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BOC > Chapter 10 - Tissue Response to Injury > Flashcards

Chapter 10 - Tissue Response to Injury Flashcards

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
Q

mononuclear phagocytes / macrophages

A

after PMN’s.

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26
Q

once debris is removed from site of injury

A

blood coagulates, exudates coagulates to form fibrin network to localize injury, epithelial cells migrate to edges and fibroblasts enter to regrow capillaries

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27
Q

granulation tissue

A

fibroblasts, collagen, capillaries

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28
Q

extracellular matrix

A

callagen, elastin, ground substance, proteoglycans, glycosaminoglycans

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29
Q

fibroblastic repair phase

A

fibroplasia - scar formation - can last 4-6 weeks

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30
Q

as the fibrin clot breaks down..

A

granulation tissue is formed. capillaries grown into the area, and fibroblasts accumulate lay down parallel to capillaries

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31
Q

fibroblasts

A

synthesize extracellular matrix and begin to randomly deposit collagen fibers to form the scar. Type III collagen is most common

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32
Q

tensile forces

A

tensile forces help strengthen the collagen and lead it into the maturation phase, presence of fibroblasts is diminished

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33
Q

maturation-remodeling phase

A

long-term process. realignment or remodeling of the collagen fibers according to the subjected tensile forces

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34
Q

types of repair

A

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

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35
Q

factors that impede healing

A

extent of injury, edema, hemorrhage, poor vascular supply, separation of tissue, muscle spasm, corticosteroids, keloids, infection, humidity, climate, health, age, nutrition

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36
Q

Vitamin C and healing

A

collagen synthesis, immune system function

37
Q

vitamin K and healing

A

clotting

38
Q

Vitamina A and healing

A

immunue system function

39
Q

zinc and healing

A

enzyme system

40
Q

oxygen tension

A

relates to neurovascularization of wound, which translates into optimal saturation and maximal tensile strength development

41
Q

microtears

A

overuse

42
Q

macro tears

A

acute

43
Q

Wolff’s law

A

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
Q

cell organelles

A

mitochondria, ribosomes, endoplasmic reticulum, centrioles, golgi apparatus, microtubules

45
Q

4 types of soft tissue

A

epitheial
connnective
muscle
nervous

46
Q

soft tissue adaptations

A

metaplasia, dysplasia, hyperplasia, atriphy, hypertrophy

47
Q

metaplasia

A

coversion of one kind of tissue into a form that is not normal for that tissue

48
Q

dysplasia

A

abnormal development of tissue

49
Q

hyperplasia

A

excessive proliferation of normal cells in the normal tissue arrangement

50
Q

cartilage healing properties

A

limited healing capacity

51
Q

ligament healing

A

first 72 hours: loss of blood and attraction of inflammatory cells

52
Q

extra-articular ligament

A

bleeding occurs in subQ

53
Q

intra-articular ligament

A

bleeding occurs inside joint capsule until clotting or pressure causes cease

54
Q

full ligament healing may take

A

12 months

55
Q

factors affecting ligament healing

A

surgery, active exercise, strengthening of surrounding muscles (all these are good for the ligament)

56
Q

Muscle healing

A

long healing time

57
Q

tendon healing

A

begins as one mass that is adhered to surrounding tissues (2nd week) eventually elongates into separate structure by the third week

58
Q

nerve healing

A

regneration is impossible
unless the injury does not affect the cell body

3-4 mm per day

59
Q

bone healing

A

affected by torsion, bending, and compression

60
Q

bone healing after fracture

A

week 1: fibroblasts laying down collagen network
weeks 3-8: immobilization
osteoblastic/clastic activity - 2-3 years after

61
Q

chondroblast cells

A

begin producing fibrocartilage, creating a callus b/w broken bones

62
Q

osteoblats

A

form cancellous bone trabeculae which eventually replaces cartilage

63
Q

osteoclasts

A

cells that resorb bone - clean up debris

64
Q

remodeling

A

fibrous cartilage replaced by fibrous bone and them lamellar bone

65
Q

referred pain

A

occurs away from a actual site of irritation

66
Q

types of referred pain

A

myofascial pain, sclerotomic pain, dermatomic pain

67
Q

myofascial pain

A

trigger points are small hyper-irritable area within a muscle in which nerve impulses bombard the CNS and are expressed as referred pain

68
Q

sclerotomic pain

A

deep, aching, poorly localized pain from area of bone or fascia,
single nerve root

can cause affective changes

69
Q

dermatomic pain

A

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
Q

nociceptors

A

pain receptors/free nerve endings, sensitive to mechanical, thermal, chemical energy

71
Q

first order-primary afferents

A

transmit impulses from nociceptor to dorsal horn of spinal cord

72
Q

a-alpha and a-beta

A

large - diameter

73
Q

a-delta and C

A

small-diameter, transmit sensation of pain and temperature

74
Q

a-deltas

A

transmit ‘fast pain’, C transmits ‘slow pain’

75
Q

secondary order afferents

A

carry sensory messages from dorsal horn to brain

input from a-betas/deltas, and C’s.

serve large receptor fields

76
Q

third order afferents

A

carry info from the thalamus to the cerebral cortex

77
Q

seratonin

A

active in descending pathways

78
Q

norephinephrine

A

inhibits pain transmission b/w first and second order neurons

79
Q

enkephalins

A

found in descending pathways

80
Q

beta-endorphins

A

found in CNS

81
Q

Gate Control Theory

A

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
Q

Central Biasing

A

‘Descending pathway pain control’

previous experience, emotional influences, sensory perception, main influence perception of pain - brain can release neurotransmitter

83
Q

Release of Beta-Endorphins

A

painful stimuli release B-endorphin opiates from hypothalamus and anterior pituitary.

strong analgesic effects

efferent pathway

84
Q

Visual Analog Scale

A

lines that represent limits of pain.

85
Q

pain charts

A

2-dimensional graphic chart to assess location of pain

86
Q

mcgill pain questionnaire

A

78 words that describe pain, which are grouped into 20 sets and divided into 4 categories representing dimensions of the pain experience

87
Q

activity pain indicators

A

64-question self report tool to assess impairment associated with pain

88
Q

numeric rating scale

A

1-10

89
Q

phagocytosis

A

disposing of injury byproducts

BOC (49 decks)

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