Injury, Inflammation, Repair Flashcards
1
Q
Acute vs chronic inflammation are distinguished by
A
Onset, duration, type of infiltrating inflammatory cells
2
Q
Signs of inflammation
A
Heat, redness, pain, swelling
3
Q
what is inflammation
A
the body’s immune system’s response to stimulus.
the bodys defense mechanism for processing foreign agents
4
Q
what causes inflammation
A
Inflammation happens when the immune system fights against something that may turn out to be harmful
5
Q
what is controlled inflammation
A
is critical in protecting the body from harmful invaders
6
Q
uncontrolled inflammation definition
A
is potentially damaging regulation is critical
7
Q
Provoked response to tissue injury:
A
chemical agents
cold
heat
trauma
invasion of microbes
cancerous cells
8
Q
Protective component of inflammation
A
destroys and contains the injurious agent
9
Q
reparative component of inflammation
A
induces and supports tissue repair
10
Q
desirable response
A
controlled and proportional
11
Q
undesirable response
A
chronic and harmful
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
13
Q
what physiological response causes heat
A
release of soluble mediators and vasodilation
14
Q
what physio response causes redness
A
release of soluble mediators and vasodilation
15
Q
what physio response causes swelling
A
release of soluble mediators and vasodilation, increased blood flow, extravasation of fluid(permeability), cellular influx(chemotaxis)
16
Q
what physio response causes pain
A
release of soluble mediators
17
Q
Vasoconstriction
A
few seconds of blanching (whiteness)
18
Q
vasodilation
A
smooth muscle relaxes called active hyperemia
19
Q
increased permeability
A
leads to vascular keagae/edema
20
Q
active hyperemia
A
accounts for redness swelling and warmth
during exercise
due to arteriolar dilation
21
Q
vascular permeability leakage: transudate
A
result of high hydrostatic pressure and low osmotic pressure clear/ low cell protein
21
Q
vascular permeability leakage: exudate
A
result of increased vascular permeability cloudy/cell/protein rich fluid
22
Q
effects of vascular permeability
A
decreased ROM and function
23
Q
exudate
A
supplies antibodies and complement protein to affected areas
contributes to swelling causes pain and decreased mobility
24
5 mechanisms that cause vascular leakiness
mediators
cytokine mediators
severe injuries
leukocutes
certain mediatory may increase transcytosis
25
mediators
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
26
cytomediators in vascular permeability
reversible endothelial cell junction retraction 4-6 hours post injury/infection, lasting 24 hours or more
27
severe injuries cause vasculae permeabilitu
Severe injuries may cause immediate direct endothelial cell damage making them leaky until they are repaired
28
how leukocytes may cause vascular leakiness
Leukocytes may adhere to and damage the endothelium through activation and release of toxic oxygen radicals and proteolytic enzymes making the vessel leaky
29
certain mediators may increase transcytosis
intracellular vesicles extend from the luminal surface to basal lamina surface of the endothelial cell
30
what is degranulation
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
30
what is diapedesis
Leukocytes leave the vasculature and enter the interstitium through the following sequence of events
Margination and rolling
Adhesion
Chemotaxis
Activation
Transmigration
31
vasoconstriction
release of vasoconstrictor substances
constriction of cells thought to be immediate response to control blood loss
blanching
<60 seconds
***
32
why vasodilation occurs
: Increased hydrostatic pressure (pressure inside the vessel pushing out) causes a decrease of blood flow rate margination of leukocytes along the blood vessel walls
33
increased vascular permeability allows..
