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inflammation Flashcards

1
Q

signs and symptoms of inflammation

A
  • Heat (calor)
  • redness (rubor)
  • swelling (tumor)
    =all due to vascular changes
  • pain (dolar)
    -loss of function due to chem mediators and leukocytes
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2
Q

length of acute inflammation

A

hours to days

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3
Q

what is the characteristis of accute inflammation

A

exudation

neurtrophil infiltration

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4
Q

length of chronic inflammation

A

days-years

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5
Q

characteristics of chronic inflammation

A
  • mononuclear inflammatory cell (lymphocytes, macrophages, plasma cells)
  • infiltration with vascular proliferation
  • fibrosis later
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6
Q

does chronic or accute inflammation cuase additional tissue damage

A

both

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7
Q

what mediates a fever

A

IL-1, TNF, PGE2

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8
Q

what happens to blood flow during acute inflmmation

A

Increased vascular permeability

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9
Q

what does the change in microvasculature do in acute inflammation

A

promote fluid (edema) and inflammatory cell accumulation in the tissue at the site of injury

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10
Q

where does vasodilation begin in acute inflammation

A

in the precapillary arterioles

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11
Q

what does vasodilation account for in acute inflammation

A

redness and heat

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12
Q

what mediates vasodilation in accute injury

A

NO from endo cells
Histamine from mast cells
maintained by prostaglandins

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13
Q

what does increased vascular permeability lead to

A
  • movement of fluid out of the microvasculature (transudate or exudeate)
  • blood concentrates and slows (statis)
  • movement of inflammatory cells out of vessels (Diapedesis) occurs at post-capillary venules
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14
Q

what leads to swelling in acute injury

A

Accumulation of fluid in the extravascular tissue (Edema)

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15
Q

what is the physical characterists of transudate

A

Low protein
Low specific gravity
clear and yellow

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16
Q

what is non inflammatory transudate casued by

A

Endothelium still intact

fluid accumation due to increased hydrostatic pressure or decreased serum oncotic pressure

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17
Q

what causes inflammatory transudate

A

early endothelial cell conctration

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18
Q

is transudate or exudate for tissue and endothelial cell damage

A

Exudate

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19
Q

what makes up exudate

A

high protein contenet
high specific gravity
contains inflammatory cells usually

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20
Q

chacteristics of fibrinous exudate

A

High protein (fibron)
Few cells
Cloudy

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21
Q

chacteristis of Purulent exudate

A

Also called pus
Contains cells (neutrophils
Opaque

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22
Q

characters of Sanguineous exudate

A

Pink and red fluid due to fluid

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23
Q

where does Fibrinous exudate occur

A

around body organs

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24
Q

what causes purulent exudate

A

BActerial

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25
Q

what causes Sanguineous exudate

A

Break down in the blood barrier

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26
Q

what may cause increased vascular permeability during inflammation

A 
Endothelial contraction
Endothelial retration
 =due to mediators
Direct injury (non-lethal injury, necrosis or detachment)
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27
Q

time frame of endothelial contraction in inflammation

A

Immediate then goes away

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28
Q

time frame for endothelial retraction in inflammation

A

Delayed then can be sustained for 24 hours

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29
Q

time frame for direct injury to endothelium in inlammation

A

Immediate or delayed and is often sustained

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30
Q

where does endothelial contraction often occur

A

post capilary venules

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31
Q

what mediates endothelial cell contraction

A

Histamine
bradykinin early, later by leukotrienes and PAF
C3a and C5a induce vasoactive amine release that leads to edema

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32
Q

what causes endothelial cell retraction

A

Restructuring of the cytoskeletal proteins

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33
Q

what mediates Endothelial cell retratction

A

IL-1
TNF
IFN-gamma

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34
Q

what may causes direct venule endothelial injury

A

Neutrophilic release of reactive ocygen species and lysosomal enzymes (proteases) during inflammation

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35
Q

what factors mediate pain

A

Bradykinin

PGE2

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36
Q

what factors mediate fever inflammation

A

IL-1
TNF
PGE2

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37
Q

what facotrs activate endothelail cells in inflammation

A 
Histamine
Thrombin
Complement factors
Cytokines - IL-1 and TND
Bacterial production
Hypoxia
VIruses
PAF
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38
Q

what do activated endothelail cells produce and why

A

PGI2 and NO to induce vasodilation

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39
Q

do endotheial cells contract of dilate during inflammation

A

Contract

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40
Q

what oes the cytoskelton of endothelial cells do during inflammation

A

Rearrange to retract

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41
Q

what does the surface of endothelial cells due during inflammation

A

INcrease expression and affininty of surface cell adhesion molecules

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42
Q

what does acitvated endothelial cells produce during inflammation

A

synth and release Inflammatory mediators

  • PGI2
  • PAF
  • IL-1
  • IL-6
  • Chemokines
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43
Q

hoe does Leukocyte etravasation occure (Steps

A 
Leukocyte margination
Leukocyte rolling
Leukocyte adhesion
Emigration
Chemotaxis
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44
Q

what leads to margination of leukocyte

A

Physical forces often due to stasis

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45
Q

what leads to rolling of leukocytes

A

Selectins (weak, transient, sticking)

