Sports Med Final

Front 1

What is a drug?

Back 1

* “ any substance, other than a normal constituent of the body or one that is required for normal bodily function (e.g. food, water, oxygen) that, when applied to or introduced into a living organism, has the effect of altering bodily function(s).”

Front 2

PHARMACODYNAMICS

Back 2

* Effects of drug on the body
* Mechanism of action
* Activation or blockage of cellular receptors
* Drugs effect receptors (effect uptake)
* It can be taken up by cells, muscle etc
* Drug companies try to find the most effective drug with the least amount of side effects

Front 3

* Dose-response curve for most drugs

Back 3

* As we increase the dose we increase the response until we have a levelling off
* At some point you will hit a max dose
* Depending on the drug the curve will change

Front 4

Adverse Drug Reactions (ADRs)

Back 4

* Side effects/Sensitivities
* Diarrhea from antibiotics, sedation from anti-histamines (allergy medication)
* Overdose toxicity
* Taking a drug above its therapeutic range
* Bleeding from oral anti-coagulants
* Allergic reactions
* Drug acts as an allergen/antigen >> immune response
* Drug interactions
* Naloxone (competitive inhibitor), drugs acting on same system, overload liver enzymes…. react with drug to keep them up and breathing until they get to hospital

Front 5

PHARMACOKINETICS

Back 5

* Study of the time course of a drug and its metabolites in the body after administration by any route
* Absorption: how it gets into our body
* Distribution: distributed in the body (crossing the BBB in the brain)
* Biotransformation
* Excretion

Front 6

ABSORPTION

Back 6

* goes from outside into the systemic circulation
* Process of drug movement from the administration site to the systemic circulation

Front 7

ABSORPTION

* Routes of Administration

Back 7

* Oral (swallowed (stomach), sublingual(right into circulation) buccal):
* Topical (eyes, ears, nose, skin)
* Vaginal, rectal
* Injection (IV (intra venous), IM (intra muscular), SQ, intra-synovial, intra-cardiac)
* Inhaled (asthma)

Front 8

Factors Affecting Absorption

Back 8

* Solubility, particle size
* Concentration
* Circulation to the site of administration (high concentration to get a small concentration to a certain part of the body ex: knee)
* Surface area at the site of administration (determined by the route of administration e.g. sublingual vs oral vs inhaled vs rectal)
* Factors affecting absorption (oral)
* Formulation (tablet, liquid, delayed release)
* Stability to acid and enzymes
* Motility of gut (don’t take pill before you go for run because blood is moved to muscle during exercise causing the motility of gut to go down)
* Food in stomach
* Degree of first-pass metabolism
* Lipid solubility

Front 9

BIOAVAILABILITY

Back 9

* If you take a drug whats the chance of you getting it to where you need it
* Extent to which – and sometimes rate at which – the active moiety (drug or metabolite) enters systemic circulation, thereby gaining access to the site of action.
* Drugs taken orally are commonly subjected to a ‘First Pass’ effect (hepatic clearance) before entering the systemic circulation

Front 10

First Pass Effect

Back 10

1. Drug taken orally
2. drug enters GI tract (esophagus to stomach)
3. Active drug is absorbed from stomach (may be attacked by acid) and small intestines >> splantic circulation
4. high blood concentration of drug is in hepatic portal vein
5. low blood levels after passing through liver (acts upon a pill)
6. Drug enters systemic circulation via inferior vena cava

Front 11

** stick something under the tongue will enter veins and go directly to the heart (systemic)

** take orally it will go straight to liver (than the systemic circulation)… alters the drug

** some drugs will be activated by the liver.. others will not

Back 11

**

Front 12

Passage Across Cell Membranes

Back 12

* Passive Diffusion: Lipid soluble, movement occurs with concentration or electrochemical gradient
* Facilitated Diffusion: Polar molecules, participation of membrane proteins with gradients
* Active Transport: Polar molecules, requires energy, uses membrane proteins

Front 13

Distribution

* After administration:

Back 13

* Interstitial fluids
* Cellular fluids

Front 14

Differences in Distribution to Tissues

* PRIORITIES OF SYSTEM

Back 14

* First minute: 3 things body prioritizes
* Heart, kidney, brain
* Up to several minutes to hours:
* Muscle, skin, fat and other internal organs
* Pattern of blood flow is the limiting factor
* E.g blood brain barrier, vascular disease (diabetes)
* vessels in the toes and hands start to close off >> ulsers
* result: ulsers become infected

Front 15

Physiochemical Factors Affecting Distribution

Back 15

* Permeability
* Lipid solubility
* Binding to plasma proteins
* Accumulation in tissues

Front 16

Physiological Factors Affecting Distribution

Back 16

* Cardiac output
* Local blood flow

Front 17

BIOTRANSFORMATION

Back 17

* Conversion by enzymes to more polar (less lipid soluble) forms
* Occurs in the smooth endoplasmic reticulum of cells in the liver
* Consists of Phase I and Phase II reactions

Front 18

BIOTRANSFORMATION Phase I

Back 18

* Conversion to polar metabolite
* Oxidation
* Reduction
* Hydrolysis
* Effects
* Inactivation of drug
* activate of drug
* Reduction of activity
* Increase activity (more rarely)

Front 19

Summary of Drug Metabolism

Back 19

* How liver effects drugs
* active drug >> metabolism >> in active drug >> elimination by kidneys, feces, air, sweat
* active drug >> less active
* inactive drug >> active
* less active drug >> to more active drug

Front 20

Conversion to a More active form

ex: Codeine

Back 20

* Liver takes codeine… goes through liver and gets converted to morphine
* Morphine is much more active than Codein
* less active to more active

Front 21

BIOTRANSFORMATION PHASE II

Back 21

* Conjugation: Coupling of drug (or its polar metabolite) with an endogenous substance
* Effects: Same as previous phase (inactivate, partial inactivate, increase)

Front 22

Factors Affecting Biotransformation

Back 22

* Genetic
* Mutation leading to gene deletion (e.g. ALDH in liver)
* you could metabolize a drug slower or faster
* Environmental
* Drug interactions (cytochrome P450 enzymes e.g decrease activity - grapefruit juice, erythromycin; increase activity - rifampin, St. John’s Wort (therefore decrease warfarin, OCPs)
* be careful with drugs you take together because they could inactivate one another
* Physiological
* Liver disease (e.g. cirrhosis)
* Change amount of drug

Front 23

Excretion

Back 23

* Unchanged drug or polar metabolites
* Urine, feces, sweat, exhalation
* sweating and exhaling are usually not good ways to eliminate
* Primary mechanism via urine/kidneys

Front 24

Elimination Kinetics

Back 24

* Important in how we dose people
* Zero Order: A constant amount of drug is eliminated per unit of time (saturation occurs)
* 1st Order: A constant fraction of the drug is eliminated per unit of time
* 2nd Order or multi-exponential Kinetics: May vary with time and dose (not specific zero or 1st order)

Front 25

Clinical Pharmacokinetics

Back 25

* how we take it in, how we does, how often we take it
* The specific quantitative pharmacokinetic properties of a drug determine its dosing schedule, dose and means of administration

Front 26

Dosing Schedule

Back 26

1. Kinetic
2. Therapeutic Window: make sure drug is at the right amount to be effective and not harmful * based off therapeutic levels and toxic levels

Front 27

Therapeutic Range (Window)

Back 27

* Lower limit:
* Concentration that produces half the greatest possible effect
* Upper limit:
* No more than 5-10% of patients experience a harmful side effect

Front 28

Definition of Therapeutic Levels

Back 28

* ED50 (Mean effective dose)
* Dose that gives the required response in 50% of subjects
* TD50 (Median toxic dose)
* Dose that produces harmful side effects in 50% of subjects
* Therapeutic index: TD50/ED50 (ratio)
* Target Level
* Maintain a steady concentration in the mid-point of the therapeutic range
* Where we want the blood level to remain at

Front 29

One Dose -pharmicokinetics

Back 29

* drug starts at zero
* drug hits a certain concentration
* body deals with it and starts to decay the concentration to a desired level

Front 30

Therapeutic Window

Back 30

* Narrow:
* important to stay within the window
* Coumadin (blood thinner, stops clotting, too much you bleed, not enough causes clot)
* Lithium ( for depression, bipolar)
* Wide:
* Some antibiotics (Penicillin)
* Some Anti-inflammatories (ibuprofen)

Front 31

Maintaining a Steady State

Back 31

* Rate of Input = Rate of loss
* barely moving within the therapeutic window

Front 32

* Drug half life (t ½)

Back 32

* how long it takes to get from max concentration to half of the concentration
* key
* Time required for the plasma concentration of the drug to be reduced by half
* Generally drugs that are given intermittently are given at the t ½ interval
* Steady state occurs in approximately 3 doses

Front 33

Alcohol Absorption

Back 33

* Occurs in gastrointestinal track by simple diffusion (small size)
* 70-80% in duodenum and jejunum
* Delayed if food in stomach (prevent from touching stomach, delay or stop absorption)

Front 34

Alcohol Distribution

Back 34

* Areas with high blood flow rapidly reach equilibrium (brain, heart (makes heart muscle smaller), lungs, liver)
* 4% into fatty tissues
* Volume of distribution less for women than for men (lean body mass)
* Therefore higher blood concentrations for female… more % body fat

Front 35

Alcohol Elimination

Back 35

* Principle elimination is by oxidation to CO2 and H2O
* urine: <1%
* lungs: 1-3 %
* Liver Oxidation: 90-95%
* alcoholics enzymes are more effective (why they can have more)

Front 36

Metabolism of Alcohol

Back 36

* Ethanol —ADH—> Acetaldehyde
* Metabolized in the liver (cytosol)
* First Pass Effect
* Alcohol Dehydrogenase (ADH)

Front 37

Alcohol Oxidation

Back 37

* Acetaldehyde —ALDH—> Acetate
* Oxidation occurs in mitochondria
* Aldehyde dehydrogenase (ALDH)
* Acetate released to blood – oxidized to CO2

Front 38

Clinical Effets

Alcohol

Back 38

* CNS depressant
* Diuretic
* Toxic effects on muscle, heart, brain (cerebellum), liver
* 50-100 (incoordination)
* 150-200 (increase reaction time)
* 200-300 (neusea/vomit/ataxia)
* >400 (coma/respiratory failure/death)

Front 39

Genetic Variations Alcohol

Back 39

* Alcohol dehydrogenase operates 5X normal
* Acetaldehyde accumulates resulting in vasodilation, facial flushing, bronchospasm and tachycardia
* 85% Asian populations, 5-10% English, 20% Swiss
* Certain genetics/cultures can’t handle alcohol
* Aldehyde dehydrogenase-2 deficiency
* 50% Asian populations
* Increase acetaldehyde production (facial flushing, tachycardia, diaphoresis, muscle weakness)

Front 40

Nonsteroidal Anti-inflammatory Drugs (NSAIDs)

