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Year 2 EMS MoD > Acute and Chronic Inflammation > Flashcards

Acute and Chronic Inflammation Flashcards

1
Q

What causes acute inflammation?

A
  • Tissue death (e.g. ischaemia, trauma, toxins)

- Infection (especially bacterial)

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2
Q

What does pyogenic mean?

A

Involving the production of pus.

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3
Q

What is suppuration?

A

The formation of pus.

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4
Q

Acute inflammation; what happens in cells can regrow?

A

Healing by regeneration.

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5
Q

Acute inflammation; what happens if cells cannot regrow?

A

Healing by repair.

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6
Q

Acute inflammation; what happens if the damaging agent persists?

A

Suppuration&raquo_space; more acute inflammation&raquo_space; chronic inflammation.

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7
Q

What is the purpose of acute inflammation?

A
  • Clear away dead tissue
  • Locally protect from infection
  • Allow access of immune system components
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8
Q

What are the 4 Celsus ‘cardinal signs’ of inflammation?

A
  • Calor (heat)
  • Rubor (redness)
  • Dolor (pain)
  • Tumor (swelling)
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9
Q

What does ‘functio laesa’ (Virchow) mean?

A

Disturbance of function.

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10
Q

What are the main types of acute inflammation? (4)

A
  • Serous
  • Fibrinous
  • Purulent (pus)
  • Pseudomembranous
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11
Q

What is serous inflammation?

A

Release of serous fluid, usually by mesothelial cells.

-e.g. skin blisters

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12
Q

What is fibrinous inflammation?

A

Increased vascular permeability allows fibrin to enter blood vessels.
-e.g. intestinal inflammation

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13
Q

What is purulent inflammation?

A

Pus formation&raquo_space; abscess formation.

-e.g. bacterial infection

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14
Q

What are the main components of acute inflammation? (3)

A
  • Vascular reaction
  • Exudative reaction
  • Cellular reaction
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15
Q

What vascular reactions are associated with acute inflammation?

A
  • Dilation (rubor)
  • Changes in flow (initially decreases then increases)
  • Increased permeability
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16
Q

What 2 processes control the vascular reaction?

A

Active control process;
MEDIATED - histamine, bradykinin, etc
NON-MEDIATED - damage e.g. toxins

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17
Q

What exudative reaction is associated with acute inflammation?

A

Formation of inflammatory exudate&raquo_space; swelling.

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18
Q

What is the composition of acute inflammatory exudate?

A

Protein rich (~50g/L).

  • immunoglobulins
  • fibrinogen
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19
Q

What is the purpose of fibrinous mesh formation as part of the exudative reaction?

A

Collects debris/bacteria.

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20
Q

What change occurs on the heart during pericarditis due to acute exudative reaction?

A

Outer surface changes from being shiny&raquo_space; rough.

-precipitated fibrin from exudate

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21
Q

What cellular reaction is associated with acute inflammation?

A

Migration of inflammatory cells out of vessels.

  • neutrophils accumulate in extracellular space
  • can form pus
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22
Q

What are systemic effects of inflammation?

A
  • Pyrexia

- Acute phase reaction

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23
Q

What is pyrexia?

A

Raised body temperature, fever.

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24
Q

What is acute phase reaction?

A

Changes in the synthesis of certain proteins during inflammation.
» non-specific protection

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25
Q

What tests are done to measure acute phase reaction?

A
  • C-reactive protein

- Erythrocyte sedimentation rate (ESR)

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26
Q

What are the commonest white blood cells?

A

Neutrophils.

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27
Q

Where are neutrophils produced?

A

Bone marrow.

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28
Q

What is amoeboid movement?

A

Crawling-like movement due to protrusion of cytoplasm&raquo_space; temporary projection.

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29
Q

One feature of neutrophils is directional chemotaxis. What is this?

A

The movement of an organism in response to a chemical stimulus.

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30
Q

What is the lifespan of neutrophils?

A

Short - hours in tissues.

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31
Q

Where do neutrophils normally flow?

A

In the axial stream - don’t interact much with the endothelium.

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32
Q

What happens to neutrophils when there’s an infection?

A

They interact with receptors on endothelial cells which are activated.
» MARGINATION and PAVEMENTING

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33
Q

What is margination?

A

Process of free-flowing leukocytes leaving axial flow and initiating leukocyte-endothelial cell interactions.

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34
Q

What is pavementing?

A

Leucocytes adhering to the linings of capillaries during inflammation.

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35
Q

What are the 2 types of mediator that control inflammation?

A
  • Cell derived

- Plasma derived

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36
Q

What half life do mediators of acute inflammation have?

A

Short half lives.

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37
Q

What is a STORED cell-derived mediator of acute inflammation?

A

Histamine.

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38
Q

Give examples of SYNTHESISED cell-derived mediators of acute inflammation. (6)

A 
Prostaglandins
Leukotrienes
PAF
Cytokines
NO
Chemokines
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39
Q

Give examples of plasma derived mediators of acute inflammation. (4)
-cascades

A

Kinin system
Clotting pathway
Thombolytic pathway
Complement pathway

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40
Q

Which processes of acute inflammation do mediators act on? (4)

A
  • Vascular dilation
  • Increased permeability
  • Neutrophil adhesion
  • Neutrophil chemotaxis
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41
Q

Give examples of anti-inflammatory drugs that interfere with the action of mediators.

