Inflammation

Content

• Inflammation

• Types of inflammation

• Changes involved in acute inflammation

Objectives

At the end of this PDF, student will be able to

• Define “inflammation”

• Classify inflammation

• Describe the etiology of inflammation

• Identify the signs of inflammation

• Describe the changes involved in acute inflammation

Inflammation

“Local response of living mammalian tissues to injury due to any agent “

• Body defence reaction to eliminate or limit the spread of injurious agent, followed by removal of the necrosed cells and tissues

• Protective response

Etiology of Inflammation

• Infective agents - bacteria, viruses and their toxins, fungi, parasites

• Immunological agents - cell-mediated and antigen antibody reactions

• Physical agents - heat, cold, radiation, mechanical trauma

• Chemical agents - organic and inorganic poisons

Signs of inflammation

4 cardinal signs of inflammation

• Rubor (redness)

• Tumor (swelling)

• Calor (heat) and

• Dolor (pain)

Fifth sign - functio laesa (loss of function) - Virchow

Types of inflammation

Depending upon the defense capacity of host and duration of response

• Acute Inflammation

• Chronic inflammation

Acute Inflammation

• Short duration

• Represents early body reaction

• Followed by repair

Main features

• Accumulation of fluid & plasma at the affected site

• Intravascular activation of platelets

• Polymorpho nuclear neutrophills (PMN) – inflammatory cells

Chronic Inflammation

• Longer duration

• If causative agent of acute inflammation persists for long periods

• Recurrent attack of acute inflammation

Main features:

• Presence of lymphocytes, plasma cells & Macrophages as inflammatory cells

Changes in Acute inflammation

Two main events involved

1. Vascular events

• Alteration of microvasculature (arteries, capillaries & venules)

2. Cellular events

• Exudation of leucocytes

• Phagocytosis

Vascular events

• Alteration in the microvasculature - tissue injury

Haemodynamic Changes

Earliest features - vascular flow change, calibre of small blood vessels

1. Irrespective of the type of injury - transient vasoconstriction of arterioles

• Mild form – blood flow - 3-5 seconds

• More severe injury the vasoconstriction - 5 minutes

Vascular changes

2. Persistent progressive vasodilatation

• Mainly arterioles

• lesser extent - venules and capillaries

• Increased blood volume - redness and warmth

3. Progressive vasodilatation

• Elevate the local hydrostatic pressure - transudation of fluid into the extracellular space – swelling

4. Stasis of microcirculation

• Increased concentration of red cells - blood viscosity

5. Leucocytic margination

• Leucocytes stick to the vascular endothelium

• Move and migrate through the gaps between the endothelial cells into the extravascular space

• Emigration

Triple response

Flush

– Appearance of red line

– Local vasodilatation of capillaries and venules

Flare

– Bright reddish appearance or flush surrounding the red line

– Vasodilatation of the adjacent arterioles

Wheal

– Swelling or oedema of the surrounding

– Transudation of fluid into the extravascular space

Pathogenesis of altered vascular permeability

Normal circumstances - fluid balance - two opposing sets of forces that causes:

Outward movement of fluid from microcirculation

– intravascular hydrostatic pressure

– colloid osmotic pressure of interstitial fluid

Inward movement of interstitial fluid into circulation

– intravascular colloid osmotic pressure

– hydrostatic pressure of interstitial fluid

Contraction of endothelial cells

• Increased leakiness - venules exclusively

• Endothelial cells - temporary gaps – contraction - vascular leakiness - release of histamine, bradykinin and others

• Response - immediately after injury – reversible - short duration (15-30 minutes)

• Example: immediate transient leakage is mild thermal injury of skin of forearm

Retraction of endothelial cells

• structural re-organisation of the cytoskeleton of endothelial cells - reversible retraction – intercellular junctions – venules - cytokines such as interleukin-1 (IL-1) and tumour necrosis factor (TNF)-α - response takes 4-6 hours after injury - lasts for 2-4 hours or more

• The example invitro experimental work only

Direct injury to endothelial cells

• Cell necrosis, physical gaps at the sites of detached endothelial cell - thrombosis at site initiated

• Affects – microvasculature - immediately after injury last for several hours or days or delay of 2-12 hours and last for hours or days