Inflammation

 Definition and brief description of Inflammation 

Inflammation:-

·        Inflammation is response of vascular connective tissue towards injury but those tissue are not vascular they will not inflammation

·       Most of the tissue of body are vascular connective tissue

·         Aim of the inflammation is to defense from increase circulation ( wbc  ,leukocytes , antibodies  etc) to the site where they are needed to eliminate of injurious agent ,followed by removal of the necrosed cells and tissue.

·        the injurious agents causing inflammation may be under .

1)    Infective agents :-

Like bacteria,viruses and their toxins, fungi, parasites

2)    Tissue necrosis :-

Caused by various agent such as ischemia, physical agent (exp- heat cold radiation mechanical trauma ) chemical agent (exp - organic & inorganic toxins)

3)    Immunological agents :-

Like cells mediated antigen antibody reactions .

4)    Inert materials :-

Such as forgein bodies dirt matter , suture etc

Sign of inflammation :-

·         The word inflammation from the latin word inflamm are means fire/burning

Celsus ,A roman writter  in first centuary AD given the four sign of inflammation.

He said  “rubor et tumor cum colore et dolare”  

Which means redness and swelling with heat pain .

Where as

Rubor – redness          ,   colore – heat

Tumor - swelling         ,    dolare - pain

·         later  Rudolf Virchow  in 19^th centuary AD added 5^th sign”functio leara” means loss of function

Steps of inflammation response- 5R

1)      Recognition – of the injurious agents

2)      Recruitment – of inflammatory cells (leucocytes)

3)      Removal – of the injurious agent

4)      Regulation (control)  - of the inflammatory response

5)      Repair /resolution /healing

Types of inflammation :- 

·          Depending upon the defence capacity of the host and duration of response.

·         Main classification of inflammation is acute & chronic

·        Inflammation on the basis of organ.

1)      Dermitis

2)      Nephritis

3)      Glomerulo-nephritis

4)      Conjunctivitis

5)      Meningitis

6)      Myocitis

7)      Arthritis

8)      Hepatitis

      *   Inflammation on the basis of duration

1) acute inflammation`

2) chronic inflammation

1) Acute inflammation:-

Acute inflammation is a short duration  less than 2 weeks and represent the early body reaction ,resolves quickly healing.

2)Chronic inflammation :-

Longer duration & occurs after a delay

Either when the causative agent of acute inflammation persist for a long time .

 

 

Basic difference B/W acute & chronic inflammation:-

                                        Acute inflammation                          Chronic inflammation

Onset           .                           Rapid in min/hrs.                                         Slow , day ,week

Cells                                       Neutrophils                                            Lymphocytes , monocytes

Tissue  injury                         Mild self limited                                       Severe & Progressive

Sign- local & systemic                      Prominent                                       Less prominent

Acute  inflammatory Response :-

Acute inflammation mechanism divided by two process

     Vascular events                                                            Cellular events

1)      Alteration of micro -                                               1)Recruitment of leucocytes

vasculature caliber                                              at the site of infection     ( arterioles , capillaries.& venules )                                                                           and  increase blood flow

                ↓

2)      To bring cells and protein                                         2)after activation of

                 to the site of injury                                                          leukocytes which leading

                                                                                                            to the process of  

                                                                                                           destruction of invaders and

                                                      production of many chemical mediator       

  3)By vasodilation & increased  

vascular permeability

Acute Inflammation in vascular changes :-

Vascular changes again divided into two changes

1) changes in the vascular flow & caliber

2) Increased vascular permeability.

 

Fig

     

 

 

 

 

 

 

       1)Changes in Vascular flow & Caliber:-

           

                    Immediate transient vasoconstriction of arterioles

                                                ↓                                                                                              Persistent progressive vasodilation of arterioles  Elevate local hydrostatic

                        pressure &  deviate osmotic pressure .

                                                ↓

                     Endothelial cells swelling & separation

                                                ↓

                           Increase oozing of fluid (Tramudate)

                                                ↓

                                                Exudate

                                                ↓

                              Leucocytes start margination

                                                ↓

                                 Leucocytes  migration

 

 

2)increased vascular permeability :-

a) increased oozing out of fluid ,blood cells & protein from the blood vessels into interstitid tissue.

b) mechanism / causes of increased vascular permeability

1) contraction of endothelial cells and leads to intracellular gap in venules.

2) retraction of endothelial cells

3) direct damage to endothelial cells

4) endothelial injury due to leukocytes

5) leakage from new blood vessels/ increased transcytocin of protein.

1) contraction of endothelial cells and leads to intracellular gap in venules.

fig

 

 

 

 

                                                                                                                          

 

·        It is  most common among all

·        It occurs immediately and its short lived (few minutes)

·        Reversible , tramient & immediate short lived

·        Contraction performed by histamine ,bradykinin & leukotrinen.

·         2) retraction of endothelial cells

·         2) retraction of endothelial cells

 

2)    retraction of endothelial cells :-

·         it is reversible mechanism

·         retraction performed by cytokinin mediation TNF( tissue necrotic factor )&IL-1(interleukin-1)

 

3)    direct damage to endothelial cells :-

·         it’s seen in severe injuries (burn, toxins, infections etc)

·         direct injury to arterioles ,capillaries & venules

·         immediate start leakage & unstained response

·         cell necropsis and detachment occurs

·         it’s develop with 2-12  hrs & persist longer.

 

fig

 

 

 

 

 

(3) endothelial injury due to leukocytes:-

·         leucocyte may accumulate during inflammatory response

·         leucocyte adhering (adhesion) to endothelial cell

·         then leucocytes may release toxic oxygen species and proteolytic enzymes causing injury

·         its act in mostly venules ,pulmonary capillaries

·         it lived long.

(4) leakage from new blood vessels/ increased transcytocin of protein:-

Fig

 

 

 

 

 

 

 

·         leakage performed by VEGF( vascular endothelial growth factor)

·         here leakage can see at the site of new vessels formation and increase of vascular permeability either it natural or unnatural

·         at this site increase transport of fluid & proteins