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clin med > inflammation repair > Flashcards

inflammation repair Flashcards

1
Q

what is inflammation

A

heal wounds and chronic conditions

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2
Q

define inflammation as it pertains to the immune system

A

the immune systems response to stimulus

when a wound swells up, turns red and hurts

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3
Q

when does inflammation happen?

A

inflammation happens when the immune system fights against something the may turn out to be harmful

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4
Q

how does the body use inflammation to protect the body?

A

protective response to cell injury and cell death

facilitates tissue repair

controlled inflammation

uncontrolled inflammation

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5
Q

what are responses from tissue injury that are noticed

A

chemical agents
cold
heat
trauma
invasion of microbes
cancerous cells

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6
Q

what is the desirable response

A

when it is controlled and proportional

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7
Q

what is a undesirable response

A

chronic and harmful

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8
Q

what does reparative mean

A

induces and supports tissue repair

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9
Q

what is the potential harm when it comes to inflammation?

A

leads to chronic bowl conditions
arthritis and chronic obstructive bowel disease

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10
Q

how can you distinguish between acute vs chronic

A

onset duration and type of infiltrating inflammatory cells

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11
Q

what are the major cells involved in acute inflammation

A

neutrophils basophils eosinophils
mononcytes and macrophages

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12
Q

what are the major cells involved in the chronic inflammation

A

monocytes
macrophages
lymphocytes
plasma cells
fibroblasts

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13
Q

what is the onset period of acute inflammation

A

onset (few days)

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14
Q

what is the onset time for chronic inflammation

A

delayed (up to many months or years)

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15
Q

what are the ourcomes associated with acute inflammatory responses

A

resolution, absess formation, chronic inflmmation

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16
Q

what are the outcomes for chronic inflammation

A

tissue destruction
fibrosis

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17
Q

what are the causative agents of acute inflammatory responses

A

pathogens irritants and damage

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18
Q

what is the causative agent for chronic inflammation

A

persistent acute inflammation due to non degradable pathogens persisitant foreign bodies or autoimmune reactions

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19
Q

what are the cardinal signs of inflammation

A

heat
redness
swelling
pain
increasing the chance of loss of function

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20
Q

give a brief recap of the inflammation response

A

foreign agent will enter the body -> local vasodilation and increased vascular permability ->
accumulation of white blood cells at the blood cells wall ->
white blood cells will exit the blood vessel ->
will be drawn to the injury area

CHEMOTAXIS

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21
Q

what are the symptoms seen with the pathological response of releasing of soluble mediators

A

heat (calor)
redness (rubor)
swelling (tumor)
pain (dolor)

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22
Q

what are the symptoms noticed with the pathological response of vasodilation

A

heat. (calor)
readness (rubor)
swelling (tumor)

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23
Q

what are the symptoms noticed with the patological response of increased blood flow

A

swelling (tumor)

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24
Q

what are the symptoms noticed with the patological response to extravasation of fluid
(increased permeability)

A

swelling (tumor)

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25
Q

what are the symptoms related to the pathological response of cellular influx (chemotaxis)

A

swelling (tumor)

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26
Q

what are physiological components of vascularity

A

vasoconstriction- few seconds of blanching
vasodilation- smooth muscle relaxes called active hyperermia
increased permeability- vascular leakage- edema

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27
Q

what are the physiological components of cellular mean

A

leukocyte accumulation and infiltration

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28
Q

where would you find active hyperemia?

A

arterial hyperemia

due to arteriolar dilatation
sympathic stimulation
the affected tissue is redder than normal because of engorgement with oxygnated blood

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29
Q

what are some examples of active hyperemia

A

at sites of inflammation
in skeletal muscle during exercise
angioneurothic- face redness

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30
Q

what does active hyperemia account for?

A

redness swelling and warmth

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31
Q

what is main difference between exudate and transudate

A

cell/ protein rich fluid vs low cell/protein fluid

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32
Q

describe some details about transudate leakage/ permeability

A

result of high hydrostatic pressure and low osmotic pressure

fluid is clear
low cell/protein fluid

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33
Q

describe some details about exudate leakage/ permeability

A

result of increased vascular permeability

cloudy
high cell/ protein fluid

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34
Q

what does exudate permeability do?

A

supplies antibodies and complement protein to affected areas contributes to swelling

causes pain and decreased mobility

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35
Q

if permeability accounts for swelling what might you also notice with the patient

A

decreased ROM and Function

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36
Q

what are the five known causes of vascular leakiness?

