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Pharmacology > Autonomic Nervous System (textbook) > Flashcards

Autonomic Nervous System (textbook) Flashcards

1
Q

What does the autonomic nervous system consist of and what does it control?

A

The autonomic nervous system consists of the sympathetic and parasympathetic nervous systems and controls various systems of the body.

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2
Q

What transmitter is released at the sympathetic nerve end?

A

Noradrenaline/norepinephrine is released at the sympathetic nerve end.

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3
Q

What receptors do noradrenaline and norepinephrine target?

A

Norepinephrine and noradrenaline target the alpha, beta 1 and beta 2 adrenoceptors.

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4
Q

Whats the difference in nerve fibres between sympathetic snd parasympathetic fibres?

A

Sympathetic fibres arise from the thoracolumbar region of the spinal cord (T1-L3) whereas the parasympathetic fibres leave via cranial nerves especially ( III, VII, IX and X) and sacral spinal roots.

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5
Q

What neurotransmitter are released by the parasympathetic nerves?

A

Postganglionic parasympathetic nerve fibres release acetylcholine.

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6
Q

What receptors does acetylcholine bind to?

A

Acetylcholine acts on muscarinic receptors.

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7
Q

Explain the difference in the inactivation of norepinephrine and acetylcholiine.

A

Norepinephrine is largely inactivated largely by reuptake into the nerve terminals. Acetylcholine is inactivated by the enzyme acetylcholinesterase.

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8
Q

What hormone mimics most sympathetic effects?

A

Adrenaline

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9
Q

What are the effects of sympathetic stimulation?

A

Sympathetic stimulation can be thought of fight or flight responses:

  1. Pupillary dilation (allows more light into the retina)
  2. Bronchiolar dilation ( facilitates increased ventilation)
  3. Heart rate and force are increased; blood pressure rises (more blood for increased activity of skeletal muscles).
  4. Vasoconstriction in skin and viscera and vasodilation to skeletal muscle (appropriate redistribution of blood go skeletal muscle
  5. To provide extra energy, glycogenolysis is activated snd the blood glucose level increases. The gastrointestinal tract and bladder relax
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10
Q

The ANS consists of motor neurons that:

A
  1. Innervate smooth muscle, cardiac muscle and glands
  2. Make adjustments to ensure optimal support for body activities
  3. Operate via subconscious control
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11
Q

What are drug designed to target ANS do?

A

Drugs in this group are designed to either enhance or mimic the actions of the ANS or to block the effects of the neurotransmitter at the receptor sites

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12
Q

Describe the basic anatomy of a parasympathetic neuron.

A

A parasympathetic neuron consists of both pre and post ganglionic neurons

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13
Q

Describe the basic anatomy of a preganglionic neuron

A

A preganglionic neuron:
Cell body in the brain or spinal cord.
Axon is a myelinated type B fiber that extends to autonomic ganglion

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14
Q

Describe the basic anatomy of a post ganglionic neuron

A

A post ganglionic neuron
The cell body lies outside the CNS in an autonomic ganglion
The axon is an unmyelinated type C fiber that terminates in a visceral recptor

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15
Q

Explain how neurotransmitters are released.

A
  1. Action potential arrives at the axon terminal
  2. This causes calcium to enter the terminal via voltage gated calcium channels
  3. This causes the neurotransmitter to be releaesd
  4. The neurotransmitter diffuses across the synaptic cleft to ehich it binds to receptors on postsynaptic target cell membranes
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16
Q

Name the different ANS neurotransmitters 7

A
  1. Acetylcholine
  2. Norepinephrine
  3. Dopamine
  4. 5HT
  5. GABA
  6. Glutamate
  7. Histamine
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17
Q

What receptors do norepinephrine and epinephrine bind to?

A

Norepinephrine binds to adrenergic receptors such as alpha, beta dopaminergic receptors

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18
Q

What receptors do acetylcholine bind to?

A

Acetylcholine binds to muscarinic and nicotinic receptors.

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19
Q

Acetylcholine is a parasympathetic neurotransmitter. Describe how it is made, broken down and remade.

A
  1. Acetylcholine is made up of choline and acetyl coA
  2. In the synaptic cleft, acetylcholine is rapidly broken down by the enzyme acteylcholinesterase.
  3. Choline is transported back into the nerve terminal where it is used to make more Ach
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20
Q

Why does Acetylcholine lack therapeutic importance?

