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Stage 2 Basic Pharmacology > 1.12 Adrenergic agonists and antagonists > Flashcards

1.12 Adrenergic agonists and antagonists Flashcards

1
Q

Where in the PNS does NA act as a neurotransmitter

A

synapse between postganglioc fibres of sympathetic NS and target organ/effector tissue

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2
Q

Noradrenaline : synthesis at junction describe:

A 
start substrate: tyrosine
1st enexyme: tyrosine hydroxylase
 1st intermediate product: DOPA
2nd enzyme: DOPA 				decarboxylase,
2nd intermediate product: DA
3rd enzyme:  DA β-hydroxylase
Final product: NA
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3
Q

Noradrenaline : release at junction describe:

A

exocytosis

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4
Q

Noradrenaline : receptor interaction at junction describe:

A

α, β, receptors

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5
Q

Noradrenaline : termination at junction describe:

A

Uptake and recycled or metabolism by monoamine oxidase into amines

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6
Q

The actions of NA are mediated via 2 main classes of NA receptor: name

A

α-noradrenergic receptors

β-noradrenergic receptors

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7
Q

What are the subclasses of α-noradrenergic receptors:

2) Where are they located
3) type of receptor
4) response time

A

1) alpha 1 and 2
2) Located in effector tissues/targets of sympathetic system

3) G-protein coupled receptors (or metabotropic receptors)
4) Slow (seconds) responses

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8
Q

Which sympathetic effects are mediated by α1-noradrenergic receptors:

1) Pupils dilate(radial muscle contracts)
2) Lens of eye adjust for far vision
3) Airways in lungs dilate
4) Heart rate increases
5) Blood vessels to limb muscles dilate
6) Blood vessels to visceral organs & skin constrict
7) Brain activity general alertness

A

1, 6 and 7

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9
Q

Which sympathetic effects are mediated by α1-noradrenergic receptors:

1) Pupils dilate(radial muscle contracts)
2) Lens of eye adjust for far vision
3) Airways in lungs dilate
4) Heart rate increases
5) Blood vessels to limb muscles dilate
6) Blood vessels to visceral organs & skin constrict
7) Brain activity general alertness
8) why? what else do they do?

A

NONE,
as they are presynaptic receptors(both NA, ACh and other neurotransmitters), role is turning off further release of neurotransmittor thus have no tole in sympathetic effects,

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10
Q

Which sympathetic effects are mediated by α2-noradrenergic receptors:

1) Pupils dilate(radial muscle contracts)
2) Lens of eye adjust for far vision
3) Airways in lungs dilate
4) Heart rate increases
5) Blood vessels to limb muscles dilate
6) Blood vessels to visceral organs & skin constrict
7) Brain activity general alertness
8) why? what else do they do?

A

NONE,
as they are presynaptic receptors(both NA, ACh and other neurotransmitters), role is turning off further release of neurotransmittor thus have no tole in sympathetic effects,

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11
Q

autoreceptor vs heteroreceptor

A

auto- means self thus, neurotransmittor bound to it is from self, heter- means different thus neurotransmittor bound to it is from another neurone.

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12
Q

Sympathetic effects mediated by Beta 1 receptors:

Pupils dilate
Lens of eye adjust for far vision
Airways in lungs dilate
Heart rate increases (and force of contraction)
Blood vessels to limb muscles dilate
Blood vessels to visceral organs & skin constrict
Brain activity general alertness

A

Heart rate increases (and force of contraction)

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13
Q

Sympathetic effects mediated by Beta 2 receptors:

Pupils dilate
Lens of eye adjust for far vision
Airways in lungs dilate
Heart rate increases (and force of contraction)
Blood vessels to limb muscles dilate
Blood vessels to visceral organs & skin constrict
Brain activity general alertness

A

Lens of eye adjust for far vision (ciliary muscle relax)
Airways in lungs dilate (bronchodilation)
Blood vessels to limb muscles dilate

