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, 7th 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 Acute inflammation INJURY

ACUTE INFLAMMATION

ACUTE INFLAMMATION

ACUTE INFLAMMATION Vasoconstriction Vasodilation SEQUENCE OF EVENTS Vasoconstriction Vasodilation Increased vascular permeability Hemoconcentration and stasis Leukocyte Adhesion Transmigration Chemotaxis Aggregation Phagocytosis

ACUTE INFLAMMATION VASODILATION

ACUTE INFLAMMATION VASODILATION

INCREASED VASCULAR PERMEABILITY ACUTE INFLAMMATION INCREASED VASCULAR PERMEABILITY Increase in Permeability Histamine (Mast Cells) Seratonin (Platelets) Time

INCREASED VASCULAR PERMEABILITY ACUTE INFLAMMATION INCREASED VASCULAR PERMEABILITY

HEMOCONCENTRATION AND STASIS ACUTE INFLAMMATION HEMOCONCENTRATION AND STASIS Normal flow Stasis

ACUTE INFLAMMATION LEUKOCYTE ADHESION

ACUTE INFLAMMATION LEUKOCYTE ADHESION

EMIGRATION (TRANSMIGRATION) ACUTE INFLAMMATION EMIGRATION (TRANSMIGRATION)

EMIGRATION (TRANSMIGRATION) ACUTE INFLAMMATION EMIGRATION (TRANSMIGRATION)

ACUTE INFLAMMATION CHEMOTAXIS

ACUTE INFLAMMATION AGGREGATION

PHAGOCYTOSIS - ATTACHMENT ACUTE INFLAMMATION PHAGOCYTOSIS - ATTACHMENT

PHAGOCYTOSIS - ENGULFMENT ACUTE INFLAMMATION PHAGOCYTOSIS - ENGULFMENT

PHAGOCYTOSIS – KILLING AND DEGRADATION ACUTE INFLAMMATION PHAGOCYTOSIS – KILLING AND DEGRADATION

ACUTE INFLAMMATION

ACUTE INFLAMMATION Serous Catarrhal Fibrinous Hemorrhagic Suppurative PATTERNS Serous Catarrhal Fibrinous Hemorrhagic Suppurative Gangrenous Pseudomembranous

ACUTE INFLAMMATION SEROUS

ACUTE INFLAMMATION SEROUS

ACUTE INFLAMMATION CATARRHAL

ACUTE INFLAMMATION FIBRINOUS

SUPPURATIVE / PURULENT ACUTE INFLAMMATION SUPPURATIVE / PURULENT

SUPPURATIVE / PURULENT - ABSCESS ACUTE INFLAMMATION SUPPURATIVE / PURULENT - ABSCESS

SUPPURATIVE / PURULENT - ABSCESS ACUTE INFLAMMATION SUPPURATIVE / PURULENT - ABSCESS

SUPPURATIVE / PURULENT - EMPYEMA ACUTE INFLAMMATION SUPPURATIVE / PURULENT - EMPYEMA

ACUTE INFLAMMATION ULCERATIVE Ulcers of tularemia

ACUTE INFLAMMATION GANGRENOUS

ACUTE INFLAMMATION GANGRENOUS Appendix Gallbladder

ACUTE INFLAMMATION PSEUDOMEMBRANOUS

ACUTE INFLAMMATION Heat Redness Swelling Pain Loss of function LOCAL MANIFESTATIONS Heat Redness Swelling Pain Loss of function

SYSTEMIC MANIFESTATIONS ACUTE INFLAMMATION SYSTEMIC MANIFESTATIONS Fever Chills Myalgia Discomfort

LABORATORY MANIFESTATIONS 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 Acute inflammation INJURY Chronic irritation Mediators Mediators Viral infection Autoimmune disease Chronic inflammation