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Pharma > Adrenergic Transmission And Its Presynaptic Modification > Flashcards

Adrenergic Transmission And Its Presynaptic Modification Flashcards

1
Q

What are sympathomimetics?

A

they are adrenergic drugs that act directly on adrenergic receptors by activating them

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2
Q

What are sympatholytics?

A

Adrenergic drugs that block the action of the NT at there receptor or they can interrupt the release of NE from adrenergic neurons

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3
Q

What is the rate limiting step of NE synthesis?

A

tyrosine hydroxylase

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4
Q

What is the co-factor of tyrosine hydroxylase?

A

Vit C

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5
Q

What is the mechanism of action of Reserpine?

A

It inhibits VMAT2

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6
Q

What is the mechanism of action of Guanethidine?

A

It inhibits the release of vesicles containing NE into the synaptic cleft

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7
Q

What is NET?

A

It is the Na+/Cl- dependent NE transporter

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8
Q

What inhibits NET?

A

TCA e.g., Imipramine

Serotonin-NE reuptake inhibitors e.g., duloxetine, cocaine

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9
Q

What is the action of methyl-p-tyrosine?

A

Inhibits tyrosine hydroxylase

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10
Q

What is the mechanism of action of MAO inhibitors?

A

it leads to increased NE in the mobile pool

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11
Q

What is the result of releasers?

A

it leads to the release of NE from the mobile poo.

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12
Q

What is the effect of an alpha 2 agonist on the pre-synaptic neuron?

A

Negative feedback

Reduced NE in the synapse

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13
Q

What is the effect of an alpha 2 antagonist on the pre-synpatic neuron?

A

Prevention of negative feedback

Increased NE synthesis and release

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14
Q

Both the skeletal muscles and vasculature have alpha and beta receptors, which predominates?

A

Beta receptors

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15
Q

What is desensitisation of adrenergic receptors?

A

Prolongued exposure to catecholamines leads to decreased responsiveness of these receptors

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16
Q

What are the possible mechanisms of desensitisation of adrenergic receptors?

A
  1. Sequestration of the receptors so that they are unavailable for interaction with the ligand
  2. Down regulation
  3. Inability to couple to H protein because the receptor has been phosphorylated on the cytoplasmic side
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17
Q

What is the result of OH substitutions in the 3rd and 4th position of the benzene ring?

A

Increased potency
Decreased absorption and distribution of the drugs
decreased lipophility

18
Q

What are the characteristics of catechomaines with 3,4-IH substituents?

A

Most potent sympathomimetics
Bad pharmacokinetics: poor absorption, bad distribution, short duration of action.
They must be given parenterally for systemic use - they don’t penetrate the BBB
They are substrates of COMT, this further decreases their bioavailability

19
Q

What are the characteristics of 3-OH, 4-OH or 3,5-OH derivatives?

A

Weaker sympathomimetics than the catecholamines but they have better pharmacokinetics
They are not substrates of COMT, but still polar drugs - they may be given orally with low bioavailability

20
Q

What are the characteristics of non-substituted derivatives?

A

They have no hydroxyl groups
Very weak direct or only indirect (NE releasing) sympathomimetic action (bad pharmcodynamics)
They have very good pharmacokinetics: good absorption and penetration through the BBB (resulting in CNS effects)

21
Q

What are the possible substitutions on the amino group?

A

Methylation

Large substitution

22
Q

What is the effect of methylation on the amino group?

A

Methylation increases the relative potency on the Beta 2 receptors (NE/EPI)

23
Q

What is the effect of large substitution of the amino group?

A

Large substitution on the amino group increases significantly the beta 2 receptor affinity

24
Q

What is a precursor substance of adrenergic synthesis?

A

Levodopa

25
Q

Name the reuptake inhibitors

A

Cocaine
TCA
Amitryptyline
Desipramine

26
Q

Name the MAO inhibitors

A

Tranylcypromine
Selegiline
Moclobemid

27
Q

What are the side edicts of guanethidine and debrisoquine?

A 
Orthostatic hypotension
Diarrhoea
Impaired Ejaculation 
Sodium and Water retention
Nasal Stuffiness
Upregulation of postsynaptic receptors
28
Q

What is the clinical indication of Guanethidine and Debrisoquine?

A

Hypertension

Limited use because of their side effects

29
Q

What is the mechanism of action of Bretylium?

A 
Acts like Guanethidine in NE nerve terminals 
It blocks K+ channels on the heart (a class 3 anti-arrhythmic action)
30
Q

What is the clinical use of Bretylium?

A

Antiarrhythmic indication

31
Q

How is Bretylium administered?

A

IV in emergency during resuscitation from ventricular fibrillation after lidocaine and cardioversion

32
Q

What are the adverse effects of Bretylium?

A 
Initial release of NE can lead to ventricular arrhythmias
Sympatholytic action (e.g., orthostatic hypertension)
33
Q

What is the mechanism of action of reserpine?

A

Blocks the uptake of biogenic amines into the synaptic vesicles. they are not stored in the vesicles and thus broken down by MAO

34
Q

What are the theoretical indications of Reserpine?

A

Hypertension

Psychosis

35
Q

What are the main side effects of Reserpine?

A 
Sympatholytic actions (diarrhoea, postural hypotension: NE depletion in the periphery) 
Mental depression (NE and serotonin depletion in the CNS)
Parkinsons (dopamine depletion in the nigrostriatal system)
36
Q

What is the effect of alpha-methyl-tyrosine?

A

Blocks the tyrosine hydroxylase enzyme, no NE synthesis, decreased alpha and beta stimulation

37
Q

What are the clinical indications of alpha-methyl-tyrosine?

A

May act synergistically with phenoxybenzamene in the treatment of pheochromocytoma

38
Q

What is the mechanism of action of Tetrodotoxin, Saxitoxin and local aesthetics?

A

Blocks voltage sensitive Na+ channels

39
Q

What is the mechanism of action of w-Conotoxin?

A

Blocks calcium channels

40
Q

What is the action of 6-OH-dopamine?

A

Destroys the nerve terminal

Pharma (23 decks)

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