Brainscape's Knowledge GenomeTM

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


See full index

03 - Body Logistics > 20 - Muscle Function and Disease > Flashcards

20 - Muscle Function and Disease Flashcards

1
Q

What is the similarities and differences between cardiac and smooth muscle contraction?

A

Similarities

  • Act as syncitium
  • Communicate through gap junctions (intercalated disc)
  • Nuclei central not peripheral
  • Act as syncitium
  • Have one contractile cell type (not 3 like skeletal)

Differences

- Smooth muscle has no sarcomeres

  • No troponins in smooth
  • Cardiac is electrical conduction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is a kranocyte?

A
  • Resides over Schwann cell and produces collagen to make membrane over whole neuromuscular junction
  • Anchors nerve to muscle cell
  • Keeps neurotransmitter in one area so doesnt affect neighboroughing muscle cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does skeletal muscle contract (5 stages)?

A
  1. Activation
  2. Calcium ion mobilisation
  3. Energy production and fibril contraction
    - Ratcheting
    - Rest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Explain in detail how the events leading to skeletal muscle contraction?

A
  1. Nerve impulse at pre-synaptic neurone
  2. Vesicles fuse with membrane and release Ach into synaptic cleft
  3. Ach binds to nicotinic receptor, depolarises membrane by voltage gated Na channels opening and Na entering cell. AchE breaks down Ach to stop continous action potentials
  4. Depolarisation spreads in t-tubules and causes Ca ion channels to open which causes ryanodine receptors to be activated and release calcium from SER, calcium spark
  5. Influx of calcium into cytoplasm, which binds to troponin, allowing tropomyosin to move and actin-myosin cross bridges to be formed
  6. Contraction, power strokes
  7. Ca release channels close and SERCA moves calcium back out, or PMCA, or mitochondria
  8. Troponin-tropomyosin slides back over acting so no more actin myosin cross bridges
  9. Muscle relaxes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the structure of a thin filament?

A

Globular actin and Troponin complex

  • Two troponin for every tropomyosin twist.
  • Troponin-Tropomyosin block actin binding sites

(can have fibrous actin)

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

What is the structure of a thick filament?

A
  • Many myosin
  • Multiple heads protuding in all directions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is special about the M section of the sarcomere?

A
  • Myosins have no heads so contraction cannot occur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is troponin made up of?

A

I, T, C

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

What happens first when there is an influx of calcium in the cytoplasm?

A
  • Binds to TnC and causes a conformational change of tropomyosin
  • Moves tropomyosin out of the actin binding site into clefts of G-actin spheres
  • Myosin can bind to actin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Explain the sliding filament theory

A
  • Calcium binds to troponin-tropomyosin complex and causes actin binding site to be exposed
  • Myosin head, that has already been energised by ATP, binds to actin to form cross bridge
  • Head tilts towards M-line in a power stroke by release of ADP and Pi, causing actin to slide over myosin
  • Myosin dissociates by ATP binding and returns to original position and is reenergised by ATP hydrolysis to form another cross bridge
  • Lots of cross bridges causes sarcomere to shorten
  • Continues as long as there is sufficient Ca and ATP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

When a muscle contracts what happens to the sarcomere?

A

Z lines get closer together so sarcomere shortens

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

How does sarcomere return to normal length after calcium is removed?

A
  • Antagonist muscles
  • Titin
  • Gravity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is a calcium spark?

A

Release of calcium from sarcoplasmic reticulum

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

What is the origin and insertion of a muscle?

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

What are the five muscle roles?

A

1. Antagonist: Prime mover

2. Antagonist: Opposite to prime mover

3. Synergist: Assist prime mover

4. Neutraliser: prevent unwanted actions of agonist

5. Fixator: hold one body part still whilst other moves

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

What are the three types of levers in the human body?

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

How are muscles separated?

A
  • Compartmentalised by thick dense fascia
  • Muscles with similar actions grouped
  • Anterior, posterior, lateral and medial
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the four compartments of the lower leg?

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

What is compartment syndrome?

A

Pressure in a compartment as constrained by fascia, which can contrict nerves, lymph and blood vessels

  • Can be caused by trauma such as internal bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the signs of compartment syndrome?

A
  • Oedema
  • Shiny swallen skin
  • Deep constant poorly localised pain
  • Paraesthesia (nerve compression)
  • Prolonged capillary refill time
  • Tense and firm
  • Passive stretch
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How do you treat compartment syndrome?

A

Fasciotomy (release pressure on deep compartments)

No fasciotomy can lead to amputation

22
Q

What is muscle tone regulated by?

A
  • Gravity
  • Use
  • Muscle elasticity
  • Motor neuron activity
23
Q

Why are muscles never fully relaxed?

A

Due to muscle tone so they are ready to react. Can improve muscle tone with exercise

24
Q

What is muscle remodelling?

A

Replacement of contractile proteins

Replacement > Destruction = Hypertrophy

Destruction > Replacement = Atrophy

25
Q

What can lead to muscle atrophy?

A
  • Disuse (bed rest, sedentary)
  • Loss of nerve supply (surgery)
  • Disease
  • Age
26
Q

What is the mechanism of muscle hypertrophy and when does it occur?

A

How?

Overstretching so I and A can no longe engage

Add sarcomeres

Produce new fibres from mesenchymal stem cells

When?

- Regular exercise

  • Pregnancy
  • Heart disease (compensate for lack of blood flow)
27
Q

What is rhabdomyolysis and what causes it?

A
  • Striated muscle breakdown

Minor: Lack of oxygen to cells, infection, hyperthermia

Serious: Crush/blast injury, prolonged immobilisation, exposure to toxins, inherited muscle disorders

28
Q

What can be seen in the blood during rhabdomyolysis and what can this cause?

