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FCA > FINAL EXAM > Flashcards

FINAL EXAM Flashcards

1
Q

what is the inflammatory process?

A

steps toward healing of injured tissue

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2
Q

what is the ultimate goal of treating an injury?

A

promote a strong, mobile scar
full, pain free movement
full strength

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3
Q

what is inflammation?

A

immediate, local response to injury & tissue damage

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4
Q

causes of tissue damage (internal / external)

A

trauma, infection, surgery, immune responses, extreme heat / cold, ischemic damage, chemical / radiation damage

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5
Q

types of healing (inflammatory process)

A

simply by replication of missing cells OR structure is created using scar tissue

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6
Q

re-epithelialization

A

-only applies if skin is damaged
-epithelial tissue lost, begins to regenerate
-if damage is superficial involving only epithelial layer, healing = regeneration of tissue
-NO scar tissue, normal tissue structure results
-regeneration possible with epithelial cells & nerve hepatic cells

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7
Q

granulation tissue

A

-part of any tissue repair where there is 1st/2nd intention healing
-adequate blood supply & nutrients must be present
-fibroblasts = important -> synthesize new collagen fibers that form loose CT matrix
-matrix replaces clot developed in acute stage
-resultant vascular CT = granulation tissue

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8
Q

NEOANGIOGENESIS (granulation tissue)

A

new blood vessels develop from venues at edge of injury

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9
Q

SCAR TISSUE (inflammatory process)

A

increases loss of epidermal tissue layers / damage to other tissue (muscle, tendon, ligaments)
-healing results from synthesis of new tissue
-requires production of CT with collagen fibers to replace area damaged
-restores structure but with different tissue than original
-MATURE COLLAGEN REPAIR

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10
Q

2 types of healing (inflammatory process)

A

first intention healing
second intention healing

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11
Q

primary / first intention healing

A

-some tissue loss, wound edges approximated (tape, sutures, staples)
-healing is efficient, with small amounts of collagen produced

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12
Q

secondary / second intention healing

A

-extensive tissue loss / large area affected
-wound edges cannot be brought together easily
-healing takes longer
-extensive re-epithelialization
-production of large amounts of granulation tissue

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13
Q

factors that affect the healing process

A

severity of injury, age, infection, presence of foreign material, nutritional support, existing conditions, adequate blood supply, wound separation, drugs, smoking

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14
Q

ACUTE STAGE (inflammatory process)

A

-from moment of injury -> 3 to 4 days post
-redness, swelling, heat, pain, loss of ROM, bruising (purple)

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15
Q

EARLY SUBACUTE STAGE (inflammatory process)

A

-within 2 days -> up to 3 weeks
-diminished inflammation, pink, warm, less painful
-muscle spasm diminished
-bruising unchanged
-primary process = filling damaged area with new tissue

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16
Q

LATE SUBACUTE STAGE (inflammatory process)

A

-2-3 weeks of subacute
-may be pocket of residual swelling
-minimal discomfort, possible loss ROM
-blood vessels developed with neoangiogenesis
-bruising changes to yellow / green
-pain with overpressure

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17
Q

WOUND CONTRACTION (inflammatory process)

A

-myofibroblasts in wound matrix contain contractile fibers
-purpose: speed healing process (peaks 2 weeks after injury)
-can result in deformation of tissue & possible dysfunction

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18
Q

SCAR REMODELING (inflammatory process)

A

-reshaping & reorganizing of healing begin as existing collagen is broken down, new collagen synthesized, cross links develop among collagen fibers
-strength of site beings to increase

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19
Q

CHRONIC STAGE (inflammatory process)

A

-overlaps with late subacute, 2-3 weeks post injury -> 1-2 years
-inflammatory process resolved, no edema
-chronic inflammation may result as part of self-perpetuating cycle

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20
Q

what is an injury?

A

disruption of the continuity of any tissue

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21
Q

epidermis

A

-outer layer
-cells have short life span (28-30) days, which results in continuous sloughing & renewal of this layer

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22
Q

dermis

A

-below epidermis
-anchors & nutritionally supports epidermis
-elastin & collagen -> flexibility & strength
-contains sebaceous (oil) & sweat glands, hair follicles, nerve receptors, blood & lymphatic vessels

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23
Q

subcutaneous layer

A

-contains adipose tissue, larger blood vessels, deep hair follicles
-below layer are muscles & bone

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24
Q

functions of skin

A

-prevent invasion of infective organisms & protects underlying tissue from injury
-nerve endings: inform body of sensory stimuli (temp, pressure, touch, pain)
-control body temp through sweating & shivering
-allows gas exchange through pores & keeps fluids & electrolytes balanced
-absorbs sunlight (vitamin D)
-subcutaneous layer stores fat = insulation & protection

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25
Q

what is a wound?

