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Pharm > PHARM; Lecture 7, 8, 9 and 10 - Cholinoceptor antagonists, SNS agonist and antagonists, NM blocking drugs > Flashcards

PHARM; Lecture 7, 8, 9 and 10 - Cholinoceptor antagonists, SNS agonist and antagonists, NM blocking drugs Flashcards

1
Q

What is the difference in potency between agonists and antagonists?

A

They both possess affinity, but only agonists possess efficacy

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2
Q

Which of the following drugs has efficacy for the muscarinic acetylcholine receptor? Acetylcholine Atropine Acetyl-cholinesterase Adrenaline Acetate

A

ACh

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3
Q

Where are nicotinic receptors located?

A

On the first ganglion of every ANS

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4
Q

What are the nicotinic receptor antagonists also called and where do they act on?

A

On the nicotinic receptor or block the ion channel (usually have 2 mechanisms, where it can block the receptor or the ion channel), so also called ganglion blocking drugs

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5
Q

What are some examples of nicotinic receptor antagonists?

A

Hexamethonium, Trimetaphan (main clinically used)

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6
Q

How do nicotinic receptor antagonists work?

A

They are use-dependent block -> most effective when channel is open as is a channel blocker not competitive antagonist so isn’t surmountable; also incomplete, slows the ion movement but doesn’t stop them

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7
Q

Which of the following effects would be observed at REST after treatment with a ganglion blocking drug? Increased heart rate Pupil constriction Bronchodilation Detrusor contraction Increased gut motility

A

Increased heart rate and bronchodilation -> NB: when using nicotinic receptor antagonists the more dominant arm of ANS is blocked causing opposite arm symptoms

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8
Q

Why do nicotinic receptor antagonists cause hypotension?

A

Due to the CVS effects as it reduces renin secretion and causes dilation of blood vessels

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9
Q

What smooth muscle effects do nicotinic receptor antagonists cause?

A

Pupil dilation, decreased GI tone, bladder dysfunction, bronchodilation

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10
Q

What exocrine effects do nicotinic receptor antagonists cause?

A

Reduced secretions

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11
Q

What is the clinical use of hexamethonium?

A

Anti-hypertensive (1st) but had loads of side effects

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12
Q

What is the clinical use of trimetaphan?

A

Causing hypotension during surgery (short-acting)

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13
Q

Where are muscarinic receptors present?

A

On effector organs of mainly PSNS (and some SNS)

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14
Q

What are some examples of muscarinic receptor antagonists?

A

Atropine and Hyoscine -> both plant based

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15
Q

Which physiological responses would be influenced by the muscarinic receptor antagonists?

A
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16
Q

What are the CNS effects of atropine?

A

Normal dose -> little effect; toxic dose -> mild restlessness and agitation (less M1 selective)

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17
Q

What are the CNS effects of hyoscine?

A

Normal dose -> Sedation, amnesia; toxic dose -> CNS depression or paradoxical CNS excitation (associated with pain)

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18
Q

What is the clinical use of Tropicamide?

A

Examination of the retina

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19
Q

What are the clinical uses of muscarinic receptor antagonists?

A

Opthalmic, anaethetic premedication, neurological

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20
Q

What are the anaesthetic premedication in muscarinic receptor antagonists?

A

Blocks constriction, blocks copious watery secretion and blocks decrease in rate and contractility -> can cause sedation

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21
Q

What are the neurological uses of muscarinic receptor antagonists?

A

For motion sickness as it controls eye movements to maintain vision whilst in motion and stopping the relay to the vomiting centre, causing sensory mismatch as your eyes are telling you one thing and the balance centre is saying something else, which is all fed back to the vomiting centre, so you feel nauseous (hyoscine patch)

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22
Q

How are muscarinic receptor antagonists used in Parkinson’s disease?

A

Cholinergic/dopaminergic balance in basal ganglia for fine control of movement -> DA neurones originitating from substantia nigra moving DA into striatum, which are massively reduced in PD -> M4 receptors have a negative effect on DA receptor, which is further trying to dampen down the DA response, which by reducing M4 effect, increases DA release as it inhibits cholinergic in basal ganglia

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23
Q

What are the respiratory uses of muscarinic receptor antagonists?

A

Asthma/obstructive airway disease -> blocks constriction - Ipratropium Bromide used as it is easier to trap in lungs as it is more difficult to cross membranes, so can only affect muscarinic receptors in the lungs

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24
Q

What are the GI uses of muscarinic receptor antagonists?

