BPK 241 Week 1

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80 Terms

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Injury Prevention

  • Reduction of Force

  • Strengthening of Body Parts

  • Screening of Participants

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Goal of Preventative Medicine

To promote health and well-being and prevent disease, disability and death

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Preventative Medicine

  • Primary prevention

  • Secondary Prevention

  • Tertiary Prevention

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Primary Prevention

Things we do to prevent injury/ illness

  • Warm-up

  • Stretching

  • Training

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Secondary Prevention

Once and injury or illness has occurred

  • Anitbiotics/ antiinflammators

  • Rehab to return to original function

  • Braces/ Taping on return to sport

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Tertiary Prevention

Things we do when original function cannot be restored

  • Reduce long-term impairment

  • Improve quality of life

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Importance of Preparation

  • Decrease incidence of injuries

  • Decrease severity of injuries

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Forms of Preparation for Physical Activity

  • General Conditioning (Endurance, Strength, Power, Flexibility)

  • Specific Training (Sport specific, Individual specific, Skills)

  • Protective Measures (Equipment, Nutrition, Hydration)

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General Conditioning

C.O. = H.R. x S.V.

  • Fitness is proportional to your resting H.R. over 1 minute

  • 20 to 60 minute exercise, HR > 150 bpm, at least 3 times per week

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Strength and Power Training

  • Resistance (weight) training (PRE)

  • Isometric (muscle contract but no length moved) vs Isotonic (eccentric, concentric)

  • Plyometrics

  • Who, when, why, how

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Flexibility Training

who, what, where, how

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Sport Specific

  • Skating, Batting, Pitching, Shooting, Golf swing, Swim stroke

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Individual Specific

  • Foot Speed, Strength, Power, Flexibility

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Skills

  • Gross vs fine motor skills

  • Open vs closed skills

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Equipment

  • Absorbs energy

  • Disperses energy

  • Deflects a blow

  • Limit excess movement

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Nutrition Six Classes

  • Protein

  • Carbohydrates

  • Fats

  • Vitamins (ADEK vs BC)

  • Minerals

  • Water/ Electrolytes

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Nutrition Role

  • Growth, repair, and maintenance of all tissues

  • Regulate body processes

  • Provide Energy

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Protein (20-25%)

  • Protein on own does not increase muscle mass

  • Complex process, related to hormones

  • Protein necessary, but not primary source of fuel

  • Extra protein consumed is burned as energy or stored as fat

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Carbohydrates (55-60%)

  • The most efficiently broken down and metabolized form energy (glucose) for the body

  • Broken down and stored as glycogen in the liver and muscles

  • Average 150 lbs athletes carries 1500-2000 calories in form of carbs

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Fats (15-20%)

  • Types: Saturated & unsaturated

  • Not the enemy and the primary fuel for light to moderate intensity exercise

  • More likely to burn fat than carbs for athletes that maintain low to mod intensity

  • Avg 150 lbs athletes carries up to 80,000 calories in fat

  • Consume more unsaturated than saturated fat (eliminates unnecessary calories, but not nutrients)

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Vitamins and Minerals

  • Play key roles in the metabolism of carbs and fats which are your primary muscle fuels during exercise

  • Involved in the repair and building of muscle protein in response to training

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Vitamins ADEK

Fat soluble, excess is stored in body fat, increased risk of toxicity, need to be careful

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Vitamins BC

Water soluble, excess is excreted in urine, therefore needs to be replenished

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Minerals

  • Dietary elements found naturally in the earth’s crust, has 20 different types in the body, mostly stored in liver and bones

  • Some are essential to our health and can only be obtained from what you eat and drink

  • Major minerals like Na, K, Cl, C, P, Mg, S need 100 mg or more daily

  • Trace minerals like Fe, Z, I, Cu, Ma, F, Se are needed in smaller amounts, usually less than 20 mg daily

