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Today’s Quranic verse

Today’s Quranic verse.

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Today’s Quranic verse

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  1. Today’s Quranic verse For each (such person) there are (angels) in succession, before and behind him: They guard him by command of God. Verily never will God change the condition of a people until they change it themselves (with their own souls). But when (once) God willeth a people's punishment, there can be no turning it back, nor will they find, besides Him, any to protect.[013:011]

  2. "You are your own raw material. When you know what you consist of and what you want to make of it, then you can invent yourself."

  3. ACUTE INFLAMMATION

  4. INFLAMMATION • Specific Objectives:  • Define inflammation. • List the causes of inflammation. • List the main components of acute inflammation. • Describe the vascular changes in acute inflammation including pattern of permeability changes. • Tabulate differences between transudate & exudates. • Describe the cellular events in acute inflammation. • Define the following terms pertaining to leukocytes involved in an inflammatory response: margination, diapedesis, emigration, exudation, chemotaxis, chemokinesis, phagocytosis, and microbiocidal substances. • Explain the type of cellular response and defects in neutrophilic responses at different levels. • List the cell-derived and plasma-derived mediators of inflammation. • Explain the main functions of cytokines released in inflammation. • Discuss the clinical aspects of acute inflammation. • Describe possible outcomes of acute inflammation.

  5. INFLAMMATION (“Inflame” – to set fire) Inflammation is the reaction of vascular and supporting elements of a tissue to injury, and results in the formation of a protein rich exudate, provided the injury has not been so severe as to destroy the area. It is usually divided into acute inflammation & chronic inflammation but in reality the two often form a continuum.

  6. ACUTE INFLAMMATION Acute inflammation may develop over minutes or hours depending on the type and severity of the tissue damage and generally lasts hours to days. It is characterized by the classical signs of pain (dolor), heat (calor), redness (rubor), swelling (tumor) and loss of function (functio laesa). The nomenclature used to describe inflammation in different tissues employs the tissue name (or its Greek or Latin equivalent) and the suffix ‘-itis’ like appendicitis, salpingitis, cellulitis, encephalitis, orchitis etc. Histologically, it involves a complex series of events, including dilatation of arterioles, capillaries, and venules, with increased permeability and blood flow, exudation of fluids, including plasma proteins, and leukocytic migration into the inflammatory focus.

  7. CAUSES OF (ACUTE) INFLAMMATION Mechanical Chemical Physical (including radiation) Biological Immunological Associated with necrosis

  8. CHANGES IN THE CALIBRE OF THE BLOOD VESSELS Transient arteriolar constriction, lasting a few seconds up to a few min. Persistent arteriolar dilatation as long as acute inflammation continues. (Hyperemia is a generic term for extra blood in an organ due to dilatation of the arterioles.)

  9. NORMAL REGULATION OF FLUID TRANSPORT STARLING’S HYPOTHESIS ( LAW ) Osmotic pressure of the blood nearly balances the outflow that is produced by hydrostatic pressure. The net result is that there is a continuous movement of fluid from the intravascular compartment into the tissues via the pre-capillary arteriole, where it is either transported away by lymphatics, or reabsorbed in the post-capillary venule

  10. The four Starling’s forces are: The balance of these forces allows calculation of the net driving pressure for filtration. Net Driving Pressure = [ ( Pc - Pi ) - ( pc - pi ) ] Arteriolar end (AE) of capillary = [(25-(-06)-(25-05)]= 11 mmHg Venous end (VE) of capillary = [(10-(-06)-(25-05)]= -4 mmHg

  11. In (acute) inflammation there is • Increased hydrostatic pressure • Increased vascular permeability • Decreased intravascular osmotic pressure • Break down of large molecules of protein • Increased extravascular osmotic pressure • Increased fluidity of ground substance  • Net result is inflammatory edema - (exudate)

  12. EXUDATE Morbid extra-vascular accumulation of fluid due to increased vascular permeability. SHOULD BE DIFFERENTIATED FROM TRANSUDATE Morbid accumulation of fluid due to hydrostatic imbalance between intravascular and extra-vascular compartments despite normal vascular permeability

  13. COMPARISON OF AN EXUDATE WITH TRANSUDATE EXUDATE TRANSUDATE  Mechanism Inflammatory No-inflammatory Total protein High <10 g/l Distribution of protein As in plasma Albumin only Fibrinogen/clotting Present / yes Not present / no Specific gravity High >1.018 Low < 1.012 Cells Many Few (inflammatory cells) (mesothelial cells)

  14. 5.Increased transcytosis of fluid

  15. PATTERNS OF PERMEABILTY CHANGES Immediate-transient response Begins at once, peaks at 5-10 minutes, and is over by 30 minutes. Involves only the venules. Causing contraction and separation of endothelial cells. It is attributed to prostaglandins, histamine, serotonin and a host of other chemical mediators.

