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Le Principles of Disease > Acute Inflammation 2 > Flashcards

Acute Inflammation 2 Flashcards

1
Q

How do you call peritoneal cavity inflammation?

A

peritonitis

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2
Q

How do you call meninges inflammation?

A

meningitis

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3
Q

How do you call appendix inflammation?

A

appendicitis

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4
Q

How do you call lungs inflammation?

A

pneumonia

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5
Q

How do you call pleural cavity inflammation?

A

pleurisy

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6
Q

How do neutrophils phagocytose?

A
  • recognition of foreign body
  • move towards it (chemotaxis)
  • adhere to organism
  • release oxidant (H2O2) and enzymes (protease) filled granules
  • foreign antigen is destroyed
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7
Q

What are the consequences of neutrophil action?

A
  • they die when granule contents are released
  • bits of cell, organisms, endogenous proteins form pus
  • may extends to other tissues progressing the inflammation
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8
Q

What plasma proteins intervene in inflammation?

A
  • fibrinogen

- immunoglobulins

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9
Q

What is fibrinogen and what does it do?

A

It is a coagulation factor which localises the inflammatory process by:

  • forming fibrin
  • clotting exudate
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10
Q

What are immunoglobulins and what do they do?

A
  • they are specific to the antigen

- they participate in humoural immune response

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11
Q

What are the mediators of acute inflammation?

A
  • molecules on endothelial cell surface membrane
  • molecules released from cells
  • molecules in the plasma
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12
Q

What are the collective effects of mediators?

A
  • vasodilatation
  • increased permeability
  • neutrophil adhesion
  • chemotaxis
  • itch and pain
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13
Q

What are the cell surface mediators? (help with diapedesis)

A
  • adhesion molecules on endothelial cells (ICAM-1) which help neutrophils stick
  • P-selectin which interacts with neutrophil surface
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14
Q

What are the molecules released from cells?

A
  • histamine
  • serotonin
  • prostaglandins
  • leukotrienes
  • omega 3 polyunsaturated FA
  • platelet-activating factor (PAF)
  • cytokines and chemokines
  • nitric oxide (NO)
  • oxygen free radicals (H2O2, OH-, O2-)
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15
Q

Where is histamine preformed?

A
  • mast cells besides vessels
  • platelets
  • basophils
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16
Q

Where is serotonin preformed?

A
  • platelets
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17
Q

What does histamine do?

A
  • vasodilatation
  • increased permeability
  • acts via H1 receptors on endothelial cells
  • IgE mediated reactions
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18
Q

What does serotonin do?

A
  • released when platelets degranulate in coagulation

- vasoconstriction

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19
Q

Where are prostaglandins preformed?

A
  • many cells including endothelium and leukocytes
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20
Q

What do prostaglandins do?

A
  • promote histamine effects and inhibits inflammatory cells
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21
Q

What do leukotrienes do?

A
  • vasoactive (dynamic effect on vessels to increase permeability and constrict smooth muscle)
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22
Q

What do omega 3 polyunsaturated FA do?

A
  • decrease synthesis of arachidonic acid derived inflammatory mediators
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23
Q

Where are platelet-activting factor preformed?

A
  • cell membranes of activated inflammatory cells
24
Q

What do platelet-activating factor do?

A
  • reduce permeability by enhancing platelet degranulation at site of injury
25
Q

Where are cytokines and chemokines preformed?

A
  • macrophages
  • lymphocytes
  • endothelium
26
Q

What do cytokines and chemokines do?

A
  • attract inflammatory cells
27
Q

Where is NO preformed?

A
  • various cells
28
Q

What does NO do?

A
  • smooth muscle relaxation
  • anti-platelet
  • regulate leukocyte recruitment to inflammatory focus
29
Q

Where do oxygen free radicals (H2O2, OH-, O2-) come from?

A
  • neutrophiles release them on phagocytosis
30
Q

What do oxygen free radicals (H2O2, OH-, O2-) do?

A
  • amplify other mediator effects
31
Q

Which are the four enzyme cascades?