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46
Q

what leads to adhesion of leukocytes

A

Integrins (ICAM, VCAM)

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47
Q

what causes emigration of leukocytes

A

PECAM

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48
Q

what do chemotactic factors do besides points cells to go in certain direction

A

stimulate leukocyte activation

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49
Q

what are the chemotactic factors for leukocyte extravasion

A 
PAF (potent)
LTB4 (Potent)
C5a
Chemokines
Bacterial lipids and peptides
Fibrin Degradation products (FDP)
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50
Q

what activates Leukocytes in an inflammatory response

A 
Bacterial products
Cellular debris
Ab-Ag complexes
Cytokines and chemokines
CHemotactic factor
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51
Q

what does a leukocyte produce when activated

A
  • Leukotrienes and prostaglandins from arachidonic acid
  • ROS
  • Cytokines
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52
Q

what does a leukocyte releases when acivated

A

Degradulation and release of lysosomal enzyme

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53
Q

what happens to the cell adhesion molecules when leukocytes are activated

A

Altered expression of cell adhesion molecules

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54
Q

How does A leukocyte do phagocytosis

A

Attachement
Engulfment into a phagocytic vacuole
Lysosomal degranulation by fusion with the phagosome
Oxidate burst releasing ROS
Other mech of intracellular killing: lysozyme, major basic protein, defensins, bactericidal permeability-increasin gprotein

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55
Q

what allows for Leukocyte attachment during phagocytosis

A

mediated by opsonins (IgG, C3b, collectins) on targets and specific leukocyte receptors (Fc receptor for IgG, complement receptors)

56
Q

what enzyme is responsible for creating NO

A

iNOS from arginine

57
Q

cells of ACute inflammation

A

Neutrophils

Monocytes (macrophages/histiocytes)

58
Q

what is the morphologic hallmark of acute inflammation

A

NEutrophils

59
Q

when do neutrophils begin to accumulate

A

within 6-24 hours after accute injury

60
Q

why do NEutrophils infiltrate tissue

A

In response to tissue necrosis, bacterial, and some fungal infection

61
Q

what does a neutrophil do after phagocytosis and digestion

A

Undergoes apoptosis and phagocytosis

62
Q

why does a neutrophil undergo apoptosis after phagocytosis and digestion

A

Release ROS and lysosomal enzymes

63
Q

when do monocytes come in

A

after Neutrophils, begining 48 hours inflammation

64
Q

when do monocytes become histiocytes or macrophages

A

after entering into a tissue

65
Q

how long are monocytes present during inflammation

A

last months (circulating monocytes only last a day)

66
Q

functions of activated macrophages

A

Phagocytize and digest cellular debris and organ
take up antigens and present to immunocompetent T cells
Elaborate various factors

67
Q

what are the various factors monocytes elaborate upon activation

A 
Enzymes (proteases)
Complement and Coagulation factors
Cytokines (IL-1, TNF)
ROS, and NO
Prostaglandins
Growth factors for healing and repair
68
Q

roll of lymphocytes

A

Immune function

69
Q

Roll of eosinophils

A

Allergic reaction, parasites

70
Q

Roll of MAst cels

A

Release Histamine

71
Q

what are the characteristics of Cellulitis inflammation

A

Diffuse, permeative infiltration of neutrophils with edema

72
Q

What are the characteristics abscess inflammation

A

Localized area of liquefactive necrosis

73
Q

what is an ulcer

A

Erosion of epithelial surface exposing underlying connective tissue

74
Q

what cells are found in acute inflammation

A

Polymorphonuclear cells (innate)

75
Q

what cells are found in chronic inflammation

A

lymph and more (addaptive)

76
Q

is accute or chronic inflammation fatal

A

Both are reversible or fatal

77
Q

Causes of Chronic Inflammation

A

Persistent Infection
prolonged exposure to a toxic agent
Immune-mediated inflammatory disease

78
Q

what type of inflamation is often associated with tissue repair

A

Non-specific chronic inflammation

79
Q

what cells are present for non-specific chronic inflammation

A 
Macrophages
Lymphocytes
Plasma cells
Eosinophils
FEw neutrophils
80
Q

what type of recation granulomatous inflmmation linked to

A

Delayed type IV hypersensitivity immune reaction (Chronic)

81
Q

what is the Morphology of granulomatous inflammation

A

Epithelioid (activated) Histiocytes)
Central Caseous necrosis often present
Epithelioid histiocytes together in a multinucleated giant cells
Collar of mononuclear cels