Back 40

* IB profeun
* Salicylates and related compounds (aspirin)
* Anti-inflammatory, anti-pyretic (against fevre, anti-platelet and analgesic
* Act by inhibiting cyclo-oxygenase

Front 41

COX 1 & 2

Back 41

* COX1: important because it produces protective prostaglandins help mucus in stomach and platelet aggregation
* not present: stomach eaten by acid, and you bleed
* COX 2: prostaglandins contribute to inflammatory process
* only with inhibitor for COX 2

Front 42

Pharmacology

Absorption & Disruption

Back 42

* Absorption: Rapidly from the stomach and upper small intestine
* Distribution: Throughout most body tissues

Front 43

Side Effects of Anti Inflammatories

Back 43

* Stomach – dyspepsia, gastritis, ulcer
* Kidneys – hypertension, fluid retention, renal failure
* Platelets – dysfunction (inhibit clotting)
* Vessels – vasoconstriction (hypertension)
* Other

Front 44

Acetaminophen (Tylenol®)

Back 44

* Other countries called ‘paracetamol’ (para-acetylaminophenol)
* Possible action through COX-3 (temperature effects)
* Modulates the endogenous cannabinoid system (pain reliever system in the pain)
* Effects – pain relief (analgesic) and anti-pyretic (fever)
* Given to kids, safe drug in safe doses
* Metabolism in liver (glucuronidation, sulfation)

Front 45

Acetaminophen (Tylenol®)

Overdose

Back 45

* causes depletion of liver of glutathione which detoxifies metabolic intermediaries
* Microvascular and cellular damage – cirrhosis
* Treat with acetylcysteine which converts to glutathione

Front 46

Conditions associated with collapse

Back 46

* Cardiac – arrest/arrhythmias
* Neurologic – CVA(stroke), IC bleed, seizure
* Resp – asthma, anaphylaxis
* Metabolic – hypoglycemia, hyponatremia, heat or cold injury
* “Other” – including benign exercise associated collapse (cross country skiing)

Front 47

Benign Exercise Associated Collapse

Back 47

* venous pooling in legs with sudden cessation of prolonged exercise
* Usually fairly immediately postrace.
* No abnormalities of vital signs (other than postural hypotension which resolves)
* Management is “postural”
* Prevention: “warm‐down”

Front 48

Heat Injury

Back 48

* Keep body temperature within in 2 degrees of baseline… when you fall out of that range your system starts to disintegrate
* Goal is to decrease body temperature
* Skin vasodilation – heat radiates from body
* Increase cardiac output to skin
* Increase respiratory rate (warm air out, cool air in)
* Sweat

Front 49

Mechanisms of heat exchange

Back 49

1. Evaporation: vaporization of sweat (or water)… how humans lose heat
2. Convection: moving air (wind or movement)
3. Conduction: heat exchange via direct contact (ice or heat packs)
4. Radiation: heat transfer from distant source (sun)

Front 50

Thermoregulation – extrinsic factors

(Ambient temp, wind, humidity/percip, insulation, activity)

Back 50

* Ambient temperature : less exchange with high temperature
* Wind: increase exchange of heat with wind
* Precipitation/Humidity: decrease evaporation… minimize sweating
* Insulation between body & environment (clothing, equipment, shade, shelter..): prevents all forms of heat exchange
* Strenuous exercise: increase heat production

Front 51

Heat injury ‐ terms

Heat cramps

Heat exhaustion

Heat stroke

Back 51

* Heat cramps: muscle cramps +/‐ fatigue, weakness with normal core temp
* Heat exhaustion: <40C core temperature, but feeling unwell.
* Heat stroke: only entity definitively related to excessively high body temperature ( >40C)
* Core’ body temperature (usually rectal temperature)

Front 52

Heat Cramps

Back 52

* Etiology poorly understood
* Tend to occur later in activity, in conjunction with muscle fatigue & in the presence of dehydration
* May be an element of electrolyte depletion?

Front 53

Heat Cramps Treatment

Back 53

* Cessation of activity
* Rehydrate as appropriate +/‐ electrolyte replacement
* Light stretch +/‐ massage for pain management
* Dietary/medical evaluation for mineral/electrolyte deficiency or other medical illness
* Return to play “as tolerated” – may have a muscle injury if severe

Front 54

Heat exhaustion

Back 54

* Most common “heat” illness among athletes
* Symptoms may include headache, fatigue, weakness, dizziness, nausea,
* Core temp <40C.

Front 55

Treatment of heat exhaustion

Back 55

* Cessation of activity and begin cooling
* If associated collapse, lay flat with legs elevated
* Imperative to check rectal temp

Front 56

Heat stroke

Back 56

* Failure of thermoregulatory mechanisms
* Core temp >40C
* Neurological symptoms of confusion, bizarre behavior,delirium, unconsciousness, seizures, coma, death.
* May or may not be preceded by more mild symptoms.
* once you get over 40 C your body doest respond
* causes a denature of protein.. organs start to die
* Muscle will produce protein that will go into system and clog Kidneys

Front 57

Treatment of Heat Stroke

* Immediate, rapid cooling

Back 57

* “COOL FIRST< TRANSPORT SECOND”
* Mortality rate & organ damage is related to length of time for cooling to occur.
* Most effective cooling is cold water immersion
* Also application of wet towels, use of fans.
* Other practical considerations such as removal of excess clothing & equipment; shade; removal from further exercise; continuous monitoring

Front 58

Prevention heat injury

Back 58

Risks in this situation:

* environmental conditions
* body size (someone with increase fat insulation = heat insulation)
* insulation (football gear)
* training (do at a time of day thats reasonable)

Front 59

Prevention and Management of Heat Injury

Back 59

* Water (critical for intake)
* ice
* towels and/or sponges
* Fans
* immersion tubs
* rectal thermometers

Front 60

Prevention of heat injury‐event organization

Back 60

* Scheduling to avoid very hot times of year & times of day.
* Minimize external factors increasing risk of heat injury.
* Educating personnel & participants re symptoms,risk & treatment of heat injury.
* Detailed knowledge of weather conditions & risk

Front 61

Prevention of heat injury‐event organization

Back 61

* Scheduling to avoid very hot times of year & times of day.
* Minimize external factors increasing risk of heat injury.
* Educating personnel & participants re symptoms,risk & treatment of heat injury.
* Detailed knowledge of weather conditions & risk

Front 62

Prevention of Heat Injury

* Ambient conditions

Back 62

* Wet bulb globe temperature:
* low risk if the WBGT is <65 o F (<18 o C)
* moderate risk if it is between 65‐73 o F (18‐23 o C)
* high risk if between 73‐82 o F (23‐28 o C)
* very high risk >82 o F (>28 o C)

Measuring absolute ambient temperature , humidity and more

Front 63

* Heat Index:

Back 63

* Propensity to heat illness based on humidity and temperature
* low humidity + low temp = low risk
* high humidity + high temp = extreme danger

Front 64

Hypothermia

Back 64

* Core Body temperature <35C
* Loss of thermoregulatory function <32C
* Body response
* Shivering to increase metabolism and heat
* Superficial blood vessels constrict reducing skin heat loss (don’t heat the skin = susceptible to frostbite)

Front 65

Symptoms of Hypothermia

Back 65

* Mild (32 – 35 C): shivering, incoordination, apathy
* Moderate (28 – 32 C): loss of shivering, decreased physiologic functioning such as HR, RR, reflexes. Cardiac arrhythmias may occur
* Severe ( < 28 C): major metabolic & physiologic abnormalities. Asystole by 18 C
* Lowest adult accidental hypothermia survival: 13.7 C
* Lowest infant survival: 14 C.

Front 66

Hypothermia treatment

Back 66

* Passive core rewarming – core body next to heat source
* Beware of worsening cardiovascular status because of too rapid external rewarming (‘afterdrop’) – blood to periphery
* Beware of refreezing frostbitten tissue
* In severe hypothermia and cardiac arrest, prolonged CPR is appropriate because of the organ preservation effect of hypothermia
* Advanced life support measures (ie. Defibrillation) may not be effective until body temp > 30 C.

Front 67

Cardiac status and hypothermia

Back 67

* Hypothermia causes cardiac arrhythmias including significant bradycardia
* Management in the field consists of NO CPR (cardiopulmonary resuscitation) unless asystolic (no pulse, no breathing)
* This may require a longer than normal length of monitoring to determine
* If asystolic in field, CPR should be started and continued until ACLS (advanced cardiac life support) can be administered

Front 68

Frostbite

Back 68

* Freezing of fluids in skin or subcutaneous tissues due to exposure to subfreezing temperature
* Crystallization (freezing of tissue) & destruction of tissue
* Superficial involves dermis & shallow subcutaneous tissue
* Deep involves subdermal tissue – skin is white, hard, insensitive.

Front 69

Superficial frostbite

Back 69

* involves dermis & shallow subcutaneous tissue
* skins red or white,cold, painful, blistering.
* Usually will recover with no permanent damage.
* Increased future susceptibility to cold injury

Front 70

Deep frostbite

Back 70

* involves subdermal tissue
* skin is white, hard, insensitive.
* Becomes black, gangrenous (no blood supply)
* Loss of tissue, loss of body part.

Front 71

Degrees of Frostbite

Back 71

* Can’t determine until several days after injury
* 1st degree: erythema, edema, mild numbness
* 2nd degree: above + clear blisters
* 3rd degree: #1 + hemorrhagic blisters
* 4th degree: bone & muscle tissue involved with necrosis

Front 72

Frostbite treatment

Back 72

* Treatment consists of rapid rewarming provided that there is no risk of refreezing as this is even more damaging.
* Refrozen tissue almost never survives.
* Important to check for other injuries, especially hypothermia.
* Rewarming with warm water immersion best (39 ‐42 C)
* Antiinflammatories, analgesics & antibiotic therapy

Front 73

Skin Cancer

Back 73

* Skin cancer the most common cause of cancer (good news not the most common cause of death)
* Prevalence increasing, particularly in older individuals but also seen in the young

Front 74

Basal Cell Carcinoma

Back 74

* Most common type of skin cancer
* Skin exposed to sun
* Non healing lesion
* Treated by excision (100% fixable if early)

Front 75

Squamous Cell Carcinoma

Back 75

* Squamous cells of outer skin
* Sun related cancer (smoking)
* Scaly, crusty, slow growing which may develop into ulcers
* Treatment based on pathology
* Excision – which may be extensive
* Rare metastases ‐ radiation

Front 76

Melanoma

Back 76

* worst type
* Melanocytes (pigment producing cells)
* Sun damage or heredity
* Recognition (ABCDE)
* A – asymmetry (not symmetrical)
* B – irregular borders
* C – variable colouring
* D – size (diameter over 6 mm)
* E – evolution – changing
* Treatment excision and commonly chemotherapy if metastases
* If late – poor prognosis

Front 77

Treatment of Skin Cancer

Back 77

* Prevention
* Protection from the sun (clothing, hats, sunscreen)
* No smoking/chewing
* Skin monitoring by a dermatologist for those at risk
* High skin damage due to sun exposure when young
* Family history

Front 78

CFL Policy for Doping

Back 78

* 1st offense – 2 game
* 2nd offense – 9 game
* 3rd offense – 1 year
* 4th offense ‐ lifetime

Front 79

Positive test: everything is wiped out, medal, times, records etc

Lie: Jail for lying to federal prosecutors about steroid use

Back 79

***

Front 80

Cocaine and Marijuana banned

Back 80

* weed stored in fat so positive test for months after

Front 81

Tampered objects

Back 81

* supplements sometimes have a protein powers but before had an energy drink with a stimulant that may be banned and cause cross contamination
* can get batch testing

Front 82

Alberta Results for Doping

Back 82

* 7,415 males and 3,110 females used steroids (1,600 males aged 11‐13)
* 40,800 used ‘pain killers’
* 13,600 used stimulants (including caffeine)

Front 83

Purposes of WADA

Back 83

* “To protect the Athletes’ fundamental right to participate in doping‐free sport and thus promote health, fairness and equality for Athletes worldwide; and
* To ensure harmonized, coordinated and effective anti‐doping programs at the international and national level with regard to detection, deterrence and prevention of doping.”

