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204 anatomy > pathophysiology of skeletal muscles > Flashcards

pathophysiology of skeletal muscles Flashcards

1
Q

what does endurance excercise respond to?

A

contractile activity

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2
Q

what does resistance training respond to?

A

loading and stretch

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3
Q

what changes occur during hypertrophy?

A
  • synthesis of myofilaments - addition of sarcomeres - satellite cell activation angiogenisis and vascularisation
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4
Q

what happens to physiology of muscles because of endurance exercise?

A
  • increased fibre diameter - increase blood supply - increase in mitochondria - increase expression of oxidative enzymes - fibres become slower- gradual transformation from type 2 fast twitch to type 1 slow switch (iiX->iiA)
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5
Q

what happens to the physiology of muscles in response to non endurance exercise (like weights)?

A

coversion to type 1 fibres from type 2 (iiA->iix) iix fibres increase because there is an increase in the number of sarcomeres and myofilaments

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6
Q

why do we heat before exercise?

A
  • to relax and losen tissue before activitities that irritate chronic injuries - increases blood flow - all preventing strain
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7
Q

what are the effects of anabolic steroids?

A
  • increases protein synthesis - decreases catabolism by opposing cortisol and glucocorticoids - reduces fat BUT abuse= increase muscle size and strength - can also cause male testicular atrophy
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8
Q

what happens to physiology of muscles in space?

A

muscles atrophy because there is decreased weight bearing muscle fibres transition from type 1 slow switch to type 2 fast twitch

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9
Q

what are the effects of bed rest on muscle physiology?

A
  • type 1 slow twitch fibres transition to type 2A - weight bearing muscles atrophy and there is a decrease in stretch because the length of the fibres is reduced
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10
Q

what is contracture?

A

if a limb is imobilised for a long period of time the growth process will be reversed sarcomeres will be removed in series from myofibrils this will cause shortening of the limb (contracture)

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11
Q

can skeletal muscles divide?

A

no- they are only enlarged by fibre enlargement and vascularisation

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12
Q

describe the nuclei of skeletal muscles

A

multinucleated

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13
Q

what is the role of myosatellite cells?

A
  • progenitor cells in the muscle - essential for regeneration and growth - most are quiecent, but activated by mechanical strain
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14
Q

what is myalgia?

A

muscle pain can be due to injury, overuse, infection and auto-immune disease can also be associated with rhabdomyolysis

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15
Q

what is myopathy?

A

muscular weakness due to muscle fibre dysfunction- can be due to neuropathy or neural disorders

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16
Q

what is muscular dystrophy?

A

can be familial or progressive stuck in degenratiion- regeneration cycle eventually regenerative ability is lost

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17
Q

what is paresis?

A

weakness of voluntary movement, or

partial loss of voluntary movement or

impaired movement

Usually referring to a limb

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18
Q

what are fasiculations?

A
  • involuntary visible twitches in single motor units (neurogenic), - commonly occur in lower motor neuron diseases such as damage to anterior horn cell bodies
  • characteristic of ALS or polio
19
Q

what are fibrilations?

A

involuntary spontaneous contractions of individual muscle fibres (myogenic)

invisible to the eye but identified by electromyography

20
Q

what is rhabdomyolysis?

A

rapid breakdown of skeletal muscle not cardio- releases myoglobin into the blood

this clogs renal glomeruli

and leads to electrolyte changes such as hyperkalaemia

urine is tea coloured and no urine is produced for 12 hours

21
Q

what is the treatment for rhabdomyolysis?

A
  • IV fluid to treat shock
  • haemodyalisis
22
Q

what are causes of rhabdomyolysis?

A
  • trauma- crush injury
  • drugs- statins or fibrates
  • hyperthermia
  • ischaemia of skeletal muscles- compartment syndrome or thrombosis
23
Q

what are signs and symptoms of rhabdomylolysis?

A

muscle pains

vomiting

confusion

dark urine

24
Q

what are the different isoforms of creatinine phosphate kinase CPK?

A

skeletal muscle- ck-MM

cardiac muscle- CK-MB

25
Q

what does elevated CK-MM mean?

A
  • probs after skeletal trauma or necrosis
  • could mean patient has….

muscular dystrophies, polymyositis and rhabdomyolysis

§Test = “Total CK” (CK-MM is not a clinical test)

26
Q

what is the role of k+ in the cause and result of rhabdomyolysis?

A

decrease serum K = cause of rhabdo,

increase K = result of rhabdo- when musces lyse they release K

27
Q
A
28
Q

why do you get rigor mortis when you die?

A

ATP depleted after death

Muscle cell does not resequester Ca2+ into SR

raised Ca2+ allows crossbridge cycle contraction

W/o ATP à myosin stops just after power stroke With myosin still bound to actin

Rigor mortis ends when muscle tissue degrades after 3 days

29
Q

what causes myasthesia gravis

A

immune system innappropiately produces anti acetyl choline receptor antibody (autoantibody)

30
Q

what are signs and symptoms of myasthenia gravis?

A

progressive muscle weakness and fatigueability- ussually starting in one eye

repeated stimulation à neuromuscular fatigue

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

proximal muscle weakness

31
Q
  • treatments for myasthenia gravis?
A

- Ache inhibitors

  • Neostigmine-* Increase ACh activity at NMJ. ACh 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

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

32
Q

what is muscular dystrophy?

A

a group of disorders that cause severe and progressive muscle wasting

is due to myopathy and not neuropathy

33
Q

what are 3 things involved in muscular distrophy?

A
  1. waddling gate
  2. contractures
  3. cardiorespiratory muscle involvement
34
Q

what gene is mutated in duchene muscular distrophy?

A

dystrophin dene

35
Q

how do you get duchennes muscular dystrophy?

A

either inherit x linked- so occurs in males

results in progressive loss of muscle tissue, which is replaced by fibrofatty connective tissue

sufferes will have grower’s sign

36
Q

what is SMA?

A
  • Floppy baby syndrome- most common cause of infant death
  • death of lower motor neurons in anterior horn of the spine

muscle atrophy-> hypotonia

37
Q

what is malignant hyperthermia

A

Genetic (rare) susceptibility to gas anaesthetics

Eg sevoflurane

38
Q

which gene is affected in SMA?

A

SNM1 gene whic is required for the survival of anterior horn neurons

inheritence is autosomal recessive

39
Q

what is the genetics of malignant hyperthermia?

A
40
Q

what is the gene involved in malignant hypethermia?

A

autosomal dominant RYR mutation;

results in release of ca2+ in response to anasthetics

SERCA works too hard to pump ca back into the SR

there is increased oxygen consumption, increased co2 production, causing acidosis.

patient becomes tachypnaeic in response and the muscles overheat, once they overheat the muscles become damadged (rhabdomylosis)- resulting in hyperkalaemia. muscles also become rigid

41
Q

what tests suggest malignant hyperthermia?

A
  • raised CKMM
  • kidney failure possible- red urine becasue myoglobin in urine
  • can also get hyperkalaemia
  • EC coupling becuase muscles go rigid
42
Q

what is given to treat malignant hyperthermia?

A

daltrolene sodium- stops abnormal calcium release by inhibiting the ryanodine receptor on the SER

43
Q

Why do you do a biopsy if you suspect SMA?

A

if have spina muscular atrophy- SMA denervation is followed by collateral reinnervation

surviving axons innervate surrounding fibres

and this results in fibre type grouping- which can be seen from biopsy and staining

204 anatomy (11 decks)

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