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lecture 1 Flashcards

1
Q

therapy=

A

science+art

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2
Q

prevention of sports injuries (3)
(preventative medicine)

A

-reduction of force
-strengthening of body parts
-screening of participants

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3
Q

reduction of force- how?

A

protective equipment, technique development, balanced opponents (ex. weight classes), preventative taping, facilities, rules & enforcement

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4
Q

screening of participants-why?

A

determine if fit, establish athlete’s health

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5
Q

preventative medicine subcategories

A

primary prevention
secondary prevention
tertiary prevention

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6
Q

primary prevention

A

=things we do to prevent injury/illness

-warmup
-stretching
-training

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7
Q

secondary prevention

A

=once an injury or illness has occurred

-antibiotics/anti-inflammatories
-rehab to return to original function
(physio, chiro, massage)
-braces/taping on return to sport

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8
Q

tertiary prevention

A

=things we do when original function can’t be restored

-reduce long term impairment
(rehab to improve existing disability)
-improve quality of life
(wheelchair basketball, sledge hockey)

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9
Q

why is preparation important for physical activity?

A

decrease incidence of injuries, decrease severity of injuries

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10
Q

forms of preparation for physical activity (3)

A
  1. general conditioning
    -endurance, strength, power, flexibility
  2. specific training
    -sport-specific, individual specific, skills
  3. protective measures
    -equipment
    -nutrition
    -hydration
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11
Q

specific training: 3 components

A
  1. sport-specific
    -skating, batting, pitching, shooting a basketball
  2. individual specific
    -foot speed, strength, power, flexibility
  3. skills
    gross vs fine motor skills
    open vs closed motor skills
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12
Q

sprain

A

stretching/tearing of ligaments or joint capsules (non-contractile)

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13
Q

what will we immediately see after injury?

A

inflammation

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14
Q

acute inflammatory phase (0-72 hours after injury)

A
  1. vascular events (minimize blood flow to area to minimize blood loss
    THEN increased blood flow to area and blood vessels get “leaky”
  2. cellular events
    increase in WBCs
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15
Q

neovascularization

A

“new blood cells”
increase blood supply to injured area

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16
Q

edema

A

excess swelling
ongoing/chronic inflammatory process
tissue damage

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17
Q

POLICE

A

protect, optimal loading, ice, compression, elevate

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18
Q

Protective measures- equipment

A
  • absorbs energy
  • disperses energy
  • deflects a blow
  • limits excess movement
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19
Q

Protein

A

-over 20-25% of cal
-protein on its own does not increase muscle mass

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20
Q

genotype/phenotype: running and confusion

A

kevin and his twin
-one developed to tolerate exercise in the heat
-possibly from playing lacrosse in the sun over the years!!!?? (kevin)

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21
Q

diaphysis

A

shaft of bone

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22
Q

metaphysis

A

transition between diaphysis (shaft) and epiphysis (head)

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23
Q

Syndesmosis joint

A

tough connective tissue between bones

(not a lot in the body)
-pubis symphysis

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24
Q

ligaments

A

connect bones together

has elastin
(a bit more stretchy than tendons)

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25
Q

tendon

A

connects muscle to bone

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26
Q

bursa

A

small fluid filled sacks

-decreases friction of tendon rubbing on the bone

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27
Q

Joint types

A

hinge, saddle, facet, pivot, gliding, ball and socket

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28
Q

Fracture types

A

-Open (compound)= bones stick out; risk of infection
-Closed (simple)= bones stay within the soft tissue

-Acute vs. stress (tiny cracks)

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29
Q

bone fracture continuum

A

=stress fracture as a healing failure continuum

Normal bone –> stress rxn –> full (acute) fracture

Osteoclastic activity> Osteoblastic activity

Decreased bone mass perpetuates the problem

30
Q

Response of bone to stress

A
  • body will lay down more calcium in response to stress
  • the shape of remodelling will depend on force, magnitude, strength, how well the muscles can stabilize the forces, and past injuries
31
Q

Bones like – forces

A

compression

they do not like shear forces (from side to side)!

32
Q

the stronger the tissue, the greater

A

magnitude of load it can withstand

33
Q

mechanical stress=

A

tissue response to forces

34
Q

Viscoelastic properties=

A

amount of resistance to stress

35
Q

Yield point=

A

elasticity of tissue can no longer hold back stress (mechanical failure– strain or sprain)

36
Q

Shock definition

A

result of decreased amount of blood for the circulatory system

37
Q

Forms of shock (6)

A
  • neurogenic (general dilation of blood vessels)
  • psychologic (temporary dilation of blood vessels to brain)
  • cardiogenic (reduced C.O leads to reduced BP)
  • septic (systemic vasodilation– dilated veins leads to reduced BP)
  • hypovolemic (reduced blood volume leads to reduced C.O/BP)
  • anaphylactic (systemic vasodilation, leads to reduced BP)
38
Q

signs and symptoms of shock

A
  • reduced BP (weak pulse)
  • hypoxia
  • reflexive increase HR (tachycardia, rapid pulse)
  • skin cool and clammy (warm and dry if septic shock)
    -anxiety, thirst, impaired consciousness
39
Q

Treatment for shock

A

-N.P.O
-ABCD’s
-maintain body temp, elevate legs
-transport to medical center!!!!

40
Q

ABCD’s

A

Airway- open?

Breathing- rate? effectiveness?

Circulation- HR? Pulses? Bleeding?

Disability- sensation? pupils? alertness? movement?

41
Q

Emergency care

A
  • keep head/neck stable
    -keep warm
    -N.P.O
    -Get help
    -Serial repetitions of ABCD’s
42
Q

most common cause of asphyxiation in unconscious patient?