Front 84

Doping Definition

Back 84

* “doping is defined as the occurrence of one or more of the anti‐doping rule violations set forth in Article 2.1 through Article 2.10 of the Code”

Front 85

Anti‐Doping Rule Violations

Back 85

1. “The presence of a Prohibited substance or its Metabolites or Markers in an Athlete’s bodily Specimen”
2. “Use or Attempted use by an athlete of a Prohibited Substance or a Prohibited Method”
3. Evading, Refusing or failing to Submit to Sample Collection.
4. Whereabouts Failures: don’t tell them where you are.. 3 missed tests and/or filing failures in a 12 month period
5. Tampering or Attempted Tampering with any part of Doping Control
6. Possession of Prohibited Substances or a Prohibited Methods
7. Trafficking or Attempted Trafficking in any Prohibited Substance or Prohibited Method
8. Administration or Attempted administration to any Athlete In‐Competition of any Prohibited Substance or Prohibited Method, or administration or Attempted administration to any Athlete Out‐of‐Competition of any Prohibited Substance or Prohibited Method that is prohibited Out‐of‐Competition,
9. Complicity: Assisting, aiding, abetting etc involving an anti‐ doping rule violation
10. Prohibited Association: Association with ineligible person, Serving as a front or intermediary for an ineligible (banned athlete, convicted doctor) person* knowing AND not reporting will not get you in trouble

Front 86

The Prohibited List Inclusion

Back 86

* Inclusion for drug or method must meet 2 of the following criteria:1. Evidence for potential of enhancement of sport performance (alone or in combination)
2. Evidence for health risk to the athlete (going over the therapeutic max can cause death for example)
3. Use “violates the spirit of sport”

Front 87

PROHIBITED SUBSTANCES

Back 87

* NEED TO KNOW WHICH EACH CATEGORY AND ONE EXAMPLE OF THE PS
* S0 Non‐approved Substances (*2011)
* S9 Glucocorticosteroids

Front 88

PROHIBITED METHODS

Back 88

* NEED TO KNOW WHICH EACH CATEGORY AND ONE EXAMPLE OF THE PM
* M1 Enhancement of Oxygen Transfer
* M2 Pharmacological, chemical and physical manipulation
* M3 Gene Doping

Front 89

Substances and Methods Prohibited at all Times (In‐and Out‐of‐Competition)

Back 89

- S0-S5

- M1-M3

Front 90

S0 Non‐approved Substances

Back 90

* New 2011
* Any pharmacological substance which is not addressed by any of the subsequent sections of the List and with no current approval by any governmental regulatory health authority for human therapeutic use
* Pre‐clinical or development or discontinued
* Drugs being made every day
* Drugs that aren’t on the list anymore but still banned

Front 91

S1 Anabolic Agents

Back 91

* Anabolic (muscle building) Androgenic (male reproducing) Steroids
* Exogenous (not produced by body)
* Endogenous (e.g. produced by the body ‐ testosterone, androstenedione)
* Beyond normal range
* T/E ratio > 4:1* in urine (testosterone to epitestosterone (mirror image) ratio)
* can be made in a petri dish
* too much testosterone can cause “changing of sex” in both M & F
*

Front 92

SIDE EFFECTS of S1

Back 92

* thinning of hair/ balding
* change mind: make more aggressive
* acne
* facial and body hair of a man (women)
* deepens/thickens vocal cords = deeper voice
* breast development (men)
* breast decrease (women)
* athrosclerois … Heart disease/stroke
* Liver damage
* testicles shrink
* increased muscle mass and weight
* increase sex drive
* enlarged clitoris
* In growing… cause growth plates to close faster and making youth stop growing

Front 93

S2 Peptide Hormones, Growth Factors Related Substances and Mimetics

Back 93

* Erythropoiesis‐Stimulating agents‐Erythropoietin (EPO), darbepoetin... (produced in kidneys and stimulates production of RBC. Increase O2 carrying capacity increase aerobic power (better at distance, increase recovery) )
* popular in 90’s and track for helping make stronger (was undetectable back than)
* $10,000/cycle
* test now
* removed from list
* originally banned
* PRP doesn’t really do anything so it was removed from the list

Front 94

S3: Beta‐2 Agonists

Back 94

* Act on respiratory smooth muscle to relax them to prevent narrowing of airways
* adrenaline like drugs = stimulatory… some can produce positive effects (banned)
* asthma medicine... some ok
*

Salbutamol,salmeterol,formoterol,serevent, advair, symbicort OK

Front 95

S4 Hormone and Metabolic Modulators

Back 95

* Things that effect physiology
* enzyme, decrease estrogen production, banned

* take these with anabolic stimulators will decrease side effects
* anastrozole,testolactone

Metabolic Modulators

Modifiers of Myostatin function (bigger muscles if you block myostanin)

Front 96

S5 Diuretics and Masking Agents

Back 96

DIURETICS

* make you pee… peeing out extra water and decrease blood pressure
* losing weight
* Problem: increase amount of fluid and decreases anything in urine (dilutes urine enough to get negative test)
* Furosemide, thiazide, acetazolamide
* Plasma expanders (albumin,dextran,hydroxyethyl starch): increase fluid in vascular system

Front 97

M1 Enhancement of Oxygen Transfer

Back 97

Blood Doping

* Autologous, homologous, or heterologous blood products
* system of taking your blood or someone else’s blood and injecting into yourself
* Increase RBC
* Products/chemicals that enhance uptake, transport or delivery of oxygen: EPO, blood substitutes, etc
* with adding a pint (of something) we can increase plasma volume which will dilute whatever is in your blood and kidney does its thing, there will be less going out of your blood and may be undetectable

Front 98

M2 Chemical and Physical Manipulation

Back 98

Catheterization, urine substitution, tampering with validity/integrity of sample, use of proteases

* urine subsitiution: catheter… “donate” urine into another’s bladder
* put enzymes into urine to breakdown illegal products in urine

*IV infusions

* Masking agents: give testosterone + epi at the same time (altering the T/E ration)

Front 99

M3 Gene Doping

Back 99

* The great frontier
* Transfer of polymers of nucleic acids or nucleic acid analogues
* Use of normal or genetically modified cells

Front 100

Substances and Methods Prohibited in‐ Competition ONLY

Back 100

S6-S9

Front 101

S6 Stimulants

Back 101

• Decrease feeling of fatigue, behavioural changes, hyperthermia, cardiac

Strychnine, amphetamines, cocaine

• Caffeine >5 micrograms per ml

Front 102

S7 Narcotics

Back 102

* Heroin (diamorphine), morphine, meperidin, fentanyl, oxycodone (percocet), etc
* Codeine permitted …no limit
* Mental alteration, slowing of CNS, pain relief

Front 103

S8 Cannabinoids

Back 103

* don’t know when it will clear system
* Marijuana, hashish
* Mental alteration

Front 104

S9 Glucocorticosteroids

Back 104

* high doses changes your ventilation… allows you to tolerate pain at a very high level
* Administered orally, rectally, IV or IM requires a TUE (note now monitored out of competition)
* Dermatological preparations are not prohibited (skin, aural/otic, nasal, buccal, ophthalmologic)
* Inhaled permitted
* Permitted on the skin and for asthmatics

Front 105

SUBSTANCES PROHIBITED IN PARTICULAR SPORTS

Back 105

* P1 Alcohol (archery, automobile/power boat/motorcycling): Violation 0.10 g/L
* P2 Beta‐Blockers (Archery, billiards, darts, golf, shooting, ski jumping, ski aerials, big air, World Underwater Federation (CMAS) (attack adrenal center and slows you down (heart).. archers shoot between heart beats)

Front 106

* Ephedrine,cannabinoids,inhaledBeta‐2agonists (not clenbuterol), beta blockers, glucocorticosteroids, alcohol, probenecid

Back 106

***

Front 107

Monitoring Program

Back 107

Stimulants

* In‐competition only: bupropion, caffeine, nicotine, phenylephrine, synephrine
* In‐competition Only: Morphine/codeine ratio, hydrocodone, tramadol, tapentadol, mitragynine
* Out‐of‐competition only
* can cause faster recovery

Front 108

International Standard Therapeutic Use Exemptions (ISTUE)

Back 108

* ISTUE
* For banned substances
* Must be pre‐approved (21 days)
* Emergency situations (e.g. Anaphylaxis)
* Must be filled out by physician
* All reviewed by a TUE Committee

Front 109

Testing – ‘Whereabouts’

Back 109

* Athletes submit whereabouts information for location purposes for no‐notice out‐of‐ competition testing.
* 1/4ly (March 15, June 15, Sept 15, Dec 15): you need to giver whereabouts, where you live, where/when practice, where your competitions you are, if your going on vacation
* 3 Whereabouts Failures is a Doping Violation

Front 110

Testing Procedure

Back 110

* Approached by DCO, proceed to room
* Informed
* Select urine collection container
* Urine specimen (Disrobe above waist to mid‐thigh, Viewed)

• 90 ml

• Select prepackaged kit

• A (most urine, important, whatt’s looked at) and B bottles

• Check pH, specific gravity

• Forms

• Sealing contents in courier bag

Front 111

Blood Sampling

Back 111

* Part of testing in endurance sports
* Evaluation of hemoglobin and hematocrit and to test for hGH
* Checks for blood doping/EPO/hemoglobin based oxygen carrier (HBOCs) use
* 2X3 ml by nurse HB/HBOCs
* 2X5 ml hGH

Front 112

Athlete Biological Passport

Back 112

* Hematological Module (urine, endocrine, and others not yet)
* Hematocrit, hemoglobin, RBC, reticulocyte count, Retic% and others
* Reviewed by expert in the field
* All your assessment for every test kept
* looks at your values and sees if there’s a specific change

