T2 L6 Intro to pathophysiology of skeletal muscle Flashcards

(60 cards)

1
Q

What does skeletal muscle respond to in endurance exercise?

A

Total contractile activity

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2
Q

What does skeletal muscle respond to in resistance training?

A

Loading and stretch

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3
Q

How many muscle fibres in biceps brachii?

A

200,000

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4
Q

What happens during hypertrophy in the muscle?

A

Synthesis of myofilaments
Addition of sarcomeres
Satellite cell activation
Angiogenesis and vascularisation

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5
Q

What is angiogenesis?

A

Physiological process through which new blood vessels form from pre-existing vessels

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6
Q

What adaptions to the muscle does endurance exercise cause?

A

Slight increase in fibre diameter
Increased blood supply to increase oxidative capacity
Increase mitochondrial content
Fibres become slower
Gradual transformation of type IIX to type IIA fibres

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7
Q

What adaptions to the muscle does non-endurance exercise cause?

A

Conversion to type IIX from IIA
Increase in numbers of sarcomeres and myofilaments causing an increase in type IIX fibre size leading to increased power
Larger muscles

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8
Q

When should ice be used on a muscle?

A

To reduce swelling by reducing perfusion
After acute injury such as a sprain
After exercise in overuse injury

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9
Q

What is a sprain?

A

Injury to a ligament

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10
Q

When should heat be used on a muscle?

A

To relax & loosen tissues
Use before activities that irritate chronic injuries such as a strain
Increases blood flow

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11
Q

What is a strain?

A

Injury to a muscle or tendon

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12
Q

What can cause a strain?

A

Chronic activities which:

  • develop over-stretching of muscle fibres
  • pulling too far on a muscle
  • pulling a muscle in one direction while it is contracting in the other direction
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13
Q

What is aspirin used for?

A

Musculoskeletal pain
Chronic disease e.g. osteoarthritis
Sports injuries - combined with ice after exercise

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14
Q

What does aspirin do?

A

NSAID

Reduces pain and inflammation

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15
Q

What is the mechanism of aspirin?

A

Inhibits COX which reduces synthesis of prostaglandins

Part of arachidonic acid pathway

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16
Q

What are the risks of aspirin?

A

Gastro-intestinal adverse effects
Stomach bleeding
Ulcers

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17
Q

What are the anabolic effects of testosterone?

A

Increases protein synthesis
Decreases catabolism by opposing cortisol and glucocorticoids
Reduces fat
- increases BMR
- increases differentiation to muscle rather than fat cells

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18
Q

What are the effects of anabolic steroid abuse in males?

A

Testes atrophy
Sterility
Baldness

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19
Q

What are the effects of anabolic steroid abuse in females?

A

Breast / uterus atrophy
Menstrual changes
Facial hair
Deepening of voice

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20
Q

What is the effect of space flight on muscles?

A

Decrease in relative muscle mass (predominantly weight-bearing muscles)
Transition of type I fibres to type IIa/X fibres

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21
Q

What is the effect of bed rest on muscles?

A
Transition of type I fibres to type IIA
Weight-bearing muscle atrophy 
 - decrease muscle protein synthesis
 - myofibrillar breakdown
 - decrease in strength 
 - loss of type I fibres
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22
Q

Why does bed rest have an effect on muscles?

A

Reduces hydrostatic pressure gradient in CVS
Reduces muscle force production
Eliminates compression on bones
Lowers total energy expenditure

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23
Q

Describe the features of type I fibres

A
Slow contraction
Small 
High fatigue resistance
Aerobic activity
Low power
High mitochondrial density
High capillary density
High oxidative capacity
Low glycolytic capacity
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24
Q

