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

Chronic Inflammation (7) Flashcards

1
Q

Inflammation

A

A protective response involving host cells, blood vessels and proteins

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2
Q

Purpose of inflammation is

A

Remove the cause of injury, remove necrosis and initiate repair

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3
Q

Problem with inflammation

A

Can be inappropriate and damage nearby tissues and be destructive

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4
Q

Onset of acute inflammation

A

Fast onset - mins-hours

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5
Q

Onset of chronic inflammation

A

Slow onset - days

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6
Q

Which cells primarily involved in acute inflammation?

A

Neutrophils

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7
Q

Which cells primarily involved in chronic inflammation?

A

Macrophages, plasma cells and lymphocytes

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8
Q

Are the signs of acute or chronic inflammation more prominent?

A

Acute

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9
Q

How severe is acute inflammation?

A

Mild, self-limiting tissue injury

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10
Q

How severe is chronic inflammation?

A

Severe, progressive

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11
Q

Infections that cause chronic inflammation

A

TB and leprosy

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12
Q

Endogenous materials that cause chronic inflammation

A

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

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13
Q

Exogenous materials that cause chronic inflammation

A

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

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14
Q

Autoimmune disease that cause chronic inflammation

A

RA, SLE, pernicious anaemia

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15
Q

Primary granulomatous diseases that cause chronic inflammation

A

Crohns, sarcoidosis

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16
Q

Acute > Chronic

A

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

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17
Q

Cholecystitis

A

Gall bladder inflammation - due to stones

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18
Q

Morphological features

A

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

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19
Q

Macroscopical features - chronic peptic ulcer

A

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

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20
Q

Macroscopical features

A

Chronic abscess cavity, granulomatous, fibrosis

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21
Q

When is fibrosis prominent?

A

Once inflammatory infiltrate has stopped

22
Q

Crohns

A

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

23
Q

What does caseating mean?

A

Necrosis with conversion of damaged tissue into a soft substance

24
Q

Microscopically

A

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

25
Q

Mast cells

A

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

26
Q

Polymorphonuclear leukocytes/granulocytes

A

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

27
Q

Neutrophils

A

Found in blood stream, most abundant phagocyte

28
Q

Eosinophils

A

Don’t phagocytose, good antigen presenting cells

29
Q

Basophils

A

Produce histamine

30
Q

Injured basophils

A

Release prostaglandins - increase blood flow to infection site

31
Q

Macrophages/histiocytes

A

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

32
Q

What is released from phagocytosis?

33
Q

What are proteases stimulated by?

A

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

34
Q

Granulation tissue

A

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

35
Q

Wound healing

A

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

36
Q

Fibrosis

A

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

37
Q

Fibroma

A

If fibrous tissue arises from 1 cell line

38
Q

Granuloma

A

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

39
Q

Epitheliod histiocytes

A

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

40
Q

Histiocytic giant cells

A

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

41
Q

Example of when histolytic giant cells form

A

Tubercle bacilli - cell walls resistant to macrophages

42
Q

Granuloma

A

Can be considered collection of macrophages

43
Q

Langhans giant cells

A

Horseshoe arrangement of peripheral nuclei (TB)

44
Q

Foreign body giant cells

A

Large cells, randomly scattered nuclei

45
Q

Examples of granulomatous inflammation

A 
Bacterial - TB, leprosy
Parasitic - Schistosomiasis
Fungal - Cryptococcus
Synthetic materials - Silicosis
Sarcoidosis, Crohn's
46
Q

TB

A

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

47
Q

Leprosy

A

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

48
Q

Silicosis

A

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

49
Q

Sarcoidosis

A

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

50
Q

Inflammation in common diseases

A

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

51
Q

Clinical outcomes of chronic inflammation

A

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

EMS - Mechanisms of Disease (21 decks)

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