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1. inflammation  with vascular events dr ashutosh kumar
 

1. inflammation with vascular events dr ashutosh kumar

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    1. inflammation  with vascular events dr ashutosh kumar 1. inflammation with vascular events dr ashutosh kumar Presentation Transcript

    • INFLAMMATION DEFINITIONINFLAMMATION IS A HOST RESPONSE TO LOCAL INJURY IN VASCULARISED TISSUES.
    • CARDINAL SIGNS OF INFLAMMATION•
    • INFLAMMATION- CARDINAL SIGNS: CELSUS RUBOR-REDNESS CALOR-HEAT TUMOR-SWELLING DOLOR- PAIN 5TH SIGN DESCRIBED BY VIRCHOW-LOSS OF FUNCTION (FUNCTIO LAESA)
    • INFLAMMATION-TYPES ACUTE CHRONICOnset Rapid SlowDuration Short LongerPredominant Neutrophil Lymphocytes andcells macrophagesChief Exudation of fluid Proliferation ofpathological and plasma blood vessels andevent proteins fibrosis
    • INFLAMMATION-STIMULI Infection- bacterial, viral , parasitic Trauma Physical/chemical injury- burns, irradiation Tissue necrosis Foreign body Immune reaction
    • ACUTE INFLAMMATION VASCULAR CHANGES:  Vascular caliber alteration.  Change in vascular structure. CELLULAR EVENTS:  leucocyte emigration
    • ACUTE INFLAMMATION- VASCULAR CHANGES IMPORTANT TO BRING ANTIBODIES AND LEUCOCYTES1. VASODILATATION  EARLIEST EVENT  ARTERIOLES- OPENING OF CAPILLARIES  INCREASED BLOOD FLOW- RUBOR AND CALOR2. INCREASED PERMEABILITY3. STASIS
    • Increased Vascular Permeability (Vascular Leakage) Contraction of endothelial cells resulting in increased interendothelial spaces is the most common mechanism of vascular leakage.
    • 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
    • Endothelial injury, resulting in endothelialcell necrosis and detachment
    • VASCULAR CHANGES-INCREASED PERMEABILITY-MECHANISMS DIRECT INJURY IMMEDIATE SUSTAINED RESPONSE ALL LEVELS NECROTIZING INJURIES (e.g.SEVERE BURN)
    • VASCULAR CHANGES-INCREASED PERMEABILITY-MECHANISMS DELAYED PROLONGED LEAKAGE VENULES,CAPILLARIES THERMAL INJURIES,X-RADIATION AFTER 2-12 HOURS,LASTS FOR HOURS OR DAYS
    • Neutrophils that adhere to the endothelium duringinflammation may also injure the endothelial cellsand thus amplify the reaction.
    • VASCULAR CHANGES-INCREASED PERMEABILITY-MECHANISMS LEUCOCYTE MEDIATED ENDOTHELIAL INJURY DELAYED PROLONGED RESPONSE COMMON IN GLOMERULI AND LUNGS
    • 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
    • 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
    • Transcytosis:may involve channels consisting of interconnected, uncoatedvesicles and vacuoles called the vesiculovacuolar organelle:located close to intercellular junctions.
    • EXUDATE Vs TRANSUDATE Exudate TransudateProtein content High LowCells & debris High LowSpecific gravity > 1.020 < 1.012Cause vascular hydrostatic permeability pressure;  osmotic pressureAssociated with Inflammation Exudate Transudate
    • 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
    • summary Inflammation-acute and chronic Acute - cardinal sign stimuli changes -vascular & cellular•vascular- vasodilation; increased vascular permeability transcytosis