A
  • blood coagulation pathways
  • fibrinolysis
  • kinin system
  • complement cascade
32
Q

What does the blood coagulation pathway do?

A
  • clots fibrinogen in exudate

- interacts widely with other systems

33
Q

What does the fibrinolysis pathway do?

A
  • breaks down fibrin, helps maintain blood supply

- fibrin breakdown products vasoactive

34
Q

What does the kinin system pathway do?

A
  • bradykinin which causes pain
35
Q

What does the complement cascade do?

A
  • ties inflammation with the immune system

- active components stimulate increased permeability, chemotaxis, phagocytosis, cell breakdown

36
Q

What are the immediate systemic effects of inflammation?

A
  • pyrexia (raised temperature) because endogenous pyrogens from white cells act centrally
  • feeling unwell (malaise, anorexia, nausea, abdominal pain and vomiting in children)
  • neutrophilia (raised white cell count) bone marrow releases/ produces
37
Q

What are the longer term effects of systemic inflammation?

A
  • lymphadenopathy (regional lymph node enlargement as an immune response)
  • weight loss (catabolic process)
  • anaemia
38
Q

What is suppuration?

A
  • outcome of acute inflammation
39
Q

What does suppuration involve?

A
  • pus formation (dead tissue, organisms, exudate, neutrophils, fibrin, red cells, debris)
  • pyogenic membrane surrounds pus (capillary sprouts, neutrophils, fibroblasts, walls of pus)
40
Q

What is an abscess?

A
  • collection of pus (suppuration) under pressure
  • single locule or multiloculated
  • ‘points’ of discharge
  • collapses then heals and repairs
41
Q

How does a multiloculated abscess form?

A
  • pus bursts through pyogenic membrane and forms new cavities
42
Q

Where would you find an empyema?

A
  • in a hollow viscus (ex: pus in gall bladder or pleural cavity)
43
Q

Where would you find a pyaemia?

A
  • in the bloodstream
44
Q

What are the physical outcomes of the acute inflammation? (except from healing)

A
  • granulation tissue characteristics

- leads to fibrosis and formation of the scar

45
Q

What is granulation tissue?

A
  • universal “repair kit” for all damage

- formed of new capillaries (angiogenesis), fibroblasts, collagen and macrophages

46
Q

Another outcome of inflammation is dissemination. What is this?

A
  • spread to bloodstream of patient infection (or septic)
47
Q

What is bacteraemia?

A
  • bacteria in blood
48
Q

What is septicaemia?

A
  • growth of bacteria in blood
49
Q

What is toxaemia?

A
  • toxic products in blood
50
Q

What is cardiac output (CO) in relation with stroke volume (SV) and heart rate (HR)?

A

CO=SVxHR

51
Q

What is blood pressure (BP) in relation with cardiac output (CO) and systemic vascular resistance (SVR)?

A

BP=COxSVR

52
Q

What is the pathogenesis of septic shock?

A
  • systemic release of chemical mediators from cells into plasma:
    ° mediators cause vasodilatation causing loss of SVR
    ° results in catecholamine release
    ° tachycardia (increased heart rate) follows to maintain (CO) because of increased heart rate to compensate
53
Q

Why does septic shock happen?

A
  • bacterial endotoxin released (interleukin1, pyrexia because of action on hypothalamus)
  • activation of coagulation (disseminated intravascular coagulation, vasoactive chemical (vasodilatation), haemorrhage skin rash)
54
Q

What happens if tachycardia due to compensation does not take place?

A
  • SVR falls so BP falls

- reduced perfusion of tissues (tissue hypoxia and loss of cell tissue and organ function)

55
Q

What are the outcomes of septic shock?

A
  • possibly fatal
  • tissue hypoxia (cell death)
  • haemorrhage
  • requires urgent intervention and support, thus the need for awareness and early recognition
  • young people may be more able to compensate (difficulty to identify)
56
Q

Summary of acute inflammation

A
  • resolution
  • suppuration
  • organisation
  • dissemination
  • chronic inflammation

Le Principles of Disease (10 decks)

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