A

IBS which are M3 selective antagonists so lose the other muscarinic side effects -> blocks increased motility and tone and secretion

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25
Q

What are the unwanted effects of muscarinic receptor antagonists?

A

Hot as hell (decreased sweating, thermoregulation), Dry as a bone (decreased secretions), blind as a bat (cyclopegia), mad as a hatter (CNS disturbance)

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26
Q

Which of the following drugs would you administer to treat an atropine overdose? Bethanechol Ecothiopate Hyoscine Physostigmine Pralidoxime

A

Bethanechol (muscarinic receptor agonist) Ecothiopate (irreversible anticholinesterase) Hyoscine (atropine-like) ^^^Physostigmine (reversible anticholinesterase)^^^ Pralidoxime (reverses anti-cholinesterase poisoning)

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27
Q

What are some other parasympatholytics?

A

Botulinum toxin - used in botox (localised and injected directly into skeletal muscle), acts interfering with SNARE complex - blocking the vesicles of ACh from joining to the presynaptic membrane

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28
Q

What are the actions of directly acting sympathomimetics on each of the receptors?

A

Mimic NA/A by binding to and stimulating adrenoceptors -> prinicpally used for action on CVS, eyes and lungs

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29
Q

What is the mechanism of action of trimetaphan?

A

Nicotinic receptor blockade (mainly, but does both)

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30
Q

What is the mechanism of action of hexamethonium?

A

Ion channel blocker (mainly, but does both)

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31
Q

What is the most potent nicotinic receptor antagonist?

A

Irreversible antagonist alpha-bungarotoxin (nicotinic receptor blocker) which can also target skeletal muscle, paralysing the prey

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32
Q

Why are atropine and hyoscine different in symptoms?

A

Due to hyoscine being more lipid-soluble and more M1 selective c.f. atropine (hence why no sedative effect in atropine)

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33
Q

How would you overcome atropine poisoning?

A

Increased ACh release to overcome it and use a reversible antagonist, like physostgmine

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34
Q

What are the response mediators of each of the adrenergic receptors?

A

Alpha1 -> PLC, IP3, DAG; A2-> decreased cAMP; beta1 -> increased cAMP; B2 -> increased cAMP

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35
Q

Which receptors cause what actions in the body?

A
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36
Q

What is the relative selectivity of NA?

A

a1=a2 > b1=b2

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37
Q

What is the relative selectivity for A?

A

b1=b2 > a1=a2

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38
Q

How is NA synthesised?

A
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39
Q

What are some examples of directly acting SNS agonists and which receptor do they act on?

A

Adrenalne (non-selective), phenylephrine (a1), clonidine (a2), dobutamine (b1), salbutamol (b2)

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40
Q

Why is adrenaline used instead of NA in treatment of anaphylaxis?

A

Adrenaline is more selective on the beta receptors so first thing it does is dilate the bronchioles (b2), which is more important than the circulation in that moment -> vasoconstrictor (a1) and tachycardia (b1) effects

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41
Q

What is glaucoma caused by?

A

Increased in IOP caused by poor drainage of aqueous humour -> untreated can permanently damage optic nerve, causing blindness

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42
Q

What is the use of adrenaline in Glaucoma?

A

By causing vasoconstriction it prevents extra release of aqueous humoour, so less is present

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43
Q

What are some other uses for adrenaline?

A
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44
Q

What are the unwanted actions of adrenaline?

A
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45
Q

How is adrenaline used in pulmonary obstructive conditions?

A

In asthma (emergencies i.m. and s.c.), acute bronchospasm associated with chronic bronchitis or emphysema -> b2 bronchodilation and suppression of mediator release

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46
Q

What is phenylephrine’s selectivity?

A

a1 >> a2 >>> b1/b2

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47
Q

What is the mechanism of action of phenylephrine?

A

Chemically related to A and resistant to COMT but not MAO

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48
Q

What are the clinical uses of phenylephrine?

A

Vasoconstriction, mydriatic, nasal decongestant

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49
Q

What is the mechanism of action of clonidine?

A

Reduces sympathetic tone by a2 mediated presynaptic inhibition of NA release, with central action in brainstem within baroreceptor pathway reducing symp outflow

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50
Q

What is the selectivity of clonidine?

A

a2 >> a1 >>> b1/2

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51
Q

WHat are the clinical uses of clonidine?

A

Treatment of hypertension and migraine, reduces sympathetic tone

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52
Q

What is the selectivity of isoprenaline?