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Anemia

Iron deficiency

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Water/ Hydration

Essential for survival - used for digestion, temperature control, eliminating waste products, prevent dehydration

Approx 60% of body weight

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Dehydration

Not enough water

  • Amount of blood pumped with each heartbeat decreases

  • Exercising muscle do not receive enough oxygen

  • By-products of exercise are not flushed out of the body as regularly as they should be

  • Exhaustion sets in and the athlete’s performance suffers

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Hyper hydration (hyponatremia)

Too much water

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Signs of dehydration

  • Early Symptoms include: Thirst, Headache, Fatigue, Weakness, Dry mouth, Loss of appetite, Muscle cramps

  • Late Symptoms include: Nausea, Hot to touch, Dizziness, Lack of coordination, Confusion, Fainting

  • Water loss of > 10 to 20% body weight may = death

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Electrolyte Minerals & Hydration

  • Ingestion of sodium during exercise may help with maintaining or restoring plasma volume during exercise and recovery

  • Consumption of sports drink helps retain water in the body and aids in hydration by increasing the absorption of fluid from the intestines into the muscles

  • Researchers suggest 6-8% carb sport drink with at least 110 mg of sodium per 8 ounce serve as a fuel of energy that water can’t provide

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Cramping

Excessive sweating with sodium/mineral loss, muscle twitching & cramps

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Heat exhaustion

Prolonged period of fluid loss via activity in high temperatures

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Heat stroke

Failure of thermoregulatory system

  • Sudden collapse, loss of consciousness, flushed, hot skin, shallow breathing and rapid pulse, core temp of 106 F or higher

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Heat stroke prevention

  • Fluid and electrolyte replacement

  • Gradual acclimization

  • monitor temp and humidity

  • identify susceptible individuals

  • weight records

  • uniforms

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ABCDs

  • Airway

  • Breathing

  • Circulation

  • Disability

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Emergency Care General Points

  • Keep head and neck stable

  • Keep warm

  • N.P.O nil per os (nothing by mouth)

  • Get help

  • Serial repetition of ABCDs- record status

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Shock Definition

  • The state of insufficient blood flow to the tissues of the body as a result of problems with the circulatory system

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Neurogenic Shock

General dilation of blood vessels

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Psychologic Shock

Temporary dilation of blood vessels to brain

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Cardiogenic Shock

Reduced C.O leads to reduced B.P

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Septic Shock

System vasodilation - dilated veins leads to reduced B.P

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Hypovolemic

Reduced blood volume leads to reduced C.O./ B. P.

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Anaphylactic

System Vasodilation - leads to reduced B.P.

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Shock Signs and Symptoms

Result of decreased amount of blood for the circulatory system

  • Reduced B.P

  • Hypoxia

  • Reflexive increase HR (tachycardia, rapid pulse)

  • Skin cool and clammy (warm and dry if septic shock)

  • Anxiety, thirst, impaired consciousness

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Shock Treatment

  • N.P.O

  • ABCDs

  • Maintain body temp ,elevate legs

  • Transport to medical center ASAP

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<p>Bone structue</p>

Bone structue

  • Diaphysis (Shaft)

  • Metaphysis

  • Epiphysis

  • Epiphyseal plate

  • Periosteum

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<p>Joint Structure</p>

Joint Structure

  • Bones (which articulate)

  • Joint capsule/ connective tissue

  • Synovial membrane and fluid

  • Cartilage (hyaline vs fibrocartilage)

  • Bursae

  • Nerves, blood vessels

  • Ligaments

  • Muscle tendons

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<p>Joint Types</p>

Joint Types

  • Hinge (elbow)

  • Saddle (thumb)

  • Facet (spine)

  • Pivot (upper C1)

  • Gliding (wrist carpal)

  • Ball-and-Socket (hip)

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<p>Fracture types</p>

Fracture types

Open (compound) vs Closed (simple)