A

Ach lacks therapeutic importance because of it’s multiplicity of actions and its rapid inactivation by acetylcholine esterase.

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21
Q

What are the actions of Ach?

A
  1. Decrease in heart rate
  2. Decreased cardiac output
  3. Decreased blood pressure (vasodilation)
  4. Increased salivation
  5. Increased sweating
  6. Increased intestinal secretions
  7. Increased motility
  8. Miosis (pupil constriction)
  9. Increased urination
  10. Increased bronchial secretions
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22
Q

How are parasympathetic drugs classified?

A

Parasympathetic drugs can be classified as either:

  1. Direct acting (muscarinic agonists)
  2. Indirect acting (reversible/ irreversible acetylcholineesterase inhibitors)
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23
Q

Name a direct acting muscarinic agonist

A

Pilocarpine

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24
Q

Name the reversible acetylcholine esterase inhibitors: 4

A
  1. Neostigmine
  2. Pyridostigmine
  3. Physostigmine
  4. Edrophonium
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25
Q

What are the irreversible acetylcholine esterase inhibitors? 3

A
  1. Organophosphates
  2. Parathion
  3. Malathion
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26
Q

When describing a drug, what are we interested in: 5

A
  1. Name:
  2. Mode of action (MOA):
  3. Therapeutic uses:
  4. Side effects (S/E):
  5. Administration:
27
Q

What does cholinergic toxicity present with? 3

A
  1. Pin point pupils ( miosis)
  2. Excessive bowel sounds
  3. Diaphoresis (excessive sweating)
28
Q

Describe how reversible indirect cholinergic agonist work?

A

Reversible cholinergic agonist promote cholinergic activity by preventing the breakdown of Ach. This is completely by temporarily binding to acetylcholine esterase for a matter of minutes to hours.

29
Q

Describe how irreversible indirect cholinergic agonists work.

A

Irreversible indirect cholinergic agonist increase cholinergic activity by forming covalent bonds with cholineseterase. Thus ach cannot be broken down. The body must make more ach-e to break down these bonds.

30
Q

What is cholinergic crisis and what are the symptoms?8

A

Cholinergic crisis is an over-activation of the muscarinic receptors. SLUD

  1. Salivation
  2. Flushing
  3. Decreased BP
  4. Abdominal pain
  5. Diarrhea
  6. Bronchospasm
31
Q

What is glaucoma?

A

Glaucoma is group of eye conditions that can cause blindness. With all types of glaucoma, the nerve connecting the eye to the brain is damaged, usually due to high eye pressure

32
Q

What is myasthenia gravis?

A

Myasthenia gravis is weakness and rapid fatigue of muscles under voluntary control. The condition is caused by the breakdown in communication between nerves and muscles.

33
Q

How is edrophonium used to diagnose myasthenia gravis?

A

Edrophonium is administered. If muscle strength improves, possible myasthenia grsvis, if no improvement it isn’t myasthenia gravis.

34
Q

How do we treat insecticide and pesticide poisoning?

A

We treat with atropine or pralidoxine (cholinesterase regenerator)

35
Q

What are anticholinergics/ cholinergic antagonists?

A

These are drugs that bind to cholinoreceptors and prevent the effects of ach and other cholinergic agonists.

36
Q

List the anti-muscarinics (4)

A
  1. Atropine
  2. Ipratopium
  3. Scopolamine
  4. Cyclopentolate
37
Q

List the neuromuscular blockers 4

A
  1. Cis-atracurium
  2. Vecuronium
  3. Rocuronium
  4. Succinylcholine
38
Q

What is a ganglionic blocker?

A

Nicotine

39
Q

What are the muscarinic antagonists?

A

Atropine and scopolamine block muscarinic receptors and thus prevent muscarinic functions

40
Q

What is mydriasis?

A

Mydriasis is pupil dilation

41
Q

What is cycloplegia?

A

Cycloplegia is the weakened contraction of the ciliary muscle; loss of the ability to accommodate (focus on near vision)

42
Q

What is xerostomia?

A

Xerostomia is dryness is the mouth

43
Q

What does the postganglionic neuron of the SNS produce?

A

The post ganglionic neuron of the SNS producds norepinephrine

44
Q

There are two places where the postganglionic neuron behaves differently, name these places.

A
  1. In sweat gland it produces Ach

2. In the adrenal medulla, norepinephrine is converted into epinephrine by phenylethanolamine-N-methyl transferase

45
Q

What are NE and epinephrine metabolized by?

