Drugs M&R Flashcards

0
Q

Where are nAChR found?

A

Post ganglionic neurones in SNS
Post ganglionic neurones in PNS
Skeletal muscle effectors

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1
Q

Describe the action of nAChR antagonist

A

These drugs bind to nAChR, thereby reducing the amount of ACh that can bind

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2
Q

What is trimethapan an example of? What is the clinical use of this drug?

A

nAChR antagonist

Controls hypotension in surgery

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3
Q

What are tubocurarine and pancuronium examples of? What is the clinical effect of these drugs?

A

nAChR antagonist

Muscle paralysis during anaesthesia

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4
Q

Describe the action of an mAChR agonist

A

These drugs bind to and stimulate mAChR

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5
Q

Where are mAChR found?

A

PNS - effectors

SNS - effectors of sweat glands only (rest are adrenoceptors)

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6
Q

What is pilocarpine an example of? What is the clinical use of this drug?

A

MAChR agonist
Major- Glaucoma
Minor- suppression of atrial tachycardia, increasing GI activity after abdominal surgery, stimulation of bladder emptying

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7
Q

Describe the action of mAChR antagonists

A

These drugs bind to mAChR, thereby reducing the amount of ACh that can bind

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8
Q

What is hyposcine an example of? What is the clinical use of this drug?

A

mAChR antagonist
Anaesthetic pre-medication - decreases bronchial and salivary secretions, prevents reflex bronchoconstriction, reduces anaesthetic induced bradycardia, sedative effect

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9
Q

What is ipratropium bromide an example of? What is the clinical use of this drug?

A

mAChR antagonist

Asthma- treats bronchoconstriction caused by increased parasympathetic discharge

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10
Q

What are homotropine and tropicamide examples of? What is the clinical use of these drugs?

A
mAChR antagonist
Ophthalmoscopic examination (eye conditions) - pupillary dilatation and paralysis of accommodation
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11
Q

What is tolteridine an example of? What is the clinical use of this drug?

A

mAChR antagonist

Over active bladder

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12
Q

Describe the action of AChEsterase inhibitors

A

These are drugs that bind to AChEsterase, preventing ACh from binding and thereby increasing the length of time ACh is available to stimulate receptors

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13
Q

What are pyridostigimine, physostigimine, dyflos and edrophonium examples of? What is the clinical use of these drugs?

A

AChEsterase inhibitor

Myesthenia gravis and glaucoma

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14
Q

What are tacrine and donepezil examples of? What is the clinical use of these drugs?

A

AChEsterase inhibitor

Alzheimer’s disease

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15
Q

Describe the action of B1 agonists

A

These drugs bind to and stimulate B1 adrenoceptors

Increase in Heart rate and Force of contraction

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16
Q

Where are B1 adrenoceptors found?

A

Heart (SAN and Myocardium)

17
Q

What is dobutamine an example of? What is the clinical use of this drug?

A

Selective B1 agonist
Positive inotropic and chronotropic effects in the heart, in treating circulatory shock (prone to causing cardiac dysrhythmias)

18
Q

Describe the action of B2 agonists

A

These drugs bind to and stimulate B2 adrenoceptors
Vasodilation in blood vessels
Bronchodilation in airways

19
Q

Where are B2 adrenoceptors found?

A

Blood vessels

Airways

20
Q

What are salbutamol and terbutaline examples of? What is the clinical use of these drugs?

A

Selective B2 agonist

Highly effective in reversing bronchoconstriction in Asthmatics

21
Q

Describe the action of a1 agonists

A

These drugs bind to and stimulate a1 adrenoceptors
Vasoconstriction in blood vessels
Dilation of pupil
Localised secretion from sweat glands

22
Q

Where are a1 adrenoceptors found?

A

Blood vessels
Pupil of eye
Sweat glands

23
Q

What are phenylephrine, oxymetazoline and adrenaline examples of? What is the clinical use of these drugs?

A

Selective a1 agonists
Nasal decongestant, may be given with a local anaesthetic injection to cause local vasoconstriction and so retard the dissipation of the anaesthetic

24
Q

Describe the action of a2 agonists

A

These drugs bind to and stimulate a2 adrenoceptors

25
Q

Where are a2 adrenoceptors found?

A

Presynaptic axons - NA reuptake

26
Q

What is clonidine an example of? What is the clinical use of this drug?

