Brainscape's Knowledge GenomeTM

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


See full index

Tissues Of The Body > Muscle > Flashcards

Muscle Flashcards

0
Q

Describe the general functions of skeletal muscle.

A
  • movement
  • posture
  • stability of joints
  • heat generation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Describe the general structure of skeletal muscle.

A

Mesoderm-derived

H & E = red fibres - intermediate fibres - white fibres

Epimysium —> Perimysium (surrounding fascicles - groups of fibres) —> Endomysium (surrounding individual fibres) —> Myofibrils —> Myofilaments

Myotendinous junctions: interdigitation of skeletal muscle fibres and tendon collagen bundles (sarcolemma in between)

T tubules within A-I band junction

Multiple peripheral nuclei

Calcium-binding protein = troponin

Stimulated by somatic & voluntary nerve supply

Cannot divide, but tissue can regenerate by mitotic activity of satellite cells

Damage = hyperplasia & hypertrophy

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

Outline the formation of skeletal muscle.

A

Myogenic stem cells —> Myoblasts —> Primary myotube (chain of central nuclei) —> Actin & myosin displace nuclei to periphery

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

What is:

  • the Z line?
  • the M line?
  • the I band?
  • the H band?
  • the A band?
A

Z line = disc between I bands (bisection of actin & myosin)

M line = myosin filaments perpendicular to muscle fibres

I band = zone of actin filaments in between myosin filaments (not superimposed with myosin filaments)

H band = zone of myosin filaments in between actin filaments (not superimposed with actin filaments)

A band = entire length of myosin filament

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

What is the definition of a sarcomere?

A

Basic unit of muscle (contractile unit of a myofibril)

Consisting of myosin and actin filaments

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

Describe the structure of an actin (thin) filament.

A

Helix of actin filaments associated with tropomyosin, which has the regulatory protein troponin (C, I & T) on its surface

Calcium binds to troponin, which changes the conformation of the actin & tropomyosin, allowing formation of myosin cross-bridges.

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

Describe the structure and function of myosin filaments.

A

2 interlocking chains

Tail region & head region (2 heads)

Myosin head binds to actin filaments during power stroke

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

Outline the sliding filament model.

A

Calcium binds to troponin

Change in conformation allows myosin head forms cross bridge with actin

Power stroke: ADP & Pi released, myosin head bends as it pulls the actin filament, sliding it towards the M line

ATP attaches to the myosin head & cross-bridge detaches

ATP hydrolysed, cocking the myosin head

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

What happens when ATP is unavailable for muscle contraction?

A

Rigor mortis = permanent contraction until decomposition breaks down the muscle fibre

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

Describe what happens during contraction at the neuromuscular junction.

A

Action potential travels down nerve

Acetylcholine released from synaptic vesicles

Acetylcholine binds to receptors on sarcolemma (acetylcholinesterase terminates binding)

Na+ entry into sarcolemma depolarises end plate

Depolarisation travels down T-tubules

Calcium released from terminal cisternae on sarcoplasmic reticulum

Calcium binds to troponin, causing contraction

Active transport removes calcium to the sarcoplasmic reticulum

Tropomyosin blocks binding site so contraction ends

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

Describe how contractions travel in the heart.

A

Myogenic cells spontaneously contract

Sino-atrial node sends electrical impulses to atrioventricular node

Atrioventricular node sends electrical impulses down Bundle of His and up the Purkinjie fibres

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

Describe the general features of cardiac muscle.

A

Mesoderm-derived

Single centrally positioned nuclei

Intercalated discs

Gap junctions & adherens-type junctions

Branching muscle fibres

T tubules in line with Z bands

Calcium-binding protein = troponin

Stimulated by myogenic cells

Incapable of regeneration

Damage -> fibroblasts lay down scar tissue

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

Describe the general features of smooth muscle.

A

Mesoderm & neural crest origin

Non-striated

Gap junctions

Spindle-shaped (fusiform) cells

Single central nuclei

No T-tubules

No sarcomeres

Capable of being stretched

Calcium binding protein = calmodulin

Stimulated by nerve signals (involuntary), hormones, drugs, [blood gases]

Cells retain mitotic activity and can form new smooth muscle cells

….+++

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

What is the definition between myoepithelia & myofibroblasts?

