ACUTE INFLAMMATION

ACUTE INFLAMMATION COMPONENTDefinition: 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

INJURY Acute inflammationMediators

ACUTE INFLAMMATION

ACUTE INFLAMMATION

VasoconstrictionVasodilationIncreased vascular

permeabilityHemoconcentration and

stasisLeukocyte AdhesionTransmigrationChemotaxisAggregationPhagocytosis

ACUTE INFLAMMATIONSEQUENCE OF EVENTS

ACUTE INFLAMMATIONVASODILATION

ACUTE INFLAMMATIONVASODILATION

Incr

ease

in P

erm

eabi

lity

Time

ACUTE INFLAMMATIONINCREASED VASCULAR PERMEABILITY

Histamine (Mast Cells)Seratonin (Platelets)

Normal flow

Stasis

ACUTE INFLAMMATIONHEMOCONCENTRATION AND STASIS

ACUTE INFLAMMATIONLEUKOCYTE ADHESION

ACUTE INFLAMMATIONLEUKOCYTE ADHESION

ACUTE INFLAMMATIONEMIGRATION (TRANSMIGRATION)

ACUTE INFLAMMATIONEMIGRATION (TRANSMIGRATION)

ACUTE INFLAMMATIONCHEMOTAXIS

ACUTE INFLAMMATIONAGGREGATION

ACUTE INFLAMMATIONPHAGOCYTOSIS - ATTACHMENT

ACUTE INFLAMMATIONPHAGOCYTOSIS - ENGULFMENT

ACUTE INFLAMMATIONPHAGOCYTOSIS – KILLING AND DEGRADATION

ACUTE INFLAMMATION

SerousCatarrhalFibrinousHemorrhagicSuppurativeGangrenousPseudomembranou

s

ACUTE INFLAMMATIONPATTERNS

ACUTE INFLAMMATIONSEROUS

ACUTE INFLAMMATIONSEROUS

ACUTE INFLAMMATIONCATARRHAL

ACUTE INFLAMMATIONFIBRINOUS

ACUTE INFLAMMATIONSUPPURATIVE / PURULENT

ACUTE INFLAMMATIONSUPPURATIVE / PURULENT - ABSCESS

ACUTE INFLAMMATIONSUPPURATIVE / PURULENT - ABSCESS

ACUTE INFLAMMATIONSUPPURATIVE / PURULENT - EMPYEMA

ACUTE INFLAMMATIONULCERATIVE

ACUTE INFLAMMATIONGANGRENOUS

ACUTE INFLAMMATIONGANGRENOUS

Appendix Gallbladder

ACUTE INFLAMMATIONPSEUDOMEMBRANOUS

Heat RednessSwellingPainLoss of

function

ACUTE INFLAMMATIONLOCAL MANIFESTATIONS

FeverChillsMyalgiaDiscomfort

ACUTE INFLAMMATIONSYSTEMIC MANIFESTATIONS

Leukocytosis

(granulocytosis vs. lymphocytosis)Elevated serum acute phase proteins

(C-reactive protein, fibrinogen, etc)Increased ESR

(erythrocyte sedimentation rate)Hypercoagulability

ACUTE INFLAMMATIONLABORATORY MANIFESTATIONS

ACUTE INFLAMMATIONSEQUELAE

INJURY

RESOLUTION

Autoimmune disease

Chronic inflammation

Acute inflammation

Viral infection

Chronic irritation

Mediators

Mediators

Mediators