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Principles of Disease-Megan > Acute Inflammation > Flashcards

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
Q

Give an example of a prostglandins and its actions

A

Thromboxane A2
Promotes platelet aggregation and vasoconstriction

Opposite to PGD2 and PGE2
PGE determines the effectiveness of non-steroidal anti-inflammatory drugs.

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26
Q

Give examples of leukotrines

A

Neutrophils

They are vasoactive so have a dynamic effect on vessels to increase permeability as well as constrict smooth muscle

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27
Q

What are prostglandins

A

Arachidonic acid metabolites from the cyclo-oxygenase pathway

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28
Q

What are leukotrines

A

Arachidonic acid metabolites from the lipoxygenase pathway

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29
Q

What do omega-3 polyunsaturated fatty acids do

A

Decrease the synthesis of arachidonic acid that is derived from inflammatory mediators

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30
Q

Where are platelet-activating factors (PAF) present

A

Cell membrane of activated inflammatory cells

31
Q

What is the function of platelet-activating factors (PAF)

A

Reduce the permeability of cell membranes through the enhancement of platelet degranulation at the site of injury

32
Q

What are cytokines and chemokines

A

Small molecules produced by macrophages, lymphocytes and endothelium in response to inflammatory stimuli

33
Q

What do cytokines and chemokines do

A

Attract inflammatory cells

34
Q

Where is nitric oxide (NO) found

A

In various cells

35
Q

What does nitric oixide do

A

Promotes smooth muscle relaxation and anti-platelets

Regulates recruitment to the inflammatory focus

36
Q

Where are oxygen free radicals released from

A

Neutrophils in phagocytosis

37
Q

What do oxygen free radicals do

A

Amplify other mediator effects

38
Q

Give examples of oxygen free radicals

A

H2O2
OH-
O2-

39
Q

Name 4 plasma mediators

A

Blood coagulation pathways
Fibrinolysis
Kinin system
Complement cascade

40
Q

What does the blood coagulation pathway do

A

Clots fibrinogen in exudate

Interacts widely with other systems

41
Q

What does fibrinolysis do

A

Breaks down fibrin to help maintain blood supply

Fibrin breakdown products are vasoactive.

42
Q

What does the kinin system do

A

Produces bradykinin to cause pain (reduce pain threshold)

43
Q

What does the complement cascade do

A

Ties inflammation with the immune system

The active components stimulate increased permeability, chemotaxis, phagocytosis and cell breakdown.

44
Q

What are the overall effects mediators can cause

A 
Vasodilatation and constriction
Altered permeability
Neutrophil adhesion
Chemotaxis
Itch and pain
45
Q

Mediators…

A

Have positive and negative effects, result is a dynamic balance, favours and inhibits acute inflammation, relative to need

46
Q

List the systemic effects of acute inflammation

A

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
Q

What is suppuration

A

Pus formation

48
Q

What does pus contain

A 
Dead tissue
Organisms
Exudate
Neutrophils
Fibrin
Red cells
Debris
49
Q

What does the pyogenic membrane surround

A

Pus (walls off pus)

50
Q

What does the pyogenic membrane contain

A

Capillary sprouts
Neutrophils
Fibroblasts

51
Q

What is an abscess

A

A collection of pus under pressure which can either be a single locule or multiloculated

52
Q

What do abscess have

A

‘Points’ and discharges

53
Q

How does a multiloculated abscess occur

A

When pus bursts through the pyogenic membrane and forms new cavities

54
Q

What is an empyema

A

A hollow viscus of pus either in the gall bladder or pleural cavity

55
Q

What is a pyaemia

A

When discharge (pus) enters the bloodstream

56
Q

What is organisation (an outcome of inflammation)

A

Granulation tissue
Healing and repair
Leads to fibrosis and formation of a scar

57
Q

What is granulation tissue

A

A ‘universal patch’ i.e. a repair kit for all damage

58
Q

What is granulation tissue formed of

A

New capillaries (angiogenesis)
Fibroblasts and collagen
Macrophages

59
Q

What is dissemination

A

An outcome of acute of inflammation where there is a spread into the bloodstream

60
Q

What is bacteraemia

A

Bacteria in the blood

61
Q

What is septicaemia

A

Growth of bacteria

62
Q

What is toxaemia

A

Toxic products in the blood

63
Q

What are the components of cardiovascular physiology

A 
Blood pressure (BP)
Cardiac output (CO) 
Stroke volume (SV)
Heart rate (HR)
Systemic vascular resistance  (SVR)
64
Q

How can cardiac output be calculate

A

CO = SV x HR

65
Q

How can blood pressure be calculated

A

BP = CO x SVR

66
Q

State the indications of early septic shock

A 
Peripheral vasodilatation
Tachycardia - high heart rate
Hypotension - low blood pressure
Often pyrexia
Sometimes haemorrhagic skin rash
67
Q

How does septic shock occur

A

Through the systemic release of chemical mediators from cells into plasma

68
Q

What do the mediators released in septic shock cause

A

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
Q

What type of bacterial toxin is released in septic shock

A

Interleukin-1 which acts on hypothalamus causing pyrexia

70
Q

What does the activation of coagulation in septic shock cause

A 
Disseminated intravascular coagulation
Vasoactive chemicals (vasodilatation)
Haemorrhagic skin rash
71
Q

What happens when the increased heart rate compensation fails

A

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
Q

What is the outcome of septic shock

A

It is rapidly fatal
Tissue hypoxia - cell death
Haemorrhage

73
Q

What does septic shock require

A

Urgent intervention and support

Principles of Disease-Megan (41 decks)

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