A

Myoepithelia = single, stellate cells forming the basketwork around secretory units of some exocrine glands to assist with secretion

Myofibroblasts = single cells at sites of wound healing which secrete collagen, but can also contract (bring wound edges together)

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

Outline how smooth muscle contracts.

A

ANS innervates

ANS releases neurotransmitters from varicosities into a wide synaptic cleft

Actin intermediate filaments attach to dense bodies

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

What is the difference between atrophy and hypertrophy? What is hyperplasia?

A

Atrophy = destruction > replacement
(muscle wasting)
e.g. bed rest, limb immobilisation, sedentary behaviour

Hypertrophy = destruction < replacement
(increased glycolysis, mitochondria, glycogen, & blood flow —> increased fibre diameter; increased sarcomeres —> increased flexibility)

Hyperplasia = increase in cell number

16
Q

What is denervation atrophy?

A

Loss of nerve supply to muscles so muscles do not receive contractile signals.

Muscle replaced with fibrous tissue

S&S = weakness, flaccidity, muscle atrophy

17
Q

What is the pathology of myasthenia gravis?

A

Autoimmune destruction of end-plate AchR, loss of junctional folds at end-plate, widening of synaptic cleft

S&S:

  • fatigue
  • sudden falling: as Ach falls over time —> muscle relaxes & loses tension
  • drooping eyelids (ptosis)
  • double vision
  • immune state affected (reduced general health & emotional state)
  • respiratory muscles affected —> DEATH

Treatment: acetylcholinesterase inhibitors

18
Q

What are the effects of botulism toxin and organophosphate poisoning on the neuromuscular junction?

A

Botulism toxin = block Ach release, therefore no transmission of action potential, therefore no muscle contraction

Respiratory muscles —> stop breathing —> DEATH

Treatment: anti-toxin

Organophosphate poisoning = inhibits Ach-ase irreversibly, therefore there is constant action potential transmission and constant muscle contraction —> fatigue, excessive secretions, cramps, confusion, paralysis, etc.

Treatment: atropine, gastric lavage, activated charcoal

19
Q

What is tetany? Why does tetanus NOT cause tetany?

A

Involuntary contraction of muscles e.g. due to action potential changes, lack of calcium, excess of phosphate etc.

Tetanus cramps are caused by a blocking of the inhibition of nerves suppling muscles

20
Q

What are muscular dystrophies? Give some examples.

A

Genetic disorders characterised by progressive muscle wasting and weakness

e.g. Duchenne’s, Becker’s

21
Q

Describe the pathology of Duchenne’s muscular dystrophy.

A

Complete absence of dystrophin (which anchors actin & myosin to the sarcolemma)

Proximal muscles affected

Sarcolemma does not move with fibres —> shearing forces tear muscle fibres during contraction —> creatine kinase released —> calcium enters muscle cells and causes necrosis —> muscle fibres replaced by fat and connective tissue (pseudohypertrophy)

S&S:

  • contractures (permanent shortening of muscles)
  • difficulty rising to feet (see Gower’s sign)
  • proximal limb weakness
  • disabled by 10yrs, dead in teens/20s

Treatment: steroids (prednisolone) to build up muscle

22
Q

Give some examples of myopathies.

A

Polymyositis (chronic inflammation of muscle by virus/auto-immune) —-> myalgia (pain)

Hypokalaemia —> hyperpolarisation —> arrhythmias (cardiac muscle)

Thryotoxicosis (hyperthyroidism) —> increased BMR —> muscle wasting

Hypoparathyroidism —> lack of PTH —> low [Ca2+] —> tetany

Malignant hyperthermia (increased [Ca2+] —> muscle contraction —> lots of heat released)

23
Q

What are some of the specialisations of the Purkinjie fibres ?

A
  • abundant glycogen
  • sparse myofilaments
  • extensive gap junctions
24
Q

Outline the mechanism of malignant hyperthermia.

A

Rare autosomal dominant disorder

Uncontrolled skeletal muscle oxidation in response to anaesthetic agents or muscle relaxant succinylcholine —> acidosis, heat production, organ failure —> circulatory collapse

Treat with dantrolene to prevent calcium release

Tissues Of The Body (15 decks)

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