A

disruption of continuity of skin

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26
Q

causes of wounds

A

-thermal sources: extreme temperatures, chemical & electrical sources
-mechanical forces: direct trauma / pressure, shear / friction force

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27
Q

ABRASION (types of wounds)

A

-superficial wound with ragged edges
-result of scrape or tear causing skin loss
-often extremely painful

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28
Q

LACERATION (types of wounds)

A

-increased tissue loss with ragged wound edges
-sutures / tape may be used to bring edges together

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29
Q

INCISION (types of wounds)

A

-clean, approximated wound edges
-result from sharp-edged object
-sutures / tape used to secure edges

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30
Q

PUNCTURE (types of wounds)

A

-clean edges with small entry
-can penetrate deeply
-can close over entry = infection

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31
Q

ANIMAL BITE (types of wounds)

A

combination of crush, laceration & puncture wound

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32
Q

what is a burn?

A

specific type of wound caused by external thermal agent

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33
Q

types of burns

A

superficial burn
partial-thickness burn
full-thickness burn

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34
Q

SUPERFICIAL BURN

A

-1st degree burn
-affects epidermis
-result of prolonged low heat / quick high heat
-redness & pain
-mild localized edema
-healing = rapid without scar tissue

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35
Q

PARTIAL-THICKNESS BURN

A

-2nd degree burn
-extends to dermis
-redness, pain, edema, BLISTERING
-increased edema & risk of infection
-decreased pain due to nerve damage
-new layer of skin can develop within 14-21 days
-can re-epithelialize with good function, minimal scar tissue

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36
Q

FULL THICKNESS BURN

A

-3rd/4th degree burn
-affects all tissue layers
-burns appear dry & inelastic, white, waxy, charred
-painless due to nerve damage
-re-epithelialization NOT possible
-skin grafts required

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37
Q

“Rule of Nines”

A

percentage of body surface damaged by burn

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38
Q

complications of burns

A

breathing, inhalation injuries, GI complications, renal complications, heterotopic calcification, burned skin, thermoregulation impairment, peripheral vascular damage, sensory impairment/ loss, subluxation & dislocation, amputation

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39
Q

what is a spasm?

A

involuntary sustained contraction of a muscle

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40
Q

what is a cramp?

A

painful, prolonged muscle spasm

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41
Q

REFLEX MUSCLE GURADING

A

-muscle spasm in response to pain, due to local injury, (present in acute)
-acts to functionally splint injured structure reducing movement & preventing further injury
-guarding stops when pain is relieved

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42
Q

INTRINSIC MUSCLE SPASM

A

-involuntary self-perpetuating pain-spasm cycle
-restricts movement of joint crossed by muscle
-lack of movement allows tissue ischemia/ circulatory stasis & metabolite retention which irritates nerve endings, registering as pain
-muscle responds to pain by staying in spasm

43
Q

what causes an intrinsic muscle spasm?

A

indirect trauma, inflammation, infection, increase SNS, stress, cold tissue

44
Q

TONE

A

resistance of a relaxed muscle to passive stretch / elongation

45
Q

TENSION

A

muscle fibers tend to shorten, causing them to perform work

46
Q

HYPERTONICITY

A

abnormally high tone usually seen with upper motor neuron disorders

47
Q

how does a muscle contract?

A

-skeletal muscle = bundle of fascicles
-fascicles = grouping of muscle fibers
-muscle fibers = thousands of fine strands called myofibrils
-myofibrils contain thick & thin filaments in units that repeat along myofibril
-units = sarcomeres (basic contractile unit)
-thick filaments (myosin) & thin filaments (actin) over lap & produce CONTRACTILE FORCE
-actin & myosin slide past each other & shorten sarcomere
-repeated actions = muscle contraction

48
Q

MUSCLE SPINDLES

A

-major sensory organ of muscles, aid in control of muscle movements
-in muscle belly
-measure degree (length) muscle is stretched & speed it happens

49
Q

GOLGI TENDON ORGAN

A

-nerve receptors located in TENDON near muscle attachments
-sensitive to tension
-when they fire, they exhibit contraction of muscle attached to tendon & protect muscle from overstretch injury

50
Q

causes of muscle spasm & cramps

A

(environmental / internal)
-pain
-circulatory stasis
-increased gamma neuron firing
-impaired nutrition supply
-lack of vitamin D

51
Q

3 techniques for muscle spasms

A

-GTO release
-O & I
-mm approximation

52
Q

what is scar tissue?

