MT Flashcards

1
Q

two main types of studies

A

descriptive (PO)
-survey and qualitative
analytic (PICO and PECO)
-experimental or observational anaytic

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2
Q

what does PICO stand for?

A

patient/problem
intervention
comparison
outcome

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3
Q

how to determine study design

A

Q1: descriptive (PO) or quantifying a relationship (PICO)?
Q2: random allocation? if yes, RCT, if not observational analytic
Q3: observational:
if outcomes determined after intervention: cohort/perspective
if at the same time, cross sectional/survey
if before exposure, case-control/retrospective

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4
Q

randomised control trial

A
comparison study where participants are randomly assigned to treatment/intervention group or control/placebo group
advantages: 
-unbiased distribution of confounders
-blinding more likely
-randomization facilitates statistical analysis
disadvantages:
-expensive (time and money)
-volunteer bias
-can be ethically problematic
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5
Q

crossover design

A

controlled trial where each participant has both therapies (randomized order)
advantages:
-subjects are their own controls and error variance is reduced (smaller sample size needed)
-all subjects receive treatment
-blinding, statistical test assuming randomization
disadvantages
-all subjects receive alternative treatment or placebo at some point
-cannot be used for treatments w/permanent effects

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6
Q

cross-sectional survey

A

-examines relationship b/t diseases and other variables in a population at one particular time
advantages: cheap and simple, ethical
disadvantages
-establishes association at most, not causality
-recall bias susceptibility
-confounders unequally distributed
-group sizes unequal

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7
Q

case-control study

A

compares patient w/a disease to controls and determines which people have been exposed to the factor under investigation
advantages
-quick and cheap
-the only feasible method for rare disorders or long lag time b/t exposure and outcome
disadvantages
-reliance on recall or records to determine exposure
-confounders
-control group selection is difficult

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8
Q

cohort

A

data from groups who have been exposed or not exxposed to new factor (from databases), no allocation of exposure made by experimenter
advantages
-ethically safe
-subjects can be matched
-can establish timing and directional of events
-standardized eligibility and outcome assesment
disadvantages
-controls may be difficult to identify
-exposure may be linked to a hidden confounder
-blinding difficult
-no randmization
-large sample size needed

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9
Q

selection bias

A

error in choosing individuals or groups taking part

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10
Q

measurement bias

A

poorly measuring outcome (calibration)

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11
Q

interviewer bias

A

opinion or predudice or influence of the interviewer, affecting behavior

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12
Q

response bias

A

respondents answer in the way they think the investigator wants them to answer

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13
Q

referral bias

A
  • preferences or local practices influencing recruitment

- eg more severe cases sent to academic centers

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14
Q

reporting bias

A

selective reporting or suppression of information (eg publication bias against negative studies)

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15
Q

sensitivity

A

of all individuals with the condition, the percentage that will test positive (true positives/all cases)
-highly sensitive tests good for ruling things OUT

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16
Q

specificity

A

off all individuals who DO NOT have he condition, the percentage that will test negative
eg true neg/true neg + false pos
-highly specific good for ruling things IN

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17
Q

three symptoms that could contribute to upper respiratory symptoms

A

anemia, anxiety, asthma

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18
Q

what does anemia not effect?

A

saturation %: it’s number of Hb, not number occupied

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19
Q

wheeze

A

strained breathing out

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20
Q

stridor

A

strained breathing in

crackling sound

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21
Q

what’s the difference b/t asthma and exercise induced asthma

A
  • asthma is chronic and brought on by many triggers
  • eg smoke, allergies, exercise could be a trigger, cold air, dry air, cats, mold
  • exercised induced bronchospasm=reaction brought on by exercise
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22
Q

asthma

A

chronic inflammatory disease of airways

-variable and recurring symptoms: reversible airflow obstruction and bronchospasm

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23
Q

EIAB

A

intermittent narrowing of airways + decrease in airflow
-wheezing, chest tightness, coughing, dyspnoea triggered by exercise
in 50-90% of asthmatics

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24
Q

how does transient airway narrowing occur?

A

thickened bronchi lining–>narrower airway

  • expiration relies more on elasticity of chest wall and pressure leads to smaller airway collapse
  • higher Ve leads to more water loss
  • changes in airway –> inflammatory cascade and sm contraction
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25
Q

what is often the first symptom of EIB?