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14
Q 
Sympathetic effects  mediated by Beta 3 receptors:
Pupils dilate 
Lens of eye adjust for far vision
Airways in lungs dilate
Heart rate increases
Blood vessels to limb muscles dilate
Blood vessels to visceral organs & skin  constrict
Brain activity general alertness
A 
lolz none , BUT does 
Increase lipolysis (breakdown of triglycerides to fatty acids)
so does have some sort of sympathetic effect
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15
Q

Which noradrenergic receptor:

increase cardiac rate and force

A

beta1 – receptors

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16
Q

Which noradrenergic receptor:

bronchodilation, ciliary muscle relaxation

A

beta2– receptors

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17
Q

Which noradrenergic receptor:

lipolysis/increased metabolism

A

beta3 – receptors

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18
Q

Which noradrenergic receptor:

inhibition of neurotransmitter release

A

alpha-2

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19
Q

Which noradrenergic receptor:

smooth muscle & vaso-constriction

A

alpha 1

20
Q

Why is adrenaline given as an injection?

A

destroyed in gut

21
Q

Adrenaline can be given subcut (locally)

  1. why
  2. what receptor is it binding to?
    3) action?
A

1) can prolong & isolate local anaesthesia.
2) alpha 1
3) vasoconstriction

22
Q

Adrenaline can be given intramusc

  1. why
  2. what receptor is it binding to?
    3) action?
A
  1. to treat anaphylactic shock. (Acute multisystem hypersensitivity reaction-cardiovascular collapse/ bronchospasm)
    2&3.
    alpha 1 - mediated smooth muscle contraction (vasoconstriction, )
    beta 1 – mediated cardiac stimulation
    beta 2 - mediated bronchiol smooth muscle relaxation:
23
Q

alpha - 2 agonist can be used for….1

and to treat…2

A

1) hypertension although mechanism is thought to also involve a central effect (nucleus tractus solitarius) which results in decrease sympathetic outflow.
2) withdrawal symptoms in morphine withdrawal (inhibits central NA release)

24
Q

selective beta 1 agonist

1) action?
2) used to treat?

A

1) increased cardiac rate and force
2) Used to treat heart failure.
 1 – mediated cardiac stimulation (increased firing rate and increased contractile force)

25
Q

selective beta 2 agonist

1) action?
2) used to treat?

A

1) bronchodilation
2) asthma
 2 – mediated bronchiol smooth muscle relaxation:

26
Q

beta 2 /beta 3 agonist)
What are the uses of beta 2?
2) What are the uses of beta 3?

A

1) Used to treat asthma (2 )

2) Increases muscle bulk in athletes/body builders/livestock (3)

27
Q

selective alpha1 -antagonist
A) how do they worK?
1) used to treat? (as causes…)
2) side effects?

A

A) blocks alpha1- mediated smooth mm vasoconstriciton

1) a) Used to treat hypertension (as causes vasodilation and decreased vascular resistance)
b) Urination problems in prostate hyperplasia (relaxation of smooth muscle in bladder neck, ease of urinary flow)
2) orthostatic or postural hypotension due to some loss in sympathetic reflex

28
Q

1) What is beta 1 and beta 2 antagonist used to treat?
2) how?
3) What is an issue with this?

A

1) hypertension and angina
2) Blocking beta1 receptors decreases cardiac output and also decreases oxygen demand
3) However blocking beta2 receptors causes bronchoconstriction. Therefore contraindicative in asthmatics .

29
Q

selective beta 1 antagonist

1) used to treat?
2) how?
3) side effects:

A

1) hypertension and angina
2) Blocking 1 decreases cardiac output and also decreases oxygen demand.
3) can cause rebound hypertension/ angina on abrupt withdrawal probably due to beta1 receptor supersensitivity

30
Q

selective beta 2 antagonist

1) used to treat?
2) how?

