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Body Logistics Revision > 10 - Muscle Diseases > Flashcards

10 - Muscle Diseases Flashcards

1
Q

True or false, smooth muscle does not contain troponins

A

True

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2
Q

How do cardiac and smooth muscle cells behave as a syncytium?

A

Network of electrically connected cells (gap junctions) allows for waves of contraction

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3
Q

What nerve provides parasympathetic supply to the heart?

A

Vagus nerve

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4
Q

What nerve provides sympathetic supply to the heart?

A

Cardiac nerve

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5
Q

Describe excitation-contraction coupling in cardiac muscle.

A
  1. Action potential carried along sarcolemma and into T-tubule
  2. Depolarisation activates DHP receptor (L-type Ca2+ channel)
  3. Ca2+ enters the cell and stimulates opening of ryanodine receptors on SR membrane, releasing Ca2+ from SR
  4. Free calcium binds to troponin C, which induces a conformation change that takes troponin I away from the myosin binding site on actin
  5. Sliding filaments can now initiate cross-bridge cycling
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6
Q

How is calcium removed from the cytoplasm when a muscle cell needs to stop contraction?

A

Calcium removed from cytoplasm by plasma membrane transporters:

  • PMCA - plasma membrane Ca2+ ATPase
  • NCX - Na+/Ca2+ exchanger

Calcium stored in SR via transporter in SR membrane:
- SERCA - S/ER Ca2+ ATPase

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7
Q

Describe excitation-contraction coupling in smooth muscle.

A
  1. Ca2+ enters through plasma membrane channels in caveoli
  2. Ca2+ release from SR by CICR and by IP3 receptor activation (Gq pathway)
  3. Calcium binds to calmodulin (CaM)
  4. Ca2+-CaM complex activates myosin light chain kinase (MLCK)
  5. MLCK phosphorylates the myosin light chains, increasing ATPase activity
  6. Rate of crossbridge cycling increases
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8
Q

Skeletal muscles are innervated at the ……………… ………………., where vesicles of ………………………. are released.

A

Neuromuscular junction

Acetylcholine

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9
Q

What is a motor unit?

A

A motor neurone and all the muscle fibres it innervates.

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10
Q

How does the number of fibres per motor unit differ depending on the function of the muscle?

A

Less fibres per motor unit allows for more fine and coordinated control (e.g. ocular muscles)

More fibres per motor unit allows broader, powerful movements (e.g. calf muscle)

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11
Q

Describe excitation-contraction coupling in skeletal muscle.

A
  1. ACh release into NMJ cleft causes local depolarisation of sarcolemma
  2. Voltage-gated Na+ channels open, Na+ enters the cell
  3. Depolarisation spreads down the T tubules and activates voltage sensors in the membrane (DHP receptors)
  4. RYRs in the SR membrane are mechanically coupled to activation of DHPRs and release Ca2+ into the sarcoplasm
  5. Ca2+ binds to TnC to initiate contraction
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12
Q

What is the difference between skeletal and cardiac excitation-contraction coupling in terms of calcium release mechanism?

A

Skeletal:

  • DHP receptors and RYR are mechanically coupled
  • Depolarisation induces charge movement and a conformational change in DHP that unblocks RYR

Cardiac:

  • DHP and RYR receptors interact via calcium-induced calcium release
  • DHP allows Ca2+ influx which activates RYRs for Ca2+ efflux from SR
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13
Q

What is myasthenia gravis? What changes are seen to the NMJ?

A

An autoimmune condition where antibodies are directed against the ACh receptors

  • Invaginations (T-tubules) are reduced or absent
  • Synaptic transmission reduced
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14
Q

Ptosis is a sign of myasthenia gravis. What is it?

A

Drooping/falling of the upper eyelid

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15
Q

A single myosin molecule contains how many fibres?

How many myosin heads does it have?

A

A single molecule consists of 2 fibres.

There are 4 heads, 2 at each end.

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16
Q

What is the structure of a thick filament

A

Each thick filament consists of many myosin molecules, with heads protruding along the whole length.

17
Q

What is the structure of actin?

A

Globular actin (G-actin) monomers polymerise to form fibrous actin (F-actin)

2 F-actin molecules wind together in a helix to form an actin filament

18
Q

What is the significance of the + and - ends of the actin filament?

