Chapter 10 - Tissue Response to Injury Flashcards

(89 cards)

1
Q

5 signs of inflammation

A
redness (rubor)
swelling (tumor)
pain (dolor)
temp (calor)
loss of function (function lease)
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2
Q

inflammatory response phase lasts

A

about 4 days

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3
Q

inflammation caused by

A

cellular injury results in altered metabolisms and liberation of materials that initiate inflammation

injury causes altered metabolisms and release of materials and chemicals that initiate inflammation

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4
Q

1st responders of inflammation

A

leukocytes, phagocytic cells, exudates

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5
Q

Phases of inflammatory response

A

vascular reaction, phagocytosis, formation of a clot

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6
Q

vascular reactions

A

immediate vasoconstriction followed by vasodilation

initial effusion last 24-36 hours

chemical mediators: histamine, leukotaxin, necrosis, leukocytes

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7
Q

histamine

A

released from mast cells; vasodilation, increased cell permeability, sensitizes pain receptors

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8
Q

Leukotaxin

A

margination; increases cell permeability locally to allow for diapedesis

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9
Q

Diapedesis

A

movement of wbc out of small arterial walls

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10
Q

Necrosin

A

phagocytic activity; amount of swelling that occurs directly related to extent of vessel damage

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11
Q

Leukocytes

A

neutrophils and macrophages - cause release of bradykinin and prostaglandin

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12
Q

Bradykinin

A

increased permeability, pain, stimulates release of prostaglandin

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13
Q

Prostaglandin

A

increases permeability of blood vessels and tissue (increased space for WBC’s to move)

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14
Q

three phases of the healing process

A

inflammatory response phase, fibroblastic repair phase, maturation-remodeling phase

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15
Q

margination

A

neutrophils and macrophages line up along the cell wall

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16
Q

cytokines

A

attrack phagocytes to site of inflammation

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17
Q

vascular reaction

A

vascular spasm, formation of a platelet plug, blood coagulation, growth of fibrous tissue

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18
Q

what state does immediate vasoconstriction cause

A

local anemia, followed by rapid hyperemia because of vasodilation

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19
Q

formation of platelet plug

A

platelets adhere to collagen fibers that stick out due to injury.. create sticky matrix that sticks to more platelets and leukocytes to eventually form a platelet plug

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20
Q

formation of a clot

A

damaged cell–>thromboplastin –>prothrombin changed to thrombin –> fibrinogen changed to fibrin –> clot shuts off blood supply to injured area

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21
Q

clot formation begins when?

A

12 hours after injury and completed within 48 hours.

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22
Q

initial flammatory phase lasts

A

2-4 days

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23
Q

Chronic inflammation

A

neutrophils present during normal acute inflammation are replaced with macrophages, lymphocytes, and fibroblasts, and plasma cells.

this causes damage to occur to the healthy cells around the dead cells - damage to the CT - causes necrosis and fibrosis.

forms granulation tissue

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24
Q

PMN’s

A

polymoprhonuclear neutrophils - first on the scene - kill bacteria - will die off and create a toxic environment

