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204-theme 2 -anatomy > T2 l6 :intro to pathophysiology of muscle > Flashcards

T2 l6 :intro to pathophysiology of muscle Flashcards

1
Q

difference between endurance exercise and resistance training

A

endurance: responds to total contractile activity

resistance training: responds to loading and stretch

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2
Q

what are the muscle plasticity adaptations

A
  • structural; size, capillarisation

- contractile properties: fibre type transitions

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3
Q

if the total number of muscle fibres are fixed at birth how do they grow

A

Hypertrophy:
-synthesis of myofilaments

  • addition of sacromeres
  • satellite cell activation
  • angiogenesis & vascularisation
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4
Q

list the effects of endurance exercise

A

fibre diameter

blood supply

mitochondrial content: express an increase in oxidative enzymes

fibres become slower-2x and 2a and type 1 eventually

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5
Q

describe the changes that occur to 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

results in much larger muscles (bulk) and leads to an increase in power

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6
Q

what type of injuries is ice used to reduce

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

what type of injury is heat used to reduce

A

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

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8
Q

describe the class, function and diseases that aspirin can be used on

A

Aspirin is an NSAID:

  • Reduces pain
  • Reduces inflammation

Mechanism:

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

Used for musc-skel pain:

  • Chronic diseases
  • –Osteoarthritis
  • Sports injuries
  • –Combined with ice
  • –Often after exercise
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9
Q

Arachidonic acid and prostaglandins

A

Gastro-intestinal adverse effects of chronic aspirin
Stomach bleeding
Ulcers

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10
Q

what are the 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

what occurs in 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

what is the effect of spaceflight on humans

A
  • Theres a decrease in weight bearing that the muscles have to undertake
  • Humans transition from type 1 to 2A/X fibres
  • decrease in the relative muscle mass- all muscles undergo some atrophy, but predominately weight-bearing muscles
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13
Q

what is the effect of bed rest on muscle

A

transition of type I fibres to type 2a

this causes weight bearing muscle atrophy

  • decrease in muscle protein synthesis
  • myofibrillar breakdown
  • decrease strength due to smaller size
  • loss of type 1 fibres
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14
Q

how do you treat the effect of bed rest

A

Add physiotherapy to prevent contractures.

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15
Q

describe contracture

A

-if limb is immobilised for a long period of time

-process of growth is reversed
sarcomeres are removed in series from myofibrils

-resulting in shortening of muscle called a contracture

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16
Q

describe the multinucleate nature of skeletal muscles

A

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

  • Skeletal muscles are enlarged by:
  • Fibre enlargement
  • Increased vascularisation
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17
Q

how does muscular regeneration occur

A

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

describe myosatellite cells

A

Progenitor cells in muscle

  • Also called “satellite cells”
  • NOT related glial satellite cells

activated by mechanical strain on muscle

activation leads to proliferation and differentiation

19
Q

what are the causes of muscle pain

A

injury
overuse
infections
auto-immune

associated with rhabdomyolysis

20
Q

describe the aetiology of myopathy

A

Muscular weakness due to muscular muscle fibre dysfunction:

  • Cf. neuropathy & neurogenic disorders
  • Failure to contract cause possibly muscle or nerve

can be systemic or familial

21
Q

describe dystrophies

A

Dystrophies: familial, progressive:

  • Stuck in degeneration-regeneration cycle
  • Eventually regenerative ability is lost
22
Q

describe paresis

A

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

Usually referring to a limb

23
Q

describe fasciculations

A

: 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

describe fibrillations

A

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

25
Q

describe rhabdomyolysis

A

Rapid breakdown of skeletal muscle

-Not cardiac muscle, not myocardial infarct

26
Q

is there An organ risk with rhabdo

A

Risk of kidney failure:

  • 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

what is the treatment for rhabdo

A
  • Intravenous fluids (to treat shock)

- possibly haemodialysis, etc

28
Q

what can cause rhabdomyolysis

A
  • Trauma: Crush injury
  • Drugs
  • -adverse effects of: statins or fibrates
  • Hyperthermia
  • Ischaemia to the skeletal muscle
  • -Compartment syndrome, thrombosis
29
Q

what are the signs and symptoms of rhabdo

A

Symptoms & signs (depending on severity):

  • muscle pains
  • vomiting and confusion
  • Dark urine
30
Q

different forms of CPK

A

skeletal muscle CPK isoform is CK-MM

 cardiac muscle CPK isoform is CK-MB
31
Q

what occurs to CPK levels when tissue damage occurs

A

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)
32
Q

how can you use myoglobin as a diagnostic test

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 serum K = cause of rhabdo,
increase K = result of rhabdo

33
Q

how is rigor mortis caused

A

ATP depleted after death

Muscle cell does not resequester Ca2+ into SR
increases 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

34
Q

what occurs in 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

35
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

36
Q

what is the treatment for MG

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

37
Q

what occurs in 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
38
Q

what is 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 (Figure A), motor units are intermingled. During reinnervation, nearby surviving neurons re-innervate the denervated fibres, resulting in clusters (Figure B)

study slide 32

39
Q

what occurs in 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)

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

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

40
Q

what occurs in 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
41
Q

what occurs in 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

42
Q

what sign is associated with Duchenne muscular dystrophy

A

Gowers sign -is a medical sign that indicates weakness of hip and thigh muscles associated with muscular dystrophy. The patient that has to use his hands and arms to “walk” up his own body from a squatting position.

204-theme 2 -anatomy (15 decks)

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