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Semester 2 > MoD Session 3 > Flashcards

MoD Session 3 Flashcards

0
Q

How long can chronic inflammation last?

A

From hours to days

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1
Q

What is chronic inflammation?

A

Chronic response to injury w/associated fibrosis

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2
Q

What does chronic inflammation overlap with?

A

Host immunity

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3
Q

Is chronic inflammation homogenous or heterogenous?

A

Very heterogenous

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4
Q

How does acute insult lead to chronic inflammation?

A

Acute insult –> acute inflammation –> more than slight damage –> chronic inflammation

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5
Q

What is the result of chronic insult and more than slight damage from acute insult?

A

Repair and scarring

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6
Q

How does chronic inflammation arise?

A

Take over form acute inflammation of damage cannot be resolved in a few days
De novo
Develop alongside acute inflammation in severe, persistent or repeated irritation

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7
Q

When does de novo chronic inflammation arise?

A

Some autoimmune conditions - RA
Some chronic infections - viral hepatitis
Chronic low level irritation (physical/microbiological)

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8
Q

What disease may cause chronic inflammation due to repeated irritation?

A

Chronic cholysytisis

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9
Q

What is the most important characteristic of chronic inflammation?

A

Type of cell present

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10
Q

Describe the microscopic appearances in chronic inflammation.

A

V. variable

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11
Q

Is chronic inflammation stereotyped?

A

Nope

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12
Q

Where are macrophages derived from?

A

Blood monocytes

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13
Q

What allows macrophages to be present in blood but not activated?

A

Various levels of activation

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14
Q

Which type of inflammation are macrophages important in?

A

Acute and chronic

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15
Q

What are the functions of macrophages?

A

Phagocytosis
Antigen presentation
Synthesis of cytokines, complement components, blood clotting factors and proteases
Control cells by cytokines release

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16
Q

Why do macrophages have a foamy appearance?

A

Abundant ER

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17
Q

What type of pathogen is macrophage phagocytosis particularly useful for?

A

Difficult to kill bacteria e.g. mycobacteria

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18
Q

How does the lifespan and replication of macrophages compare to that of neutrophils?

A

Live for moths and can replicate unlike neutrophils

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19
Q

What effects do macrophages have in chronic inflammation?

A 
Stimulate angiogenesis
Induce fibrosis
Fever
Acute phase reaction
Cachexia
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20
Q

Hen are lymphocytes seen?

A

Normal component of many tissues but always present in chronic inflammation

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21
Q

What is needed in addition to lymphocyte presence to indicate chronic inflammation?

A

Tissue damage

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22
Q

What is the function of B lymphocytes?

A

Mature in bone marrow to form plasma cells to release antibodies

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23
Q

What are the functions of T lymphocytes?

A

Process antigens
Secrete cytokines to influence inflammatory cells
Differentiate into NK cells which attack virus infected and some tumour cells

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24
Q

Where do T lymphocytes mature?

A

In the bone marrow

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25
Q

What do B lymphocytes and T lymphocytes provide together?

A

Coordinated immune response

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26
Q

How does the chromatin in a plasma cell appear after it has been phenotypically changed from a B lymphocyte?

A

‘Clock face’ - clear background w/blobs

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27
Q

Why do plasma cells have abundant cytoplasm?

A

For antibody production and secretion

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28
Q

What do the presence of plasma cells imply?

A

Chronicity as they take a longer time to develop

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29
Q

Describe the distribution of eosinophils.

A

Normally present but scattered, accumulate in certain circumstances

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30
Q

What circumstances cause accumulation of eosinophils?

A

Parasite infestations
Some tumours
Immune response
Allergic reactions

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31
Q

What circumstance are eosinophils predominant in?

A

Parasite infestations

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32
Q

What do demotactic stimuli do?

A

Secreted by macrophages and other inflammatory cells to recruit fibroblasts and myofibroblasts

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33
Q

What do fibroblasts and myofibroblasts secrete?

A

Collagen
Elastin
Glucosaminglycans (fibroblasts only)

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34
Q

Why do myofibroblasts differentiate?

A

So they can contract

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35
Q

What are the three types of giant cells?

