Dani - ch 5 Flashcards

1
Q

____: vascular and cellular responses whose purpose is to localize or eliminate the injurious agents

A

inflammation

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2
Q

2 types of inflammation

A

acute

chronic

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3
Q

___ inflammation: transient process that occurs within a few minutes of injury and lasts for a short time; usually described by -itis preceded by the organ/tissue

A

acute

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4
Q

5 causes of acute inflammation

  • ____ agents: bacteria, virus, parasites, protozoa
  • ____ reaction
  • ____ agents: trauma, hot, cold, radiation
  • ____ agents: acids, alkalis or bacterial toxins
  • tissue ____
A
infectious
hypersensitivity
physical
chemical
necrosis
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5
Q

____: due to blood vessels dilation; redness

A

rubor

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6
Q

___: due to increased pressure by exudate and by the following mediator; bradykinin and prostaglandins; pain

A

dolor

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7
Q

___: due to increased blood flow; increased heat

A

calor

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8
Q

___: due to accumulation of exudate; swelling

A

tumor

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9
Q

___ ___: due to pain and tissue damage; loss of function

A

functio laesa

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10
Q

___: fluid, protein, and blood cells escape from the vascular system –> interstitial tissue

A

exudation

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11
Q

___: ultrafiltrate of blood and plasme, result from imbalance across the vascular endothelium

A

transudate

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12
Q

___: excess of fluid in the interstitial tissue or body cavities; can be exudate or transudate

A

edema

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13
Q

___: purulent inflammatory exudate abundant in leukocytes and cell debris

A

pus

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14
Q

transudate

  • ____ permeability
  • ___ hydrostatic pressure
A

normal

increased

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15
Q

transudate

- ___ or ___ protein

A

no

low

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16
Q

transudate

- only ____ (ultra filtrate)

A

albumin

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17
Q

transudate

- cells = _____

A

0

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18
Q

transudate

specific gravity is ____

A

low

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19
Q

exudate

- ___ permeability

A

increased

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20
Q

exudate

- ___ protein content

A

high

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21
Q

exudate

- all proteins except ___

A

fibrinogen

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22
Q

exudate

- ___ cells

A

inflammatory

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23
Q

exudate

- specific gravity is ___

A

high

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24
Q

4 steps in acute inflammation

A

white line
flush
flare
wheal

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25
Q

3 phases of the triple response

A

flush
flare
wheal

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26
Q

1st step in triple response:

red line = ____

A

flush

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27
Q

flush is due to ____ ___

A

capillary dilation

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28
Q

momentary white line before triple response is due to ___ ___

A

arteriolar vasoconstriction

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29
Q

2nd step in triple response:

- red irregular area = ____

A

flare

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30
Q

flare is due to ___ ___

A

arteriolar dilation

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31
Q

3rd step in tripe response

- a swelling = ____

A

wheal

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32
Q

wheal is due to ____ caused by ___ permeability

A

edema

increased

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33
Q

hemodynamics

  • changes in blood flow
  • transient ____ of arterioles –> ___ of precapillary sphincters –> ___ of arterioles leads to blood flow and opening of new capillary bed
A

vasoconstriction
relaxation
vasodilation

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34
Q

____: opening of new capillary bed

A

hyperemia

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35
Q

slowing of circulation:
- vascular permeability and outpouring of fluid into intersitial tissue –> ____ blood viscosity –> ___ rate of blood flow

A

increased

decreased

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36
Q

hemodynamics - increased vascular permeability

- arteriolar dilation and increased blood flow –> ____ intravascular hydrostatic pressure –> ____

A

increased

transudate

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37
Q

immediate transient leakage due to ____ injury and ___ reactions

A

mild

hypersensitivity

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38
Q

immediate transient leakage mediated by ____, ___, and ___

A

histamine
serotonin
bradykinin

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39
Q

immediate transient leakage

- contraction of endothelial cells –> widening of ___ junctions (gapping)

A

intercellular

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40
Q

immediate transient leakage

- ____ leakage, ___ lived(___-___min)

