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Medical-20230325-WA0004..pptx

  1. GOVT. AUTONOMOUS AYURVEDA COLLEGE AND HOSPITAL NIPANIYA REWA(M.P.) • NAME – NAVEEN PARIHAR • TOPIC – INFLAMMATION • BATCH 2019
  2. 🔆 INFLAMMATION 🛑 INTRODUCTION • INFLAMMATION IS DEFINED AS THE LOCAL RESPONSE OF LIVING MAMMALIAN TISSUES TO INJURY DUE TO ANY AGENT. BODY DEFENSE REACTION ELIMINATE OR LIMIT THE SPREAD OF INJURIOUS AGENT.
  3. CAUSE OF INFLAMMATION 1. INFECTIVE AGENTS :- BACTERIA, VIRUSES AND THEIR TOXINS, FUNGI, PARASITES. 2. IMMUNOLOGICAL AGENTS :- CELL-MEDIATED AND ANTIGEN ANTIBODY REACTIONS. 3.PHYSICAL AGENTS :- HEAT, COLD, RADIATION, MECHANICAL TRAUMA. 4. CHEMICAL AGENTS :- ORGANIC AND INORGANIC POISONS. 5. INERT MATERIALS :- SUCH AS FOREIGN BODIES
  4. SIGNS OF INFLAMMATION 4 CARDINAL SIGNS(CELSUS) • - RUBOR (REDNESS); • - TUMOR (SWELLING); • - CALOR (HEAT); • - DOLOR (PAIN) • 5TH SIGN FUNCTION - LAESA (LOSS OF FUNCTION) R VIRCHOW
  5. Types of inflammation 1. ACUTE INFLAMMATION- - SHORT DURATION - REPRESENTS THE EARLY BODY REACTION - FOLLOWED BY HEALING - EDEMA - MAINLY NUTROPHILS • 2. CHRONIC INFLAMMATION - LONGER DURATION - LYMPHOCYTES AND MACROPHAGES PREDOMINATE - FIBROSIS
  6. ACUTE INFLAMMATION • THE MAIN FEATURES OF ACUTE INFLAMMATION ARE:- - ACCUMULATION OF FLUID AND PLASMA AT THE AFFECTED SITE. - INTRAVASCULAR ACTIVATION OF PLATELETS; - POLYMORPHONUCLEAR NEUTROPHILS AS INFLAMMATORY CELLS.
  7. THESE INFLAMMATORY CHANGES INVOLVE TWO MAIN COMPONENT – Vascular Reaction Cellular Reaction Changes in Blood vessels Changes in Leucocytes (blood cells)
  8. Changes in blood vessels involve following steps 1. Vasodilation 2. Change in vascular permeability 3. Change in vascular Flow
  9. VASODILATION • VASODILATION IS THE ONE OF THE EARLIEST MANIFESTATION OF ACUTE INFLAMMATION. SOMETIME IT FOLLOWS TRANSIENT CONSTRICTION OF ARTERIOLE. THIS VASOCONSTRICTION LASTING FOR A FEW SECONDS. • VASODILATION FIRST INVOLVE ARTERIOLE AND THEN RESULTS IN OPENING OF NEW CAPILLARY BEDS IN THE AREA.
  10. CHANGE IN VASCULAR PERMEABILITY • INCREASED VASCULAR PERMEABILITY IS THE HALLMARK OF ACUTE INFLAMMATION. • DUE TO VASCULAR PERMEABILITY ESCAPE OF PROTEIN RICH FLUID [EXUDATE] AND LEUKOCYTE INTO EXTRA VASCULAR SPACE.INTRAVASCULAR OSMOTIC PRESSURE REDUCES DUE TO EXUDATION OF PROTEIN AND OSMOTIC PRESSURE OF INTERSTITIAL FLUID IS INCREASED. • TOGETHER WITH INCREASED HYDROSTATIC PRESSURE AND DECREASED INTRAVASCULAR OSMOTIC PRESSURE LEADS TO FURTHER OUTFLOW OF FLUID AND ACCUMULATE IN THE INTERSTITIAL FLUID.
