Definition, Types & Vascular Events of Acute Inflammation

Veer Prabhakar Choollun

Roll no.1Pathology23/02/15

Contents

• InflammationDefinitionCausesTypes

• Acute InflammationDefinitionEvents of Acute InflammationVascular Events of Inflammation

Definition

• Inflammation is defined as a complex reaction elicited in the vascularised connective tissue of the body caused by various stimuli that can cause cell injury. It is a protective response that tends to eliminate or isolate the causative agent and necrotic tissues resulting from the original damage. It is interwoven with the process of healing and repair.

Causes of Inflammation

Inflammation

Physical Agents

Chemical Agents

Infectious agentsImmunological

Nutritional

Tissue Necrosis

Types of Inflammation

• Depending on the nature of stimulus & the effectiveness of the initial response to neutralize the causative agent, Inflammation can be divided into 2 types: AcuteChronic

• An inflammatory lesion thus can be denoted with the prefix, Acute or Chronic & suffix –itis along with the site or organ involved.

Acute Inflammation –Definition

• It can be defined as an immediate or early response to an injurious stimulus, microbe or foreign body, the critical function of which is to deliver leukocytes, plasma proteins and antibodies to the site of injurious stimulus.

• It is a rapid , non-specific response to cell injury. It is of shorter duration lasting for minutes to hours to few days.

• Since all these components are present in blood, certain phenomenon takes place:Alteration in vascular calibre (↑blood flow) &

structural alteration in the microvasculatureEmigration of leucocytes & their accumulation

at site of injury.

Events

•Vascular Events

•Cellular Events

Vascular Events

Vascular Events

Alteration in Calibre & Flow

Alteration in Vascular Permeability

Alteration in Calibre & Flow

Transient Vasoconstriction

•Of arterioles for a few sec. Following injury•Due to smooth m. Cell contraction

Vasodilatation•First involving arterioles + opening of new capillary beds which were previously carrying little or no blood •↑Blood flow by x10•Known as ACTIVE HYPEREMIA

Slowing of Circulation •Due to increasing vascular permeability with outflow of fluid into interstitium•↑ in viscosity of blood, microvasculature becomes packed with RBCs•Known as STASIS

Alteration in Vascular PermeabilityVasodilatation ↑Blood Flow

↑ in Vascular permeability with more outflow of fluid having a different consistencyFluid known as Exudate

Transudate

It is an ultra filtrate of plasma formed in the earliest phase of inflammation due to RAISED HYDROSTATIC PRESSURE or due to DECREASED ONCOTIC PRESSURE WITHOUT THE ALTERATION IN VASCULAR PERMEABILITY.

Exudate It is an inflammatory extra vascular fluid formed due to

an INCREASE IN VASCULAR PERMEABILITY.

Transudate & Exudate formation

Differences between Transudate and Exudate

Transudate Exudate

Formed in the earliest phase of inflammation

Formed after Transudate formation

Low protein content High protein content

Low content of HMW proteins High content of HMW

Low cell count High cell count

Low content of fibrinogen ( low tendency to clot)

High content of fibrinogen ( High tendency to clot)

Low specific gravity (<1.012) High specific gravity (>1.020)

Mechanisms of Increased Vascular permeability

1. Endothelial Cell Contraction

2. Junctional Retraction

3. Direct Endothelial cell Damage

4. Leukocyte mediated Endothelial Cell Damage

5. Transcytosis or via Vesiculovacuolar pathway

Endothelial Cell contraction

• In response to mediators like Bradykinin, Substance P & Histamine.

• Onset is few seconds and lasts for 15-30 minutes.• More effective in post capillary venules because of more

receptors• Endothelial cells contract widening inter-endothelial

junction.• Response is known as IMMEDIATE TRANSIENT

RESPONSE.

Junctional Retraction

• In response to cytokines like IL-1 & TNF-α• Onset in 2 to 4 hours and lasts for about 24 hours• Cytokines cause structural re-organisation in

endothelial cell causing disruption of inter- endothelial junctions.

Direct Endothelial Cell Damage• There is 2 types of responses possible:

Immediate Sustained Response• There is endothelial cell necrosis & detachment. • Seen in severe trauma like burns, lytic bacterial infections or

septicaemia. • In this leakage begins immediately through necrosed cell &

sustained at a high level until vessel is repaired or thrombosed.

Delayed Prolonged Response• In mild to moderate thermal injury ( X rays, U.V.)• Onset is in 12-24 hrs and lasts for days• Due to endothelial cell damage and replacement by

apoptosis.

Leukocyte Mediated Endothelial cell Damage

• During inflammation, there is stasis and hence leukocytes being larger have a tendency to fall out from the central axial column into periphery lying closer to endothelial cells.

• Such activated leukocytes produce ROS/ RNS & proteolytic enzymes like collagenases which damage endothelial cells.

Transcytosis or Vesiculovacuolar Pathway

• In the process of healing & repair, there is subsequent angiogenesis mediated by VEGF-A and FGF-2.

• The newly formed capillary sprouts have leaky inter- endothelial junctions and also, fluid can also traverse into tiny vesicles or vacuoles through immature endothelial cells.

Cardinal Signs of Inflammation

• These events give rise to the 5 Cardinal Signs of Inflammation:RUBOR ( redness) due to ↑Blood flowCALOR ( Heat) due to ↑Blood flowTUMOR ( Swelling) due to oedemaDOLOR (pain) due to chemical mediatorsLoss of function due to tissue damage