A

fibrous, collagen based tissue that results from inflammatory process
-replaces normal tissue that has been destroyed
-weaker than tissue it replaces

53
Q

who is more likely to produce increased amounts of scar tissue?

A

younger people -> due to greater rate of collagen synthesis

54
Q

what areas of the body are hypertrophic scars more likely to be developed?

A

sternum, upper back, shoulder / deltoid region, buttocks, dorsal surface of foot

55
Q

what areas of the body are keloid scars more likely to be developed?

A

from ear level to waist & from shoulder to elbow

56
Q

effects of massage on scar tissue

A

-before scar tissue develops, massage decreases edema
-removal of excess interstitial fluid can reduce amount of tissue that develops
-enough pressure applied to create blanching followed by hyperemia
-helps desensitize scars through tactile stimulation

57
Q

CI’s for scars

A

FRICTIONS: anti-inflammatory medication & proud flesh / keloid scars

58
Q

scar tissue is avascular …

A

no hair, sebaceous or sweat glands

59
Q

who developed cross fiber frictions? what does it do?

A

James Cyriax
-intended to disrupt & break down existing & forming adhesions in muscles, tendons, ligaments using compression & motion

60
Q

what is a trigger point?

A

-hyperirritable spot within discrete taut band of skeletal muscle or its fascia that produces local / referred pain
-point tender on site & often has predictable pain pattern
-causes affected muscle to shorten

61
Q

theory of what causes a trigger point

A

-interaction of calcium & ATP on myofascial tissues that have been stressed in some way, causes tissue to shorten & produce taut band
-generates localized & uncontrolled metabolic activity in area, localized acidic fluid environment, makes nerve endings hyperirritable

62
Q

perpetuating factors of trigger points

A

reflexive
mechanical
systemic

63
Q

ACTIVE TRIGGER POINTS

A

-painful at rest & with active / passive movements
-prevents muscle from fully lengthening & reduces its strength
-local tissue exhibits ischemia
-tender upon palpation & refers pain
-produce LOCAL TWITCH response & possible referred autonomic phenomena

64
Q

LATENT TRIGGER POINTS

A

-produces pain only when palpated
-more common
-opposite to active

65
Q

PRIMARY TRIGGER POINTS

A

directly activated by acute / chronic mechanical strain or overload of affected muscle

66
Q

SECONDARY TRIGGER POINTS

A

activated in the overworked synergistic or antagonist muscles

67
Q

SATELLITE TRIGGER POINTS

A

found in muscles that lie within referral pattern of another trigger point

68
Q

what is EDEMA?

A

local / general accumulation of fluid in interstitial tissue spaces
-result of altered physiological function in the body

69
Q

function & anatomy of lymphatic system

A

-blood: RBCs, WBCs, various proteins
-circulatory capillaries: fluid pumped through arterial ends into interstitial spaces than absorbed at venous ends
-excess clear, watery interstitial fluid collected, filtered & returned to circulation by lymphatic system

70
Q

what is fluid called once it is in the lymphatic system?

A

LYMPH

71
Q

what does lymph contain?

A

WBCs, plasma proteins, fats & debris

72
Q

how is equilibrium maintained in lymphatic system

A

as long as fluid entering interstitial tissues via arterioles EQUALS fluid leaving through venules & lymphatics
-EDEMA results if equalibrium is upset

73
Q

lymphatic vessels contractibility

A

-have minor contractile capability & pulse of 1-30 beats per minute
-stimulated by stretching of vessels internally by vessels filling / externally by massage

74
Q

how is majority of lymphatic flow stimulated?

