Acute Inflammation Flashcards

1
Q

Define acute inflammation

A

A fundamental response to maintain the integrity of organism

A series of protective changes occurring in living tissue as a response to injury

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2
Q

What are the cardinal signs of inflammation

A
Rubor - redness
Calor - heat
Tumor - swelling
Dolor - pain
Loss of function
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3
Q

What are the causes of acute inflammation

A

Microorgansims -including bacteria, fungi, viruses, parasites
Mechanical trauma - injury to tissues even in surgery
Chemical - unstable environment e.g. upset pH or bile and urine causing irritation when in inappropriate places
Physical - extreme conditions e.g. heat, cold, ionising radiation
Dead tissue - cell necrosis irritates adjacent tissue
Hypersensitivity - causes several classes of reaction

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4
Q

What changes occur in acute inflammation

A

Changes in:
Vessel radius (flow)
The permeability of the vessel wall (exudation)
And movement of neutrophils from the vessel to the extravascular space

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5
Q

What are the benefits of acute inflammation

A

A rapid response to non-specific insult
Cardinal signs and loss of function (allowing transient protection of the inflamed area)
The neutrophils destroy organisms and denature antigens for macrophages
Plasma proteins localise the process
It can be resolved and return to normal

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6
Q

What is acute inflammation

A

Series of microscopic events occur which are localised to the affected tissue
They take place in the microcirculation
Result in the clinical symptoms and signs of acute inflammation

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7
Q

What happens in the process of exudation

A

There is a net movement of plasma from capillaries to extravascular space causing fluid to be leaked which is exudate

Exudate fluid is rich in protein and plasma and it includes Ig and fibrinogen

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8
Q

What can exudation cause

A

Oedema - the accumulation of fluid in the extravascular space

Presents as the swelling of tissue in acute inflammation which cause pain and reduce function

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9
Q

How are inflammation at various anatomical positions named

A

“Structure”-itis
e.g. peritoneal cavity inflammation is peritonitis, meninges inflammation is meningitis, appendix inflammation is appendicitis.

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10
Q

What is an exemption to the rule of how inflammation is named

A

Lungs which is known as pneumonia

Pleural cavity is known as pleurisy

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11
Q

What is the role of neutrophils

A
They are mobile phagocytes
Recognise foreign antigen
Adhere to organism
Release granule contents 
Phagocytose and destroy foreign antigen
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12
Q

What do the granules in neutrophils contain

A

Oxidants (e.g. H202)

Enzymes

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13
Q

What happens to the neutrophil when the granule contents are released

A

They die

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14
Q

What is produced from a neutrophil

A

A ‘soup’ of fluid
Bits of cell
Organisms
Endogenous proteins

This is known as pus

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15
Q

What is fibrinogen

A

A coagulation factor which forms fibrin and colts exutade

It localises inflammatroy processes

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16
Q

What is the role of immunoglobulins in plasma

A

They are specific for the antigen

Involved in the humoural immune response

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17
Q

Name the type of mediators in acute inflammation

A

Molecules on endothelial cell surface membrane,
Molecules released from cells
Molecules in the plasma

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18
Q

What are the collective effects of mediators

A
Vasodilatation
Increased permeability
Neutrophil adhesion
Chemotaxis
Itch and pain
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19
Q

What are cell surface mediatiors

A

Adhesion molecules which appear on endothelial cells

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20
Q

Give example of cell surface mediatiors

A

ICAM-1 which help neutrophils stick

P-selectin which interact with the neutrophil surface

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21
Q

Give examples of the molecules released from cells

A

Histamine
5-hydroxytryptamine (serotonin)
Prostgladins (arachidonic acid metabolites via cyclo-oxygenase pathway)
Leukotrienes (arachidonic acid metabolites via lipoxygenase pathway
Omega-3 polyunsaturated fatty acids
Platelet-activating factor (PAF)
Cytokines and chemokines (e.g. TNFα, IL-1)
Nitric oxide (NO)
Oxygen free radicals (H2O2, OH-, O2-)

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22
Q

Describe histamine

A

Preformed in mast cells beside vessels, platelets and basophils
Released due to local injury which cause IgE mediated reactions
Cause vasodilatation
Increase permeability
Act via H1 receptors on endothelial cells

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23
Q

Describe 5-hydroxytryptamine (serotine)

A

Preformed in platelets

Released when platelets degranulate in coagulation causing vasoconstriction

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24
Q

Describe prostglandins (arachidonic acid metabolites via cyclo-oxygenase pathway)

