Inflammation: Local Defense and Response

Study Notes

Living irritants include bacteria, fungi, viruses, parasites, and their toxins.
Non-living irritants include chemicals, physical agents, mechanical forces, and hypersensitivity reactions.

Acute inflammation: Rapid onset, short duration (minutes to days), characterized by fluid, plasma proteins, and neutrophils (PNL) in the tissue.
Subacute inflammation: Rarely occurs, intermediate between acute and chronic.
Chronic inflammation: Slow onset, longer duration (days to months), characterized by lymphocytes, plasma cells, macrophages, and fibroblasts in the tissue.

Polymorphonuclear leukocytes (PMNs): Neutrophils, which become pus cells when they die.
Monocytes or histocytes: Macrophages.
Giant cells: Formed by the fusion of macrophages.
Lymphocytes: B and T lymphocytes.
Plasma cells: Developed from activated B cells.
Eosinophils: Involved in allergic and parasitic infections.
Fibroblasts: Involved in tissue repair.

Local destruction of tissue: Necrosis in the area of maximal irritant concentration, leading to the release of chemical mediators like histamine.
Local vascular changes:
- Initial temporary vasoconstriction for a few seconds.
- Active vasodilatation of arterioles and capillaries (induced by histamine) and passive dilatation of venules.
- Increased capillary permeability (fluid exudate to the extravascular tissue), resulting in blood cell concentration and slowed blood flow (stasis).
- Pavementing and margination of leukocytes.
- Emigration of leukocytes, fluid, and plasma proteins outside the blood vessels into the surrounding tissue (forming inflammatory fluid exudate).
- In some cases, red blood cells may also pass through (Diapedesis).
- Dilatation of lymphatic vessels to accelerate lymph flow and drain fluid exudate.
Reaction of tissue histiocytes: Proliferation of tissue histocytes (normally present in connective tissue and organs) to phagocytose remaining bacteria, cellular debris, and fibrin.

Phagocytosis: neutrophils engulf and destroy microbes.
- Steps of phagocytosis include recognition, ingestion, vacuole formation, digestion, and exocytosis.
- Opsonins, like Fc and C3b receptors, aid in recognizing and binding microbes.

Redness: Caused by increased blood flow.
Hotness: Caused by increased blood flow.
Swelling: Caused by fluid exudate accumulating in the tissue.
Pain and tenderness: Caused by pressure on nerve endings by the swelling and by chemical mediators.
Loss of function: Caused by pain and swelling.

Fever: Caused by release of pyrogenic compounds and increased tissue metabolism.
Leucocytosis: Increase in white blood cell count above 10,000/cm3, caused by the liberation of leucocytosis promoting factor from injured tissue.
Toxic effects: Anorexia, headache, etc.

Suppurative or purulent inflammation: Characterized by pus formation (pus cells, neutrophils, and other debris).
- Localized: Abscesses (walled-off collections of pus)
- Diffuse: Cellulitis (widespread inflammation of subcutaneous tissue)
Non-suppurative inflammation:
- Catarrhal inflammation: Characterized by mucus production.
- Serous inflammation: Characterized by thin, watery fluid exudate.
- Fibrinous inflammation: Characterized by a fibrinous exudate (thick, sticky fluid).
- Membranous inflammation: Characterized by a membrane-like exudate (fibrin and inflammatory cells).
- Hemorrhagic inflammation: Characterized by bloody exudate.

May follow acute inflammation or begin chronically.
Results from increased resistance of the causative agent to phagocytosis or a depressed immune response.
Shows lower vascular and exudative responses compared to acute inflammation.
Characterized by an accumulation of lymphocytes, plasma cells, macrophages, and fibroblasts.

Characterized by the formation of granulomas.
Granulomas are specialized inflammatory structures that form when the body is unable to eliminate a foreign agent.
Common causes include tuberculosis, leprosy, and fungal infections.