Lecture 24

Question 1

Cardiac and smooth muscle differences?

Answer 1

No troponin in smooth muscle

No sarcomere in smooth muscle

No specialised electrical conduction mechanisms in smooth muscle

Commonalities are central nuclei, one contractile cell type and communicate through gap junctions/intercalated disks

Question 2

Cardiac innervation and contraction?

Answer 2

Depolarisation opens DHP receptor channel and allows calcium in. The ryanodine receptor is activated and more calcium enters cell and binds troponin C to reveal actin binding site and allows contraction.

Question 3

Smooth muscle contraction?

Answer 3

Neurotransmitter released from varicosities or hormones can bind to receptors on cell. Calcium enters and contraction results. Contraction will continue as long as calcium is present

Question 4

How is skeletal muscle innervated?

Answer 4

If fine control is required each motor unit will innervate just a few muscle fibres. If less fine control is required each motor unit will innervate a large number of fibres

Question 5

T tubule function?

Answer 5

Allows membrane depolarisation to quickly reach cell centre

Question 6

Skeletal muscle contraction events?

Answer 6

Nerve impulse arrives at neuromuscular junction.

Acetylcholine released and sarcolemma depolarised

Na+ channels open

General depolarisation into T tubules

Gated calcium channels sarcoplasmic reticulum activated

Ca2+ ions released into sarcoplasm

Ca2+ binds TnC subunit of troponin and contraction cycle is initiated

Ca2+ ions returned to terminal distal of sarcoplasmic reticulum

Question 7

What happens in myasthenia gravis?

Answer 7

Antibodies block ACh receptor.

Endplate invaginations in synaptic cleft reduced.

Results in muscle weakness

Question 8

Explain the sliding filament theory?

Answer 8

Tropomyosin-troponin complex sits over the actin binding sites. Myosin heads extend over actin filaments in regions of potential overlap.

On calcium binding the tropomyosin moves away from the actin binding sites and the myosin heads can bind to the actin.

1 Myosin head with ADP and P binds to actin myofilament.

2 power stroke occurs and ADP and P are released

3 ATP attaches and cross bridge detaches

4 ATP hydrolysed into ADP and P. Cocking of myosin head occurs

Question 9

Do actin and myosin shorten?

Answer 9

No, just the Z bands come closer together

Question 10

Muscle roles in movement?

Answer 10

Agonists

Antagonists

Synergistic

Neutralisers

Fixators

Question 11

What are the three types of levers?

Answer 11

First class “see saw”

Second class “wheelbarrow”

Third class “fishing rod”

Question 12

What are compartments?

Answer 12

What limbs are divided into and delineated by fascia

Question 13

What is compartment syndrome?

Answer 13

Trauma in one compartment can cause internal bleeding which exerts pressure on blood vessels and nerves. Eg lymphatic that go through tissue- can get lympodema

Question 14

What is muscle tone?

Answer 14

Tension in a muscle at rest.

Question 15

Muscle remodelling?

Answer 15

Destruction greater than replacement= atrophy

Replacement greater than destruction= hypertrophy

Question 16

How does muscle hypertrophy work?

Answer 16

Over stretching results in no more overlap between actin and myosin so new fibrils are produced. New muscle fibres arise from mesenchymal cells

Question 17

Muscle atrophy mechanism?

Answer 17

Disuse- bed rest

Surgery- denervation- no stimulus for contraction. Takes 3 months for regeneration

Disease- muscular dystrophies

50% of muscle lost by the age of 80

Question 18

What is denervation?

Answer 18

Loss of nerve supply

Question 19

Duchene muscular dystrophy?

Answer 19

X linked recessive disease. Absence of dystrophin allows excess calcium into cell. Calcium taken up by mitochondria along with water. Causes them to burst and muscle cell bursts (rhabdomyolysis). Creatine kinase and myoglobin levels are extremely high in blood. Muscle replaced by adipose tissue.

Seen as arched back and shoulders and arms held back. Walk on tip toes and poor balance etc.

Question 20

Creating kinase

Answer 20

Was used for MI diagnosis but largely replaced by troponin 1 assay

Question 21

What is rhabdomyolysis?

Answer 21

Death of muscle fibres and the release of their contents into the blood stream

Question 22

Troponin assay for MI

Answer 22

Released within an hour of MI and must be measured within 20 hours for absolute accuracy. Troponin quantity not necessarily proportional to degree of muscle damage.

Question 23

Botulism toxin and Botox?

Answer 23

Toxin blocks neurotransmitter release at motor end plate.

Prevents contraction of skeletal muscle. Used clinically to treat muscle spasms and used cosmetically to treat wrinkles.

If given incorrectly can get into nerves and stop them from working.

Question 24

What are fasciculations?

Answer 24

Brief spontaneous contractions affecting a small number of muscle fibres, often causing flickering under the skin

Question 25

Organophosphate poisoning?

Answer 25

Prevents acetylcholinesterase from working. Sustained receptor stimulation.

Effects different at muscarinic and nicotinic receptors.

SLUDGE at muscarinic and MTWTF at nicotinic

Muscle cramps
Tachycardia
Weakness
Twitching
Fasciculations