A

Formed from many cells including endothelium and leukocytes

Many of the cells promote histamine effects and inhibit inflammatory cells

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25
Give an example of a prostglandins and its actions
Thromboxane A2 Promotes platelet aggregation and vasoconstriction Opposite to PGD2 and PGE2 PGE determines the effectiveness of non-steroidal anti-inflammatory drugs.
26
Give examples of leukotrines
Neutrophils | They are vasoactive so have a dynamic effect on vessels to increase permeability as well as constrict smooth muscle
27
What are prostglandins
Arachidonic acid metabolites from the cyclo-oxygenase pathway
28
What are leukotrines
Arachidonic acid metabolites from the lipoxygenase pathway
29
What do omega-3 polyunsaturated fatty acids do
Decrease the synthesis of arachidonic acid that is derived from inflammatory mediators
30
Where are platelet-activating factors (PAF) present
Cell membrane of activated inflammatory cells
31
What is the function of platelet-activating factors (PAF)
Reduce the permeability of cell membranes through the enhancement of platelet degranulation at the site of injury
32
What are cytokines and chemokines
Small molecules produced by macrophages, lymphocytes and endothelium in response to inflammatory stimuli
33
What do cytokines and chemokines do
Attract inflammatory cells
34
Where is nitric oxide (NO) found
In various cells
35
What does nitric oixide do
Promotes smooth muscle relaxation and anti-platelets | Regulates recruitment to the inflammatory focus
36
Where are oxygen free radicals released from
Neutrophils in phagocytosis
37
What do oxygen free radicals do
Amplify other mediator effects
38
Give examples of oxygen free radicals
H2O2 OH- O2-
39
Name 4 plasma mediators
Blood coagulation pathways Fibrinolysis Kinin system Complement cascade
40
What does the blood coagulation pathway do
Clots fibrinogen in exudate | Interacts widely with other systems
41
What does fibrinolysis do
Breaks down fibrin to help maintain blood supply | Fibrin breakdown products are vasoactive.
42
What does the kinin system do
Produces bradykinin to cause pain (reduce pain threshold)
43
What does the complement cascade do
Ties inflammation with the immune system | The active components stimulate increased permeability, chemotaxis, phagocytosis and cell breakdown.
44
What are the overall effects mediators can cause
``` Vasodilatation and constriction Altered permeability Neutrophil adhesion Chemotaxis Itch and pain ```
45
Mediators...
Have positive and negative effects, result is a dynamic balance, favours and inhibits acute inflammation, relative to need
46
List the systemic effects of acute inflammation
Pyrexia (raised temperature) - the endogenous pyrogens from white cells will act centrally Feeling unwell – this can include: malaise, anorexia and nausea (abdominal pain and vomiting in children) Neutrophilia (raised white cell count) - bone marrow releases/produces more Lymphadenopathy (regional lymph node enlargement) – this is due to an immune response Weight loss – catabolic process Anaemia Shock – inability to perfuse tissues
47
What is suppuration
Pus formation
48
What does pus contain
``` Dead tissue Organisms Exudate Neutrophils Fibrin Red cells Debris ```
49
What does the pyogenic membrane surround
Pus (walls off pus)
50
What does the pyogenic membrane contain
Capillary sprouts Neutrophils Fibroblasts
51
What is an abscess
A collection of pus under pressure which can either be a single locule or multiloculated
52
What do abscess have
‘Points’ and discharges
53
How does a multiloculated abscess occur
When pus bursts through the pyogenic membrane and forms new cavities
54
What is an empyema
A hollow viscus of pus either in the gall bladder or pleural cavity
55
What is a pyaemia
When discharge (pus) enters the bloodstream
56
What is organisation (an outcome of inflammation)
Granulation tissue Healing and repair Leads to fibrosis and formation of a scar
57
What is granulation tissue
A 'universal patch' i.e. a repair kit for all damage
58
What is granulation tissue formed of
New capillaries (angiogenesis) Fibroblasts and collagen Macrophages
59
What is dissemination
An outcome of acute of inflammation where there is a spread into the bloodstream
60
What is bacteraemia
Bacteria in the blood
61
What is septicaemia
Growth of bacteria
62
What is toxaemia
Toxic products in the blood
63
What are the components of cardiovascular physiology
``` Blood pressure (BP) Cardiac output (CO) Stroke volume (SV) Heart rate (HR) Systemic vascular resistance (SVR) ```
64
How can cardiac output be calculate
CO = SV x HR
65
How can blood pressure be calculated
BP = CO x SVR
66
State the indications of early septic shock
``` Peripheral vasodilatation Tachycardia - high heart rate Hypotension - low blood pressure Often pyrexia Sometimes haemorrhagic skin rash ```
67
How does septic shock occur
Through the systemic release of chemical mediators from cells into plasma
68
What do the mediators released in septic shock cause
Vasodilation causing loss of systemic vascular resistance (SVR) Results in catecholamine release Tachycardia follows to maintain cardiac output because the increased heart rate compensates
69
What type of bacterial toxin is released in septic shock
Interleukin-1 which acts on hypothalamus causing pyrexia
70
What does the activation of coagulation in septic shock cause
``` Disseminated intravascular coagulation Vasoactive chemicals (vasodilatation) Haemorrhagic skin rash ```
71
What happens when the increased heart rate compensation fails
The raised HR is insufficient to maintain the cardiac output so SVR is low and BP falls. This means there is reduced perfusion of the tissues causing tissue hypoxia and the loss of cell tissue and organ functions
72
What is the outcome of septic shock
It is rapidly fatal Tissue hypoxia - cell death Haemorrhage
73
What does septic shock require
Urgent intervention and support