, regeneration, Patology repair, and scarring

lecture 2

prof dr hab. n. med. Andrzej Marszałek

Inflammation (1)

• is a complex reaction to injurious agents such as microbes, chemical or physical agents and damaged (usually necrotic) cells that consists of: inflammations – vascular responses – migration and activation of leukocytes – and systemic reactions – release of madiators of (IL-1/TNF, IL-6, C-reactive protein, )

• -itis → gastritis, hepatitis, dermatitis, appendicitis, colitis

Inflammation (2) Inflammation (3)

• the unique feature of the inflammatory • acute i. process is the reaction of the blood – is a rapid onset (seconds or minutes) and is of vessels, leading to the accumulation of relatively short duration, lasting for minutes, several fluid and leukocytes in extravascular tissue hours, or a few days • the inflammatory response is closely • chronic i. intertwined with the process of repair: – is of longer duration and is associated histologically with the presence of: – regeneration • lymphocytes and – scarring • the proliferation of blood vessels – or combination of those two (most commonly) • the proliferation of fibroblasts • and tissue necrosis

1 Inflammation (4) Inflammation (5)

• Clinical signs of i. • steps of i. – rubor - redness – 1. Initiation – calor - heat – 2. Amplification – tumor - swelling – 3. Termination – dolor - pain – functio laesa - impaired function

Inflammation (6)

• Types of outcome: – Resolution (ideal) - normal tissue architecture and physiologic function are restored – Abscess - the area is walled off, and additionally we acute inflammation 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 cell- mediated immune reaction

Ac. inflammation Ac. inflammation

• Inflammatory edema - one of the earliest • Important steps: responses to tissue injury → alterations – transient vasoconstriction of arterioles (seconds to within microvasculature may promote minutes) → • is mediated by neurogenic and chemical mediators fluid accumulation in tissue – 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

2 Ac. inflammation

• Important steps: – transient vasoconstriction of arterioles (seconds to minutes) • is mediated by neurogenic and chemical mediators chronic inflammation – 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

Chr. inflammation granulomatous inflammation

• foreign body type • type • Inflammation of prolonged duration : (weeks or months) in which active granulomas: inflammation, tissue destruction, and attempts at repair are proceeding simultaneously.

– tuberculosis • In this type of inflammation usually – lepra – syphilis macrophages, lymphocytes and plama – around sutures – cat scratch disease cells predominate. – around talc – tularemia – periapical – sarcoidosis – berylosis

(inflammatio alterativa) (inflammatio serosa)

3 (inflammatio catarrhalis) (inflammatio fibrinosa)

(inflammatio purulenta) (inflammatio haemorrhagica)

(inflammatio gangrenosa) (inflammatio ulcerativa)

4 (inflammatio pseudomembranosa) (inflammatio proliferativa/productiva)

inflammatio granulomatosa

healing

Healing

• process induced by local injury, • labile cells: • begins very early in the process of – surface epithelia inflammation and in the end results in – lining mucosa of excretory ducts/glands repair and the replacement of dead or – columnar epithelium damaged cells by healthy cells. – transitional epithelium – 1) regeneration – splenic, lymphoid, hematopoetic tissue • (parenchymal cells, epithelial tissue) – 2) replacement by the connective tissue.

5 • permanent cells: • stabile cells (normally do not replicate) – nerve cells – liver – skeletal muscle – kidney – cardiac muscle – pancrease – osteoblasts – chondroblats – vascular endothelium

repair by the connective tissue

• tissue injury – → Neutrophils ↓ • necrotic debris repair (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)

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

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