Place : Thiruchirappalli at Aroggya Ayurveda Hospital
Date : 09/06/2014
Inflammation is defined as the local response of living mammalian tissues to injury due to any agent. It is a body defense reaction in order to eliminate or limit the spread of injurious agents as well as to remove the necrosed cells and tissues.
CAUSES :
Physical agents like heat, cold, radiation, mechanical trauma
Chemical agents like organic and inorganic poisons
Infective agents like bacteria, viruses and other toxins
Immunologic agents like cell mediated and antigen antibody reactions
PROCESSES :
Early inflammatory response
Healing
SIGNS OF INFLAMMATION
Rubor
Tumor
Calor
Dolor
Functioleasa
TYPES OF INFLAMMATION
Acute &
Chronic
ACUTE INFLAMMATION
The changes in acute inflammation can be conviniently described under the following two headings :
Vascular Events
Cellular Events
VASCULAR EVENTS
Alteration in the micro vasculature(arterioles, cappillaries and venules) is the earliest response to tissue injury. These alterations include :
Haemodynamic changes
Changes in vascular permeability
HAEMODYNAMIC CHANGES
The earliest features of inflammatory response results from changes in the vascular flow and calibre of small blood vessels in the injured tissue.
Transient vaso constriction-3 to 5 seconds maximum 5 minutes
Persistent progressive vasodilation-mainly arterioles, 1/2 an hour of injury redness and warmth
Elevation of local hydrostatic pressure-transudation of fluid into ECF resulting in swelling
Slowing or stasis-due to increased permeability of microvasculature
Leucocytic margination-emigration
LEWIS EXPERIMENT
Features of haemodynamic changes. The triple response or Red line response :
Red Line-local vasodilation of cappillaries & venules
Flare-bright reddish appearance, vasodilation of adjacent arterioles
Wheal-swelling or oedema, transudation of fluid into the extravascular space
CHANGES IN VASCULAR PERMEABILITY
The appearance of inflammatory oedema due to increased vascular permebility of microvasculature bed is explained on the basis of starlings hypothesis. In normal circumstances, the fluid balance is maintained by two opposing forces :
-forces causing outward movement of fluid from microcirculation namely intravascular hydrostatic pressure and osmotic pressure of interstitial fluid
-forces causing inward movement of interstitial fluid into circulation namely intravascular osmotic pressure and hydrostatic pressure of interstitial fluid
MECHANISMS IF INCREASED VASCULAR PERMEABILITY
-Endothelial cell contraction, involving venules, immediate transient(15 to 30 min)response type, histamine, bradykinin others act as mediators, ex: during mild injury.
-Endothelial cell retraction, also involves venules, which is somewhat delayed(in 4 to 6 hrs) or prolonged (for 24 hrs or more), where IL-1, TNF act as mediators, happens in vitro only.
-Direct endothelial cell injury, where arterioles, venules, cappillaries are involved, immediate prolonged(hrs to days) or delayed prolonged(2-12 hrs, hrs to days), results in cell necrosis and detachment, ex : as in moderate to severe burns, severe bacterial infection, radiation injury.
-Leucucyte mediated endothelial injury,where venules and cappillaries are involved, which may be a delayed or prolonged process/response, where leucocyte activation release proteolytic enzymes, mostly happens in pulmonary venules & cappillaries.
-Neovascularisation, all levels are involved, which may be of any type, involving angiogenesis and vasculo endothelial growth factor usually seen in healing and tumors.
CELLULAR EVENTS
The cellular phase of inflammation consists of two processes
Exudation of leucucytes
Phagocytosis
EXUDATION OF LEUCOCYTES
Margination due to slowing and stasis results in exudation
Pavementing-neutrophil of central column come closer to vessel wall
Rolling of marginated and pavemented neutrophils
Transient bond between leucocytes and endothelial cells adhesion phase
Simultaneous to emigration of leucocytes,, escape of red cells through gaps between the endothelial cells , diapedesis takes place.
The chemotactic factor mediated transmigration of leucocytes after crossing several barriers to reach the interstitial tissues is called chemotaxis. Leukotriene B4 LTB4, Platelet factor 4 PF4, Complement system C3C5 in particular, Cytikines interleukins IL-1, IL-5, IL-6, Soluble bacterial products, Monocyte chemoattractant protein MCP-1, Chemotactic factor for CD4+T cells, Exotoxin chemotactic for eosinophils are the CHEMOKINES.
