Pathophysiology For Pharmacy students

Classification Several points of view Length: acute × chronic (+ subacute, hyperacute) According to predominant component 1. alterative (predominance of necrosis - diphtheria) 2. exudative (pleuritis) 3. proliferative (cholecystitis - thickening of the wall by fibrous tissue) According to histological features nonspecific (not possible to trace the etiology) - vast majority specific (e.g. TB) According to causative agent aseptic (sterile) - chemical substances, radiation septic (caused by living organisms) - inflammation has a protective character

Causes of inflammation: •A. Exogenous •Mechanical •Physical •Chemical •Biological trauma, surgery, infection, extremes of heat and cold, irradiation •B. Endogenous •Circulatory disorder, hypoxia (ischemia) •Endogenous protease release •Immune complex formation

Example of chemical mediators : 1- Histamine & serotonin → Mast cells , basophils & platelets 2- Lysosomal enzymes → monocytes 3- Prostaglandins → endothelial cells 4- Platelet activation factor → monocytes & platelets 5- O2 – free radical → leucocytes. 6- Colony stimulating factor → macrophage Q: what are the most important cells against inflammation ? In bacterial infection → neutrophils In viral infection → lymophocytes

Types and

Acute Inflammation

1. HYPERAEMIA Tissue injury damages cells, Mast cells and platelets release chemical mediators such as histamine, serotonin, prostaglandins and leukotrienes into the interstitial fluid and blood. These chemicals affect blood vessels and nerves in the area causing vasodilatation. HYPERAEMIA explains the classical signs of REDNESS and HEAT. Note: many anti-inflammatory drugs and antihistamines reduce the effects of some of these chemical mediators

2. Exudation Exudation is the increased passage of protein-rich fluid through the vessel wall into the interstitial tissue.

3- Emigration of leucocytes During the "cellular response leukocytes are attracted (by chemotaxis) to the area of inflammation as damaged cells release their contents. The chemicals at the site of injury act like magnets for cells. First neutrophils and later monocytes and macrophages collect along the capillary wall and then move through the wider separations in the wall into the interstitial area. There they destroy and remove foreign material, microorganisms, and cell debris by phagocytosis, thus preparing the site for healing.