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Y2B2 - Musculoskeletal πŸ“— > Physiology 🫁 > Flashcards

Physiology 🫁 Flashcards

1
Q

skeletal muscle innervation

A
  • The skeletal ms fibers are innervated by thick myelinated nerve fibers (type A alpha)
  • originate from the motor neuron pools located in either the spinal cord (AHCs) or the brain stem.
  • Neuromuscular junction is the point of contact between the motor nerve and ms fiber.
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2
Q

what innervates skeletal muscle fibers?

A

thick myelinated nerve fibers (type A alpha)

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3
Q

where do thick myelinated nerve fibers (type A alpha) originate from?

A

originate from the motor neuron pools located in either the spinal cord (AHCs) or the brain stem.

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4
Q

what is the point of contact between the motor nerve and ms fiber called?

A

Neuromuscular junction

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5
Q

what is a motor unit?

A

It consists of a motor neuron and the ms fibres supplied by it.

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6
Q

compare between number of muscle fibers of a motor unit in muscles producing delicate & coarse movements

A

Number of ms fibres in each unit is variable:

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7
Q

what is the site of Neuromuscular junction (NMJ)?

A

is the region of contact between the motor nerve ending and ms fiber nearly at the middle of the ms fiber

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8
Q

what are the parts of Neuromuscular junction (NMJ)?

A
  • The axon terminal of motor neuron (presynaptic part)
  • Synaptic cleft
  • Motor end plate (MEP) (postsynaptic part)
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9
Q

what are the contents of The axon terminal of motor neuron (presynaptic part) of NMJ?

A

Vesicles
- Contain the chemical transmitter acetylcholine (Ach)

Mitochondria
- provides the ATP for the synthesis of Ach and Na - K pump

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10
Q

what does the synaptic cleft separate?

A

It separates the muscle plasma membrane from the axonal terminal

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11
Q

length of synaptic cleft

A

It is about 10-30 nm

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12
Q

what are the contents of the Motor end plate (MEP) (postsynaptic part) of NMJ?

A
  • Junctional folds
  • Cholinergic receptors for Ach
  • Cholinesterase enzyme
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13
Q

what is the function of Junctional folds at NMJ?

A

which ↑ the surface area of MEP.

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14
Q

what is the type of Cholinergic receptors for Ach? and what is their action?

A
  • they are nicotinic receptors (Nm type), which act as ligand- gated ion channels.
  • Normally, the receptor is not permeable to ions, but when Ach is attached to the binding sites, Na and K ions can pass through these chemically activated channels.
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15
Q

what is the function of cholinestrase?

A

hydrolyzes Ach to choline and acetic acid

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16
Q

Biosynthesis and storage of Ach

A
  • Ach is synthesized in axonal terminal from choline and acetyl-coA by choline acetyltransferase (CAT) enzyme
  • Once Ach is synthesized, it is stored in vesicles (each vesicle contains 5000 -10000 molecules)
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17
Q

steps & mechanism of neuromuscular transmission

A
  • When the nerve impulse in a motor neuron reaches its axon terminal, it opens the voltage-gated Ca+2 channels allowing the Ca+2 ions to diffuse into the axon terminal.
  • The high intracellular Ca+2 ion causes the synaptic vesicles to move towards the membrane, and to fuse with it with rupture of vesicles and release their content into the synaptic cleft by exocytosis.
  • Ach diffuses across the cleft to the postsynaptic membrane (motor end plate) where it binds with its specific binding sites on nicotinic receptors (Nm) and this open the ligand gated ion channels that allow Na influx and K efflux
  • Na+ influx is more than K+ efflux due to the differences in electrochemical gradients across the membrane, producing a local depolarization of motor end plate known as the motor end plate potential (EPP).
  • The end plate potential causes small local currents which depolarize the adjacent ms plasma membrane to the threshold level for generation of an action potential.
  • This action potential propagates on both sides of the motor end plate to the whole length of the ms fibres leading to its contraction.
  • Once Ach produces its action, it is rapidly hydrolyzed by the cholinesterase enzyme into choline and acetic acid. Choline is reuptaken by axonal terminal for resynthesis of Ach and acetic diffuse into blood.
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18
Q

what is miniature end plate potential? and what are its characteristcs?