A

b1=b2 >>>> a1/2

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53
Q

What is the difference between isoprenaline and adrenaline?

A

Isoprenaline is chemically similar but less susceptible to uptake 1 and MAO breakdown with t1/2 of 2h

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54
Q

What are the clinical uses of isoprenaline?

A

Cardiogenic shock, acute heart failure, MI

55
Q

What do you have to worry about with isoprenaline?

A

b2-stimulation in VSM in skeletal muscle results in fall in venous BP which triggers a reflex tachycardia via stimulation of baroreceptors

56
Q

What is the clincial use of dobutamine?

A

Cardiogenic shock, lacks isoprenaline’s reflex tachycardia; admin by iv, with plasma t1/2 2min (met by COMT)

57
Q

What are some indirectly acting SNS agonists?

A

Cocaine and tryramine

58
Q

What is the mechanism of cocaine?

A

Release of DA with blocking of uptake 1 receptor

59
Q

What are the actions and side effects of cocaine on the CNS and CVS?

A
60
Q

What is the selectivity of salbutamol?

A

b2>>b1>>>a1/2

61
Q

What is salbutamol?

A

Synthetic catecholamine derivative with relative resistance to MAO and COMT

62
Q

What are the clinical uses of salbutamol?

A

Treatment of Asthma (b2 relaxation of bronchial SM, inhibition of release of bronchoconstrictor substances from mast cells); Treatment of threatened premature labour (b2-relaxation of uterine SM)

63
Q

What is tyramine?

A

Dietary amino acid -> acts as a false NT

64
Q

What is the mechanism of action of tyramine?

A

If MAO inhibitors are taken causes a hypertensive crisis as the metabolites aren’t broken down

65
Q

What are the side effects of salbutamol?

A

Reflex tachycardia, tremor, blood sugar dysregulation

66
Q

What are the types of adrenoceptors and their functions?

A

a1- Vasoconstriction, Relaxation of GIT. a2 - Inhibition of transmitter release, contraction of vascular smooth muscle, CNS actions. b1- Increased cardiac rate and force, relaxation of GIT, renin release from kidney. b2- Brochodilation, vasodilation, relaxation of visceral smooth muscle, hepatic glycogenolysis b3- Lipolysis.

67
Q

Name a non-selective A1/B1 antagonist?

A

Labetalol

68
Q

Name an a1/2 antagonist?

A

Phentolamine

69
Q

Name an a1 antagonist?

A

Prazosin

70
Q

Name a b1/2 antagonist

A

Propranolol

71
Q

Name a b1 antagonist?

A

Atenolol

72
Q

When would you use an SNS antagonist?

A

Hypertension, cardiac arrhythmias, angina, glaucoma

73
Q

What is hypertension?

A

Increased BP associated with an increased risk of other diseases -> Diastolic arterial pressure greater than 90mmHg (140/90 - NICE, ABPM - 135/85))

74
Q

Which elements contribute to hypertension?

A

Blood volume, Cardiac Output and Peripheral vascular tone

75
Q

Which tissues are targets for antihypertensives?

A

Symp nerves that release NA -> kidney (blood vol/vasoconstriction), heart, arterioles (determine peripheral resistance), CNS (determines BP set point and regulates some systems involved in BP control and ANS)

76
Q

What are the b adrenoceptor antagonists which are cardioselective, nonselective and with additional a1 antagonist activity?

A

x

77
Q

How do beta antagonists work?

A

Act in CNS to reduce sympathetic tone -> Heart (b1) to reduce heart rate and CO but disappears in chronic treatment; kidneys (b1) to reduce renin production with common long term feature is reduction in TPR

78
Q

What are the presynaptic effects of beta antagonists?

A

Blockade of facilitatory effects of presynaptic beta receptors on NA release may also contribute to antihypertensive effect

79
Q

What are some unwanted effects of b-adrenoceptors?

A

Bronchoconstriction (in asthmatics can be dramatic/life threatening), cardiac failure (patients with heart disease may rely on symp drive to heart to maintain an adequate CO and removal by blocking b-ceptors produces degree of cardiac failure); hypoglycaemia (masks symptoms of hypoglycaemia, using non-selective ones is more dangerous as they block B2 receptor driven glycogenolysis); fatigue (due to reduced CO and muscle perfusion), cold extremities (loss of b-ceptor mediated vasodilation in cutaneous vessels); bad dreams

80
Q

What is propanolol - selectivity, effect, side effects?

