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Mechanisms of disease > Session 3 > Flashcards

Session 3 Flashcards

1
Q

What is chronic inflammation?

A

Chronic response to injury with associated fibrosis

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2
Q

In what three ways can chronic inflammation develop?

A

May ‘take over’ from acute inflammation if damage too severe to be resolved within a few days, may arise ‘de novo’, or may develop alongside acute inflammation in severe persistent/repeated irritation

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3
Q

What are the most important characteristic in chronic inflammation?

A

The type of cells present (chronic inflammation is much more heterogeneous than acute inflammation)

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4
Q

What cells are found in chronic inflammation?

A

Macrophages (derived from blood monocytes), lymphocytes, eosinophils, fibroblasts/myofibroblasts

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5
Q

What are macrophages derived from?

A

Blood monocytes

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6
Q

Describe the histological appearance of macrophages (blood monocytes)

A

Large, folded nucleus; grey/blue granular cytoplasm

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7
Q

Describe the difference in phagocytosis between macrophages and neutrophils

A

Macrophages are better with dead tissue, polymorphs are better with bacteria

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8
Q

What are the functions of macrophages?

A

Phagocytosis, antigen presentation, synthesis of cytokines, complement components, blood clotting factors and proteases (signalling), and the control of other cells by this cytokine release

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9
Q

What are the functions of lymphocytes?

A

Complex, mainly immunological; B cells produce antibodies (plasma cells), T cells are involved in the control of the immune action, and some cytotoxic actions. The presence of lymphocytes is not necessarily indicative of inflammation

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10
Q

How long does plasma cell appearance usually take in an immune reaction?

A

Around a week

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11
Q

What is the appearance of plasma cells likened to?

A

A clock-face

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12
Q

What situations are eosinophils commonly found in?

A

Allergic reactions, parasite infections, some tumours

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13
Q

What are the predominant cells in rheumatoid arthritis?

A

Plasma cells

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14
Q

What are the predominant cells in chronic gastritis?

A

Lymphocytes

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15
Q

What are the predominant cells in leishmaniasis (a protozoal infection)?

A

Macrophages

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16
Q

What are giant cells? What is the commonest theory for their formation?

A

Multinucleate cell made by the fusion of macrophages; frustrated phagocytosis

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17
Q

What are the three types of giant cells commonly seen?

A

Langhans, foreign body type, Touton

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18
Q

What are Langhans giant cells commonly seen in? Describe their structure

A

Tuberculosis (can be seen in other diseases); usually a horseshoe shaped nuclei arrangement, around granular cytoplasm

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19
Q

What is the function of foreign body type giant cells?

A

Prevent spread by localisation of foreign body

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20
Q

What situation are Touton giant cells commonly seen in?

A

Fat necrosis; the gat like foam is due to the emptiness of the cells

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21
Q

What are the four principle effects of chronic inflammation?

A

Fibrosis, impaired function (rarely increased), atrophy, stimulation of immune response

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22
Q

What is chronic cholecystitis?

A

Inflammation of gall bladder most commonly due to gallstone in cystic duct; the acute inflammatory response causes the gallstone to pop out, the gallstone blocks the duct again and the process continues

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23
Q

Why does chronic inflammation occur in cholecystitis?

A

The repeated acute inflammatory response results in chronic inflammation

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24
Q

Why does the wall of the gallbladder appear white in colour in cholecytitis? What is the normal colour?

A

Translucent; chronic inflammation results in formation of fibrous tissue

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25
Q

What does the cystic duct connect the gallbladder with?

A

The common bile duct

26
Q

What are some causes of acute gastritis and chronic gastritis respectively?

A

Acute: alcohol, drugs e.g. aspirin
Chronic: helicobactor pylori

27
Q

Why gastric ulceration occur?

A

Imbalance of acid production and mucosal defence, acid causes damage to the mucosa stimulating an acute inflammatory response forming an ulcer

28
Q

What is an ulcer?

A

An area of necrosis through the mucosa

29
Q

What is the potential result of an untreated gastric ulcer?