A
  • Glucocorticooid steroids
  • NSAIDs
  • Leukotriene receptor anatagonists
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42
Q

How do glucocorticoid steroids interfere with inflammatory mediators?

A

Bind to glucocorticoid receptors and up-regulate the expression of anti-inflammatory proteins in the nucleus.

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43
Q

How do NSAIDs interfere with inflammatory mediators?

A

COX inhibitors.

-decreased formation of prostaglandins and thromboxane

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44
Q

How do leukotriene receptor antagonists interfere with inflammatory mediators?

A

Leukotrienes are inflammatory mediators.

-prevents their production/action

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45
Q

What components of a FBC can be used to assess inflammation?

A
  • Haemoglobin (increase with lung disease)
  • WBC (increase with infection)
  • Platelets (increase with inflammation)
46
Q

How is erythrocyte sedimentation rate (ESR) used to assess inflammation?

A

ESR increases with inflammation.

-high proportion of fibrinogen in the blood

47
Q

Give an example of an acute phase protein.

A

C-reactive protein.

48
Q

How can C-reactive protein be used as a marker of inflammation?

A

Protein produced by the liver, which increases when there is inflammation anywhere in the body.

49
Q

What are the main processes that trigger endothelial activation? (2)

A
  • Tissue damage

- Neutrophil activation

50
Q

What does resolution mean?

A

Reduction of inflammation and the removal of waste products.

51
Q

List 5 conditions in which the inflammatory pathway has gone wrong.

A
  • Systemic inflammatory response syndrome (SIRS)
  • Acute adult respiratory distress sydrome
  • Chronic granulomatous disease of childhood
  • Hereditary angio-oedema
  • Amyloidosis
52
Q

What is systemic inflammatory response syndrome(SIRS)?

A

Non-specific systemic inflammation caused by ischaemia/trauma/infection.

53
Q

What is acute respiratory distress syndrome(ARDS)?

A

Severe inflammation of the lungs due to infection/injury&raquo_space; difficulty breathing.

54
Q

What is hereditary angio-oedema?

A

Autosomal dominant disorder&raquo_space; episodic swelling in airways/face/extremities/genitals.
-can be life-threatening

55
Q

What is amyloidosis?

A

Accumulation of amyloid in the body, often in kidney and heart.

56
Q

What bacteria is the main cause of pneumonia?

A

Streptococcus pneumoniae.

57
Q

How do the lungs become inflamed with pneumonia?

A

WBCs try to fight the infection&raquo_space; inflammation in the alveoli.

58
Q

What are the main differences between acute and chronic inflammation? (4)

A

ACUTE

  • fast onset (mins-hours)
  • neutrophils
  • mild and self-limiting
  • prominent signs

CHRONIC

  • slow onset (days)
  • macrophages/lymphocytes/plasma cells
  • severe and progressive
  • subtle signs
59
Q

What is the difference between cells types involved with acute and chronic inflammation?

A

ACUTE - mainly neutrophils

CHRONIC - mainly macrophages, plasma cells and lymphocytes

60
Q

What is the basic process of acute inflammation?

A

Vessels dilate and become leaky&raquo_space; protein rich exudate.

61
Q

What are the main outcomes of acute inflammation? (4)

A
  • Resolution
  • Suppuration (abscess)
  • Organisation
  • Chronic inflammation
62
Q

Is chronic inflammation normally primary or secondary?

A

Usually primary.

-but can be sequential from acute

63
Q

Is granulation and scar tissue more abundant in acute or chronic inflammation?

A

Chronic inflammation.

64
Q

What are the main primary causes of chronic inflammation? (5)

A
  • Infection
  • Endogenous material
  • Exogenous material
  • Autoimmune
  • Primary granulomatous diseases
65
Q

Give an example of an infection that causes chronic inflammation.

A

TB

Leprosy

66
Q

What is the difference between endogenous and exogenous material?

A

ENDOGENOUS has internal origin within the body.

EXOGENOUS has external origin outside the body.

67
Q

Give an example of endogenous material that causes chronic inflammation.

A

Necrotic adipose tissue

Uric acid crystals

68
Q

Give an example of exogenous material that causes chronic inflammation.

A

Asbestos
Sutures
Implanted prostheses

69
Q

Give an example of an autoimmune condition that causes chronic inflammation.

A

Arthritis
SLE
Pernicious anaemia

70
Q

Give an example of a primary granulomatous disease that causes chronic inflammation.

A

Crohn’s

Sarcoidosis

71
Q

What is the most common type of acute inflammation to turn into chronic inflammation?

A

Suppurative (pus forming) inflammation.

72
Q

How does acute suppurative inflammation lead to chronic inflammation?

A

Pus can form an abscess
» walls thicken
» granulation and fibrous tissue
» recurrent acute can lead to chronic

73
Q

Give an example of acute suppurative inflammation becoming chronic inflammation.