A

Actin has a + and - end from the polarity of the G-actin monomers making up the chain

This determines the direction of travel of myosin heads along the molecule

19
Q

What molecules form the thin filament?

A
  • Actin
  • Tropomyosin
  • Troponin (I, C & T)
20
Q

Where are tropomyosin and troponin found?

A
  • Tropomyosin coils around the actin helix, reinforcing it

- A troponin complex is attached to each tropomyosin molecule

21
Q

What effect does increasing Ca2+ have on tropomyosin and troponin?

A
  1. Ca2+ binds to TnC, which moves TnI away
  2. This conformational change moves tropomyosin out of the myosin binding site on actin
  3. Myosin heads now bind to actin
22
Q

How are muscles compartmentalised?

A
  • Muscles with similar actions are grouped into compartments

- Surrounded by thick, dense fascia

23
Q

What is compartment syndrome? What are the signs/symptoms?

A

Trauma in one muscle compartment can cause internal bleeding and put pressure on blood vessels and nerves

  • Deep, poorly-localised pain
  • Paresthesia (altered sensation)
  • Tense/firm compartment
  • Swollen, shiny skin (sometimes bruising)
  • Prolonged capillary refill
24
Q

How can compartment syndrome be treated?

A

Fasciotomy to release the pressure

Subsequently needs to be covered by a skin graft

25
Q

What is muscle tone? How is it regulated?

A
  • Tension in a muscle at rest - healthy muscles are never fully relaxed
  • Makes muscles ready to react

Regulated by:

  • Motor neurone activity
  • Muscle elasticity
  • Use
  • Gravity
26
Q

How long does it take to replace the contractile proteins in muscle remodelling?

A

2 weeks

27
Q

How does muscle hypertrophy occur?

A
  • New muscle fibrils are produced - arise from mesenchymal stem cells
  • New sarcomeres added in the middle of existing sarcomeres
28
Q

How is muscle overstretching defined in terms of the sarcomere?

A

When the A band and I band no longer engage - i.e. actin and myosin no longer overlap

29
Q

What causes muscle atrophy?

A
  • Disuse (e.g. bed rest, immobilisation)
  • Surgery (e.g. denervation of muscle)
  • Disease (e.g. muscular dystrophies)

Loss of protein –> reduced fibre diameter

30
Q

What is Duchenne Muscular Dystrophy (DMD)?

A
  • X-linked recessive mutation in the dystrophin gene

- Muscle cells are replaced by adipose tissue

31
Q

In DMD, what does the absence of dystrophin do?

A
  • Excess calcium can enter the cell
  • Calcium taken up by mitochondria and water taken with it
  • Mitochondria burst
  • Muscle cells burst (rhabdomyolysis)
32
Q

What is rhabdomyolysis? What can be detected in the blood as a result?

A

Muscle cell bursting (seen in DMD)

Can detect creatine kinase (CK) and myoglobin in the blood

33
Q

What is creatine kinase?

A
  • An important enzyme in metabolically active tissues (e.g. muscle)
  • Released into the blood by damage to the muscle or brain
  • Formerly used to diagnose heart attacks
34
Q

CK assays were formerly used to diagnose heart attacks. What is now used as a marker for cardiac damage?

A

Troponin I & T (as cardiac muscle has specific isoforms of these)

  • Released from ischaemic cardiac muscle within one hour
  • Quantity of troponin is not always proportional to the size of the infarct
35
Q

What effect does botulinum toxin (botox) have on skeletal muscle?

A
  • Blocks neurotransmitter release at NMJ
  • Causes a non-contractile state
  • Clinical use - treat muscle spasms
  • Cosmetic use - wrinkles
36
Q

What effect does organophosphate (pesticide) poisoning have on the neuromuscular junction?

A
  • Inhibits ACh esterase
  • ACh activity is potentiated
  • Leads to multiple different signs and symptoms, both somatic and autonomic
37
Q

What are the signs and symptoms of organophosphate poisoning from MUSCARINIC receptors?

A 
S - Salivation
L - Lacrimation
U - Urination
D - Defecation
G - GI cramping
E - Emesis
38
Q

What are the signs and symptoms of organophosphate poisoning from NICOTINIC receptors?

A 
M - Muscle cramps
T - Tachycardia
W - Weakness
T - Twitching
F - Fasciculations (muscle flickering)

Body Logistics Revision (25 decks)

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