acute inflammation Flashcards Preview

Undeleted > acute inflammation > Flashcards

Flashcards in acute inflammation Deck (49):
1

what is inflammation

complex, non-specific tissue reaction

2

2 purposes of inflam

1. remove necrotic/damaged tissue
2. elim. foreign invaders

3

2 times of inflammatiokn

acute, chronic, or acute on chronic

4

3 main features of inflammation

1. blood flow (vasodilation)
2. vascular permeability
3. recruitment and activation of leukocytes

5

2 types of fluid in swelling

1. tranudate
2. exudate

6

what is mech of transudate

fluid leaks out by osmosis due to lack of plasma proteins

7

3 features of transudate fluid

1. low protein
2. low cellularity
3. low specific gravity

8

mech of exudate

increased vascular permeability means everything leaks out

9

3 features of exudate fluid

1. high protein
2. high cellularity
3. high specific gravity

10

4 mechs of vasc. permeability

1. endothelial retraction (NO and histamine) - rapid and shortlived
2. direct endothelial injury - rapid and possibly long lived
3. leukocyte-induced endo injury - delayed onset, long lived
4. transcytosis - interconnected, uncoated vessicle and vacuoles

11

what does type of fluid tell you

tranudate - no inflammation
exudate - inflammation

12

what is acute lymphangitis

when inflammation affects lymph nodes

13

5 cardinal signs of inflammation

1. rubor
2. calor
3. tumor
4. dolor
5. loss of function

14

what are steps of leukocyte reactions in inflammation

1. injury activates macrophages to secrete TNF and IL-1
2. leukocytes bind lightly to selectins on cell wall
3. chemikine activation leads to integrin binding on cell wall (tight)
4. diapedis occurs, where leukocyte squeezes through vessel wall
5. chemotaxis - causes migration of leukocytes along chemokine gradient in interstitial tissues

15

3 examples of chemokines

1. bacterial products
2. leukotrine B4
3. complement 5a

16

what is goal of chemotaxis

bring leukocyte close to offending agents

17

what are steps to phagocytosis

1. binding of agent to membrane wall
2. engulfment into lysosome
3. destruciton of microbes

18

2 ways to destroy microbes

1. digestion by lysosomal enzymes
2. free radicals

19

3 deficits of leukocyte function

1. chediak-higashi syndrome - failure to fuse with lysosome leads to accumulation in vacuoules
2. chronic granulomatous disease - failure of oxidative burst leading to accumulation
3. myeloperoxidase deficiency - deficient halogenation

20

what are qualities of a neutrophil

early response
1. lower phagocytic activity
2. more lysosomal enzymes
3. enzymes secreted into interstitial space causing further tissue damage

21

what are qualities of a macrophage

1. later response
2. lower quantitiy of lysosomal enzymes
3. more phagocytic activity
4. would repair and clean up

22

2 types of macrophages and their jow

M1 - via micorbes and IFN-G - inflammation
M2 - via IL13 and IL4 - anti inflammatory

23

2 types of inflammatory mediators and their features

1. preformed, stored in granules for rapid release and action
2. synthesized de-novo - delayed onset of action

24

3 features of pro-inflammaroty mediators

1. activated by wide variety of stim with lots of crosstalk
2. short lived and quick to decay
3. 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

Decks in Undeleted Class (589):