PHAGOCYTOSIS
Two main types of phagocytic cells
Polymorphonuclear neutrophils PMNs-microphages
Circulating monocytes-macrophages
Involves following four steps :
Recognition & attachment or opsonisation, IgG opsonins, C3b opsonins, Lectins.Opsonins coat microorganisms, occur naturally in serum
Engulfment stage
Degranulation stage
Killing or degradation stage
CHEMICAL MEDIATORS OF INFLAMMATION
CELL DERIVED MEDIATORS
Vasoactive amines like histamine , serotonin
Arachindonic acid metabolites, Prostaglandins PGs like PGD2, PGE2, PGF2 PGI2, TXA2 and Leukotrienes like LTB4, LTC4, LTD4, LTE4 etc...via the cyclo oxygenase pathway and lipo oxygenase pathway respectively.
Lysosomal components, granules of neutrophils, monocytes & tissue macrophages
Platelet Activating Factor
Cytokines which are polypeptide substances produced by activated lymphocytes and activated monocytes, namely IL-1, TNF alpha, TNF beta, IF alpha, IL 8, PF4, MCP 1
Nitirc oxide and oxygen derived derivatives
PLASMA DERIVED MEDIATORS
The kinin system
Clotting system
Fibrinolytic system
Complement system
FACTORS DETERMINING VARIATION IN INFLAMMATORY RESPONSE
Factors involving organisms
Factors involving host
Type of exudation
Cellular proliferation
Necrosis
MORPHOLOGY OF ACUTE INFLAMMATION
Pseudomembranous inflammation
Ulcer
Suppuration
Cellulitis
Bacterial infection of blood-Bactraemia, Septicaemia and Pyaemia : pyeamic abscess & septic infarcts.
SYSTEMIC EFFECTS
Fever
Leucocytosis
Lymphangitis-lymphadenitis
Shock
Fate of acute inflammation
Resolution
Healing of scarring
Progression to suppuration
Progression to chronic inflammation.
THANK YOU FOR SPENDING YOUR VALUABLE TIME READING. HAVE A GOOD DAY. GOD BLESS YOU.
INITIATIVE TO SPREAD KNOWLEDGE OF PATHOLOGICAL PROCESS AMONG AYURVEDIC PEERS.
Dr.Prasanth.K.P. B.A.M.S.
Date : 09/06/2014
Inflammation is defined as the local response of living mammalian tissues to injury due to any agent. It is a body defense reaction in order to eliminate or limit the spread of injurious agents as well as to remove the necrosed cells and tissues.
CAUSES :
Physical agents like heat, cold, radiation, mechanical trauma
Chemical agents like organic and inorganic poisons
Infective agents like bacteria, viruses and other toxins
Immunologic agents like cell mediated and antigen antibody reactions
PROCESSES :
Early inflammatory response
Healing
SIGNS OF INFLAMMATION
Rubor
Tumor
Calor
Dolor
Functioleasa
TYPES OF INFLAMMATION
Acute &
Chronic
ACUTE INFLAMMATION
The changes in acute inflammation can be conviniently described under the following two headings :
Vascular Events
Cellular Events
VASCULAR EVENTS
Alteration in the micro vasculature(arterioles, cappillaries and venules) is the earliest response to tissue injury. These alterations include :
Haemodynamic changes
Changes in vascular permeability
HAEMODYNAMIC CHANGES
The earliest features of inflammatory response results from changes in the vascular flow and calibre of small blood vessels in the injured tissue.
Transient vaso constriction-3 to 5 seconds maximum 5 minutes
Persistent progressive vasodilation-mainly arterioles, 1/2 an hour of injury redness and warmth
Elevation of local hydrostatic pressure-transudation of fluid into ECF resulting in swelling
Slowing or stasis-due to increased permeability of microvasculature
Leucocytic margination-emigration
LEWIS EXPERIMENT
Features of haemodynamic changes. The triple response or Red line response :
Red Line-local vasodilation of cappillaries & venules
Flare-bright reddish appearance, vasodilation of adjacent arterioles
Wheal-swelling or oedema, transudation of fluid into the extravascular space
CHANGES IN VASCULAR PERMEABILITY
The appearance of inflammatory oedema due to increased vascular permebility of microvasculature bed is explained on the basis of starlings hypothesis. In normal circumstances, the fluid balance is maintained by two opposing forces :
-forces causing outward movement of fluid from microcirculation namely intravascular hydrostatic pressure and osmotic pressure of interstitial fluid
-forces causing inward movement of interstitial fluid into circulation namely intravascular osmotic pressure and hydrostatic pressure of interstitial fluid
MECHANISMS IF INCREASED VASCULAR PERMEABILITY
-Endothelial cell contraction, involving venules, immediate transient(15 to 30 min)response type, histamine, bradykinin others act as mediators, ex: during mild injury.