A

by movement of skeletal muscles, diaphragm when breathing, peristalsis, contraction of arteries in contact with lymphatic vessels

75
Q

lymphatic flow

A

initial vessels
precollectors
collectors
ducts

76
Q

INITIAL VESSELS (lymphatic flow)

A

-begin as tiny, delicate lymphatic capillaries
-LACK VALVES
-form dense, overlapping network in skin for maximum drainage

77
Q

PRECOLLECTORS (lymphatic flow)

A

connect subcutaneously to deeper vessels in limbs & trunk
HAVE VALVES

78
Q

COLLECTORS (lymphatic flow)

A

connect to larger vessels
HAVE VALVES

79
Q

DUCTS (lymphatic flow)

A

-largest lymph vessels which collectors connect to
-drain into venous system at subclavian veins just before vena cava

80
Q

LYMPHATIC DUCTS (right & left)

A

RIGHT lymphatic duct: drains right arm, anterior & posterior right shoulder, right side of head
LEFT (thoracic) duct: drains rest of body

81
Q

CATCHMENTS

A

-clustering of several lymph nodes together that form a “bed” or collection
-collect lymph from specific body region
-found at “hinge” areas
-rate of flow = slower than other vessels
-susceptible to blockage

82
Q

2 main catchments in the body

A

axilla (upper limbs)
inguinal (lower limbs)

83
Q

WATERSHEDS

A

-boundary line that gives regional organization to multiple lymphotomes
-form single pathway for lymph flow
-high concentration of anastomoses between body regions

84
Q

watersheds of the torso

A

one at level of clavicles & scapular spines
one at umbilicus
vertical line at midsagittal

85
Q

types of edema

A

circulatory
lymphedema
traumatic

86
Q

CIRCULATORY EDEMA

A

-caused by dysfunction/ disease in cardiovascular system
-imbalance between dynamic forces of capillary filtration & reabsorption
-causes: hypertension, venous insufficiency, kidney dysfunction, obesity

87
Q

LYMPHEDEMA

A

dysfunction / failure in lymphatic system
opposite to circulatory
-primary & secondary

88
Q

PRIMARY LYMPHEDEMA

A

-congenital/ genetic defect in lymphatic system
-results in insufficient fluid return
-evident in early childhood -> begins as swelling in legs

89
Q

SECONDARY LYMPHEDEMA

A

-when nodes / vessels are damaged or destroyed
-scar tissue develops / catchment damaged & lymph movement compromised
-swelling covers ENTIRE body
-causes: surgery, radiation, virus/ infection, repeated compression

90
Q

TRAUMATIC EDEMA

A

localized & temporary swelling of tissue associated with soft tissue injury & exertion of exercise
-primary & secondary

91
Q

PRIMARY TRAUMATIC EDEMA

A

amount of fluid actually spilled out of stretched & torn soft tissue

92
Q

SECONDARY TRAUMATIC EDEMA

A

amount of fluid drawn into area of damage due to increased interstitial oncotic pressure of that arm

93
Q

causes of edema

A

increased permeability of capillaries
obstruction of lymphatic flow
increased capillary pressure
decrease of plasma protein

94
Q

what is lymphedema?

A

chronic accumulation of interstitial fluid spaces

95
Q

who developed MLD?

A

Emil Vodder, Danish PT
1930’s

96
Q

what is a contusion?

A

a crush injury to a muscle
-damage of muscle fibers & bleeding into subcutaneous tissue & skin
-skin over contusion is intact

97
Q

HEMATOMA

A

-large area of local hemorrhage following trauma
-pooling of blood causes swelling & pain
-swelling more rapid than edema

98
Q

MYOSITIS OSSIFICANS

A

-complication following hematoma where blood within muscle CALCIFIES
-fibroblasts replaced by osteoblasts which lay down new bone over 6 weeks
-may form within muscle or existing bone

99
Q

causes of contusions

A

DIRECT BLOW TO A MUSCLE
-contact sports
-MVA
-a fall

100
Q

mild, moderate, severe loss of ROM (contusions)

A

MILD: 5-20%
MODERATE: 20-50%
SEVERE: more than 50%

101
Q

why should you avoid stretching & vigorous massage within 7-10 days of a moderate to severe contusion?

A

risk of rebleeding
(heat & contrast also CI’d for same reason)

102
Q

non-pitted edema

A

firm & discoloured
results from coagulation of serum proteins in interstitial spaces, usually following local trauma / infection

103
Q

pitted edema

A

boggy to touch
tissue retains indentation after pressure is applied
accumulation of fluid exceeds absorption rate

104
Q

MLD techniques - pressure & repetition

A

pressure of 20-40mmHg
each stroke repeated 5-7x
strokes = unidirectional toward the heart -> start proximal & work distally to site

FCA (5 decks)

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