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CLIN MED > Injury, Inflammation, Repair > Flashcards

Injury, Inflammation, Repair Flashcards

1
Q

Acute vs chronic inflammation are distinguished by

A

Onset, duration, type of infiltrating inflammatory cells

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2
Q

Signs of inflammation

A

Heat, redness, pain, swelling

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3
Q

what is inflammation

A

the body’s immune system’s response to stimulus.
the bodys defense mechanism for processing foreign agents

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4
Q

what causes inflammation

A

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

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5
Q

what is controlled inflammation

A

is critical in protecting the body from harmful invaders

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6
Q

uncontrolled inflammation definition

A

is potentially damaging  regulation is critical

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7
Q

Provoked response to tissue injury:

A

chemical agents
cold
heat
trauma
invasion of microbes
cancerous cells

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8
Q

Protective component of inflammation

A

destroys and contains the injurious agent

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9
Q

reparative component of inflammation

A

induces and supports tissue repair

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10
Q

desirable response

A

controlled and proportional

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11
Q

undesirable response

A

chronic and harmful

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12
Q

timeline of imflammation

A

Foreign agent enters the body

Local vasodilation and increased vascular permeability

Accumulation of WBC in blood vessels

WBC exit the blood vessels

Drawn to an area of foreign agent/injury = Chemotaxis

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13
Q

what physiological response causes heat

A

release of soluble mediators and vasodilation

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14
Q

what physio response causes redness

A

release of soluble mediators and vasodilation

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15
Q

what physio response causes swelling

A

release of soluble mediators and vasodilation, increased blood flow, extravasation of fluid(permeability), cellular influx(chemotaxis)

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16
Q

what physio response causes pain

A

release of soluble mediators

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17
Q

Vasoconstriction

A

few seconds of blanching (whiteness)

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18
Q

vasodilation

A

smooth muscle relaxes called active hyperemia

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19
Q

increased permeability

A

leads to vascular keagae/edema

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20
Q

active hyperemia

A

accounts for redness swelling and warmth
during exercise
due to arteriolar dilation

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21
Q

vascular permeability leakage: transudate

A

result of high hydrostatic pressure and low osmotic pressure  clear/ low cell protein

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21
Q

vascular permeability leakage: exudate

A

result of increased vascular permeability  cloudy/cell/protein rich fluid

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22
Q

effects of vascular permeability

A

decreased ROM and function

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23
Q

exudate

A

supplies antibodies and complement protein to affected areas
contributes to swelling causes pain and decreased mobility

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24
Q

5 mechanisms that cause vascular leakiness

A

mediators
cytokine mediators
severe injuries
leukocutes
certain mediatory may increase transcytosis

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25
Q

mediators

A

histamines, bradykinins, leukotrienes cause an early, brief (<30 min) immediate response in the form of reversible endothelial cell contraction that widens intercellular gaps of venules, specific to allergic reaction

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26
Q

cytomediators in vascular permeability

A

reversible endothelial cell junction retraction 4-6 hours post injury/infection, lasting 24 hours or more

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27
Q

severe injuries cause vasculae permeabilitu

A

Severe injuries may cause immediate direct endothelial cell damage making them leaky until they are repaired

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28
Q

how leukocytes may cause vascular leakiness

A

Leukocytes may adhere to and damage the endothelium through activation and release of toxic oxygen radicals and proteolytic enzymes making the vessel leaky

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29
Q

certain mediators may increase transcytosis

A

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

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30
Q

what is degranulation

A

is 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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30
Q

what is diapedesis

A

Leukocytes leave the vasculature and enter the interstitium through the following sequence of events
Margination and rolling
Adhesion
Chemotaxis
Activation
Transmigration

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31
Q

vasoconstriction

A

release of vasoconstrictor substances
constriction of cells  thought to be immediate response to control blood loss
blanching

<60 seconds ***
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32
Q

why vasodilation occurs

A

: Increased hydrostatic pressure (pressure inside the vessel pushing out) causes a decrease of blood flow rate  margination of leukocytes along the blood vessel walls

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33
Q

increased vascular permeability allows..

A

allows fluid, WBC, and protein to move to the interstitial tissue causing a decrease in osmotic pressure in the blood vessels and increase in osmotic pressure in the interstitial tissue

34
Q

the results of increased vascular permeability is

A

Edema or increased fluid in the interstitial tissue

35
Q

endothelial relaxation mechanism of increased vascular permeability

A

HBP, fluid leakage –> transudate

36
Q

endothelial contraction mechanism of increased vascular permeability

A

: Immediate response –> exudate
immediate up to 30 mins

37
Q

endothelial cell retraction of vascular permeability

A

delayed response –> exudate
4-6 hours

38
Q

direct endothelial injury mechanism of vascular permeability is

A

immediate-sustained response

39
Q

chemoattraction/chemotaxis stage of inflammation

A

Activation of macrophages by pathogens cause a release of cytokines  release of cytokines causes endothelial cells of local blood vessels to secrete adhesion molecules local leukocytes are attracted to the presence of cytokines and adhesion molecules

40
Q

rolling stafe of acute inflammation

A

Circulating leukocytes bind to adhesion molecules with moderate affinity
Causes leukocytes in the blood to slow down and begin ‘rolling’ along the inner surface of blood vessel walls

41
Q

firm adhesion & tight adhesion stage of acute inflammation

A

Release of chemokine by macrophages to transition moderate affinity to high affinity bonding to endothelial cells

41
Q

transmigration stage of acute inflammation

A

Cytoskeleton reorganization in conjunction with leukocyte pseudopod extensions leukocytes pass through gaps in endothelial cells