A
  1. mediators
  2. cytokine mediators
  3. severe injuries
  4. leukocytes adhering and damaging the endothelium
  5. certain mediators may increase transcytosis
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37
Q

describe what occurs with the mediators that causes vascular leakiness

A

hisamines bradykinis and leukotrienes cause a <30 minute response in the form of reversible endothelial cell contraction

this will widen the gaps of venules that is specific to allergic reactions

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38
Q

describe what occurs with the cytokine mediators that causes vascular leakiness

A

reversible endothelial cell junction retraction
happens 4-6 hours post injury or infection

last up to 24 hours or more
where brusing can be noticed

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39
Q

how will severe injuries cause vascular leakiness

A

immediate direct endothelial cell damage making them leaky until they are repaired

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40
Q

vascular permeability follows what process

A

flows vasodilation

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41
Q

vascular permeability causes what type of dysfunction

A

endothelial cell dysfunction

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42
Q

how does leukocytes that adhere and damage the endothelium cause vascular permeability

A

through activation and release of toxic oxygen radicals and proteolytic enzymes making the vessel leaky

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43
Q

how does mediators increasing transcytosis cause vascular permeability

A

intracellular vesicles extend from the luminal surface to basal lamina surface of the endothelial cells

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44
Q

what is meant by degranulation?

A

a cellular process that releases: neutrophils
basophils
eosinophils
mast cells
cytotoxic cells
natural killer cells

main purpose is to destroy pathogens

innate immune system

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45
Q

what is meant by diapedesis

A

leukocytes leave the vasculature and enter the interstitium through a sequence

if you know the sequence say it now

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46
Q

what is the sequence followed by diapedesis

A

margination and rolling
adhesion
chemotaxis
activation
transmigration

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47
Q

after the sequence of diapedesis what can the leukocytes participate in

A

degranulation
phagocytosis- macrophage
leukocyte/cytokine - protects and repair (controlled)
leukocyte/ cytokine ‘storm’ induced tissue injury (uncontrolled or chronic)

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48
Q

what is special about the cytokine storm

A

long covid and disproportionallity to the response which creates a chronic disease
cells of the enate immune system

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49
Q

explain the vasoconstriction stage of acute inflammation stage

A

release of vasoconstrictor substances

constriction of cells- thought to be immediate response to control blood loss BLANCHING

<60 seconds

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50
Q

explain the vasodilation stage of acute inflammation stage

A

Mechanism of action- cellular release of mediators
relaxation of the blood vessel walls

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51
Q

what relax the blood vessels walls in the vasodilation stage of acute inflammation

A

histamine, prostacyclin and nitric oxide relax the blood vessel walls

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52
Q

why does the vasodilation stage happen in acute inflammation

A

increased hydrostatic pressure (pressure inside the cell pushing out) causes a decrease in blood flow rate
leukocytes will marginate among the blood vessel wall

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53
Q

what is the mechanism of action in the increased vascular permeability stage of acute inflammation

A

increased vascular permeability occurs through release of histamine and leukotrienes

54
Q

why does increased vascular permeability occur

A

allows fluid, WBC, and proteins to move the interstitial tissue

this will decrease the osmotic pressure in the blood vessels and increase osmotic pressure in the interstitial space

55
Q

what is the result of the increased vascular permeability stage of acute inflammation

A

edema or increased fluid in the interstitial tissue

56
Q

what are the physiological mechanisms that increase vascular permeability?

A

endothelial relaxation and contraction

57
Q

provide a defintion of endothelial relaxation

A

HBP cause fluid leakage. the fluid leakage is transudate

58
Q

provide a definition of endothelial contraction

A

immediate response that is exudate fluid leakage

initiated by the cell mediators: histimine and leukotrines

time: immediate up to 30 minutes

59
Q

Provide a definition for endothelial cell retraction

A

Delayed response that is a exudate leakage

Happens in 4 to 6 hours, but is long lasting

60
Q

what are the physical mechanisms of increased vascular permeability

A

direct endothelial injury

61
Q

what is direct endothelial injury

A

immediate -sustained response

time: IMMEDIATE

62
Q

give a detailed depiction of what happens during chemotaxis

A

pathogens charge macrophages that secrete cytotines. The release of cytotines causes the endotheilal cells to secrete adhession molecules. luekocytes are atracted to the presence of cytokines and adhession molecules

