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Year 1- Principles of Disease (FOM) > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

Define acute inflammation

A

The fundamental response maintaing integrity of the organism.

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2
Q

What is acute inflammation.

A

Series of protective changes occuring in living tissue as a response to injury.

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3
Q

List some cardinal signs of inflammation.

A

rubor - redness, darkening
calor - heat
tumor - swelling
dolor - pain
loss of function

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4
Q

Rubor?

A

Redness or darkening.

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5
Q

Calor?

A

Heat

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6
Q

Tumour?

A

Swelling

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7
Q

Dolor?

A

Pain

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8
Q

Name some causes of acute infammation.

A

-Microorganisms
-Mechanical/trauma/injury to tissue (all injuries, even sterile ones like surgery).

-Chemcial- upsets stable environment (acid, alkali, bile, urine)

-Physical- extreme conditions

Dead tissues cell necrosis irritates adjacent tissue

-Hypersensitivity

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9
Q

Name the microorganiss which cause acute inflammation.

A

(bacteria, fungi, viruses, parasites)

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10
Q

Describe some extreme conditions which may cause acute inflammation.

A

heat=suburn,
cold= forstbite,
ionising radiation

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11
Q

Describe the process of acute inflammation.

A

-Series of microscopic events localised to affected tissue
-Results in the clinical symptoms and signs of acute inflammation - the cardinal signs

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12
Q

wHAT ARE CAPILLARY BEDS OF THE MICROCIRCULATION FED BY?

A

Arterioles

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13
Q

What are the cappilary beds of the mircocirculation drained by?

A

Venules

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14
Q

What is in the extracellular compartment of the microcirculation?

A

Fluid and molecules

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15
Q

How quicly does the microcirculation respond to stimuli?

A

Very quickly

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16
Q

What is microcirculation?

A

Circulation of the blood in the smallest blood vessels

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17
Q

Describe the process of increased flow.

A

-changes in vessel radius - flow

-change in the permeability of the vessel wall - exudation

-movement of neutrophils from the vessel to the extravascular space

-increased arteriolar radius causes increased local tissue blood flow

-results in observed redness and heat

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18
Q

Describe the process of Increased permeability

A

-Localised vascular response
-Microvascular bed
-Endothelial leak - fluid and protein not held in vessel lumen (imbalance of Starling forces)
-Locally produced chemical mediators

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19
Q

What is ecudate?

A

A fluid which is rich in protein and contains mostly plasma. Cotains immunogloblin and fibrinogen.

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20
Q

What is the effect of increased permeability?

A

-Net movement of plasma from capillaries to extravascular space
-Exudation

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21
Q

What is leaked in exudation?

A

Ecudate

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22
Q

What are the effects of exudation?

A

-Oedema formed

-Swelling causes pain - reduce function

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23
Q

What is an oedema?

A

Oedema is accumulation of fluid in the extravascular space- this explains swelling of tissue in acute inflammation

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24
Q

What does stasis produce?

A

Change in flow characteristics in the vessel

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25
Q

What is the most important cell in inflammation?

A

Neutrophil polymorphonuclear leukocyte

->call them either neutrophils, polymorphs or NPLs

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26
Q

What happens f you lose normal laminar flo?

A

Red blood cells are aggravated in the centre of the lumen and neutrophils get pushed out to the endothelium

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27
Q

Naame the phases of the emigration of neutrophils.

A

Margination
Pavementing
Emigration

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28
Q

Describe Margination

A

Neutrophils move endothelial saspect of the lumen.

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29
Q

Describe Pavementing

A

Neutrophils adhere to endothelium

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30
Q

Define diapedesis

A

The passive movement of red blood cells through the intact walls of the capillaries, typically accompanying inflammation

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31
Q

Describe Emigration

A

Neutrophils squeeze between endothelial cells - active process - to extravascular tissues

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32
Q

What is the ideal outcome (resolution) of accute inflammation?

A
  1. inciting agent isolated & destroyed
  2. macrophages move in from blood and phagocytose debris; then leave
  3. epithelial surfaces regenerate
  4. inflammatory exudate filters away
  5. vascular changes return to normal
  6. inflammation resolves
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33
Q

What are the benefits of acute inflmmation?

