Chronic Inflammation (7) Flashcards Preview

EMS - Mechanisms of Disease > Chronic Inflammation (7) > Flashcards

Flashcards in Chronic Inflammation (7) Deck (51):
1

Inflammation

A protective response involving host cells, blood vessels and proteins

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Purpose of inflammation is

Remove the cause of injury, remove necrosis and initiate repair

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Problem with inflammation

Can be inappropriate and damage nearby tissues and be destructive

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Onset of acute inflammation

Fast onset - mins-hours

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Onset of chronic inflammation

Slow onset - days

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Which cells primarily involved in acute inflammation?

Neutrophils

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Which cells primarily involved in chronic inflammation?

Macrophages, plasma cells and lymphocytes

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Are the signs of acute or chronic inflammation more prominent?

Acute

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How severe is acute inflammation?

Mild, self-limiting tissue injury

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How severe is chronic inflammation?

Severe, progressive

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Infections that cause chronic inflammation

TB and leprosy

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Endogenous materials that cause chronic inflammation

Have an internal original e.g. necrotic adipose tissue, uric acid crystals

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Exogenous materials that cause chronic inflammation

External origin e.g. asbestos fibres, sutures, implanted prostheses

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Autoimmune disease that cause chronic inflammation

RA, SLE, pernicious anaemia

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Primary granulomatous diseases that cause chronic inflammation

Crohns, sarcoidosis

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Acute > Chronic

Most common in supportive (pus forming) acute inflammation, if deep enough walls thicken, granulation and fibrous tissue and recurrent acute

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Cholecystitis

Gall bladder inflammation - due to stones

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Morphological features

Infiltration with mononuclear cells (macrophages, lymphocytes, plasma cells), tissue destruction, healing by fibrosis

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Macroscopical features - chronic peptic ulcer

Mucosal breach, granulation tissue base, fibrous tissue extends through wall

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Macroscopical features

Chronic abscess cavity, granulomatous, fibrosis

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When is fibrosis prominent?

Once inflammatory infiltrate has stopped

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Crohns

Chronic inflammation with non-caseating granulomas, Diarrhoea, mucus, blood, weight loss, pain

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What does caseating mean?

Necrosis with conversion of damaged tissue into a soft substance

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Microscopically

Cellular infiltrate of lymphocytes, plasma cells and macrophages, production of new fibrous tissue from granulation, exudation of fluid not prominent

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Mast cells

Release histamine - increases permeability of blood vessels to WBCs and proteins

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Polymorphonuclear leukocytes/granulocytes

(Neutrophils, Basophils, Eosinophils, Mast cells) Eliminate microbes and dead tissues (acute)

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Neutrophils

Found in blood stream, most abundant phagocyte

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Eosinophils

Don't phagocytose, good antigen presenting cells

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Basophils

Produce histamine

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Injured basophils

Release prostaglandins - increase blood flow to infection site

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Macrophages/histiocytes

Increase inflammation, already at site of damage release cytokines signal to monocytes, monocytes enter damaged tissue from endothelium of blood vessel (leukocyte extravasion), proliferate locally in damaged tissue, immobilisation

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What is released from phagocytosis?

Proteases

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What are proteases stimulated by?

Low oxygen content > induce angiogenesis and cells to re-epitheliase the wound and create granulation tissue

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Granulation tissue

New connective tissue and blood vessels that form on surface of wound during healing, grows from base up (light red/pink due to capillaries)

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Wound healing

Repair by replacement of injured tissues by fibrous tissues - granulation tissue, angiogenesis, fibroblasts deposit collagen and inflammatory cells

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Fibrosis

Formation of excess fibrous connective during repair, scarring, macrophage induced laying down of connective tissue (collagen)

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Fibroma

If fibrous tissue arises from 1 cell line

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Granuloma

Aggregate/nodule of epithelioid histiocytes, lymphocytes, histolytic giant cells

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Epitheliod histiocytes

Large vesicular nuclei and eosinophilic cytoplasm, in clusters, secrete angiotensin converting enzyme

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Histiocytic giant cells

Form where material is indigestible to macrophages, multinucleate (>100) giant cells, not phagocytic

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Example of when histolytic giant cells form

Tubercle bacilli - cell walls resistant to macrophages

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Granuloma

Can be considered collection of macrophages

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Langhans giant cells

Horseshoe arrangement of peripheral nuclei (TB)

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Foreign body giant cells

Large cells, randomly scattered nuclei

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Examples of granulomatous inflammation

Bacterial - TB, leprosy
Parasitic - Schistosomiasis
Fungal - Cryptococcus
Synthetic materials - Silicosis
Sarcoidosis, Crohn's

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TB

Night sweats, weight loss, haemoptysis, cough, caseous (cheese-like) necrosis, TNFa and INF-y important information and function of granuloma

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Leprosy

Granulomas of nerve, respiratory tract, skin and eyes > loss of pain sensation, weakness, poor eyesight

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Silicosis

Occupational lung disease from inhailing silica dust, forms scarring and granulomas in upper lobes of lungs

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Sarcoidosis

Granulomas form in multiple organs (lungs and lymph nodes), fatigue, weight loss, joint aches and pains, cough, bilateral hilar lymphadenopathy

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Inflammation in common diseases

MI, atheroma formation, MS (plasma cells and T seen in white matter where macrophages break down myelin)

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Clinical outcomes of chronic inflammation

Persistence of infection, prolonged exposure to toxic agents, autoimmune disease