Acute Inflammation

Living tissues are characterized by:

1. Reproduction.

2. Reaction to injury.

Reaction to injury could be generalized or localized.

Generalized reactions include:

1. Hormonal reaction.

2. Neural reaction.

3. Metabolic.

4. Proliferative e.g. leukocytosis.

• Local reaction is called inflammation or vital reaction.

• Inflammare: to set on fire “Latin”.

• Conventionally it was divided into three types depending on duration of the

inflammatory process:

1. Acute: Days.

2. Subacute: Weeks.

3. Chronic: Months & yrs.

• Classification of inflammation, nowadays, depends on cellular components,

rather than duration.

Acute inflammation:

Local vascular response of a living tissue to injury.

• It is induced & controlled by chemical mediators.
 • Tissue + itis. Eg……….

Aetiology:
1. Chemical injury: Acids, bases, phenols, etc.

2. Physical injury: Trauma, heat, cold, electricity, radiation, etc.

3. Microbial injury: Micro organisms like bacteria, viruses & fungi.

4. Immunological injury: Ag-Ab complexes, allergic reaction, etc.

5. Injury associated with necrosis.

Cardinal signs:

1. Swelling “tumour”.

2. Hotness “calor”.

3. Pain “dolor”

4. Redness “rubor”

5. Loss of function.

Vascular Changes
1. Transient vasoconstriction followed by permanent vasodilatation, bringing
more blood into the area.

Mediated mainly by histamine & nitric oxide.

2. Increased hydrostatic pressure:

• Arteriolar end of capillaries:

32 to 60 mmHg.

• Venular end: From 12 to 30 mmHg.

• The osmotic pressure is 25 mmHg.

 • This forces fluids to pass out to the tissues.

3. Increased vascular permeability, Allowing passage of large proteins from

the intravascular compartment to the extra vascular compartment.

This will add excess protein to the fluid passing to tissue.

This protein rich fluid is called exudate & its protein content is usually more
than 3 gm/dl “usually 3.5 – 5 gm/dl”.

4. The lymphatic channels are widely open to accommodate the exudated

fluids.

5. The capillary endothelial cells contract & become covered with sticky
gelatinous layer.

6. The axial blood flow is lost & the cells become scattered haphazardly in the
capillary lumen.

7. Margination of the neutrophils:

The neutrophils polymorphs occupy the periphery of the capillary & some of them
will passively adhere to the gelatinous layer.

Later on the monocytes start marginating.

8. Emigration:

The stuck neutrophils start active amoeboid movement across the capillary wall to
reach the extravascular tissue.

The polymorphs are the most characteristic cells of acute inflammation.

Several hours later, the monocytes start emigration, called macrophages.

The neutrophils never go back to the intravascular compartment.

9. Chemotaxis:

Directional movement of leukocytes in response to a chemical gradient.

It enables the white cells to move towards the site of injury.

It is mediated by chemotaxins.

They react with cell receptors to stimulate movement of cells towards the injury.

Important chemotaxins include: Bacteria, dead tissues, C3a, C5a, C567 &
leukotrien B4.

Chemotaxis leads to accumulation of cells into the injury site.

The neutrophils are the dominant cells in acute inflammation.

Eosinophils predominate in allergic reactions & parasitic infections.

10.Phagocytosis:

Engulfment of particulate materials.

Opsonisation is necessary for phagocytosis of virulent organisms.

Opsonins include; immunoglobulins, fibronectin & some complement components.

Both neutrophils & macrophages are phagocytic cells.

The phagosome is lysed by lytic enzymes.

The macrophages are long living cells & can replenish their enzyme system.

The neutrophils are short living cells & cannot replenish their enzyme system,
therefore, they die with the lysis of the phagosome.

11.Demolition:

Is achieved by macrophages. They remove all tissue debris from the site of
inflammation.

Therefore, the macrophages are called scavenger cells.

Termination of acute inflammatory response

 The inflammatory response must be actively terminated when no longer
needed to prevent unnecessary damage to tissues.
 It is a complex process that is brought about by:

1. Cessation of chemical mediators. Mediators of inflammation have short half

lives, therefore, they are degraded shortly after release.

2. cholinergic neural impluses that inhibit production of TNF in macrophages.