A

poor performance for given level of conditioning

-season and climate related

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26
Q

EIB signs and symptoms

A

wheeze, cough, dyspnoea, chest tightness
for 1-2 hrs after exercise
-chlorine and exhaust are aggravators

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27
Q

EIB test

A

field test: make symptoms occur, then measure lung function

also chemical ways to trigger attack (insensitive)
and osmotic challenge, which causes drying of lungs and mimics exercise

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28
Q

eucapnic voluntary hyperpnea

A

mimic exercise breathing
-breathe in some CO2 so they can breathe at the same rate as heavy level
exercise
-sensitive and specific

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29
Q

treatment for EIB

A
  • ideal activities in warm, humid environment
  • extend warm-up, low to moderate intensity
  • use refractory period (less risk of attack after 1 attack)
  • increase intensity in steps
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30
Q

asthma treatment

A

stabalize w/bronchodilators, corticosteroids

-salbutabol b/f exercise and as rescue medication

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31
Q

what should be considered when EIB treatment fails?

A

vocal chord dysfunction

pulmonary embolism

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32
Q

vocal chord dysfunction

A

paradoxical vocal chord adduction obstructing inspiration

-females and younger patients more common

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33
Q

vocal chord dysfunction signs and symptoms

A

throat tightness, stridor, chest tightness, air hunger, coughing/hoarseness
-often at very high exercise intensity

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34
Q

how is VCD treated?

A

treatment of aggravating factors (eg gerd, post nasal drip) may be enough
-vocal chord resynchronization w/coughing or panting, RMT?
-postural techniques and stress
management

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35
Q

pulmonary embolism

A

rare cause of exertional dyspnoea
axillary vein thrombosis common (more so in elite athletes and throwers) is possible
-clot goes from R side of heart through hole (20% of ppl have it)

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36
Q

thromboembolism risk factors

A

use of elicit substances
ritual dehydration (lightweight, boxers)
effort-induced thrombosis (trauma to vessel wall?)

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37
Q

symptoms of pulmonary embolism

A
  • pain, swelling, numbness in distal limb
  • poor exercise performance
  • profound arterial desaturation during exercise
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38
Q

distinguishing factors of pulmonary embolism

A

no wheeze, stridor, or abnormal spirometry

-affects blood, not lungs

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39
Q

possible adverse effects of pollution

A

cancer, heart disease, stroke

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40
Q

pollution componenets

A

gaseous: ozone, CO, oxides of N
particulate: eg diesel

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41
Q

does increased exercise intensity add to effects of pollution?

A

no, increases in Ve and O2 consumption at low but not high as a result of exposure
no effect on norepinephrine, endothelial function, heart rate variability

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42
Q

concussion considerations

A

short term impact
post concussion syndrome
dementia, parkinsons, depression/suicide
cost to professional sports teams

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43
Q

concussion

A

functional head injury w/symptoms that usually last a short period of time.
acute clinical symptoms reflect functional disturbance, not structural injury
may not involve loss of consciousness

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44
Q

mechanisms of concussion

A

direct blow to head
coup contrecoup
-whiplash motion of head results in axonal shearing and damage to neurons/release of chemicals
-acceleration/decceleration of brain w/in skull

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45
Q

final determination regarding concussion diagnosis

A

based on clinical judgement

  • there are no grades
    1. can’t prove someone has it so certainly can’t prove how severe
    2. initial injury doesn’t correlate to symptoms so grading is even more useless
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46
Q

SCAT assessment

A
  • LOC
  • balance/coordination
  • disorientation or confusion
  • loss of memory
  • blank or vacant look
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47
Q

Maddocks score

A

for sideline assessment

-questions about game + game last week

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48
Q

SCAT 3

A

for further assessment
-involves orientation questions (month/year/time)
concentration task (count digits or months backward)
-memory task (repeat words)
-balance test

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49
Q

when to refer to emergency

A
  • worsening headache
  • very drowsy
  • can’t recognize ppl or places
  • significant nausea/vomitting
  • confusion/irritability
  • seizures
  • weakness in limbs
  • slurred speech or unsteadiness
  • pupils would be UNCHANGED (no swelling or bleeding)
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50
Q

reasons for not returning to sports the same day

A
  1. brain may be in state of neurometabolic crisis, increased energy demand slowing healing
  2. window of vulnerability for second worse injury
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51
Q

how long does concussion recovery take?