A
  1. rapid response to non-specific insult
  2. cardinal signs and loss of function
  3. transient protection of inflamed area
  4. neutrophils destroy organisms and denature antigen for macrophages
    plasma proteins localise process
  5. resolution and return to normal
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34
Q

Name the four outcomes of acute inflammatoion.

A
  1. Resoluation
  2. Suppuration
  3. Organisation
  4. Chronic inflammation
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35
Q

Ho inflmaHow is acute inflammation named?

A

‘Structure’itis

Meninges= menigitis
Appendix= appendicitis

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36
Q

Name some inflammations which do not follow this ule.

A

lungs = -pneumonia
pleural cavity = -pleurisy

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37
Q

What do neutrophils do and how do they do it?

A

Mobile phagocytes

They recognise foreign antigens, move towards it and adhere to it.

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38
Q

What do granules conatin?

A

Oxidants (H2O) and enzymes (e.g. proteases).

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39
Q

What heppens when the neutrophils adhere to anitgens?

A

They release the granules which pahgocytise and destroyy the foreign antigen.

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40
Q

What is the consequence of neutrophil action?

A

Neutophils die when granule contents released and produce a “soup” of fluid, bits of cell, organisms, endogenous proteins - pus.
This pus might extend into other tissues, progressing the inflammation

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41
Q

What is pus made of?

A

Fluid, bits of cell, organisms, endogenous proteins.

42
Q

What is fibrinigon?

A

Coagulation factor- forms fibrin and clotes exudate.
This localises inflammatory process.

43
Q

What are immunoglobulins?

A

Specialised moleucles which help us destroy antigens. They are specific to the antigen they are developed against.
Part of the immune system.

44
Q

What are the types of mediators regardingacute inflammation??

A

Molecules that appear on surfaces of endothelial cells.

Molecules released from cells.

Molecules in the plasma.

molecules inside cells.

45
Q

hat are the collective effects of Mediators?

A

-Vasodilation
-Increased permeability
-Neutrophil adhesion
-Chemotaxis
-Itch and pain

46
Q

What do cell surface modulaters do?

A

Makes cell surfaces ‘sticky’ which helps neurphils adhere.

47
Q

Give an axample of a surface cell modulator.

A

P-selectin
ICAM-1

48
Q

Give examples of modulators which is a molecules released from and cell and what happens.

A

Histamine- REleased as a result of local injury which causes vasodilation and increased permeability.
Acts via H1 rrecpotros on endothlial cells.

5-hydroxytryptamine (serotonin)-preformed in platelets and released when platelets degranulate in coagulation. Causes vasoconstriction

49
Q

Molecules inside cells- signalling

A

Look over this slide again and make cue cards

(got my AH english grade so got distracted lol)

50
Q

What is MAPK

A

Mitrogen-activated proteins kinases

51
Q

How is MAPK stimulated?

A

Stimulated in inflammation via surface receptors eg toll-like receptors (TLRs)

52
Q

What does MAPK regulate?

A

Regulates pro-inflammatory cytokine production and inflammatory cell recruitMENT

53
Q

What does blood coagulation pathways do?

A

Clots fibrinogen in exudate
which interacts widely with other systems

54
Q

What does fibrinolysis do?

A

Breaks down fibrin, helps maintain blood supply
fibrin breakdown products vasoactive

55
Q

What do complement cascades do?

A

Ties inflammtation with the immune system.

->active components stimulate increased permeability, chemotaxis, phagocytosis, cell breakdown

56
Q

Wat is the outcome of the effect of vasodilation and constrcition?

A

Mediators have positive and negative effects.

57
Q

What is the oucome of the effect of altered permeabilty?

A

Results in a dynamic balance.

58
Q

What is the outcome of the effect of neutrophil adhesion?

A

favours and inhibits acute inflammation

59
Q

What is pyrexia?

A

Raised temperature.

60
Q

What is neutrophillia?

A

Raised white blood cell count.

61
Q

What is lympahdenpathy?

A

regional lympth nodes enlargement. N

62
Q

Name some immediate systemic effects of inflammation

A

Pyrexia
Neutrophillia
Feeling unwell

63
Q

Name some long term effects of inflammation.

A

lympahdenpathy
weight loss
anaemia

64
Q

What are the outcomes of acute inflammation.

A

Pus formation
Pyogenic membrane surrounds pus

65
Q

What is the pyogenic membrane which surrounds pus composed of?