A

Both NE and epinephrine are metabolized by:

  1. Catechol-o-methyl transferase (COMT)
  2. Monoamineoxidase (MAO)
46
Q

Name the types and there subtypes of the adrenergic receptors.

A
  1. α1 α2

2. β1 β2 β3

47
Q

What are drugs that activate adrenergic receptors known as?

A

Drugs that activate adrenergic receptors are known as sympathomimetics

48
Q

What are drugs that inhibit adrenergic receptors known as?

A

Drugs that inhibit adrenergic receptors are known as sympatholytics

49
Q

Explain NE transmission:

A
  1. Synthesis of NE: hydroxylation of tyrosine is a rate limiting step
  2. Uptake into storage vesicles: dopamine enters a vesicle and is converted to NE
  3. Release of neurotransmitters: an influx of calcium causes fusion of vesicle with cell membrane in a process known as exocytosis
  4. Binding to a receptor: post synaptic receptor is activated by binding of neurotransmitter
  5. Metabolism: NE and E is metabolized by COMT and MAO
  6. Removal of NE: released NE is rapidly taken into the neuron. Re-uptake is inhibited by cocaine and imipramine
50
Q

What does NE activate?

A

NE is direct acting and activates the following receptors>

α1, α2 β1

51
Q

What receptors does epinephrine activate?

A

Epinephrine is direct acting and activates:

α1,α2, β1 β2

52
Q

What does ephidrine (low blood pressure medication)act on?

A

Ephidrine acts on all adrenergic receptors (direct acting) and indirect (mixed) by weakly stimulating the release of NE and E from nerve endings in the SNS

53
Q

What does amphetamine (CNS stimulant used to treat narcolepsy and obesity) do?

A

Amphetamine acts indirectly by strongly stimulating the release of NE and Epinephrine

54
Q

What does cocaine do?

A

Cocaine is an indirect acting drug that inhibits the re-uptake of NE and dopamine

55
Q

Where are α1 receptors located and are they stimulatory or inhibitory? 3

A

α1 receptors are located on the post synaptic membrane of:

  1. Vascular smooth muscle
  2. The eye

α1 receptors have stimulatory effect

56
Q

Where are α2 receptors located and are they stimulatory or inhibitory? 3

A

α2 receptors are located on the presynaptic nerve endings and have an inhibitory effect on the release of NE:

  1. GIT
  2. Pancreas
  3. Platelets
57
Q

Where are β1 receptors located? 3

A

β1 receptors show an equal affinity for NE and E and can be located in cardiac tissue

58
Q

Where are β2 receptors located? 3

A

β2 receptors have a greater affinity for E than NE. These receptors are found in the:

  1. Respiratory
  2. Uterus
  3. Vascular smooth muscle (VSM)
  4. Liver
59
Q

Where are β3 receptors located? 3

A

β3 receptors are involved in lipolysis and the detrusor muscle of the bladder

60
Q

Discuss α1 receptor activation

A

α1 receptors are found in most VSM, pupillary dilator muscle, pilomotor smooth muscle, prostate and heart. Activation increases IP3 2nd messenger which results in vasoconstriction as well as:

  1. Pupil dilation
  2. Erect hair
  3. Prostate contraction
  4. Increase in the force of contraction of the heart
61
Q

Discuss α2 receptor activation

A

α2 receptors are located in post synaptic CNS adrenoreceptors, platelets, adrenergic and cholinergic nerve terminals and fat cells. Activation leads to decreased CAMP production resulting in decreased NE release. This leads to:

  1. Platelet aggregation
  2. VSM contraction
  3. Inhibtion of lipolysis
62
Q

Discuss β1 activation

A

β1 receptors are located in the heart and juxtglomerular apparatus. Activation leads to an increase in CAMP resulting in:

  1. Increased HR, contractility, conduction and velocity
  2. Increased renin release
63
Q

Discuss β2 activation

A

β2 receptors are located in the respiratory, uterine, VSM, skeletal muscle and liver. Activation results in increased CAMP redulting in vasodilation and bronchodilation as well as:

  1. Smooth muscle relaxation
  2. Skeletal muscle potassium uptake
  3. Glycogenolysis
64
Q

Discuss β3activation

A

β3 receptors are found in fat cells and activation results in lipolysis.

Pharmacology (13 decks)

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