1. Inflammation - Introduction
On inury, the cells either undergo adaptation or necrosis depending upon its severity. At the
same time, the whole tissue will mount a response and is known as inflammation.
INFLAMMATION - DEFINITION
Inflammation is a reaction of a living vascularised tissue to an injury.
e.g., a boil, an acute appendicitis.
Inflammation serves to destroy, dilute or wall of injurious agents.
It closely intertwined with the process of repair.
i.e., Regeneration / Scarring
INFLAMMATION - TYPES
The inflammation is broadly divided in to two types.
ACUTE INFLAMMATION
is of short duration
is stereotypic
is characterised by oedema & migration of neutrophils
CHRONIC INFLAMMATION
Long duration
less uniform
ACUTE INFLAMMATION
CAUSES
Acute inflammation can be caused by many agents which include...
Physical: Trauma, Heat, cold, Radiation etc.
Chemical : Toxins, acid etc.
Biological : Bacteria, Virus, Parasite etc

2. Immunological: Antibody mediated , Cell mediated
Necrotic tissue : Necrotic tissue [as in myocardial infarction]
LOCAL SIGNS OF INFLAMMATION
At the site of injury, the following CHARACTERISTIC signs develop.
CARDINAL SIGNS
Rubor: Red
Calor: Heat
Tumour: Swelling
Dolar : Pain
Functiolaesa : loss of function (may or may not present)
PATHOGENESIS
The pathogenesis of acute inflammation can be studied conveniantly under the following
three headings.
1. Changes in vascular flow & caliber
2. Changes in vascular permeability
3. Cellular events : Leukocyte exudation & phagocytosis
1. CHANGES IN VASCULAR FLOW AND CALIBER
- produce hyperaemia
'Blood flow in normal area'

3. 'Blood flow in inflammed area'
2. CHANGES IN VASCULAR PERMEABILITY
produce local oedema
MECHANISM: (of increased permeability of vessel wall)
1. Endothelial contraction
• occurs in mild injury
• begin directly after injury (Imm.transient leakage)
• peak within 5 to 10 mts. & phases out within 15 to 30 mts

4. • mediated by histamine & other chem. mediators
• inhibited by antihistamine -leak exclusively from venules.