  16. Immediate-sustained reaction ("immediate prolonged") Seen only when the injury is severe enough to cause direct endothelial cell damage, and persists until thrombosis or regeneration ends it. Can affect any blood vessel.

  17. Delayed-prolonged leakage phenomenon Seen only after hours or days, Venules and capillaries exude protein, due to widening & separation of endothelial junctions Underlying mechanism is apoptosis of the endothelial cells Swelling that accompanies a sunburn, radiation therapy, and thermal burns.  

  18. In acute inflammation whenever blood flow is slowed, loss of axial flow causes neutrophils to exhibit: Margination,white cells falling out of central column and assuming a peripheral position along the endothelial surface) Rolling transient adherence of rows of tumbling white cells along the endothelium Adhesionto the walls of vessels, especially venules, (adhesion receptor: selectin, immunoglobulin & integrin) Emigration of neutrophils from the vessels into the tissues occurs when the cells squeeze through the widened endothelial cell gaps, then get through the basement membrane by digesting it with enzymes.The other white cells also leave vessels by this route.

  19. (Diapedesis is passive movement of RBCs as a result of increased hydrostatic pressure through the defects created by WBCs) The final key event in acute inflammation is the accumulation of neutrophils in the injured tissue. (Most of the time, these predominate for the first 24-48 hours after injury, and are more or less replaced by macrophages after this time.)

  20. ROLLING: In rolling selectins transiently bind to receptors, neutrophils bounce or roll along. ADHESION: Mediated by Integrins ICAM-1 and VCAM-1 TRANSMIGRATION: Mediated by PECAM-1

  21. Once the cells are in extra-vascular space they exhibit Chemokinesis increased random locomotion (of an organism-WBC) Chemotaxis directional movement of an organism (WBC) in response to chemical gradient. Chemotactic agents Bacterial breakdown products, Complement components, Leukotriene B4. Chemokines (certain lympohokines and monokines)

  22. (Most small molecules which are chemotactic for neutrophils are also chemotactic for macrophages and vice versa.) Mast cells, activated in parasitic infestations and classic IgE-mediated allergy, release "eosinophilic chemotactic factor of anaphylaxis

  23. Leukocyte Activation • Chemokines also “activate” PMN’s characterized by: • AA metabolite production • Degranulation and Secretion of lysosomal enzymes • Oxidative burst • Modulation of adhesion molecules

  24. Once they have found their way to the tissues, the neutrophils exhibit ENDOCYTOSIS It is vesicular engulfment of extracellular material by a cell. It includes both phagocytosis (ingestion of particles) and pinocytosis (ingestion of fluid phase material, i.e., "cell drinking"). The engulfing cells degranulate, releasing enzymes into phagocytic vacuoles or into the interstitial fluid.

  25. PHAGOCYTOSIS Recognition & Attachment (Opsonin -Fc fragment of IgG, C3b/C3bi) Engulfment (Phagosome, lysosome, phagolysosome)  Killing or Degradation of phagocytized bacteria H2O2-myeloperoxidase-halide system, Oxygen-dependent and oxygen-independent systems the latter less effective like BPI, lysozyme, lactoferrin, MBP etc.

  26. Bactericidal activity in phagocytic cells • Activated oxygen species • Superoxide (.O2) • (formed via NADPH oxidase) • Hydrogen peroxide (H2O2) • (formed via spontaneous dismutation of superoxide) • Hydroxyl radical (.OH) • H2O2-Myeloperoxidase-halide system leading to formation of Hypochlorous acid (HOCl) [Probably the primary bactericidal agent in neutrophils]

  27. Non-oxidative bacterial killing

  28. Neutrophil Granules Primary (azurophilic granules) - contain serine proteases, lysozyme and phospho-lipase A2 etc. Secondary (specific granules) - similar to primary, but also contain lactoferrin and collagenase etc. Tertiary (small storage granules) - present at the leading edge of migrating PMNs, contain gelatinases that are capable of degrading basement membrane

  29. ` "Frustrated phagocytosis" This is a phenomenon where neutrophil products, including lysosomal enzymes, H2O2, free radicals, and arachidonic acid metabolites are released into the interstitium during the process by "regurgitation during feeding", (i.e., the neutrophil tries to eat something too big, such as a huge immune complex or a splinter). This leads to endothelial injury, tissue damage and amplification of the effects of the initial inflammatory stimulus. This type of leukocyte dependant tissue injury underlies many human diseases like rheumatoid arthritis and certain forms of chronic lung diseases,

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