A
  • It is a weak depolarization of the MEP caused by spontaneous rupture of few vesicles at rest.
  • It is localized at the MEP and disappears rapidly and occurs on an average of about one per second
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19
Q

what are the characters of neuromuscular transmission?

A
  • One-way conduction
  • Synaptic delay
  • Fatigue
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20
Q

why is NMT one-way directional?

A
  • NMT occurs only from the nerve to the ms and not in the opposite direction
  • because the chemical transmitter (Ach) is present only in the terminal parts of the nerve fibre (presynaptic terminals) and not in the ms (postsynaptic membrane)
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21
Q

what is the definition of synaptic delay?

A

It is the time interval (about 0.5 msec) between the arrival of nerve impulse to the NMJ and the action potential generated in the ms.

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22
Q

what causes synaptic delay?

A
  • Release of Ach from the presynaptic terminals
  • Ach diffusion across the synaptic cleft
  • Combination of Ach with the receptors
  • Opening the channels leading to diffusion of ions.
  • Depolarization of MEP (EPP)
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23
Q

fatigue in NMT

A
  • Rapid repeated stimulation of the motor nerve caused ms fatigue or weakness of ms
  • Due to depletion of the Ach vesicles
  • O2 lack facilitates the onset of fatigue because it ↓es the metabolic reactions needed to reform Ach.
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24
Q

what modifies NMT?

A

NMT is modified by ions or drugs or diseases

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25
Q

how do Ca++ ions and hypercalcemia affect NMT?

A

Ca+2 ions helps NMT but hypercalcemia (increase blood Ca+2) decreases the NMT by blocking Na+ channels in neurons and preventing depolarization in nerve fibers and vice versa.

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26
Q

how do Mg++ ions affect NMT?

A

It inhibits NMT by stabilizing the Ach vesicles, so prevent the release of Ach

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27
Q

how do K+ ions affect NMT?

A

It has anticurare action on the motor end plate.

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28
Q

what are drugs that stimulate NMT?

A
  • Methacholine
  • Neostigmine
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29
Q

what is the action and effect of methacholine?

A

Action
- Stimulate Nm receptors at MEP directly

Effect
- Stimulate NMT and produce ms spasm

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30
Q

what is the action and effect of neostigmine?

A

Action
- Inhibit cholinesterase

Effect
- Prolong the action of Ach at MEP, stimulate NMT

31
Q

what are examples of NMT blockers?

A
  • Botulinum toxin
  • Hemicholinium
  • Curare
  • Succinylcholine
32
Q

action and effect of botulinum toxin

A

Action
- Prevent synthesis and release of Ach

Effect
- Causes presynaptic block of the NMT and ms paralysis

33
Q

action and effect of hemicholinium

A

Action
- Interfere with choline uptake

Effect
- Causes presynaptic block of the NMT and ms paralysis

34
Q

action and effect of curare

A

Action
- Competes with Ach nicotinic (Nm) receptors at motor end plate

Effect
- Causes postsynaptic block of the NMT and ms paralysis

35
Q

action and effect of succinylcholine

A

Action
- Bind to Nm receptors to produce initial depolarization of MEP followed by maintained depolarization of MEP

Effect
- Causes initial ms contraction followed by postsynaptic block of the NMT and ms paralysis

36
Q

what is the definition of Myasthenia gravis?

A

Myasthenia gravis is a rare autoimmune disease that affect neuro-muscular junction and characterized by marked muscle weakness and rapid onset of fatigue

37
Q

incidence of Myasthenia gravis

A

Common in young females

38
Q

mechanism of Myasthenia gravis

A
  1. ↓ ed number of Ach vesicles in axonal terminals
  2. ↓ed Ach content of synaptic vesicles.
  3. Widening of synaptic cleft.
  4. ↓ed number of junctional folds, so decrease the surface area for action of Ach.
  5. ↓ed number of Ach receptors on MEP due to production of auto antibodies against them (curare like substance) which compete with Ach at receptor site.
39
Q

how is Myasthenia gravis treated?

