1. inflammation with vascular events dr ashutosh kumar
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INFLAMMATION
DEFINITION
INFLAMMATION IS A HOST RESPONSE TO LOCAL INJURY IN VASCULARISED TISSUES.
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CARDINAL SIGNS OF INFLAMMATION
•
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INFLAMMATION- CARDINAL SIGNS: CELSUS
RUBOR-REDNESS
CALOR-HEAT
TUMOR-SWELLING
DOLOR- PAIN
5TH SIGN DESCRIBED BY VIRCHOW-LOSS OF FUNCTION
(FUNCTIO LAESA)
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INFLAMMATION-TYPES
ACUTE CHRONIC
Onset Rapid Slow
Duration Short Longer
Predominant cells
Neutrophil Lymphocytes and macrophages
Chief pathological event
Exudation of fluid and plasma proteins
Proliferation of blood vessels and fibrosis
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INFLAMMATION-STIMULI
Infection- bacterial, viral , parasitic
Trauma
Physical/chemical injury- burns, irradiation
Tissue necrosis
Foreign body
Immune reaction
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ACUTE INFLAMMATION
VASCULAR CHANGES:
Vascular caliber alteration.
Change in vascular structure.
CELLULAR EVENTS:
leucocyte emigration
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ACUTE INFLAMMATION- VASCULAR CHANGES
IMPORTANT TO BRING ANTIBODIES AND LEUCOCYTES
1. VASODILATATION EARLIEST EVENT
ARTERIOLES- OPENING OF CAPILLARIES
INCREASED BLOOD FLOW- RUBOR AND CALOR
2. INCREASED PERMEABILITY
3. STASIS
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Increased Vascular Permeability (Vascular Leakage)
Contraction of endothelial cells resulting in increased interendothelial spaces is the most common mechanism of vascular leakage.
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VASCULAR CHANGES-INCREASED PERMEABILITY-MECHANISMS
FORMATION OF ENDOTHELIAL GAPS IN VENULES
RAPID,SHORT LIVED
Agent: Histamine,bradykinin
MECHANISM: Phosphorylation Of Cytoskeletal
Proteins Contraction
IMMEDIATE TRANSIENT RESPONSE
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Endothelial injury, resulting in endothelial cell necrosis and detachment
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VASCULAR CHANGES-INCREASED PERMEABILITY-MECHANISMS
DIRECT INJURY
IMMEDIATE SUSTAINED RESPONSE
ALL LEVELS
NECROTIZING INJURIES (e.g.SEVERE BURN)
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VASCULAR CHANGES-INCREASED PERMEABILITY-MECHANISMS
DELAYED PROLONGED LEAKAGE
VENULES,CAPILLARIES
THERMAL INJURIES,X-RADIATION
AFTER 2-12 HOURS,LASTS FOR HOURS OR DAYS
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Neutrophils that adhere to the endothelium during inflammation may also injure the endothelial cells and thus amplify the reaction.
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VASCULAR CHANGES-INCREASED PERMEABILITY-MECHANISMS
LEUCOCYTE MEDIATED ENDOTHELIAL INJURY
DELAYED PROLONGED RESPONSE
COMMON IN GLOMERULI AND LUNGS
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VASCULAR CHANGES-INCREASED PERMEABILITY-MECHANISMS
INCREASED TRANSCYTOSIS
ACROSS ENDOTHELIAL CYTOPLASM
INCREASE IN NO: AND SIZE OF TRANSENDOTHELIAL CHANNELS
LEAKAGE FROM NEW BLOOD VESSELS
IMPORTANT DURING EARLY PHASES OF HEALING
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VASCULAR CHANGES-INCREASED PERMEABILITY
ESCAPE OF PROTEIN RICH FLUID AND BLOOD CELLS - FORMATION OF EXUDATE
TRANSUDATE FLUID WITH LOW PROTEIN
DUE TO OSMOTIC OR HYDROSTATIC IMBALANCE
VASCULAR PERMEABILITY INTACT
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Transcytosis:
may involve channels consisting of interconnected, uncoated vesicles and vacuoles called the vesiculovacuolar organelle: located close to intercellular junctions.
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EXUDATE Vs TRANSUDATE
Exudate Transudate
Protein content High Low
Cells & debris High Low
Specific gravity > 1.020 < 1.012
Cause vascular
permeability
hydrostatic
pressure;
osmotic pressure
Associated with Inflammation
Exudate Transudate
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Responses of Lymphatic Vessels
lymph flow is increased and helps drain edema fluid, leukocytes, cell debris, as well as microbes.
Lymphatic vessels also proliferate.
+/-(lymphangitis),+/-(lymphadenitis).
Inflamed lymph nodes are often enlarged because of hyperplasia of the lymphoid follicles and increased numbers of lymphocytes and macrophages. This constellation of pathologic changes is termed reactive, or inflammatory, lymphadenitis
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summary
Inflammation-acute and chronic
Acute - cardinal sign
stimuli
changes -vascular & cellular
•vascular- vasodilation;
increased vascular permeability
transcytosis
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