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MSAP Week 2 > Physiology Week 2 > Flashcards

Physiology Week 2 Flashcards

1
Q

Somatic motor neurons are _____ and _____. They always release _____.

A
  1. Long and Myelinated

2. ACh

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2
Q

In the Autonomic NS, Preganglionic neurons are _____, and always release ____, while Postganglionic neurons are _____ and can release ______.

A
  1. Myelinated
  2. ACh
  3. Un-myelinated
  4. ACh OR NE
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3
Q

Somatic motor neurons synapse ______, and therefore do not have _____.

A
  1. On their target effectors

2. Ganglia

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4
Q

The Enteric NS is the 3rd division of the ________.

A

ANS

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5
Q

The major neurotransmitter in the SYMPATHETIC NS is _______.

A

NorEpinephrine

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6
Q

If your skin is very warm, is there more sympathetic or parasympathetic activity occurring in your body?

A

Parasympathetic: Because blood vessels are relaxed and filled with more blood as BP is reduced.

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7
Q

List the 6 organs/glands/muscles/tissues that are ONLY innervated by the Sympathetic NS and NOT the Parasympathetic NS:

A
  • Vascular Smooth Muscle
  • Sweat glands
  • Pilo-erector Muscles
  • Liver
  • Adipose Tissue
  • Kidney
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8
Q

List the 2 organs/glands/muscles/tissues that are ONLY innervated by the Parasympathetic NS and NOT the Sympathetic NS:

A
  • Gastric/Pancreatic Secretions

- Lacrimal Glands

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9
Q

Sympathetic trunk Ganglia are also called ________.

A

ParaVertebral Ganglia

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10
Q

Pre-Ganglionic released ACh binds to ______ receptors, and post-ganglionic released ACh binds to ________, while Epinephrine/NE bind to ________ receptors.

A
  1. Nicotinic
  2. Muscarinic
  3. Adrenergic (alpha and beta)
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11
Q

The Adrenal Medulla is considered to be a __________.

A

Modified Post-Ganglionic Neuron

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12
Q

Which cells on the Adrenal Medulla do the pre-ganglionic neurons synapse with?

A

Chromaffin Cells which release Catecholamines

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13
Q

The majority of vascular smooth muscle uses ________ as its neurotransmitter.

A

NE

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14
Q

Metabolic rate will _________ with generalized sympathetic activity.

A

INCREASE

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15
Q

Somatic motor neurons release ________ that binds to ______ receptors.

A
  1. ACh

2. Nicotinic

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16
Q

Sympathetic post-ganglionic neurons release NE which binds to ________ receptors, but also release ACh which binds to _______.

A
  1. Alpha/Beta/1/2 Receptors

2. Muscarinic

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17
Q

Parasympathetic post-ganglionic neurons release ACh that ALWAYS binds to _______ receptors.

A

Muscarinic

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18
Q

All NICOTINIC cholinergic receptors are _________, meaning when they are bound, they allow ________. When ACh binds these, the response is ALWAYS ________.

A
  1. Ligand-Gated Cation-selective channels
  2. The movement of Sodium and Potassium
  3. Stimulatory
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19
Q

All MUSCARINIC cholinergic receptors are _________, meaning when they are bound, they allow __________.

A
  1. GPCR’s

2. Activation of second messenger systems

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20
Q

List the 3 places that Nicotinic receptors are found:

A
  1. Motor End Plates of Skeletal Muscle (Somatic System)
  2. ALL autonomic Post-Ganglionic Neurons (Ganglia)
  3. Chromaffin Cells of Adrenal Medulla
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21
Q

When ACh binds Muscarinic receptors, the effect is described as ___________.

A

EITHER stimulatory or inhibitory

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22
Q

List the 2 places that Muscarinic receptors are found:

A
  1. ALL effector organs of the Parasymp. NS
  2. Certain effector organs of the Symp. NS
    i. e. Sweat Glands, vascular smooth muscle OF skeletal muscle.
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23
Q

Where are Adrenergic receptors found?

