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SEM > Week 3 - Medical and environmental issues > Flashcards

Week 3 - Medical and environmental issues Flashcards

1
Q

What is over training syndrome (aka unexplained underperformance syndrome)

A

A neuroendocrine disorder that may result from the process of overtraining and reflects accumulated fatigue during periods of excessive training with inadequate recovery. Leads to impaired performance.

FOR = Functional overreaching

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2
Q

Precipitating factors to OTS

A

Training:
* Intensive Interval Training
* Large Volume and Monotonous
* Sudden Increases
* Step up in class
* Excessive training load
* Inadequate recovery
* Decreased rest time

Competition stress
* Physical stress
* Glycogen Depletion
* Dehydration
* Psychological stress (monitor POMS)
* Injury or other illness

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3
Q

Symptoms of OTS

A
  • Fatigue, underperformance, heavy muscles,
  • Depression,
  • Sleep disturbance,
  • Frequent minor infections
  • Loss of appetite
  • Increased anxiety and irritability
  • Loss of competitive drive
  • Loss of libido
  • Excessive Sweating ( ?autonomic response catecholamine mediated)

Pattern persists despite 2/52 rest

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4
Q

Signs of OTS

A
  • HR
    Increased resting HR
    Increased HRV BJSM Sept 2008 (Likely too small to be of clinical significance)
    Slow return of HR after exercise
    Decreased maximal HR
    Increased HR at sub maximal loads
  • Postural BP drops
  • Performance decrements
  • Reduced VO2 Max
  • Increase in sub maximal O2 consumption
  • Reduced maximal power output
  • Reduced lactate conc at max work rate
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5
Q

Assessment of the fatigued athlete

A
  • Exclude organic causes
  • Iron deficiency anaemia
  • EIA - exercise induced asthma, quite strict TUE for this
  • Viral infections Monoculeosis Parvo Toxoplasma
  • Diabetes
  • Malabsorption probs
  • Cardiac issues
  • Must not misses (malignancies, cardiac issues, infection Hep A/B HIV, diabetes, pregnancy, post concussion syndrome)
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6
Q

History from a fatigued athlete

A

Usual and related to symptoms described above

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7
Q

Examination of fatigued athlete

A
  • Pulse / BP
  • HS and rhythm / Apex beat
  • Lungs ?PFR / Spirometry
  • Lymphadenopathy
  • Liver / Spleen
  • Thyroid
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8
Q

Investigations in the fatigued athlete

A
  • FBC ESR Ferritin Transferrin Sats, CRP, Us+Es, LFT’s, TFT’s Fasting Gluc
  • Vit B12 / Folate
  • U&E’s
  • Viral Titres EBV CMV etc
  • Lactate profiling??
  • Urinalysis

?CK

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9
Q

What hormonal tests might you test for in the fatigued athlete

A

Adrenaline and cortisol may be raised, lowTestosterone/cortisol ratio

Glutamine

Serotonin, TSH, GH, trytophan

(this is all pretty hypothetical)d

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10
Q

Assessment of psychological changes in athletes

A

POMS (profiling of mood states)  a validated psychological test
* Daily monitoring used in USA swimmers
* Training decreased when mood deteriorated and increased when mood improved
* Decreased incidence of overtraining and burnout

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11
Q

Management of OTS

A
  • Rest (not total )
  • Very low level exercise aids recovery
  • Aerobic even few mins daily
  • Slow increase over 6-12 weeks
  • Programme must be individually designed
  • Best avoid own sport
  • Increase volume before intensity
  • Increase intensity when tolerating 20 mins light exercise Eg 10 second sprints with 3 min recovery
  • Reduce stress
  • Consider antidepressants no evidence for multivits chromium zinc magnesium selenium etc etc etc
  • Beware of performers excelling at 12 weeks

Usually an excellent prognosis

PREVENTION BEST !!!! - Education, good coaching. Non specific - POMS, labs, HR

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12
Q

Discuss cardiac screening

A

Wilsons criteria - is screening appropriate? E.g. important condition, early detectable, early treatment beneficial, intervals for repeating test determined, risks less than benefits, costs balanced against benefits

“Screening debate” – BJSM 2012 (Asptar hospital in Qatar) highlighted differences between USA and Europe where Europe like investigative but USA likes history and examination, eg echo screening no great for HOCM – unlikely to develop – “optics”. Worry about false positives/false negatives.