A

Foreign body type
Langhans
Touton

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36
Q

How are small and large foreign bodies dealt with?

A

Small foreign bodies are engulfed

Giant cells stick to the surface of large foreign bodies

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37
Q

How are the nuclei arranged in foreign body type giant cells?

A

Randomly

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38
Q

How are giant cells formed?

A

Fusion of macrophages

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39
Q

What appearance do Langhans giant cells have?

A

Foamy centre w/peripheral horseshoe shared nuclei

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40
Q

What disease are Langhans cells associated with?

A

TB

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41
Q

What are Touton cells associated with?

A

Fat necrosis

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42
Q

What do Touton cells form in high lipid content?

A

Lesions

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43
Q

What cells are seen with Touton cells?

A

Foam cells

44
Q

Which type of cells form xanthomas?

A

Touton

45
Q

How are the nuclei arranged in Touton cells?

A

Ring towards centre

46
Q

What is ‘frustrated phagocytosis’?

A

Formation of giant cells

47
Q

How is the morphology of most chronic inflammatory reactions described?

A

Non-specific

48
Q

Give the main cell types present in RA, chronic gastritis and Leishmaniasis.

A

RA = plasma cells
Chronic gastritis = lymphocytes
Leishmaniasis = macrophages

49
Q

What cell type can be used in chronic inflammation to help diagnosis?

A

Giant

50
Q

What is Leishmaniasis?

A

Protozoal infection

51
Q

What are the effects of chronic inflammation?

A

Fibrosis
Impaired function
Atrophy
Stimulation of immune response

52
Q

How is fibrosis caused?

A

Cytokines stimulate fibroblasts to produce excess fibrous tissue

53
Q

How is fibrosis initially helpful?

A

Walls off infected area

Scar needed for wound healing

54
Q

How can fibrosis be problematic?

A

Can replace parenchymal tissue and impair organ function

55
Q

What determines the consequences of fibrosis?

A

Position

56
Q

How does chronic cholecystitis causes fibrosis?

A

Repeated obstruction by gall stones –> repeat acute inflammation causing chronic inflammation –> fibrosis of gall bladder wall as the muscle thickens to try and push stone out

57
Q

How do peptic ulcers appear?

A

Inflamed w/central acute inflammation causing the submucosa to be washed in acid causing pure acute inflammation

58
Q

What can cause acute gastritis leading to peptic ulcers?

A

Alcohol

NSAIDs

59
Q

What can cause chronic peptic ulcers?

A

Helicobacter pylori

60
Q

What is ulceration due to in peptic ulcers?

A

Imbalance of acid production and mucosal defence

61
Q

What protects the gastric mucosa?

A

Mucus

Prostaglandins

62
Q

How can myofibroblasts cause further problems in chronic inflammation?

A

Can slowly contract

63
Q

What disease is impaired function due to chronic inflammation seen in?

A

Chronic inflammatory bowel disease

64
Q

Give three diseases in which fibrosis due to chronic inflammation is seen.

A

Chronic cholecystitis
Peptic ulcers
Cirrhosis

65
Q

Give two examples of increased function caused by chronic inflammation.

A

Increased mucus secretion

Thyrotoxicosis in Grave’s disease

66
Q

Why is Crohn’s said to have a ‘cobblestone’ appearance?

A

Characterised by islands of mucosa surrounded by inflammation

67
Q

What do both Crohn’s and Ulcerative Collitus result in?

A

Scarring

68
Q

Give two examples of sites of atrophy caused by chronic inflammation.

A

Adrenal glands

Gastric mucosa

69
Q

What happens in atrophy of gastric mucosa caused by chronic inflammation?

A

Thickness and density of gastric bands decrease due to lymphocyte degeneration

70
Q

What interactions stimulate immune response in chronic inflammation?

A

Macrophage-lymphocyte

71
Q

What does stimulation of the immune response in chronic inflammation attack?

A

Innocuous targets

Autoimmune

72
Q

What leads to a disease process?

A

Stimulation of immune response by chronic inflammation

73
Q

How do patients with idiopathic inflammatory disease affecting large and small bowel present?

A

Diarrhoea

Rectal bleeding

74
Q

What are the characteristics of Ulcerative Colitis?

