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Fundamentals of pharmocology and physiolgy > Adrenergic effects > Flashcards

Adrenergic effects Flashcards

1
Q

What are the nerve fibres like in the sympathetic nervous system

A

There are short pre-ganglionic nerve fibres and long post-ganglionic nerve fibres

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2
Q

What receptors do sympathetic nerves have

A

nicotinic acetylcholine receptors

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3
Q

What is the main neurotransmitter in the sympathetic nervous system and where does it act

A

Noradrenaline

It acts on the adrenergic G coupled receptors

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4
Q

How is DOPA (dihydroxyphenylalanine) made

A

Tyrosine is converted to DOPA by the action of tyrosine hydroxylase
This is the rate determining step

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5
Q

How is dopamine made

A

DOPA is converted to dopamine by the action of DOPA decarboxylase

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6
Q

What is dopamine used for

A

Its a neurotransmitter in the brain

Its involved in many pathways especially reward-motivated behaviour

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7
Q

How is noradrenaline made

A

Dopamine is converted to noradrenaline by the action of dopamine beta-hydroxylase

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8
Q

Where and how is adrenaline made

A

In the adrenal medulla, noradrenaline is converted to adrenaline by the action of phenylethanolamine N-methyltransferase (PNMT)

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9
Q

What is sympathomimetics

A

A drug that mimics or looks like you’ve stimulated the sympathetic nerves

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10
Q

What is indirect sympathomimetics

A

These drugs overstimulate the sympathetic nervous system

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11
Q

What is direct sympathomimetics

A

When the drug is an agonist which will bind to the receptor taking the place

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12
Q

What is isoprenaline

A

A synthetic stimulator

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13
Q

What is the order in sensitivity of stimulators on alpha receptors

A
  1. Noradrenaline
  2. Adrenaline
  3. Isoprenaline
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14
Q

What is the order in sensitivity of stimulators on beta receptors

A
  1. Isoprenaline
  2. Adrenaline
  3. Noradrenaline
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15
Q

What type of receptor is an alpha 1 receptor

A

Gq protein coupled receptor

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16
Q

What happens when alpha 1 receptors are activated

A

Phospholipase C is activated
Splits PIP2 into IP3 and DAG
IP3 causes calcium release from smooth ER
DAG causes kinase C production

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17
Q

What are the physical outcomes of alpha 1 receptor stimulation

A

Vascular smooth contraction; vasoconstriction in blood vessels
Contraction of seminal vesicles; iris muscle (pupil dilation) and pilomotor muscle

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18
Q

What are alpha 1 agonists

A

Phenylephrine and oxymetazoline

19
Q

What are alpha 1 antagonists

A

Prazosin, doxazosin and tamsulosin

20
Q

What type of receptor is an alpha 2 receptor

A

Gi protein coupled receptor

21
Q

What happens when alpha 2 receptors are activated

A

Inhibits adenylate cyclase

therefore decreases cAMP production so protein kinase A production reduced

22
Q

What are the physical outcomes of alpha 2 receptor stimulation

A

Inhibition of transmitter release from sympathetic nerves
The likely hood of the calcium channels on the adrenergic neurone opening is less even if depolarisation occurs since there is a lack of protein kinase A

23
Q

What are alpha 2 agonists

A

Clonidine

24
Q

What are alpha 2 antagonists

A

Yohimbine

25
Q

What type of receptor is a beta 1 receptor

A

Gs protein coupled receptor

26
Q

What happens when beta 1 receptors are stimulated

A

Activates adenylate cyclase therefore increases cAMP production so protein kinase A production is increased

27
Q

What are the physical outcomes of beta 1 receptor stimulation

A

Positive chronotropy - Heart rate increases
Positive inotropy - Force increases
Positive lusitropy - Rate of relaxation increases
Positive dromotropy - Conduction velocity of atrioventricular node increases

28
Q

What does cAMP do after beta 1 stimulation

A

Will interact with a pacemaker channel in the SAN that open up by hyperpolarisation

29
Q

What does protein kinase A do after beta 1 stimulation

A

Makes calcium channels have a higher sensitivity to voltage therefore there is a larger influx of calcium ions
Stimulates potassium channels so the action potential depolarises quicker therefore there is a shorter action potential
Will affect calcium release channels, increases the uptake of calcium back into the sarcoplasmic reticulum - contraction is bigger but briefer

30
Q

Where is the juxta glomerular apparatus (JGA) located

A

Between afferent and efferent renal arteries

31
Q

What does the JGA do

A
  1. Increases renin release
  2. Renin converts inactive angiotensinogen to active angiotensin I
  3. This is turned into angiotensin II
32
Q

What are the effects of angiotensin II

A
  1. Contracts vascular smooth muscle itself
  2. Increases the release of noradrenaline from sympathetic nerves
  3. Stimulates aldosterone which reabsorbs more water so you have an increase in circulating volume
33
Q

What type of receptor is a beta 2 receptor

A

Gs protein coupled receptor

34
Q

What happens when beta 2 receptors are stimulated

A
  1. Increased cAMP production

2. Increased K+ channel activity and decreased Ca release

35
Q

What are the physical outcomes of beta 2 receptor stimulation

A
  1. Vascular dilation/airway relaxation

2. Decreased myosin light chain kinase and decreased contraction

36
Q

What are beta 2 agonists

A

Salbutamol, salmeterol and clenbuterol

37
Q

What are beta 2 antagonists

A

Propanolol

38
Q

What type of receptor is a beta 3 receptor

A

Gs protein coupled receptor

39
Q

What are beta 3 agonists

A

Mirabegron

40
Q

What are the physical outcomes of beta 3 receptor stimulation

A

Enhancement of lipolysis in adipose tissue

41
Q

Whats the treatment of an overreactive bladder

A

The beta 3 agonist mirabegron

42
Q

What is a nasal decongestant

A

The alpha 1 agonist phenylephrine and ephedrine

43
Q

Use of adrenoreceptor blockers

  1. Heart
  2. Kidneys
  3. Eye drops
A
  1. Atenolol
  2. Atenolol, less renin production
  3. Timolol

Fundamentals of pharmocology and physiolgy (12 decks)

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