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
the results of increased vascular permeability is
Edema or increased fluid in the interstitial tissue
35
endothelial relaxation mechanism of increased vascular permeability
HBP, fluid leakage --> transudate
36
endothelial contraction mechanism of increased vascular permeability
: Immediate response --> exudate
immediate up to 30 mins
37
endothelial cell retraction of vascular permeability
delayed response --> exudate
4-6 hours
38
direct endothelial injury mechanism of vascular permeability is
immediate-sustained response
39
chemoattraction/chemotaxis stage of inflammation
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
rolling stafe of acute inflammation
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
firm adhesion & tight adhesion stage of acute inflammation
Release of chemokine by macrophages to transition moderate affinity to high affinity bonding to endothelial cells
41
transmigration stage of acute inflammation
Cytoskeleton reorganization in conjunction with leukocyte pseudopod extensions leukocytes pass through gaps in endothelial cells
42
acute inflammation characteristics
Rapid onset
Lasts minutes to days
Exudation of fluid and protein from vessels
Emigration of WBCs
43
purpose of acute inflammation
quick attack on foreign agents and initiate the repair process
44
cardinal signs of acute inflammation
Rubor, heat, edema, pain, tumor, and loss of function
45
causes of acute inflammation
Infection, trauma, physical and chemical agents, necrosis, foreign bodies, and immune reaction
46
outcomes of acute inflammation
resolution, chronic inflammation, healing by scarring
47
chronic inflammationcan lead to
cancer, CVD, pulmonary diseases, diabetes, autoimmune diseases, arthritis, neurological disease, alzheimers
48
chronic inflammation occurs when
acute phase cannot be resolved
49
chronic inflammation
lymphocytes, plasma cells, macrophage, fibroblasts
50
acute inflammation
neutrophils, macrophage
51
phases of inflammatory process
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
chronic inflammation 3 characteristics
- 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
what is angiogenesis
new vasculature, critical to wound repair
54
causes of chronic inflammation
Viral, microbial infection, prolonged exposure to toxin, autoimmune
Undesirable movement patterns***
55
lymphocytes involvement in chronic inflammation
stimulate fibroblasts to produce collagen (scarring)
56
requirements of resolution
Affected tissue is capable of healing
Body capable of removing the irritating agent
57
abscess
collection of pus
neutrophils are primary responders
58
requirements for formation of abscess
Body unable to eliminate the irritant
Tissue injury rate>>tissue repair
59
ulcer description
Loss of mucosa, basement membrane and deeper tissue
60
erosion description
loss of mucosa only, basement membrane intact
61
requirements for formation of ulcer
Body unable to eliminate the irritant
Tissue injury rate>>tissue repair
62
fistula
abnormal connection between two organs
63
requirements for formation of fistula
Full thickness opening of walls of adjacent organs, vessels, ducts due to the inflammatory process
Communication between the two structures
64
scar formation
Disorganized connective tissue>>healing and repair
Loss of parenchyma
65
requirement for scar formation
Loss of basement membrane = loss of regenerative tissue, loss of resoluti
can lead to loss of function
66
granulation tissue
2-5 days post wounding, starts
as early as 24 hours
perforating fibroblasts
wound progressing from inflammatory phase to proliferative phase of healing
66
pt implications to repair phase scar tissue
manual therapy, concentric/eccentric strengthening to promote organization
scar tissue = descres function and increased injury risk
67
regneration of parenchyma
complete regeneration of tissue
-involves restitution of tissue identical to that lost by injury
68
repair/healing
regeneration combined with scaring and fibrosis
- fibro-proliferative response that ‘patches’ a tissue defect by laying down connective tissue; fibrosis and scar formation
69
partial regeneration or repair
Replacement of damaged or lost tissue with fibrosis tissue
70
complete regeneration
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
timeline of repair and granulation tissue
within 24 hrs to 10 days
72
process of repair
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
wound contraction timeline
3 to 20 days
74
wound contraction
Migration and proliferation of fibroblasts: fibroblasts within granulation tissue produce collagen fibers & contractile proteins to pull edges of damaged tissue together
75
scar formation
> 7 days
76
wound healing timeline phases
inflammation
granulation tissue formation
epithelial healing
wound contraction
scar formation
77
primary healing
Wound with clean edges, close approximation of margins, and minimal tissue disruption
Small to nonexistent scar
78
secondary healing
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
wound strength 1 week
wound/incision is about 10% strength compared to normal skin
80
wound strength 2 months
scar is fully healed about 75% of normal skin strength
81
factors that may impair wound healing
Infection, nutritional deficiency (Vit C), steroids
Re-injury/Reopening
Decrease blood flow to the area
82
potential complications of wound healing
Ulceration as a result of reinjury/reopening
Keloid scars scar tissue forms beyond the boundaries of the wound
Contractures
