lecture 1 Flashcards
therapy=
science+art
prevention of sports injuries (3)
(preventative medicine)
-reduction of force
-strengthening of body parts
-screening of participants
reduction of force- how?
protective equipment, technique development, balanced opponents (ex. weight classes), preventative taping, facilities, rules & enforcement
screening of participants-why?
determine if fit, establish athlete’s health
preventative medicine subcategories
primary prevention
secondary prevention
tertiary prevention
primary prevention
=things we do to prevent injury/illness
-warmup
-stretching
-training
secondary prevention
=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
tertiary prevention
=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)
why is preparation important for physical activity?
decrease incidence of injuries, decrease severity of injuries
forms of preparation for physical activity (3)
- general conditioning
-endurance, strength, power, flexibility - specific training
-sport-specific, individual specific, skills - protective measures
-equipment
-nutrition
-hydration
specific training: 3 components
- sport-specific
-skating, batting, pitching, shooting a basketball - individual specific
-foot speed, strength, power, flexibility - skills
gross vs fine motor skills
open vs closed motor skills
sprain
stretching/tearing of ligaments or joint capsules (non-contractile)
what will we immediately see after injury?
inflammation
acute inflammatory phase (0-72 hours after injury)
- vascular events (minimize blood flow to area to minimize blood loss
THEN increased blood flow to area and blood vessels get “leaky” - cellular events
increase in WBCs
neovascularization
“new blood cells”
increase blood supply to injured area
edema
excess swelling
ongoing/chronic inflammatory process
tissue damage
POLICE
protect, optimal loading, ice, compression, elevate
Protective measures- equipment
- absorbs energy
- disperses energy
- deflects a blow
- limits excess movement
Protein
-over 20-25% of cal
-protein on its own does not increase muscle mass
genotype/phenotype: running and confusion
kevin and his twin
-one developed to tolerate exercise in the heat
-possibly from playing lacrosse in the sun over the years!!!?? (kevin)
diaphysis
shaft of bone
metaphysis
transition between diaphysis (shaft) and epiphysis (head)
Syndesmosis joint
tough connective tissue between bones
(not a lot in the body)
-pubis symphysis
ligaments
connect bones together
has elastin
(a bit more stretchy than tendons)
tendon
connects muscle to bone
bursa
small fluid filled sacks
-decreases friction of tendon rubbing on the bone
Joint types
hinge, saddle, facet, pivot, gliding, ball and socket
Fracture types
-Open (compound)= bones stick out; risk of infection
-Closed (simple)= bones stay within the soft tissue
-Acute vs. stress (tiny cracks)
bone fracture continuum
=stress fracture as a healing failure continuum
Normal bone –> stress rxn –> full (acute) fracture
Osteoclastic activity> Osteoblastic activity
Decreased bone mass perpetuates the problem
Response of bone to stress
- 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
Bones like – forces
compression
they do not like shear forces (from side to side)!
the stronger the tissue, the greater
magnitude of load it can withstand
mechanical stress=
tissue response to forces
Viscoelastic properties=
amount of resistance to stress
Yield point=
elasticity of tissue can no longer hold back stress (mechanical failure– strain or sprain)
Shock definition
result of decreased amount of blood for the circulatory system
Forms of shock (6)
- 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)
signs and symptoms of shock
- 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
Treatment for shock
-N.P.O
-ABCD’s
-maintain body temp, elevate legs
-transport to medical center!!!!
ABCD’s
Airway- open?
Breathing- rate? effectiveness?
Circulation- HR? Pulses? Bleeding?
Disability- sensation? pupils? alertness? movement?
Emergency care
- keep head/neck stable
-keep warm
-N.P.O
-Get help
-Serial repetitions of ABCD’s
most common cause of asphyxiation in unconscious patient?
tongue obstructing the oropharynx
Stress/Strain relationship: tendon and ligament
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
Ligaments and tendons have a high
collagen content
ligaments also have elastin
Soft tissue injury repair (3 phases)
- Acute inflammatory phase (0-72 hours)
- Proliferation/repair phase (2 days- 6 weeks)
- Remodeling/maturation phase (4 weeks- 6 months…)
Cardinal signs of inflammation
Rubor= redness (incr blood flow)
Calor= heat (incr blood flow)
Tumor= swelling (fluid accumulation)
Dolor= pain
Functio laesa= loss of function
Actute inflammatory phase: vascular events
Vasoconstriction: minimize blood loss (seconds)
Vasodilation: incr blood flow (minutes)
AND increased vascular permeability: oedema formation
Acute inflammatory phase: cellular events
increase in WBC
macrophages eat away at the damaged tissue/destroy viruses if the skin is pierced
Why are tendon injuries harder to heal than muscular injuries?
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
fibroblasts make
collagen
which is why it is important that fibroblasts come to the damaged tissue
Inflammation and swelling
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
Systemic manifestations of inflammation
fever, leukocytosis, myaligia (muscle aches), arthralgia (joint pain), malaise (fatigue), chills (in response to fever)
Treatment for inflammation
- Remove underlying cause
- incise and drain abscess, antibiotics, remove foreign body, remove mechanical stress - Treat local effects
- POLICE then heat
-NSAID drugs
-physio, chiro, RMT, acupuncture… - Treat systemic effects
- Antipyretic (acetaminophen, ASA)
- Analgesics (NSAIDS, narcotics)
- Antibiotics
“itis” means
inflammation
myositis, arthritis, tendonitis, bursitis, vasculitis, dermatitis
Proliferation/Repair phase
(2 days- 6 weeks)
- 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
what is scar tissue (or granulation tissue) made of
collagen and extracellular matrix with a cross-linking
Proliferation phase scar tissue:
what type collagen,
vascularization,
organization?
early scar tissue is more type 3, less type 1
poorly vascularized
disorganized
Remodeling/Maturation phase
want to load tissue in this phase!!! increased stress
body will reorient collagen fibres into the correct direction (parallel to the line of tension)
Movement in the Remodeling/Maturation phase
- increases synthesis and lysis
-reorganizes collagen
–> decrease in weaker type 3, increase in type 1
Which stage of soft tissue injury repair is often overlooked?
Remodeling/maturation
-“rehabilitation” isn’t done for a year or more
-stopping before that increases risk of reinjury
Would healing: mechanisms
- scar tissue formation
- regeneration (labile cells/stable cells)
Types of tissues (regeneration)
Labile cells= regenerates
Stable cells= doesn’t normally regenerate but can if needed
Permanent= can’t regenerate
Would healing- Skin
Types of unions? (2)
primary= clean incision, smaller scar, rapid healing, edges well-approximated
secondary= large irregular wound, contamination, larger scar, slower healing, dysfunction
Local factors that influence healing
-location of wound
-hemorrhage
-edema
-extent of injury
-separation of tissue
-muscle spasm
-atrophy
-infection
Systemic factors that influence healing (3)
-blood supply (smoking decreases blood supply)
-corticosteroids (inhibit collagen synthesis)
-heath/age/nutrition
Ice can decrease… (3)
Decrease swelling,
Decrease inflammation (controversial),
Decrease pain
Why would we need ice to decrease inflammation if we already have blood supply there??
minimizes inflammation to allow FRESH blood and oxygen to get in there
Ice benefits (7)
- 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!!)
Implications of pain on performance
-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!!!
Heat effects (7) on injury
-vasodilation (incr blood flow)
-incr inflammatory response
-incr swelling
-decr pain
-decr muscle spasm
-decr stiffness of soft tissues
-incr metabolism in warmed cells
critical temp threshold for beneficial effects of heat
39 deg C
can be achieved through 15 min dynamic warmup
