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Year 2 > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

Define ‘inflammation’

A

A reaction to injury or infection involving cells such as neutrophils and macrophages

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2
Q

In what two instances is inflammation good

A
  1. Infection

2. Injury

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3
Q

In what two instances is inflammation bad

A
  1. Autoimmunity

2. Over-reaction to a stimulus

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4
Q

In what two ways is inflammation classified as?

A

Acute and Chronic

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5
Q

Three characteristics of an acute condition

A
  1. Sudden Onset
  2. Short Duration
  3. Usually resolves
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6
Q

Three characteristics of chronic inflammation

A
  1. Slow onset or sequel to acute
  2. Long Duration
  3. May never resolve
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7
Q

Name five cells involved in inflammation

A
  1. Neutrophil Polymorphs
  2. Macrophages
  3. Lymphocyte
  4. Endothelial Cell
  5. Fibroblasts
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8
Q

How long do macrophages survive for

A

Weeks to months

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9
Q

Role of macrophages (3)

A
  1. Ingest bacteria and debris
  2. Carry debris away
  3. Present antigen to lymphocyte
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10
Q

How long do lymphocytes last

A

Years (almost as long as we can do!)

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11
Q

Role of lymphocyte

A

Produce chemicals which attract in other inflammatory cells

Immunological memory

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12
Q

What lymphocyte produces antibodies

A

Plasma cells

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13
Q

What lymphocyte produces cytokines

A

T-cells

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14
Q

Where are endothelial cells found

A

Lining capillary blood vessels in areas of inflammation

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15
Q

What happens to endothelial cells in areas of inflammation (3)

A
  1. Become sticky so inflammatory cells adhere to them
  2. Become porous to allow inflammatory cells to pass into tissues
  3. Grow into areas of damage to form new capillary vessels
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16
Q

What is produced by fibroblasts and under what condition is this produced

A

Collagen in areas of chronic inflammation and repair

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17
Q

Give an example of an acute inflammation

A

Acute Appendicitis

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18
Q

What causes acute appendicitis

A

Unknown why it happens

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19
Q

Name four things that happen when acute inflammation takes place

A
  1. Neutrophils appear
  2. Blood Vessels Dilate
  3. Inflammation of serosal surface occurs
  4. Pain felt
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20
Q

Give an example of chronic inflammation

A

Tuberculosis

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21
Q

At what point during TB does inflammation occur

A

Later on - does not appear initially

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22
Q

What four things occur during chronic inflammation

A
  1. Mycobacteria ingested by macrophages
  2. Lymphocytes appear
  3. Macrophages appear
  4. Fibrosis
    ( Macrophages often fail to kill kill mycobacteria)
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23
Q

When does acute inflammation occur

A

Initial tissue reaction to injury

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24
Q

What two things happen during acute inflammation

A
  1. Vascular component: Dilatation of vessels

2. Exudative component: Vascular leakage of protein-rich fluid

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25
Q

How long does acute inflammation last

A

Few hours to a few days

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26
Q

What suffix is given to conditions caused by inflammation

A

-itis

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27
Q

5 causes of acute inflammation

A
  1. Microbial Infections
  2. Hypersensitivity reactions
  3. Physical Agents
  4. Chemicals (acids and alkalis)
  5. Tissue necrosis
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28
Q

What is the most common cause of inflammation

A

Microbial infection

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29
Q

How are microbial infections caused

A
  1. Bacteria release specific exotoxins which initiate inflammation or endotoxins which are associated to the cell walls
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30
Q

What is a hypersensitivity reaction

A

An excess immune reaction that damages tissues

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31
Q

What physical agents cause acute inflammation

A

UV Lights and ionising radiation

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32
Q

How do irritants cause acute inflammation

A

By tissue damage or directly releasing specific chemical irritants

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33
Q

How does tissue necrosis cause acute inflammation

A

Death of tissues from lack of oxygen or nutrients

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34
Q

What factors are indications of acute inflammation

A 
Redness 
Heat
Swelling (oedema)
Pain (stretching of tissues)
Loss of function
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35
Q

What are the early stages of acute inflammation

A

Odema fluid accumulates in extracellular space

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36
Q

What is the cellular component of oedema fluid called

A

Neutrophil polymorph

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37
Q

What happens to the microcirculation during acute inflammation

A
  1. Smooth muscle of arteriolar walls form pre capillary sphincters which regulate blood flow through the capillary bed.
  2. Flow through some capillaries shut down
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38
Q

