Inflammation:

 The local response of living tissues to injury due to any agent. (Or)
 A process by which the body's immune system malfunctions (failure to function normally).
 Eg. Diseases like,
o Arthritis.
o Diabetes.
o Myasthenia gravis.

Etiology:

Exogenous causes:-

 Physical agents:
o Mechanical agents:
 Fractures, foreign corps, sand, etc..,
o Thermal agents:
 Burns, freezing.
 Chemical agents:
o Toxic gases.
o Bases.
o Acids.
 Biological agents:
o Bacteria.
o Viruses.
o Parasites.

Endogenous causes:-

 Circulation disorders:
o Thrombosis.
o Infarction.
o Hemorrhage.
 Enzyme activation:
o Acute pancreatitis.
 Metabolic products:
o Uric acid.
o Urea.

Types of inflammation:

 Acute inflammation.
 Chronic inflammation.

Acute inflammation:

 Rapid onset.
 Short duration.
  Fluid accumulation.
 Plasma protein exudation.
 Neutrophils.

Mechanism of inflammation:

 The two main events of the acute inflammation are,

o Vascular events.
o Cellular events.

Vascular events:

Initial transient vasocontraction of arterioles

Persistent progressive vasodilation

Elevation of local hydrostatic pressure

Increase in vascular permeability

Transudation of fluid into the extracellular space

Slowing (or) stasis of microcirculation

Leukocyte margination

Cellular events:

 Leukocyte recruitment to site injury.

o Extravasation – sequence of events in the recruitment of leukocytes from the vascular
lumen to the extravascular space.
 Leukocyte activation at the site of injury.
 Phagocytosis of particles
o Process of engulfment of.
 Solid particulate material by the leukocytes. (Neutrophils & monocytes)

Fate of acute inflammation:

 Resolution:
o Complete return to normal tissue following acute inflammation.
 Repair:
 o Healing by regeneration in case of superficial tissue loss.
o Healing by fibrosis in case of extensive tissue loss.
 Suppuration:
o Result of extensive tissue necrosis by pyogenic bacteria.
o Intense neutrophil infiltration with fragments of necrosis tissue, cell debris & fibrin.
o Pus/abscess.

Signs of inflammation:

 Five cardinal signs of inflammation as,

o Rubor(redness).
o Tumour(swelling).
o Calor(heat).
o Dolor(pain).
o Functio laesa(loss of function).

Examples of acute inflammation:

 Acute appendicitis.
 Acute meningitis.
 Acute pyelonephritis.
 Lobar pneumonia,
o May spill to involve pleural cavity- Empyema.

Chronic inflammation:

 Onset – insidious.
 Longer duration.
 Lymphocytes, macrophages, plasma cells are inflammatory cells.

Causes of chronic inflammation:

 Persistent infection:-
o Bactria.
o Viruses.
o Fungi.
o Parasites.
 Prolonged exposure to potentially toxic agent:-
o Endogenous (atherosclerosis) .
o Exogenous (particulate silica-sclerosis) .
 Autoimmunity:
o Occurs in,
 Rheumatoid arthritis.
 Lupus erythematosus.

Morphological features of chronic inflammation:

  These are characterized by,
o Infiltration by mononuclear cells.
o Tissue destruction.
o Removal of damaged tissue(healing).

Infiltration by mononuclear cells:

 The mononuclear cells are predominant at 48 hours.

 These include,
o Macrophages.
o Lymphocytes.
o Plasma cells.
o Eosinophils.
o Mast cells.

Tissue destruction:

 Occurs due to,

o Inflammatory cells.
o Persistent infecting material.

Removal of damaged tissue(healing) :

 Occurs by proliferation of small blood vessels (angiogenesis).

 Proliferation of fibroblast(fibrosis-repair).