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Foundations of Medicine > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

Define acute inflammation

A

Physiological response to tissue damage.

A series of protective changes occurring in living tissue as a fundamantal response to injury to maintain the integrity of the organism

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2
Q

What are the cardinal signs of inflammation?

A

Rumor - redness
Calor - heat
Tumour -swelling
Dolor - pain
Loss of function

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3
Q

What are the causes of acute inflammation?

A

Microorganisms
Trauma
Chemical
Physical - extreme conditions such as heat, cold, radiation
Necrosis (Dead tissues irritating adjacent tissues)
Hypersensitivities

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4
Q

Features of the process of acute inflammation

A

Series of microscopic events
Localised to affected tissue
Takes place in microcirculation
Results in the cardinal signs

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5
Q

What is microcirculation?

A

Capillary beds (fed by arterioles and drained by venules)

Extracellular space and fluid and molecules within

Lymphatic channels and drainage

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6
Q

What creates dynamic balance?

A

Hydrostatic and colloid osmotic pressures
Compartments and physical constants

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7
Q

Define hydrostatic pressure

A

Pressure exerted by a fluid

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8
Q

Define oncotic pressure

A

Pressure exerted by proteins in the blood vessel plasma

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9
Q

What are the step in acute inflammation pathogenesis?

A
  1. Change in vessel radius
  2. Change in the permeability of the vessel wall - exudation - endothelium becomes more or less permissive which changes the amount of fluid that can go through the membrane
  3. Movement of neutrophils from the vessel to the extravascular space
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10
Q

What is exudation?

A

Plasma (fluid) moves from the capillary(vessel) to the extracellular space

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11
Q

What is exudate?

A

The fluid that is leaked - rich in plasma proteins (immunoglobulin and fibrionogen)

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12
Q

What does increased arteriolar radius cause?

A

Increased local tissue blood flow which causes:

Redness - Rubour
Heat - Calor

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13
Q

Features of increased permeability

A

Localized vascular response occurring in the microvascular bed

Endothelial leak - fluid and protein not held in the vessel lumen

Locally produced chemical mediators

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14
Q

What is the effect of exudation?

A

Oedema - accumulation of fluid in the extravascular space - is formed

There is swelling, pain and reduced function

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15
Q

What is the effect of exudation on blood viscosity?

A

Increased viscosity - rate of blood slows down aka stasis

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16
Q

Describe the structure of the blood flow in inflammation

A

RBC’s aggregate in the center of the lumen and neutrophils are found near the endothelium

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17
Q

How are the components of blood laid out?

A

Plasma sits on the outside because it is the smallest

The erythrocytes, the red cells are the next layer.

Then the white cells, particularly neutrophils in the centre.

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18
Q

What is the most important cell in the flow in inflammation?

A

Neutrophil (polymorphonuclear leukocyte)

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19
Q

What do we see in flow in inflammation?

A

Loss of nromal laminar flow
Red cells aggregate in the centre of the lumen
Neutrophils found near endothelium

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20
Q

What are the phases of emigration of neutrophils?

A

Margination - neutrophils move to the endothelial aspect of the lumen

Pavementing - neutrophils adhere to the endothelium

Emigration - neutrophils squeeze between endothelial cells - active process - to extravascular tissues

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21
Q

What does diapedesis mean?

A

Passage of blood cells through the intact walls of the capillaries, typically accompanying inflammation.

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22
Q

What are the benefits of acute inflammation?

A

Rapid response to non-specific injury
Protection in the inflamed area from cardinal signs
Neutrophils destroy organisms and denature antigens for macrophages
Plasma proteins localise process
Resolution and return to normal

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23
Q

What are the outcomes of acute inflammation?

A

Resolution
Suppuration - pus formation
Organization -tissue growth
Chronic infection

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24
Q

Name inflammation at the following sites:

Peritoneal cavity
Meninges
Appendix
Lungs
Pleural cavity

A

Peritonitis
Meningitis
Appendicitis
Pneumona
Plearisy

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25
Q

What do neutrophils do?

A

Recognise foreign antigen and move towards it - chemotaxis

Adhere to the organism

They are mobile phagocytes

Phagocytose and destroy the foreign antigen

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26
Q

What do the granules that contain neutrophils release the contents of?

A

Possess oxidants - H202 and enzymes (proteases)

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27
Q

When does a neutrophil die?

A

When granule contents are released

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28
Q

What is pus?

A

Produced by neutrophils - its a fluid made up of bits of cells, organisms, endogenous proteins

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28
Q

What is fibrinogen?

A

A plasma protein - coagulating factor forming fibrin which clots exudate, localises inflammatory process

29
Q

What plasma protein is responsible for humoural immune response?

A

Immunoglobulins

30
Q

What does humoural mean?

A

Relates to the immune response that involves the release of antibodies in circulating bodily fluids

31
Q

Where are the mediators of acute inflammations?

A

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

32
Q

What are endothelial cells?

A

Linings of the walls of blood vessels

33
Q

What the collective effects of mediators?

A

Vasodilation
Increased permeability
Neutrophil adhesion - mediators from different cells adhere because of their mediators
Chemotaxis
Itch and pain

34
Q

Describe the action of adhesion molecules that appear on endothelial cells

A

Help neutrophils stick
ICAM - 1

35
Q

Describe the function of P-Selectin

A

Interacts with neutrophil surface

36
Q

What releases histamine?