Where are blood cells located in the capillary

A

Centre of the lumen (axial flow)

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39
Q

Where does plasma flow along the capillaries

A

The plasmatic zone (outer part of the lumen)

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40
Q

Why does axial flow exist

A

Keeps blood cells away from and adhering to the blood wall

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41
Q

What are fenestrations

A

Areas of the capillaries where the wall gets thinner than the rest of the vessel

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42
Q

What happens to vascular permeability during acute inflammation

A
  1. High colloidal osmotic pressure causes fluid to be ejected into extravascular space.
  2. Colloidal proteins also pushed into extracellular fluid which increases oncotic pressure at venule end (exudation).
  3. Less fluid re-enters capillary at venule end
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43
Q

What can be found in fluid exudate

A

Immunoglobulins

Coagulation factors

44
Q

What are acutely inflamed organ surfaces covered by

A

Fibrin

45
Q

Are endothelial cells damaged during inflammation

A

No

46
Q

Why are endothelial cells not damaged during inflammation

A

They contain a protein called actin which causes contraction of endothelial cells, opening transient pores when stimulated by inflammatory mediators

47
Q

Example of an inflammatory mediator

A

Histamine

48
Q

How do chemicals like x-rays contribute to inflammation

A

By delaying prolonged leakage which CAN damage endothelial cells

49
Q

How does tissue sensitivity impact inflammation

A

Tissues in different parts of the body respond to inflammatory mediators in different ways (e..g those in the CNS are very insensitive to them)

50
Q

What is the diagnostic histological feature of acute inflammation

A

Accumulation of neutrophil polymorphs

51
Q

What happens to neutrophils during inflammation

A
  1. Margination of neutrophils
  2. Adhesion of neutrophils
  3. Neutrophil emigration
  4. Diapedesis
52
Q

What is the margination of neutrophils

A

Cells usually confined to axial flow end app in plasmatic zone near to endothelium due to loss of fluid

53
Q

What is the adhesion of neutrophils

A

Neutrophils adhere to endothelium which doesn’t normally happen

54
Q

Do neutrophils make contact with the endothelial walls normally

A

Yes, randomly but don’t adhere to it

55
Q

Along with neutrophils what other cell adheres to endothelial walls

A

Leucocytes

56
Q

What is neutrophil emigration

A

They move through opened pores formed by endothelial cells (the actin contractions in response to inflammatory mediator) through basal lamina into adventitia.

57
Q

What is diapedesis

A

Red blood cells escape passively through vessels due to hydrostatic pressure.

58
Q

When does diapedesis occur

A

Major damage to blood vessels

59
Q

What happens to neutrophils in later stages of acute inflammation

A

Chemotaxis

60
Q

What is chemotaxis

A

Neutrophil polymorphs are attracted to chemical substances in solution

61
Q

What two substances early in the inflammatory response are released by inflammatory stimulus

A

Histamine and Thrombin

62
Q

Role of thrombin and histamine in inflammation

A

Up-regulation of adhesion molecules on surface of endothelial cells

63
Q

What is the result of adhesion molecules increasing on surface of endothelial cells to neutrophils

A

They have a firm adhesion to the endothelial surface

64
Q

Role of Histamine

A
  1. Vascular dilatation

2. transient phase of increased vascular permeability

65
Q

Where are histamines stored

A

Mast Cells

66
Q

What components stimulate the release of histamine

A

C3a and C5a
Lysosomal proteins released from neutrophils
Serotonin
Chemokines

67
Q

How many cascade systems are in place in the plasma flow to produce chemical mediators

A 
4:
Kinin
Fibrinolytic
Coagulation
Complement
68
Q

What factor activates the kinin, fibrinolytic and coagulation systems

A

Hageman factor (XII)

69
Q

What are the most important cytokines that stimulate inflammation due to injury

A
  1. IL-1

2. TNF - alpha

70
Q

When do IL-1 and TNF-alpha have an effect

A

Following histamine and thrombin’s effects

71
Q

What is E-selectin

A

An adhesion molecule that binds + activates neutrophils

72
Q

Role of IL-8

A

Chemotaxins for neutrophil polymorphs

73
Q

What is the effect of IL-8 and TNF-alpha on endothelial cells

A

Cause secretion of MCP-1 which is chemotactic for neutrophil polymorphs

74
Q

What is the role of lymphatics in inflammation

A
  1. Channels become dilated as they drain fluid away from inflamed site.
  2. Limits oedema collection in tissues
75
Q