63
Q

give a detailed depiction of what happens during rolling and rolling adhession

A

luekocytes bind to adhession molicules with moderate affinity

causes leukocytes in the blood ro slow down and begin rolling among the inner surface of blood vessel walls

64
Q

give a detailed depiction of what happens during firm and tight adhessions

A

release of chemokine by machrophages to transition modetate affinity to high bonding to endotheilial cells

65
Q

give a detailed depiction of what happens during transmigration

A

cytoskeleton reorganization in conjunction with leukocyte pseudopod extensions

leukocytes pass through gaps in endothelial cells

66
Q

what should you KNOW about diapedesis?

hint: COPS AND ROBBERS

A

diapedesis is blood vessel escape

67
Q

how do leukocytes move to injury and infection

A

through chemotactic gradients

68
Q

what details can you associate with acute inflammation

A
  1. rapid onset
  2. lasts minutes to days
  3. exudation of fluid and proteins from vessels
  4. emigration of WBC
69
Q

what is the purpose of acute inflammation

A

quick attack on foreign agents and initiate the repair process

70
Q

what are the cardinal signs associated with acute inflammation

A

rubor
heat
edema
pain
tumor
loss of function

71
Q

whats the cause of acute inflammation

A

infection
trauma
physical and chemical agents
necrosis
foreign bodies
immune reaction

72
Q

what are the outcomes of acute inflammation

A

resolution
abscess
ulcer
chronic inflammation
scar formation

73
Q

Contributors in scar formation for acute inflammation

A

neurophils and macrophages

74
Q

contributors in scar formation for chronic inflammation

A

lymphocytes, plasma cells, macrophage, fibroblasts

75
Q

Scar formation on acute inflammation is connected to what

A

calcification

76
Q

what are the phases of the inflammatory process

A
  1. acute phase
  2. tissue formation (proliferation)
  3. remodeling phase
77
Q

describe the acute phase of inflammatory process

A

inflammatory response lasts 2-4 days but complete in 2 weeks

78
Q

describe the tissue formation phase of the inflammatory process

A

-subacute phase tissue rebuilding, approximately 2-3 weeks
-this does not include chronic inflammation

79
Q

describe the remodeling phase of the inflammatory process

A

-adapt to original tissue
-continues for up to 1 year post injury

80
Q

describe chronic inflammation

A
  • lasts week to years
  • involves lymphocytes and macrophages
    -tissue repair and tissue injury happen simultaneously
81
Q

describe active inflammation for chronic inflammation

A

lymphocyte, macrophage, plasma cell infiltration

81
Q

what are the three characteristics of chronic inflammation?

A
  1. active inflammation
  2. tissue destruction by inflammatory cells and stimuli
  3. tissue healing
82
Q

describe tissue destruction by inflammatory cells and stimuli when it comes to chronic inflammation

A

lack of complete resolution

83
Q

describe tissue healing when it comes to chronic inflammation

A

fibrosis + regeneration
both require angiogenesis

84
Q

what does angiogenesis mean

A

new vasculature, critical to wound repair

85
Q

what does regeneration mean

A

formation of new tissue

86
Q

Give a description for what chronic inflammation is

A
  • simultaneously active inflammation- lymphocytes
  • tissue destruction - tissue repair
    injuries stimulus that the body cannot remove
87
Q

what are the causes of chronic inflammation

A

viral micronial infection, prolonged exposure to toxin, autoimmune
UNDESIRABLE MOVEMENT PATTERNS

88
Q

what are the cells involved in chronic inflammation?

A

macrophage- produce enzymes and mediators
Lymphocytes- stimulate fibroblasts to produce collagen

scarring

89
Q

discribe the resolution stage of inflammation

A

irritating agent is removed
damage is repaired
inflammatory process completed

90
Q

what are the requirements for the resolution phase of inflammation

A

-affected tissue is capable of healing
- body capble of removing the irrritating agent

91
Q

what are the important points in the resolution phase of inflammation

A

intact epithelium
basement membrane must be intact in order to guide the healing process in laying down new tissue

92
Q

what happens if the basement membrane is destroyed

A

new tissue is unorganized and otherwise known as scare tissue
causing tissue repair

93
Q

what is an abscess?