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25
mononuclear phagocytes / macrophages
after PMN's.
26
once debris is removed from site of injury
blood coagulates, exudates coagulates to form fibrin network to localize injury, epithelial cells migrate to edges and fibroblasts enter to regrow capillaries
27
granulation tissue
fibroblasts, collagen, capillaries
28
extracellular matrix
callagen, elastin, ground substance, proteoglycans, glycosaminoglycans
29
fibroblastic repair phase
fibroplasia - scar formation - can last 4-6 weeks
30
as the fibrin clot breaks down..
granulation tissue is formed. capillaries grown into the area, and fibroblasts accumulate lay down parallel to capillaries
31
fibroblasts
synthesize extracellular matrix and begin to randomly deposit collagen fibers to form the scar. Type III collagen is most common
32
tensile forces
tensile forces help strengthen the collagen and lead it into the maturation phase, presence of fibroblasts is diminished
33
maturation-remodeling phase
long-term process. realignment or remodeling of the collagen fibers according to the subjected tensile forces
34
types of repair
resolution: little no damage - normal restoration granulation: initially laying down of type III - changes to type 1 in 2 weeks regneration: new cells of same type are generation and capable of performing same function
35
factors that impede healing
extent of injury, edema, hemorrhage, poor vascular supply, separation of tissue, muscle spasm, corticosteroids, keloids, infection, humidity, climate, health, age, nutrition
36
Vitamin C and healing
collagen synthesis, immune system function
37
vitamin K and healing
clotting
38
Vitamina A and healing
immunue system function
39
zinc and healing
enzyme system
40
oxygen tension
relates to neurovascularization of wound, which translates into optimal saturation and maximal tensile strength development
41
microtears
overuse
42
macro tears
acute
43
Wolff's law
bone and soft tissue will respond to the physical demands placed on them, causing them to remodel or realign along line of tensile force
44
cell organelles
mitochondria, ribosomes, endoplasmic reticulum, centrioles, golgi apparatus, microtubules
45
4 types of soft tissue
epitheial connnective muscle nervous
46
soft tissue adaptations
metaplasia, dysplasia, hyperplasia, atriphy, hypertrophy
47
metaplasia
coversion of one kind of tissue into a form that is not normal for that tissue
48
dysplasia
abnormal development of tissue
49
hyperplasia
excessive proliferation of normal cells in the normal tissue arrangement
50
cartilage healing properties
limited healing capacity
51
ligament healing
first 72 hours: loss of blood and attraction of inflammatory cells
52
extra-articular ligament
bleeding occurs in subQ
53
intra-articular ligament
bleeding occurs inside joint capsule until clotting or pressure causes cease
54
full ligament healing may take
12 months
55
factors affecting ligament healing
surgery, active exercise, strengthening of surrounding muscles (all these are good for the ligament)
56
Muscle healing
long healing time
57
tendon healing
begins as one mass that is adhered to surrounding tissues (2nd week) eventually elongates into separate structure by the third week
58
nerve healing
regneration is impossible unless the injury does not affect the cell body 3-4 mm per day
59
bone healing
affected by torsion, bending, and compression
60
bone healing after fracture
week 1: fibroblasts laying down collagen network weeks 3-8: immobilization osteoblastic/clastic activity - 2-3 years after
61
chondroblast cells
begin producing fibrocartilage, creating a callus b/w broken bones
62
osteoblats
form cancellous bone trabeculae which eventually replaces cartilage
63
osteoclasts
cells that resorb bone - clean up debris
64
remodeling
fibrous cartilage replaced by fibrous bone and them lamellar bone
65
referred pain
occurs away from a actual site of irritation
66
types of referred pain
myofascial pain, sclerotomic pain, dermatomic pain
67
myofascial pain
trigger points are small hyper-irritable area within a muscle in which nerve impulses bombard the CNS and are expressed as referred pain
68
sclerotomic pain
deep, aching, poorly localized pain from area of bone or fascia, single nerve root can cause affective changes
69
dermatomic pain
area of skin supplied by a single nerve root; pain is sharp and well-localized, projects mainly to thalamus and is relayed directly to the the cortex (skips autonomic and affective responses)
70
nociceptors
pain receptors/free nerve endings, sensitive to mechanical, thermal, chemical energy
71
first order-primary afferents
transmit impulses from nociceptor to dorsal horn of spinal cord
72
a-alpha and a-beta
large - diameter
73
a-delta and C
small-diameter, transmit sensation of pain and temperature
74
a-deltas
transmit 'fast pain', C transmits 'slow pain'
75
secondary order afferents
carry sensory messages from dorsal horn to brain input from a-betas/deltas, and C's. serve large receptor fields
76
third order afferents
carry info from the thalamus to the cerebral cortex
77
seratonin
active in descending pathways
78
norephinephrine
inhibits pain transmission b/w first and second order neurons
79
enkephalins
found in descending pathways
80
beta-endorphins
found in CNS
81
Gate Control Theory
sensory inför from alpha-beta fibers overrides or inhibits the 'pain info' carried along a-deltas and C affront fibers, thus inhibiting or 'closing the gate' to the transmission of pain info to 2nd order neurons T-cell (located in dorsal horn) only lets one sensation through at a time, so strong sensory information traveling along alpha-beta fibers can affect the SG(substantial gelintinosa) which can send inhibitory signals to the T-cell and close the gate before the pain stimuli (a-deltas or C fibers) can be transmitted to 2nd order neurons occurs at spinal cord level. afferent pathway
82
Central Biasing
'Descending pathway pain control' previous experience, emotional influences, sensory perception, main influence perception of pain - brain can release neurotransmitter
83
Release of Beta-Endorphins
painful stimuli release B-endorphin opiates from hypothalamus and anterior pituitary. strong analgesic effects efferent pathway
84
Visual Analog Scale
lines that represent limits of pain.
85
pain charts
2-dimensional graphic chart to assess location of pain
86
mcgill pain questionnaire
78 words that describe pain, which are grouped into 20 sets and divided into 4 categories representing dimensions of the pain experience
87
activity pain indicators
64-question self report tool to assess impairment associated with pain
88
numeric rating scale
1-10
89
phagocytosis
disposing of injury byproducts