ACUTE INFLAMMATION ACUTE INFLAMMATION COMPONENT Definition Acute inflammation
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ACUTE INFLAMMATION
ACUTE INFLAMMATION COMPONENT Definition: Acute inflammation is a rapid response to an injurious agent that serves to deliver mediators of host defense-leukocytes and plasma proteins-to the site of injury. Acute inflammation has three major components: (1) alterations in vascular caliber that lead to an increase in blood flow; (2) structural changes in the microvasculature that permit plasma proteins and leukocytes to leave the circulation; (3) emigration of the leukocytes from the microcirculation, their accumulation in the focus of injury, and their activation to eliminate the offending agent. (Robbins, 7 th ed. ) When a host encounters an injurious agent, such as an infectious microbe or dead cells, phagocytes that reside in all tissues try to get rid of these agents. At the same time, phagocytes and other host cells react to the presence of the foreign or abnormal substance by liberating cytokines, lipid messengers, and the various other mediators of inflammation.
PLASMA PROTIEN & ACUTE INFLAMMATION Plasma proteins leave the vessels, most commonly through widened interendothelial cell junctions of the venules. The redness (rubor), warmth (calor), and swelling (tumor) of acute inflammation are caused by the increased blood flow and edema. Circulating leukocytes, initially predominantly neutrophils, adhere to the endothelium via adhesion molecules, transmigrate across the endothelium, and migrate to the site of injury under the influence of chemotactic agents. Leukocytes that are activated by the offending agent and by endogenous mediators may release toxic metabolites and proteases extracellularly, causing tissue damage. During the damage, and in part as a result of the liberation of prostaglandins, neuropeptides, and cytokines, one of the local symptoms is pain (dolor. (
Plasma proteins leave the vessels, most commonly through widened interendothelial cell junctions of the venules. The redness (rubor), warmth (calor), and swelling (tumor) of acute inflammation are caused by the increased blood flow and edema. Circulating leukocytes, initially predominantly neutrophils, adhere to the endothelium via adhesion molecules, transmigrate across the endothelium, and migrate to the site of injury under the influence of chemotactic agents. Leukocytes that are activated by the offending agent and by endogenous mediators may release toxic metabolites and proteases extracellularly, causing tissue damage. During the damage, and in part as a result of the liberation of prostaglandins, neuropeptides, and cytokines, one of the local symptoms is pain (dolor. (
ACUTE INFLAMMATION Mediators INJURY Acute inflammation
ACUTE INFLAMMATION
ACUTE INFLAMMATION
ACUTE INFLAMMATION SEQUENCE OF EVENTS Vasoconstriction Vasodilation Increased vascular permeability Hemoconcentration and stasis Leukocyte Adhesion Transmigration Chemotaxis Aggregation Phagocytosis
ACUTE INFLAMMATION VASODILATION
ACUTE INFLAMMATION VASODILATION
ACUTE INFLAMMATION Increase in Permeability INCREASED VASCULAR PERMEABILITY Histamine (Mast Cells) Seratonin (Platelets) Time
ACUTE INFLAMMATION HEMOCONCENTRATION AND STASIS Normal flow Stasis
ACUTE INFLAMMATION LEUKOCYTE ADHESION
ACUTE INFLAMMATION LEUKOCYTE ADHESION
ACUTE INFLAMMATION EMIGRATION (TRANSMIGRATION)
ACUTE INFLAMMATION EMIGRATION (TRANSMIGRATION)
ACUTE INFLAMMATION CHEMOTAXIS
ACUTE INFLAMMATION AGGREGATION
ACUTE INFLAMMATION PHAGOCYTOSIS - ATTACHMENT
ACUTE INFLAMMATION PHAGOCYTOSIS - ENGULFMENT
ACUTE INFLAMMATION PHAGOCYTOSIS – KILLING AND DEGRADATION
ACUTE INFLAMMATION
ACUTE INFLAMMATION PATTERNS Serous Catarrhal Fibrinous Hemorrhagic Suppurative Gangrenous Pseudomembranous
ACUTE INFLAMMATION SEROUS
ACUTE INFLAMMATION SEROUS
ACUTE INFLAMMATION CATARRHAL
ACUTE INFLAMMATION FIBRINOUS
ACUTE INFLAMMATION SUPPURATIVE / PURULENT
ACUTE INFLAMMATION SUPPURATIVE / PURULENT - ABSCESS
ACUTE INFLAMMATION SUPPURATIVE / PURULENT - ABSCESS
ACUTE INFLAMMATION SUPPURATIVE / PURULENT - EMPYEMA
ACUTE INFLAMMATION ULCERATIVE
ACUTE INFLAMMATION GANGRENOUS
ACUTE INFLAMMATION GANGRENOUS Appendix Gallbladder
ACUTE INFLAMMATION PSEUDOMEMBRANOUS
ACUTE INFLAMMATION LOCAL MANIFESTATIONS Heat Redness Swelling Pain Loss of function
ACUTE INFLAMMATION SYSTEMIC MANIFESTATIONS Fever Chills Myalgia Discomfort
ACUTE INFLAMMATION LABORATORY MANIFESTATIONS Leukocytosis (granulocytosis vs. lymphocytosis) Elevated serum acute phase proteins (C-reactive protein, fibrinogen, etc) Increased ESR (erythrocyte sedimentation rate) Hypercoagulability
ACUTE INFLAMMATION SEQUELAE RESOLUTION Mediators INJURY Acute inflammation M Mediators rs o at i ed Chronic irritation Viral infection Autoimmune disease Chronic inflammation
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- Acute inflammation definition
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- Morphological pattern of acute inflammation
- Cellular events of acute inflammation
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- Cellular events of acute inflammation
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- Acute inflammation
- Morphological pattern of acute inflammation
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