ACUTE INFLAMMATION

Inflammation

Dr Mustafa Salah Fadhil

Chemical Mediators of Inflammation

A substances which play a role in genesis and modulation of inflammatory reaction

They are responsible for:

1. Vasodilatation
2. Increased permeability
3. Emigration of WBC (Chemotactic agent).

Chemical Mediators of Inflammation

Chemical Mediators of Inflammation

A/ Vasoactive Amines


1) Histamine: secreted from mast cells, basophils & platelets

2) Serotonin: secreted from platelets

Effects: arteriolar vasodilation & increase vascular permeability

B/ Arachidonic Acid (AA) Metabolites

AA present in the cell membrane phospholipids

Release from phospholipids through the action of phospholipase enzyme by mechanical, chemical & physical stimuli

AA metabolism proceeds along 1 of 2 pathways

Cyclooxygenase pathway---------- Postoglandins
Lipooxygenase pathway------------Leukotriens

Arachidonic Acid Metabolites

Thromboxane A2
Vasoconstriction
Platelet aggregation
Protacyclin (PGI2)
Vasodilatation
Inhibits Platelet aggregation
PGD2, PGE2 & PGF2
VD & edema
PGE2:
Fever
Pain



5-HETE:
Chemotaxis

LTB4:

Chemotaxis
Aggregation of neutrophils
LTC4, LTD4, LTE4
Vasoconstriction
Bronchospasm
Increase vascular permeability

Cyclooxygenase pathway

Lipooxygenase pathway

C) Cytokines

Polypeptides produced by activated lymphocytes & macrophages.
Involved in cellular immunity & inflammatory responses.
• IL-1 & TNF
• IL-6
• IL-8
Chemotactant & neutrophil activating agent


D) Nitric Oxide (NO)

Soluble free radical gas synthesized by endothelial cells, macrophages & specific neurons in the brain

Effects:

Vascular smooth muscle relaxation causing VD

Decreased platelet aggregation & adhesion

Microbicidal agent

E) Oxygen Free Radicals

Superoxide (O2-), OH-, H2O2 & NO

Effects

kill bacteria

Endothelial cell damage causing increase vascular permeability

Activation of proteinases

Injury to surrounding cells

F) Complement System

Present as inactive form in the plasma

Vascular effect (anaphylotaxins): C3a, C5a & C4a causing VD & increase vascular permeability

Leukocyte adhesion, chemotaxis & activation: C5a

Phagocytosis: C3b & C3b1 act as opsonins

Microscopic appearance of acute inflammation

Congestion of blood vessels


Exudation of fluid

Exudation of inflammatory cells mainly neutrophils

Special macroscopic appearances of acute inflammation

1. Serous inflammation:
There is abundant protein-rich fluid exudate with a relatively low cellular content. Examples include inflammation of the serous cavities, such as peritonitis, and inflammation of a synovial joint, acute synovitis.

2. Catarrhal inflammation:

When mucus hypersecretion accompanies acute inflammation of a mucous membrane. The common cold is a good example.

3. Fibrinous inflammation :

When the inflammatory exudate contains plentiful fibrinogen, this polymerises into a thick fibrin coating. This is often seen in acute pericarditis and gives the parietal and visceral pericardium a 'bread and butter' appearance.


Special macroscopic appearances of acute inflammation
4. Suppurative (purulent) inflammation:
Means: pus
Consists of dying and degenerate neutrophils, infecting organisms and liquefied tissues and exudate.
Abscess (a localised collection of pus in a tissue).
Empyema is accumulationof pus in a hollow viscus, e.g. empyema of the gallbladder or of the appendix

5. Membranous inflammation:

An epithelium becomes coated by fibrin, desquamated epithelial cells and inflammatory cells. e.g. grey membrane seen in pharyngitis or laryngitis due to Corynebacterium diphtheriae.

Fates (outcomes) of acute inflammation

1. Complete resolution: return to normal
It involve:
removal of the exudate, fibrin & debris
reversal of the microvascular changes
regeneration of lost cells
2. Healing & organization: connective tissue replacement.
Occurs in:
substantial tissue destruction
tissue cannot regenerate
extensive fibrinous exudate
3. Suppuration:
(It may be diffuse in tissue, localized in tissue (abscess) , on the surface of a wound, or in serous cavity)
4. Progression to chronic inflammation:
when there is persistent infection
when there is foreign body, …etc

Complete resolution

Effects of Acute Inflammation

Dilution of toxins
Entry of antibodies
Drug transport
Fibrin formation
Delivery of nutrient & O2
Stimulation of immune system

Digestion of normal tissue

Swelling & pain
Inappropriate inflammatory response


BENIFITIAL EFFECTS
HARMFUL EFFECTS

THANKS