A

Prostigmine inhibits cholinesterase enzyme, so prolongs the action of Ach at MEP

40
Q

What do muscles convert?

A

Muscles are machines which convert the stored chemical energy into mechanical energy (work) and heat.

41
Q

what do muscles represent (concerning the whole body weight)?

A
42
Q

what are the functions of the skeletal muscles?

A
  1. Movements of the body as a whole or part of it e.g. one limb.
  2. Maintenance of the body posture by their tonic contraction and muscles tone.
  3. Control of body temperature: 50% of heat production in the body during rest is due ms tone and during ms exercise heat production is much increased.
43
Q

structure of skeletal muscles

A
  • Each skeletal ms consists of many fasciculi
  • Each fasciculus is composed of many ms fibers (myofibers) or ms cells.
44
Q

Who is the structure of skeletal muscle fiber?

A
  • It is elongated multinucleated cells (vary in length and 10-100 um in diameter)
  • Surrounded by cell membrane called sarcolemma
  • Sarcoplasm contains cytoplasmic organelles e.g. sarcosomes (mitochondria), sarcoplasmic (endoplasmic) reticulum (SR), Golgi Apparatus, Ribosomes, Glycogen granules and myofibrils
  • the sarcolemma has tubular extensions called transverse (T) tubules
45
Q

what is the structural unit of skeletal muscles?

A

muscle fiber

46
Q

what is the Definition of transverse (T) tubules?

A
  • They are tubular extensions of sarcolemma extend deep into the ms fiber (at junction of the A and I bands).
  • Its lumen is continuous with the ECF around ms fibers.
47
Q

what are the functions of transverse (T) Tubules?

A

A. ↑ the surface area of the sarcolemma many folds.

B. Help the movement of ions and other substances into and out of the cell.

C. Help the spread of depolarization wave to inside the interior of ms fiber.

48
Q

what is the definition of Sarcoplasmic reticulum?

A
  • Is a network of anastomosing longitudinal tubules
  • The ends of these tubules are dilated and called the terminal cisternae (TC).
49
Q

What are the functions of sarcoplasmic reticulum?

A
  • Help longitudinal distribution of ions and substances within the sarcoplasm
  • TC releases Ca+2 ions during ms contraction and stores it during ms relaxation.
50
Q

what is a triad?

A

A group of the T tubule and two terminal cisternae on either side called a triad.

51
Q

what does a muscle fiber consist of?

A

ms fibre contains several hundred myofibrils (fibril =little fiber)

52
Q

What is the diameter of myofibrils?

A

1 ΞΌm

53
Q

what causes longitudinal and transverse striation of myofibrils?

A
  1. Myofibrils extend from one end of the ms fiber to the other to give it its longitudinal striation
  2. each myofibril consists of alternate light and dark bands→ give the skeletal ms fibre its characteristic transverse striation:
    - The dark bands are called A bands (anisotropic),
    - whereas the light bands are called I bands (Isotropic).
54
Q

what do myofibrils consist of?

A

Each myofibril is composed of filaments: thick and thin filaments.

55
Q

where are Z lines found and what do they divide the myofibril into?

A

Z lines (discs) cross the center of each I band and divide the myofibril into smaller units called sarcomeres.

56
Q

what is the definition of sarcomere?

A

It is the part of the myofibril present between the 2 Z lines

57
Q

what is the functional unit of the skeletal muscle?

A

sarcomere

58
Q

what is the structure of sarcomere?

A

It is formed of contractile proteins:
- Thick filaments→consist of the contractile protein myosin
- Thin filaments β†’ consist of contractile proteins actin, troponin and tropomyosin

59
Q

structure of thick filaments of sarcomere

A

Each one consists of many myosin molecules which consists of 2 parts:

  • Head of cross-bridges β†’ act as ATPase and binding sites for actin and for ATP.
  • Tail of myosin
60
Q

Thin filaments of sarcomere

A

Consists of 3 types of protein molecules:

1) Actin:
- consists of 2 rows of actin molecules wrapped around each other.
- It contains binding sites for myosin.