A

collection of pus
neutrophils are primary responders

94
Q

what are the requirements for abscess formation

A

body is unable to elimminate the irritant
tissue injury rate» tissue repair

95
Q

where can an abscess occur

A

in all tissue

96
Q

what is the potential sequelae for an abscess

A

pain, fever, rupture, and swelling

97
Q

what is an ulcer

A

loss of mucosa, basement membrane and deeper tissue

98
Q

Erosion that occurs with an ulcer means what excatly

A

loss of mucosa only
basement membrane is still intact

99
Q

what are the requirements for a an ulcers formation

A

body is unable to eliminate the irritant
tissue injury rate» tissue repair

100
Q

where would you find and ulcer

A

most often in the GI tract

101
Q

what is the potential sequelae of an ulcer

A

pain, hemorrhage, pertonitis

102
Q

what is a fistula

A

abnormal connection between two organs

103
Q

what are the requirements for the formation of a fistula

A

Full thickness opening of walls of adjacent organs, vessels, ducts due to the inflammatory process
Communication between the two structures
Potential Sequelae
Structure dependent➔ infection, hemorrhage

104
Q

what is scar formation from chronic inflammation?

A

disorganized connective tissue&raquo_space; healing and repair

loss of parenchyma cells

105
Q

what is the requirement for scare tissue

A

loss of basement membrane= loss of regenerative tissue, loss of resolution

106
Q

what is the potential sequelae for scare tissue

A

loss of finction

107
Q

give a breif review defintion for resoulution

A

original tissue

108
Q

give a breif review defintion for tissue repair

A

tissue healing
regeneration and replacement (fibrosis/scare tissue)

109
Q

give a breif review defintion for regeneration

A

restoration of damaged tissue to the original state

110
Q

give a breif review defintion for replacement

A

laying down of collegen

111
Q

whats the process of granulation on a young scar

A

granulation tissue is highly vascularized connective tissue that is composed of newly formed capilliaries proliferating fibroblasts and residual inflammatory cells.

112
Q

whats the time frame for granulation tissue

A

2-5 days post wounding, starts as early as 24 hours.

113
Q

what type of growth pattern does granulation take

A

granulation tissue normally fills the base of the wound new tissue. Then fills the wound.

114
Q

what are the physcial therapy implications for repair

A

manual therapy, concetric and eccentric stregthening to promote organization

115
Q

repair =

A

regeneration + replacement

116
Q

scare tissue will

A

decrease functions and increased risk of reinjury

117
Q

what is the difference between regeneration and repair and healing

A

regeneration of parenchyma calls complete regeneration of tissue

repair/healing= regeneration combined with scaring and fibrosis

118
Q

what is the process of complete regeneration

A
  1. process of renewal, restoration, and growth of parenchyma cells
  2. new tissue is the same as the lost or damage tissue- no scare formation
  3. requires cells that can divide
  4. requires an intact basement membrane
  5. requires an intact connective tissue scaffolding
119
Q

what occurs during partial regeneration or healing/ repair

A

replacement of damaged or lost tissue with fibrosis tissue

120
Q

how long does the repair process take

A

begins in early inflammation within 24 hours to 10 days

121
Q

what happens in the repair process

A

fibroblasts and vascular endothelial cells begin to proliferate to form granulated tissue

pink, soft, and granular

122
Q

give a defintion of angiogenesis

A

angiogenesis- formation of new blood vessels; granulation tissue lays down a new capillary bed
-new vessels are leaky allowing protein and RBC passage.

123
Q

what does proliferation of fibroblasts secrete

A

collagen

124
Q

How would you describe the makeup of the extracellular matrix

A

the extra cellular matrix is edematous

granulation tissue - soft infrastructure

125
Q

explain wound contraction

A

approximation of wound edges
3 days to 20 days

126
Q

quickly describe the migration and proliferation of fibroblasts

A

fibroblasts within granulation tissue produce collagen fibers and contractile proteins to pull edges of damaged tissue together

127
Q

How do parenchyma cells regenerate

A

parenchyma cells regenerate to the extent possible

they are capable of cell division

128
Q

Scar formation take how many days

A

> 7 days

129
Q

how long does the reogranization of fibrous tissue take

A

remodling for weeks to months even years

130
Q

give a breif overview of the wound healing timeline

A
  1. inflammation: dilute or neutralize the injurious agent
  2. granulation tissue formation : regeneration of damaged connective tissue
  3. epithelial healing : regeneration of damaged epitheilial tissue
  4. wound contraction: approximation of wound edges
  5. scar formation and remodling: provide strength and return tissue to uninjured states
131
Q
A

clin med (19 decks)

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