Define and differentiate acute and chronic inflammation

Acute Inflammation - initial, rapid response to infections and tissue damage; typically develops within
minutes or hours and is of short duration, lasting several hours or few days; main characteristics are the
exudation of fluid and plasma proteins (edema) and emigration of leukocytes, predominantly neutrophils.
Chronic inflammation - of longer duration and is associated with more tissue destruction, and the presence of
lymphocytes and macrophages, the proliferation of blood vessels, and the deposition of connective tissue.
FEATURE

ACUTE

CHRONIC

Onset

Fast: minutes or hours

Slow: days

Cellular infiltrate

Mainly neutrophils

Monocytes/macrophages amd
lymphocytes

Tissue injury, fibrosis

Usually mild and self-limited

Often severe and progressive

Local and systemic signs

Prominent

Less

Type of host defense

Innate immunity

Adaptive immunity

Cells

Neutrophil
Eosinophil

Mononuclear cells
Fibroblast

Hallmarks

None

Blood vessel proliferation

Fibrosis
Granuloma

Course

Resolution
Abscess formation

Scarring
Amyloidosis

List causes of inflammation; discuss steps in pathogenesis of acute inflammation.

Causes of inflammation:
1. Infections (bacterial, viral, fungal, parasitic) and microbial toxins
2. Tissue necrosis secondary to cell death
3. Foreign bodies
4. Immune reactions
Pathogenesis of acute inflammation
1. Dilation of small vessels leading to an increase in blood flow
2. Increased permeability of tje microvasculature enabling plasma proteins and leukocytes to.leave circulation
3. Emigration of the leukocytes from the microcirculation, their accumulation in the focus of injury and their
activation to eliminate the offending agent.

Define and differentiate exudate and transudate

An EXUDATE is an extravascular fluid that has HIGH protein concentration and CONTAINS cellular debris.
Its presence implies that there is an INCREASE IN THE PERMEABILITY OF SMALL BLOOD VESSELS
triggered bu some sort of tissue injury and ongoing inflammatory reaction. It is formed in inflammation because
vascular permeability increases as a result of increased interendothelial spaces.
A TRANSUDATE os a fluid with LOW protein content (most of which is albumin), LITTLE OR NO cellular
material, and LOW specific gravity. It is formed when fluid leaks out because of increased hydrostatic pressure
or decreased osmotic pressure. It is essentially an ultrafiltrate of the blood plasma that is produced as a result of
osmotic or hydrostatic imbalance across the vessel wall WITHOUT AN INCREASE IN VASCULAR

PERMEABILITY.

Discuss the steps in vascular reactions, leukocyte migration amd mediators involved.
Steps in vascular reactions
1. Vasoconstriction of arterioles
due to a neurogenic reflex that lasts only a few seconds
2. Vasodilation of arterioles
histamine and other vasodilators relax vascular smooth muscle, causing increased blood flow
3. Increased permeability of venules
histamine and other mediators contract endothelial cells in venukes, producing endothelial gaps exposing
bare basement membrane
transudates (fluid low in proteins and cells) move through the intact venular basement membrane into the
interstitial tissue because of the increased hydrostatic pressure
4. Swelling of tissueflow
tumor, edema
net outflow of fluid from the venules surpasses the capacity of lympatics to remove fluid; hence there oss
swelling of the tissue
5. Reduced blood flow
reduced blood flow eventually occurs because of the outflow of fluid into the interstitial tissue and increased
uptake of fluid by lympatics.
Leukocyte migration
1. Leukocyte Adhesion to the Endothelium
involves
1.1 Margination - process of leukocyte redistribution where hemodynamic conditions change (wall shear syress
decreases), and more white cells assume a peripheral position along the endothelial surface as a result of
slowing of blood flow early in inflammation (stasis)
1.2 Rolling - mediated by a family of proteins selectins (characterized by weak binding) and intergrins
(responsible for stable adhesion) to slow down leukocytes and give them the opportunity to bind more firmly to
the endothelium.
1.3 Adherance
2. Leukocyte Migration Through Endothelium
transmigration or diapedesis - Chemokines act on the adherent leukocytes and stimulate the cells to migrate
through interendothelial spaces toward the chemical concentration gradient, that is, toward the site of injury or
infection where the chemokines are being produced.
3. Chemotaxis of Leukocytes
locomotion along a chemical gradient. The leukocyte moves by extending filodopia that pull the back of the
cell in the direction of extension, much as an automobile with the front-wheel drive is pulled by the wheels in
front.
Mediators involved
comprehensive presentaion in tabular form c/o Dr. Aznar's powerpoint lecture