Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Body Logistics > Muscle Tissue - Function and Disease > Flashcards

Muscle Tissue - Function and Disease Flashcards

1
Q

What are the main differences between cardiac muscle and smooth muscle?

A

Smooth muscle has no sarcomeres.
The electrical conduction is different. In cardiac muscle it’s specialised cells (purkinje)
There are no troponin in smooth muscle
There are intercalated discs in cardiac muscles due to the sarcomeres. Due to the absence of sarcomeres in smooth muscle there are no intercalated discs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What do smooth muscle and cardiac muscle have in common?

A

Nuclei are central and not peripheral as in skeletal muscle.
Only one contractile cell type
They act as a syncytium as a wave-like function.
Myocytes communicate through gap junctions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does cardiac innervation and contraction work?

A

Via the sympathetic nervous system an action potential travels from the cardioacceleratory centre through the spinal cord to the sympathetic preganglionic to the designated ganglia. Here it turns postganglionic and unmyelinated. The sympathetic postganglionic nerve now carries the action potential and impacts the ventricles. The action potential travels via the sarcolemma of cardiomyocytes until it reaches the T-tubule and goes in that gap to reach a receptor that is activated by the action potential. This causes an influx of calcium into the cardiomyocyte. The sudden spark of calcium activated ryanoidine receptors on the sarcoplasmic reticulum releasing even more calcium into the sarcoplasm. The calcium now binds to troponin-C and contraction starts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is a t-tubule?

A

A large gap that is about 100x larger than the synaptic cleft found in skeletal muscle. Note that t-tubules are also present in skeletal muscle, just that they are 100x smaller.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Why are the t-tubules important?

A

The neurotransmitter has a chance to spread across a large number of cells to activate the cardiac muscle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are varicosities?

A

Structures found in smooth muscle instead of synapses. The varicosities contain mitochondria and synaptic vesicles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How are neurotransmitters released from varicosities in smooth muscle?

A

By the release of calcium from the mitochondria in the varicosities.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do varicosities relate to the t-tubules in cardiac muscle?

A

The gaps between the muscle and the varicosity is around 100x larger than that of a skeletal muscle here as well.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Explain the ultrastructure of a smooth muscle cell.

A

A central nucleus. No sarcomeres. No intercalated discs. Gap junctions can be found here as well.
You can find 3 special units:
thick filaments
thin filaments
Dense bodies also called focal adhesion plaques

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why are the gap junctions important in smooth muscle?

A

Allows transportation of important ions but also of actin filament (thin filament).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the innervation ratio regarding skeletal muscle?

A

The more nerve fibres per motor unit of a muscle the more power. A motor unit with less nerve fibres means more fine control.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Give an example of a muscle with a low amount of nerve fibres per motor unit.

A

The inferior rectus which moves the eyeball.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Give an example of a muscle with a high amount of nerve fibres per motor unit.

A

The gastrocnemius which is the calf muscle. Needs a lot of power to lift the body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is a triad in skeletal muscle?

A

The combination of t-tubule and sarcoplasmic reticulum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the important neurotransmitter that causes contraction of a skeletal muscle?

A

Acetylcholine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Explain the events leading to contraction of skeletal muscle.

A

An action potential is conducted along the motor neuron axon and arrives at the neuromuscular junction.
This action potential causes calcium to come into the synapse and release the vesicles containing acetylcholine into the synaptic cleft. This causes local depolarisation of sarcolemma.
Voltage-gated Na+ channels open and sodium ions enter the cell.
General depolarisation spreads over the sarcolemma into t tubules.
Voltage sensor Proteins of t tubule membrane change their conformation.
Gated ca2+ ion release channels of adjacent terminal cistern are activated.
Ca2+ ions are rapidly released into the sarcoplasm.
Calcium ions no bind to troponin-C and contraction is initiated.
Calcium ions then return to the terminal cistern of SR.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Explain the pathophysiology of myasthenia gravis.

A

An autoimmune disease where antibodies are directed to the acetylcholine receptor and blocks it by binding to it.
Only a 30% reduction in the receptors available is enough to cause symptoms.
This causes the endplate invaginations in the synaptic cleft to be reduce meaning ‘die off’.
This means there is less synaptic transmission
The reduced synaptic transmission results in muscle weakness where ptosis is a symptom of myasthenia gravis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is titin?

A

A spring like protein that is important in muscle contraction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the two protein components of actin?

A

F-actin fibres and G-acting globules.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What else can be found on a thin filament (actin)?

A

Tropomyosin running along the actin.

Also two troponin complexes can be found for every twist.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What does the troponin complex consist of?

A

Troponin-C
Troponin-T
Troponin-I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What can be found in the centre of the sarcomere?

A

This is the M line. Here only c-proteins and myomesin can be found except for myosin. The important take away message here is that you can only find thick filament, no thin filament and there are no myosin heads there as well.

23
Q

What does the absence of myosin heads and thin filament in the centre of the sarcomere mean?

A

That the centre cannot contract.

24
Q

Why is the tropomyosin important in the thin filament?

A

It blocks the binding site for myosin to bind to the actin molecules. If this structure wasn’t there the muscle would always contract. Also it provides strength to the structure of the thin filament.

25
Q

Why is the troponin complex important in the thin filament?

A

Calcium ions bind to troponin-C. This causes the troponin complex along with the tropomyosin to undergo conformational change and move away from the binding site of the actin/myosin. This causes contraction.

26
Q

Explain the sequence of events in contraction.

