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Phase 1 - S2 Pathology > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

What is acute inflammation

A

Response of living tissue to injury. It is innate, immediate, stereotypes and short lived

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2
Q

Give 5 causes of acute inflammation

A
  1. Microbial infections
  2. Hypersensitivity reactions
  3. Physical agents
  4. Chemicals
  5. Tissue necrosis
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3
Q

What are the clinical signs of acute inflammation

A 
Rubor (redness)
Tumour (swelling)
Dolor (pain)
Calor (heat)
Loss of function
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4
Q

What changes in the tissue occur as a result of inflammation

A
  1. Changes in blood flow
  2. Exudation of fluid into tissues
  3. Infiltration of inflammatory cells
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5
Q

What is exudation of fluid

A

Fluid that filters from the circulatory system into lesions (areas of tissue suffering from damage) or areas of inflammation

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6
Q

What are the changes in the changes of blood flow

A
  1. Vasoconstriction of arterioles occurs for a few seconds
  2. Vasodilation then occurs
    There is an increased permeability of blood vessels
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7
Q

How does the blood flow change in acute inflammation

A

It increases due to vasodilation

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8
Q

What does an increase in permeability of blood vessels cause

A

Exudation of protein rich fluid

Slowing down of the circulation

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9
Q

What are the 2 types of chemical mediators of acute inflammation

A

Immediate response mediators

Mediators giving a persistent response

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10
Q

Give an example of an immediate chemical mediator

A

Histamine, cytokines and chemokines

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11
Q

What cells release histamine

A

Mast cells, basophils and platelets

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12
Q

When is histamine released

A

In response to physical damage, complementary factors C3a and C5a, interleukin and neutrophils

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13
Q

What does histamine cause

A

Vasodilation, increased permeability of blood vessels and pain

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14
Q

Give an example of a persistent chemical mediator of acute inflammation

A

Leukotriene and Proteases (bradykinin, complement proteins C3a and C5a, fibrin)

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15
Q

What 2 pressure determine fluid flow across vessel walls

A

Hydrostatic and oncotic pressure

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16
Q

If there is an increased oncotic pressure in the interstitum what happens to fluid in the vessels

A

It will move out of the vessels in to the interstitium

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17
Q

What is oedema

A

Increased fluid in the tissues

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18
Q

True or false: arteriolar dilation leads to an increase in hydrostatic pressure

A

True as there is more blood flow through the capillaries increasing the pressure. This forces more fluid out

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19
Q

What does transudate mean

A

The fluid outside of the vessels has the same protein content as the plasma

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20
Q

What is the protein content like in an exudate

A

Greater than in the plasma

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21
Q

True or false: fluid loss in inflammation is a transudate

A

False - it is an exudate

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22
Q

What are the 5 mechanisms of increasing vessel permeability

A
  1. Endothelial contraction
  2. Cytoskeleton reorganisation
  3. Direct injury
  4. Leukocyte dependant injury
  5. Increased transcytosis
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23
Q

What is transcytosis

A

When fluid moves across the endothelial cytoplasm through cells and not between cells

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24
Q

What causes endothelial contraction

A

Histamine and leukotrienes

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25
Q

What does endothelial contraction causes

A

Gaps inbetween the endothelial making the vessels more leaky

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26
Q

What causes cytoskeleton reorganisation

A

Cytokines interleukin and TNF

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27
Q

What does cytoskeleton reorganisation cause

A

Gaps in the vessel walls

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28
Q

How can leukocyte dependant injury occur

A

When neutrophils release toxic oxygen species and enzymes

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29
Q

What causes an increase in transcytosis

A

VEGF

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30
Q

What is the primary type of white blood cell involved in inflammation

A

Neutrophils

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31
Q

Describe the appearance of a neutrophil

A

Granular, multi-lobed nucleus

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32
Q

What are the 4 stages in neutrophil infiltration

A
  1. Margination
  2. Rolling
  3. Adhesion
  4. Emigration
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33
Q

What occurs in migration in the infiltration of neutrophils

A

Neutrophils line up at the edge of the blood vessel along the endothelium

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34
Q

What is rolling in the infiltration of neutrophils

A

Neutrophils roll along the endothelium, sticking to it loosely

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35
Q

What is the adhesion stage of the infiltration of neutrophils into blood vessels

A

When neutrophils tightly adhere to the endothelial lining the blood vessel

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36
Q

What occurs in the emigration stage of the infiltration of neutrophils into the blood vessels

A

Neutrophils move through the blood vessel wall

37
Q

What allows neutrophils to bind onto the endothelial wall of the blood vessel

A

Inflammatory mediators cause a change to the endothelial receptors which allows the neutrophils to bind

38
Q

How to the neutrophils move through the endothelial wall

A

There is relaxation of inter-endothelial cell junction, digestion of the vascular basement membrane which then allows the neutrophil to move across

39
Q

What is chemotaxis

A

Movement along concentration gradients of chemoattractants

40
Q

What process do neutrophils do

A

Phagocytosis

41
Q

What facilitates phagocytosis by neutrophils

A

Opsonins (C3b)

42
Q

What happens during phagocytosis

A

Opsonins allows the neutrophil to recognise and make contact with the particle. The cytoskeleton then changes to allow endocytosis of the particle. Lysosomes fuse