Describe the features of type IIA fibres

A
Moderately fast contraction
Medium 
Long-term anaerobic activity
Medium power
High mitochondrial density
Intermediate capillary density
High oxidative capacity
High glycolytic capacity
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25
Describe the features of type IIX fibres
``` Fast Large Short-term anaerobic High power Medium mitochondrial density Low capillary density Intermediate oxidative capacity High glycolytic capacity ```
26
Describe the features of type IIB fibres
``` Very fast contraction Very large Low resistance to fatigue Short-term anaerobic activity Very high power Low mitochondrial density Low capillary density Low oxidative capacity High glycolytic capacity ```
27
How do muscles regenerate during inflammation & degeneration of damaged muscle tissue?
Previous quiescent myogenic cells (satellite cells) are activated Proliferate, differentiate and fuse on extant fibres Contribue to forming multinucleate myofibres
28
What is HGF?
Hepatocyte growth factor | Paracrine cellular factor important in myogenesis and muscle regeneration
29
What is caveolin 1?
Integral membrane protein which is involved in receptor-independent endocytosis
30
What are myosatellite cells?
Progenitor cells in muscles (satellite cells) Essential for regeneration and growth Most are quiescent and activated by mechanical strain to proliferate and differentiate
31
What is myalgia?
Muscle pain
32
What causes myalgia?
Injury Overuse Infections Auto-immune
33
What is myopathy?
Muscular weakness due to muscular muscle fibre dysfunction
34
What is paresis?
Weakness of voluntary movement or partial loss of voluntary movement or impaired movement
35
What are fasciculations?
Involuntary visible twitches in single motor units Commonly occur in motor neuron disease Appear as brief ripples under skin
36
What are fibrillations?
Involuntary spontaneous contractions of individual muscle fibres
37
What is rhabdomyolysis?
Rapid breakdown of skeletal muscle
38
What are the causes of rhabdomyolysis?
``` Trauma Drugs - statins or fibrates Hyperthermia Ischaemia to skeletal muscle - compartment syndrome - thrombosis ```
39
What is compartment syndrome?
Increased pressure within one of body's compartments which contains muscles & nerves
40
What are the symptoms of rhabdomyolysis?
Myalgia Vomiting & confusion Darkened urine
41
Why is there a risk of kidney failure in rhabdomyolysis?
Cellular proteins (especially myoglobin) is released into the blood and clots renal glomeruli Urine becomes tea coloured, no urine production 12h after injury Leads to hyperkalaemia
42
What is the treatment for rhabdomyolysis?
Intravenous fluids to treat shock | Haemodialysis
43
What is the CPK isoform in skeletal muscle?
CK-MM
44
What is the CPK isoform in cardiac muscle?
CK-MB
45
What does myoglobin do?
Buffers O2
46
Why does rigor mortis occur?
ATP is depleted after death Muscle cell doesn't re-sequester Ca2+ in SR leading to increase in cytosolic Ca2+ Ca2+ allows cross-bridge cycle contraction until ATP and creatine-phosphate run out. Without ATP the myosin stops after the power stroke and is still bound to actin
47
When does rigor mortis end?
When muscle tissue degrades after 3 days
48
What is myasthenia gravis?
Progressive muscle weakness and fatiguability | Depletion of nicotinic acetylcholine receptor
49
What are the symptoms of myasthenia gravis?
Ptosis Diplopia Weakness in eyelid and extraoccular muscles Dysphagia
50
What are the treatment options for myasthenia gravis?
``` AChE inhibitors e.g. neostigmine Edrophonium Thymectomy Immunosuppressive drugs Plasmapheresis ```
51
How does neostigmine help myasthenia gravis?
Increases ACh activity at NMJ --> ACh released from nerve terminals into synapse aren't catabolised --> bind to remaining AChR for a long time
52
What is plasmapheresis?
Removal of anti-AChR antibodies from bloodstream
53
What is spinal muscular atrophy?
Floppy baby syndrome | Death of lower motor neurons in anterior horn of spine
54
What causes spinal muscular atrophy?
Genetic defect SMN1 gene Autosomall recessive
55
What is malignant hyperthermia?
Rare genetic susceptibility to gas anaesthetics | Mutation in RyR + gas anaesthetic leads to Ca2+ release
56
Describe the process occurring in malignant hyperthermia
Ca2+ release SERCA works too hard to pump Ca2+ back into SR Increase O2 consumption --> increased CO2 --> acidosis, tachypnoea, muscles & body overheat --> muscles are damaged --> hyperkalaemia --> muscles become rigid
57
What treatment can be used in malignant hyperthermia?
Dantrolene sodium can stop abnormal calcium release by inhibiting ryanodine receptor
58
What are muscular dystrophies?
Group of inherited disorders | Severe and progressive muscle wasting
59
What is Duchenne muscular dystrophy?
Progressive loss of muscle tissue which is replaced by fibrofatty connective tissue Mutation of gene for dystrophin protein X-linked Gower's sign
60
What is Gower's sign?
Patient has to use hands and arms to walk up own body to stand up Indicates weakness of hip and thigh muscles associated with muscular dystrophy