A

In the target tissues of the SNS

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24
Q

Alpha-1 Adrenergic Receptors:

  1. Where are they found? (6)
  2. What physiological effect do they elicit?
  3. What mechanism do they use to elicit it?
A
  1. Found in:
    - Vascular S.M.
    - Skin
    - GI Tract
    - Bladder
    - Sphincters
    - Radial Muscle/Iris
  2. S.M. Contraction/Constriction
  3. Increase of IP3 to Increase Ca2+
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25
Q

Alpha-2 Adrenergic Receptors:

  1. Where are they found? (2)
  2. What physiological effect do they elicit?
  3. What mechanism do they use to elicit it?
A
  1. Found in:
    -GI Tract WALL
    -ON Post-ganglionic motor neurons
  2. Relaxation and DECREASE NE release
  3. Inhibition of Adenylyl Cyclase to DECREASE cAMP
    (serve as negative feedback)
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26
Q

Beta-1 Adrenergic Receptors:

  1. Where are they found? (4)
  2. What physiological effect do they elicit?
  3. What mechanism do they use to elicit it?
A
  1. Found in:
    -Heart (mainly)
    -Salivary Glands
    -Adipose Tissue
    -Kidney
  2. Increase Heart Contractility/Rate/Contraction and lipolysis, and Renin secretion from kindey
  3. Stimulation of AC to INCREASE cAMP
    (opposite of Alpha-2 receptors)
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27
Q

Beta-2 Adrenergic Receptors:

  1. Where are they found? (5)
  2. What physiological effect do they elicit?
  3. What mechanism do they use to elicit it?
A
  1. Found in:
    -Vascular S.M. OF Skeletal Muscle
    -GI Tract WALL
    -Bladder
    -Bronchioles
    -Uterus
  2. Relaxation of Smooth Muscle/Dilation
  3. Stimulation of AC to INCREASE cAMP
    (Same as Beta-1 receptors)
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28
Q

Nicotinic Cholinergic Receptors:

  1. Where are they found? (3)
  2. What physiological effect do they elicit?
  3. What mechanism do they use to elicit it?
A
  1. Found in:
    - Motor End Plate of Skeletal Muscle (Somatic)
    - Ganglia (Post-ganglionic neurons of ANS)
    - Adrenal Medulla
  2. Various Effects
  3. Ionic: Depolarization via opening of Na+ and K+ channels
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29
Q

Muscarinic Cholinergic Receptors:

  1. Where are they found? (3)
  2. What physiological effect do they elicit?
  3. What mechanism do they use to elicit it?
A
  1. Found in:
    - ALL effector organs of PNS
    - Sweat Glands
    - Vascular S.M. of Skeletal Muscle
  2. Various Effects
  3. Increase IP3 to Increase Ca2+
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30
Q

What is the difference between N1/Nm receptors and N2/Nn receptors?

A

N1 receptors are Nicotonic Cholinergic receptors of the SOMATIC NS, while N2 receptors are Nicotinic Cholinergic receptors of the Autonomic NS.

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31
Q

Describe how ACh can negatively feedback on itself:

A

If it binds to Muscarinic receptors, only the M1, M3, and M5 receptors are stimulatory and activate PLC with a G-subQ. The M2 and M4 receptors are inhibitory and will use a G-sub-i to inhibit AC and decrease cAMP.

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32
Q

How is ACh recycled after eliciting its effect?

A

Cholinesterases hydrolyze it into acetate and choline. That Choline can then be taken back up by the Na+-coupled Choline symporter in pre-ganglionic neurons to be acetylated and packaged into secretory vesicles as de novo ACh.

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33
Q

What is required for ACh to elicit its effect on its nicotinic receptor?

A

2 molecules of ACh must bind to 2 alpha-subunits of the 5-subunit cholinergic receptor to allow the movement of Na+ and K+.

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34
Q

What type of GPCR G-subunit do each of the 5 muscarinic receptor types bind?

A

Gq: M1 and M5 —> Increases IP3–> PLC
Gi: M2 and M4 –> Decreases AC –> cAMP (in heart)
Gs: M3 –> Increases AC –> cAMP

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35
Q

The most discussed muscarinic receptors are the M2, which is found in ________, and the M3 which is found in ________.

A
  1. The HEART (SA and AV nodes)

2. Smooth muscle, Glands, etc.

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36
Q

What is the main enzyme required for the synthesis of ACh?

A

Choline transaminase in the Cholinergic Neurons

37
Q

What is the rate-limiting step in Catecholamine synthesis?

A

Tyrosine —> L-DOPA

Catalyzed by Tyrosine hydroxylase

38
Q

How does Tyrosine enter Adrenergic Cells?

A

Via a Na+-coupled symporter, just like Choline does.

39
Q

After dopamine is formed, how does it enter the secretory vesicle?

A

The VMAT (Vesicular Monoamine Transporter) moves it into the vesicle in exchange for an H+ ion.

40
Q

What happens AFTER dopamine enters its secretory vesicle?

A

It is converted into NE by Dopamine B-hydroxylase

41
Q

What enzyme is required for conversion of NE to Epinephrine and where is it found?