82
Q

what do epithelioid (Activated) histiocytes look like

A

Granular pink cytoplasms with indistinct cell borders

83
Q

What do older granulomas eventually develop

A

A rim of fibroblasts and connective tissue

84
Q

how does Granulomatous inflammation heal

A

Heal by fibrosis

85
Q

what can causes granuloma

tous inflammation

A 
BActerial infection
Parasitic infection
Fungal infection
Inorganic matter
Unknown
86
Q

what bacterial infection can cause granulomatous inflammation

A

Tuberculosis

Cat scratch fever

87
Q

what parasitic infection can cause granulomatous inflammation

A

Schistosomiasis

Toxoplasmosis

88
Q

what fungal infection can cause granulomatous inflammation

A

Coccidioimycosis

Histoplasmosis

89
Q

What inorganic matter can cause granulomatous inflammation

A

Silicosis

Inert foreign material

90
Q

what are some unkown causes that can cause granulomatous inflammation

A

Saecoidosis

Crohn’s

91
Q

what cells secerete Histamine

A

Mast cells

92
Q

where does Bradykinin come from

A

Plasma protein

93
Q

where does NO come from

A

Endothelial cells + others

94
Q

Where do prostaglandins come from

A

MEmbrane phospholipids

95
Q

where do leukotrienes C4, D4, E4 come from

A

Membrane phospholipids

96
Q

where does Leukotriene B4 come from

A

MEmebrane phospholipids

97
Q

where does PAF come from

A

Leukocytes

endothelial cells

98
Q

where does IL-1 and TNF come from

A

Macrophages

Endothelial cells

99
Q

Where does C5a and C3a come from

A

Plasma protein

100
Q

Roll of Histamine

A

Vasodilation and increased vascular permeability

101
Q

Roll of bradykinin

A

increased vascular permeability and pain

102
Q

roll of NO

A

Vasodilation

103
Q

roll of Prostaglandins

A

Vasodilation
Pain
fever
Potenetiate other mediators

104
Q

roll of leukotriene C4, D4, and E4

A

Increase vsacular permeabilty
Vasoconstricition
Bronchoconstriction

105
Q

Roll of Leukotriene B4

A

Leykocyte activation

Chemotaxis

106
Q

Roll of PAF

A

Increaed vascular permeability

Chemotactic

107
Q

Roll of Il-1 and TNF

A

EC and leukocyte activation
Fever
Pain

108
Q

Roll of C5a and C3a

A

Chemotaxis (C5a)
Increased Vascular permeability (C3aand C5a)
Phagocytosis (C3b)

109
Q

what causes histamine release

A

Physical injury
Ag-IgE
C3a and C5a
Cytokines

110
Q

what are prostaglandins and leukotrienes drerived from

A

Arachidonic acid

111
Q

how are prostaglandins made from arachidonic acid

A

Cyclo-oxygenase

112
Q

how are leukotrienes made from arachidonic acid

A

lipo-oxygenase

113
Q

how does Asprin and non-steroidal anti-inflmmatory drugs reduce inflammmation

A

Blocking cyclo-oxygenase activity

- inhibit release of arachidonic acid from cell membrane phospholipids

114
Q

what prostaglandins don;t cause vasodilation

A

thromboxane A2 (vasoconstriction)

115
Q

action of thromboxane on platelet aggregation

A

Promotes platelet aggregation

116
Q

action of prostacyclin on platelet aggregation

A

Inhibits platelet aggregation

117
Q

what are the consequences of Injury

A

Regeneration or repair

118
Q

what does regenetaion include

A

REnewing tissues

Stable tissues

119
Q

what is renewing tissue

A

Complete regeneation after injury

120
Q

what does renewing tissues when injured

A

Epidermis
GI tract
Epithelium
hematopoietic system

121
Q

what is regenration via stable tissues

A

Compensatory growth

122
Q

what does Compensatory growth

A

Liver and kidney

123
Q

what are possibilities of repair

A

Wound

Chronic inflammation

124
Q

Would healing leads to what

A

Scar formation

125
Q

chronic inflammation leads

A

Fibrosis

126
Q

what cells are continuously dividing

A

Hematopoietic cels

Surface epithelium

127
Q

what are stable cells

A

Minimal replicating in normal conditions, but can proliferate in response to injury

128
Q

what cells are considered to be stable cells

A

Parenchymal cells of most solid organs
Smooth muscle
Fibroblasts

129
Q

what are permanent cels

A

No capacity for proliferation

130
Q

what are permanent cells in the body

A

Neurons

Cardiac muscle

131
Q

steps of Healing by first(primary) intention

A

Blood clot (minutes)
neutrophils (24 hours)
Early proliferation/migration of epithelial cells (24-48 hours)
Macrophages replace neutrophils; early granulation tissue (day 3)
Peak neovascularization (Day5)
Progressive collagen deposition (During 2nd week(
Increased wound stregnth (next 4 months)

132
Q

differnece between 1st and second healing by intention

A

Second has more inflammation, more granulation tissue

wound contraction due to myofibroblasts

133
Q

what causes wound contaction in second intension

A

Mycofibroblasts

134
Q

what factors affect wound healing

A 
Infection
Nutrition (protein and vitamins)
Steroids
Mech factors
Poor perfusion
 - Diabetes mellitus
 -athreosclerosis
135
Q

what is the number one cause of delayed healing

A

Infection

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