Front 113

WADA

Back 113

* First violation – 4 years
* Second violation – based on previous and current type of Anti‐Doping violation (Article 10.7.1 of WADA Code)
* Third violation – always a lifetime except in certain circumstances
* Substances susceptible to unintentional anti‐ doping
* First ‐ minimum warning and reprimand to maximum two years
* Second ‐ 2 years
* Third ‐ lifetime
* WADA Trafficking, Administration, etc – Minimum 4 years to lifetime
* WADA whereabouts violation: Minimum 1 year to maximum 2 years

Front 114

Gene doping definition

Back 114

* Narrow definition: Misuse of techniques of gene therapy and cell therapy
* WADA definition: “Non-therapeutic use of cells, genes, genetic elements, or of the modulation of gene expression, having the capacity to improve athletic performance.
* can effect/change: DNA, protein, mRNA, affect translation and transcription etc.. effect at every level

Front 115

* Recombinant genes

Back 115

* change gene
* Introduced in tissues
* Introduced in embryo

Front 116

* Recombinant protein

Back 116

* effect from recombinant gene
* From recombinant genes

Front 117

Genetic Polymorphisms (SNPs) and Mutations

Back 117

* A case-control study will test for a significant association between allele (polymorphism) ratios and phenotype. SNP – single nucleotide plymorphism
* amino acid change, introduce a stop codon, codon deletion
* can inject DNA that already has these changes etc

Front 118

Specific gene changes (mutations)

Back 118

* Double Muscling in Cattle
* 20-25% increase in muscle mass relative to conventional cattle Reduction size internal organs
* Reduction in female fertility, lower viability of offspring, and delay in sexual maturation
* Myostatin (GDF8): member of transforming growth factor-beta superfamily; control of skeletal muscle mass

Front 119

Myostatin

Back 119

* Growth Differentiation Factor 8 (GDF-8)
* Protein produced by myocytes
* MSTN gene
* Inhibits muscle production/growth
* NOT PRODUCED – BIG MUSCLES

Front 120

Female Physiology is designed for pregnancy

Back 120

* hypothalamus is connected to the pituitary gland
* Vascular supply = circle of willis
* Pituitary is fixed but the brain is not
* Concussion: can cause disruption between hypo and pit. Causing dysfunction

Front 121

Female Feedback system

Back 121

* CNS >> hypothalamus (generates GNRH) >> Pituitary ( FSH + LH) >> ovary (effect the oocytes >> follicles (E) and Corpus (P)) ( P + E) >> endometrium thicken
* estrogen prepares for implantation
* progesterone finishes preparation for implantation
* P + E have negative feedback when pregnant

Front 122

Menses

Back 122

* Follicular development: increase in Lh and FSH and overtime the FSH diminished… as the follicle develops it produces estrogen it thickens the endometrium
* mid cycle = LH serge = Ovulation
* Day 14: Ovulation, body temp high
* Progesterone from corpus makes lining secretory
* If no pregnancy than endometrium is sloughed off for Menes
* Restart cycle

Front 123

Ovary + Menses

Back 123

* oocytes/follicles
* every cycle a number start to develop into primary and secondary… one wins releases an egg the rest fall off an die
* once egg release = remaining the corpus lutem which produces progesterone
* Egg goes down the F tubes into the uterus

Front 124

Oocyte in middle

Back 124

* theca cells on outside
* granulosa cells on the inside
* LH acts on the Theca cells = production of androgen …
* androgen + FSH goes to granules cells to produce estrogen

Front 125

Female Athlete Triad

Back 125

* Disordered eating (energy imbalance)
* Amenorrhea
* Osteoporosis
* energy imbalance makes body think its starving its self and than makes the body shut off the ability to get pregnant.. hormones aren’t working causing thin bones
* not absolute

Front 126

Female Athlete SPECTRUM

Back 126

* optimal energy >> eumenorrhea (normal period) >> optimal bone health
* reduced energy >> subclinical menstrual disorders/ may still have normal periods >> low bone mass
* low energy >> amenorrhea >> osteoporosis

Front 127

* ‘Relative Energy Deficiency in Sport’

Back 127

* Reflects the issue that males are also involved
* Physiological dysfunction – metabolic rate, menstration, cardiovascular health, immunity
* Risk Assessment and Return to Play Model (problematic)
* takes away from the Much bigger issue in Females

Front 128

Who Is At Risk for Triad

Back 128

* Teens or young women
* Endurance sport and sport that requires a lean physique
* 15‐62% female athletes have pathologic weight‐control behaviours (1‐ 3% of normal female population)
* Key time – when entering college

Front 129

* Eating disorders have a ____% mortality rate in female non‐athletes

Back 129

- 10‐18%

Front 130

Consequences of Triad

Back 130

* Eating disorders
* Osteoporosis related problems at an early age
* Stress fracture risk increases
* G‐I, C‐V disorders
* Thermoregulatory dysfunction

Front 131

Avoidant/Restrictive Food Intake Disorder

Back 131

* An eating or feeding disturbance as manifested by persistent failure to meet appropriate nutritional/energy needs associated with one of the following
* results in weight lose, nutrient deficiency, interferes with psychological functioning
* * not because of lack of food
* no disturbance in view of body,
* these people feel normal just not eating

Front 132

Anorexia Nervosa

Back 132

* - (0.5‐ 1.0% of population)
* Two types (restricting + binge eating)
* Energy restriction
* Intense fear of gaining weight or fat
* Lack of recognition of the seriousness of the current low body weight
* removed DSM‐V
* At risk young women under stress
* Mortality 5% per decade for female
* Mortality 80% per decade for males

Front 133

* Restricting type AN
* Binge eating type

Back 133

* last 3 months, individual is engaged in recurrent episodes of binge eating or purging behaviour

Front 134

Bulimia Nervosa

Back 134

* - 1- 1.5 %
* Recurrent binge eating
* Self‐evaluation unduly influenced by body shape and weight
* Inappropriate compensatory behaviours (vomiting)
* 1X/week for 3 months
* Problem not just during episodes of anorexia nervosa
* Young affected, mortality 2% per decade for both males and females

Front 135

Binge‐Eating Disorder

Back 135

* Recurrent binge eating
* 1X/week for 3 months
* Sense of lack of control and feeling of distress
* Ashamed of problem ‐ conceals
* no compensatory behaviour

Front 136

Detection of Disorder

Back 136

* High index of suspicion
* Screening questionnaires
* Eating history
* Menstrual history
* Life stressors (include competition and goals)
* Stress fracture history

Front 137

Warning Signs of Anorexia

Back 137

* Significant weight loss
* Preoccupation with food and weight
* Wears clothing that hides body figure (baggy clothes, layered clothes)
* Excessive exercise
* Avoids social activities that involve food

Front 138

Warning Signs of Bulemia

Back 138

* Noticeable weight loss or gain
* Overly concerned about weight
* After meals – visits bathroom
* Mood fluctuations – depressive
* Dieting (strict)/binging cycles
* Criticism of one’s body

Front 139

Detection of Physical observations:

Back 139

* Thin
* Low pulse rate and hypotension
* Lanugo hair
* Parotid gland enlargement (bulimia)
* Tooth enamel erosion (bulimia)
* Nail and finger changes (Russell’s sign)

Front 140

Amenorrhea

Back 140

* PRIMARY: No periods by age 15 yr
* SECONDARY: Absence of 3‐6 consecutive cycles or <3 cycles per year after onset of menstruation
* PREVALENCE: 2‐5% General Population, 1‐44% in Athletes (depends on sports)

Front 141

Causes of Amenorrhea

Back 141

* Pregnancy
* Hypothalamic‐pituitary (GnRH deficiency)
* Hyperprolactinemia (pituitary tumour)
* Premature ovarian failure: none of the eggs are able to mature into follicles
* Polycystic ovary syndrome: most common,

Front 142

Hypothalamic Amenorrhea (Athletic amenorrhea)

Back 142

* Problem of caloric levels… too thin
* Stress and ‘starvation’ act on the hypothalamus >> decrease GnRH amplitude
* Result: pre‐pubertal state
* Loss of FSH, LH therefore no follicle development
* NO ESTROGEN (no endometrial development + no stimulation of bone development >. stress fractures)
* No progesterone
* return of fat mass by increase caloric intake plus decrease exercise
* Vitamin D and calcium for bones
* Estrogen supplementation (e.g. BCP) does not increase bone mass but may slow the decline

Front 143

Polycystic Ovary Syndrome (PCO)

Back 143

* 5‐10% of all women
* Hyperandrogenism (hirsuit, acne, alopecia) – theca cells produce too much
* Result too much estrogen >> suppresses FSH/LH
* Anovulatory therefore no progesterone therefore very irregular periods
* BCP (E + P): Progesterone more important
* Aid for ovulation for fertilization if pregnancy desired

Front 144

Bone Mineral Density

(T score, Z score)

Back 144

* T‐score compares individuals to average peak adult BMD
* Z‐score compares individuals of same age and sex
* Athletes USUALLY have high BMD
* Low BMD Z‐score between ‐1.0 and ‐2.0 with other risk factors
* Osteoporosis Z‐score < ‐2.0

Front 145

* Females hit their peak bone mass around ___ years
* There is a significant bone mass reduction at age

Back 145

- 20-25

- 50 (menopause)

Front 146

Treatment Female Athlete Triad

Back 146

* Early detection is key
* Psychological and nutritional counseling
* Medical intervention (bone preservation) (Calcium, D, Estrogen)
* Reduce training
* energy balance

Front 147

Female Birth Control Pills

Back 147

* Fools the hypothalamic‐pituitary‐ovary axis by turning off the pituitary
* Synthetic estrogen and progestin agents
* Quadraphasic – estrogen/progestin (represents females cycle the most

Front 148

Male Endocrinology

Back 148

* Production of sperm
* production of testosterone
* LH stimulates Leydig cells to produce testosterone
* testosterone crosses the membrane and goes into the sertoli cells
* FSH + Testosterone produces various growth factors to mature and release sperm
* Males have pulsative GnRH, as they hit puberty ( low to high GnRH causes the FSH + LH release >> causes sperm production)

Front 149

Testosterone

Back 149

* Slow decrease with age
* Secondary sexual characteristics

Front 150

Iron in Humans

Back 150

* Stores( 55 mg/Kg body weight Males + 45 mg/Kg body weight Females)
* 60‐75% Heme Oxygen (Hb, Mb).. whats affected when you start to lose iron
* 15‐30% protein bound (free iron)… free iron destroys things, causing chemical reactions that effect cell membrane
* 1% Enzymes in Redox functions

Front 151

Iron Uses

Back 151

energy production

* O2 transport (Hb, Mb)
* Enzymes
* Electron transport chain
* Citric acid cycle
* Glycolytic cycle

Front 152

O2 Binding to Heme

Back 152

* O2 binding to Fe changes local shape, which changes globin shape thus making it easier for more O2 molecules to bind
* 02 binds to hemoglobin changes shape and creates higher affinity

Front 153

Transferrin

Back 153

* Glycoprotein (produced in liver )
* 2 iron binding sites
* Prevents uncontrolled oxidation
* Allows iron into solution
* Facilitates transport into cells
* TIBC – total binding sites for Fe
* Transports iron in circulation

