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BSMS204 Theme 2 Musculoskeletal > 6. Pathophysiology of skeletal muscle > Flashcards

6. Pathophysiology of skeletal muscle Flashcards

1
Q

Plasticity of skeletal muscle: exercise

A

muscle is extremely plastic
adapts to changes in functional demand:

Endurance exercise
Responds to total contractile activity

Resistance training
Responds to loading & stretch

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2
Q

muscle plasticity: adaptations

A

adaptations:

	- structural
	  e. g. size, capillarisation

	- contractile properties
	  e. g. fibre type transitions

adaptability occurs from embryogenesis
into maturity

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3
Q

Structural adaptation

A

total number of muscle fibres fixed at birth:

	- e.g. 200,000 – biceps brachii

muscle growth: hypertrophy

		- synthesis of myofilaments
		- addition of sarcomeres
		- satellite cell activation
		- angiogenesis & vascularisation

some muscles enlarge by between 15-50%

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4
Q

effect of endurance exercise

A

E.g. distance running, cycling or swimming
(low force, high contractile frequencies)

increased:

		- fibre diameter (slight)
		- blood supply (Increased oxidative capacity)
		- mitochondrial content

will express increase in oxidative enzymes
fibres become slower
gradual transformation of type IIX to type IIA (or to type I?)

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5
Q

Non-endurance exercise

A

conversion to type IIX
from type IIA
greater muscle force & strength

increase in type IIX fibre size due to increase in numbers of sarcomeres & myofilaments -> increase in power

results in much larger muscles (bulk)

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6
Q

Ice

A 
To reduce swelling
By reducing perfusion
After an acute injury
Sprain
After exercise in overuse injury
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7
Q

Heat

A

To relax and loosen tissues
Use before activities that irritate chronic injuries
Strain
Increases blood flow

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8
Q

Aspirin and MSK pain

A

Aspirin is an NSAID
Reduces pain
Reduces inflammation

Used for musc-skel pain
Chronic diseases
Osteoarthritis
Sports injuries
Combined with ice
Often after exercise
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9
Q

Mechanism of aspirin

A

Mechanism
Inhibits COX
Reduces synthesis of prostaglandins
Part of arachidonic acid pathway

Arachidonic acid and prostaglandins have many effects
Gastro-intestinal adverse effects of chronic aspirin
Stomach bleeding
Ulcers

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10
Q

Anabolic effects of testosterone

A

Anabolic effects of testosterone:
Increases protein synthesis
Decreases catabolism (by opposing cortisol & glucocorticoids)
Reduces fat: increase BMR, increase differentiation to muscle (rather than fat cells)

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11
Q

Effects of anabolic steroid abuse

A

anabolic steroid abuse - used to increase muscle size and strength

large doses required – leads to damaging side effects (kidney, liver, heart, mood changes)

male – testes atrophy, sterility, baldness

female – breast/uterus atrophy, menstrual changes, facial hair, deepening of voice

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12
Q

Effect of spaceflight

A

Decreased weight-bearing

Humans – transition of type I fibres to type IIA/X fibres

Decreased relative muscle mass - all muscles undergo some atrophy, but predominantly weight-bearing muscles

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13
Q

Effect of bed-rest

A

transition of type I fibres to type IIA

weight-bearing muscle atrophy:

  • Decreased muscle protein synthesis
  • myofibrillar breakdown
  • Decreased strength (due to decreased size)
  • Loss of type I fibres

Treat by resuming minor activity early. Add physiotherapy to prevent contractures.

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14
Q

Contracture

A

if limb immobilised for long periods:

process of growth is reversed
sarcomeres are removed in series from myofibrils
resulting in shortening of muscle called a contracture
patients with paralysed limbs must have physical therapy to prevent contractures occurring

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15
Q

Skeletal muscle cells structure

A

Skeletal muscle cells are multinucleate

They develop as myoblasts which are mononucleate
Then the myoblasts fuse

The nuclei are peripheral

The multinucleate cells do not divide
Mitosis with multiple nuclei usually impossible

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16
Q

What enlardes skeletal muscle

A

Skeletal muscles are enlarged by:
Fibre enlargement
Increased vascularisation

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17
Q

Muscle regeneration

A

During inflammation and degeneration of damaged muscle tissue

previous quiescent myogenic cells, called satellite cells, are activated
These proliferate, differentiate and fuse onto extant fibres
They contribute to forming multinucleate myofibers

18
Q

Myosatellite cells

A 
Progenitor cells in muscle
Also called “satellite cells”
NOT related glial satellite cells
Essential for regeneration & growth
Most are quiescent
Activated by mechanical strain
Activation —> proliferation & differentiation
19
Q

Myalgia

A

Muscle pain
Causes of myalgia:
Injury, overuse, infections, auto-immune

Can by associated with Rhabdomyolysis

20
Q

Myopathy

A

Muscular weakness due to muscular muscle fibre dysfunction
Cf. neuropathy & neurogenic disorders
Failure to contract cause possibly muscle or nerve
Systemic vs. familial
Dystrophies: familial, progressive
Stuck in degeneration-regeneration cycle
Eventually regenerative ability is lost

Myo + pathy = “muscle disease”
Dys + trophy = “incorrect nourishment/growth”

21
Q

Paresis

A

weakness of voluntary movement, or
partial loss of voluntary movement or
impaired movement

Usually referring to a limb

From Greek “to let fall”

22
Q

Involuntary twitches

A

Fasciculations and fibrillations

23
Q

Fasciculations

A

fasciculations : involuntary visible twitches in single motor units (neurogenic), which commonly occur in lower motor neuron diseases such as damage to anterior horn cell bodies characteristic of ALS or polio
clinically appear as brief ripples under the skin