A
immediate
short (15-20)
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41
Q

immediate sustained leakage

- caused by ___ injury

A

sever

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42
Q

immediate sustained leakage

- ___ leakage, ___ for long time till damaged vessel is repaired or thrombosed

A

immediate

sustained

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43
Q

delayed sustained leakage

- caused by ____ or ___ injury

A

mild

moderate

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44
Q

severe injury example

A

burn

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45
Q

mild/moderate injury examples

A

sunburn
x-ray
bacterial toxins

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46
Q

delayed sustained leakage

- endothelium is injured ___ or ____ causing intracellular gaps

A

direct

indirect

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47
Q

delayed sustained leakage

- leakge begins after __-__ hours and lasts for several ___ or ___

A

2-12
hours
days

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48
Q

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

A

margination

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49
Q

___ of neutrophils: neutrophils adhere to endothelium by surface adhesioin molecules

A

pavementing

adhesion

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50
Q

____ of neutrophils: neutrophils insert pseudopods in intercellular junctions, squeeze their way, traverse basement membrane and escape to extravascular space

A

diapedesis

emigration

51
Q

____: passage of blood cells through intact capillary walls and into the surrounding tissue

A

diapedesis

52
Q

____: neutrophils move toward site of injury along concentration gradient of chemotactic agents

A

chemotaxis

53
Q

neutrophils emigrate 1st in the first 12-24 hours

- later replaced by ___

A

monocytes

54
Q

RBCs coalesce into ___ at central axis

A

rouleaux

55
Q

____ - like a stack of coins

A

rouleaux

56
Q

types of cells in acute inflammation are ____

A

neutrophils

57
Q

neutrophils are present __-__hrs

A

6-24

58
Q

types of cells in chronic inflammation are ____ and ____

A

monocytes

macrophages

59
Q

monocytes and macrophages are present ___-___hrs

A

24-48

60
Q

life span of a neutrophil is __-__ hrs

A

24-48

61
Q

recognition of phagocytosis is through attachment to agen either directly or indirectly ____ or complement — this is called ____

A

IgG

opsinization

62
Q

engulfment in phagocytosis happens when the cytoplasm surrounds an agent, encloses it into a membrane-bound vacuole called a ____

A

phagosome

63
Q

intracellular killing - oxygen DEPENDENT mechanism
- phagocytosis stimulates other cellular oxidative mechanism (____ ___) –> microbicidal derivatives and antimicrobil (___,___ and ___)

A

respiratory burst
O2
H2O2
HOCl

64
Q

intracellular killing - oxygen INDEPENDENT mechanism

- phagosome fuses with ____(phagolysosome) –> release of ____ enzymes –> ___ agent

A

lysosome
lysosomal
degrade

65
Q

inflammation process –> ___ to stop damage –> still alive bacteria is carried to ___ ___ to be filtered –> if fails –> lymph system –> ventricular circulation –> ____ or ____

A

fails
lymph node
bacteremia
septicemia

66
Q

neutrophils account for ___-___% of all WBCs

A

60-70

67
Q

neutrophils

  • ___ nucleus
  • __-__ lobes
A

segmented

1-4

68
Q

___ are the 1st acute inflammatory cell

A

neutrophils

69
Q

function of neutrophils is ____

A

phagocytosis (oxygen dependent and independent)

70
Q

monocyte = _____ = ____ ____

A

macrophage

tissue histiocyte

71
Q

monocyte accounts for ___-___ of all WBCs

A

4-8

72
Q

monocyte has a ___ shaped nucleus

A

kidney

73
Q

monocytes are ___-lived; replace neutrophils after __-__ days

A

long

1-2

74
Q

monocytes are in the blood for ___ days and the tissues for ____ months

A

4

several

75
Q

function of monocytes: ____

A

phagocytosis (large particles)

76
Q

lymphocytes account for __-__% of all WBCs

A

25-30

77
Q

lymphocytes are present in ___ inflammation and ___ viral or fungal infections

A

chronic

acute

78
Q

eosinophils account for __-__% of all WBCs

A

1-4

79
Q

eosinophils are present in ___ and ___ infections

A

allergy

parasitic

80
Q

2 vasoactive amines

A

histamine

serotonin

81
Q

3 sources of vasoactive amines

A

mast cells
basophils
platelets

82
Q

action of vasoactive amines

  • ___ of arterioles
  • ___ permeability (intercellular gaps)
A

dilation

increased

83
Q

duration of vasoactive amines

  • ___ release
  • ____ lived
A

immediate

short

84
Q

bradykinin causes ___ of arterioles, ___ permeability, ___ and is __ lived and deactivated by ____

A
dilation
increased
pain
short
kininase
85
Q

bradykinin is made through ____

A

kallikrein

86
Q

fibrinopeptides

  • ___ permeability
  • ____ for neutrophils
A

increased

chemotactic

87
Q

C3b: favors ____ (____)

