INFLAMMATION PHYSIOLOGY
0 likes313 views
The document discusses inflammation, including its causes, types, components, and mechanisms. It describes the vascular and cellular components of acute inflammation. The vascular component involves vasodilation, increased permeability and exudation. The cellular component involves the emigration of white blood cells from blood vessels to tissue through a process of margination, rolling, tight adhesion, and diapedesis. Together these components work to destroy pathogens and initiate healing through removal of dead cells and debris.
INFLAMMATION PHYSIOLOGY
- 1. Kamal Ch. Upreti Pharmaceutical marketing INFLAMMATION
- 2. INFLAMMATION GOOD SIDE BAD SIDE
- 3. INFLAMMATION “A dynamic response of vascularised tissue to injury.” Host ImmunityHost Immunity
- 5. TYPES OF INFLAMMATION ACUTE INFLAMMATION CHRONIC INFLAMMATION Rapid Development & Short life Slow Development & Last will long
- 6. ACUTE INFLAMMATION Non-specific response to any cell injury Involves blood vessels, chemical mediators, and white blood cells Purposes Destroy an organism Limit damage to a certain area Prevent reproduction of an organism Virus, bacterium Clear debris and lay groundwork for healing
- 7. Heat Redness Swelling Pain Loss Of Func. The 5 Cardinal Signs of ACUTE INFLAMMATION
- 8. Inflammation is characterized by five cardinal signs:- Rubor (redness), Calor (increased heat), Tumor (swelling), Dolor (pain), and Functio laesa (loss of function). Cardinal Signs (primary or major clinical sign)
- 9. Vascular component Cellular component Two components ACUTE INFLAMMATION Arteriolodilation Microcirculation EXUDATION
- 10. Inflammation - Mechanism 1. Vasodilatation 2. Exudation - Edema 3. 4. Emigration of cells 5. Chemotaxis Vascular component Cellular component
- 11. Vascular Events Initial vasoconstriction near site of injury Vasodilation of arterioles and capillaries Increased blood flow to the area Increased hydrostatic pressure
- 13. NORMAL BLOOD FLOW Hydrostatic Pressure Osmotic Pressure Vascular Events
- 14. DURING INJURY PLASMA PROTEIN LEAKOUT Hydrostatic Pressure Osmotic Pressure Vascular Events
- 16. Vascular Events Increased capillary permeability Secondary to tight junction disruption in endothelial layer of blood vessels Plasma moves out of the blood vessels (exudate) Exudate = large amount of protein Transudate = relatively little protein
- 17. ENDOTHELIAL CELL HISTAMIN PROSTAGLANDINS NITRIC OXIDE TNF CYTOKINES THROUGH GENOMIC PROGRAMME OF PR-CEL CONTRECTION Short Time RETRECTION Long Time NORMAL CELL Vascular Events
- 18. Fluid environment surrounding inflammation is thick with cells and debris Cells and debris will become purulent over time Vascular Events
- 19. Rubor, Calor, Tumor Vascular Events
- 20. Kinin cascade Group of plasma proteins that stimulate the vascular component of inflammation Bradykinin is most important kinin Kinins and prostaglandin E cause pain at site Chemical Mediator
- 21. Histamine Stimulates vascular component of inflammation Nitrous oxide -Promotes vasodilation , Blocks platelet clumping and clot formation , Cytotoxic. Aracodonic acid metabolites from cell membrane phospholipids Leukotrienes (C-4, D-4, E-4) maintain inflammation in cellular and vascular inflammation Prostaglandins prolong inflammatory process PGD2, E2, F2 - Vasodilation and increased capillary permeability PGI2 – vasodilation, inhibits platelet clumping Chemical Mediator
- 22. Vascular component Cellular component Two components Microcirculation EXUDATION Arteriolodilation WBCs Chemotaxis Emigration of cells
- 23. Cellular component How WBC pass through Vascular component to Interstitial component ?
