acute inflammation Flashcards
1
Q
what is inflammation
A
complex, non-specific tissue reaction
2
Q
2 purposes of inflam
A
- remove necrotic/damaged tissue
2. elim. foreign invaders
3
Q
2 times of inflammatiokn
A
acute, chronic, or acute on chronic
4
Q
3 main features of inflammation
A
- blood flow (vasodilation)
- vascular permeability
- recruitment and activation of leukocytes
5
Q
2 types of fluid in swelling
A
- tranudate
2. exudate
6
Q
what is mech of transudate
A
fluid leaks out by osmosis due to lack of plasma proteins
7
Q
3 features of transudate fluid
A
- low protein
- low cellularity
- low specific gravity
8
Q
mech of exudate
A
increased vascular permeability means everything leaks out
9
Q
3 features of exudate fluid
A
- high protein
- high cellularity
- high specific gravity
10
Q
4 mechs of vasc. permeability
A
- endothelial retraction (NO and histamine) - rapid and shortlived
- direct endothelial injury - rapid and possibly long lived
- leukocyte-induced endo injury - delayed onset, long lived
- transcytosis - interconnected, uncoated vessicle and vacuoles
11
Q
what does type of fluid tell you
A
tranudate - no inflammation
exudate - inflammation
12
Q
what is acute lymphangitis
A
when inflammation affects lymph nodes
13
Q
5 cardinal signs of inflammation
A
- rubor
- calor
- tumor
- dolor
- loss of function
14
Q
what are steps of leukocyte reactions in inflammation
A
- injury activates macrophages to secrete TNF and IL-1
- leukocytes bind lightly to selectins on cell wall
- chemikine activation leads to integrin binding on cell wall (tight)
- diapedis occurs, where leukocyte squeezes through vessel wall
- chemotaxis - causes migration of leukocytes along chemokine gradient in interstitial tissues
15
Q
3 examples of chemokines
A
- bacterial products
- leukotrine B4
- complement 5a
16
Q
what is goal of chemotaxis
A
bring leukocyte close to offending agents
17
Q
what are steps to phagocytosis
A
- binding of agent to membrane wall
- engulfment into lysosome
- destruciton of microbes
18
Q
2 ways to destroy microbes
A
- digestion by lysosomal enzymes
2. free radicals
19
Q
3 deficits of leukocyte function
A
- chediak-higashi syndrome - failure to fuse with lysosome leads to accumulation in vacuoules
- chronic granulomatous disease - failure of oxidative burst leading to accumulation
- myeloperoxidase deficiency - deficient halogenation
20
Q
what are qualities of a neutrophil
A
early response
- lower phagocytic activity
- more lysosomal enzymes
- enzymes secreted into interstitial space causing further tissue damage
21
Q
what are qualities of a macrophage
A
- later response
- lower quantitiy of lysosomal enzymes
- more phagocytic activity
- would repair and clean up
22
Q
2 types of macrophages and their jow
A
M1 - via micorbes and IFN-G - inflammation
M2 - via IL13 and IL4 - anti inflammatory
23
Q
2 types of inflammatory mediators and their features
A
- preformed, stored in granules for rapid release and action
- synthesized de-novo - delayed onset of action
24
Q
3 features of pro-inflammaroty mediators
A
- activated by wide variety of stim with lots of crosstalk
- short lived and quick to decay
- present in bloods ad inactive precursors
25
2 types of preformed mediators
1. vasoactive
| 2. lysosomal contsituents of leukocytes
26
2 types of vasoactive mediators and their funct
1. histamines - mast cells - vasodilation and endothelial retraction
2. serotonin - platelets and neuroendocrine cells - endothelial contraction - link between clotting and inflammation
27
what are lysossomal constituents of leukocytes
enzymes stores in neutrophils and macrophages that activate C3 and C5
28
what are de novo snythesized mediators
1. arachndonic acid metabolites - eiconasoids
29
4 key actions of eiconasoids
1. vasodilation - prostcyclin, PGE1 and2
2. vasoconstriciton - thromboxane
3. vasc. permeability - leukotrienes C4 E4 D4
4. chemotaxis and cellular adhesions - leukotiene B4
30
3 classes of de novo made mediators
1. arachnadonic acids
2. NO
3. cytokines
31
where is NO from and what is the function
1. from endothelium, macrophages
| 2. microbial killing, vasodilation, anti-inflammatory
32
what are cytokines
proteins produced by many cell types that madulate the functions of other cell types
33
2 main cytokines
TNF and IL1
34
what are local and systemic effects of cytokines
1. local - activation of leukocytes
| 2. systemic, fever, leukocytosis, acute phase proteins, sleep
35
what are 2 main systems of plasma protein derived inflammation
1. complement system
| 2. coagulation and kinin systems
36
what are complement proteins
C3 an C5 - involved in innate and adaptive immunity - circulate in inactive form
37
what are 3 ways to activate complement proteins
1. from microbes (alternate path)
2. antibody mediated (classical path)
3. mannose binding (lectin path)
38
4 possible outcomes of active complement proteins
1. recruitment of leukocytes to destroy microbes
2. bind to microbe to imporve recognition for phag.
3. form a membrane attack complex (MAC) which cause fluid filling an explosion
4. C5a activates lipoxygenase pathway - anti-inflammatory
39
what is coagulation and kinin system
hageman factor (factor XII) activated intrisic clotting pathway, kinin cascade - activates COX and get proinflammatory
40
what is main product of kinin cascade activation
bradykinin - mediated pain - hyperalgesia
41
3 major mediators of vasodilation
1. protaglandin
2. NO
3. histamine
42
3 major mediators of permeability
1. H and 5 HT
2. leukotiens
3. C3a and C5a
43
4 major mediators of chemotaxis and activation
1. TNF
2. IL-1
3. C3and 5a
4. leukotriene B4
44
2 mediators of fever
1. TNF
| 2. IL-1
45
mediator of pain
bradykinin
46
3 mediators of tissue damage
1. NO
2. lysosomal enzymes
3. ROS
47
2 morphological hallmarks of acute inflammation
1. dilation of vessels
| 2. exudation
48
3 morphological patterns acute inflammation
1. serous
2. fibrinous
3. pruulent (abscess)
49
3 morphological patterns acute inflammation depends on
1. nature of injury
2. severity of injury
3. site of injury