43
Q

What are the 2 mechanisms of phagocytosis

A

Oxygen dependant and independant

44
Q

What occurs in oxygen dependant phagocytosis

A

Enzymes produce superoxide and hydrogen peroxide

45
Q

Which type of phagocytosis is particularly good for killing bacteria

A

Oxygen dependant

46
Q

What occurs in oxygen independant phagocytosis

A

Lysozymes and hydrolases break down the particle

47
Q

Why is the response by neutrophils not always 100% reliable

A

Neutrophils may release toxic metabolites and enzymes causing damage to host tissue

48
Q

Give 2 examples of cytokines

A

Interleukin and TNF alpha

49
Q

What chemicals mediators cause increased blood flow

A

Histamine

50
Q

What chemicals mediators cause vascular permeability

A

Histamine and leukotrienes

51
Q

What chemicals mediators cause neutrophil chemotaxis

A

C5a, bacterial peptides, lnterleukin

52
Q

What chemicals mediators cause phagocytosis

A

C3b

53
Q

How does the exudation of fluid combat injury?

A
  1. Delivers plasma proteins, immunoglobulins, inflammatory mediators and fibrinogen to area of injury
  2. Dilutes toxins
  3. Increases lymphatic drainages
54
Q

Why is an increased lymphatic drainage advantageous in an inflammatory response

A

Delivers microorganisms to phagocytes and antigens in the immune system through the lymph nodes

55
Q

How does the infiltration of cells combat injury

A

Removes pathogenic organisms and debris

56
Q

How does vasodilation help combat injury

A
  1. Increases delivery of helping components (plasma proteins, immunoglobin, fibrinogen, mediators)
  2. Increases temperature
57
Q

How does an increased temperature help combat injury

A

The cells work more efficiently at higher temperatures

58
Q

How does pain and loss of function help combat injury

A

Reduces chance of further damage

59
Q

What complications can occur due to local inflammation

A
  1. Swelling can block tubes
  2. Exudate can cause compression
  3. Pain and loss of function
60
Q

What is serositis

A

Inflammation of serous membranes

61
Q

What are systemic effects of inflammation

A
  1. Fever

2. Leukocytosis

62
Q

What causes a fever

A

Endogenous pyrogens

63
Q

Give 2 examples of endogenous pyrogens

A

Interleukin 1 and TNF alpha

64
Q

What chemical mediators are found in aspirin to reduce fever

A

Prostaglandins

65
Q

What is leukocytosis

A

An increase in the number of white cells in the blood normally as a response to infections

66
Q

What type of white cell increases in the blood due to bacterial infections

A

Neutrophils

67
Q

What type of white cell increases in the blood due to viral infection

A

Lymphocytes

68
Q

What are acute phase proteins

A

Plasma proteins that increase in infections

69
Q

Give 3 examples of acute phase proteins

A

C reactive protein
Alpha 1 antitrypsin
Fibrinogen

70
Q

What is the acute phase physiological responses of acute inflammation

A

Decreased appetite, raised pulse rate, altered sleep pattern and changes in plasma concentrations of acute plasma proteins

71
Q

What does it mean by acute

A

Rapid onset

72
Q

What is shock

A

Clinical syndrome of systemic circulatory failure

73
Q

What are the 4 outcomes of acute inflammation

A
  1. Complete resolution
  2. Continued acute inflammation with chronic inflammation (abscess)
  3. Chronic inflammation and fibrous repair giving scarring
  4. Death
74
Q

How is the plasma levels of fibrin reduced

A

Degraded by plasmin and proteases

75
Q

How is the exudate reduced

A

Drained to the lymphatics

76
Q

When is complete resolution not possible

A

If cell architecture is destroyed

77
Q

True or false: mediators of acute inflammation have short half lives

A

True

78
Q

How are the amount of mediators reduced when resolving inflammation

A
  • short half lives
  • inactivated by degradation
  • inhibited
  • diluted in exudate
79
Q

What is lobar pneumonia

A

Inflammation of the pulmonary lobe

80
Q

What organism causes lobar pneumonia

A

Streptococcus pneumoniae (pneumococci)

81
Q

What systems are seen with lobar pneumonia

A

Fever, hypoxaemia, dry cough and breathlessness

82
Q

What is bacteria meningitis

A

Acute inflammation of the meninges (membrane outlining the brain and spinal cord) causing vascular thrombosis and reduced cerebral perfusion

83
Q

What causes bacterial meningitis

A

Streptococcus pneumoniae

84
Q

What is an abscess

A

Collection of pus (inflammatory exudate) in the tissues due to bacterial infection. This causes high pressure giving pain and can damage adjacent tissue

85
Q

What type of necrosis is associated with an abscess

A

Liquefactive in the centre

86
Q

What occurs if the inflammatory exudate pours into serous cavities

A

Ascites, pleural or pericardial effusion

87
Q

What is pericarditis

A

Swelling of the pericardium with fibrin deposits there

88
Q

List 4 examples of inflammation disorders

A
  1. Hereditary angiotensin-oedema (attacks of swelling)
  2. Alpha-1 antitrypsin deficiency
  3. Inherited complementary deficiencies
  4. Defects in neutrophil number and size
89
Q

What is diapedesis

A

Passage of blood cells through the capillary walls

Phase 1 - S2 Pathology (13 decks)

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