A

S: non-selectvie for beta adrenoceptors; effect: at rest causes very little change in HR, CO or arterial pressure, but reduces effect of exercise/stress on variables; SE: typical non-selective adverse effects

81
Q

What is atenolol - selectivity, effect, side effects?

A

S: b1 (cardio-selective drug); effect: antagonises effects of NA on heart but will affect any tissue with b1; SE: less effect on airways that non-selective drugs but still not safe with asthmatic patients with selectivity conc dependent

82
Q

What is labetalol - selectivity, effect, side effects?

A

S: dual acting B1/A1 (4:1) antagonist, E: lowers BP by reduction in PR; SE: Induces change in HR/CO but effect wanes with chronic use

83
Q

When are alpha adrenoceptor antagonists used?

A

Non-selective, so used in fall in arterial pressure like postural hypotension, CO/HR increases (reflex response to fall arterial pressure), blood flow through cutaneous and splanchic vascular beds increased but effects on SM are slight

84
Q

What is phentolamine - selectivity, effect, side effects?

A

Non-selective alpha; E: causes vasodilatation and fall in BP due to blockade of A1 - BUT a2 blockade tends to increase NA release which enhances reflex tachycardia occurring with any BP lowering agent, increased GIT motility, diarrhoea (problem)

85
Q

What is prazosin - selectivity, effect, side effects?

A

Highly selective for A1; E: vasodilation and fall in arterial pressure, less tachycardia than non-selective antagonist as don’t increase NA release from nerve terminals (no A2), CO decreases due to fall in venous pressure as result of dilation of capitance vessels

86
Q

What is methyldopa?

A

False transmitter -> antihypertensive agent which is taken up by noradrenergic neurons -> decarboxylated and hydroxylated to form false transmitter, alpha-methylNA; not deaminated within neuron by MAO so tends to accumulate in larger quantities than NA so displaces it

87
Q

What is the mechanism of action of methyldopa?

A

Released in same way as NA, but differs in 2 impoertant respects in action on adrenoceptors -> less active than NA on A1 so less effective at vasoconstriction, more active on presynaptic A2 receptors, autoinhibitory feedback mechanism operates more strongly, reduces transmitter release below normal levels; also some CNS effects, stimulates vasopressor centre in brainstem to inhibit symp outflow

88
Q

What are some benefits of methyldopa?

A

Renal and CNS blood flow is well maintained so is used in hypertensive patients with renal insufficiency/Cerebrovascular disease, recommended in hypertensive pregnant women as has no adverse effects on fetus despite crossig blood-placenta barrier

89
Q

What are some adverse effects of methyldopa?

A

Dry mouth, sedation, orthostatic hypotension, male sexual dysfunction

90
Q

What is arrhythmia and its cause?

A

Abnormal/irregular heart beats with Myocardial ischaemia as main cause

91
Q

What are class II antiarrhythmics?

A

Increase in symp drive to heart via B1 can precipitate/aggravate arrhythmias - AV conductance depends on symp activity and refractory period is increased by b-antagonists, interfering with AV conduction in atrial tachys and to slow ventricular rate

92
Q

What is an example of a Class II antiarrhythmic with effects?

A

Propanolol -> non-selective beta antagonist class II drug with effects mainly attributed to b1 antagonism -> reduces mortality of patients with MI, particularly successful in arrhythmias that occur during exercise or mental stress

93
Q

What is angina?

A

Pain that occurs when O2 supply to myocardium is insufficient for its needs -> distribution on chest, arm and neck; brought on by exertion/excitement

94
Q

What are the 3 types of angina?

A

Stable, unstable, variable

95
Q

What is stable angina?

A

Pain on exertion -> increased demand on heart and is due to fixed narrowing of coronary vessels

96
Q

What is unstable angina?

A

Pain with less and less exertion, culminating with pain at rest -> platelet-fibrin thrombus associated with a ruptured atheromatous plaque but without complete occlusion of vessel - risk of infarction

97
Q

What is variable angina?

A

Occurs at rest caused by coronary artery spasm - associated with atheromatous disease

98
Q

What is a good type of adrenoceptor antagonist to use for angina and why?

A

Beta antagonists because reduce myocardial oxygen demand -> decrease HR, SBP, cardiac contractile activity; at low doses b1-selective agents (metoprolol) reduce HR and myocardial contractile activity without affecting bronchial smooth muscle -> reduce O2 demand whilst maintaining the same degree of effort

99
Q

What are some adverse effects of beta blockers (metoprolol)?