A

Phenylethanolamine N-Methyltransferase, found in the Adrenal Medulla

42
Q

The release of neurotransmitter secretory vesicles is dependent on _______.

A

Ca2+ for exocytosis

43
Q

Which of the Adrenergic receptors is found both on the target effector cells AND the post-ganglionic neuron releasing it (to act as a negative feedback regulator)?

A

Alpha-2 Adrenergic receptors

44
Q

How is NE removed from the synaptic cleft to terminate its effects? (4 mechanisms)

A
  1. Re-uptake into the Post-ganglionic neuron by a Na+-coupled NE symporter OR first degraded by MAO.
  2. Uptake by Target: Metabolism to inactive metabolite AFTER uptake. NE is degraded by MAO or Catechol-O-Methyltransferase (COMT) within the target cell.
  3. Diffuses away from synaptic cleft into circulation
  4. Vesicular Uptake: VMAT takes NE back up into vesicles for re-use.
45
Q

The “balloon” shape of the bladder is called the _______. It is surrounded by the _______, also called the ______. It is also surrounded by an ______.

A
  1. Detrusor Muscle
  2. Internal Sphincter
  3. Trigone
  4. External Sphincter
46
Q

Bladder contraction and penile erection are both controlled by __________ receptors.

A

Muscarinic

47
Q

Describe the structure of Myosin:

A

Contains 6 Polypeptide chains:

  • 2 PAIRED heavy chains
  • 4 PAIRED light chains (2 on each heavy chain)
48
Q

The heavy chains of myosin form its ________, which exhibits _______ and _____.

A
  1. Secondary Alpha-Helical Structure

2. A Coiled Tail and 2 Globular Heads (cross-bridges)

49
Q

What 2 important structures are located on the cross-bridges of myosin?

A
  1. The Actin-Binding Site

2. The ATP-Hydrolase

50
Q

Actin Filaments are made up of: ________ (3 proteins)

A
  1. Actin
  2. Tropomyosin
  3. Troponin
51
Q

Each molecule of ______ has a myosin binding site, but these molecules polymerize to form _______, which possesses a ________ arrangement.

A
  1. G-actin
  2. F-actin
  3. Helical
52
Q

Tropomyosin Function:

A

Filamentous protein that BLOCKS myosin-binding sites on actin molecules in a filament.

53
Q

Troponin is made up of 3 ______ called : _____, _____, and ____.

A
  1. Globular Proteins

2. Troponin T, Troponin I, and Troponin C

54
Q

Troponin Function:

A

Upon binding Ca2+, Troponin rotates Tropomyosin (into the F-actin cleft) to expose myosin-binding sites on F-actin.

55
Q

Define “Rigor” in terms of the Cross Bridge Cycle:

A

The presence of Ca2+, BUT lack of ATP prevents myosin from releasing actin so muscles STIFFEN.

56
Q

Explain the Sliding Filament Theory:

A

Actin slides over Myosin (as Myosin acts as a motor and pulls it) to cause shortening of the sarcomere, and ultimately the muscle as a whole. The Sliding Filament Theory refers to the COLLECTIVE sliding of all sarcomeres in a muscle simultaneously causing its contraction.

57
Q

Muscle Contraction is initiated by _________.

A

An elevation of intracellular Ca2+ ions

58
Q

Describe the 2 types of muscle contractions:

A
  1. Isometric: No length change in muscle during contraction, but change in FORCE over time.
  2. Isotonic: No force change in muscle during contraction, but change in LENGTH.
59
Q

Muscle Contraction is initiated by _________.

A

An elevation of intracellular Ca2+ ions

60
Q

What does the Length-Tension curve explain?

A

The highest number of myosin head groups (cross bridges) overlapping with actin in sarcomeres to create an optimal force/tension.

61
Q

What does Active Force refer to?

A

The optimal level of actin-myosin overlapping in sarcomeres to create an optimal force/tension.

62
Q

Passive Force:

A

The force that a muscle generates when it is RESISTING being stretched. NO CONTRACTION involved. (No actin-myosin activity)

63
Q

Total Isometric Force:

A

The total force that a muscle can generate at varied specific lengths WHEN STIMULATED to contract. (AND resisting stretch)

64
Q

Equation for Active Force:

A

Total Isometric - Passive = Active Force

65
Q

Equation for Active Force:

A

Total Isometric - Passive = Active Force

66
Q

Why is Pre-Load important to the Force-Length curve?

A

A higher pre-load (more stretch) will contribute some of the force required to move the after-load. So actin-myosin force won’t need to be as strong.