A

Cholecystitis.

-gall bladder inflammation due to stones can become chronic

74
Q

How does chronic inflammation lead to fibrosis?

A

Infiltration by mononuclear cells
» tissue destruction
» healing by fibrosis

75
Q

What is fibrosis?

A

The thickening and scarring of connective tissue during repair of injured tissue.

76
Q

Which mononuclear cells are involved in chronic inflammation?

A

Macrophages
Lymphocytes
Plasma cells

77
Q

What are the main macroscopic appearances of chronic inflammation? (4)

A
  • Ulcer
  • Granulomatous
  • Chronic abscess cavity
  • Fibrosis
78
Q

What cells are present in connective tissue during inflammation? (3)

A

Macrophages
Plasma cells
Mast cells

79
Q

What is the function of mast cells?

A 
Release mediators (e.g. histamine).
>> increased vessel permeability to WBCs and proteins
80
Q

What is the main function of macrophages during inflammation?

A

Engulf and digest cellular debris and microbes.

81
Q

What are the main polymorphonuclear leukocytes (granulocytes)?

A

Neutrophils
Basophils
Eosinophils
Mast cells

82
Q

Where are granulocytes produced?

A

Bone marrow.

83
Q

What is the most abundant phagocyte?

A

Neutrophils.

84
Q

What is the main function of eosionophils during inflammation?

A

Antigen presenting cells.

-don’t phagocytose

85
Q

What are the main functions of basophils during inflammation?

A
  • Produce histamine

- Release prostglandins when injured

86
Q

What is the main function of prostaglandins in inflammation?

A

Vasodilation.

-increase blood flow to the site of injury

87
Q

What is the main function of macrophages in chronic inflammation?

A
  • Increase inflammation (phagocytose bacteria)
  • Release cytokines to signal monocytes
  • Fibrosis
88
Q

What stimulates macrophages to produce factors that induce angiogenesis?

A

Low oxygen content.

89
Q

What happens when macrophages release cytokines to signal monocytes to the site of injury?

A

Monocytes enter damaged tissue from blood (RECRUITMENT).
» macrophages PROLIFERATE locally in damaged tissue
» IMMOBILISATION of macrophages in tissue

90
Q

What is granulation tissue?

A

New connective tissue and blood vessels that form on the surface of a wound during healing. Grows up from the base of the wound.

91
Q

What structures does granulation tissue contain?

A
  • New blood vessels (angiogenesis)
  • Fibroblasts (deposit collagen)
  • Inflammatory cells
92
Q

What is the aim of granulation tissue?

A

To repair and replace injured tissues with fibrous tissues.

93
Q

What is the appearance of granulation tissue?

A

Light red/dark pink.

-due to capillaries

94
Q

What is angiogenesis?

A

The formation of new blood vessels.

95
Q

What is a fibroma?

A

A benign fibrous tumour of connective tissue.

-arises from 1* cell line

96
Q

What type of cell induces fibrosis?

A

Macrophages.

97
Q

What is a granuloma?

A

An aggregate/nodule of epithelioid histiocytes and other cells (lymphocytes, histiocytic giant cells).

98
Q

What can macrophages be known as when in tissues?

A

Histiocytes.

99
Q

What are the main structural features of epitheloid histiocytes?

A
  • Large vesicular nuclei

- Eosinophilic cytoplasm

100
Q

What enzyme do epitheloid histiocytes secrete?

A

Angiotensin converting enzyme.

101
Q

What are histiocytic giant cells and where do they form?

A

Multinucleated giant cells that form where material is indigestible to macrophages.
-e.g. tubercle bacilli with cell walls resistant to macrophages

102
Q

What is a giant cell?

A

Mass formed from the union of several cells (usually macrophages), often forming a granuloma.

103
Q

Give an example of a giant cell seen in TB.

A

Langerhans giant cells.

  • nuclei form peripheral horseshoe arrangement
  • found at the centre of granulomas
104
Q

Are solitary giant cells called granulomas?

A

No, not in the absence of epitheloid histiocytes.

105
Q

Give 2 examples of bacterial granulomatous diseases.

A
  • TB (lungs)

- LEPROSY (nerves, airways, skin, eyes)

106
Q

Give an example of a parasitic granulomatous disease.

A

Schistosomiasis.

-urinary tract and intestines

107
Q

Give an example of a fungal granulomatous disease.

A

Cryptococcus.

108
Q

Give an example of a granulomatous disease caused by synthetic materials.

A

Silicosis.
-inhaling silica dust
»scarring and granulomas in upper lobes of lungs

109
Q

Give 2 examples of granulomatous disease of unknown causes.

A
  • Sarcoidosis

- Crohn’s

110
Q

What is the general mechanism of granuloma formation in TB?

A
  • Alveolar macrophages release cytokines&raquo_space; recruit more macrophages.
  • Dendritic cells present antigens to T cells&raquo_space; T cell respeonse.

> > granuloma formation

111
Q

What type of granuloma forms in TB?

A

CASEOUS GRANULOMA.

-macrophages, epitheloid cells and Langherans cells surrounded by T cells

Year 2 EMS MoD (20 decks)

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