Pathology Lecture: Types of Acute Inflammation PDF

Pathology lecture (7) TYPES OF ACUTE INFLAMMATION  Pathology –  Associated with pus formation  NOT associated with pus formation Caused by staphylococcus Aureus Caused by streptococci  Produce coagu...

Pathology lecture (7) TYPES OF ACUTE INFLAMMATION  Pathology –  Associated with pus formation  NOT associated with pus formation Caused by staphylococcus Aureus Caused by streptococci  Produce coagulase enzyme leads to fibrin  Produce hyalurinidase and streptokinase coagulation and deposition that help (fibrinolysin) that dissolve fibrin and help localization : spread : 1- Abscess. 1. Cellulitis 2- Furuncle (Boil). 2. Suppurative appendicitis. 3- Carbuncle. Severest form caused by strong pyrogenic bacteria as staphylococcus aureus and streptococcus haemolyticus 1. Strong pyogenic Bacteria cause marked necrosis 2. Attraction of large number of neutrophils that die due to high virulence of bacteria 3. Presence of sufficient amount of proteolytic enzymes Mainly produced by dead neutrophils (= pus cells) and to less extent by necrotic tissue make liquefaction of of necrotic tissue and fibrin Liquefied material mixed with pus cells and fluid exudate to form pus. Pathology  Localized suppurative inflammation resulting in the formation of an irregular pus-containing cavity.  Anywhere commonly subcutaneous (commonest) or deep organs  Early the abscess shows two zones, a central necrotic zone surrounded by a zone of acute inflammation containing large number of neutrophils then abscess then shows three zones: a- Central necrotic core. b- Mid zone containing pus, abscess cavity usually formed by 48 hours. c- Peripheral zone of inflamed tissue called pyogenic membrane. 1. The abscess enlarges by further necrosis and liquefaction of the surrounding inflamed zone until the staphylococci produce the coagulase enzyme which helps fibrin formation that localizes the inflammation. 2. A subcutaneous abscess appears as localized tender swelling covered by red edematous skin with opaque yellow center. 3. The covering epidermis may undergo necrosis and separates 4. (A slough is a separated necrotic tissue) and the pus is evacuated. an ulcer is formed. 5. An internal abscess as lung, liver or kidney opens in a hollow organ as in bronchi, ureter, intestine Pathology 1- Small abscess:  Pus may be absorbed and followed by healing. 2- Large abscess:  Pus is very slowly absorbed & its high osmotic pressure absorb water & increase in size → throbbing pain.  If not surgically evacuated, pointing & rupture occur (spontaneous evacuation) on the skin or hollow organs of abscess of internal organs followed by healing by 2ry intention. 1- Ulcer 2- Sinus 3- Fistula 4- Hemorrhage Keloid (excessive projecting scar).  Surrounded by fibrosis, the pus dries with addition of cholesterol crystals & dystrophic calcification may occur. e.g. chronic breast abscess.  lead to enlargement of the abscess.  leads to lymphangitis & lymphadenitis.  Toxemia: Bacterial toxins circulating in the blood.  Septicemia: large No. of virulent bacteria with their toxins circulating in blood.  Pyemia: Multiple small abscesses caused by septic emboli derived from septic thrombi due to septic inflammation of a nearby vein (septic thrombophlebitis). Ulcers Keloid Sinus Fistula Pathology  Small abscess related to hair follicle, sebaceous or sweat gland.  Staphylococci.  Mainly hairy parts as face, axilla.  Multiple neighboring boils are called furunculosis.  Acute localized suppurative inflammation forming multiple communicating suppurative foci in the skin and S.C. fat discharging pus through several openings.  Staphylococci.  Common in diabetes  Areas where the skin and S.C. tissue are thick and tough as the back of the neck, scalp and buttocks.  When bacteria invade S.C. fat it will result in the formation of multiple communicating suppurative foci developing in the same way as the abscess.  The open on the surface at multiple points particularly at the base of hair follicles. Pathology  Acute diffuse suppuration inflammation.  streptococcus hemolyticus which produces two enzymes: 1. Fibrinolysin (streptokinase) enzyme: Dissolves fibrin. 2. Hyaluronidase enzyme: Dissolves hyaluronic acid of ground substances helping spread of bacteria.  Loose connective tissue as areaolar tissue of orbit, scrotum & wall of appendix.  Lymphatic spread: leads to acute lymphangitis and lymphadenitis.  Blood spread: leads to septicemia and pyemia.  Thin and bloody  Contains many sloughs (necrotic depris) due to more necrosis Pathology  In skin blister after burnwith  Excess watery fluid exudate. watery vesicles are seen/ skin  Poor in fibrin vesicles due to viral infection  Excess fluid exudate rich in  Serous membranes as pleura, fibrin peritoneum and pericardium  hypersensitivity eg urticaria,  Fluid exudate rich in bronchial asthma, allergic eosinophil's rhinitis, contact dermatitis Pathology  excess mucous secretion.  Catarrhal rhinitis  Pseudomembrane consisting of fibrin, desquamated epithelium and inflammatory cells  Diphtheria  Complications :  Bacillary dysentery caused by 1. Toxemia most common Shigella bacilli. 2. Suffocation by detached membranes as in Diphtheria  Vascular damage and  Meningococci. hemorrhage in the exudate  Oral mucosa in debilitated  Extensive tissue necrosis malnourished children