Acute Inflammation 2 Flashcards
1
Q
How do you call peritoneal cavity inflammation?
A
peritonitis
2
Q
How do you call meninges inflammation?
A
meningitis
3
Q
How do you call appendix inflammation?
A
appendicitis
4
Q
How do you call lungs inflammation?
A
pneumonia
5
Q
How do you call pleural cavity inflammation?
A
pleurisy
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
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
8
Q
What plasma proteins intervene in inflammation?
A
- fibrinogen
- immunoglobulins
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
10
Q
What are immunoglobulins and what do they do?
A
- they are specific to the antigen
- they participate in humoural immune response
11
Q
What are the mediators of acute inflammation?
A
- molecules on endothelial cell surface membrane
- molecules released from cells
- molecules in the plasma
12
Q
What are the collective effects of mediators?
A
- vasodilatation
- increased permeability
- neutrophil adhesion
- chemotaxis
- itch and pain
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
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-)
15
Q
Where is histamine preformed?
A
- mast cells besides vessels
- platelets
- basophils
16
Q
Where is serotonin preformed?
A
- platelets
17
Q
What does histamine do?
A
- vasodilatation
- increased permeability
- acts via H1 receptors on endothelial cells
- IgE mediated reactions
18
Q
What does serotonin do?
A
- released when platelets degranulate in coagulation
- vasoconstriction
19
Q
Where are prostaglandins preformed?
A
- many cells including endothelium and leukocytes
20
Q
What do prostaglandins do?
A
- promote histamine effects and inhibits inflammatory cells
21
Q
What do leukotrienes do?
A
- vasoactive (dynamic effect on vessels to increase permeability and constrict smooth muscle)
22
Q
What do omega 3 polyunsaturated FA do?
A
- decrease synthesis of arachidonic acid derived inflammatory mediators
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
Where are cytokines and chemokines preformed?
- macrophages
- lymphocytes
- endothelium
26
What do cytokines and chemokines do?
- attract inflammatory cells
27
Where is NO preformed?
- various cells
28
What does NO do?
- smooth muscle relaxation
- anti-platelet
- regulate leukocyte recruitment to inflammatory focus
29
Where do oxygen free radicals (H2O2, OH-, O2-) come from?
- neutrophiles release them on phagocytosis
30
What do oxygen free radicals (H2O2, OH-, O2-) do?
- amplify other mediator effects
31
Which are the four enzyme cascades?
- blood coagulation pathways
- fibrinolysis
- kinin system
- complement cascade
32
What does the blood coagulation pathway do?
- clots fibrinogen in exudate
| - interacts widely with other systems
33
What does the fibrinolysis pathway do?
- breaks down fibrin, helps maintain blood supply
| - fibrin breakdown products vasoactive
34
What does the kinin system pathway do?
- bradykinin which causes pain
35
What does the complement cascade do?
- ties inflammation with the immune system
| - active components stimulate increased permeability, chemotaxis, phagocytosis, cell breakdown
36
What are the immediate systemic effects of inflammation?
- 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
What are the longer term effects of systemic inflammation?
- lymphadenopathy (regional lymph node enlargement as an immune response)
- weight loss (catabolic process)
- anaemia
38
What is suppuration?
- outcome of acute inflammation
39
What does suppuration involve?
- pus formation (dead tissue, organisms, exudate, neutrophils, fibrin, red cells, debris)
- pyogenic membrane surrounds pus (capillary sprouts, neutrophils, fibroblasts, walls of pus)
40
What is an abscess?
- collection of pus (suppuration) under pressure
- single locule or multiloculated
- 'points' of discharge
- collapses then heals and repairs
41
How does a multiloculated abscess form?
- pus bursts through pyogenic membrane and forms new cavities
42
Where would you find an empyema?
- in a hollow viscus (ex: pus in gall bladder or pleural cavity)
43
Where would you find a pyaemia?
- in the bloodstream
44
What are the physical outcomes of the acute inflammation? (except from healing)
- granulation tissue characteristics
| - leads to fibrosis and formation of the scar
45
What is granulation tissue?
- universal "repair kit" for all damage
| - formed of new capillaries (angiogenesis), fibroblasts, collagen and macrophages
46
Another outcome of inflammation is dissemination. What is this?
- spread to bloodstream of patient infection (or septic)
47
What is bacteraemia?
- bacteria in blood
48
What is septicaemia?
- growth of bacteria in blood
49
What is toxaemia?
- toxic products in blood
50
What is cardiac output (CO) in relation with stroke volume (SV) and heart rate (HR)?
CO=SVxHR
51
What is blood pressure (BP) in relation with cardiac output (CO) and systemic vascular resistance (SVR)?
BP=COxSVR
52
What is the pathogenesis of septic shock?
- 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
Why does septic shock happen?
- bacterial endotoxin released (interleukin1, pyrexia because of action on hypothalamus)
- activation of coagulation (disseminated intravascular coagulation, vasoactive chemical (vasodilatation), haemorrhage skin rash)
54
What happens if tachycardia due to compensation does not take place?
- SVR falls so BP falls
| - reduced perfusion of tissues (tissue hypoxia and loss of cell tissue and organ function)
55
What are the outcomes of septic shock?
- 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
Summary of acute inflammation
- resolution
- suppuration
- organisation
- dissemination
- chronic inflammation
