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semester 1 > Acute Inflammation 2 > Flashcards

Acute Inflammation 2 Flashcards

1
Q

What is the name of inflammation at these various sites?
Peritoneal cavity
Meninges
Appendix
Lungs
Pleural cavity

A

Peritonitis
Meningitis
Appendicitis
Pneumonia
Plearisy

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2
Q

What do neutrophils do?

A

Recognise foreign antigen
Move towards it - chemotaxis
Adhere to the organism

They are mobile phagocytes

Phagocytose and destroy foreign antigen

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3
Q

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

A

Possess oxidants - H202 and enzymes (proteases )

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4
Q

When does a neutrophil die?

A

When granule contents are released

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5
Q

What is pus?

A

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

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6
Q

What is fibrinogen?

A

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

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7
Q

What plasma protein is responsible for humoural immune response?

A

Immunoglobulins

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8
Q

What does humoural mean?

A

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

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9
Q

Where are the mediators of acute inflammations?

A

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

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10
Q

What are endothelial cells?

A

Line the walls of blood vessels

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11
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

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12
Q

Describe the action of adhesion molecules that appear on endothelial cells

A

Help neutrophils stick
ICAM - 1

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13
Q

Describe the function of P-Selectin

A

Interacts with neutrophil surface

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14
Q

What releases histamine?

A

Mast cells beside vessels, platelets, basophils

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15
Q

When is histamine released?

A

As a result of local injury

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16
Q

What is the effect of histamine?

A

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

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17
Q

What is another name for serotonin?

A

5 - hydroxytryptamine

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18
Q

Where is seratonin released from?

A

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

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19
Q

What are the immediate systemic effects of 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

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20
Q

What are the long term effects of inflammation?

A

Lymphadenopathy - lymph node enlargements
Weight loss - catabolic process
Anaemia

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21
Q

Describe what suppuration is

A

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

22
Q

What is an abscess?

A

Collection of pus under pressure

23
Q

What is a multiloculated abscess?

A

Pus burts through the pyogenic membrane - forms new cavities

24
Q

What is empyema

A
  • pus in a hollow viscus (gall bladder, pleural cavity)
25
Q

What is pyaemia

A

Discharge of pus to the blood stream

26
Q

What is organisation?

A

Healing and repair - leads to fibrosis and formation of scar

Granulation tissue characteristic

27
Q

What is granulation tissue?

A

Universal patch

It is formed of new capillaries
Fibroblasts and collagen
Macrophages

28
Q

Describe the outcome of dissemination

A

Spreads to the bloodstream - patient is now described as septic

29
Q

What is the difference between bacteraemia and septicaemia?

A

Bacteria in blood versus the growth of bacteria in blood

30
Q

What is toxaemia?

A

Toxic products in the blood

31
Q

How do you calculate cardiac output?

A

Stroke volume multiplied by heart rate

32
Q

How can you calculate blood pressure?

A

Cardiac output multiplied by systemic vascular resistance

33
Q

Define SVR

A

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

34
Q

What is the effect of systemic infection?

A

Shock - inability to perfuse tissue

35
Q

What is the clinical picture of early septic shock

A

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

36
Q

What is the effect of bacterial endotoxin?

A

Interleukin- 1 is released - acts on hypothalamus - pyrexia

37
Q

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

A

Histamine effects and inhibit inflammatory cells

Thromboxan A2 - promotes platelet aggregation and vasoconstriction

38
Q

What is a leukotriene? (archidonic acid metabolite)

A

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

39
Q

Are leukotrines vasoactive?

A

Yes, they increase permeability and constrict smooth muscle

40
Q

What is the effect of omega 3 polyunsaturated fatty acids?

A

Decreases synthesis of archidonic acid derived inflammatory mediators

41
Q

What is the function of platelet - activating factor?

A

Produced especially by mast cells and basophils, It is a lipid molecule responsible for platelet aggregation degranulation, releasing factors such as histamine and seratonin

42
Q

What are cytokines and chemokines?

A

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

They attract inflammatory cells

43
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

44
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

45
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

46
Q

What are the key effects of the mediators?

A

Vasodilation and constriction
Altered permeability
Neutrophil adhesion
Chemotaxis
Itch and pain

47
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)

48
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

49
Q

What is the outcome of septic shock

A

Rapidly fatal
Tissue hypoxia
Haemorrhage
Requires immediate intervention and support

50
Q

What are the outcomes of acute inflammation?

A

Resolution
Suppuration
Organisation
Dissemination
Chronic inflammation

semester 1 (105 decks)

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