- 24. Cellular Components of Inflammation Primary circulating WBC's are granulocytes 1.) Neutrophils 2.) Eosinophils 3.) Basophils Other components: platelets, monocytes (precursors of macrophages), and lymphocyte-like natural killer cells (NK cells)
- 25. Neutrophils and monocytes (phagocytes) move to the inflammatory site Margination Phagocytes adhere to the blood vessel walls
- 26. Emigration (diapedesis) Phagocytes slip out of the blood vessels through endothelial junctions Neutrophils arrive the earliest – 6-24 hours Monocytes arrive approx. 24-48 hours after injury
- 27. Phagocytosis WBC recognizes and attaches to the organism or antigen The organism is engulfed Degranulation (release of lysosomes) leads to death of the organism Platelet clumping at the site of injury
- 28. Cellular Events Emigration of Leukocytes from Vascular components to cellular components Chemotaxis Leukocyte movement towards the source of Inflammation
- 29. How the WBC pass the vascular compartment to Interstitial Components ?
- 33. Vascular Events Hydrostatic PressureHydrostatic Pressure Protein Rich Fluid -ExudationProtein Rich Fluid -Exudation More Viscus BloodMore Viscus Blood Less blood velocityLess blood velocity Coming blood increaseComing blood increase Normal Blood Flow- DisturbedNormal Blood Flow- Disturbed
- 34. RBC start sticking to each other Protein rich fluid - Exudation Increase Blood viscosity
- 35. 1- Margination WBC now hit the endothelial cell
- 36. Chemical Mediator act on the endothelial cell— Activation The sticky molecule of WBC –SIALATED SUGAR (oligisaccharide) Adhesion of WBC with Endothelial cell But the conjugation is not longer
- 37. 2- ROLLING Sticky WBC rolling with Endothelial cell
- 38. 3- Tight Adhesion Chemokines released from inflammatory area, attached with Endothelial cell surface- IL8- Induced
- 39. Activated INTEGRINE (peptide) Non activated INTEGRINE Chemomkines ICAM- Inter Cellular Adhesion Molecule VCAM- Vascluar Cellular Adhesion Molecule Chemokine stimulate the INTEGRINE and this INTEGRINE bind with ICAM, VCAM Strong Bonding of WBC with Endothelial cell -Tight adhesion
- 40. 4- DIAPEDIASIS (Imigration, Extravassation, Migration ) PECAM- Platelet Cell Adhesion Molecule Homophilic Interaction Collegenase -Make a hole on endothelial lining
- 42. Gprotein C-Receptor - IP3-ER-Activation – Proteinkinase-C - Polymer Chemoattractant Chemotaxis
- 44. Systemic effects of inflammation ● Fever ● Effects of pyrogen from neutrophils and macrophages ● Effects of interleukin-1 on hypothalamus ●Increased temp is harmful to some organisms (good) ●Some organisms release endotoxins when killed(bad)
- 45. Leukocytosis ● Stimulated by complement (C3a) ● Large release of stored neutrophils ● Production of leukocytes by bone marrow Loss of appetite Increased deep sleep Weight loss Weakness Systemic effects of inflammation
- 46. Benefits of Inflammation 1.) CONTROLS TISSUE DAMAGE ●The clotting systems and WBC's (i.e. eosinophils)
- 47. 2.) PREVENTS INFECTION The plasma protein systems that help destroy and contain bacteria (i.e. complement & clotting systems) and the influx of WBC's Benefits of Inflammation
- 48. 3.) INITIATES THE ADAPTIVE IMMUNE RESPONSE 4.)INITIATES HEALING THRU REMOVAL OF DEAD CELLS Benefits of Inflammation
- 49. Return to normal vascular permeability Removal of edema and plasma proteins by lymphatics and macrophages Phagocytosis by macrophages Cellular debris and dead neutrophils removed Resolution of inflammation
- 51. THANK YOU