inflammation repair Flashcards

(132 cards)

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
what are the symptoms related to the pathological response of cellular influx (chemotaxis)
swelling (tumor)
26
what are physiological components of vascularity
vasoconstriction- few seconds of blanching vasodilation- smooth muscle relaxes called active hyperermia increased permeability- vascular leakage- edema
27
what are the physiological components of cellular mean
leukocyte accumulation and infiltration
28
where would you find active hyperemia?
arterial hyperemia due to arteriolar dilatation sympathic stimulation the affected tissue is redder than normal because of engorgement with oxygnated blood
29
what are some examples of active hyperemia
at sites of inflammation in skeletal muscle during exercise angioneurothic- face redness
30
what does active hyperemia account for?
redness swelling and warmth
31
what is main difference between exudate and transudate
cell/ protein rich fluid vs low cell/protein fluid
32
describe some details about transudate leakage/ permeability
result of high hydrostatic pressure and low osmotic pressure fluid is clear low cell/protein fluid
33
describe some details about exudate leakage/ permeability
result of increased vascular permeability cloudy high cell/ protein fluid
34
what does exudate permeability do?
supplies antibodies and complement protein to affected areas contributes to swelling causes pain and decreased mobility
35
if permeability accounts for swelling what might you also notice with the patient
decreased ROM and Function
36
what are the five known causes of vascular leakiness?
1. mediators 2. cytokine mediators 3. severe injuries 4. leukocytes adhering and damaging the endothelium 5. certain mediators may increase transcytosis
37
describe what occurs with the mediators that causes vascular leakiness
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
38
describe what occurs with the cytokine mediators that causes vascular leakiness
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
39
how will severe injuries cause vascular leakiness
immediate direct endothelial cell damage making them leaky until they are repaired
40
vascular permeability follows what process
flows vasodilation
41
vascular permeability causes what type of dysfunction
endothelial cell dysfunction
42
how does leukocytes that adhere and damage the endothelium cause vascular permeability
through activation and release of toxic oxygen radicals and proteolytic enzymes making the vessel leaky
43
how does mediators increasing transcytosis cause vascular permeability
intracellular vesicles extend from the luminal surface to basal lamina surface of the endothelial cells
44
what is meant by degranulation?
a cellular process that releases: neutrophils basophils eosinophils mast cells cytotoxic cells natural killer cells main purpose is to destroy pathogens innate immune system
45
what is meant by diapedesis
leukocytes leave the vasculature and enter the interstitium through a sequence if you know the sequence say it now
46
what is the sequence followed by diapedesis
margination and rolling adhesion chemotaxis activation transmigration
47
after the sequence of diapedesis what can the leukocytes participate in
degranulation phagocytosis- macrophage leukocyte/cytokine - protects and repair (controlled) leukocyte/ cytokine 'storm' induced tissue injury (uncontrolled or chronic)
48
what is special about the cytokine storm
long covid and disproportionallity to the response which creates a chronic disease cells of the enate immune system
49
explain the vasoconstriction stage of acute inflammation stage
release of vasoconstrictor substances constriction of cells- thought to be immediate response to control blood loss BLANCHING <60 seconds
50
explain the vasodilation stage of acute inflammation stage
Mechanism of action- cellular release of mediators relaxation of the blood vessel walls
51
what relax the blood vessels walls in the vasodilation stage of acute inflammation
histamine, prostacyclin and nitric oxide relax the blood vessel walls
52
why does the vasodilation stage happen in acute inflammation
increased hydrostatic pressure (pressure inside the cell pushing out) causes a decrease in blood flow rate leukocytes will marginate among the blood vessel wall
53
what is the mechanism of action in the increased vascular permeability stage of acute inflammation
increased vascular permeability occurs through release of histamine and leukotrienes
54
why does increased vascular permeability occur
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
what is the result of the increased vascular permeability stage of acute inflammation
edema or increased fluid in the interstitial tissue
56
what are the physiological mechanisms that increase vascular permeability?
endothelial relaxation and contraction
57
provide a defintion of endothelial relaxation
HBP cause fluid leakage. the fluid leakage is transudate
58
provide a definition of endothelial contraction
immediate response that is exudate fluid leakage initiated by the cell mediators: histimine and leukotrines time: immediate up to 30 minutes
59
Provide a definition for endothelial cell retraction
Delayed response that is a exudate leakage Happens in 4 to 6 hours, but is long lasting
60
what are the physical mechanisms of increased vascular permeability
direct endothelial injury
61
what is direct endothelial injury
immediate -sustained response time: IMMEDIATE
62
give a detailed depiction of what happens during chemotaxis
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
give a detailed depiction of what happens during rolling and rolling adhession
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
give a detailed depiction of what happens during firm and tight adhessions
release of chemokine by machrophages to transition modetate affinity to high bonding to endotheilial cells
65
give a detailed depiction of what happens during transmigration
cytoskeleton reorganization in conjunction with leukocyte pseudopod extensions leukocytes pass through gaps in endothelial cells
66
what should you KNOW about diapedesis? hint: COPS AND ROBBERS
diapedesis is blood vessel escape
67
how do leukocytes move to injury and infection
through chemotactic gradients
68
what details can you associate with acute inflammation
1. rapid onset 2. lasts minutes to days 3. exudation of fluid and proteins from vessels 4. emigration of WBC
69
what is the purpose of acute inflammation
quick attack on foreign agents and initiate the repair process
70
what are the cardinal signs associated with acute inflammation
rubor heat edema pain tumor loss of function
71
whats the cause of acute inflammation
infection trauma physical and chemical agents necrosis foreign bodies immune reaction
72
what are the outcomes of acute inflammation
resolution abscess ulcer chronic inflammation scar formation
73
Contributors in scar formation for acute inflammation
neurophils and macrophages
74
contributors in scar formation for chronic inflammation
lymphocytes, plasma cells, macrophage, fibroblasts
75
Scar formation on acute inflammation is connected to what
calcification
76
what are the phases of the inflammatory process
1. acute phase 2. tissue formation (proliferation) 3. remodeling phase
77
describe the acute phase of inflammatory process
inflammatory response lasts 2-4 days but complete in 2 weeks
78
describe the tissue formation phase of the inflammatory process
-subacute phase tissue rebuilding, approximately 2-3 weeks -this does not include chronic inflammation
79
describe the remodeling phase of the inflammatory process
-adapt to original tissue -continues for up to 1 year post injury
80
describe chronic inflammation
- lasts week to years - involves lymphocytes and macrophages -tissue repair and tissue injury happen simultaneously
81
describe active inflammation for chronic inflammation
lymphocyte, macrophage, plasma cell infiltration
81
what are the three characteristics of chronic inflammation?