Screening would include history, exam, ECG, echo, stress test, holter, cardiac MRI/CT angio

History
* FH of cardiac event
* Diabetic hypertensive valvular disease
* Smoker
* Symptoms of chest pain/palpitations/dizziness/SOB/collapse/syncope

Exam (low sensitivity and low specificity)
* Pulse
* BP
* ?murmers, apex beat

ECGs: have low specificity with a high false positive rate, influence of ethnicity on normal athlete ECG variation. Rely on interpretation.

Echo: wall thickness assessment, heterogeneity of wall thickening, septal thickness, diastolic cavity small in most patients with HOCM - may be used in those with suggestive symptoms or wit abnormal ECG

ESC guidelines help with decision making regarding safety of exercise in those with CVD

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13
Q

Discuss SCD

A

SCD over 35 years:
IHD commonest cause
Check FH of premature death
Consider predisposing symptoms and need for screening

In those U35
Hypertrophic cardiomyopathy the most common cause, then coronary anomaly, myocarditis

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14
Q

Discuss HCM (hypertrophic cardiomyopathy)

A

AD inheritance ?genetic testing, with high degree of penetrance
Incidence 1 in 500
Increased prevalence in African Americans

Screening - as above, look for LV hypertrophy (nearly always greater than 15mm)

Symptoms may include chest pain, palpitates, syncope and dyspnoea, inappropriate BP response to exercise
Signs - jerky pulse, double apex beat, fourth heart sound. ESM at left sternal border

Increased risk of death if FH of sudden death, extreme LV wall thickness, predisposition to supra ventricular and ventricular arrhythmias

Echo - hypertrophied non dilated left ventricle with no predisposing cause for LVH, chamber size reduced, impaired diastolic filling

Athletes heart - “Grey zone thickness” between 13 and 15mm, LV cavity >55mm, reduction of LV mass with deconditioning, cardiac MRI would give most detailed.
Change in threshold for “normal” more being referred to cardiology .

Treatment:
* no cure… prevent complications
* B Blockers
* Surgical myomectomy
* Alcohol septal ablation
* ICD devices

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15
Q

Discuss ARVC (Arrhythmogenic right ventricular cardiomyopathy)

A
  • AD pattern of inheritance - strong genetic link to certain parts of Europe (Veneto region north eastern Italy)
  • Develops in early adulthood
  • Genetic defect in “glue”
  • Usually affects small areas of R ventricles
  • Repeat testing of family members - more subtle than HOCM so may notice change overtime
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16
Q

What are exercise recommendations based on?

A

ESC risk score (European society of cardiology)
Low <4%, moderate 4-6%, high >6%
(10 year risk for fatal CVD)

Exercise Recommendations based on:
* Presence of symptoms
* ESC Risk Score
* Presence of resting or inducible LVOT obstruction 9left ventricular outflow tract obstruction)
* BP response to exercise especially hypotension suggesting above
* Presence of resting or inducible arrhythmias (NSVT)

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17
Q

Discuss dilated cardiomyopathy

A
  • Failure of pumping chambers
  • Commonest cause IHD but 50% unknown
  • Excessive alcohol, persistent high BP, valvular heart disease, viral infections, AI disease
  • Possible genetic link in 25%
  • Symptoms include SOB, ankle swelling, dizziness, fatigue and palpitations
  • Medical management
  • Ace inhibitors, diuretics, B blockers, inotropes
  • Specialised pacemakers. Resynchronisation therapy
  • ICD
  • ?Cardiac Transplant –> needed to extend life
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18
Q

Discuss myocarditis

A
  • Inflammation of heart muscle. ?viral, ?SLE, ?drug abuse
    Lymphocytic infiltration with focal necrosis leading to cardiac dysfunction and conduction problems
  • Feverish, flu like, tachycardia
  • Blood tests ECG (non specific ST wave change, may show heart block)and Echo (may show chamber dysfunction)
  • Athletes with fever and tachycardia should not be exercising
  • 75% recover in 2 weeks . 10% go on to develop DCM
19
Q

Discuss premature CAD

A
  • Atherosclerosis
  • Genetic Link
  • High BP Smoking Familial Hypercholesterolaemia
  • ECG, Exercise ECG, CT angiography
  • Interventions aimed at trying to reduce the risk of MI
20
Q

List ion channelopathies

A
  • Long QT syndrome
  • Brugada Syndrome
  • Progressive cardiac Conduction defects
  • Catecholaminergic PVT
  • Short QT syndrome
  • Idiopathic VF
21
Q

