AUTO - B. SKELETAL MUSCLE-COVERED

Question 1

Skeletal muscle

Answer 1

• large cells extend length of muscle (smaller cells fused together, specialised junctions to get calcium into skeletal muscle)
• multiple nuclei
• no gap junctions as don’t need to talk to neighbouring cell and whole cell contracts to move muscle
• myosin and actin
• actin connected to Z lines
• Troponin/tropomyosin complex

Question 2

Cardiac muscle

Answer 2

• small cells so don’t need special junction to get calcium into cell
• single nuclei
• connected by gap junctions to communicate with each other to get unified contraction
• myosin and actin
• actin connected to Z-lines
• Troponin/tropomyosin complex

Question 3

Smooth muscle

Answer 3

• small cells so don’t need special junction to get calcium into cell
• single nuclei
• connected by gap junctions to communicate with each other to get unified contraction
• myosin and actin
• actin connected to dense bodies
• no Troponin/tropomyosin complex

Question 4

what is contraction dependent on in cardiac and skeletal muscle

Answer 4

troponin C - tropomyosin complex
calcium binding to troponin C
confirmation changes in proteins, tropomyosin moves and uncovers actin binding site to allow myosin to bind to actin

*smooth muscle: need phosphorylation of myosin head domain to allow myosin to interact with actin

Question 5

what is a motor unit

Answer 5

• single myelinated axon coming out of axon that can be 1 metre in length
• branches close to targets
• allows 1 motor neurone to control many muscle fibres at 1 time
• nerve fibre ends in neuromuscular junction

Question 6

what factors affect muscle force contraction

Answer 6

• size (cross-sectional area)
• frequency of stimulation (force of contraction increases with increased freq of APs)

*skeletal muscle can’t maintain tension
would get lockjaw (tetanus) - botulinum toxin

Question 7

manipulation of neuromuscular transmission

Answer 7

• neuromuscular blockade (paralysis/muscle relaxation)
• acute procedures: dislocations
• surgery
• cosmetic: botox
• movement disorders: tics
• increases function
• myasthenia graves: muscle weakness due to NMJ dysfunction (autoantibodies against NMJ receptor so can’t activate it as well and get weakness)

Question 8

Non-depolarising NM blockers
nACh-R antagonists
eg - atracurium, vecuronium

Answer 8

• block NM transmission - paralysis
• block post-synaptic nACh receptors
• block = competitive
• 3-5 mins onset, 30+ min duration = good for surgery as prevents transmission and muscle contracting
• not preceded by stimulation ie no contraction
• block antagonised by agents that depolarise muscle membrane or increase ACh release
• block reversed by anticholineesterases (acetylcholine esterase inhibitor)

can overcome antagonism through agonist - ACh
can increase antagonist by preventing break dose of ACh - acetylcholine esterase inhibitor
competes with antagonist

Question 9

Depolarising blockers
nACh-R agonists
ie - mimic ACh/nicotine
eg - suxamethonium, decamethonium

Answer 9

• persistent activation of nACh-R causes inactivation of voltage-gated Na channels
• can no longer open in response to brief depolarisation
• block preceded by muscle twitches
• activate receptor for longer

Question 10

Botox (Botulinum toxin Type A)

Answer 10

• blocks ACh release - paralysis
• produced by clostridium botulinum (part of toxin)
• destroys SNARE proteins involved in vesicular docking and ACh release
• 10 molecules enough to block a synapse
• long-term action
• irons out wrinkles
• tics
• eye twitch
• excessive sweating

Question 11

Myaesthenia gravis

Answer 11

• autoimmune disorder of NM transmission
• autoantibodies against nicotinic ACh-R which decrease activation and lack of contraction in skeletal muscle
• muscle weakness
• inability to prolong muscle contraction
• ptosis = droopy upper eyelid
• increase ACh in end plate
• short-acting anticholineesterase (for diagnosis), Edrophonium
• long-acting anti cholinesterase, Neostigmine, Pyridostigmine