Pathology Inflammation-2

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Transcript Pathology Inflammation-2

Pathology
Inflammation-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).
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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.
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• 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
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Furuncle:
• Small abscess in a hair follicle or sebaceous
gland.
• The commonest sites are:
– Face.
– Neck.
– Axilla.
Furuncle, gross appearance
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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
Cause: Staphylococcus Aureus
Cellullitis
Group A Streptococci
The organism secretes: coagulase enzyme Fibrinolysin
Hyaluronidase
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
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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:
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Some viral infections.
Mycobacteria (TB and Leprosy).
Parasitisc infestations (e.g. Schistosomiasis).
Some fungal infections.
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– Auto-immune diseases.
– Response to a foreign material.
– Response to a malignant tumor.
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Important cells in chronic inflammation:
• Macrophages:
– Monocytes of blood, the most commonly present
during inflammation .
– Other cells derived from the tissues:
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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:
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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 Emediated 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.
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• 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
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• Granulomatous diseases:
– Tuberculosis.
– Syphilis.
– Leprosy.
– Fungal infections.
– Parasitic infections.
– Foreign body reaction.
– Sarcoidosis.