A

about 10 days
symptom free w/daily activity before sports
gradual return
-go back one step if symptoms return

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52
Q

how many canadians have pre or type II diabetes

A

9 mil

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53
Q

legacy effect

A

early knowledge and control (being talked to about prevention) usually puts people in a better situation
early control results in fewer complications 10 years later

54
Q

what’s blood sugar for diabetes diagnosis

A

7mmol/L

55
Q

practical advice for reducing diabetes risk

A

150min of exercise/week
5-7% weight loss
-reduces risk by 60%!!!

56
Q

metabolic syndrome

A

elevated waist circumference + any 2 other risk factors (elevated TG, BP, or fasting glucose, reduced HDL)

57
Q

normal values

A

men: <93 waist
women: <79cm waist
BP <130/85
HDL >1 for males, 1.3 for females
glucose <5.6
triglycerides <1.7

58
Q

why is glycated hemoglobin a good measure for prediabetes diagnosis?

A

Hb picks up coating

59
Q

glucose and FFA metabolism in obesity and IR

A

inc. adipose tissue results in increase FFA and FFA oxidation
- ->decreased glucose oxidation and increased gluconeogenesis
- ->insulin resistance

60
Q

beta cell dysfunction

A

overstimulation of cells leads to overproduction of insulin
-glucose desensitization/toxicity
-lipotoxicity
-amyloid deposition
leads to beta cells crapping out and blood sugar skyrocketing
50% are gone at diabetes diagnosis

61
Q

screening recomendations

A

screen ALL ppl over 40 yrs every 3 yrs
-earlier and more w/risk factors
recommend medication if 1 risk factor is present + glucose 5.6-6.9

62
Q

long term diabetes complications

A
  • retinopathy, neuropathy, nephropathy
  • atherosclerosis
  • NAFLD fatty liver/liver cirrhosis
63
Q

short term diabetes complications

A

hypoglycemia, hyperglycemia

comorbidities are hypertension, elevated cholesterol

64
Q

targets for glycemic control

A

pre meal: 4-7 (6 in normal)

2 hours post meal : 5-10 (8 in normal)

65
Q

vascular protection checklist

A
  1. glycemic control
  2. blood pressure control
  3. cholesterol LDL less than 2
  4. drugs to protect heart
  5. exercise/diet
  6. smoking cessation
66
Q

nutrition basics

A
  • more fat from things that grow and less from things w/mothers
  • weight loss with IR is harder b/c it drives hunger
  • NO muffins, chinese takeout, juicing, cheerios
  • double veg
  • plan afternoon snack
67
Q

nutrition starting advice

A
  1. breakfast
  2. where carbs come from + labels
  3. focus on biggest meal
  4. for weight loss: no starch at dinner, plate, food tracking
68
Q

areas for nutritional improvement

A
  1. balanced meals (breakfast lunch and dinner)
  2. fueling need for instant energy
  3. calorie dense foods (muffins, scones, beverages)
  4. eating from bordom/habit/stress
  5. less filling foods (low fiber/bulk)
69
Q

what must the body compensate for at altitude?

A

ambient pressure decreases, so O2 levels and saturation decrease
-50% at everest base camp

70
Q

4 points

A

respiratory: increased frequency and volume
cardiovascular: increased HR and volume and increases BP
haematological: reduced plasma volume–>eventual new blood cells
renal: increased bicarbonate to acidify blood and compensate for mild respiratory alkalosis

71
Q

acute mountain sickness

A

2-12 hours after ascent

  • headache
  • sleep disturbance, insomnia
  • anorexia, nausea, vomiting
  • light-headedness, dizzy
  • fatique
72
Q

AMS Risk factors

A

rate of ascent
exertion
obesity
possible other factors
-previous neck dissection (chemoreceptor damage)
-dehydration: poorer water quality + GI symptoms at altitude + lose water through breathing
-infection-have to melt snow

73
Q

other possible causes of AMS symptoms

A

dehydration, hangover, migraine, overexertion, virus, subarachnoid hemmorhage, CO exposure
*diagnosis of exclusion

74
Q

treatment of AMS

A

stop ascent until symptoms resolve

  • tylenol, rest and rehydrate
  • mod to severe: descent, O2, hyperbaric bag, dexamethasone (lower inflammation), acetaxolamide (doesn’t work)
75
Q

gamow bag

A
simulated descent (1600m)
by inflation
76
Q

high altitude cerebral aedema

A
  • severe end of AMS spectrum

- AMS symptoms + lethargy, confusion, altered LOC

77
Q

HACE treatment

A
descent
O2
hyperbaric bag
drugs
evacuation
78
Q

high altitude pulmonary adema

A
onset 2-5 days
aggravated by cold and exertion
shortness of breath, bloody cough, poor exercise tolerance, tachypnoea
crackles in lungs
may be febrile
low O2 sat
79
Q

HAPE risk factors

A
rate of ascent
exertion
previous history
primary pulmonary hypertension
unilateral pulmonary artery
80
Q

non risk factors for altitude

A
age
gender
fitness
asthma-although other considerations like wood smoke exposure and puffer dysfuntion
hypertension
81
Q

how slowly should people ascend?

