Inflammation

Inflammation :

Mechanism of self defense. Latin word Inflammo = ignite.

The reaction of the living tissues to irritant or the reactive process which begins following sub lethal injury to tissue and ends with complete healing.

Irritant can be physical, chemical or biological agent. Physical like trauma, cold, heat and electricity. Chemical like acid , alkali or toxin. Biological microbes like bacteria, virus, parasites and fungus.

Cardinal signs of inflammation are given by Celsus are Rubor,  Calor, Dolar and sign funtio laesa was given by Galon.

Classification of Inflammation:

1.	According to the acuteness of onset, intensity of symptoms, duration of course
2.	Etiology
3.	Depending on location
4.	Extent of tissues involoved
5.	According to nature of exudates
6.	Based on sequelae or tissue changes

 

1.  According to the acuteness of onset, intensity of symptoms, duration of course:

A) Acute inflammation		B) Sub acute inflammation	C) Chronic Inflammation
Severe irritant			Mild irritant
Pronounced symptoms			Not so severe symptoms
Marked exudation			Least exudate
Neutrophils			Macrophages,Fibroblasts
			Characteristic feature is fibrous tissue formation.

2. Based on etiology

A) Exogenous			B)Endogenous
Physical	Chemical	Biological	Circulatory Disoders	Enzyme Activation	Metabolic Products
Eg: Mechanical Trauma,Heat,Cold, Electricity	Eg: Acid,Alkali, Toxins	Eg: Microbes like bacteria, virus,fungus, allergens and parasites	Eg: Thrombosis, Infarction, hemorrhage	Eg: Acute pancreatitis	Eg: Urea, uric acid.

 

 

3. Depending on the location:

A) Reactive	B) Metastatic
It is around a foreign body Eg: Traumatic pericarditis	It is produced at a distant part infection conveyed by blood or lymph. Eg: Streptococal Valvular Endocarditis

 

4. Extent of tissues involoved:

A) Focal	B) Diffused	C) Disseminated	D) Interstitial	E) Paranchymatous
In particular spot or area. Eg: Focal inflammatory disease of liver, Traumatic pericarditis, white matter lesions of brain.	Large area of interstitial and parenchmatous tissues involoved. Eg: Diffuse proliferative glomerulonephritis, Diffuse inflammatory bowel disease.	Large number of distinct foci. Eg: Haemolytic uremic syndrome, Disseminated gonococcal infection.	Primarily affects the stroma of an organ. Eg: Interstitial nephritis, Interstitial pneumonia in H.S.	It affects essential tissue parenchyma. Eg: Obstructive pulmonary disease in which small airways and lung parenchyma is involoved.

 

5. According to nature of exudates:

1. Serous inflammation	Only serous exudates in serous membranes like peritoneum or pleura. Or Simple blister by hot water.
2.Haemmorhagic infl.	RBC in exudates Eg. Haemmorhagic pneumonia or enteritis
3.Fibrinous(Croupus) infl.	Fibrin in exudates with bread butter appearance in Fibrinous pericarditis.
4. Purulent(Suppurative) infl.	Pus in exudates in purulent pleuritis.
5.Phlegmonous infl.	When pyogenic organisms are present in semipurulent or purulent exudates.
6.Catarrhal infl	Mucous membrane inflammation in sinusitis with discharge of mucous and epithelial debris.
7. Membranous(Diphtheritic) infl	Mucous membranes inflamed with false membrane formation in diphtheritic form of fowl pox.
8. Mucopurulent or Serofibrinous	Mucopurulent cervicitis by chlamydial infection. Acute serofibrinous pericarditis, or serofibrinous pleuritis or acute rheumatic heart disease.

 

 

 

6. Based on sequelae or tissue changes:

1. Adhesive infl.	Which bring the adhesion of opposing surfaces.Eg: Ischemic cerebrovasular disease.
2.Obliterative infl.	Infl. of lining membrane of a cavity or a vessel which causes adhesion between surfaces or obliteration of lumen. Eg: Brochiolitis obliterans lung disease in which airway is obstructed by inflammation, Atherosclerosis.
3.Hyperplastic infl.(Productive or proliferative infl)	Formation of new connective tissue in abundance.Eg: Inflammatory papillary hyperplasia and Nodular regenerative hyperplasia in Inflammatory bowel disease.
4. Atrophic infl.(cirrhotic, fibroid, sclerosing inf)	Infl resulting in atrophy and deformity. Eg: Cirrhotic liver in gin drinkers disease.
5.Granulomatous infl.(tumor like granulation tissue)	Infl of tissues resemble granulation tissue. Eg:Actinomyces or TB.
6. Necrotic infl.	Infl. With death of affected tissue. Eg: Inflammatory bowel disease, Ulcerative colitis.

