Patology. Inflammation (1) inflammations. Inflammations, regeneration, repair, and scarring. lecture 2

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1 Patology Inflammations, regeneration, repair, and scarring lecture 2 prof dr hab. n. med. Andrzej Marszałek Inflammation (1) inflammations is a complex reaction to injurious agents such as microbes, chemical or physical agents and damaged (usually necrotic) cells that consists of: vascular responses migration and activation of leukocytes and systemic reactions release of madiators of inflammation (IL-1/TNF, IL-6, C-reactive protein, histamine) -itis gastritis, hepatitis, dermatitis, appendicitis, colitis

2 Inflammation (2) the unique feature of the inflammatory process is the reaction of the blood vessels, leading to the accumulation of fluid and leukocytes in extravascular tissue the inflammatory response is closely intertwined with the process of repair: regeneration scarring or combination of those two (most commonly) Inflammation (3) acute i. is a rapid onset (seconds or minutes) and is of relatively short duration, lasting for minutes, several hours, or a few days chronic i. is of longer duration and is associated histologically with the presence of: lymphocytes and macrophages the proliferation of blood vessels the proliferation of fibroblasts and tissue necrosis Inflammation (4) Clinical signs of i. rubor - redness calor - heat tumor - swelling dolor - pain functio laesa - impaired function steps of i. 1. Initiation 2. Amplification 3. Termination Inflammation (5)

3 Inflammation (6) Types of outcome: Resolution (ideal) - normal tissue architecture and physiologic function are restored Abscess - the area is walled off, and additionally we can observed accumulation of inflammatory cells and tissue destruction Scar - despite elimination of the initial pathogen, the normal tissue is replaced by scar Persistent inflammation - elimination of pathologic insult fails and can be associated with a cellmediated immune reaction acute inflammation Ac. inflammation Inflammatory edema - one of the earliest responses to tissue injury alterations within microvasculature may promote fluid accumulation in tissue Ac. inflammation Important steps: transient vasoconstriction of arterioles (seconds to minutes) is mediated by neurogenic and chemical mediators vasodilatation of precapillary arterioles is known as a hyperemia; caused by release of specific mediators; redness and warmth an increase in the permeability of the endothelial call barier (minutes - hours) leakage of fluids edema

4 Ac. inflammation Important steps: transient vasoconstriction of arterioles (seconds to minutes) is mediated by neurogenic and chemical mediators vasodilatation of precapillary arterioles is known as a hyperemia; caused by release of specific mediators; redness and warmth an increase in the permeability of the endothelial call barier (minutes - hours) leakage of fluids edema Selektyny: - L-selektyny (CD62L) limfocyty i inne leukocyty - E-selektyny śródbłonki (po aktywacji przez cytokiny) - P-selektyny wiążą neutrofile, limfocyty T oraz monocyty Chr. inflammation chronic inflammation Inflammation of prolonged duration (weeks or months) in which active inflammation, tissue destruction, and attempts at repair are proceeding simultaneously. In this type of inflammation usually macrophages, lymphocytes and plama cells predominate.

granulomatous inflammation foreign body type granulomas: epithelioid cell type granulomas: healing around sutures around talc periapical granuloma tuberculosis lepra

results in repair and the replacement of dead or damaged cells by healthy cells.

5 granulomatous inflammation foreign body type granulomas: epithelioid cell type granulomas: healing around sutures around talc periapical granuloma tuberculosis lepra syphilis cat scratch disease tularemia sarcoidosis berylosis Healing process induced by local injury, begins very early in the process of inflammation and in the end results in repair and the replacement of dead or damaged cells by healthy cells. 1) regeneration (parenchymal cells, epithelial tissue) 2) replacement by the connective tissue. labile cells: surface epithelia lining mucosa of excretory ducts/glands columnar epithelium transitional epithelium splenic, lymphoid, hematopoetic tissue

6 permanent cells: nerve cells skeletal muscle cardiac muscle stabile cells (normally do not replicate) liver kidney pancrease osteoblasts chondroblats vascular endothelium repair by the connective tissue repair tissue injury Neutrophils necrotic debris (dead parenchymal cells, dead neutrophils) survived organisms (24-48hrs) macrophages (3-5d)proliferation of: fibroblasts endothelial cells formation of granulation tissue (histology def.: proliferation of new small blood vessels and fibroblasts)

7 histology: 1) neovascularisation 2) fibroblasts: RER (synthesis of proteoglycans, collagen) myofibroblasts (acquire features of smooth muscle cells) 3) macrophages are ridding area of: extracellular debris fibrin foreign mater 4) neutrophils 5) eosinophils 6) lymphocytes extracellular constituents No. of active fibroblats No of new vessels (thrombosis, degeneration) FORMATION OF THE SCAR: (hist.: spindle-shaped fibroblasts, dens collagen, fragments of elastic tissue, extracellular matrix, few vessels) fibroblasts produce: collagen elastic fibers (elastin, elastic mcrofibrils) laminin proteoglycans GAGs hyaluronic acid heparine chondroitin dermatan keratan heparan sulfate

Chronic inflammation. 07-Dec-15. Macrophage Tissue destruction

Chronic inflammation. 07-Dec-15. Macrophage Tissue destruction Chronic inflammation DR. M. TARIQ JAVED PROFESSOR DEPARTMENT OF PATHOLOGY FACULTY OF VETERINARY SCIENCE UNIVERSITY OF AGRICULTURE, FAISALABAD. Other types of cells present B & T lymphocytes (antibody and