42
Q

acute inflammation characteristics

A

Rapid onset
Lasts minutes to days
Exudation of fluid and protein from vessels
Emigration of WBCs

43
Q

purpose of acute inflammation

A

quick attack on foreign agents and initiate the repair process

44
Q

cardinal signs of acute inflammation

A

Rubor, heat, edema, pain, tumor, and loss of function

45
Q

causes of acute inflammation

A

Infection, trauma, physical and chemical agents, necrosis, foreign bodies, and immune reaction

46
Q

outcomes of acute inflammation

A

resolution, chronic inflammation, healing by scarring

47
Q

chronic inflammationcan lead to

A

cancer, CVD, pulmonary diseases, diabetes, autoimmune diseases, arthritis, neurological disease, alzheimers

48
Q

chronic inflammation occurs when

A

acute phase cannot be resolved

49
Q

chronic inflammation

A

lymphocytes, plasma cells, macrophage, fibroblasts

50
Q

acute inflammation

A

neutrophils, macrophage

51
Q

phases of inflammatory process

A

phase 1 - acute phase 2-4 days complete in 2 weeks
phase 2 - tissue formation (proliferation) 2-3 weeks
phase 3 - remodeling phase up to 1 yr

52
Q

chronic inflammation 3 characteristics

A
  • Active Inflammation  lymphocyte, macrophage, plasma cell infiltration
  • Tissue destruction by inflammatory cells & stimuli  lack of complete resolution
  • Tissue healing  fibrosis + regeneration  both require angiogenesis
53
Q

what is angiogenesis

A

new vasculature, critical to wound repair

54
Q

causes of chronic inflammation

A

Viral, microbial infection, prolonged exposure to toxin, autoimmune
Undesirable movement patterns***

55
Q

lymphocytes involvement in chronic inflammation

A

 stimulate fibroblasts to produce collagen (scarring)

56
Q

requirements of resolution

A

Affected tissue is capable of healing
Body capable of removing the irritating agent

57
Q

abscess

A

collection of pus
neutrophils are primary responders

58
Q

requirements for formation of abscess

A

Body unable to eliminate the irritant
Tissue injury rate»tissue repair

59
Q

ulcer description

A

Loss of mucosa, basement membrane and deeper tissue

60
Q

erosion description

A

loss of mucosa only, basement membrane intact

61
Q

requirements for formation of ulcer

A

Body unable to eliminate the irritant
Tissue injury rate»tissue repair

62
Q

fistula

A

abnormal connection between two organs

63
Q

requirements for formation of fistula

A

Full thickness opening of walls of adjacent organs, vessels, ducts due to the inflammatory process
Communication between the two structures

64
Q

scar formation

A

Disorganized connective tissue»healing and repair
Loss of parenchyma

65
Q

requirement for scar formation

A

Loss of basement membrane = loss of regenerative tissue, loss of resoluti
can lead to loss of function

66
Q

granulation tissue

A

2-5 days post wounding, starts
as early as 24 hours
perforating fibroblasts
wound progressing from inflammatory phase to proliferative phase of healing

66
Q

pt implications to repair phase scar tissue

A

manual therapy, concentric/eccentric strengthening to promote organization
scar tissue = descres function and increased injury risk

67
Q

regneration of parenchyma

A

complete regeneration of tissue
-involves restitution of tissue identical to that lost by injury

68
Q

repair/healing

A

regeneration combined with scaring and fibrosis
- fibro-proliferative response that ‘patches’ a tissue defect by laying down connective tissue; fibrosis and scar formation

69
Q

partial regeneration or repair

A

Replacement of damaged or lost tissue with fibrosis tissue

70
Q

complete regeneration

A

Process of renewal, restoration, and growth of parenchyma cells
New tissue is the same as the lost or damaged tissue no scar formation
Requires cells that can divide
Requires an intact basement membrane
Requires an intact connective tissue scaffolding

71
Q

timeline of repair and granulation tissue

A

within 24 hrs to 10 days

72
Q

process of repair

A

Fibroblast and vascular endothelial cells begin to proliferate to form granulation tissue pink, soft, and granular

Angiogenesis  Formation of new blood vessels: granulation tissue lays down a new capillary bed  new vessels are leaky allowing protein and RBC passage

Proliferation of fibroblasts  secrete collagen

Extracellular Matrix (ECM) is edematous = Granulation Tissue  soft infrastructure

73
Q

wound contraction timeline

A

3 to 20 days

74
Q

wound contraction

A

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

75
Q

scar formation

A

> 7 days

76
Q

wound healing timeline phases

A

inflammation
granulation tissue formation
epithelial healing
wound contraction
scar formation

77
Q

primary healing

A

Wound with clean edges, close approximation of margins, and minimal tissue disruption
Small to nonexistent scar

78
Q

secondary healing

A

Large wounds where edges cannot be drawn together

Fibroblasts help bring the edges together – granulation results in a broad scar

large more prominant scar

79
Q

wound strength 1 week

A

wound/incision is about 10% strength compared to normal skin

80
Q

wound strength 2 months

A

scar is fully healed about 75% of normal skin strength

81
Q

factors that may impair wound healing

A

Infection, nutritional deficiency (Vit C), steroids

Re-injury/Reopening

Decrease blood flow to the area
82
Q

potential complications of wound healing

A

Ulceration as a result of reinjury/reopening
Keloid scars scar tissue forms beyond the boundaries of the wound
Contractures

CLIN MED (9 decks)

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