 

Termination of inflammation:

1. Disappearance of symptoms,

2. Resolution of inflammation after irritant is removed,

3. Exudate absorbed by lymphatics,

4. Damaged cells phagocytosed.

5.Tissue regenerated or replaced by fibro connective tissue leading to fibrous thickening or induration.

6. In pyogenic inflammation pus formation takes place leading to abscess formation.

7. In severe inflammation massive tissue death occurs enmass leading to gangrene formation.

 

Mechanism which serve to terminate inflammation:

After entering tissues, granulocytes promote the switch of arachidonic acid– derived  prostaglandins and leukotrienes to lipoxins, which initiate the termination  sequence. Neutrophil recruitment thus ceases and programmed death by apoptosis is engaged. These events coincide with the biosynthesis, from omega-3 polyunsaturated fatty acids, of resolvins and protectins, which critically shorten the period of neutrophil infiltration by initiating  apoptosis. Consequently, apoptotic neutrophils undergo phagocytosis by macrophages, leading to  neutrophil clearance and release of anti-inflammatory and reparative cytokines such as transforming  growth factor-β1. The anti-inflammatory program ends with the departure of macrophages through the lymphatics

Short half-life of inflammatory mediators in vivo.

Production and release of Transforming growth factor (TGF) beta from macrophages^[18][19][20]

Production and release of Interleukin 10 (IL-10)^[21]

Production of anti-inflammatory lipoxins^[22]

Downregulation of pro-inflammatory molecules, such as leukotrienes.

Upregulation of anti-inflammatory molecules such as the Interleukin 1 receptor antagonist or the soluble tumor necrosis factor receptor (TNFR)

Apoptosis of pro-inflammatory cells^[23]

Outcome of inflammation:

A) Resolution	B) Fibrosis	C)Abscess formation	D) Chronic inflammation
Vasodilatation, Chemical production and leucocyte infiltration stops then parenchymatous tissue regenerates.	With large tissue destruction, tissue not regenerated leading to fibrous scarring with deposition of collagen there will be functional impairment.	A cavity is formed with pus which is opaque liquid with dead WBC and bacteria with general debris from destroyed cells.	If injurious agent persists it will lead to chronic inflammation.Inflammation will continue for many months leads to dominating presence of macrophages which are powerful defensive agents of the body. Macrophages release toxins like reactive oxygen species which are injurious to own tissues and also invading agents. Chronic inflammation always leads to tissue destruction.

 

 

 

Treatment of Inflammation:

1.  The irritant cause to be removed.

2.  Exudation suppressed by cold/Astringent application

3. Compression  and application of pressure bandages to minimize inflammatory swelling.

4. If tissue is threatened by gangrene, warm fomentation is advised, which improves proper circulation and resorbtion of exudates. Dry heat or moist heat is to be applied by heated bran/sand or hot water. Moist heat is soothening.

5. For superficial lesion local anaesthetic is applied.

6. Scarification to remove dead tissues leads to slight bleeding, to be covered by antiseptic preparation.

7. Septic inflammation requires antiseptic application, antibiotic therapy and Biers hyperemia.

8. Cortisones or NSAIDS as anti inflammatory agents to alleviate symptoms.

9. Anti inflammatory foods: Prostaglandins are hormone-like substances that affect the body in variety of ways, also regulating inflammatory mediation. An anti-flammatory diet includes less foods that create inflammation-causing prostaglandins (PGE2) in the body, and more foods that create anti-flammatory prostaglandins (PGE1 and PGE3).^[23]

Suggested diets to reduce inflammation include those rich in vegetables and low in simple carbohydrates and fats, such as saturated fatsand trans fats. Anti-inflammatory foods include most colorful fruits and vegetables, oily fish (which contain higher levels of omega-3 fatty acids), nuts, seeds, and certain spices, such as ginger. Extra-virgin olive oil contains the chemical oleocanthal that acts similarly to ibuprofen. Those following an anti-inflammatory diet will avoid refined oils and sugars, and show a preference for so-called anti-inflammatory foods in their meal choices.

10. Exercise:

Developing research has demonstrated that many of the benefits of exercise are mediated through the role of skeletal muscle as an endocrine organ. That is, contracting muscles release multiple substances known as myokines which promote the growth of new tissue, tissue repair, and various anti-inflammatory functions, which in turn reduce the risk of developing various inflammatory diseases.