Post on 19-Jan-2016
transcript
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
Inflammation-2
• 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.
Inflammation-2
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
Inflammation-2
• Serous inflammation:– There is serous exudate with low fibrin content.– Examples are:• Blisters of superficial burns.• Herpes simplex infection.
Herpes simplex
Inflammation-2
• Serofibrinous inflammation:– There is serous fluid & fibrin secretion.– Occurs in serous and synovial membranes.– Examples: • Pericarditis, • Pleurisy, • Arthritis.
Inflammation-2
• Fibrinous inflammation:– Characterized by excess fibrin secretion.– The causative organism: Pneumococci.– The best example: • Lobar pneumonia (fibrinious exudate fills the alveoli).
Lobar pneumonia
Inflammation-2
• Hemorrhagic inflammation:– Presence of large number of RBCs in the exudate
due to vascular damage:– Examples:• Plague.• Anthrax.
Inflammation-2
• Membranous inflammation:– There is severe damage to the mucosa.– Examples:• Diphtheria.• Bacillary dysentery.
Inflammation-2
• Necrotizing inflammation:– There is severe tissue damage by the virulent
organisms.– Examples:• Necrotizing fasciitis.• Necrotizing pharyngitis.
Inflammation-2
• Allergic inflammation:– The exudate is serous or serofibrinous.– There is excess eosinophils.– Examples:• Bronchial asthma.• Urticaria.
Inflammation-2
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.
Inflammation-2
– Chemotactic factors for monocytes: • C5a, • MCP-1, • PDGF, • TGF-β.
– Macrophages secrete a wide variety of active products “monokines”.
Inflammation-2
• Lymphocytes:– B cells and plasma cells.– T cells.– They secrete chemokines (lymphotaxin).
Inflammation-2
• 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.
Inflammation-2
• 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
Inflammation-2
• Chronic granulomatos inflammation:– It is special type of chronic inflammation with a
distinctive histologic appearance.– Characterized by granuloma formation.
Inflammation-2
• 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.