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

Acute Inflammation Flashcards

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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
What is the most important cell in inflammation?
Neutrophil polymorphonuclear leukocyte ->call them either neutrophils, polymorphs or NPLs
26
What happens f you lose normal laminar flo?
Red blood cells are aggravated in the centre of the lumen and neutrophils get pushed out to the endothelium
27
Naame the phases of the emigration of neutrophils.
Margination Pavementing Emigration
28
Describe Margination
Neutrophils move endothelial saspect of the lumen.
29
Describe Pavementing
Neutrophils adhere to endothelium
30
Define diapedesis
The passive movement of red blood cells through the intact walls of the capillaries, typically accompanying inflammation
31
Describe Emigration
Neutrophils squeeze between endothelial cells - active process - to extravascular tissues
32
What is the ideal outcome (resolution) of accute inflammation?
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
33
What are the benefits of acute inflmmation?
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
34
Name the four outcomes of acute inflammatoion.
1. Resoluation 2. Suppuration 3. Organisation 4. Chronic inflammation
35
Ho inflmaHow is acute inflammation named?
'Structure'itis Meninges= menigitis Appendix= appendicitis
36
Name some inflammations which do not follow this ule.
lungs = -pneumonia pleural cavity = -pleurisy
37
What do neutrophils do and how do they do it?
Mobile phagocytes They recognise foreign antigens, move towards it and adhere to it.
38
What do granules conatin?
Oxidants (H2O) and enzymes (e.g. proteases).
39
What heppens when the neutrophils adhere to anitgens?
They release the granules which pahgocytise and destroyy the foreign antigen.
40
What is the consequence of neutrophil action?
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
41
What is pus made of?
Fluid, bits of cell, organisms, endogenous proteins.
42
What is fibrinigon?
Coagulation factor- forms fibrin and clotes exudate. This localises inflammatory process.
43
What are immunoglobulins?
Specialised moleucles which help us destroy antigens. They are specific to the antigen they are developed against. Part of the immune system.
44
What are the types of mediators regardingacute inflammation??
Molecules that appear on surfaces of endothelial cells. Molecules released from cells. Molecules in the plasma. molecules inside cells.
45
hat are the collective effects of Mediators?
-Vasodilation -Increased permeability -Neutrophil adhesion -Chemotaxis -Itch and pain
46
What do cell surface modulaters do?
Makes cell surfaces 'sticky' which helps neurphils adhere.
47
Give an axample of a surface cell modulator.
P-selectin ICAM-1
48
Give examples of modulators which is a molecules released from and cell and what happens.
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
Molecules inside cells- signalling
Look over this slide again and make cue cards (got my AH english grade so got distracted lol)
50
What is MAPK
Mitrogen-activated proteins kinases
51
How is MAPK stimulated?
Stimulated in inflammation via surface receptors eg toll-like receptors (TLRs)
52
What does MAPK regulate?
Regulates pro-inflammatory cytokine production and inflammatory cell recruitMENT
53
What does blood coagulation pathways do?
Clots fibrinogen in exudate which interacts widely with other systems
54
What does fibrinolysis do?
Breaks down fibrin, helps maintain blood supply fibrin breakdown products vasoactive
55
What do complement cascades do?
Ties inflammtation with the immune system. ->active components stimulate increased permeability, chemotaxis, phagocytosis, cell breakdown
56
Wat is the outcome of the effect of vasodilation and constrcition?
Mediators have positive and negative effects.
57
What is the oucome of the effect of altered permeabilty?
Results in a dynamic balance.
58
What is the outcome of the effect of neutrophil adhesion?
favours and inhibits acute inflammation
59
What is pyrexia?
Raised temperature.
60
What is neutrophillia?
Raised white blood cell count.
61
What is lympahdenpathy?
regional lympth nodes enlargement. N
62
Name some immediate systemic effects of inflammation
Pyrexia Neutrophillia Feeling unwell
63
Name some long term effects of inflammation.
lympahdenpathy weight loss anaemia
64
What are the outcomes of acute inflammation.
Pus formation Pyogenic membrane surrounds pus
65
What is the pyogenic membrane which surrounds pus composed of?
capillary sprouts, neutrophils, fibroblasts
66
aWhat does the pyogenic membrane hich surrounds pus do?
Walls off pus
67
What is an abscess?
Collection of pus (suppuration) under pressure
68
Discuss abscesses.
-single locule, multiloculated -“points” and discharges -collapses - healing and repair
69
Discuss the suppuration of an abscess.
Ingrowth of granulation tissue (pyogenic membrane) under the epithelial surface. Discahrge of pus from surface.
70
What happens in Multiloculated abscess?
Pus bursts through pyogenic membrane and forms new cavities
71
Define empyema.
Pockets of pus that have collected inside a body cavity
72
Name two places you might find an empyema.
Gall bladder Pleural cavity
73
Define pyaemia
Blood poisoning (septicaemia) caused by the spread in the bloodstream of pus-forming bacteria released from an abscess.
74
Discuss the organisation of the outcome of acute inflammation.
-granulation tissue is characteristic -healing and repair -leads to fibrosis and formation of a scar
75
What is granulation tissue?
“universal patch” – repair kit – for all damage
76
What is granulation tissue formed of?
-new capillaries - angiogenesis -fibroblasts and collagen -macrophages
77
Define dissemination.
The spread of something.
78
What is bacteraemia?
Bacteria in blood.
79
What is septicaemia?
Growth of bacteria in blood
80
What is toxaemia?
Toxic products in blood
81
BP?
Blood pressure
82
CO?
Cardiac output
83
SV?
Stroke volume
84
HR?
Heart rate
85
Cardiac ouput=
CO=SVxHR
86
SVR=?
Systemic vascular resistance
87
Blood pressure =?
BP = CO x SVR
88
Name an effect of of systemic infection.
Shock resulting in an inability to perfuse tissues
89
List some clinical picture of early septic shock
-peripheral vasodilatation -tachycardia - high heart rate -hypotension - low blood pressure -often pyrexia -sometimes haemorrhagic skin rash
90
How does septic shock occur?
Systemic release of chemical mediators from cells into plasma Increased heart rate compensates - CO = SV x HR Bacterial endotoxin released Activation of coagulation
91
What do mediators do and what does this cause in regards to septic shock?
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
What bacterial endotoxin is released regarding septic shock? What does this act on?
Interleukin-1 released Acts on hypothalamus - pyrexia
93
What does the coagulation step of septic shock involve?
Disseminated intravascular coagulation Vasoactive chemical - vasodilatation Haemorrhagic skin rash
94
What can occur when compensation fails?
-Raised HR insufficient to maintain cardiac output -SVR low; so, BP falls -Reduced perfusion of tissues
95
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?
Tissue hypoxia Loss of cell tissue and organ function
96
What is the outcome of septic shock?
Potentially fatal. Tissue hypoxia - cell death Haemorrhage Requires urgent intervention and support
97
Name the five outcomes of acute inflammation.
-Resolution -Suppuration -Organisation -Dissemination -Chronic inflammation
98
Where does acute inflammation occur?
Microcirulation
99
What is chemotaxis regarding neutrophils?
The neutrophils move towards the foreign sntigen
100
Are neutrophils specific or non-specific?
Non-specific
101
Are immunoglobulins specific or non=specific?
Specific

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

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