A

It can burn through the wall of the GI tract (perforation) allowing digestive juices and food to leech into the abdominal cavity

30
Q

What causes inflammatory bowel disease?

A

It is idiopathic

31
Q

With what two symptoms will a patient with inflammatory bowel disease commonly present?

A

Diarrhoea and rectal bleeding

32
Q

What is the typical site of ulcerative colitis?

A

Large intestine, however small intestine may show inflammation in some people

33
Q

How much of the bowel wall is affected by ulcerative colitis?

A

It is superficial and inflammation tends to be continuous throughout inflamed areas

34
Q

How does ulcerative colitis appear histologically?

A

No granulomas, mucosa ulcerated, crypt architecture distorted; presence of inflammatory cells

35
Q

What is the typical site of Crohn’s disease?

A

Inflammation can occur anywhere along the digestive tract, and tends to do so in patches

36
Q

Why is Crohn’s disease described as ‘transmural’?

A

It affects the full thickness of the bowel wall

37
Q

What does Crohn’s disease cause in the bowel?

A

Strictures, fistulae and cobblestoning

38
Q

What are ‘strictures’?

A

Narrowing of the bowel

39
Q

What are ‘fistulae’?

A

Connection between 2 mucosal surfaces that shouldn’t otherwise be linked

40
Q

What is cobblestoning?

A

Deep ulceration around surviving areas of mucosa, and the thickening of the mucosal wall; there is a distinct appearance

41
Q

What is a key indicator of Crohn’s in a biopsy?

A

Presence of granulomas

42
Q

What are possible treatments of inflammatory bowel disease?

A

Corticosteroids, anti-inflammatories, surgery

43
Q

What is cirrhosis a consequence of?

A

Chronic liver disease

44
Q

What are common causes of cirrhosis?

A

Alcohol, infection (hep B/C), immunological, fatty liver disease, drugs and toxins

45
Q

What is a typically seen in cirrhotic liver histology?

A

Nodules of fibrosed tissue, caused by damage to the architecture with attempted regeneration; there is disruption to blood flow as a result

46
Q

What is the pathophysiology of Grave’s disease?

A

Antibodies produce that stimulate TSH receptors, mimicking TSH; there is chronic inflammation

47
Q

Why can atrophy cause hypochloridia in the stomach?

A

Chronic inflammatory cells replace glands

48
Q

What is a granuloma?

A

Mixture of chronic inflammatory cells; macrophages (epitheloid histiocytes) group together and lymphocytes (T cells predominate) are usually associated

49
Q

What are the main causes of granulomatous inflammation

A

Mildly irritant ‘foreign’ material, infections, unknown causes

50
Q

Why do granulomas arise?

A

Persistent, low grade antigenic stimulation

51
Q

Name three diseases in which the cause of granulomatous inflammation is unknown?

A

Sarcoidosis, Wegener’s granulomatosis, and Crohn’s (around 50% of cases have granulomas)

52
Q

Which common vaccination results in the formation of a granuloma?

A

BCG (for tuberculosis)

53
Q

What causes sarcoidosis?

A

It is idiopathic

54
Q

What structures does sarcoidosis affect?

A

Lungs, lymph nodes

55
Q

What are the granulomas like in sarcoidosis?

A

Beautiful! Neat, tight groups of macrophages (non-caseating)

56
Q

Why do giant cells form with tuberculosis?

A

The organism is very resistant to phagocytosis by macrophages

57
Q

How does tuberculosis cause disease?

A

Persistence and induction of cell-mediated immunity; granulomas are a localisation of this and last for a very long time

58
Q

What do tuberculosis granulomas contain?

A

Central caseous necrosis, macrophages (epitheloid histiocytes), lymphocytes and Langhans type giant cells

59
Q

What is tuberculosis empymena?

A

Infection of pleural space caused by tuberculosis

60
Q

Why can tuberculosis be seen on an X-ray?

A

It causes fibrosis and scarring in the lungs?

61
Q

What is tuberculosis called when it affects many organs?

A

Miliary tuberculosis

Mechanisms of disease (3 decks)

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