Learn about Inflammation PowerPoint Presentation

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Medical Pathology By Dr: Yara Shamikh

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Pathology Pathology: is the study of diseases. Diseases are the deviations from normal. The concept of diseases: For the pathologist: structural changes that are accompanied by functional changes. For a patient For a physician

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The Scope of Human Pathology Pathology deals with recognition of diseases, their causes (aetiology), and their progression. Pathologists study structural changes (gross, or microscopic), etiology and mechanisms of diseases (pathogenesis) Most diseases can be placed in one of these categories: Inflammatory Neoplastic Degenerative conditions Developmental conditions

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Inflammation Inflammation: Local defense and protective response against cell injury or irritation or Local vascular and cellular reaction, against an irritant. Irritating or injurious agents (Irritant) Living: Bacteria, Fungi, Virus, Parasite or their toxins Non-Living: Chemical Physical Mechanical Inflammation is designated by adding the suffix (itis) to the end of the name of the inflamed organ or tissue.

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Types of inflammation Acute inflammation 3) Chronic inflammation 2) Sub acute inflammation: rarely occur.

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1. Acute inflammation Microscopic signs: Inflammatory response Macroscopic signs: Symptoms 1) Redness: 2) Hotness: 3) Swelling: 4) Pain and tenderness: 5) Loss of function: 1. Local vascular change 2. Formation of inflammatory exudate

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Inflammatory response: (microscopic signs) Normal Inflammation First: Local vascular changes: 1. Initial temporary vasoconstriction for few seconds. 2. Active vasodilatation of arterioles and capillaries (by chemical mediators: Histamine) and passive dilatation of venules. Increase in capillary permeability (fluid exudate to the extravascular tissue) thus concentration of blood cells, slowing of blood flow (stasis) 3. Pavmentation: the margination of leukocytes.

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Second: Formation of inflammatory exudates: Immigration or infiltration of the various leukocytes, fluid and plasma proteins outside the blood vessels into the surrounding tissue without injury of the blood vessels. Leukocytes seem to leave the smallest blood vessels by inserting pseudopodia into the interendothelial junctions and sliding through the wall by amoeboid movement. This is also due to the increased capillary permeability caused by the high osmotic pressure of the surroundings. The early stages are marked by the predominance of polymorphs especially neutrophils migration, particularly when the inflammation is caused by pyogenic cocci, later on monocytes infiltration occurs. ****In some cases RBCs may also pass (Diapedesis)

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Function of inflammatory exudates 1- Dilute the invading microorganism and its toxins. 2- Bring antibodies through the plasma to the inflamed area. 3- Bring leukocytes that engulf the invading microorganisms. 4- Bring fibrinogen through the plasma, which is converted, to fibrin mesh, helping in trapping the microorganism and localize the infection.

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Blood stem cell

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Cells of inflammatory response 1) Polymorphonuclear leukocytes: are basophils, neutrophils and eosinophils; lobed nucleus and grainy cytoplasm (granulocyte). Microphages (small eaters) 2) Monocytes or histocytes: macrophages. (big eaters) 3) Lymphocytes: leukocyte of fundamental importance; they determine the specificity of the immune response to infectious microorganisms and other foreign substances. 4) Plasma cells: A type of immune cell that makes large amounts of a specific antibody, developed from activated B cells (Derived from lymphocytes originate in the bone marrow). It is a type of WBCs and also called plasmacyte.

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Neutrophil Eosinophil Basophil Lymphocyte Plasma cell Monocyte

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Monocytes Plasma cell Plasma cell

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Phagocytosis Process by which Phagocytic cell (microphages and macrophages) engulf and kill foreign particles (bacteria) Two main types of phagocytes: 1- Motile phagocytes found in the blood stream and migrate to the inflamed area (microphages) 2- Histocytes (macrophages) of the reticuloendothelial system (RES) which remove bacteria that escapes from the inflamed area.

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Normal cell

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Phagocytosis

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Phagocytosis

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Steps of Phagocytosis 1. Recognition 2. Ingestion- pseudopods engulf microbe through endocytosis 3. Vacuole Formation- vacuole contains microbe 4. Digestion- vacuole merges with enzymes to destroy microbes 5. Exocytosis- microbial debris is released

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It occurs in two subsequent stages 1. Ingestion of the m.o. 2. Intracellular killing of the m.o. (digestion): Increased glycolysis and the PH drop to 4 -4.5 As a result, the proteolytic enzymes, phagocytin, lysozyme and other hydrolytic enzymes (lipase, esterase, nuclease … etc.) are released and digest the ingested microorganism. Some species of bacteria e.g. tuberculosis are not killed within the phagocyte and even multiply within it.

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Ingestion stage Methods of Intracellular killing of the m.o. (digestion) Oxygen-dependent intracellular killing: Production of a superoxide. Use of the enzyme myeloperoxidase from neutrophil granules Oxygen-independent intracellular: 1. electrically charged proteins 2. lysozymes 3. lactoferrins 4. proteases and hydrolytic enzymes

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Chemotaxis Positive directional response to chemical stimuli (chemotactic subs) The migration of leukocytes (by amoeboid movement) toward the injurious agent and the injured cells due to chemical stimuli (chemotactic subs). Chemotactic subs: Exogenous (Specific): Polysaccharide secreted by m.o. Endogenous (General): Reaction product of the antigen-antibody reaction .

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Chemotaxis

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Types of acute inflammation (based on type of exudates) 1- Catarrhal inflammation: 2- Serous inflammation: 3- Fibrinous inflammation: 4- Membranous inflammation: 5- Hemorrhagic inflammation: 6- Gangrenous inflammation: 7- Allergic inflammation: 8- Suppurative or purulent inflammation:

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Lobar Pneumonia due to Streptococcus pneumonia is associated with massive fibrinous exudates in the lung alveoli. Pseudomembranous inflammation in diphtheria showing network of fibrin entangling inflammatory cells. Bacteria forming pseudo-membrane (left). 3. Fibrinous type: 4. Membranous type 5. Suppurative or purulent Pyemic abscess in myocardium. Abscess containing necrotic cell debris, colonies of bacteria, and large number of neutrophils, many of them degenerate. Myocardium is on the right.

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Suppurative or purulent inflammation Pus: thick fluid containing viable and necrotic polymorph and necrotic tissue Localized: ex. Abscess: Abscess is the localized collection of pus, commonly seen solid block of tissue - Example: dermis, liver, kidney, brain etc. Pus consists of partly or completely liquefied dead tissue mixed with dead or dying neutrophils and living or dead bacteria, formed of 3 zones Small abscess is called boil or furuncle Large one carbuncle Fistula 2. Diffused: Spreading of pus to adjacent areas e.g. cellulites occurring in subcutaneous tissue . Usually caused by streptococci.

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Abscess:

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Fate of acute inflammation 1- Resolution: exudates are reabsorbed and tissue becomes normal again. 2- Healing: by repair and regeneration. 3- Spread: through lymphatics or blood stream. 4- Chronicity

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Chronic inflammation: (granulomatous) Results from increased resistance of the causative agent to phagocytosis or the body defense mechanism is depressed. Shows lower vascular and exudative response The inflammatory cells are mainly macrophages, plasma cells, giant cells, lymphocytes, fibroblasts. Occurs in the form of granuloma. Chronic inflammation usually occur with granulomatous infections; e.g. leprosy, tuberculosis and fungal infections.

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Phagocytosis

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Acute inflammation