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Flashcards in 1. wk 5 inflammation Deck (66):
1

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

inflammation

2

what are the two types of inflammation

acute
chronic

3

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

acute inflammation

4

infectious agents are (4)

bact
viruses
parasites
protozoa

5

name 5 causes of inflam

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

6

___: redness due to blood vessel dilation

rubor

7

___: pain due to incr. pressure by exudate

dolor

8

___: increa. heat due to increase in blood flow

calor

9

___: swelling due to acc of exudate

tumor

10

___: loss of fxn due to pain and tiss damage

funtio laesa

11

What are two mediators of dolor

bradykinin
prostaglandin

12

what are the 5 cardinal signs of acute inflam

rubor
dolor
calor
tumor
functio laesa

13

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

exudation
(aka edema)

14

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

transudate

15

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

edema

16

______: purulent inflam exudate abundant

pus
(abundant in leukocytes and cell debris)

17

edema can be ___ or ___

exudate or transudate

18

_____ will only form in a bact. infection

pus

19

There is normal permeability and increa. hydrostatic pressure in ______

trandsudate

(increase permeability in exudate)

20

There is an increase in permeability in _____

exudate

21

_____ only has albumin

trandsudate

22

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

arteriolar vasoconstriction

23

What is involved in "triple Response"

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

24

the flush during triple response is due to _____

capillary dilation

25

the flare during triple response is due to ____

arteriolar dilation

26

the wheal during triple response is due to _____

edema caused by incr. permeability

27

vascular changes is called _____

hemohynamics

28

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

immediate leakage , sustained for a long time

29

leakage begins after ___ & lasts for _____ during "delayed systained leakage"

begins 2-12 hrs
lasts: several hrs or days

lates awhile to begin and a while to end

30

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

neutrophils

31

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

pavementing

32

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

emigration

33

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

diapedesis

34

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

IgG or complement (opsonization )

35

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

phagosome

36

_____emigrate first, and then are later replaced by monocytes

neutraphils

37

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

chemotaxis

38

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

venous circulation
(bad!)
--> bacteremia septicemia

39

what is the first line of defense after damage

inflam process

40

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

lymph node to be filtered

41

fxn of neutrophils

phagocytosis

42

_____ make up the majority of WBC

neutrophils (60-70%)

43

what is the 1st inflam cell to respond

neutrophils

44

_____ respond to allergy and parasitic infections

eosinophils

45

____ make up 1-4% of total WBC

eosinophils

46

_____cyte respond to chronic inflam & acute viral or fungal infections

lymphocytes
(25-30% of WBC)

47

_____cyte make up 25-30% of WBC

lymphocytes

48

fxn of monocytes is ____

phagocytosis

49

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

monocyte

50

What is the plasmatic zone during inflm

layer of plasma protecting endoth.

51

RBC sludging during inflam is called ___

Rouleaux formation

52

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

oxygen dependent mechanism

53

_____mechanism of intracellular killing: phagosome fuses with lysosome

oxygen independent

54

What are 2 vasoactive amines

histamine and serotonin
source: mast cells, basophils, platets

55

Action of histamine and serotonin (vasoactive amines)

dilation of arterioles
incr permeability

short lived , immediate

56

Fxn of plasma proteaase bradykinins

dilation of arterioles
incr permeability
** pain
short lived

57

activation of ____ leads to production of thrombin from prothrombin

factor XII (hageman factor)

58

What arachidonic acid cycle is blocked by aspirin and ibuprofen

cyclooxygenase cycle

59

fxn of the lipoxygenase cycle (under the arachidonic acid)

leukotrienes : increase permeability , chemotasix

60

fxn of the cyclooxygenase cycle

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

61

what are 4 products released by leukoproducts

02 derived free radicals
lysosomal enzymes
platlet activating factor
cytokinase

62

tumor necrosis agent

TNF

63

fxn of the hageman factor activation

clotting system
kinin system

64

What cells are histamine and serotonin derived from

mast cells
blood basophils
blood platelets

65

3 systemic clinical signs of inflammation

fever
change in WBC count
incr. erythrocyte sedimentation rate

66

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

complete resolution
healing by scar
progression to chronic inflam