Lecture: Inflammation (Veterinary Medicine) - King Salman University - 20/10/2024 PDF

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King Salman International University

2024

Mohamed M.M. Metwally

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inflammation veterinary medicine pathology biology

Summary

These lecture notes from King Salman University, delivered on October 20, 2024, detail inflammation in veterinary medicine. It covers the different types, causes, and functions/responses of inflammation.

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Faculty of veterinary medicine Veterinary medicine program Lecture: Inflammation Dr: Mohamed M.M. Metwally Date: 20/ 10 /2024 Professor of veterinary pathology Definition Nomenclature Causes Functions Contents: Cla...

Faculty of veterinary medicine Veterinary medicine program Lecture: Inflammation Dr: Mohamed M.M. Metwally Date: 20/ 10 /2024 Professor of veterinary pathology Definition Nomenclature Causes Functions Contents: Classifications Types Acute inflammation Inflammatory cells Gross and microscopic picture Types Chronic Inflammatory cells inflammation Gross and microscopic picture ❑ Definition: Inflammation is a progressive reaction of vascularized living tissue to injury. - Inflammation comes from the root inflame, from the Latin word inflammare meaning " setting something on fire" ❑ Nomenclature: - - Inflammation of a specific organ or tissue is usually systematically signalized by adding the suffix "-itis" after the Latin name of the organ. E.g., dermatitis is inflammation of the skin, and hepatitis is inflammation of the liver. ▪ -itis: - is a word-forming element in medicine denoting "diseases characterized by inflammation" (inflammation of-). ▪ A few words denoting inflammation and do not end with the suffix -itis including pleurisy (inflammation of pleura), and pneumonia (inflammation of lung) ❑ Causes of inflammation; causes of inflammation are too many and include; 1. Infectious agents, bacteria, viruses, fungi, and parasites 2. Physical irritants, e.g., excessive heat or cold, ionizing radiation, heatstroke 3. Chemical irritants, e.g., caustic agents, poisons, venom 4. Nutritive irritants, e.g., ischemia- vitamin deficiencies 5. Endogenous causes, e.g., Hypersensitivity, and autoimmune reactions Functions of Inflammation - Inflammation is often a protective mechanism. Its main purposes are 1- Dilute, isolate, and eliminate the causative agent. 2- Repair tissue damage resulting from the injury. Without inflammation, animals would not survive their daily interactions with environmental microbes, foreign materials, and trauma and with degenerate, senescent, and neoplastic cells. Classification of inflammation - Inflammation could be classified according to: I. Distribution: - What is the location of the lesion within an organ ① Focal: - Single inflamed area within a tissue Size: Varies from 1 mm to several centimeters in diameter ② Multifocal: - Several foci are separated from one another by an intervening zone of relatively normal tissue Size: Variable. ③ Locally extensive (focally extensive): - Involvement of a considerable area within an organ. ④ Diffuse inflammation: - Involve all the tissue or organ in which the inflammation is present II. Severity (How severe is the inflammatory process?) - mild, moderate, and severe. III. Duration (How long does the inflammation persist?) ① Peracute inflammation - Usually caused by a potent stimulus, as in the cases of African swine fever, clostridial infection, Avian influenza, African horse sickness, and anthrax. - Usually, the animal has no time to respond morphologically (very short course) to a disease process (sudden death often occurs). - Lesions: usually include hyperemia, slight edema, hemorrhage, and few inflammatory cells. -N.B., Lesion is a pathologic structural change in the tissue derived from the Latin laesio "injury"). It includes macroscopic (gross) and microscopic changes. ② Acute inflammation Acute inflammation is a short-term process (a few hours to a few days) that usually appears within a few minutes or hours after exposure to the causative agent and progresses rapidly to resolution or chronic inflammation. - Lesions: A. Gross lesions Cardinal signs of inflammation 1. Redness (Rubor) 2. Hotness (Calor) 3. Swelling (Tumor) 4. Pain (Dolor) 5. Loss of function (Functiolaesa) B. Microscopic lesions 1. Vascular congestion 2. Leukocytic infiltration 3. Presence of exudate ① Redness (Rubor): The inflamed area usually appears red due to a great increase of blood in the inflamed part due to the dilatation of capillaries and arterioles with the opening of all collapsed capillaries (hyperemia). ② Hotness (calor): The inflamed area feels warmer than the adjacent normal area due to the increased metabolic rate of the inflamed area " as if it is catching fire’’. ③ Swelling (tumor): The inflamed area usually appears swollen due to hyperemia, and the formation of exudate. ④Pain (Dolor): The pain sensation in the inflamed area results from stimulation of the sensory nerve endings by: a. Pressure due to swelling. b. Irritated chemical mediators e.g., bradykinin. c. Changes in the Ph of the inflamed area. ⑤Loss of function (functiolaesa): The function of the inflamed area is decreased or abolished due to: 1. Pain 2. Tissue destruction 3. Mechanical disability B. Microscopic lesions (Microscopic picture of acute inflammation) 1. Vascular congestion; distension of blood vessels with blood 2. Leukocytic infiltration - it is the migration of blood leukocytes to the extravascular tissue in a cascade of processes including leukocyte margination, rolling, adhesion to the endothelial surface, and transendothelial cell migration. 3. Presence of exudate (inflammatory fluid) ❖ Acute inflation is of an exudative, and the character of exudate depends on the causative agent, the anatomic site, and the animal species. ❖ According to the character of exudate, most types of acute inflammation can be classified into: 1) Serous inflammation 2) Catarrhal inflation 3) Purulent (suppurative) inflammation 4) Hemorrhagic inflammation 5) Fibrinous inflammation 1. Serous inflammation - Grossly, the tissue contains excessive clear to slightly yellow, watery fluid that leaks from the tissue on the cut section or forms raised fluid-filled vesicles protruding above the surface. - Microscopically, fine granular or homogenous eosinophilic material within the tissue spaces (albumen) may be seen. 2. Catarrhal inflammation = This inflammation occurs in the digestive, respiratory, and urogenital tracts (mucous membranes) due to infectious and/or noninfectious agents. - Grossly, the surface or cut surface of affected tissue may be covered with or contain mucous (a clear to slightly opaque, thick gelatinous fluid). - Microscopically, hyperemia, leukocytic infiltration, and presence of mucin. 3. Purulent (suppurative) inflammation = Mostly caused by pyogenic bacteria. = Turpentine oil induces abscesses if injected I/M. = Suppurative means causing the production of pus. = Purulent means consisting of pus. - Grossly, the surfaces and/or connective tissues of affected organs are covered by or contain pus. In general, pus is a creamy fluid but varies in its consistency according to the causative agent and species due to the variance of the proteolytic enzymes present inside neutrophils (liquid in dogs, viscid in bovine, and caseous in birds). The color of pus varies from white, yellow, green, red, and black to blue according to the species of animal and type of bacteria; Strep. and Staph. usually produce white or yellow pus. Corynebacterium, particularly in bovine produces greenish pus. Pseudomonas aeroginosa produces bluish-green pus. Erythrocytes turn pus red. Hydrogen sulfide produced by saprophytic bacteria, as in hoof injury, turns the pus black. - Microscopically, pus appears as a deep bluish structure composed of numerous living and dead neutrophils, some red cells, necrotic tissue, and fibrin. N.B., the appearance of considerable numbers of neutrophils justifies a diagnosis of purulent inflammation. 4. Hemorrhagic inflammation = occurs due to severe irritants that induce severe vascular injury producing an exudate with a high erythrocyte content. ▪ Grossly, blood-colored material, sometimes fluid or semisolid appears on the surface or in the tissue spaces. N.B. blood whether as an exudate or as hemorrhage coming from the stomach or anterior portion of the intestine stains feces brown or black due to the formation of acid hematin but if it comes from the posterior portion (colon and rectum) will be bright red. ▪ Microscopically, RBCs are the main constituent of exudate. 