A

Calcium binds to troponin-C. The troponin complex along with the tropomyosin moves away from the binding site.
This means that the myosin head can now bind to the actin. A high energy myosin head with ADP and inorganic phosphate can now ‘pull back’ the thin filament, this causes the thin filament to slide towards the M-line. This causes ADP and inorganic phosphate to release. ATP now binds to he myosin head and this causes the myosin head to dissociate from the thin filament.
ATP hydrolysis occurs and ADP and inorganic phosphate is once again bound to the myosin head to make a high energy configuration again in order to once again bind to the thin filament. Rinse and repeat.

27
Q

How do the lengths of actin and myosin relate to the contraction of a skeletal muscle?

A

The lengths remain the same, they are always constant. The sarcomeres are the units that shorten as the Z-lines come closer.

28
Q

What are compartments?

A

Muscles with similar actions are grouped together. For example agonists are grouped together and separated from grouped up antagonists.

29
Q

What are compartments separated by?

A

A thick dense fascia.

30
Q

What is compartment syndrome?

A

Since the compartments are divided up and separated by a thick dense fascia this fascia acts as a constrainer like the fibrous capsule that surrounds the parotid gland or the cranium of the brain.
When trauma happens to one compartment it can swell and cause internal bleeding. The internal bleeding can exert pressure on adjacent compartments and/or blood vessels and nerves as well as lymphatics.

31
Q

What are some symptoms of compartment syndrome?

A 
Deep constant poorly localised pain
Paresthesia
Compartment may feel tense and firm
Swollen shiny skin and oedema
Prolonged capillary refill time.
32
Q

How is compartment syndrome treated?

A

By fasciotomy where the skin is deliberately cut open to release the pressure.

33
Q

Why is fasciotomy important?

A

Because if you don’t do it you might have to amputate.

34
Q

Define muscle tone.

A

The tension in a muscle at rest.

35
Q

Define muscle strength.

A

The muscle’s ability to contract and create force in response to resistance.

36
Q

What is muscle tone regulated by?

A 
Motor neuron activity
Muscle elasticity
Use
Gravity
Remember that healthy muscles never fully relaxed
37
Q

How long does the replacement of contractile proteins in muscle remodelling take?

A

Around 2 weeks.

38
Q

Explain atrophy.

A

When the destruction of muscle outweighs the replacement of new muscle.

39
Q

Explain hypertrophy.

A

When replacement of new muscle outweighs the destruction.

40
Q

Explain the mechanism of hypertrophy.

A

Overstretching has occurred to begin with such that the A and I bands can no longer re-engage.
This causes new muscle fibrils to be produced and new sarcomeres to be added in the middle of existing sarcomeres.
New muscles fibres arise from MSCs.

41
Q

How does muscle atrophy happen?

A

By the diseases of the muscle. Bed rest or limb immobilisation.
Also by surgery where denervation of muscle happens.
Also by disease such as muscular dystrophies.

42
Q

Briefly explain Duchenne muscular dystrophy.

A

X-linked recessive
Mutation of the dystrophin gene.
The absence of dystrophin causes a series of events:
Excess calcium is taken up by cell.
Excess calcium in cell is taken up by mitochondria
Water goes into mitochondria and mitochondria burst
All the substance is released into cytoplasm and more water goes into cell.
Muscle cell bursts
This causes an increased level of creatine kinase and myoglobin levels in blood.
The dead muscle cells are then replace with adipose tissue instead.

43
Q

What is rhabdomyolysis?

A

Condition where muscle cells are broken down rapidly.

44
Q

What is creatine kinase and why is it important?

A

It is an enzyme that is found in metabolically active tissues such as muscles.

45
Q

How can creatine kinase be used clinically?

A

You can measure the level of creatine kinase in blood or urine in order to diagnose heart attacks (myocardial infarctions).

46
Q

Why might you not use creatine kinase assay to determine whether someone has had a heart attack?

A

Because it is not restricted to muscle damage from cardiac muscle. Also skeletal muscle or brain damage can be a cause of elevated creatine kinase levels.

47
Q

What are some causes of elevated creatine kinase levels?

A 
Vaccinations
Physical exercise
A fall
Rhabdomyolysis
Muscular dystrophies
Acute kidney injury
48
Q

So if Creatine kinase is not always the appropriate assay for diagnosis what else can be used?

A

Something that is only found in cardiac muscle:

A special isoform of troponin-I.

49
Q

What is the disadvantage of only using troponin-I assay?

A

Troponin-I levels cannot show the level of the infarction.
Creatine kinase levels are largely proportional to the size and severity of the infarction.
It also needs to be measure within 20 hours for absolute accuracy.

50
Q

Explain how botulism toxin and botox work.

A

It blocks neurotransmitter release at the motor end plate.
The causes non-contractile state of skeletal muscle.
This is clinically used to treat muscle spasm but also cosmetically used to treat wrinkles.

51
Q

Why is the depth of injection of botox important?

A

Because wrong depth or wrong amount means that the toxin can end up in the CNS instead.

52
Q

Explain organophosphate poisoning.

A

Organophosphates are used as pesticides.
When these are found in the body they inhibit the normal function of acetylcholine esterase.
The act esterase that is supposed to stop signalling process does not work anymore so signalling keeps going and is potentiated (added on).

53
Q

What are muscarinic symptoms of organophosphate poisoning?

A 
SLUDGE:
Salivation
Lacrimation
Urination
Defecation
GI - cramping
Emesis (vomiting)
54
Q

What are nicotinic symptoms of organophosphate poisoning?

A 
MTWTF:
Muscle cramps
Tachycardia
Weakness
Twitching
Fasciculations

Body Logistics (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions