Response to inflammation

Acute inflammation is the immediate and early response to an introus agent. This response which serves to control and eliminate the source of injury occurs in 2 phases.

1 Vascular phase = leads to an increase in blood flow and changes in the small blood vessels of the microcirculation

2 Cellular phase = leads to immigration of leukocytes from the microcirculation and their activation to eliminate the injurious agent.

Vascular Phase

            Vasoconstriction

                Vasodilation

Cellular Phase

Margination:	The process by which leukocytes slow their movement and accumulate along the endothelial surface. – line up on vessel
Emigration:	Leukocytes change shape and squeeze through interendothelial junctions into the extravascular space. – move thru vessels walls to injury
Chemotaxis:	The process by which migrate in response to a chemical signal. – drawn to injured cells
Phagocytosis :	Elimination of the injurious agents by cell eating – eats up bacteria and cellular debris by digesting it

 Chemical mediators of inflammatory response

Mast cell degranulation – increase capillary permeability, histamine seratonin

Mast cell synthesis – prostaglandins increase cap. perm stimulate pain and produce fever, leukotrienes initiate inflammatory response

Plasma proteases – plasma proteases Fibrinogen stimulates clot formation to seal the injured site Kinins and Complements stimulate pain and increase capillary permeabality

Vascular stage process : acute inflammation= changes in the small blood vessels, begins with the momentary vasoconstriction followed rapidly by vasodilation. Vasodilation involves the arterioles and venules with a resultant increased capillary blood flow causing heat and redness. (Two of the cardinal signs of inflammation.)

This is accompanied by an increase in vascular permeability with outpouring of protein rich fluid, termed exudate into the extravascular spaces. The loss of proteins reduces the capillary osmotic pressure and increase the intrastitial osmotic pressure. This coupled with an increase in capillary pressure causes the marked outflow of fluid and its accumulation of fluid in the tissue spaces producing swelling, pain and impaired function.  (Other cardinal signs of inflammation)

As fluid moves out of the vessels stagnation of flow and clotting of blood occurs, this aids in localizing the spread of infectious microorganisms.

Cellular stage

Cells involved with inflammation stimulate other cells They do this by secreting -          Lymphokines -          Interferon -          Interleukins

Movement of white blood cells or leukocytes into the area of injury 2 types of leukocytes participate in the acute inflammatory response: granulocytes and monocytes. Rapid response also requires the release of chemical mediators from tissue cells such as mast cells and microphages that are prepositioned in the tissues. - white blood cells enter the injured tissue à destroying infective organisms à removing damaged cells àreleasing more inflammatory mediators to control further inflammation and healing. Leukocytes enter the injured area (mainly neutrophils) à leukocytes express adhesive proteins à attach to the blood vessel lining à squeeze between the cells à follow the inflammatory mediators to the injured area.

Physiologic response

Local	Systemic
Redness Edema Heat Pain	Fever Leukocytosis Malaise (fatigue)

Mechanisms of fever (pyerexia)
1 release of endogenous pyrogen from inflammatory cells
2 resetting of the hypothalamic temperature set point to a higher level (prodome)
3 generation of hypothalamus-mediated responses that raise body temperature (chill)
4 development of fever with elevation of body temperature to new thermostatic set point
5 production of temperature lowering responses (flush and defervescence) and return of body temperature to a lower level.

Interleukin 1-s induce fever

Take temperature and pulse in case high temperature