A

tongue obstructing the oropharynx

43
Q

Stress/Strain relationship: tendon and ligament

A

same graph except ligaments can tolerate a but more stress as they have elastin

increased stress= increased strain (linear relationship)

microtears in the collagen fibres

44
Q

Ligaments and tendons have a high

A

collagen content

ligaments also have elastin

45
Q

Soft tissue injury repair (3 phases)

A
  1. Acute inflammatory phase (0-72 hours)
  2. Proliferation/repair phase (2 days- 6 weeks)
  3. Remodeling/maturation phase (4 weeks- 6 months…)
46
Q

Cardinal signs of inflammation

A

Rubor= redness (incr blood flow)
Calor= heat (incr blood flow)
Tumor= swelling (fluid accumulation)
Dolor= pain
Functio laesa= loss of function

47
Q

Actute inflammatory phase: vascular events

A

Vasoconstriction: minimize blood loss (seconds)

Vasodilation: incr blood flow (minutes)
AND increased vascular permeability: oedema formation

48
Q

Acute inflammatory phase: cellular events

A

increase in WBC

macrophages eat away at the damaged tissue/destroy viruses if the skin is pierced

49
Q

Why are tendon injuries harder to heal than muscular injuries?

A

muscles have a good blood supply, tendons do not (same w ACL: that is why we usually need surgery)

tendons get neovascularization: new blood vessels grow into the damaged tissue

fibroblasts come to that area at the end of the inflammatory phase

50
Q

fibroblasts make

A

collagen

which is why it is important that fibroblasts come to the damaged tissue

51
Q

Inflammation and swelling

A

local inflammation is local, beneficial and usually short-lived

BUT
accumulation of cells (WBCs, macrophages, leukocytes, antibodies..) can be very painful

an ongoing inflammatory process= chronic= edema and swelling= decreased blood supply to area= tissue damage and death

52
Q

Systemic manifestations of inflammation

A

fever, leukocytosis, myaligia (muscle aches), arthralgia (joint pain), malaise (fatigue), chills (in response to fever)

53
Q

Treatment for inflammation

A
  1. Remove underlying cause
    - incise and drain abscess, antibiotics, remove foreign body, remove mechanical stress
  2. Treat local effects
    - POLICE then heat
    -NSAID drugs
    -physio, chiro, RMT, acupuncture…
  3. Treat systemic effects
    - Antipyretic (acetaminophen, ASA)
    - Analgesics (NSAIDS, narcotics)
    - Antibiotics
54
Q

“itis” means

A

inflammation

myositis, arthritis, tendonitis, bursitis, vasculitis, dermatitis

55
Q

Proliferation/Repair phase
(2 days- 6 weeks)

A
  • proliferation of capillaries (neovascularization) and fibroblasts which synthesize scar tissue (granulation tissue)

-collagen is laid down randomly and is mostly type 3

  • as the amount of collagen increases at the injured site, the number of fibroblasts decrease
56
Q

what is scar tissue (or granulation tissue) made of

A

collagen and extracellular matrix with a cross-linking

57
Q

Proliferation phase scar tissue:
what type collagen,
vascularization,
organization?

A

early scar tissue is more type 3, less type 1

poorly vascularized

disorganized

58
Q

Remodeling/Maturation phase

A

want to load tissue in this phase!!! increased stress

body will reorient collagen fibres into the correct direction (parallel to the line of tension)

59
Q

Movement in the Remodeling/Maturation phase

A
  • increases synthesis and lysis
    -reorganizes collagen
    –> decrease in weaker type 3, increase in type 1
60
Q

Which stage of soft tissue injury repair is often overlooked?

A

Remodeling/maturation

-“rehabilitation” isn’t done for a year or more
-stopping before that increases risk of reinjury

61
Q

Would healing: mechanisms

A
  • scar tissue formation
  • regeneration (labile cells/stable cells)
62
Q

Types of tissues (regeneration)

A

Labile cells= regenerates

Stable cells= doesn’t normally regenerate but can if needed

Permanent= can’t regenerate

63
Q

Would healing- Skin
Types of unions? (2)

A

primary= clean incision, smaller scar, rapid healing, edges well-approximated

secondary= large irregular wound, contamination, larger scar, slower healing, dysfunction

64
Q

Local factors that influence healing

A

-location of wound
-hemorrhage
-edema
-extent of injury
-separation of tissue
-muscle spasm
-atrophy
-infection

65
Q

Systemic factors that influence healing (3)

A

-blood supply (smoking decreases blood supply)

-corticosteroids (inhibit collagen synthesis)

-heath/age/nutrition

66
Q

Ice can decrease… (3)

A

Decrease swelling,
Decrease inflammation (controversial),
Decrease pain

67
Q

Why would we need ice to decrease inflammation if we already have blood supply there??

A

minimizes inflammation to allow FRESH blood and oxygen to get in there

68
Q

Ice benefits (7)

A
  • vasoconstriction
    -decr bleeding into injured tissue
    -decr inflammatory response
    -decr swelling
    -decr pain (decr excitability of nociceptors)
    -decr muscle spasm
    -decr cellular damage (decr secondary tissue hypoxia!!)
69
Q

Implications of pain on performance

A

-decr pain sensation
-GTO less sensitive
-muscle spindles less sensitive
-incr stiffness

if you don’t warm up properly after ice, you are increasing injury risk!!!

70
Q

Heat effects (7) on injury

A

-vasodilation (incr blood flow)
-incr inflammatory response
-incr swelling
-decr pain
-decr muscle spasm
-decr stiffness of soft tissues
-incr metabolism in warmed cells

71
Q

critical temp threshold for beneficial effects of heat

A

39 deg C

can be achieved through 15 min dynamic warmup

241 (13 decks)

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