A

Mast cells beside vessels, platelets, basophils

37
Q

When is histamine released?

A

As a result of local injury

38
Q

What is the effect of histamine?

A

Vasodilation, increases permeability, acts via H1 receptors (histamine receptors) on endothelial cells

39
Q

What is another name for serotonin?

A

5 - hydroxytryptamine

40
Q

Where is seratonin released from?

A

Platelets, when they degranulate in coagulation
Vasoconstriction - to keep useful materials in the correct place

41
Q

What are the immediate systemic effects of acute inflammation?

A

Pyrexia - endogenous pyrogens from white blood cells act centrally

Feel unwell - malaise, anorexia, nausea, abdominal pain, vomiting in chilrdren

Neutrophilia - raised WBC count

42
Q

What are the long term effects of inflammation?

A

Lymphadenopathy - lymph node enlargements
Weight loss - catabolic process
Anaemia

43
Q

Describe what suppuration is

A

Pus formation

Pyogenic membrane surrounds pus (capillary sprouts neutrophils, fibroblasts - walls off pus)

44
Q

What is an abscess?

A

Collection of pus under pressure

45
Q

What is a multiloculated abscess?

A

Pus burts through the pyogenic membrane - forms new cavities

46
Q

What is empyema?

A

Pus in a hollow viscus (gall bladder, pleural cavity)

47
Q

What is pyaemia?

A

Discharge of pus to the blood stream

48
Q

What is organisation?

A

Healing and repair - leads to fibrosis and formation of scar

Granulation tissue characteristic

49
Q

What is granulation tissue?

A

Universal patch

It is formed of new capillaries
Fibroblasts and collagen
Macrophages

50
Q

Describe the outcome of dissemination

A

Spreads to the bloodstream - patient is now described as septic

51
Q

What is the difference between bacteraemia and septicaemia?

A

Bacteria in blood versus the growth of bacteria in blood

52
Q

What is toxaemia?

A

Toxic products in the blood

53
Q

How do you calculate cardiac output?

A

Stroke volume multiplied by heart rate

54
Q

How can you calculate blood pressure?

A

Cardiac output multiplied by systemic vascular resistance

55
Q

Define SVR

A

An index of arteriolar constriction throughout the body, calculated by dividing the blood pressure by the cardiac output.

56
Q

What is the effect of systemic infection?

A

Shock - inability to perfuse tissue

57
Q

What is the clinical picture of early septic shock

A

Peripheral vasodilation
Tachycardia
Hypotension
Often pyrexia
Sometimes haemorrhagic skin rash - blood vessels leaking

58
Q

What is the effect of bacterial endotoxin?

A

Interleukin- 1 is released - acts on hypothalamus - pyrexia

59
Q

What is the effect of prostglandins? (archidonic acid metabolite)

A

Histamine effects and inhibit inflammatory cells

Thromboxan A2 - promotes platelet aggregation and vasoconstriction

60
Q

What is a leukotriene? (archidonic acid metabolite)

A

Any substance which is derived from a leucocyts (white blood cell)

61
Q

Are leukotrines vasoactive?

A

Yes, they increase permeability and constrict smooth muscle

62
Q

What is the effect of omega 3 polyunsaturated fatty acids?

A

Decreases synthesis of archidonic acid derived inflammatory mediators

63
Q

What is the function of NO?

A

Released by various cells.

Responsible for smooth muscle relaxation, anti-platelet, regulate functional activity, growth and death of many cell types including macrophages, T lymphocytes, antigen presenting cells, mast cells, neutrophils and natural killer cells.

It regulates leukocyte recruitment to inflammatory focus

64
Q

What are the effects of oxygen free radicals and what are their names?

A

H2O2, OH-, O2-

Released by neutrophils on phagocytosis

Amplify other mediator effects

65
Q

What are the different plasma enzymes involved?

A

Blood coagulation pathways - clotting fibrinogen in exudate

Fibrinolysis - breaks down fibrin maintaining blood supply. The breakdown products are vasoactive

Kinin system - bradykinin is responsible for pain

Complement cascade -
Increase permeability, chemotaxis, phagocytosis, cell breakdown

66
Q

What is the pathogenesis of septic shock?

A

There is a release of chemical mediators from cells into plasma

Mediators cause vasodilation
Vasodilation results in loss of systemic vascular resistance

This results in catecholamine (adrenaline and noradrenaline release)

Tachycardia follows to maintain cardiac output

Bacterial endotoxins are released (interleukin- 1 - pyrexia)

67
Q

The increased heart rate is insufficient to maintain cardiac output during septic shock, what is the effect of this?

A

Blood pressure drops due to reduced SVR

There is a reduced perfusion of tissues, hypoxia and loss of cell tissue and organ function

68
Q

What is the outcome of septic shock?

A

Rapidly fatal
Tissue hypoxia
Haemorrhage
Requires immediate intervention and support

69
Q

What are the outcomes of acute inflammation?

A

Resolution
Suppuration
Organisation
Dissemination
Chronic inflammation

Foundations of Medicine (56 decks)

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