A

Selective a2 agonist
Antihypersensitivity agents
(Stimulation of inhibitory presynaptic receptors which decrease NA release via a centrally mediated action)

27
Q

Describe the action of a adrenoceptor antagonists

A

These drugs bind to a adrenoceptors, thereby reducing the amount of NA that can bind

28
Q

What are phentolamine and phenoxybenzamine (irreversible) examples of? What is the clinical use of these drugs?

A

a adrenoceptor antagonist
Cause peripheral vasodilation in PVD (oppose sympathetically mediated vasoconstriction)
Not used to treat hypertension as they can cause postural hypotension and reflex tachycardia
Pheochromocytoma- block the effect of excess secreted NA by tumour

29
Q

Describe the action of selective a1 antagonists

A

These drugs bound to a1 adrenoceptors, thereby reducing the amount of NA that can bind

30
Q

What is prazosin an example of? What is the clinical use of this drug?

A

Selective a1 antagonist

Hypertension (but postural hypotension and impotence are unwanted side effects)

31
Q

Describe the action of B antagonists

A

These drugs bind to B adrenoceptors, thereby preventing NA from binding

32
Q

What are atenolol and propranolol examples of? What is the clinical use of these drugs?

A

B adrenoceptor antagonists

Hypertension, cardiac dysrhythmias, angina and MI

33
Q

What are the major unwanted side effects of B antagonist drugs?

A

Bronchoconstriction, bradycardia, cold extremities, insomnia, depression

34
Q

What are aprenolol and oxprenolol examples of? What is the clinical use of these drugs?

A

Partial B adrenoceptor agonists
Believed to cause fewer side effects than B antagonists, when treating hypertension, cardiac dysrhythmias, angina and MI
This is because they provide a low tonic stimulation of B adrenoceptors while still blocking receptor stimulation by NA

35
Q

How does a-methyl tyrosine work? What is its clinical effect?

A

Competitively inhibits tyrosine hydroxylase and therefore blocks de novo synthesis of NA. Its only clinical use is to inhibit NA synthesis in pheochromocytoma.

36
Q

How does a-methyl DOPA work? What is its clinical effect?

A

Taken up by adrenergic neurones and is converted to a-methyl-NA. Unlike the true neurostransmitter, it is poorly metabolised and therefore accumulates in the synaptic vesicles of noradrenergic terminals. When released by Ca2+ mediated exocytosis, it preferentially activates pre-synaptic a2 receptors. The bg subunit of the a2 receptor inhibits the VOCC, reducing Ca2+ mediated neurotransmitter release.

37
Q

How does Carbi-DOPA work? What is its clinical effect?

A

Inhibits DOPA decarboxylase in the periphery, but not in the CNS (Does not cross the BBB). It is used in combination with L-DOPA in the treatment of Parkinson’s disease.

38
Q

How do adrenergic blocking drugs work? What are their clinical effects? What are some examples?

A

Selectively concentrated in terminals by Uptake 1. They act via a variety of mechanisms, including a local anaesthetic action reducing impulse conduction & Ca2+ mediated exocytosis, partial blocking action on reputable of neurotransmitter and depletion of NA from synaptic vesicles. Rarely used therapeutically because of severe side effects (postural hypotension).
Guanethidine, Bretylium

39
Q

How do indirectly acting sympathomimetic agents (IASAs)? What are their clinical effects? What are some examples?

A

Structurally related to NA. Because they are only weak agonists at adrenoceptors, they are though to exert their actions by additional/other methods. IASAs are recognised and transported into the adrenergic terminal by Uptake 1 and taken up into Synaptic Vesicles. The displaced NA can leak into the synaptic cleft by a mechanism unrelated to Ca2+ mediated exocytosis. The extent to which the NA leaks into the synaptic cleft can be greatly enchanced by inhibition of the NA-degrading enzyme MAO.
Tyramine, Amphetamine, Ephedrine

40
Q

How do uptake 1 inhibitors work? What are their clinical effects? What is an example?

A
Comprise an important class of therapeutic agents, the tricyclic antidepressants. These agents exert their therapeutic actions centrally and their possible peripheral actions (e.g. tachycardia and cardiac dysrhythmias) are unwanted side effects, avoided by choice of drug and dose.
Amitryptyline