1. active inflammation 2. tissue destruction by inflammatory cells and stimuli 3. tissue healing
82
describe tissue destruction by inflammatory cells and stimuli when it comes to chronic inflammation
lack of complete resolution
83
describe tissue healing when it comes to chronic inflammation
fibrosis + regeneration both require angiogenesis
84
what does angiogenesis mean
new vasculature, critical to wound repair
85
what does regeneration mean
formation of new tissue
86
Give a description for what chronic inflammation is
- simultaneously active inflammation- lymphocytes - tissue destruction - tissue repair injuries stimulus that the body cannot remove
87
what are the causes of chronic inflammation
viral micronial infection, prolonged exposure to toxin, autoimmune UNDESIRABLE MOVEMENT PATTERNS
88
what are the cells involved in chronic inflammation?
macrophage- produce enzymes and mediators Lymphocytes- stimulate fibroblasts to produce collagen scarring
89
discribe the resolution stage of inflammation
irritating agent is removed damage is repaired inflammatory process completed
90
what are the requirements for the resolution phase of inflammation
-affected tissue is capable of healing - body capble of removing the irrritating agent
91
what are the important points in the resolution phase of inflammation
intact epithelium basement membrane must be intact in order to guide the healing process in laying down new tissue
92
what happens if the basement membrane is destroyed
new tissue is unorganized and otherwise known as scare tissue causing tissue repair
93
what is an abscess?
collection of pus neutrophils are primary responders
94
what are the requirements for abscess formation
body is unable to elimminate the irritant tissue injury rate>> tissue repair
95
where can an abscess occur
in all tissue
96
what is the potential sequelae for an abscess
pain, fever, rupture, and swelling
97
what is an ulcer
loss of mucosa, basement membrane and deeper tissue
98
Erosion that occurs with an ulcer means what excatly
loss of mucosa only basement membrane is still intact
99
what are the requirements for a an ulcers formation
body is unable to eliminate the irritant tissue injury rate>> tissue repair
100
where would you find and ulcer
most often in the GI tract
101
what is the potential sequelae of an ulcer
pain, hemorrhage, pertonitis
102
what is a fistula
abnormal connection between two organs
103
what are the requirements for the formation of a fistula
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
what is scar formation from chronic inflammation?
disorganized connective tissue >> healing and repair loss of parenchyma cells
105
what is the requirement for scare tissue
loss of basement membrane= loss of regenerative tissue, loss of resolution
106
what is the potential sequelae for scare tissue
loss of finction
107
give a breif review defintion for resoulution
original tissue
108
give a breif review defintion for tissue repair
tissue healing regeneration and replacement (fibrosis/scare tissue)
109
give a breif review defintion for regeneration
restoration of damaged tissue to the original state
110
give a breif review defintion for replacement
laying down of collegen
111
whats the process of granulation on a young scar
granulation tissue is highly vascularized connective tissue that is composed of newly formed capilliaries proliferating fibroblasts and residual inflammatory cells.
112
whats the time frame for granulation tissue
2-5 days post wounding, starts as early as 24 hours.
113
what type of growth pattern does granulation take
granulation tissue normally fills the base of the wound new tissue. Then fills the wound.
114
what are the physcial therapy implications for repair
manual therapy, concetric and eccentric stregthening to promote organization
115
repair =
regeneration + replacement
116
scare tissue will
decrease functions and increased risk of reinjury
117
what is the difference between regeneration and repair and healing
regeneration of parenchyma calls complete regeneration of tissue repair/healing= regeneration combined with scaring and fibrosis
118
what is the process of complete regeneration
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
what occurs during partial regeneration or healing/ repair
replacement of damaged or lost tissue with fibrosis tissue
120
how long does the repair process take
begins in early inflammation within 24 hours to 10 days
121
what happens in the repair process
fibroblasts and vascular endothelial cells begin to proliferate to form granulated tissue pink, soft, and granular
122
give a defintion of angiogenesis
angiogenesis- formation of new blood vessels; granulation tissue lays down a new capillary bed -new vessels are leaky allowing protein and RBC passage.
123
what does proliferation of fibroblasts secrete
collagen
124
How would you describe the makeup of the extracellular matrix
the extra cellular matrix is edematous granulation tissue - soft infrastructure
125
explain wound contraction
approximation of wound edges 3 days to 20 days
126
quickly describe the migration and proliferation of fibroblasts
fibroblasts within granulation tissue produce collagen fibers and contractile proteins to pull edges of damaged tissue together
127
How do parenchyma cells regenerate
parenchyma cells regenerate to the extent possible they are capable of cell division
128
Scar formation take how many days
>7 days
129
how long does the reogranization of fibrous tissue take
remodling for weeks to months even years
130
give a breif overview of the wound healing timeline
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