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Unit 14 > Tevald: MSK changes and respiration with SCI > Flashcards

Tevald: MSK changes and respiration with SCI Flashcards

1
Q

Diaphysis is made of what kind of bone?

A

cortical which is hard

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2
Q

Epiphysis is made of what kind of bone?

A

trabecular/cancellous/spongey

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3
Q

What happens to bone with SCI
Epiphysis ?
Diaphysis?
Spine?

A

Epiphysis: BMD loss

Diaphysis: thinning of the cortex from the inside

Spine: BMD stays the same because they’re still able to load through it

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4
Q

Does bone stiffness increase or decrease at the dipahysis with SCI?

A

decrease it thins from the inside out.

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5
Q

two phases of the bone getting weaker

what % per month initially?

What % overall?

A

1) initial rapid decline in the first 2 years. 2-4% per month during this phase
2) persistent decline over decades. 60% decline overall

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6
Q

_____ fold increase in risk of fracture compared to age matched norms for able bodied individuals

A

5-23

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7
Q

Cumulative fracture rate for SCI?

What does it mean and what %

A

Number of fractures by the number of people across time

> 40%

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8
Q

What is the big deal with weak bone?

A

risk of fractures with minimal trauma

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9
Q

What are the most commonly fractured bones?

A

distal femur, proximal tibia, ankle

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10
Q

What is a risk for skin breakdown with fractures for SCI that is not a concern in able bodied individuals

A

casts on an insensate body part

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11
Q

Resorption and formation of bone with SCI. And what is the catalyst?

A

Resorption&raquo_space;> formation and this occurs because there is no loading going on!

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12
Q

osteoclast resorption or formation?

A

resorption = breaking down

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13
Q

Two things that happen to muscle after SCI

A

1) atrophy

2) fat and CT infiltration

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14
Q

CSA of muscles with SCI

A

goes way down over 25 week period, and its possible that acutely its even more, the study we looked at took data 6 weeks after injury

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15
Q

name positive and negative regulators of muscle

A

+ regulators: growth factors, anabolic horomones, mTORC1. These are DECREASED

  • regulators: inflammation, protein breakdown FoxO. These are INCREASED
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16
Q

Type one vs. type two fibers

Kind of activity and fatiguability

A

Type one: endurance, fatigue resistant, running

Type two: power, quick movements

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17
Q

what is the fiber type change in muscle post SCI?

Consequences of this?

A

type one –> type two; muscles start forming cross bridges more rapidly, it takes a lot higher frequency to get a fully fused tetanic contraction/the amount of torque

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18
Q

Does type one or type two fibers need a higher frequency for tetanic contractions?

why do we care?

Implications for practice?

A

type two

We care: after SCI muscle fiber type changes from type one to type two therefore cross bridges are forming more rapidly and it takes a higher frequency to get a tetanic contraction.

implications for practice: you have to set the stimulator at a higher frequency to get the same % of peak torque/relative force

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19
Q

Muscle fatiguability with stimulation post SCI vs. control

A

the control didn’t even have a 10% drop in force

The SCI had a crazy drop in force

MUSCLE BECOMES MORE FATIGUABLE.

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20
Q

T2 weighted image what color is water? What does water suggest?

A

T2 weighted image water is white and suggests inflammation

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21
Q

Describe control vs. SCI T2 weighted images 72 hrs post activation?

A

control looks about the same at baseline, only a little white suggesting inflammation

SCI looks very bright, inflammation stemming from contraction induced muscle damage.

22
Q

What do the T2 weighed images of the muscles 72 hours post tell us about SCI muscles?

A

there is prolonged force loss and damage (1/4 of individuals after 72 hours)

23
Q

What are the three factors of total energy expenditure and what is compromised in SCI

A

total energy expenditure = resting + PA + diet

In SCI resting (due to muscle atrophy) and PA is influenced

24
Q

How do muscle changes in SCI affect how we think about treatment if a cure for SCI was developed

A

they still wouldn’t be good candidates because their muscles have already undergone physiologic changes

25
Q

how do muscle changes with SCI affect use of FES

A

higher frequency needed to get same contraction. This may cause muscle damage and fatiguability

26
Q

Why do we care about energy expenditure in SCI population?

