Pathology Lecture 5: Acute Inflammation PDF

Pathology lecture (5) ACUTE INFLAMMATION  Pathology Local response of living vascularized connective tissue to injurious agents That brings cells & molecules of host defense from circulation to sites of injury. The suffix "itis" is adde...

Pathology lecture (5) ACUTE INFLAMMATION  Pathology Local response of living vascularized connective tissue to injurious agents That brings cells & molecules of host defense from circulation to sites of injury. The suffix "itis" is added to the organ to indicate its inflammation.  Appendicitis  Tonsillitis  Colitis 1. Destroy, dilute, remove or localize injurious agents. 2. Prepare the tissue for repair process 1. Bacteria 1. Physical irritants (trauma, excess heat, excess cold) 2. Viruses 2. Chemical irritants (strong acids or alkalies, toxins) 3. Fungi 3. Necrotic tissue 4. Parasites. 4. Immune mechanism (Ag/Ab reaction) Strong Mild Sudden Gradual Short Long Lymphocytes, plasma cells, Neutrophils and macrophages macrophages and giant cells. Followed by repair Associated with repair  Pathology  Necrosis.  Degeneration (sick cell).  a s irritant is at a maximum concentration.  as irritant is of lesser intensity.  Necrotic cells and degenerated cells release chemical substances called chemical mediators which help the vascular changes 1. Transient arteriolar vasoconstriction (for seconds) (by direct action of irritant) 2. Permanent arteriolar V.D --- increase blood flow to the area (action of chemical mediators (histamine) → redness & hotness. 3. Increased vascular permeability( widening of interendothelial gaps by direct injury of endothelium) → fluid exudate & swelling. 4. Slowing of blood flow (escape of plasma→⇧ blood viscosity (hemoconcentration). with escape of WBCs (leukocytes) from blood to tissue → cellular exudate.  Pathology  Accumulation of protein-rich fluid at the  Escape of leucocytes (neutrophils, area of inflammation macrophages) from blood into the area of inflammation 1- Dilutes the irritant specially chemical and  Phagocytosis. bacterial toxins. 2- Brings antibodies to the site of inflammation.  Accumulation of extracellular protein-rich  Accumulation of extracellular fluid due to fluid at the area of inflammation. any cause other than inflammation  Mainly due to increased capillary  Mainly due to increased hydrostatic permeability pressure  High protein content 4-8 gm%  Protein: Less than 4gm%  High Specific gravity.  Low specific gravity.  It clots on standing (fibrin content)  Does not clot on standing  It contains inflammatory cells.  Absent inflammatory cells Pathology  Leukocytes cross the peripheral plasmatic zone then stick to the endothelium of the venules forming a layer (margination)  Characteristic rolling movement of leucocytes along the endothelial surface (rolling) then Firm adhesion of leukocytes to endothelial cells.  The marginated cells then actively move outside the blood vessel through inter-endothelial gaps (emigration).  It is the directional movement of leucocytes towards the irritant within the area of acute inflammation by chemical substances (called chemotactic agents) e.g. complement system.  It is the recognition, engulfment & destruction of bacteria or necrotic tissue by phagocytic cells. The first cell appear in acute Produced by fusion of Macrophage/histiocytes inflammation macrophages Pathology 1) Redness due to V.D. 2) Hotness due to V.D. and increased blood flow. 3) Swelling due to presence of inflammatory exudate. 4) Pain and Tenderness due to:  Pressure of exudate on the sensory nerves.  Release of bradykinin & prostaglandins in inflammatory area. 5) Loss of function due to pain & tissue damage. 1) Fever 2) Leucocytosis: Chemical mediators as interleukin 1 (IL-1) & tumor necrosis factor (TNF). 3) Loss of appetite and weight