A

Superficial
More likely to cause acute problems than Crohn’s
Causes diarrhoea and bleeding

75
Q

What are the characteristics of Crohn’s Disease?

A

Transmural
Stricture and fistulae formation
Can be considered as ‘regional enteritis’

76
Q

What two effects of chronic inflammation is cirrhosis and example of?

A

Fibrosis

Impaired function

77
Q

What are common causes of cirrhosis?

A 
Alcohol
Infection with HBV or HCV
Fatty liver disease
Immunological
Drugs and toxins
78
Q

How does chronic inflammation lead to cirrhosis?

A

Fibrosis –> disorganisation of architecture –> attempt regeneration –> abnormal collagen deposits –> nodules formed disrupting bile path giving green colour

79
Q

What causes rheumatoid arthritis?

A

Autoimmune localised and systemic immune response causing joint destruction

80
Q

What effects can rheumatoid arthritis have in organs?

A

Beta-pleated sheet deposited causing amyloidosis

81
Q

What produces rheumatoid factor in RA?

A

Lots of lymphoid tissue

82
Q

What shows lymphoid aggregates in RA?

A

Fronds of synovium

83
Q

How can the link between chronic inflammation, immune response and immune disease sometimes be described?

A

Overlapped and circular

84
Q

What is granulomatous inflammation?

A

Chronic inflammation w/granulomas

85
Q

What is a granuloma?

A

Aggregate of active macrophages

86
Q

What is a hypersensitivity reaction?

A

Immunological reaction that damages self

87
Q

What are the cells present in a foreign body granuloma?

A

Macrophages
Foreign body cells
Epitheloid (tightly packed)
Some peripheral fibroblasts

88
Q

Are lymphocytes present in foreign body granulomas?

A

Probably not - few if any

89
Q

What are foreign body granulomas found around?

A

Not antigenic material e.g. Surgical thread causing persistent, low-grade stimulation

90
Q

How does breakdown of an artificial joint cause fluorescence in polarised light?

A

Foreign material from breakdown of artificial joint –> giant cells form holes that shouldn’t be in the joint –> foreign material fluoresces

91
Q

What cells are present in a hypersensitivity/immune reaction?

A 
Macrophages
Langhans
Epitheloid
Peripheral fibroblasts
Lymphocytes
92
Q

What does central caseating necrosis in an immune reaction indicate?

A

TB

93
Q

How does caseating necrosis damage organs?

A

Forms around insoluble antigenic particles and occupy parenchymal space

94
Q

What are two idiopathic causes of granulomatous inflammation via hypersensitivity reactions?

A

Xanthogranulomatous pyelonephritis

Malakoplakia

95
Q

What can cause granulomatous inflammation via immune reaction?

A 
Fungi
Sarcoids
Crohn's - seen in ~50% of cases
'Cat-scratch disease'
Leprosy
Syphilis
TB
Wegener's granulomatosis
96
Q

How are BCG and TB differentiated?

A

Look similar but BCG has no caseous necrosis

97
Q

What does Wegener’s granulomatosis affect?

A

Lungs

Kidneys

98
Q

How do sarcoids present?

A

Common in young adult women affecting lungs and lymph with non-caseating granulomas

99
Q

How does TB spread from the lungs?

A

Arrest, fibrosis and scarring in lungs
Erosion –> bronchus causing bronchopneumonia and TB in GI tract
Infects pleura
Erodes into bloodstream

100
Q

Why does it take 6 weeks to receive a +/-ve result for TB?

A

M.tuberculosis difficult and slow to culture

101
Q

Why can M. tuberculosis survive inside macrophages?

A

Has mycoside wall lipids

102
Q

Does M. tuberculosis have toxins or lyric enzymes?

A

Nope

103
Q

How does TB cause scarring in lungs?

A

Persistence and induction of cell-mediated immunity

104
Q

What causes miliary TB?

A

Many M. tuberculosis present therefore affects multiple organs

105
Q

What causes single organ TB?

A

Few M. tuberculosis present

106
Q

In miliary TB what percentage of lung tissue is taken over by granulomas?

A

50%

107
Q

Which type of TB is often fatal?

A

Miliary

Semester 2 (45 decks)

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