Front 154

* Ferritin

Back 154

* main storage for iron
* mostly in bone marrow
* Large glycoprotein
* Binds iron for storage (centrally Fe+++ and released as Fe++)
* Good representative of bone marrow iron stores
* In balance with circulation

Front 155

Where iron goes in the body

Back 155

* In the gut.. eat iron… transferrin picked up iron and taken around in transferrin which it go to bone marrow
* as i goes around it will hit bone marrow it will either from it for RBC for hemoglobin or give it to Ferritin (store it)
* Its iron free and goes back into circulation
* RBC goes around circulation and than broken down into spleen and the iron is picked up by Transferrin and brought into circulation

Front 156

Iron Loss

Back 156

- Menses

- Pregnancy

- Sweat

- RBC destruction

- urine

Front 157

Athletes Loss of Iron

Back 157

* Increase turn‐over (Turn‐over rate, intravascular hemolysis, increase body temp, low pH)
* Increase utilization ( Increase RBC production + Increase enzyme requirements)
* Increase sweat

Front 158

Athletes at Risk for Iron Deficiency

Back 158

* Females (menses)
* Endurance athletes (increase pounding)
* Sports at risk for disordered eating
* Vegetarians

Front 159

Stages of Iron Deficiency

Back 159

* Prelatent (iron depletion): Low ferritin, normal Hb
* Latent (iron deficiency erythropoiesis): Low ferritin, Hb structure changes
* Anemia: Low ferritin, low Hb
* Hb level is a key factor for aerobic performance

Front 160

Ferritin as an indicator of iron stores

Back 160

* <10 μgm/l – iron stores essentially nil (0)
* <20 μgm/l – low iron stores (banging on empty)
* <34 μgm/l – difficulty benefiting from altitude training

Front 161

* red meat has the highest source and highest absorbed (way more than an iron supplement)

Back 161

**

Front 162

Iron Supplementation Side Effects

Back 162

Contraindications

* Hemochromatosis
* Oral and parenteral together
* Ulcer disease
* Decrease absorption of medication (e.g. tetracycline)
* Nausea, vomit, ulcer
* Constipation
* Diarrhea
* Black stools

Front 163

Depression

Back 163

* ‘Vegetative signs’: changes in eating, sleeping, pleasure
* Hopelessness, worthless, guilty, angry, empty, irritable
* self harm or suicide
* Athletes don’t seek help: stigma

Front 164

Depression Prevalence

Back 164

* 6.7% prevalence in adult population
* Higher rates in 18‐25 (8.7%) and older adults
* College athletes depression rates in USA 15.6‐21% (women>men)
* Suicide: male > female (as per general population)

Front 165

Depression Treatment

Back 165

* Exercise
* Counselling
* Anti‐depressants (change brain chemistry, takes a while)

Front 166

Substance Abuse

Back 166

* Higher alcohol use (binge pattern)
* Illicit drug use lower than in general population of same age (drug testing?)
* Some sports: ’culture’ (of alcohol use, weed etc depends on sports)

Front 167

Injury and psychosocial factors ‐ initial

Back 167

* Athletes identify as sportspeople, sport is a major part of their life
* Injury – initial emotion (mood, anxiety and fear) high but improved as completion of rehab improved with some anxiety as time to return to play occurred

Front 168

Injury and rehabilitation process

Back 168

* Psychosocial factors (thinks, feels and acts) are associated with the outcomes of rehab
* Female, young limited experience of injury, negative emotion, perception of isolation – less successful rehab outcomes
* how you approach the rehabilitation will affect how well the outcome is

Front 169

Injury and return to sport

Back 169

* Injury‐related behaviour – sport injury rehabilitation outcomes – need for social interaction with team, staff, coaches important issues around return to sport
* Athlete’s psychological readiness to return to play related to fear, anxiety, confidence in performing well and remaining uninjured
* progressive matter

Front 170

Concussion: definition

Back 170

* COMPLEX PATHOPHYSIOLIGCAL PROCESS AFFECTING THE BRAINE INDUCED BY BIOMECHANICS FORCES
* any direct or indirect force to the head, neck or body that results in symptoms that may develop over minutes to hours

Front 171

Concussion Diagnosis

Back 171

* results in functional, not structural, disturbance ( no findings on imaging)
* diagnosis and management is CLINICAL

Front 172

Pathophysiology

Back 172

* Multiple theories
* second impact syndrome? combination of cellular ionic disturbances, decreased cerebral blood flow (CBF), and glucose metabolic dysfunction hypothesized to cause cerebral edema and cause pt to be vulnerable to more severe neurologic dysfunction or even death
* CBF: alterations in cerebral blood flow ? Triphasic ( down, up, down in immediate days following injury)
* Diffuse axonal damage:
* Glucose metabolism

Front 173

Neurometabolic cascade after traumatic injury.

Cellular Events

Back 173

1. nonspecific depolarization and initiation of action potentials,
2. release of excitatory neurotransmitters (EAAs),
3. massive efflux of potassium,
4. increased activity of membrane ionic pumps to restore homeostasis,
5. hyperglycolysis to generate more ATP,
6. lactate accumulation,
7. calcium influx and sequestration in mitochondria, leading to impaired oxidative metabolism
8. decreased energy (ATP) production,
9. calpain activation and initiation of apoptosis.

Front 174

Neurometabolic cascade after traumatic injury.

Axonal events

Back 174

1. axolemmal disruption and calcium influx,
2. Neurofilament compaction via phosphorylation or sidearm cleavage,
3. microtubule disassembly and accumulation of axonally transported organelles,
4. axonal swelling and eventual axotomy.

Front 175

Biomechanics

Back 175

* concussion may be caused either by aa direct blow with impulsive force transmitted to the head
* force, acceleration and velocity
* Forces: direct contact or inertial ( impulsive)
* Direction of force may also impact symptoms and severity (lateral, rotational,

Front 176

Concussion Signs + Symptoms

(physical, cognitive, emotional, energy)

Back 176

* physical: head ache, blurred vision, dizziness, vomiting, sensitivity, disorientation
* cognitive: feeling slowed, difficulty remembering/concentration
* emotionaL: personality change, anxiety, irritability, sadness
* sleep/energy: fatigue, excess sleep, drowsiness

Front 177

Diagnosing a concussion can be a challenge

Back 177

* no definitive imaging or blood work
* clinical effects are often subtle
* may have immediate or delayed onset symptoms
* symptoms vary in individuals
* underreport symptoms from student athletes

Front 178

When a player shows ANY features of a concussion

Back 178

1. The player should be evaluated by a physician or other licensed healthcare provider
2. The appropriate disposition of the player must be determined by the treating healthcare provider in a timely manner. If no healthcare provider is available, the player should be safely removed from practice or play and urgent referral to a physician arranged.
3. an assessment of the concussive injury should be made using the SCAT3
4. The player should not be left alone following the injury and serial monitoring for deterioration is essential over the initial few hours following injury.
5. A player with diagnosed concussion should not be allowed to RTP on the day of injury.

Front 179

Red Flags

Back 179

* *SUDDEN CHANGE
* vomiting > 2 times
* drowsiness/ difficulty cousins
* seizures/convulsions
* severe/worsening headache
* unusual behaviour
* double visions
* unsteadiness
* slurred speech
* Indications to be seen urgently in ER, consideration of CT head to rule out intracranial bleed

Front 180

Post Injury evaluation

Medical professional should:

Back 180

* Complete medical history including prev concussion history
* Complete physical exam: full neuro exam, cervical exam
* SCAT3 included in initial evaluation
* Determination if imaging required

Front 181

Child SCAT3 –

Back 181

more age appropriate questions and symptoms reporting, also has component for parent to weigh in

Front 182

Recovery

Back 182

* majority recover in 7-10 days
* some left with persistent symptoms (31% NHL, 72% elite youth ice hockey, 14% still symptomatic at 3 months)
* Need to consider Modifiers, appropriate relative rest and return to play.

Front 183

Treatment Strategies

Back 183

* relative rest
* addressing modifiers
* treat underlying issues (sleep, mood, neck pain, teaches, dizziness )
* education + counselling
* step wise progression

Front 184

Return to Play

Back 184

* Pacing: use of timer - goal to gradually progress tolerance while staying within sub-symptoms threshold
* Rest (cognitive and physical) >> graduated exertion >> return to play
* asymptomatic at rest and with light physical activity
* full return to learn achieved
* not relying on pharmacologic therapy
* cleared to start RTP progression by medical staff

Front 185

Special Populations

Back 185

Children/ Adolescents

* Age appropriate testing
* RTP/recovery
* patient and parent involvement
* all concussions care should be standard
* resources/logistics

Front 186

Baseline Screening

Back 186

* no evidence to support mass baseline screening
* significant costs, questionable clinical utility

Front 187

Chronic Traumatic Encephalopathy (CTE)

Back 187

* specific tauopathy, progressive neurodegenerative disease
* Clinical areas affected: cognition, mood, behaviour and motor
* diagnosis currently only possible on autopsy
* no cause and effect yet proven
* significant medico-legal concerns
* Localised brain atrophy and deposition of Tau protein and neurofibrillary tangles in the cerebral cortex, basal ganglia, or brainstem in a distinctive pattern

Front 188

Primary Prevention

Back 188

1. Helmets

* decrease incidence of structural head trauma
* role in alpine skiing
* prevention of orofacial/dental injury
* NCAA
* minor soccer
* Heading in minor soccer in US and contact practice limits in NCAA football

Front 189

T or F

if you weren't knocked to the you don’t have a concussion?

Back 189

* Myth..less than 10% of concussions income LOC

Front 190

T or F

having multiple concussions in sport increases your risk of having another concussion?

Back 190

* True… an athlete experiencing 1 concussion is 2-8.5x more likely to sustain another concussion

Front 191

T or F

helmets prevent concussions?

Back 191

* true if its properly fit

Front 192

T or F

a normal CT scan rules out a concussion:

Back 192

* false… Ct looks at structural only not functional

Front 193

T or F

If there are no instant symptoms right after event then there is no concussion:

Back 193

* False

Front 194

T or F

any contact to the head or body causing rapid head movement can cause a concussion?

Back 194

* True

Front 195

Take Home Points

* complex pathophysiology
* recognize + remove
* diagnostic challenges, clinical diagnosis - Err on the side of caution
* no same day return to play
* intimal period of relative rest >> return to learn >> return to play
* no return to play until full return to learn and appropriate RTP progression

Back 195

**

Front 196

SCAT 3

Back 196

* Symptoms: need to look at the baseline of the individual. They might already have the symptoms when they were healthy
* immediate memory: read word at 1 word per second
* digits backwards: if you get a level wrong twice don’t do it again
* balance test: you cannel do one error at a time to a max of ten

Front 197

Primary difference between adult and children scale on SCAT

Back 197

* the symptoms scale different
* parent scale and child scale
* no one leg stance
* no month backwards
* serious issues that need to be addressed (differences in score, and normal symptoms)

Front 198

Pre‐departure Planning

Back 198

• 22%–64% of travellers to the developing world self‐ report travel‐related health problems

• 8% of travellers to developing regions seek health care, either while abroad or upon returning home

Who (Who is going? Who’s there?)

