There is severe tissue damage by the virulent

organisms.– Examples:• Necrotizing fasciitis.• Necrotizing pharyngitis.

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• Allergic inflammation:– The exudate is serous or serofibrinous.– There is excess eosinophils.– Examples:• Bronchial asthma.• Urticaria.

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Chronic inflammation:• Causes of chronic inflammation:– May follow acute inflammation.– Persistence of the agent.– Infections with certain organisms:• Some viral infections.• Mycobacteria (TB and Leprosy).• Parasitisc infestations (e.g. Schistosomiasis).• Some fungal infections.

Inflammation-2

– Auto-immune diseases.– Response to a foreign material.– Response to a malignant tumor.

Inflammation-2

Important cells in chronic inflammation:• Macrophages:– Monocytes of blood, the most commonly present

during inflammation .– Other cells derived from the tissues:• Histiocytes of connective tissue.• Alveolar macrophages.• Kupffer cells of the liver.• Osteoclasts of the bone.• Microglia of the brain.

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– Chemotactic factors for monocytes: • C5a, • MCP-1, • PDGF, • TGF-β.

– Macrophages secrete a wide variety of active products “monokines”.

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• Lymphocytes:– B cells and plasma cells.– T cells.– They secrete chemokines (lymphotaxin).

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• Eosinophils:– Have a role in parasitic infections and Ig E-

mediated reactions.– Secrete eosinophilic chemokines (eotaxin).– Its granules contain major basic protein (MBP),

toxic to parasites.

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• Basophils:– Tissue-based basophils are called mast cells.– They are present in high numbers in the lung and

skin.– Play an important role in Ig E mediated reactions.– Secrete histamine.

Inflammatio-2

• Morphology of chronic inflammation:– The reaction is more proliferative than exudative.– The cellular reaction is pleomorphic, containing:• Macrophages.• Lymphocytes.• Plasma cells, etc.

– The arterioles, gradually show thick wall and narrow lumen.

– Fibrosis is a common feature.

Chronic inflammation, microscopic

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• Chronic granulomatos inflammation:– It is special type of chronic inflammation with a

distinctive histologic appearance.– Characterized by granuloma formation.

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• Composition of a granuloma: – Epithelioid cells: derived from macrophages by

the effect of INF-γ, closely backed large cells with abundant cytoplasm (epithelial-like).

– Giant cells formed by fusion of epithelioid cells:• Langhan’s type with peripheral arrangement of nuclei.• Foreign body type with central nuclei.

– Lymphocytes and plasma cells.

Granulomatous inflammation, microscopic

Inflammation-2

• Granulomatous diseases:– Tuberculosis.– Syphilis.– Leprosy.– Fungal infections.– Parasitic infections.– Foreign body reaction.– Sarcoidosis.