Pathophysiology of Inflammatory Response

Etiology: Infection/ Mechanical Damage/

Ischemia/ Nutritional Deprivation/ Extremes Tissue Injury
Temperature/ Radiation/ etc.

Release of chemical
mediators (histamine, Release of
complement, kinins, leukocytosis-inducing
prostaglandins) factors

Vasodilation Increased Attract neutrophils,

capillary Leukocytosis
of arterioles monocytes & lymphocyte to
permeability area (chemotaxis) (increased of WBC
in blood stream)
Local hyperemia Capillaries leak
fluid (exudate Migration to
formation) injury area
Heat Redness
Increased Blood flow
oxygen & Leaked protein-rich slows
Leaked
Increased nutrients fluid in tissue Margination
clothing
temperature spaces (leukocytes cling to
proteins
increases metabolic capillary walls)
rate of cells
Pain Swelling
Walling-off process(blood clots Diapedesis (leukocytes pas
wall off area to prevent injury to through capillary walls)
surrounding area
Possible temporary limitation
of joint movement
Phagocytosis of pathogen & dead
Temporary fibrin tissue cells (by neutrophils, short
patch forms term; by macrophages, long term)
scaffolding for
repair Pus may
Area cleared of form
debris

Prepared by:
Czarina Sales, RN Healing
Student Name