A

capillary sprouts, neutrophils, fibroblasts

66
Q

aWhat does the pyogenic membrane hich surrounds pus do?

A

Walls off pus

67
Q

What is an abscess?

A

Collection of pus (suppuration) under pressure

68
Q

Discuss abscesses.

A

-single locule, multiloculated
-“points” and discharges
-collapses - healing and repair

69
Q

Discuss the suppuration of an abscess.

A

Ingrowth of granulation tissue (pyogenic membrane) under the epithelial surface. Discahrge of pus from surface.

70
Q

What happens in Multiloculated abscess?

A

Pus bursts through pyogenic membrane and forms new cavities

71
Q

Define empyema.

A

Pockets of pus that have collected inside a body cavity

72
Q

Name two places you might find an empyema.

A

Gall bladder
Pleural cavity

73
Q

Define pyaemia

A

Blood poisoning (septicaemia) caused by the spread in the bloodstream of pus-forming bacteria released from an abscess.

74
Q

Discuss the organisation of the outcome of acute inflammation.

A

-granulation tissue is characteristic
-healing and repair
-leads to fibrosis and formation of a scar

75
Q

What is granulation tissue?

A

“universal patch” – repair kit – for all damage

76
Q

What is granulation tissue formed of?

A

-new capillaries - angiogenesis
-fibroblasts and collagen
-macrophages

77
Q

Define dissemination.

A

The spread of something.

78
Q

What is bacteraemia?

A

Bacteria in blood.

79
Q

What is septicaemia?

A

Growth of bacteria in blood

80
Q

What is toxaemia?

A

Toxic products in blood

81
Q

BP?

A

Blood pressure

82
Q

CO?

A

Cardiac output

83
Q

SV?

A

Stroke volume

84
Q

HR?

A

Heart rate

85
Q

Cardiac ouput=

A

CO=SVxHR

86
Q

SVR=?

A

Systemic vascular resistance

87
Q

Blood pressure =?

A

BP = CO x SVR

88
Q

Name an effect of of systemic infection.

A

Shock resulting in an inability to perfuse tissues

89
Q

List some clinical picture of early septic shock

A

-peripheral vasodilatation
-tachycardia - high heart rate
-hypotension - low blood pressure
-often pyrexia
-sometimes haemorrhagic skin rash

90
Q

How does septic shock occur?

A

Systemic release of chemical mediators from cells into plasma
Increased heart rate compensates - CO = SV x HR
Bacterial endotoxin released
Activation of coagulation

91
Q

What do mediators do and what does this cause in regards to septic shock?

A

Mediators cause vasodilation causing loss of systemic vascular resistance (SVR) - BP = CO x SVR.
This results in catecholamine release.
Tachycardia (increased heart rate) follows to maintain (CO) because increased heart rate compensates - CO = SV x HR

92
Q

What bacterial endotoxin is released regarding septic shock?

What does this act on?

A

Interleukin-1 released

Acts on hypothalamus - pyrexia

93
Q

What does the coagulation step of septic shock involve?

A

Disseminated intravascular coagulation
Vasoactive chemical - vasodilatation
Haemorrhagic skin rash

94
Q

What can occur when compensation fails?

A

-Raised HR insufficient to maintain cardiac output
-SVR low; so, BP falls
-Reduced perfusion of tissues

95
Q

What can reduced perfusion (passage of fluid through the circulatory system or lymphatic system to an organ or a tissue, usually referring to the delivery of blood to a capillary bed in tissue) of tissues lead to?

A

Tissue hypoxia
Loss of cell tissue and organ function

96
Q

What is the outcome of septic shock?

A

Potentially fatal.
Tissue hypoxia - cell death
Haemorrhage
Requires urgent intervention and support

97
Q

Name the five outcomes of acute inflammation.

A

-Resolution
-Suppuration
-Organisation
-Dissemination
-Chronic inflammation

98
Q

Where does acute inflammation occur?

A

Microcirulation

99
Q

What is chemotaxis regarding neutrophils?

A

The neutrophils move towards the foreign sntigen

100
Q

Are neutrophils specific or non-specific?

A

Non-specific

101
Q

Are immunoglobulins specific or non=specific?

A

Specific

Year 1- Principles of Disease (FOM) (40 decks)

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