INFLAMMATION- TYPES, CAUSES, IMMUNE RESPONSE AND RECTIFYING METHODS

Inflammation is not a diseases but it is a process. Inflammation is a complex response to local injury or other trauma; it is characterized by redness, heat, swelling, and pain.It is immediate.It is non-specific defense. TYPES OF INFLAMMATION: Acute Inflammation Chronic Inflammation Acute Inflammation: Acute inflammation is a rapid response to an injurious agent that serves to deliver mediators of host defenseleukocytes and plasma proteinsto the site of injury. Causes- Acute: Infections (bacterial, viral, parasitic) and microbial toxins Trauma (blunt and penetrating) Physical and chemical agents (thermal injury, e.g., burns or frostbite; irradiation; some environmental chemicals) Tissue necrosis (from any cause) Foreign bodies (splinters, dirt, sutures) Immune reactions (also called hypersensitivity reactions)

Differences between normal and inflamed blood vessels

Process of acute inflammation: When a host encounters an injurious agent, such as an infectious microbe or dead cells, phagocytes that reside in all tissues try to get rid of these agents. At the same time, phagocytes and other host cells react to the presence of the foreign or abnormal substance by liberating cytokines, lipid messengers, and the various other mediators of inflammation. Some of these mediators act on endothelial cells in the vicinity and promote the efflux of plasma and the recruitment of circulating leukocytes to the site where the offending agent is located. As the injurious agent is eliminated and anti-inflammatory mechanisms become active, the process subsides and the host returns to a normal state of health. Acute is Characteristic by.. The redness (rubor), warmth (calor), and swelling (tumor) of caused by the increased blood flow and edema. pain Chronic Inflammation: Chronic inflammation is considered to be inflammation of prolonged duration (weeks or months) in which active inflammation, tissue destruction, and attempts at repair are proceeding simultaneously.It may cause tissue damage in some of the most common and disabling human diseases such as rheumatoid arthritis, atherosclerosis, tuberculosis, and chronic lung diseases. Chronic inflammation arises in the following settings: Durning, Persistent infections (ulcer, TB) Prolonged exposure to potentially toxic agents, either exogenous or endogenous (silica) Autoimmunity (RA, SLE)

Chronic inflammation is characteristic by.. Infiltration with mononuclear cells, which include macrophages, lymphocytes, and plasma cells. Tissue destruction, induced by the persistent offending agent or by the inflammatory cells. Attempts at healing by connective tissue replacement of damaged tissue, accomplished by proliferation of small blood vessels (angiogenesis) and, in particular, fibrosis. Local symptomatology of Inflammation: Classical 5 symptoms (Celsus 1st c. B.C., Virchow 19th c. A.D.) 1. calor - heat 2. rubor - redness 3. tumor - swelling 4. dolor - pain 5. function laesa - loss (or impairment) of function Systemic symptomatology of Inflammation: Fever (irritation of centre of thermoregulation) TNF, IL-1 IL-6 high erythrocyte sedimentation rate Leucocytosis - increased number of WBC bacteria neutrophils parasites eosinophils viruses - lymphocytosis Leucopenia - decreased number of WBC viral infections, salmonella infections, rickettsiosis Immunologic reactions - increased level of some substances (C-reactive protein)

Process of Inflammation: When there is injury, the aterioles (minute blood vessels) in the surrounding tissue dilate (widen). This allows an increased blood flow to the area (redness). Vasoactive substances also increases the permeability (increase pore size) of these arterioles which allows blood cells, chemical mediators, blood proteins and fluid to accumulate in the area. This fluid accumulation causes swelling and may compress nerves in the area resulting in pain. Furthermore, the main chemical mediators of inflammation like prostaglandins, which are produced by cells, may also cause irritation of the nerves and further contribute to pain.

Table 34. Types of Acute Inflammation.

Type
Classic type

Features
Hyperemia; exudation with fibrin and neutrophils; neutrophil leukocytosis in blood. Paucity of neutrophils in exudate; lymphocytes and plasma cells predominant; neutropenia, lymphocytosis in blood.