24
Q

Fibrillations

A

fibrillations : involuntary spontaneous contractions of individual muscle fibres (myogenic) invisible to the eye but identified by electromyography

25
Q

Rhabdomyolysis

A

Rapid breakdown of skeletal muscle

Risk of kidney failure

Treatment:
Intravenous fluids (to treat shock)
possibly haemodialysis, etc

26
Q

Why is there risk of kidney failure in rhabdomyolysis

A 
Cellular proteins (esp myoglobin) released into blood can “clog” renal glomeruli
Urine is “tea coloured”, no urine produced 12 hours after injury
Leads to electrolyte changes: hyperkalaemia
27
Q

Causes of rhabdomyolysis

A 
Causes of rhab (ie when cell membrane loses integrity)
Trauma: Crush injury
Drugs
adverse effects of: statins or fibrates
Hyperthermia
Ischaemia to the skeletal muscle
Compartment syndrome, thrombosis
28
Q

rhabdomyolysis symptoms and signs

A

Symptoms & signs (depending on severity)
muscle pains
vomiting and confusion
Dark urine

29
Q

Serum levels CPK: diagnostic

A

Creatine Phosphokinase
CK or CPK abbreviations used interchangeably
The enzyme, not creatine phosphate

distinct forms of CPK found in different tissues

skeletal muscle CPK isoform is CK-MM
cardiac muscle CPK isoform is CK-MB

when tissue damaged and cells lyse there is a release of tissue specific CK from cells into blood
Elevations in CK-MM occur after skeletal muscle trauma or necrosis
muscular dystrophies, polymyositis and rhabdomyolysis
Test = “Total CK” (CK-MM is not a clinical test)

30
Q

Myoglobin: diagnostic

A 
“Buffers O2”
Protein + Haem group
“tea coloured”
In plasma indicates rhabdomyolysis or MI
Can lead to renal failure
Urine tested for myoglobin

Diagnostic: Hyperkalaemia
When muscle cells lyse
They release K+
This increases serum K+

Nb: decrease in serum K = cause of rhabdo,
Increase in K= result of rhabdo

31
Q

Rigor mortis

A

ATP depleted after death
Muscle cell does not resequester Ca2+ into SR
Increase in Cytosolic Ca2+
Ca2+ allows crossbridge cycle contraction
Until ATP & creatine-P run out
W/o ATP -> myosin stops just after power stroke
With myosin still bound to actin
Rigor mortis ends when muscle tissue degrades after 3 days

32
Q

Myasthenia gravis

A

progressive muscle weakness and fatigability
Often starts with eye muscles

Caused by depletion of nAChR

arises as the immune system inappropriately produces auto-antibodies against nAChR

33
Q

Pathophysiology of myasthenia gravis

A

less depolarisation of muscle fibres
many fibres do not reach threshold

repeated stimulation -> neuromuscular fatigue

symptoms include ptosis, diplopia,
with weakness in eyelid and extraocular muscles

proximal muscle weakness

34
Q

MG: treatment and diagnosis

A

AChE inhibitors
Neostigmine
Increase ACh activity at NMJ. ACh released from nerve terminals into synapse not rapidly catabolised but can bind to the remaining AChRs for longer time

Edrophonium (a/k/a tensilon): short-lived AChE inhibitor for diagnosis, temporarily improves symptoms eg ptosis

Other category of treatment is directed at immune system

Thymectomy – reduces symptoms in 70% of patients. Exact mechanism unknown. Rebalance immune system?

use of immunosuppressive drugs e.g. corticosteroids

plasmapheresis = removal of anti AChR antibodies from blood stream

35
Q

Spinal muscular atrophy

A

a/k/a Floppy Baby Syndrome
One of most common genetic causes of infant death
Severity and time of onset can vary greatly

death of lower motor neurons in anterior horn of spine
Muscle atrophy —> hypotonia & muscle weakness
Via apoptosis
Fibre type grouping
Sensory system is spared (b/c not in anterior horn)

Caused by genetic defect 
SMN1 gene
Required for survival of anterior horn neurons
Autosomal recessive
Other genes cause similar syndromes
36
Q

Fibre type grouping

A

During spinal muscular atrophy
Cycles of denervation are followed by collateral reinnervation
surviving axons innervate surrounding fibres
resulting in fibre type grouping
In healthy muscles, motor units are intermingled. During reinnervation, nearby surviving neurons re-innervate the denervated fibres, resulting in clusters

37
Q

Malignant hyperthermia

A

Genetic (rare) susceptibility to gas anaesthetics
Eg sevoflurane

Mutation in RyR means gas anaesthetic -> Ca2+ release
Autosomal Dominant
Channel is susceptible if any of subunits are

Result: SERCA works too hard (to pump Ca back into SR)

increased O2 consumption, increased CO2, acidosis, tachypnea, muscles overheat, the body overheats, muscles are damaged (rhabdomyolysis), hyperkalaemia, muscles become rigid

38
Q

How does malignant hyperthermia occur?

A

Muscle cells open and leak their contents

Plasma CK-MM increases

Kidney failure possible: urine red from myoglobin

dantrolene sodium can stop the abnormal calcium release
Inhibits ryanodine receptor

39
Q

Muscular dystrophies

A 
group of inherited disorders 
 severe and progressive wasting of muscle 
muscle weakness
Due to myopathy, not neuropathy
 waddling gate 
 contractures 
 cardiorespiratory muscle involvement
40
Q

Duchenne muscular dystrophy

A 
x-linked disease
 affects 1:3500 live male births
one third of cases arise spontaneously 
 progressive loss of muscle tissue
 replaced by fibrofatty connective tissue
 Mutation: gene for dystrophin protein

BSMS204 Theme 2 Musculoskeletal (22 decks)

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