A

Energy balance is off, energy in is the same, energy out is decreasing leading to an increase in adiposity

27
Q

Increase in adiposity leads to what two things?

A

1) intramuscular adipose tissue doubles

2) increase in visceral adipose tissue

28
Q

risk of overweight/obesity in CHRONIC SCI population?

A

66%

29
Q

BMI for assessing obesity in SCI population?

How do “normal” BMI and fat mass correlate?

A

no! grossly underestimates obesity

BMI and fat mass correlation: poor! half of those with “normal” BMI had 30% fat mass which is over the 20% to be qualified as obese

30
Q

what is the gold standard for assessing obesity in SCI population

A

DEXA looking at fat mass >20%

31
Q

Looking at waist dircumference with assessing obesity in SCI?

A

underestimates again bc they have a greater visceral adiposity

32
Q

Suggested SCI specific obesity cutoff for BMI? (if you’re going to use it even though its not great)

A

≥ 22 kg/m2

33
Q

Describe glucose, insulin action leading to what with gluconeogenesis in response to increased adiposity.

All leading to _______

A

decreased glucose uptake into liver and muscle

decrease insulin action leading to increased gluconeogenesis in the liver

All leading to hyperglycemia

34
Q

What two things bring about diabetes

A

hyperglycemia

insulin resistance

35
Q

Insulin resistance % in chronic SCI

A

60%

36
Q

Diabetes % in chronic SCI

A

50%

37
Q

Metabolic syndrome % in chronic SCI

A

55%

38
Q

Metabolic syndome leads to what overall disease?

A

CVD

39
Q

Risk of CAD in paraplegia

A

70% higher

40
Q

____ fold risk of cerebrovascular disease in tetraplegia

A

5 fold

41
Q

What is the primary cause of death in chronic SCI

A

CV disease!

42
Q

What are three out of the four risk factors of metabolic syndrome that SCI individuals undergo?

A

Abdominal obesity, dylipidemia, hyperlglycemia

the other is HTN

43
Q

Describe

  • how much compression load to the bone was dosed
  • the findings of the long term boot NMES trial.
  • Big picture
A

Compression to the bone =1.5xBW

a lot more trabecular bone in the trained limb 31% increase at distal tibia.

By loading muscle they were able to load the bone. Appropriately dosed NMES can reverse bone loss.

44
Q

What can NMES do

A 
reverse bone loss
increase muscle size
reduce fatiguability 
- preventing loss in acute injury 
- reversing loss in chronic injury
Reverse fiber type shift
Improve metabolic profile
45
Q

Explain the findings of the knee extension protocol and CSA of the muscle

A

increase in muscle CSA at 6 weeks and 6 months (up to 37%)

46
Q

NMES reducing fatiguability what protocol was used and what outcome were they looking at to look at fatiguability?

What did they find?

A

boot protocol

they were looking at the endurance of the muscle

NMES can prevent the loss of endurance in acute SCI

NMES can recovery the loss of endurance in chronic SCI

47
Q

FES cycling can what in terms of muscle changes?

fiber changes?
thigh muscle mass?
VO2?

A

reduce fiber type shift

increase thigh muscle mass

increase in VO2

48
Q

After 10 weeks of FES cycling how did the metabolic profile of the muscles change, two things

A

Increase in lean muscle mass

Decrease in inflammatory markers

49
Q

Glucose control post FES cycling?

Insulin sensitivity?

A

Better glucose control, better insulin sensitivity

50
Q

in 8 week FES cycling literature what was used to categorize people in to normal, DM and insulin resisstance?

What happened after training

A

glucose tolerance

After training: None had DM, fewer were in the insulin resistance, majority were normal

Unit 14 (6 decks)

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