A

300-400m/day, rest every 1000m for a day

  • w/adequate hydration and not overexerting themselves
  • avoid alcohol and slow descent if GI symptoms occur
82
Q

acetazolamide

A

carbonic anhydrase inhibitor

  • increase Ve by acidifying blood through kidneys
  • MAY be good for AMS prevention
83
Q

HAPE prevention

A

nifedipine 90% effective for recurrent

salmeterol (2 puffs) 50% effective for recurrent

84
Q

considerations for competing at altitude

A
  • high exertion in low O2 environment-decrease aerobic capacity and poor recovery
  • UV exposure
  • jet lag, disturbed sleep
  • increased breathing, dyspnoea during exercise
  • vaccinations
  • supplements and medication
85
Q

for brief acclimatization

A

-overcome: dehydration and sleep deprivation
reset training intensity
-respiratory and renal acclimatization
-rule out iron-deficiency anemia and other anemia

86
Q

diffuse cerebral edema

A

also secondary-impact syndrome

  • post-concussive symptoms following head injury and then return to play and secondary injury
  • may be fatal
87
Q

skull fracture

A

not always visible

-swelling and tenderness around impact, facial bruising, and bleeding from nose/ears

88
Q

intracranial hemorrhage

A

=accumulation of blood in skull cavity

  • sub, epi (middle meningeal artery) dural (bridging veins) hemmorhage
  • intraventricular hemmorhage
  • or hemmorhagic stroke
89
Q

epidural hematoma

A

may have initial lucidity followed by decline in function

  • may have LOC
  • pupilary reaction changes
90
Q

subdural hematoma

A

more in older adults
symptoms take longer
nausea, headache, vomiting, etc.

91
Q

prevention of head injuries

A
  • head gear
  • technique in contact sports
  • education on concussion and symptoms
92
Q

hyperglycemia symptoms

A
flushed skin
frequent urination
irregular breathing
nausea
drowsiness
fruity breath
93
Q

hypoglycemia

A
hunger
shakiness
nervousness
pallor
cool skin
sleepiness
confusion anxiety
weakness
94
Q

prevention of diabetes emergencies

A
  • wear ID bracelet
  • adhere to meds
  • inform other staff
  • eat regular meals and snacks, hydrate
  • check glucose before and during activities
95
Q

when should a diabetic avoid exercise??

A

if less than 100mg/dL

if greater than 250 w/ketones or 300 w/out

96
Q

treatment of diabetic emergency (hypoglycemia)

A

if conscious: administer CHO high GI, hydrate, monitor

if unconscious-activate EMS, if trained, administer glucagon

97
Q

c-spine suspected

A
  • LOC
  • bilateral neurological findings
  • significant pain along spine
  • obvious deformity
  • stabalize in neutral position and maintain airways
  • manually re-align if treating airway is difficult but NOT if it causes inc. pain, neurological symptoms, or mm spasm
98
Q

what’s the cause of death from head down tackling

A

cervical fx above C4

  • vulnerable in 30deg flexion
  • cause of fx=axial loading
99
Q

exertional sickling

A

SCT associated with sudden death from exertional sickling collapse
**usually in heat

100
Q

sickle cell trait

A

1 copy of the gene is usually benign but may be provoked w/ intense exercise, altitude, or heat
-they usually maintain normal Hb, some are affected

101
Q

sickle cell anemia

A

=two copies of gene
RBC’s get sickled and trapped in spleen
-spleen can’t replace w/ new RBC’s fast enough
–>body becomes anemic