Discuss long QT

A
  • 1:2000 genetic testing identify 70%
    >0.44s
  • Most potassium channel defects though some affect sodium channels
  • Great variation in severity
  • Males more likely pre puberty Females adolescence and early adulthood
  • ECG non specific repeated testing exercise ECG and Holter monitoring.
    Can lead to VT incl tornadoes de pointes
  • Provocation testing
  • Drugs to avoid, Avoid hypokalaemia. beta blockers may be used, surgical sympathectomy if this fails.
22
Q

Discuss brugada

A
  • More common men SE Asia
    Commonest cause of SD in young men without underlying cardiac disease
    AD inheritance
  • Abnormal function of sodium channels
  • ECG changes can come and go
  • Genetic testing not useful
  • Avoid medications and fevers
  • ICD
23
Q

Discuss WPW

A
  • Accessory pathway 1:300 to 1:500
  • Rarely inherited
  • Palpitations main symptoms if any
    Commonest tachycardia
  • ECG delta wave, shortened PR interval
  • RF ablation
24
Q

Discuss coronary artery anomalies

A
  • Anomalous coronary origin 1:100
  • Small numbers squashing or kinking during exercise
  • Chest discomfort ,blackouts with exercise
  • Cardiac MRI
  • Surgery can be life saving
25
Q

Discuss MVP

A

5% population many people have trivial degrees of MV regurgitation
* Dizziness, syncope, palpitations, SOB or significant FH
* If none of above criterion met can be cleared for play

26
Q

Discuss MVP

A

5% population many people have trivial degrees of MV regurgitation (ie normal variant)
* Dizziness, syncope, palpitations, SOB or significant FH
* If none of above criterion met can be cleared for play

27
Q

Describe heat gain and what loss

A

Heat gain
* Endogenous production - muscle activity other metabolic processes (so a lot to lose when exercising)
* Exogenous - transfer occurs when environmental conditions exceed body temp

Heat loss
* conduction - water
* convection - rest
* radiation - rest
* evaporation - >35 degrees C only method

Humidity –> rapid increase in core temp, loose ability to appropriately regulate, worse in heavier athletes

28
Q

What is heat stroke

A
  • Metabolic rate function of speed and body mass – bulkier, faster runners more at risk eg 8-21km range
  • Rectal temp 41 degrees and above
  • Asymptomatic rectal temp at 40.5 degrees not uncommon
  • Core temp rises –> cellular damage –> SIRS –> multi organ failure –> death

Rectal temp above 41 degrees

29
Q

Symptoms and signs of heatsroke

A

Nausea, headache, confusion, dizziness, aggression, irrational behaviour, drowsiness,

Altered mental state (confusion -> seizures -> coma), tachycardia, hypotension (note sweating no influence on diagnosis), rectal temp >40

Altered glucose, altered Na, weight change

30
Q

Risk factors for heatstroke

A
  • Men – oestrogen reduces inflammatory response
  • Conditions
  • Febrile illness
  • Dehydration
  • Increasing age
  • Lack fitness
  • Lack sleep or food
  • Obesity
  • Previous episode
  • Skin diseases
  • Clothing
  • Genetics RyR1 and calsequestran

Drugs
* Alcohol
* Amphetamine
* Antihistamine
* Benzodiazepines
* Beta Blockers
* Cocaine
* Diuretics
* Laxatives
* Thyroid agents
* TCA’s

31
Q

Management of heat stroke

A

Rapid cooling to 38 degrees eg ice bath for 5-10 mins (no rationale with going slow)
Note that rectal temp lags core temp (watch for hypothermia)
IV fluids 1-1.5L saline

32
Q

Complications of heatstroke

A

Malignant hyperthermia  rhabdomylosis
MI/pulmonary oedema
Coma/convulsions/stroke
Liver bleeds/ulcers
DIC
Rhabdomylosis
Acute renal failure

33
Q

Discuss exercise associated collapse

A
  • Mainly a drop in BP
  • Postural hypotension
  • Blood pooling in periphery (second heart action stops, splanchnic vein filling)
  • Dehydration unlikely to be factor
  • Rectal temp not high enough

Mx
* Drink glucose 4-8%
* Trendelenberg
* Spontaneous recovery only 10-20 mins

34
Q

Discuss hyponatraemia

A
  • Athlete in an ultra endurance event with an altered conscious state and rectal temp below 41`C must have serum sodium measured
  • Dehydration does not cause unconsciousness till renal failure
  • 50KG athlete run for 10 hours sweating at 1L/hour with no fluids

Signs - altered consciousness, confused, check bracelets and watch straps (tightness), Na <129mmol, 2L-6L overhydrated

