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acute inflammation Flashcards

1
Q

what is inflammation

A

complex, non-specific tissue reaction

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2
Q

2 purposes of inflam

A
  1. remove necrotic/damaged tissue

2. elim. foreign invaders

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3
Q

2 times of inflammatiokn

A

acute, chronic, or acute on chronic

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4
Q

3 main features of inflammation

A
  1. blood flow (vasodilation)
  2. vascular permeability
  3. recruitment and activation of leukocytes
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5
Q

2 types of fluid in swelling

A
  1. tranudate

2. exudate

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6
Q

what is mech of transudate

A

fluid leaks out by osmosis due to lack of plasma proteins

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7
Q

3 features of transudate fluid

A
  1. low protein
  2. low cellularity
  3. low specific gravity
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8
Q

mech of exudate

A

increased vascular permeability means everything leaks out

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9
Q

3 features of exudate fluid

A
  1. high protein
  2. high cellularity
  3. high specific gravity
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10
Q

4 mechs of vasc. permeability

A
  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
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11
Q

what does type of fluid tell you

A

tranudate - no inflammation

exudate - inflammation

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12
Q

what is acute lymphangitis

A

when inflammation affects lymph nodes

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13
Q

5 cardinal signs of inflammation

A
  1. rubor
  2. calor
  3. tumor
  4. dolor
  5. loss of function
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14
Q

what are steps of leukocyte reactions in inflammation

A
  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
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15
Q

3 examples of chemokines

A
  1. bacterial products
  2. leukotrine B4
  3. complement 5a
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16
Q

what is goal of chemotaxis

A

bring leukocyte close to offending agents

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17
Q

what are steps to phagocytosis

A
  1. binding of agent to membrane wall
  2. engulfment into lysosome
  3. destruciton of microbes
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18
Q

2 ways to destroy microbes

A
  1. digestion by lysosomal enzymes

2. free radicals

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19
Q

3 deficits of leukocyte function

A
  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
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20
Q

what are qualities of a neutrophil

A

early response

  1. lower phagocytic activity
  2. more lysosomal enzymes
  3. enzymes secreted into interstitial space causing further tissue damage
21
Q

what are qualities of a macrophage

A
  1. later response
  2. lower quantitiy of lysosomal enzymes
  3. more phagocytic activity
  4. 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
  1. preformed, stored in granules for rapid release and action
  2. synthesized de-novo - delayed onset of action
24
Q

3 features of pro-inflammaroty mediators

A
  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
Q

2 types of preformed mediators

A
  1. vasoactive

2. lysosomal contsituents of leukocytes

26
Q

2 types of vasoactive mediators and their funct

A
  1. histamines - mast cells - vasodilation and endothelial retraction
  2. serotonin - platelets and neuroendocrine cells - endothelial contraction - link between clotting and inflammation
27
Q

what are lysossomal constituents of leukocytes

A

enzymes stores in neutrophils and macrophages that activate C3 and C5

28
Q

what are de novo snythesized mediators

A
  1. arachndonic acid metabolites - eiconasoids
29
Q

4 key actions of eiconasoids

A
  1. vasodilation - prostcyclin, PGE1 and2
  2. vasoconstriciton - thromboxane
  3. vasc. permeability - leukotrienes C4 E4 D4
  4. chemotaxis and cellular adhesions - leukotiene B4
30
Q

3 classes of de novo made mediators

A
  1. arachnadonic acids
  2. NO
  3. cytokines
31
Q

where is NO from and what is the function

A
  1. from endothelium, macrophages

2. microbial killing, vasodilation, anti-inflammatory

32
Q

what are cytokines

A

proteins produced by many cell types that madulate the functions of other cell types

33
Q

2 main cytokines

A

TNF and IL1

34
Q

what are local and systemic effects of cytokines

A
  1. local - activation of leukocytes

2. systemic, fever, leukocytosis, acute phase proteins, sleep

35
Q

what are 2 main systems of plasma protein derived inflammation

A
  1. complement system

2. coagulation and kinin systems

36
Q

what are complement proteins

A

C3 an C5 - involved in innate and adaptive immunity - circulate in inactive form

37
Q

what are 3 ways to activate complement proteins

A
  1. from microbes (alternate path)
  2. antibody mediated (classical path)
  3. mannose binding (lectin path)
38
Q

4 possible outcomes of active complement proteins

A
  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
Q

what is coagulation and kinin system

A

hageman factor (factor XII) activated intrisic clotting pathway, kinin cascade - activates COX and get proinflammatory

40
Q

what is main product of kinin cascade activation

A

bradykinin - mediated pain - hyperalgesia

41
Q

3 major mediators of vasodilation

A
  1. protaglandin
  2. NO
  3. histamine
42
Q

3 major mediators of permeability

A
  1. H and 5 HT
  2. leukotiens
  3. C3a and C5a
43
Q

4 major mediators of chemotaxis and activation

A
  1. TNF
  2. IL-1
  3. C3and 5a
  4. leukotriene B4
44
Q

2 mediators of fever

A
  1. TNF

2. IL-1

45
Q

mediator of pain

A

bradykinin

46
Q

3 mediators of tissue damage

A
  1. NO
  2. lysosomal enzymes
  3. ROS
47
Q

2 morphological hallmarks of acute inflammation

A
  1. dilation of vessels

2. exudation

48
Q

3 morphological patterns acute inflammation

A
  1. serous
  2. fibrinous
  3. pruulent (abscess)
49
Q

3 morphological patterns acute inflammation depends on

A
  1. nature of injury
  2. severity of injury
  3. site of injury

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