• What (Reason for travel, what sport/event?)

• Where (Country, rural vs urban, climate, time zones, etc.)

• When (Time of year, how long, how soon?)

• How (Transportation, medical emergencies, etc.)

Front 199

Vaccinations Routine

Back 199

• Tetanus:(Td) booster (booster every 10 years)

• Polio: booster every 10 years, if injected

• Measles/mumps: rubella booster (x1)

• Influenza: 3 viruses (yearly)

Front 200

Vaccinations ‐ Recommended

Back 200

Hepatitis A Vaccine (Havrix)

• Hepatitis B Vaccine (Energix‐B) (from touch)

• Meningitis (Menactra)

• Pneumococcus: usually only older

• Traveller’s Diarrhea

* Others – destination dependant

Front 201

Hepatitis A Vaccine (Havrix)

Back 201

* Two injections at 0 and 6 ‐ 12 months
* First injection at least 2 weeks before exposure
* Effective x 10 years
* Age 2 and older
* high in Africa and south america, south Asia
* Hepatitis A endemic areas
* Person‐to‐person contact (child/health care, food service)
* Contaminated water and food

Front 202

Hepatitis B Vaccine (Energix‐B)

Back 202

* 3 injections at 0, 1, and 6 months
* 4 weeks before exposure
* Effective x 10 years
* Any age
* Hepatitis B endemic areas for > than 6 months
* Medical work
* Blood or sexual contact
* Chronic liver disease
* high in colder areas, eastern Europe, south america, Africa

Front 203

Hepatitis Combined A and B Vaccine (Twinrix)

Back 203

* 3 injections at 0, 1, and 6 months
* 4 weeks before exposure

Front 204

CDC Yellow Book on Travel

Back 204

• Pre‐travel Consultation

• Infectious Disease

• Destination Specific Information

• Post‐Travel evaluation

• Conveyance and Transportation Issues

• Travel with Infants and Children

* Travellers with Specific Needs

Front 205

* jet lag
* Travel fatigue:

Back 205

* travel across time zones
* being tired after a flight
* Jet lag + travel fatigue = overtraining + under recover

Front 206

Sleep Gate

Back 206

* melatonin goes up at start of darkness
* body temp goes up by day and down by night
* cortisol increases during day and decrease at night

Front 207

Jetlag

Back 207

* result of rapid desynchronization of normal circadian rhythms (“the body clock”) with exogenous time cures, termed zeitgebers (“time givers”)”*
* Results in GI disturbance, sleep disturbance, fatigue and cognitive/concentration impairment
* Traversing time zones = circadian dysrhythmia

Front 208

Environmental Clues (‘zeitgebers’)

Back 208

• Light

• Meals

• Physical Activity

* Temperature

Front 209

Jetlag Early Symptoms

Back 209

• Fatigue

• Sleep disturbances

• Disorientation

• Reduced physical ability

• Headaches

• Tired muscles

• Reduced mental activity

• Poor psychomotor coordination

• Gastrointestinal symptoms

* General malaise

Front 210

Jet lag Delayed Symptoms

Back 210

• Reduced physical capacity

• Reduced motor coordination & reflexes

• Slowed response to stimulation

• Loss of appetite, constipation or diarrhea

• Lack of sexual interest

• Mood problems, irritability

• Interference with prescription drugs

• Day time fatigue, sleepiness

• Sleep disturbance

Front 211

Individual Factors

Back 211

Age (older as more troubles)

• Personal health

• Circadian type (owls + larks)

• Personality – flexibility temperament

• Sleep quality/ability to sleep

• Sleep loss

Front 212

* Owls travels easier ____ward
* Larks travel easer ____ward

Back 212

* Owls (peaks late): easier westward
* Larks (peaks early): easier eastward (older person moves towards ‘Larks’)

Front 213

Time Zone Dependent Factors

Direction of travel:

Back 213

• W> E (phase advance, shortened day) = MOST JETLAG

• E> W (phase delay, lengthened day) = 30‐5‐% less jet lag

• N>S or S>N (no phase shift) no desynchronization. (travel fatigue not jetlag)

* Number of time zones travelled: ONE DAY PER TIME ZONE TRAVELLED… arrive 7-8 days in advance to competition

Front 214

Travel Fatigue

Back 214

* Results in persistent fatigue, recurrent illness, behavioural change, motivation loss
* Training history/monitoring

Front 215

Travel Management Program

Back 215

* direction of travel + distance of travel = jet lag
* distance of travel + frequency of travel + length of season = travel fatigue

Front 216

Preflight

Back 216

• Rule out significant sleep disorders

• Change sleep timing

• Change practice time

• Change timing of eating

• No ‘Red Eye

Front 217

In‐Flight

Back 217

* Set watch/clocks to destination time
* Rest/sleep to destination time
* Eyeshades, ear plugs, cancellation ear phones
* Compression Socks/Stockings
* Sedatives (short to medium acting)
* Meals to destination schedule if possible
* Hydration (no caffeine or alcohol)

Front 218

* Meals to destination schedule if possible

**

Back 218

* High protein/low CHO increase CNS tyrosine and adrenaline = increase arousal
* Low protein/High CHO decrease CNS tryptophan and serotonin = increase drowsiness/sleep

Front 219

Post flight

Back 219

* Move to ‘new’ time
* Exercise once off the plane
* Training sessions progressive in intensity/contact
* Short nap (30 minutes) post lunch
* Medium half‐life hypnotics (sleep)

Front 220

Post flight Light

Back 220

East Travel

* Mid morning light exposure (30‐60 minutes)
* Mid afternoon light avoidance (sunglasses)
* Late afternoon light exposure (30‐60 minutes)
* Late evening light avoidance

Front 221

Post flight Melatonin

Back 221

* Phase advance before sleep (3‐5 mg 30 minutes before sleep)
* Side effects:
* Immediate cognitive performance decrements but short lived (caution using sustained‐release)
* Decrease blood pressure
* GI and nightmares
* BEWARE SUPPLEMENTS!!

Front 222

Post flight Stimulant

Back 222

Caffeine 50‐200 mg

* East travel: Morning on waking and just before a nap
* West travel: Late afternoon and just before a nap

Front 223

Successful Infection

Back 223

* Attach >> enter body
* Local/general spread
* Multiplication (bug needs to multiple to come into effect)
* Evasion of host defences
* Shed from body
* Damage to host

Front 224

Barriers to Infection

Back 224

* Skin/mucous membranes/cilia (hairs in respiratory system)/acid/IgA
* Skin damage common in athletes
* Skin infection very common
* PMNs, macrophages, complement
* B and T lymphocytes

Front 225

Routes of Transmission

Back 225

* Latent: in which the usual symptoms are not yet manifest.
* Immunosuppresion: the partial or complete suppression of the immune response of an individual. It is induced to help the survival of an organ after a transplant operation.

Front 226

VIRUS

Back 226

* Replicate only in living cells (that they recognize)
* Inert in extracellular environment
* Enter through mucosa of Respiratory tract, GI, GU or blood stream injection
* Components (nucleic acid, protein coat + membrane envelope)

Front 227

Bacteria

Back 227

* Remain alive in extracellular environment
* live and reproduce outside of the cell
* Classified by: how they move, shape, stain
* Components: DNA, plasma membrane, cell wall

Front 228

* Stain under H&E

Back 228

* Gram Positive take up purple die
* Gram Negative take up red die
* Modified cell wall no staining (mycobacterium, chlamydia, mycoplasma)

Front 229

Fungi

Back 229

* Plant Kingdom
* Eukaryotic (Nucleus (ER and tRNA etc))
* Sexual and Asexual (bud)
* Classification (yeast, mycelium)

Front 230

Parasites

Back 230

* Animal Kingdom
* Eukaryotic (Nucleus)
* ex: Malaria
* Worms
* Symbiotic relationship

Front 231

Upper Resp Tract Infection

Back 231

* COMMON: up to 6/person/year
* Pathogens: viral because of sneezing, coughing etc
* Clinnical: runny nose, sore through, fevers, cough
* course: 3-7 days

Front 232

* TREATMENT for Upper Resp Infection

Back 232

* antibiotics don’t help
* Supportive (fluids, pain control)
* Decrease training ‐ faster recovery
* Prevention – gloves, hand washing

Front 233

Neck Check for Athlete

Back 233

* Symptoms below the neck? Vomiting, diarrhea, fever, myalgia...Not ok to play ..Rest

Front 234

Pharyngitis

Back 234

* COMMON
* PATHOGENS:
* Viral (Majority ~ 70%)
* Influenza,parainfluenza
* Rhinovirus, adenovirus
* EBV,HIV,enterovirus
* Bacterial
* Group A Strep (10%): most common, treat with penicillin
* Neisseria Gonorrhoea
* Cornyebacterium
* Chlamydial

Front 235

Pharyngitis Symptoms

Back 235

* Fever, edema, erythema
* Pustonsils,lymphadenopathy
* Chills
* Aches
* Cough (viral),
* Conjunctivitis (viral)
* Rhinorrhea (viral) (runny nose)

Front 236

Strep Throat

Back 236

* Bacterial: GroupA Streptococcus (we treat)
* Fever
* Anterior Cervical lymphadenopathy
* Tonsillar exudates
* No cough
* Diagnosis: throat swab

Front 237

Pharyngitis Treatment:

Back 237

* Supportive
* NSAIDs/Tylenol
* Fluid
* Salt water gargles

Front 238

* Strep Throat: Treatment

Back 238

* Antibiotics: Penicillin
* treat Strep to Prevent complications not to just help throat
* Reduce secondary spread
* Shorten by one day

Front 239

Complications

* Strep Throat:

Back 239

* Acute Rheumatic Fever: rash or heart infection (effect valves and need to get a valve replacement later)
* Return to play:
* Contagious until Antibiotics for 24 hours
* Play if anbx for 24 hrs, no fever, no systemic sx

Front 240

Complications

* Viral Pharyngitis:

Back 240

* Myocarditis: inflammation of heart muscle…can kill you or permanently damage your heart

Front 241

* glandular fever

Back 241

* Fever, pharyngitis, lymphadenopathy
* 90% adults immune
* Less severe in younger
* 30‐50% college students susceptible
* Humans are the only source

Front 242

EPSTEIN BARR VIRUS

Back 242

* Transmission: Oral secretions/saliva (“Kissing disease”, Reported seminal fluid; cervical epithelial cells) or close contact (sneezing, sharing)
* Incubation period: 30‐50 days, Virus shed 32 wks (decades)
* Duration: 4-8 weeks
*

Front 243

Infectious Mono

* COMMON

Back 243

* 90% exposed by age 30
* First year 20% have been exposed
* Final year 80% have been exposed

Front 244

Infectious Mono

Back 244

* Epstein Barr Virus (EBV)
* Fatigue, achy, anorexia
* DIAGNOSIS: blood work (WBC) + Monospot test (Positive at one week of symptoms)

Front 245

Mono Complications

Back 245

* Hepatitis
* Pericarditis
* Myocarditis
* Neuro (encephalitis, Guillaine‐ Barre)
* • Bone marrow suppression
* SPLENIC ENLARGEMENT
* SPLENIC RUPTURE (not related to sport usually)

Front 246

Mono Symptoms + Recovery

Back 246

* Acute symptoms 5‐15 days
* Recovery 4‐6 weeks… can have post viral syndrome (sense of fatigue)
* May take > 12weeks
* If abrupt onset may recover in shorter period 10 days
* Might not know you have mono

Front 247

* Athletes at same risk of contracting IM as non‐athletes

Back 247

* Overtraining‐ decreased immunity may increase risk
* May recover more quickly
* Elite may take 3‐6m to reach pre‐illness function

Front 248

SPLENOMEGALY

Back 248

* Enlarged Spleen
* Average 8.9 x 8.5 cm
* Imaging: X‐ray; Ultrasound; CT
*

*

Front 249

SPLENIC RUPTURE

Back 249

- Uncommon

* Increased in 3rd ‐4th week of illness, Most between 4‐21days, Rare beyond 4weeks
* Spontaneous 50%
* Trauma (Sport)
* Can be potential emergency (ultrasound + CT imaging)

Front 250

TO ULTRASOUND OR NOT?