5. Fibrinous inflammation = Characterized by exudation of fibrin-rich fluid. This response occurs due to severe irritants that induce severe endothelial cell injury which allows leakage of large molecular weight proteins such as fibrinogen which polymerizes outside of the vessels to fibrin that is deposited in the extracellular space. - Grossly, the surfaces of affected tissue are covered with a thick, stringy, elastic, white-gray to yellow exudate that can be removed from the surface of the tissue (in contrast to a fibrous response). ❖ Fibrinous pseudomembrane: It is a distinct film of fibrinous exudate on the inflamed surface, It may be; - 1. Croupous or pseudo-diphtheritic membrane: If the fibrinous exudate can be removed, leaving an intact mucosa. 2. Diphtheritic or fibrinonecrotic membrane: if the fibrinous exudate is difficult to be removed and leaves an ulcerated mucosa. - Microscopically, The stromal connective tissue or the mesothelial surfaces of the affected organ contains or is covered by fibrin which appears as an eosinophilic meshwork of threads or sometimes as an amorphous coagulum. Hemorrhagic inflammation Hemorrhage - The cardinal signs of inflammation are present - Absence of cardinal signs -The inflammatory cells are abundant - Normal number of leukocytes - The blood vessels are dilated - No dilated blood vessels - The degenerative and necrotic changes usually - The degenerative and necrotic changes are seen usually absent ③ Chronic inflammation - Chronic inflammation is inflammation of prolonged duration (weeks to months to years) and characterized by chronic inflammatory cell infiltration and fibroplasia. Causes: 1. Failure of the acute inflammatory response to eliminate the causative agent. 2. Repeated episodes of acute inflammation. 3. Unique biochemical characteristics and/or virulence factors in the causative agents. Gross picture: 1. Color: gray to white due to the infiltrates of macrophages and lymphocytes, proliferation of fibroblasts, and deposition of fibrous connective tissue. 2. Consistency: firm due to the proliferation of fibroblasts, and deposition of fibrous connective tissue, and the solidification of the exudate. 3. Shape: irregular due to a. Haphazard accumulation of leukocytes b. Fibrosis c. Contraction of the lesion by myofibroblasts within the fibrous connective tissue. Microscopic picture: a. Chronic inflammatory cell infiltrate: lymphocytes, macrophages, plasma cells, epithelioid cells, and sometimes multinucleate giant cells b. Fibroplasia: proliferation of fibroblasts and deposition of collagen. ❑ Neutrophils are the first type of leukocyte recruited into the Acute inflammatory cells inflammatory exudate and constitute the major cell type involved in suppurative inflammations. ❑ Mast cells are the initiator of the acute inflammatory response ❑ Eosinophils play a crucial role in allergic and parasitic ❑ Basophils play a critical role in allergic diseases diseases. Chronic inflammatory cells ❑ Epithelioid cells are larger than activated macrophages, having abundant cytoplasm but with diminished phagocytic ❑ Macrophages capacity. Their physiologic activity is poorly understood but is 1. The primary effectors in granulomatous inflammation suggested that their main function may be extracellular in granulomatous inflammation. secretion 2. Differentiate to epithelioid cells 3. Fuse to form multinucleate giant cells (MGCs). ❑ Multinucleated giant cells formed by fusing two or more activated macrophages into one large cell with two or ❑ Lymphocytes are the cornerstone of the adaptive more nuclei. immune response and the basis of immunological memory. ❖The main differences between acute and chronic inflammation Criteria Acute inflammation Chronic inflammation Duration Short Long Cardinal sings Present Usually, absent Inflammatory cells Neutrophils, eosinophils, Macrophages, lymphocytes, basophils, and sometimes plasma cells and sometimes lymphocytes, and/or MGCs macrophages Vascular changes Vasodilatation with increased Absent permeability Fluid exudate Present Usually, absent Fibroplasia Absent Present

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