  • Varieties (Transverse, Oblique, Comminuted, Spiral, Greenstick, Epiphyseal plate, Segmental, Avulsed, Impacted, Torus)

  • Acute vs Stress (elastic vs plastic range)

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<p>Bone Fracture Continuum</p>

Bone Fracture Continuum

  • Normal Bone → Stress reaction → Stress Fracture → Full (Acute) Fracture

  • Osteoclastic activity > Osteoblastic activity

  • Decreased bone mass perpetuates the problem

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<p>Response of bone to stress</p>

Response of bone to stress

  • Structure (strength and stiffness)

  • Load (magnitude, duration, direction, repetitions)

  • Support (muscle activation, equipment)

  • Past history

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<p>Response of joints to stress</p>

Response of joints to stress

  • Structure (bone stability, flexibility, capsule, ligaments)

  • Load (magnitude, duration, direction, repetitions)

  • Support (muscle activity, braces, tape)

  • Past history

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<p>Response of Tissues to Stress</p>

Response of Tissues to Stress

The stronger the tissue, the greater magnitude of load it can withstand:

  • Load = outside or internal forces acting on body

  • Mechanical stress = tissue responses to forces

  • Viscoelastic properties = amount of resistance to stress

  • Yield Point = elasticity of tissue can no longer hold back stress = mechanical strain (strain or sprain)

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Soft Tissue Injury Repair

  • Acute Inflammatory Phase (0-72 hours)

  • Proliferation/ Repair Phase (2 days- 6 weeks)

  • Remodelling/ Maturation Phase (4 weeks - 6 months, longer?)

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Inflammation

  • Protective tissue reaction

  • “Clinical” if causes pain or disability

  • Usually a localized, beneficial response to tissue injury

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Cardinal Signs of Inflammation

  • Rubor: increased blood flow

  • Calor: Increased blood flow

  • Tumor: fluid accumulation

  • Dolor: local tissue pressure

  • Functio laesa: swelling and tenderness

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Acute Inflammatory Phase

Consists of two primary events:

  • Vascular evnets

  • Cellular events

Vascular and cellular reactions are mediated by chemical mediators, derived from plasma proteins or cells (cytokines) and are produced in response to OR activated by stimuli

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Vascular events (minutes to several hours)

Changes in vascular flow (Vasoconstriction and Stasis)

Tissue damage activates the coagulation cascade: Thromboplastin → prothrombin → thrombin → Fibrinogen → Insoluble clot (Quickly followed by Vasodilation → increased blood flow AND increased vascular permeability)

Increased Vascular permeability - Hallmark of acute inflammation and protein and fluid leakage from artery

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Vasoconstriction

Blood vessels constrict for a brief period

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Stasis

Increased blood viscosity

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Cellular Events

Initiated by chemical mediators:

  • Release from invading organism, damaged tissue, WBC’s involved in inflammatory response

  • Margination

  • Rolling

  • Adhesion

  • Migration (diapedesis/extravasation

  • Migration → chemotaxis

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Inflammation Benefits

Supplies things to injury site

  • Clotting factors

  • Anti-infection materials & processes:

    • Leukocytes

    • Phagocytes (macrophages) - eat damaged/destroyed cells

    • Antibodies

    • Stick micro-organisms to phagocytes

    • Attack foreign cells (e.g., put holes in their membranes)

    • Nutrients (O2, amino acids, glucose)

  • Stimulates proliferation of endothelial cells (neovascularization) & fibroblasts (cells that synthesize collagen and extracellular matrix)

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Edema

  • Restrict blood flow if no room for swelling

  • Produce pain, which can limit movement

  • Excessive or chronic inflammation may → tissue destruction, fibrosis, and necrosis (death)

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Acute vs Chronic inflammation

Acute: immediate, few days and resolution, abscess formation

Chronic: delayed, up to many months or years, tissue destruction, fibrosis, necrosis

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Systemic Manifestations

  • Fever

  • Leukocytosis

  • Myalgia

  • Arthralgia

  • Malaise

  • Chills

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Inflammation Treatment

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, Naturopath

Treat systemic effects

  • Antipyretics (ASA, acetaminophen)

  • Analgesics (NSAIDS, narcotics)

  • Antibiotics

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Inflammation types

  • Myositis

  • Arthritis

  • Tendonitis

  • Bursitis

  • Vasculitis

  • Dermatitis

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Proliferation/Repair Phase (2 days- 6 weeks)

  • Characterized by proliferation of capillaries (neovascularization) and fibroblasts which synthesize granulation tissue aka scar tissue (a collagen and extracellular matrix with cross-linking)

  • Collagen initially is laid down in random fashion and is predominantly Type III collagen

  • As the quantity of collagen at the injury site increases, the number of fibroblasts decrease

  • More Type III, less Type I collagen. Weak (H-bonds), rather than covalent bonds, between collagen fibres) and susceptible to re-injury

  • Poorly vascularized and Disorganized

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Remodelling/Maturation Phase (4 weeks - 12-24 months)

  • Starts 1 to 2 weeks post injury

  • Long term process that involves realignment & maturation of collagen fibres that make up scar tissue

  • Myofibroblasts re-orient collagen fibrils in the direction of loading

    • Increased stress and strain causes collagen fibres to realign to position of maximum efficiency

    • Parallel to lines of tension

    • Gradually assumes more normal appearance and function

  • Lasts 10-12 months, total maturation phase may take years to be fully complete

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Remodelling/ Maturation Phase Movement

  • Increases synthesis

  • Increases lysis

  • Reorganizes - decrease in weaker type III collagen, increase in stronger type I collagen

  • Importance of this stage overlooked since patients stop doing rehab exercises once acute pain and disability are gone

  • Rehab isn’t done for a year or more; stopping before complete increases risk of re-injury

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Phases of Soft Tissue Injury Repair

  1. Inflammation (days to several weeks)

  2. Proliferation (several weeks to month)

  3. Remodelling aka Maturation (a year+)

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Wound Healing Mechanisms

Scar tissue formation and Regeneration

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Wound Healing Tissue Types

  • Labile

  • Stable (smooth muscle, glands, connective tissue)

  • Permanent (cardiac and skeletal muscle, neurons)

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Primary Union

  • Clean incision

  • Edges well - approximated

  • Smaller scar, rapid healing

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Secondary union

  • Large, irregular wound

  • Contamination

  • Larger scar, slower healing, dysfunction

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Factors that influence Healing

Local:

  • Location of wound, Extent of Injury, Edema, Hemorrhage, Poor Vascular Supply, Separation of Tissue, Muscle Spasm, Atrophy, Infection

Systemic:

  • Blood Supply

  • Corticosteroids

  • Health/Age/Nutrition

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Ice

  • Vasoconstriction (Hunting Response)

  • Decreased bleeding into injured tissue

  • Decrease in inflammatory response

  • Decreased swelling

  • Decrease pain - decreases excitability of free nerve endings (nociceptors)

  • Decreased muscle spasm

  • Decreased cellular damage - low secondary tissue hypoxia

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Implications of Cold on Performance

  • Decreased pain sensation

  • Golgi Tendon organs less sensitive

  • Muscle spindles less sensitive

  • Increase stiffness at myotendinous junction

  • Muscle more susceptible to fatigue if cooled below 25 C

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Heat

  • Vasodilation - increased blood flow

  • Increase in inflammatory response

  • Increased swelling

  • Decreased pain

  • Decreased muscle spasm

  • Decreased stiffness of soft tissues

  • Increased metabolism within cells that are warned

  • Critical temp threshold for beneficial effects is 39 C

  • Can be achieved by 15 min of general exercise

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Types of vascular events

  1. Vasoconstriction (seconds)

  2. Vasodilation (minutes)

  3. Permeability Increase - oedema formation