A

- Myoglobin: kidney damage

- Na: swelling

- Ca: sustained muscle contraction

- K: Electrolyte imbalance as lots in muscle cells, prevent electrical conduction of cardiomyocytes

- Uric acid

- CK

COMA OR DEATH

29
Q

Why might CK be high in the blood?

A
  • Rhabdomyolysis
  • MI
  • Kidney injury (myoglobin not cleared)
  • Intramuscular injection
  • Vigorous exercise
  • A fall
  • Muscular dystrophy
30
Q

What is used to test for MI but what is the disadvantage to it?

A
  • Test troponin I and t levels as cardiac isoforms only found in cardiac
  • Release an hour after MI and remain high for over 20 hours, unlike CK
  • Can’t measure extent of MI, like you can with CK. Not proportionate
31
Q

What is rigor mortis?

A
  • After death muscles go into period of sustained contraction due to chemical changes in muscle.
  • 6hours after death - several days, starting with eyelids, jaw and neck.
  • Quicker onset if environment is cold or deceased performed hard physical work before death
  • Due to lack of ATP to break actin-myosin cross bridges
32
Q

What is the cause of myasthenia gravis?

A
  • Autoimmune
  • Antibodies block or destroy Ach receptors
  • Endplate invaginations reduced (less receptors)
  • Reduced synaptic transmission by 30% causes symptoms like muscle weakness
33
Q

What are the symptoms of myasthenia gravis?

A
  • Drooping eyelid (ptosis)
  • Blurred vision
  • Difficulty swallowing
  • Impaired speech (dysarthria)
  • Weakness in arms, hands, legs, fingers, neck
  • Shortness of breath
  • Change in facial expression
34
Q

What is muscular dystrophy?

A
  • Group of muscle disease that result in weakening and breakdown of skeletal muscles over time.
  • Generally they are inherited.
  • Mutation in dystrophin gene, where dystrophin normally tethers actin to membrane and controls calcium concentration so loss of muscle stability
35
Q

How do you diagnose muscular dystrophy?

A
  • Muscle biopsy (more fat)
  • Increased levels of CK in blood
  • Genetic tests
  • Electromyography
36
Q

What is the most common MD and why is it caused?

A

Duchenne MD

- X-LINKED RECESSIVE (mainly m but f carriers have some symptoms)

  1. Mutation in dystrophin gene
  2. XS calcium enters cell and taken up by mitochondria
  3. Causes water to enter, causing swelling
  4. Rhabdomyolysis due to bursting
  5. Muscle cells replaced by adipose
37
Q

What are the symptoms of Duchenne MD?

A
  • Mainly boys
  • Lifespan 15-45
  • Braces age 10
  • Can’t walk by age 12
38
Q

What is malignant hyperthermia?

A

Severe reaction to medications used during general anaesthesia. Triggers cells to release stored Ca ions, causing muscle contraction and this generates lots of heat and causes metabolic acidosis

39
Q

What are the signs of malignant hyperthermia?

A
  • Tachycardia
  • Muscle rigidity
  • High fever
  • High blood K levels due to rhabdomyolysis
40
Q

Why do old people get cold?

A

Muscle atropy

Less muscle, less heat generation

41
Q

Why can pesticides lead to death?

A

ORGANOPHOSPHATE POISONING

- Absorbed by inhaling, ingesting or dermal absorption

  • Inhibit AchE
  • Continuous muscle contraction
42
Q

What are the signs of cholinergic toxidrome and what can they be caused by?

A
  • Snake venom
  • Pesticides
  • Both inhibit AchE
43
Q

What is botulism?

A
  • Toxin produced by bacteria clostridium botulinum
  • Blocks neurotransmitter release at end plate
  • Flaccid paralysis

SIGNS: VOMITING, WEANESS, FEELING TIRED, TROUBLE SPEAKING, DIARROHEA, SWELLING OF ABDOMEN (no fever or loss of consciousness)

44
Q

What is botox used for clinically?

A
  • Overreactive bladder
  • Treat wrinkles
  • Underarm sweating
  • Cervical dystonia
  • Blepharospasm

Lasts 3-12 months by paralysing muscles and blocking nerves. Can cause issues if gets to diaphragm so trained professional has to do it

45
Q

How is the cardiac muscle innervated?

A
  • From medulla oblongata
  • One pre-synaptic, many post-synaptic as synapse is a gap

Paramsympathetic: Vagus nerve, synapse in ventricle wall. Slows heart down

Sympathetic: Spinal nerve. Increases heart rate

46
Q

How is smooth muscle stimualted to contract?

A
  • Varicosities releasing neurotransmitters
  • Hormones
47
Q

If a agonist hormone bound to smooth muscle what would happen?

A
  • Stopped when Ca runs out or active myosin dephosphorylated back to circular
48
Q

If a neurotransmitter bound to smooth muscle how would it contract?

A

Same as with hormone but calcium spark would be released from mitochondria instead of sarcoplasmic reticulum

49
Q

What is the unit of contraction in a smooth muscle?

A
50
Q

What is a gap junction and what is the importance of them in smooth muscle cells?

A

Two hexamers of connexin on two membranes that come together to form a hole between the two cells.

Actin can travel between the two muscle cells

51
Q

How are skeletal muscles innervated?

A
  • Each motor unit is specific to one type of muscle fibre (I,IIa,IIB)
  • Boutons at the end of each axon bound to muscle cells
  • Boutons contain acetylcholine that they release when there is a nervous impulse
52
Q

What is the significance of the number of nerve fibres on a single muscle?

A
  • Less nerve fibres, more control
  • More fibres, stronger contraction
  • Eyes least, calf most

03 - Body Logistics (20 decks)

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