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Integrated Physiology and Pharmacology > Muscles > Flashcards

Muscles Flashcards

1
Q

Describe the sliding filament theory

A

Contraction of muscles is caused by the myosin heads pulling on the actin filaments which reduces the size of the sarcomere
It is dependent on the rise of intracellular calcium as calcium allows cross-bridge formation
The muscle action potential controls intracellular calcium

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2
Q

What is the motor unit?

A

The motor neuron and the muscle fibre it innervates

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3
Q

Integration and regulation of muscles is dependent on what?

A

The number of motor units and the number of muscle fibres it innervates

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4
Q

What type of receptors are the nicotinic Ach receptors?

A

Non- selective ligand-gated cation channels

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5
Q

What is the Nernst potential of nicotinic Ach receptors?

A

0mV - they are permeable to both Na and K

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6
Q

Describe the structure of the nicotinic Ach recetor

A

It is a pentameric structure (5 sub units) of 4 different types of subunits- alpha, gamma, beta and delta
There are two alpha subunits, and 1 of each other type
The binding sites for Ach are between alpha-gamma and alpha-delta
Two Ach receptors have to bind for the channel to open

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7
Q

What are the different types of Nicotinic Ach Receptors (CHRNA/ CHRNAB) and where are the found?

A

CHRNA 1 to 9 have alpha subunit variations
1 is found in skeletal muscle
2 to 8 are found in neuronal tissue
CHRNB 1 to 4 have beta subunit variations
1 is found in skeletal muscle
2 to 4 found in neuronal tissue

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8
Q

What is Myasthenia Gravis?

A

An autoimmune disease where antibodies are produced against Ach receptors on the postsynaptic membrane of neuromuscular junctions causing them to be blocked and causing a reduction in their numbers
Patients show a weakness in their skeletal muscle

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9
Q

What is the risk of Myasthenia Gravis with respect to men and women?

A

Women have a risk in their 30s whereas men have a bigger risk in their 60s/70s

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10
Q

Describe to pieces of evidence that show antibodies are involved in Myasthenia Gravis

A

1) Normal individuals have fewer antibodies but 87% of patients with the disease test positive for the antibodies
2) Mice injected with antibodies for Ach receptors have weak skeletal muscle and fewer firing of action potentials compared to the control

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11
Q

How can acetylcholinesterases treat Myasthenia Gravis?

A

Used for mild cases, they prevent the break down of Ach so enhance levels in the synpase, eg Pyridastigmine

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12
Q

How can corticosteroids treat Myasthenia Gravis?

A

Used in moderate to severe cases they are an immunosuprresant which reduces the patient’s levels of antibodies, eg prednistolone

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13
Q

How can IV immunogoblins treat Myasthenia Gravis?

A

In severe cases patients are given 400mg/kg for five days, which mops up the extra antibodies, reducing levels

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14
Q

How can plasmapheresis treat Myasthenia Gravis?

A

This is used when acute intervention is required ie in life threatening situations, it is similar to dialysis; it filters out antibodies from the plasma in a process called immunoadsortpion

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15
Q

How can a thymectomy treat Myasthenia Gravis?

A

The removal of tumour or in severe cases, the removal of the thyroid glands has unclear mechanisms as to why this works but it may be due to the removal of antibody secreting B cells in the thyroid

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16
Q

What is the ‘triad’?

A

The sarcoplasmic reticulum (source for calcium) sandwhiches the transverse tubules

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17
Q

Where is calcium induced calcium release essential?

A

Cardiac muscle - it is not necessary in skeletal muscle

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18
Q

Depolarisation in the t-tubule activates which channels?

A

L-type calcium channels

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19
Q

Name two calcium binding proteins

A

Calrectulin and calsequestrin

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20
Q

What is myotonia?

A

Hyper-excitability of skeletal muscle which causes stiffness
Is a result of either too many action potentials or delayed relaxation after an action potential
Myotinic seizures impact on balance and occur every now and again

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21
Q

What is the incidence of myotinia?

A

Approx 1 in every 23,000 to 50,000 (rare)

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22
Q

What are the two main forms of myotonia?

A

Congenita- loss of function mutations in chloride channels

Paramyotonia/potassium aggravated- gain of function mutation in potassium channels

23
Q

What are the two myotonia congenita categories?

A

Thomsen’s - autosomal dominant, shows milder symptoms

Becker’s - autosomal recessive, more severe with earlier onset

24
Q

How can mutations in CLC1 cause the symptoms of myotonia congenita?

A

The mutations affect the open probability of the channel so they open at a higher potential- usually open CLC1 channels will reduce the membrane potential
For a muscle action potential you need a certain amount of Ach but in myotonic patients you don’t need as much as the action potential is more likely to be fired causing increased muscle contraction

25
Q

Why is mexilitene used to treat myotonia congenita?

A

It blocks some action potentials by blocking sodium channels - however, dosage is important as you don’t want all action potentials to be blocked

26
Q

How does the potassium channel mutation in paramyotonia cause symptoms?

A

Issues with the inactivation gate of the potassium channels do not close as properly as they should so the pore does not close
More sodium enters the cell so the depolarisation is prolonged so the cells do not repolarise

27
Q

Why can the cold be a trigger for paramyotonia?

A

The cold impacts on gating so the sodium concentration in the cell remains higher for longer

28
Q

How does advice between treating congenita myotonia and paramyotonia differ?

A

Congenita patients are told to move there muscles more, but in paramyotonia patients movement can worsen stiffness

29
Q

What triggers malignant hyperthermia?

A

Patients will only see symptoms after they have an operation and are given a general anaesthetic such as halothene

30
Q

What is the incidence of malignant hyperthermia?

A

Approx 1 in every 10,000 to 50,000 people

31
Q

What is the death rate of malignant hyperthermia if it is a) untreated
b) treated

A

a) 80%

b) 10%

32
Q

List the symptoms of malignant hyperthermia

A

Increase in body temperature by 1 degree every 5 minutes
Rapid breathing
Low plasma oxygen/ high plasma carbion dioxide
Tachycardia
Excessive muscle contraction and rigidity
Sweating
Shifts in body temperature

33
Q

What causes the death of patients with malignant hyperthermia if they are not treated in time?

A

Respiratory acidosis and lactic acidosis have an additive effect
Muscle rigidity causes the break down of muscle fibres which causes a release of potassium
Severe hyperkalaemia causes excess neuronal and cardiac excitability = death

34
Q

What are the reasons behind the rise in temperature in malignant hyperthermia?

A

Uncontrolled muscle contraction causes excessive ATP hydrolysis causing excess heat production

35
Q

What mutation causes malignant hyperthermia?

A

A mutation in the ryanodine receptor in skeletal muscle.
It is a gain of function mutation increases the open probability of this channel, so more calcium enters the skeletal muscle cells

36
Q

What amino acids are mutated in the RyR1 mutation for malignant hyperthermia?

A

Arg to Cyst at point 614 (615 in pigs)

37
Q

What two things can activate ryanodine receptors?

A

Caffeine and Halothene

38
Q

How is malignant hyperthermia treated?

A

Before any operation time is always allowed to check for any problems
Dantrolene is used to inhibit the RyR1 receptors
IV hydration
Diuretics are given to stop kidney damage occuring as a result of muscle breakdown products
NaHCO3 given to counter acidosis
Mechanical hyperventilation to remove carbon dioxide

39
Q

List sources of tetrodotoxin

A

Produced by marine bacteria- these bacteria may be in a symbiotic relationship with invertebrates, fish and amphibians - this may be ingested eg in organs from puffer fish
Bites can occur from blue ringed octopus

40
Q

What are the symptoms of ingesting tetrodotoxin

A

Facial parasthesia, headache, nausea, dizziness, diarrhoea, vomiting, increasing paralysis, respiratory paralysis eventually leads to death (can occur in 20 minutes to 8 hours)

41
Q

How can tetrodotoxin be treated?

A

Mechanical ventilation

42
Q

What is the antidote to tetrodotoxin?

A

There isn’t one

43
Q

What does tetrodotoxin inhibit?

A

Voltage gated sodium channels on the muscle and the neuron
Inhibition on the neuron reduces the neurotransmitter release so there is a loss of sensation
This leads to respiratory paralysis

44
Q

Which sodium channels are sensitive to tetrodotoxin?

A

1, 2, 3, 4, 6 and 7

insensitive 5, 8 and 9

45
Q

Which type of garter snake is sensitive to tetrodotoxin?

A

The Bear Lake Garter snake

46
Q

Which type of garter snake is insensitive to tetrodotoxin? why?

A

The Willow Creek Garter Snake

They eat salamanders which produce tetrodotoxin

47
Q

Dendrotoxins affect which type of channel and how?

A

They inhibit the Kv channels, this inhibits repolarise

48
Q

What are the symptoms of dendrotoxin poisoning?

A

Early weakness and numbness in the bitten extremity, ptosis (drooping eyelid), opthalmoplegia, paralysis of eye muscle, disphagia, paresis, respiratory failure leading to death

49
Q

How do dendrotoxins affect potassium channels?

A

They block them so there is an excess release of Ach from pre-synaptic stores due to the lack of repolarisation
This causes the failure of subsequent neurotransmission causing problems in muscle control leading to respiratory paralysis and death

50
Q

What species produces conotoxin?

A

Cone snails

51
Q

What does conotoxin target?

A

Nociceptor nerve endings for pain sensation for pain sensation

52
Q

What are the possible targets for pain therapy using conotoxins?

A

Nociceptor nerve endings - Ca2.2 or Na1.8

Dorsal Root Ganglia - Ca2.2, Ca3.2 and Na1.8

53
Q

What are they symptoms of conotoxin poisoning?

A

Burning pain, swelling at injection site, numbness throughout body, cardiac respiratory distress, muscle weakness, loss of coordination, ptosis, headache, nausea, stomach cramps, stiff lips (associated with fatal cases), blurred vision, paralysis and coma

Integrated Physiology and Pharmacology (17 decks)

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