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T3- Patho unit 1 > 1. wk 5 inflammation > Flashcards

1. wk 5 inflammation Flashcards

stopped at S; 37

1
Q

___: vascular and cellular response whose purpose is to localize / elimainate the injurious agents

A

inflammation

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2
Q

what are the two types of inflammation

A

acute

chronic

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3
Q

___: transient process that occurs within few min of injury and lasts for short time

A

acute inflammation

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4
Q

infectious agents are (4)

A

bact
viruses
parasites
protozoa

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5
Q

name 5 causes of inflam

A
  1. infectious agents
  2. hypersensitivity rxn
  3. physical agents
  4. chem agents
  5. tiss necrosis
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6
Q

___: redness due to blood vessel dilation

A

rubor

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7
Q

___: pain due to incr. pressure by exudate

A

dolor

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8
Q

___: increa. heat due to increase in blood flow

A

calor

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9
Q

___: swelling due to acc of exudate

A

tumor

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10
Q

___: loss of fxn due to pain and tiss damage

A

funtio laesa

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11
Q

What are two mediators of dolor

A

bradykinin

prostaglandin

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12
Q

what are the 5 cardinal signs of acute inflam

A 
rubor 
dolor 
calor
tumor 
functio laesa
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13
Q

____: fluid, protein, and blood escaping from the vascular system into tiss

A

exudation

aka edema

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14
Q

____: ultrafiltrate of blood and plasma, results from imbalance across vascular endothelium

A

transudate

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15
Q

____: excess of fluid in the interstitial tis of body cavitites (can be exudate or transudate)

A

edema

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16
Q

______: purulent inflam exudate abundant

A

pus

abundant in leukocytes and cell debris

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17
Q

edema can be ___ or ___

A

exudate or transudate

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18
Q

_____ will only form in a bact. infection

A

pus

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19
Q

There is normal permeability and increa. hydrostatic pressure in ______

A

trandsudate

increase permeability in exudate

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20
Q

There is an increase in permeability in _____

A

exudate

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21
Q

_____ only has albumin

A

trandsudate

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22
Q

After a strike to the skin there is a white line bc of _______

A

arteriolar vasoconstriction

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23
Q

What is involved in “triple Response”

A
  1. flush (due to cap. dialation)
  2. flare (due to arteriolar dilation
  3. wheal (due to edema caused by incr. permeability )
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24
Q

the flush during triple response is due to _____

A

capillary dilation

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25
Q

the flare during triple response is due to ____

A

arteriolar dilation

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26
Q

the wheal during triple response is due to _____

A

edema caused by incr. permeability

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27
Q

vascular changes is called _____

A

hemohynamics

28
Q

there is ____ leakage , ___ for a long time till damage vessel is repaired during “immediate sustained (prolonged) leakage

A

immediate leakage , sustained for a long time

29
Q

leakage begins after ___ & lasts for _____ during “delayed systained leakage”

A

begins 2-12 hrs
lasts: several hrs or days

lates awhile to begin and a while to end

30
Q

as blood flow slows, ___ fall out of the central column and roll along the endothelium

A

neutrophils

31
Q

______: is the neutrophils adhering to endothelium by surface adhesion mole

A

pavementing

32
Q

during _______ neutophils insert pseudopods in intercellular jxn , squeeze their way, & exscpe into extravascular space

A

emigration

33
Q

____: the passage of blood cells (WBC) through intact cap. walls and into surrounding tis

A

diapedesis

34
Q

there is recognition of the phagocyte by attachment to agent either directly or indirectly by ____

A

IgG or complement (opsonization )

35
Q

cytoplasm of a phagocyte surrounds agent, encloses it into a membrane bound vacuole called _____

A

phagosome

36
Q

_____emigrate first, and then are later replaced by monocytes

A

neutraphils

37
Q

______: neutrophils mnove toward site of injury along conc. gradient of chemotact agents

A

chemotaxis

38
Q

if inflam process and lynmph nodes fail to defend against bact. it goes into the ______

A

venous circulation
(bad!)
–> bacteremia septicemia

39
Q

what is the first line of defense after damage

A

inflam process

40
Q

if the inflam process fails to stop the damage , the bact. is carried to the _____

A

lymph node to be filtered

41
Q

fxn of neutrophils

A

phagocytosis

42
Q

_____ make up the majority of WBC

A

neutrophils (60-70%)

43
Q

what is the 1st inflam cell to respond

A

neutrophils

44
Q

_____ respond to allergy and parasitic infections

A

eosinophils

45
Q

____ make up 1-4% of total WBC

A

eosinophils

46
Q

_____cyte respond to chronic inflam & acute viral or fungal infections

A

lymphocytes

25-30% of WBC

47
Q

_____cyte make up 25-30% of WBC

A

lymphocytes

48
Q

fxn of monocytes is ____

A

phagocytosis

49
Q

___cyte are long lived. they replace neutrophils 1-2 days later

A

monocyte

50
Q

What is the plasmatic zone during inflm

A

layer of plasma protecting endoth.

51
Q

RBC sludging during inflam is called ___

A

Rouleaux formation

52
Q

_____ mechanism of intracellular killing: phagocytosis stim cellular oxidative mechanism (respiratory burst)

A

oxygen dependent mechanism

53
Q

_____mechanism of intracellular killing: phagosome fuses with lysosome

A

oxygen independent

54
Q

What are 2 vasoactive amines

A

histamine and serotonin

source: mast cells, basophils, platets

55
Q

Action of histamine and serotonin (vasoactive amines)

A

dilation of arterioles
incr permeability

short lived , immediate

56
Q

Fxn of plasma proteaase bradykinins

A

dilation of arterioles
incr permeability
** pain
short lived

57
Q

activation of ____ leads to production of thrombin from prothrombin

A

factor XII (hageman factor)

58
Q

What arachidonic acid cycle is blocked by aspirin and ibuprofen

A

cyclooxygenase cycle

59
Q

fxn of the lipoxygenase cycle (under the arachidonic acid)

A

leukotrienes : increase permeability , chemotasix

60
Q

fxn of the cyclooxygenase cycle

A

prostagladin (vesodil)
thromboxane (vasocon)
prostacyclin (vasodilation)

61
Q

what are 4 products released by leukoproducts

A

02 derived free radicals
lysosomal enzymes
platlet activating factor
cytokinase

62
Q

tumor necrosis agent

A

TNF

63
Q

fxn of the hageman factor activation

A

clotting system

kinin system

64
Q

What cells are histamine and serotonin derived from

A

mast cells
blood basophils
blood platelets

65
Q

3 systemic clinical signs of inflammation

A

fever
change in WBC count
incr. erythrocyte sedimentation rate

66
Q

healing as a result of inflammation will result in (3)

A

complete resolution
healing by scar
progression to chronic inflam

T3- Patho unit 1 (14 decks)

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