-Endothelial cell retraction, also involves venules, which is somewhat delayed(in 4 to 6 hrs) or prolonged (for 24 hrs or more), where IL-1, TNF act as mediators, happens in vitro only.
-Direct endothelial cell injury, where arterioles, venules, cappillaries are involved, immediate prolonged(hrs to days) or delayed prolonged(2-12 hrs, hrs to days), results in cell necrosis and detachment, ex : as in moderate to severe burns, severe bacterial infection, radiation injury.
-Leucucyte mediated endothelial injury,where venules and cappillaries are involved, which may be a delayed or prolonged process/response, where leucocyte activation release proteolytic enzymes, mostly happens in pulmonary venules & cappillaries.
-Neovascularisation, all levels are involved, which may be of any type, involving angiogenesis and vasculo endothelial growth factor usually seen in healing and tumors.
CELLULAR EVENTS
The cellular phase of inflammation consists of two processes
Exudation of leucucytes
Phagocytosis
EXUDATION OF LEUCOCYTES
Margination due to slowing and stasis results in exudation
Pavementing-neutrophil of central column come closer to vessel wall
Rolling of marginated and pavemented neutrophils
Transient bond between leucocytes and endothelial cells adhesion phase
Simultaneous to emigration of leucocytes,, escape of red cells through gaps between the endothelial cells , diapedesis takes place.
The chemotactic factor mediated transmigration of leucocytes after crossing several barriers to reach the interstitial tissues is called chemotaxis. Leukotriene B4 LTB4, Platelet factor 4 PF4, Complement system C3C5 in particular, Cytikines interleukins IL-1, IL-5, IL-6, Soluble bacterial products, Monocyte chemoattractant protein MCP-1, Chemotactic factor for CD4+T cells, Exotoxin chemotactic for eosinophils are the CHEMOKINES.
PHAGOCYTOSIS
Two main types of phagocytic cells
Polymorphonuclear neutrophils PMNs-microphages
Circulating monocytes-macrophages
Involves following four steps :
Recognition & attachment or opsonisation, IgG opsonins, C3b opsonins, Lectins.Opsonins coat microorganisms, occur naturally in serum
Engulfment stage
Degranulation stage
Killing or degradation stage
CHEMICAL MEDIATORS OF INFLAMMATION
CELL DERIVED MEDIATORS
Vasoactive amines like histamine , serotonin
Arachindonic acid metabolites, Prostaglandins PGs like PGD2, PGE2, PGF2 PGI2, TXA2 and Leukotrienes like LTB4, LTC4, LTD4, LTE4 etc...via the cyclo oxygenase pathway and lipo oxygenase pathway respectively.
Lysosomal components, granules of neutrophils, monocytes & tissue macrophages
Platelet Activating Factor
Cytokines which are polypeptide substances produced by activated lymphocytes and activated monocytes, namely IL-1, TNF alpha, TNF beta, IF alpha, IL 8, PF4, MCP 1
Nitirc oxide and oxygen derived derivatives
PLASMA DERIVED MEDIATORS
The kinin system
Clotting system
Fibrinolytic system
Complement system
FACTORS DETERMINING VARIATION IN INFLAMMATORY RESPONSE
Factors involving organisms
Factors involving host
Type of exudation
Cellular proliferation
Necrosis
MORPHOLOGY OF ACUTE INFLAMMATION
Pseudomembranous inflammation
Ulcer
Suppuration
Cellulitis
Bacterial infection of blood-Bactraemia, Septicaemia and Pyaemia : pyeamic abscess & septic infarcts.
SYSTEMIC EFFECTS
Fever
Leucocytosis
Lymphangitis-lymphadenitis
Shock
Fate of acute inflammation
Resolution
Healing of scarring
Progression to suppuration
Progression to chronic inflammation.
THANK YOU FOR SPENDING YOUR VALUABLE TIME READING. HAVE A GOOD DAY. GOD BLESS YOU.
INITIATIVE TO SPREAD KNOWLEDGE OF PATHOLOGICAL PROCESS AMONG AYURVEDIC PEERS.
Dr.Prasanth.K.P. B.A.M.S.
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