102
Q

sickle cell disease symptoms

A

painful episodes
swelling in hands and feet
joint pain
blood clots

103
Q

prevalence of SCD

A
  • most common inherited blood disorder

- 1 in 12 black people have the trait, 1 in 500 the disease

104
Q

symptoms of exertional sickling collapse

A
  • mm WEAKNESS, not pain, which distinguishes it from heat cramps
  • athletes “slump” to the ground
  • initially communicative (distinguishable from grave cardiac arrhthmia)
  • muscles look and feel normal (unlike locked up from heat cramps)
  • rapid tachypnea from lactic acidosis but good air movement breathing
  • rectal temp less than 103
105
Q

Prevention of SC emergencies

A
  • allow longer rest periods
  • allow exclusion from intense tests or if feeling ill
  • adjust work-rest cycles in heat
  • hydrate and altitude
  • control asthma if applicable
106
Q

exertional heat stroke

A
rectal temp above 104 post collapse
CNS dysfunction
-headache
-confusion
-GI upset
-dehydration, mm cramps
-collapse, staggering
-profuse sweating
-rapid pulse, low BP, rapid breathing
107
Q

exercising in heat

A
  • blood transported to periphery for cooling–>central fluid deficit
  • smaller SV and increased HR for given intensity
  • splachnic vasoconstriction to compensate for blood going to periphery
  • ->leads to GI and kidney issues
108
Q

heat stroke treatment

A
  • remove equipment and excess clothing
  • cool via whole body immersion/towels if not available
  • 911
  • vitals (rectal temp)
  • cease cooling when 101-102
109
Q

RTP after heat stroke

A

after 1 week
longer if more severe
w/clearance and normal lab values and symptoms
graduated return

110
Q

should you exercise w/ a fever?

A

no.
- mm strength and endurance decreased
- fatigue increased
- ability to regulate temp impaired

111
Q

hyponatremia

A

over-hydration

-Na<135mmol/L

112
Q

early signs hyponatremia

A

bloating, puffiness, nausea, vomiting, headache

113
Q

serious hyponatremia signs

A

altered mental status, obtundation, coma, seizures, respiratory distress (PE)
**should be suspected if an athlete collapses where heat is not a factor

114
Q

hyponatremia risk factors

A
  • excessive drinking
  • low body weight
  • female
  • slow performance pace
  • event inexperience
  • NSAID use
115
Q

treatment for hyponatremia

A
  • if severe, 3% hypertonic saline due to risk of cerebral edema
  • if not, salty foods
116
Q

lightning

A
  • are safe to touch and should be moved to safer environment
  • ABCs, CPR and defib if needed
  • then orthopedic, burn, wound, neurological assessments
117
Q

sudden cardiac arrest risks

A
  • personal or family history of heart disease
  • congenital heart defect
  • drugs that affect heart rhythm (cocaine)
  • fever may be (viral infections w/fever may cause myocarditis)
  • history of syncope
118
Q

hypertrophic cardiomyopathy

A
  • ventricle wall thickens
  • may obstruct blood flow and cause disruption of electrical signals
  • may be asymptomatic but have ECG abnormalities
  • in in 500 ppl
119
Q

what would be a more sensitive test for serious heart conditions?

A

ECG

120
Q

Cardiac event symptoms

A
  • unexpected collapse + unresponsive
  • myoclonic jerking may be present
  • occasional breathing may be present (but not normal)
121
Q

Commotio cordis

A

sudden death from direct impact to chest wall that triggers a fatal arrythmia
-happens during vunerable period in cardiac cycle just before T-wave

122
Q

female triad

A
  • disordered eating
  • menstrual dysfunction
  • osteoporosis (influenced by mensstrual halt)
123
Q

amenorrhea causes

A

high levels of growth hormone and cortisol
low levels of insulin and leptin
primary (delayed getting period) and 2ndary(stops for 3 mo)

124
Q

functional hypothalamic amenorrhea

A

loss of period from lack of energy

-supression of ovarian response w/out a identifiable anatomic or organic cause

125
Q

what effect do leptin levels have?

A

levels the GnRH pulse further

126
Q

what is estrogen’s function in terms of bone health?

A

protects from bone reabsorbtion (osteoblast-clast)

127
Q

osteopenia

A

reduced bone mass

128
Q

osteoporosis

A

brittle bones from tissue loss, more severe

129
Q

screening for triad

A

if one is present, look for other two (especially diet)

  • examine for bradycardia, hypotension, hypothermia
  • signs of disordered eating (ie decaying enamal)
  • palpate (stress fx common on spine and shins)
130
Q

what (besides eat more, train less) can be part of triad treatment?

A

Vit D/Ca2+ supplimentaion
-hormones
leptin injections