By Dr. Ghada Ahmed Lecturer of pathology Benha Faculty of Medicine
Part I Objectives 1- Define inflammation 2- Classify types of inflammation 3- Explain mechanism of acute inflammation 4- Enumerate the cardinal signs of acute inflammation
Definition Irritant Reaction of living tissue Aims to: 1- prevent tissue damage 2- localization of irritant 3- destruction of irritant 4- preparing for repair lymphatic cellular vascular Irritant
Irritant (types & effects)
Inflammation Acute Subacute Chronic
Acute inflammation Mild/ severe irritant Short duration Rapid tissue response Acute inflammation
Cardinal signs of inflammation
Mechanism of acute inflammation Local changes 1- Tissue destruction 2- Vascular phenomenon 3- Rx of tissue histiocytes General changes 1- changes in blood cells 6- degenerative changes 7- septicemia 5-hyperplasia of draining LN 4- liver secretes proteins 3- loss of appetite 2- fever 8- pyemia
1- Local tissue destruction Injurious agent Chemical mediators Local tissue destruction
2. Local Vascular phenomenon Dilatation of lymphatic vessels Transient VC VD Stasis Inflammatory exudate Dilatation of lymphatic vessels
Fluid exudate: = inflammatory extravascular fluid capillary HP cap permeability tissue OP Cellularity Sp gravity Protein content (fibrinogen- clot)
Fluid exudate
Function of fluid exudate Formation of fibrin network Dilutes bacterial toxins Brings antibodies to destruct irritant
N.B: Chemotaxis & Phagocytosis Inflammatory exudate Cellular Margination Migration Activation Diapedesis Fluid N.B: Chemotaxis & Phagocytosis
Cellular exudate
Function of cellular exudate PNLs enzymes attak, phagocytose, kill the organism Later : phagocytosis by macrophages
Attraction of leucocytes towards the irritant by chemotactic factors Chemotaxis Attraction of leucocytes towards the irritant by chemotactic factors
Phagocytosis Ingestion and destruction of foreign body and bacteria by phagocytic cells
2. Local Vascular phenomenon Dilatation of lymphatic vessels Transient VC VD Stasis Inflammatory exudate Dilatation of lymphatic vessels
3. Local reaction of tissue hiseocytes By macrophages: Proliferate Phagocytosis: dead bacteria, necrotic debris Clean the area of inflammation
Part II Objectives 1- Explain mechanism of acute inflammation 2- Define chemical mediators and discuss their role in acute inflammation 3- Discuss the fate of acute inflammation 4- Classify then discuss types of acute inflammation
Mechanism of acute inflammation Local changes 1- Tissue destruction 2- Vascular phenomenon 3- Rx of tissue histiocytes General changes 1- changes in blood cells 6- degenerative changes 7- septicemia 5-hyperplasia of draining LN 4- liver secretes proteins 3- loss of appetite 2- fever 8- pyemia
Cells of Acute inflammation PNLs Macrophages RBCs Pus cells
Chemical mediators of acute inflammation Chemical factors derived from plasma and cells (e.g. PNLs, monocytes, endoth cs, macrophages, fibroblasts) Found as precursors in inactive forms. Inflammatory stimulus triggers their release, activation, de novo synthesis Act by binding to specific receptors on target cells
Chemical mediators of acute inflammation Examples: PGs: VD, fever, pain Histamine, serotonin: increased permeability C5a: increased permeability, chemotaxis Cytokines: chemotaxis, leukocyte activation Lysosomal enz of PNLs & macrophages: tissue damage
Fate of acute inflammation Resolution Spread Chronicity
Quiz Mark TRUE or FALSE: 1- Histamine release causes increased capillary permeability. 2- Diapedesis is an energy-dependent process. 3- Acute inflammation is a rapid tissue response against severe irritants only. 4- Opsonization is covering leucocytes with opsonin to target it for phagocytosis.
Acute inflammation Suppurative Localized Diffuse Non-suppurative
Suppurative inflammation Definition: Acute inflammation chch by PUS formation Cause: Pyogenic organism (staph, strept,……)
Suppurative inflammation Chch of pus Composition of pus
Localizes suppurative inflammation (Abscess ) Definition Sites Cause
Pathogenesis of abscess
Pathogenesis of abscess opening Cavity containing pus Pyogenic membrane
Complications of abscess Chronicity Spread Complications of healing
Complications of abscess healing keloid
Furuncle (boil) Carbuncle Diabetes
Diffuse suppurative inflammation Cellulitis Definition Sites Cause Differs from abscess….
Complications of diffuse suppurative inflammation Spread Acute Lymphangitis Acute Lymphadenitis Thrombophlebitis Septicaemia
Non-suppurative inflammation Types: (according to features of exudate) 1- Catarrhal infl. 2- Membranous infl. 3- Fibrinous 4- Serous 5- Serofibrinous infl. 6- Hemorrhagic 7- Necrotizing 8- Allergic
Catarrhal inflammation Definition: Sites Morphology Fate
Catarrhal inflammation
Membranous (pseudomembranous) inflammation Definition Examples Pathogenesis Morphology Complications Exotoxin
Membranous (pseudomembranous) inflammation
Part III Objectives 1- classify then discuss types of acute inflammation 2- define chronic inflammation, its causes, features and types 3- compare between acute and chronic inflammation
Non-suppurative inflammation Types: (according to features of exudate) 1- Catarrhal infl. 2- Membranous infl. 3- Fibrinous 4- Serous 5- Serofibrinous infl. 6- Hemorrhagic 7- Necrotizing 8- Allergic
Fibrinous inflammation Serous inflammation Serofibrinous inflammation
Serofibrinous inflammation
Serofibrinous inflammation
Hemorrhagic infl. Necrotizing infl. Allergic infl.
Non-suppurative inflammation Types: (according to features of exudate) 1- Catarrhal infl. 2- Membranous infl. 3- Fibrinous 4- Serous 5- Serofibrinous infl. 6- Hemorrhagic 7- Necrotizing 8- Allergic
Chronic inflammation
Chronic inflammation Prolonged duration Active inflammation Tissue destruction Attempts of healing
Chronic inflammation When???? Persistent infections: Acute infl. fail to cure Repeated acute infl. Start de novo (T.B.) Prolonged exposure to toxic agents Autoimmunity
Morphology of chronic inflammations Tissue destruction Blood vessels Fluid exudate Cellular exudate
Cells of chronic inflammation Esinophils Lymphocytes Plasma cells Giant cells Fibroblasts
Microscopic picture of chronic inflammation EAO EAO Perivascular infiltrate
Microscopic picture of chronic inflammation (cellular exudate)
Chronic inflammation (granuloma) Specific Non-specific
Compare between acute & chronic inflammation Onset Sudden Gradual Duration Short Prolonged Vascular phenomenon Present Slight/ absent Cardinal signs Cells PNLs, pus cs, macrophages Lymphocytes, plasma cs, macrophages, giant cs, fibroblasts Bl.vessels Thin, dilated, congested EAO