What is the role of neutrophil polymorph

A
  1. Movement
  2. Adhesion to microorganisms
  3. Phagocytosis
76
Q

How do neutrophil polymorphs cause movement

A

Contraction of cytoplasmic microtubules bring about amoeboid movement allowing chemotaxis

77
Q

What does the amoeboid movement of neutrophil polymorphs depend on

A

Calcium ions and intracellular concentrations of cyclic nucleotides

78
Q

define chemotaxis

A

Movement of a compound in one direction in response to inflammation

79
Q

How are microorganisms opsonised

A

By immunoglobulins or complement compounds

80
Q

How do neutrophils carry out phagocytosis

A

Phagocytes become pseudopodia shaped
:
1. Neutrophils produce H2O2 which reacts with myeloperoxidase in cytoplasmic granules
2. Produces microbicidal agent

81
Q

Why are lysosomal products released from neutrophils

A
  1. Damages local tissues by proteolysis
  2. Activates coagulation factor XII
  3. Attracts leucocytes in the area
82
Q

Role of mast cells in acute inflammation

A

Metabolise arachidonic acid to inflammatory mediators

83
Q

What are mast cells stimulated by

A

C3a/C5a complement factors

84
Q

Why is inflammation beneficial (6)

A
  1. Dilution of toxins
  2. Entry of antibodies due to increased intravascular permeability
  3. Transport of antibiotics
  4. Fibrin formation traps microbes facilitating phagocytosis
  5. Delivery of nutrients and oxygen
  6. Stimulation of immune response by drainage of this fluid into lymphatics allows soluble antigens to reach local lymph nodes
85
Q

What other cells drive at the site of inflammation

A

Blood macrophages

86
Q

What happens to blood macrophages upon leaving the blood vessels

A

Transform into macrophages by becoming more metabolically active

87
Q

Role of macrophages

A

Clearing away tissue debris and damaged cells

88
Q

Three harmful effects of inflammation

A
  1. Digestion of normal tissues (by collagenases and proteases)
  2. Swelling in certain areas
  3. OTT inflammatory response
89
Q

What happens during resolution of acute inflammation

A
  1. Minimal cell death + tissue damage
  2. Occurrence in an organ that has regenerative capacity
  3. Rapid destruction of causal agent
  4. Rapid removal of fluid + debris
90
Q

What are the three sequence of events that lead to resolution

A
  1. Phagocytosis of bacteria by neutrophils
  2. Fibrinolysis
  3. Phagocytosis of debris by macrophages
  4. Carry debris through lymphatics
  5. Disappearance of vascular dilatation
91
Q

What is Suppuration

A

Formation of Pus (mixture of living, dying and dead neutrophils and bacteria)

92
Q

What must happen in order for suppurating to occur

A

Causative stimulus must be persistent and always caused by an infective agent (pyogenic bacteria)

93
Q

Describe Suppuration process

A
  1. Puss accumulates in tissue
  2. Puss surrounded by pyogenic membrane consisting of sprouting capillaries, neutrophils and fibroblasts
  3. Forms an abscess
94
Q

What is problematic about an abscess

A

Bacteria within abscess are inaccessible to antibodies and antibiotics

95
Q

How does an abscess close up

A
  1. It bursts
  2. Cavity collapses
  3. Cavity obliterated by organisation and fibrosis
  4. Scar formation
96
Q

What happens if pus accumulates inside a hollow viscus

A

Mucosal layers of the outflow tract are covered by fibrin resulting in an empyema

97
Q

Where is pus from an abscess discharged

A

Into the sinus tract

98
Q

What is the sinus tract

A

A layer between the abscess and skin or mucosal surface

99
Q

When does a fistula form

A

When sinus tract pus connects two mucosal surfaces together

100
Q

What is organisation

A

Replacement by granulation tissue as part of repair

101
Q

What three circumstances favour this outcome

A
  1. Large amounts of fibrin are formed which can’t be removed by fibrinolytic enzymes
  2. Large volumes of tissues become necrotic
  3. Exudate and debris can’t be removed
102
Q

Describe organisation

A
  1. New capillaries grow into the inert material, macrophages migrate into the zone
  2. Fibroblasts proliferate under the influence of TGF-beta resulting in fibrosis
103
Q

Where does organisation typically occur

A

lung parenchyma

104
Q

What is the consequence of fibrin not being easily removed

A

Capillaries grow into fibrin

105
Q

What stage follows on from suppuration

A

Organisation

Year 2 (155 decks)

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