Management – catheterise and aim of urine output 500ml/L, NaCL (3-5%) 50-100ml/hr, diuretics, no fluids by mouth, salt containing foods

Consensus is that its due to over drinking >750mls/hour for 4 hours.
Failure to supress ADH
Failure to mobilise osmotically inactive Na stores (Hew Butler et al (2015)

35
Q

Discuss heat acclimatisation

A
  • Earlier onset sweating
    Decreases Na concentration
  • Increased amount sweating
  • Increased dilution sweat
  • Greater peripheral sweating
  • Heat and Humidity training for at least 2 weeks
  • 24 hour exposure
  • Sleep only time for AC
36
Q

Discuss hypothermia

A

Rectal temp < 35, shivering, quickly depletes energy stores, lessens as glycogen stores fall, loss of muscle coordination

37
Q

How is heat loss minimised

A
  • Fat
  • Peripheral vasoconstriction (you don’t vasoconstrict your head - hat!
  • Clothing
  • Curling into a ball body position
  • Minimising movement
38
Q

Effects of hypothermia

A

Cardiovascular:
* Vasoconstriction fluid shift
* Cold diuresis
* Decrease circulatory volume
* Cold myocardium - Decreased HR, J waves, AF, VF
* Warming causes fluid shift

Respiratory
* Hyperventilation
* Heat and water loss
* Bronchospasm
* Increased risk aspiration

Neuromuscular
* Numbness
* Muscle stiffness
* Poor coordination
* Increase in muscle damage

Renal function

Coagulopathies

39
Q

Clinical features hypothermia

A

Mild 33-35 Degrees
* Cold
* Shivering
* Tachycardia
* Urinary urgency
* Incoordination

Moderate 31-32 Degrees
* Apathy
* Decreased shivering
* Weakness and clumsiness
* Slurred speech
* Amnesia
* Dehydration
* Increased coordination issues

Severe < 31 Degrees
* Inappropriate behaviour
* Loss of shivering
* Arrythmias
* Oedema
* Decrease in pulse rate and BP
* Decreased conscious level
* Rigidity

40
Q

Management of hypothermia

A

–> need gentle rewarming (fluid shift risk makes it far more dangerous than rapid cooling in hyperthermia)
* Remove from wet and windy condition
* Core temp
* Insulate
* Nutritional and fluid support
* Assess for frostbite
* Rewarm
* Transfer to medical facility

Methods of Rewarming

Passive
* Clothing
* Covering body
* Penguin affect
* Little value in space blanket

Active (External)
* Hot air
* Water blankets
* Hot packs

Active (Internal)
* EC blood warming ,full bypass,warm IV infusions
* Needs ITU monitoring

Rx Mild
* Remove from cold
* Insulate where possible
* Warm sweet drink
* Heat to torso axilla and groins
* Mild activity if temp>35

Rx Moderate
* Remove from cold
* Insulate
* In Field No active rewarming till temp 34
* In Hospital active rewarming
* Close monitoring of cardiac status

Severe Hypothermia
* Minimal handling as risk of VF
* Quick transfer to hospital (extra-corneal warming)
* May appear dead
* HR can be as low as 6bpm
* Warm and Dead - warming efforts should continue until the body temp exceeds 35 since a person with hypothermia is not “cold and dead” until they are shown to be “warm and dad”

Also note Vfib is a common compilation of treatment for hypothermia esp during rapid re-warming

41
Q

Causes of hypothermia

A
  • Accident or Injury
  • Exhaustion
  • Dehydration
  • Immersion
  • Cyclists and skiers generate own wind chill
42
Q

Specific management immersion hypothermia

A
  • Rapid cooling ensues
  • Remove in horizontal position – avoiding catastrophic drop in BP
  • Temp < 31`C same protocol
  • Temp 32`C and in water < 3 hours rapid rewarming can occur (because they’ve cooled so quickly)
43
Q

Discuss frostbite

A
  • Superficial (skin and sc tissue only)
  • Deep (full skin thickness and deeper layers)
  • Crystallisation of fluids in skin and tissue
  • Peripheral sites (fingers, toes, nose, ears,and cheeks)
  • Skiing postponed if temp lower than -20`C
44
Q

What is athletes heart?

A

An increase in cardiac mass due to systematic training.

“Grey zone thickness” between 13 and 15mm, LV cavity >55mm, reduction of LV mass with deconditioning, cardiac MRI would give most detailed. Change in threshold for “normal” more being referred to cardiology

SEM (17 decks)

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