A

phagocytosis

opsonin

88
Q

C3a, C4a, C5a:

  • ____ and ___ permeability
  • ____
  • stimulate mast cells to release ____
A

vasodilation
increase
anaphylatoxins
histamine

89
Q

C5a: ___ to neutrophils and macrophages

A

chemotactic

90
Q

cell membrane phospholipids release ___ __ which are activated by ____

A

arachidonic

phospholipase

91
Q

____ inhibit phospholipase

A

corticosteroids

92
Q

lipoxygenase cycle of AA produce ____

A

leukotrienes

93
Q

leukotienes

  • ___ permeability
  • _____
A

increase

chemotaxis

94
Q

cyclooxygenase cycle of AA produce 3 things

A

prostaglandin
thromboxane
prostacyclin

95
Q

prostaglandin favors ____
thromboxane favors ____
prostacyclin favors ____

A

vasodilation
vasoconstriction
vasodilation

96
Q

leukocyte product:
- oxygen derived free radicals
___ damage –> ___ permeability

A

endothelial

increased

97
Q

leukocyte product:
- lysosomal enzymes
neutral proteases
____ damage –> ___ leakage

A

capillary

sustained

98
Q

leukocyte product:
- acid proteases
___ bacteria and ___ debis

A

degrade

cellular

99
Q

leukocyte product
- platelet activating factor:
____ of platelets –> release of ___ and ___ –> _____ vascular permeability

A

aggregation
histamine
serotonin
increase

100
Q

2 cytokines

A

Interleukin - 1 (IL-1)

tumor necrosis factor (TNF)

101
Q

IL-1 and TNF are produced by ____ and ___

A

lymphocytes

macrophages

102
Q

action of cytokines:

- ___ effect: ___ synthesis of endothelial ___ molecules and ____

A

endothelial
adhesion
prostaglandins

103
Q

action of cytokines

- release of ___ from basement membrane

A

neutrophils

104
Q

action of cytokines

- ____ phase reaction

A

acute

105
Q

3 acute phase reactions due to cytokines

A

fever
sleepiness
anorexia

106
Q

endothelial cells make ____

A

prostaglandins

107
Q

3 systemic clinical signs

A

fever
changes in WBC count
increased erythrocyte sedimentation rate

108
Q

3 sequelaes of acute inflammation

  • complete ____
  • healing by ___
  • progression to ___ ____
A

resolution
scar
chronic inflammation

109
Q

serous acute inflammation

  • ___ type
  • excess thin ___ __ __ fluid
A

mildes

watery clear serous

110
Q

examples of serous acute inflammation

  • ____ in burn
  • ___ ___ in herpes
  • ___ of serous sacs
A

blisters
skin vesicles
inflammation

111
Q

fibrinous inflammation:
____ form, virulent bacteria
rich in ___

A

severe

fibrinogen

112
Q

examples of fibrinous inflammation

  • lobar ___
  • ____ of serous sacs
A

pneumonia

inflammation

113
Q

catarrhal inflammation
___ inflammation of ___ ____
exudate rich with ____

A

mild
mucous membrane
mucus

114
Q

exmaple of catarrhal inflammation

A

common cold

115
Q

allergic inflammation

  • ____
  • many ____
A

hypersensitivity

eosinophils

116
Q

2 examples of allergic inflammation

A

bronchial asthma

urticaria

117
Q

pseudomembranous inflammation

  • ___, affect mucous membrane, by ____ bacteria
  • necrotic epithelium and inflammatory exudate –> ___ membrane replacing mucosa
A

severe
toxigenic
false

118
Q

example of pseudomembranous inflammation

A

diphtheria

119
Q

hemorrhagic inflammation

  • ____, by highly virulent bacteria, viral or fungal agents
  • excessive tissue ___ and ____
A

severe
necrosis
hemorrhage

120
Q

3 examples of hemorrhagic inflammation

A

anthrax
plague
herpes simplex

121
Q

suppurative inflammation

  • ___ bacteria
  • aggregation of neutrophils, tissue ____ and ____ into pus
A

necrosis

liquefaction

122
Q

acute inflammation without neutrophils

- ___ and ___ infections

A

viral

rickettsial

123
Q

inflammatory cells in acute inflammation without neutrophils

A

lymphocytes
plasma cells
lyphocytosis
neutropenia