Lecture 8 (P) PDF

Lecture 3 PMED-DENT-PHRM Pathology Team By the end of this session students should be able to: ◦ Discuss briefly the plasma derived chemical mediators of inflammation. Session’s Objectives ◦ Enumerate the morphologic patterns of inflammation, and its systemic effects. ◦ List the outcomes of acute in...

Lecture 3 PMED-DENT-PHRM Pathology Team By the end of this session students should be able to: ◦ Discuss briefly the plasma derived chemical mediators of inflammation. Session’s Objectives ◦ Enumerate the morphologic patterns of inflammation, and its systemic effects. ◦ List the outcomes of acute inflammation. ◦ Discuss inflammation induced injury. 1. Complement System: ◦ Consists of 20 circulating proteins. Plasma Derived Mediators: ◦ Activation is initiated by microorganisms. ◦ Their activation produces membrane attack complex (MAC), which can destroy invading microorganisms. ◦ C3a & C5a are anaphylotoxins and act in anaphylaxis or shock. ◦ C5b – 9 is membrane attack complex (MAC). Plasma Derived Mediators: 2. Coagulation cascade & fibrinolytic cascade: ◦ All these are triggered on by Hageman Factor i.e. Factor XII. ◦ Bradykinin has a role in inflammation and produces pain. EFFECTS MEDIATORS Vasodilation Prostaglandins, Nitric oxide Histamine Increased vascular permeability Pain Histamine and serotonin C3a and C5a Bradykinin Leukotrienes C4, D4, E4 PAF Substance P TNF, IL-1 Chemokines C3a, C5a Leukotriene B4 (Bacterial products, IL-1, TNF, Prostaglandins Prostaglandins, Bradykinin, Neuropeptide Tissue damage Lysosomal enzymes, Reactive oxygen species, Nitric oxide Leukocyte recruitment and activation Fever 1. SEROUS INFLAMMATION: Morphologic Types of Acute Inflammation: ◦ Response to mild injury, only fluid escapes into the tissue spaces. ◦ Example: Watery fluid in the blister of mildly burned skin. ◦ Serosal cavities - Effusion. Skin blister: Epidermis separated from the dermis by collection of serous effusion. Types of Acute Inflammation: 2. FIBRINOUS INFLAMMATION: ◦ Seen in severe injuries due to fibrinogen leak and fibrin deposition. ◦ Seen with inflammation in body cavities, such as meningies, pericardium & pleura ◦ Fibrin appears as eosinophilic mesh work. When incompletely removed leads to fibrosis (scarring). A: Deposits of fibrin on pericardium. B: A pink meshwork of fibrin exudate Fibrinous pericarditis with strands of stringy pale fibrin between visceral and parietal pericardium Types of Acute Inflammation: 3. PURULENT OR SUPPURATIVE INFLAMMATION: ◦ Large amount of purulent exudate (pus). ◦ Consists of neutrophils, necrotic cells. ◦ Staphlococcus Aures, fungi - Pyogenic organisms ◦ Localized suppuration – Abscess. ◦ Diffuse suppurative inflammation - Cellulitis. ◦ Ulcer is a local defect or excavation of the surface, produced by necrosis of cells and sloughing of inflammatory necrotic tissue. crater with an acute inflammatory exudate in the base. in the lung in bronchopneumonia. Abscess contains neutrophils & cellular debris. 4. HEMORRHAGIC INFLAMMATION: Types of Acute Inflammation: ◦ Large number of RBCs in the inflammatory exudate. ◦ Hemosiderin laden macrophages are seen. 1. RESOLUTION: ◦ Seen in short lived injury with minimal tissue damage. Outcomes of Acute Inflammation: ◦ Outcome is complete restoration of tissue histologically & functionally. ◦ Involves: ◦ Neutralization of chemical mediators ◦ ◦ ◦ ◦ Return of normal vascular permeability Cessation of leukocytic infiltration Death of neutrophils Removal of edema, proteins, leukocytes, necrotic debris by phagocytes Events in the Process of Resolution 2. Progression to chronic inflammation: Outcomes of Acute Inflammation: ◦ If the offending agent is not removed chronic inflammation follows. 3. Scarring and fibrosis: ◦ Seen after extensive tissue destruction or when inflammation occurs in tissues which do not regenerate. Outcomes of Acute Inflammation Summary