2) Tropomyosin:
- cover the biding sites of myosin on actin β†’relaxing protein.

3) Troponin
- consists of 3 subunits:
➒ Troponin C β†’ binds to Ca ions.
➒ Troponin T β†’ binds to Tropomyosin.
➒ Troponin I β†’ binds to actin.

61
Q

what is the definition of excitation-contraction coupling in the skeletal muscles?

A

Is the process by which an action potential in motor nerve initiates the ms contraction

62
Q

what are the steps of excitation-contraction coupling in the skeletal muscles?

A
  1. Propagation of the AP and release of Ca ions
  2. Binding of the cross-bridges between myosin and actin
  3. Cycling of cross-bridges
  4. Relaxation
63
Q

Propagation of the AP and release of Ca ions

A
  • Propagation of the action potential (AP) in the motor nerve β†’ production of end plate potential (EPP) at motor end plate β†’ generation of action potential at the adjacent areas of ms cell membrane β†’ AP spreads on both sides of the motor end plate and spreads along the T tubules which extend deep into the ms fibre β†’ release Ca+2 ions from the terminal cisternae of SR via dihydropyridine (DHP) receptors in T tubules and ryanodine receptor (RyR) in sarcoplasmic reticulum (SR).
64
Q

Binding of the cross bridges between myosin and actin

A
  • The released Ca+2 ions combine with troponin C molecules β†’ causes the tropomyosin to move away from its blocking position and thus exposing the binding sites present on actin molecules.
  • So, the cross bridges are formed from the head of myosin with actin molecules
65
Q

what are the steps of cycling of cross-bridges?

A
  • occurs in the following steps:
    1. binding
    2. Bending
    3. Detachment
    4. Return to original position
66
Q

steps of cycling of cross-bridges

A

Binding
- cross-bridges of myosin bind to actin.

Bending
- The energized head of myosin split ATP to ADP and P by myosin ATPase, thus producing angular movement of the cross bridges and sliding of the actin filaments across the thick filaments.

Detachment
- When ATP molecule bind to the head of myosin, this decreases the affinity of the head to actin molecules causes detachment of the cross-bridges from the thin filament.

Return to original position
- The cross-bridge returns to its original position and another cycle can occur by binding to another actin molecule and so on.

67
Q

when does cross-bridge cycling occur?

A

Cross-bridge cycling occurs as long as Ca+2 ions combine with Troponin C and ATP is available

68
Q

what does lack of ATP lead to (concerning actin and myosin)?

A

Lack of ATP leads to failure of detachment between actin and myosin as occurs after death due to depletion of ATP resulting in rigors mortis (ms stiffening after death)

69
Q

Relaxation in (excitation-contraction coupling in the skeletal muscles)

A
  • It occurs when Ca+2 ions are transported into the SR by an active process using ATP and Ca+2-ATPase (SERCA)
  • Removal of Ca+2 ions makes troponin to return to its original state which causes tropomyosin to move back and cover the binding sites on actin
  • The thin filaments to slide back again to their original position.
70
Q

when is malignant hyperthermia seen?

A

commonly seen during anesthesia.

71
Q

explain malignant hyperthermia

A

During anesthesia with sevoflurane some patients developed spams of jaw muscles with tachypnea and tachycardia with elevation of body temperature due to excessive heat production from ms spasms.

72
Q

what is the nature of malignant hyperthermia?

A

It is an inherited disease characterized by β†’ defect in ryanodine receptors that allow some anesthetic drugs to cause continuous release of Ca+2 from SR resulting in continuous ms contraction and spams

73
Q

compare between skeletal muscles, smooth muscles, and cardiac muscles in terms of:

  • Appearance
  • regulation
  • Action potential
  • Regulatory proteins
  • Source of calcium
  • Speed of contraction
A

Y2B2 - Musculoskeletal πŸ“— (8 decks)

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