67
Q

Differentiate between the two types of summation:

A
  1. Temporal: Increasing the FREQUENCY of stimulation of the muscle to increase force.
  2. Spatial: Increasing the AMOUNT of muscle fibers utilized in contraction to increase force.
68
Q

Tetanus:

A

The maximal force produced by a high frequency of stimulation of muscle contraction.

69
Q

Motor Unit:

A

A neuron AND the muscle fiber that it innervates

70
Q

What does Excitation-Contraction Coupling describe?

A

How Action Potential energy is rapidly propagated acroos an entire muscle to be utilized/converted into synchronous Muscle Contraction.

71
Q

What allows release of ACh from the axon terminal for action potentials to occur?

A

Depolarization of the terminal causes opening of L-type Ca2+ channels in the terminal that allow entry of Ca2+. This Ca2+ causes fusion of the ACh synaptic vesicles with the membrane and release of ACh into the NMJ.

72
Q

What is meant by the term “Safety Factor”?

A

The excessive release of ACh by the neurons at the NMJ to ensure a large enough depolarization for an AP to occur.

73
Q

Describe the 5 possible causes of NMJ dysfunction:

A
  1. Atrophy: Disuse of a muscle or a severed nerve
  2. Inhibition of ACh release (Botulism)
  3. Inhibition of ACh degradation (Physotigmine, Edroph.)
  4. Inhibition of ACh binding to receptors (Curare)
  5. Inhibition of ACh receptors (Myasthenia Gravis)
74
Q

Cardiac muscle cells are extremely _______, and their ends are held together by ______.

A
  1. Branched

2. Intercalated Discs

75
Q

While skeletal muscle uses _______ and ______ to increase force of contraction, cardiac muscle uses ______ to increase force.

A
  1. Temporal summation
  2. Spatial Summation
  3. GAP Junctions (Neither temporal nor spatial summation)
76
Q

What allows the cardiac muscle cells to act in syncitium?

A

GAP junctions connect all cardiac muscle cells and allow rapid propagation of electrical signals and all cells to act as a single unit.

77
Q

Why can’t cardiac muscle use temporal summation? Why is this essential and desirable?

A
  1. Because cardiac action potentials last almost as long as the actual contraction, so increasing frequency of stimulation has no effect.
  2. Because this prevents the heart from ever experiencing tetanus (tetany).
78
Q

How does the heart control its own force of contraction? (2 ways)

A
  1. It controls intracellular Ca2+ levels, to which cardiac contractions are proportional.
  2. Frank-Starling Mechanism
79
Q

Explain how Cardiac muscle can have graded action potentials:

A

In skeletal muscle action potentials, intracellular Ca2+ is high enough to saturate all troponin and give 100% cross-bridge efficiency, giving an ALL OR NONE response. In cardiac muscle, only enough Ca2+ for about 40% efficiency is used in normal conditions, so the heart can increase or decrease Ca2+ availability in the cytoplasm to give a GRADED response.

80
Q

Define Inotropic:

A

The ion conditions within a cell, referring to Ca2+, Na+, or K+ typically.

81
Q

Explain the Frank-Starling Law:

A

Increase in pre-load (blood volume entering the heart) will result in a proportional increase in force of contraction. This is the auto-regulation mechanism of the heart.

82
Q

Give the 2 reasons why increased pre-load to the heart causes greater contractile force:

A
  1. Force-Length Curve: Greater over-lapping of cross-bridge activity.
  2. Passive Force/Tension: Greater passive force created due to the rigidity of cardiac muscle contributes some force to the overall contractile strength.
83
Q

Describe the arrangement of ultra-structural components in smooth muscle:

A

Actin and myosin filaments are criss-crossing and forming a lattice-like network.

84
Q

Instead of using Tropinin as a Ca2+-binding component, as in skeletal muscle, Smooth muscle utilizes ________.

A

Calmodulin

85
Q

How are smooth muscle cross-bridges “side polar”?

A

Cross-bridges are exhibited over the entire length of myosin thick filaments.

86
Q

The myo-filaments that form a lattice-like network in smooth muscle are held together by ________. These structures are analogous to ______ in striated muscle.

A
  1. Dense Bodies

2. Z-Discs

87
Q

Why is it important that smooth muscle myosin is side polar?

A

It means that actin filaments do not interfere with each other upon shortening, so contractile force can be maintained over long periods of time (which is very important in the organs they supply).

88
Q

Which type of muscle exhibits GAP junctions?

A

Cardiac AND Smooth Muscle

MSAP Week 2 (3 decks)

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