Back 250

* One time imaging of the spleen for assessment of splenomegaly at the time of illness is NOT recommended d/t variability encountered in normal values
* Without baseline values unique to individuals, a single ultrasound CANNOT be reliably used to determine splenomegaly

Front 251

MANAGEMENT of IM

Back 251

* Supportive
* Rest
* Activities as tolerated
* NO PHYSICAL/STRENUOUS for 3 weeks
* no alcohol
* Fluids, analgesia, throat care
* Stool softener

Front 252

Medications IM

Back 252

* ACYCLOVIR (Zovirax)
* NO CLINICAL BENEFIT
* May decrease viral shedding
* There are NO pharmacologic measures that will speed recovery

Front 253

RETURN to PERFORMANCE (RTP) for Im

Back 253

Usually at 3‐4 weeks after diagnosis‐ light, non‐contact

• Good energy level

• No associated clincal abnormalities

Front 254

Mumps

Back 254

• Paramyxovirus

• Parotid gland infection plus usual viral illness symptoms of headache, fever, unwell

• PREVENTION – vaccine MMR, need to rest

• Tx – symptomatic

* Complications in adult : orchiditis
* can attack testes and ovaries

Front 255

INFLUENZA (flu)

Back 255

* Virus
* Seasonal Outbreaks: Oct ‐ March

• PATHOGENS: Orthomyxoviridae (RNA virus)

• TRANSMISSION:: Direct Contact, air

Front 256

Flu • CLINICAL: + Complications

Back 256

• CLINICAL:

* Sudden acute onset
* Fever, headache, myalgia, malaise, nausea and vomiting
* Cough, sore throat
* COMPLICATIONS:
* Dehydration
* Bronchitis/asthma
* Pneumonia
* Rhabdomyositis

Front 257

Flu Treatment + RTP

Back 257

* TREATMENT:
* Rest
* Humidifier
* Fluid – dehydration is common
* NSAIDs, Tylenol
* Bronchodilator
* anti‐virals: may help a little bit
* SPORT/RETURN TO PLAY
* Highly contagious, isolate athlete for 5 days from sx onset
* Return to full activity when all sx resolved ((No fever, dehydration, SOB, wheeze)
* highly contagious and lasts for a while

Front 258

EAR INFECTION

Back 258

* eustachian tube goes to throat
* Tympanic membrane goes out… plugged ear

Front 259

Otitis Externa

Back 259

* ear outside
* swimmers ear
* Usually bacterial
* Treatment: Antibiotic drops + NSAIDs for pain

Front 260

Otitis Media

Back 260

* middle ear
* when you're young Eustachian tube is too flat and doesn’t drain very well
* effects tympani membrane (red, fluid)
* Pathology: Viral and potentially bacterial

Front 261

Otitis Media Treatment

Back 261

* Wait and see with analgesia
* Antibiotics
* Tympanosotomy tubes for chronic/recurrent.. goes through tympanic membrane and drains fluid into ear canal
* Rupture – no swimming, etc

Front 262

Impetigo

Back 262

* Bacteria: Staphylococcus or Streptococcus
* Skin break down
* Lesions: Tender (early). Vesicles or pustules with surrounding redness, Honey crust’ will form around them (late) (yellow)
* Common on head, face and neck but can be anywhere
* Rare on palms and soles
*

Front 263

Impetigo Treatment + RTP

Back 263

* TREATMENT:
* Keep skin clean
* Local lesions: Topical ointment (Bactroban cream for 7 days)
* Wide spread lesions (oral antibiotics for 7 days)
* Gets better in 7 to 10 days
* Return to Play
* High Risk (Contact or Collision Sport)
* No new lesions in 48 hours
* 72 hours of antibiotics completed
* No moist or draining lesions

Front 264

Herpes Simplex

Back 264

* 30% risk of transmission with sparring with an infected partner
* Common in contact sports
* HSV‐1: Herpes labialis… cold sores
* HSV‐2: Urogenital herpes… genitals
* Re‐activation: Triggered by physical stress, emotional stress, UV radiation, fever
* Primary: Fever, chills, headache, sore throat then rash

Front 265

Herpes Treatment + RTP

Back 265

* Treatment
* General: Prevention: Gloves, clean mats, skin checks
* Anti‐virals:
* Prophylaxis:
* Before tournaments/games
* >3 episodes per year
* Return to Play
* Free of systemic symptoms for 72 hours
* No new lesions for 72 hours
* No moist or active lesions
* Treated with antivirals for 120 hours

Front 266

Anatomy of Lung

Back 266

* right lung has 3 lobes
* because the heart leans to the left… 2 lobes on left
* lung muscle inverted by the phrenic nerve
* intercostal muscles inverted by intercostal nerves
* I

Front 267

Inspiration vs Expiration

Back 267

* inspiration: external intercostals contract and bring ribs up diaphragm contracts.. volume increases and brings in air
* expiration: external intercostals relax, internal intercostal + abdominal contract for active expiration

Front 268

Ventilation During Exercise

Back 268

* RR 12 >> 45 BPM
* Tidal volume to 4 L/min
* Pulmonary Ventilation 10 >> 200 L/min
* Oxygen consumption 0.3 L/min >> 4 L/min

Front 269

Bronchitis

Back 269

* inflammation of the mucous membrane in the bronchi
* Acute: viral vs bacterial
* Chronic: airway changes associated with COPD (chronic obstructive pulmonary disease) causes changes of bronchi (no more elastic recoil
* Smoking
* Genetic
* Treatment: Asthma – inhalers + Anti‐biotics

Front 270

* Pneumonia:

Back 270

* lung inflammation, air sac fill with pus and can become solid
* Lobe infection
* Viral vs bacterial (fungal)
* Treat – antibiotics vs anti‐virals

Front 271

Pneumothorax

Back 271

* air escapes from lungs/lobe, air will leak outside of lung and take up space outside
* Commonly spontaneous
* Trauma – broken rib
* Treat
* Small : watch, it can fix itself, but have to make sure it doesn’t get worse
* Large: chest tube
* Tension
* Shift mediastinum so vena cava kink
* Decrease oxygenation, decrease venous return
* Emergency

Front 272

Hemothorax

Back 272

* Blood in the chest cavity from Broken rib, bleeding vessels in thorax, sharp trauma
* Sport – broken rib(s), Marfan syndrome – aortic aneurysm
* Decrease oxygenation, blood loss
* Hospital – chest tube

Front 273

SYMPTOMS OF ASTHMA

Back 273

* Wheezing (expiratory)
* Cough, wheeze, chest tightness with exercise

* if you breathe in and there is wheezing this is an UPPER respiratory… stridor (inspiration)

Front 274

PATHOLOGY of Asthma

Back 274

* Characterized by inflammation, increase mucous production and airway narrowing
* increased resistance against air going out
* Net effect is expiratory resistance and air trapping
* Long term results include denudation of epithelium, collagen deposition and airway remodeling

Front 275

Asthma Steps

Back 275

* normal: inside epithelium, cilia and around smooth muscle, little glands that produced mucous to clean air way
* asthmas: inflammation increase mucous secretion and increase smooth muscle contraction and increase hypertrophy and more contraction narrowing the airway

Front 276

Asthma Prevalence

Back 276

* 5000 die/year (US)
* In cold outdoor sports (X‐country ski) – up to 50% of athletes

Front 277

resting tidal volume

Back 277

* resting, siting =

Front 278

air left after expiration

Back 278

* functional residual capacity:

Front 279

residual volume:

Back 279

* whats left even if you blow everything out

Front 280

vital capacity

Back 280

* breathe in all the way and breath out =

Front 281

total lung capacity

Back 281

* = deep breath in and breath out all the way

Front 282

PFT's

Back 282

* FEV1: forced expired volume in 1 second; related to the size of your tubes
* when your tubes narrow the amount you can blow out in 1 sec will diminish (asthmatics)
* Residual volume is increased in asthmatics
* FEV1% <= 65% ( normally would be 80%) … this means airway narrowing

Front 283

Treatment

Asthma

Back 283

* anticholinegerics: stop simulatory
* B agonist: relaxes smooth muscle
* Mast cell release inflammatory chemicals

Front 284

* Corticosteriods

Back 284

* main, inhalation for Asthmastics

Front 285

Electrical Conduction in Heartb

Back 285

* SA node: pacemaker, sends stimulus, right atrium
* causes left and right atrium to contract
* goes to AV node (left atrium), bundle of hiss takes the signal to the right and left ventricles
* Heart disease: one bundle not working, not as strong contraction
* atrium depolarizes = p wave
* depolarization of ventricle = QRS
* T wave = ventricles repolarization of ventricles

Front 286

12‐Lead Electrocardiogram (ECG/EKG)

Back 286

* specific pattern related to contraction of the heart
* ECG: your heart

Front 287

Rate and Rhythm

Back 287

* normal heart rate = 60-100
* Tachycardia ‐ >100 bpm
* Bradycardia ‐ <60 bpm (commonly seen in athletes)
* Heart rate (lowers) and blood pressure (increases) changes with age

Front 288

Premature Atrial Contraction (PAC)

Back 288

* Premature atrial (ectopic) depolarization
* Related to anxiety, stimulants (caffeine), Beta agonists (asthma)
* ‘skipped beat’, palpitations
* Very common, no treatment
* seen in my age group

Front 289

Echocardiogram

Back 289

* looks at architecture of the heart

Front 290

Athlete Heart

Back 290

* Bradycardia: slow heart rate, good stroke volume, cause murmur
* Systolic murmurs
* heart muscle might get bigger