Common Causes
Bacterial infections; response to cell necrosis of any cause. Viral and rickettsial infections (immune response contributes).

Acute inflammation without neutrophils

Allergic acute inflammation

Serous inflammation (inflammation in body cavities) Catarrhal inflammation (inflammation of mucous membranes) Fibrinous inflammation Necrotizing inflammation, hemorrhagic inflammation Membranous (pseudomembranou s) inflammation

Marked edema and numerous eosinophils; eosinophilia in blood.

Marked fluid exudation.

Certain hypersensitivity immune reactions

Burns; many bacterial infections.

Marked secretion of mucus.

Infections, eg, common cold (rhinovirus); allergy (eg, hay fever).

Excess fibrin formation. Marked tissue necrosis and hemorrhage.

Many virulent bacterial infections. Highly virulent organisms (bacterial, viral, fungal), eg, plague (Yersinia pestis), anthrax (Bacillus anthracis), herpes simplex encephalitis, mucormycosis. Toxigenic bacteria, eg, diphtheria bacillus (Corynebacterium diphtheriae) and Clostridium difficile.

Necrotizing inflammation involving mucous membranes. The necrotic mucosa and inflammatory exudate form an adherent membrane on the mucosal surface. Exaggerated neutrophil response and liquefactive necrosis of parenchymal cells; pus formation. Marked neutrophil leukocytosis in blood.

Suppurative (purulent) inflammation

Pyogenic bacteria, eg, staphylococci, streptococci, gramnegative bacilli, anaerobes.

Patterns of acute and chronic inflammation: Serous Watery, protein-poor effusion (e.g., blister) Fibrinous Fibrin accumulation Either entirely removed or becomes fibrotic Suppurative Presence of pus (pyogenic staph spp.) Often walled-off if persistent Ulceration

Immune Response Cells involved in inflammation: Leukocytes Neutrophils Macrophages Eoisnophils Basophils Neutrophils: Account for 67% of WBC Function: Phagocytosis of foreign particles Mature neutrophils are called segs, polys. Immature neutrophils are called band, stabs. They are the first line of defense. They take 12 14 days to mature. Only live about 12 14 days. Only take part in one episode of phagocytosis.

Monocytes: 3% of WBC. When matured they are called macrophages. Can live for months to year. Can be involved in multiple episodes in phagocytosis. Eosinophils: 1.5% of WBC Main Function: to release chemicals which control inflammation. Elevated in allergic reactions/ parasitic Infection. Basophils: .5% of WBC They are non phagocytic cells that function by releasing specific compounds from their cytoplamic granules. They are histamine, prostaglandins, serotonin and leukotrienes.

Treatment for Inflammation: Once the cause of the injury has been neutralized or the integrity of the living tissue has been secured, inflammation gradually subsides.Inflammation is a process and not a disease, however it may require treatment if it continues to persist. Drugs involved in treatment as follows: NSAIDs (Non-Steroidal Anti inflammatory Drugs): These drugs, like paracetamol, usually act by inhibiting the cells from producing prostaglandins, the main chemical mediator of inflammation. Corticosteroids: Steroids also inhibit prostaglandin formation by the cells as well as inhibiting the function of white blood cells which play an essential role in the inflammatory process.

Anti-Histamines: Histamine is a chemical produced by the white blood cells like basophils and mast cells and is usually secreted in allergic responses. Histamine causes local inflammation and an antihistamine drug blocks basophils and mast cells from producing and secreting histamine. Hot & Cold Therapy: Cold applications cause constriction (narrowing) of the blood vessels thereby inhibiting inflammation.Hot applications usually aggravate (worsen) inflammation but may help with easing the cause of inflammation like spasms or cramping of muscles. Major drug prescribed by physicians involves: CROMOGLICATE NEDOCROMIL SODIUM COLCHICINE Functions of Inflammation: Destroy and remove pathogens If destruction is not possible, to limit effects by confining the pathogen and its products.

Repair and replace tissue damaged by pathogen and its products.