  11. CHANGE IN VASCULAR FLOW • THE LOSS OF FLUID RESULTS IN CONCENTRATION OF RED CELLS AND INCREASED VISCOSITY OF BLOOD. WHICH SLOW THE BLOOD FLOW CALLED AS STASIS. • किसी भी बाह्य िारि ि े प्रवेश िरने पर प्रकिकिया स्वरूप में प्रभाकवि उत्ति ों से किस्टाकमन स्त्राकवि ि िा िै। किससे सबसे पिले VASODILATION ि िा िै।
  12. • HISTAMIN SMOOTH MUSCLES ि RELAX िरिा िै, किससे VASODILATION ि िा िै। RUBOR (RED), COLOR (HEAT) ARTERIOLES व CAPPILARIES में रक्त िा प्रवाि बढ िािा िै। HYDROSTATIC PRESSURE बढ़ने ि े िारण TRANSUDATE बािर आिा िै। (बाह्य िारि ों िी प्रकिकिया स्वरूप) िथा CAPPILARY PERMEABILITY बढ़ने ि े िारण ARTERIOLE OR CAPPILARIES से प्र टीन बािर INTERSTITIAL SPACE में आने लगिा िै। ि कशिाओों से EXUDATE (प्र टीन आकिक्य स्राव बािर आिा िै।
  13. • ि े कशिाओों में रक्त प्रवाि िम ि ने पररक्त ि कशिाओों में पररवितन प्रारम्भ ि िे िै।
  14. • CELLULAR CHANGES :- A CRITICAL FUNCTION IS TO DELIVER LEUKOCYTE TO THE SITE OF INJURY AND TO ACTIVATE THE LEUKOCYTE TO PERFORM THEIR NORMAL FUNCTION IN HOST DEFENCE • THE SEQUENCE OF EVENTS IN THE JOURNEY OF LEUKOCYTE FROM THE VESSEL LUMEN TO INTERSTITIAL TISSUE IS CALLED EXTRAVASATION. Cellular reaction involve following changes
  15. 1. In the vessel 2. Diapedesis 3. Chemotaxis 4. Leukocyte Activation 5. Phagocytosis A) Migration B) Rolling C) Adhesion D) Pavementing Extravasatio n Extravasation involved following steps.
  16. 1. IN THE VESSEL MIGRATION – AS STASIS DEVELOPS, LEUKOCYTE PRINCIPALLY NEUTROPHIL ACCUMULATE ALONG THE VASCULAR ENDOTHELIUM. THIS IS CALLED MIGRATION. ROLLING – THE ROWS OF LEUKOCYTE MOVE SLOWLY ALONG THE ENDOTHELIUM A PROCESS CALLED ROLLING. ADHESION – FINALLY COMING AT REST, LEUKOCYTE ADHERE FIRMLY TO ENDOTHELIUM THIS MECHANISM CALLED ADHESION. PAVEMENTING – THE ENDOTHELIUM CAN BE LINED BY WHITE CELLS, PROCESS CALLED- PAVEMENTING
  17. • IT IS THE PROCESS OF TRANSMIGRATION OF LEUCOCYTE ACROSS THE ENDOTHELIUM. • AFTER FIRM ADHESION, LEUKOCYTE MIGRATE THROUGH INTER ENDOTHELIAL JUNCTION AND ASSUME A POSITION BETWEEN ENDOTHELIUM CELLS AND THE BASEMENT MEMBRANE. • EVENTUALLY THEY PIERCE THE BASEMENT MEMBRANE BY SECRETING COLLAGENASE AND ESCAPE INTO THE EXTRAVASCULAR SPACE. 2. Diapedesis
  18. 3. CHEMOTAXIS :- • AFTER EXTRA VASATION, LEUKOCYTE EMIGRATE INTO TISSUE TOWARDS THE SITE OF INJURY, ALONG A CHEMICAL GRADIENT A PROCESS KNOWN AS CHEMOTAXIS.THE SUBSTANCE THAT ACT AS A CHEMO ATTRACTANT MAY BE EXOGENOUS [BACTERIAL PRODUCTS] OR ENDOGENOUS [INTERLEUKINS- 8] 4. Leucocyte Activation :- • At the site of inflammation, cytokines induce defensive function of leukocyte and are referred as leukocyte activation.
  19. 5. PHAGOCYTOSIS • RELEASE OF ENZYME BY NEUTROPHILS AND MACROPHAGES ARE RESPONSIBLE FOR ELIMINATING THE INJURIOUS AGENTS • IN PHAGOCYTOSIS, ENGULFMENT AND KILLING AND DEGRADATION OF INJURIOUS AGENT TAKE PLACE.
  20. • WBC रक्त िा वेग िम ि ने पर नाकिय ों िी किवार िी ओर िाने लगिी िै किसे MIGRATION िििे िैं। • WBC उन्ीोंकिवार ों पर घूमने लगिी िै, किसे ROLLING िििे िै • एि स्थान कवशेष पर किपि िािी िै किसे ADHESION िििे िै। • ित्पश्चाि् ि कशिायें रक्ति कशिाओों िी किवार ों से बािर कनिलिर INTERSTIAL SPACE में आ िािी िै विााँ िीवाणु आकि ि े द्वारा स्त्राकवि कवष (TOXIN) ि े प्रभाव से रक्त ि कशिायें िीवाणुओों िी िरफ गकिमान ि िी िै व उन्ें PHAGOCYTS द्वारा भक्षण िर लेिी िै।
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