A

1) glaucoma

2) antagonism of 2– receptors cause ciliary contraction, and decreased intraocular pressure

31
Q

What is the action of the noradrenergic agonist is used to:

1) locally to prolong local anaesthesia
2) to treat hypertension)
3) (to treat heart failure
4) to treat asthma
5) to treat anaphylactic shock

A

1) adrenaline btw, vasoconstriction alpha1 – mediated

2) alpha2 mediated inhibition of NA release
3) cardiac stimulation beta 1 - mediated
4) bronchiol smooth muscle relaxation beta 2 - mediated
5) smooth muscle contraction alpha 1
cardiac stimulation, beta 1
bronchiol smooth muscle relaxation beta 2

32
Q

What is the actions of different noradrenergic antagonists used to treat hypertension

A
  1. vasodilation alpha-1 - mediated

2. cardiac inhibition beta 1 –mediated (can be non-selective to beta 1&beta2 or selective to beta 1)

33
Q

What are the 2 different ways of controlling salivary excretion, explain (which receptor and effect):

A

Directly: a1,b1and 2
(increases secretion)
INdirectly: a2
(inhibits NA realease= xerostomia)

34
Q

Why does the following increase salivary excretion:

1) beta 1 receptor activation
2) beta 2 receptor activation
3) alpha 1 receptor activation

A

1) b1 stimulates protein secretion
2) Beta 2 role uncertain
3) a1 stimulates water electrolyte secretions

35
Q

1) When intefering with synthesis of product do you interfering with something upstream or downstream?
2) what is the rate limiting enzyme in
3) What enzymes are downstream of this enzyme?
4) What is added as a false substrate to substitute DOPA (formed after tyrosine)?

A

1) downstream
2) tyrosine hydroxylase
3) DOPA decarboxylase and DA beta-hydroxylase
4) meDOPA

36
Q

What does tyrosine hydroxylase convert tyrosin into?

2) WHat is the next enzyme and what is the next substrate?
3) WHat is the next enzyme and what is the next substrate?

A

1) DOPA
2) DA, DOPA decarboxylase
3) NA, beta-hydroxylase

37
Q

meDOPA .inhibits enzyme activity, What is it used to treat?

A

• Used in the treatment of hypertension (in pregnancy as few side effects)

38
Q

what does reserpine effect about NA at synapses?

2) What is it used to treat?
3) What else relating to autoinhibitory control can also treat this condition?

A

Reserpine disrupts storage, so there is an overall decrease in available NA for release thus NA transmission also decreases.

2) hypertension
3) alpha2 agonist

39
Q

NA uptake can be blocked by __A__

This will __B__ the action of NA in the synapse, used to treat ___C____

A

A) NA reuptake inhibitors
B) prolong
C) depression
`

40
Q

What is • desipramine tricyclic ?

What is reboxetine

A
  • desipramine tricyclic antidepressants

* reboxetine selective noradrenaline reuptake inhibitors

41
Q

After reuptake NA is metabolised by the enzymes ___A____, and ___B____.
• By blocking these enzymes the amount of NA available for release is ___C___.

A

A) monoamine oxidase (MAO)
B) catecholamine transferase (COMT)
C) increased

42
Q

tranylcypramine blocks __A___and allows ___B___ NA to be recycled so ___C___ NA neurotransmission

A

A) MAO
B) more
C) increases

43
Q

What do the following inhibit:

a) methyldopa
b) reboxetine

A

a) synthesis

b) uptake

44
Q

What do the following inhibit:

a) reserpine
b) tranylcypramine

A

a) storage

b) metabolism

45
Q

What is the cheese reaction?

A
  • Tranylcypramine and other MAOIs not only block the metabolism of NA but also block the metabolism of dietary amines (e.g. commonly found in cheese, marmite) and amines found in popular cold remedies.
  • Accumulation of dietary amines can have a sympathomimetic effect and result in hypertension

Stage 2 Basic Pharmacology (16 decks)

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