Front 291

Sudden Cardiac Death in Sport

Back 291

* TRAGIC – receive disproportionate degree of public scrutiny
* RARE event
* Commonly death is the first indication of a problem
* Male to female 2:1 (males more prone)
* High school age and a little older (most prone)
* 1 in 50‐100,000 athletes per year (3X higher than non athletes

Front 292

Cardiovascular causes of sudden cardiac deaths in 1435 young competitive athletes

Back 292

* 36% = HCM
* Coronary artery anomalies = 7%
* Myocarditis = 6%

Front 293

HYPERTROPHIC CARDIOMYOPATHY (HOCM)

Back 293

* About 1 in 500
* myocyte hypertrophy, myocyte disorganization and disarray, and myocardial fibrosis
*

Front 294

HOCM

* LV wall thickening

Back 294

* causes the aorta
* limited outflow of the ventricles, no blood supply, cant supply heart
* Asymmetric wall thickening
* Distorted cellular architecture
* Abnormal intramural coronary arteries

Front 295

Commotio Cordis

Back 295

* Blunt chest trauma over heart (sternum)
* Hits just before T wave – VF (Ventricular fibrillation)… need to cause electrical stimulation
* Potential prevention by wearing padding to attenuate impact
* need to hit at the right time
* biggest cause inn females in softball who catch

Front 296

Coronary Artery Anomalies

Back 296

* Coronary arteries are either absent or run an abnormal course
* Abnormal stress on the coronary artery and its endothelium
* Results in damage and atherosclerosis – blockage
* Heart Attack

Front 297

Myocarditis

Back 297

* inflammation of the heart cause by almost always of a viral infection
* 5‐19% with a viral infection will develop mild myocardial inflammation
* Coxsackie B virus often involved
* Difficult to determine problem
* Treatment : prolonged period of rest (6 months)

Front 298

Atherosclerosis

Back 298

* creating plaque in arteries
* Related to:
* Genetics
* LDL cholesterol
* Triglycerides
* Tobacco
* Lack of exercise and obesity
* Diabetes
* Hypertension
* Older age

Front 299

Angina (angina pectoris)

Back 299

* Pressure, heavy, squeezing, pain in chest
* May radiate into jaw (to L arm)
* Common – nausea, sweating (dizzy), short of breath

Front 300

Angina

* Treatment

Back 300

* Address co‐morbidities (diabetes, high LDL/triglyceride, smoking, obesity etc)
* Maintain low heart rate (beta blocker) – decrease energy requirements by decreasing work
* Prevent clotting (Aspirin, other clot preventers)
* Exercise
* Angioplasty and Stent
* Coronary bypass

Front 301

4 Pillars to Athletic Success

Back 301

* training
* nurturing
* sport psych
* recovery (sleep is the foundation of recovery)

Front 302

Stage 1: When we first fall asleep

Back 302

* Transition from wake to sleep
* Muscles relax, may twitch
* Slow (rolling) eye movements
* 4-5% of sleep time
* Non Rem sleep

Front 303

Stage 2: Most Common Stage

Back 303

* Breathing + heart rate regular
* Body temperature drops
* K-complexes and sleep spindles
* 45-55% of sleep time
* K complex wave: high amplitude waves, signals its the start of the stage of sleep
* Spindle wave: indicative of learning

Front 304

Stage 3: Energy is restored

Back 304

* Tissue grows and repairs
* Hormones are released
* Most occurs in first half of the night
* 15-25% of sleep time
* Most important stage for athletes
* large delta waves

Front 305

Stage 4: Rapid Eye Movement (REM)

Back 305

* Irregular breathing and heart beat
* Muscles are paralyzed
* Most occurs in second half of the night
* 20-25% of sleep time
* low amplitude chin EMG

Front 306

Group Comparison Smokers vs Controls

Back 306

* Smokers:
* irregular pattern, more awakening occurring during the night
* takes them longer to fall asleep (nicotine)
* once they start the quit attempt there is a more similar pattern to control
* smokers take longer to get into N3 and N2
* smokers have longer 1 stage
* smoking negatively affects sleep

Front 307

* 50% if athletes were found to be poor sleepers

Back 307

* Athletes need more sleep
* athletes more susceptible to sleep apnea

Front 308

How do elite athletes compare to a control group?

Back 308

* Sleep quality: athletes more at risk for lower sleep quality
* Sleep disturbances: Athletes outnumber control for every signal reason ( wake up, use bathroom, feel too hot, bad dreams etc) higher risk for athletes
* other self reported sleep parameters: similar between athletes and controls ( time in bed, sleep duration, betimes, wake times)
* morningness/eveningness: controls have normal distribution, athletes lean to morningness
* Evening Types More Likely to Have Sleep Problems for athletes

Front 309

Limitations to PSQI

Back 309

* PSQI not validated in an athlete sample
* No information specific to athletes
* No napping
* No travel
* Difficult to score
* Looks at sleep quality, not sleep disorders
* Does not look at timing of sleep

Front 310

Athlete Sleep Screening Questionnaire (ASSQ)

Back 310

* 15 items, <5 min to complete, global questionnaire
* Designed to flag athletes for sleep problems
* Information specific to athletes
* Evaluates sleep quantity, quality, timing, sleep disordered breathing, and travel disturbance

Front 311

**

Back 311

How satisfies are you with the quality of your sleep

* NT Skate Canada Results: 70% satisfiesdm 30% dissatisfied
* NT FSS Results: 15 minutes or less majority
* WNT Field Hockey Results: have troubles staying asleep… 5-7 sevens is a concern
* NT Golf Results: how often do you take medicine to help you sleep about 15% 1 or twice a week, 85% none

Front 312

Sleep Dose-Response and Attention

Back 312

* the less sleep you have the more lapses in attention

Front 313

Effects of Sleep Extension on Athletic Performance

Back 313

* Baseline period – sleep as normally would 6.7h sleep/night
* Sleep extension period – Be in bed for 10 h 8.5 sleep/night
* showed increase performance in athletes

Front 314

During the recent pas how many hours of sleep did you get at night

Back 314

* NT FSS Results: majority 7-8 hr, still 25% getting less that 6
* NT Golf Results: majority 7-8, 30% getting less than 7
* NT Alpine Results: majority getting above 7 hrs

Front 315

What can naps do?

Back 315

* Heightens alertness
* Increases concentration
* Enhances motor performance
* Boosts mood

Front 316

How should I nap?

Back 316

* Best time: between 1-4 pm
* Best duration for training/competition days: 20 min
* Best duration for days off: 90 min

Front 317

Electronic Devices

Back 317

* Blue light from screens tells brain to wake up
* Reduces melatonin, delays sleep phase, and wakes you up more during night
* Content is exciting
* decreases melatonin and delays sleep phase

Front 318

Why you should eliminate bad light

Back 318

* decrease melatonin
* blue light blocking glasses best
* book vs iPad: difference in brain wave activity… normal delta activity in book,

Front 319

Sleep Interventions During Olympics

Back 319

1. Nighttime sleep extension of +1 hour above sleep need
2. Daily 20 min nap
3. Technology curfew 1 hour before bedtime
4. Blue light blocking glasses

Front 320

Strategy #1: Monitoring Sleep

Back 320

Comprehensive Sleep Screening

* Athlete Sleep Screening Questionnaire
* Set a sleep schedule
* Think in terms of weekly need

Front 321

Strategy #2: Sleep Extension

Back 321

Strategy: Extend sleep/bank sleep as much as possible

* Sleep extension on days off (no more than 1-2h)
* Sleep extension during travel on plane
* Bank sleep 1 week prior to important competition

Front 322

Strategy #3: Nap Everyday

Back 322

* Strategy: Incorporate daily naps into your routine!!!

Front 323

Strategy #4: Eliminate Bad Light

Back 323

* Strategy: Blue blocking glasses 2 h before bed
* Strategy: Technology curfew 1 h before bed
* Install f.lux technology on your computers, phones, etc.
* Strategy: Dim lights 1 h before bed

Front 324

ABCs

Back 324

* A: Airway, Breathing, Circulation
* make sure there is an open Airway
* get oxygen into blood stream and lungs with effective Breathing
* oxygen pumped around body through Circulation
* Cant have C without B and cant have B without A
* *** OPEN AIRWAY IS ABSOLUTE PRIORITY

Front 325

Unconscious, head-injured players

Back 325

* can’t tell you about other symptoms
* treat all as if they all have neck injury
* manual in line stabilization” (MILS) that simply shields and stabilizes the head and neck from accidental movement
* make sure tongue isn't cover air way

Front 326

Distracting Injuries

Back 326

* visually dramatic injury that may distract you from the lifesaving aspects of looking after an injured player such as a brain or neck injury, an obstructed airway or are whether they are breathing normally.
* ex: broken limbs or wounds bleeding

Front 327

DR ABC

Back 327

* Danger: ensure field is safe to approach
* Response: check responsiveness by speaking… if they don't respond lightly touch them… call for help if the don’t respond
* Airway, Breathing, Circulation

Front 328

Manual in-line stabilisation (MILS)

Back 328

* approach from in front for an injured player who may have a head or neck injury.
* using his hands and forearms to cocoon the injured player’s head and neck and make an assessment of DR ABC in greater detail.

Front 329

Management of seizures

Back 329

* Take control.
* Ensure an ambulance is on its way.
* Move all dangerous objects away from the casualty.
* Assess for DR ABC. Provide open airway for casualty until assistance arrives.

Front 330

Who should be treated as having a serious neck injury?

Back 330

* Anyone who is unconscious.
* Anyone with an injury above the collarbone.
* Anyone who has a pain in the neck.
* Anyone who has loss of movement in the arms or legs and/or difficulty breathing.
* Anyone you are unsure about

Front 331

* At rest, most people will breathe around __ breaths per minute

Back 331

15

Front 332

Cyanosis

Back 332

* Lack of oxygen is known as hypoxia and hypoxic people can die.
* central cyanosis is a sign of inadequate oxygen

Front 333

* (pneumothorax).

Back 333

* Rib fractures Can cause bleeding in lung (haemothroax) or puncture lung causing it the collapse (pneumothorax).

Front 334

* haemorrhagic shock).

Back 334

* Not enough blood or fluid in the circulation (most commonly due to bleeding –
* Signs

1. Pale and clammy (not enough blood in circulation).
2. Signs of organs under stress (brain – confusion; lungs - breathing fast).
3. Clues as to where the blood may be (pain in abdomen, chest movement asymmetrical).

Front 335

Neurogenic shock

Back 335

* spinal cord injury interrupting the nerve supply that normally constricts the arteries to support the blood pressure. Hence, they dilate and blood pressure falls (neurogenic shock)
* the skin appears pink and warm, but with evidence of organ dysfunction,

Front 336

* Chest compressions start with __compressions to __ breaths

Back 336

30 - 2

Front 337

* Each minute’s delay in failing to use the AED results in a __% decrease in the chance that it will be successful

Back 337

10