A

Fatigue, insomnia, dizziness, sexual dysfunction, bronchospasm, bradycardia, heart bock, hypotension, decreased myocardial contractility

100
Q

Which cases should you avoid giving beta blockers to?

A

Patients with bradycardia (HB of less than 55bpm), bronchospasm, hypotension (SBP less than 90mmHg), AV block/severe CHF

101
Q

What is glaucoma and its cause?

A

Increase in IOP, caused by poor drainage of aqueous humour -> untreated could permanently damage optic nerve (blindness)

102
Q

What is aqueous humour and where is it produced?

A

Produced by blood vessels in ciliary body via actions of carbonic anhydrase - flows into posterior chamber through pupil to anterior chamber, drains into trabecular network and into veins and canal of Schlemm with production indirectly related to BP and blood flow in ciliary body

103
Q

Which beta antagonists are used in glaucoma?

A

Non-selective B1 and 2; carteolol hydrochloride, levobunolol hydrochloride, timolol maleate

104
Q

What is the function of the beta antagonists in glaucoma?

A

Reduce rate of aqueous humour production by blocking receptors on ciliary body -> selective B1 antagonist betaxolol hydrochloride is also effective

105
Q

In which other conditions can you use B-antagonists?

A

Anxiety states - to control somatic symptoms associated with symp over reactivity, such as palpitations and tremor; migraine prophylaxis; benign essential tremor

106
Q

Summary of sites of drug action in propagation of action potential in the muscles -> presynaptic action (all skeletal muscle relaxants - intentional or not)

A
107
Q

Which drugs act on the central process in a NMJ?

A

Spasmolytics (anti-spastic: used in CF, CP) -> diazepam, baclofen -> have central action and reduce generation of AP in the cell body

108
Q

Which drugs act on the conduction of nerve AP in motor neurone?

A

Local anaesthetics -> inhibit Na influx, reducing generation and propagation of AP (injecting near nociceptic neurones, with unintentional muscle relaxation)

109
Q

Which drugs act on the release of ACh?

A

Hemicholinium, Ca2+ entry blockers (reduces exocytotic release of Ca), neurotoxins (reduces release of ACh) -> NOT NEEDED TO KNOW (yet)

110
Q

Which drugs act on depolarisation of motor end-plate -> AP initiation?

A

Tubocurarine, suxamethonium

111
Q

Which drugs act on the propagation of AP along muscle fibre and muscle contraction?

A

Spasmolytics -> dantrolene

112
Q

Which drugs cause a nondepolarising effect (postsynapse)?

A

Competitive antagonists like Tubocurarine and atracurium -> NB: large molecules with less flexibility around the bonds

113
Q

Which drugs cause a depolarising effect (postsynapse)?

A

Agonists -> Suxamethonium

114
Q

What are some important things to note about pain, consciousness and respiration about postsynaptic neuromuscular blocking drugs?

A

They don’t affect pain sensation (not analgesic) or consciousness and always assist respiration (can affect breathing muscles) until drug is inactive or antagonised

115
Q

What is the method of action of suxamethonium?

A

Extended EP depolarisation (depolarisation block, phase 1), fasciculations -> flaccid paralysis

116
Q

What is the pharmacokinetics of suxamethonium?

A

Administration = IV, duration of paralysis = 5 min, metabolised by pseudocholinesterase in liver and plasma

117
Q

What are the uses of suzamethonium?

A

Endotracheal intubation, muscle relaxant for ECT

118
Q

What are the unwanted effects of suxamethonium?

A

Post-op muscle pains, bradycardia (direct muscarinic action on heart - atropine), hyperkalaemia (soft tissue injuries/burns, ventricular arrhythmias/cardiac arrest), increases IOP (avoid for eye injuries, glaucoma)

119
Q

What is tubocurarine?

A

Prototype -> naturally occurring alkaloid found in S. american plant

120
Q

What is the method of action of tubocurarine?

A

Competitive nAChR antagonist, needing 70-80% block

121
Q

What are the effects of tubocurarine?

A

Flaccid paralysis: first of extrinsic eye muscles (double vision), small muscles of face, limbs and pharynx and lastly, resp muscles and then recovery occurs

122
Q

What are the uses of tubocurarine?

A

Relaxation of skeletal muscles during surgical operations and permits artificial ventilation (NB: can be reversed by anticholinesterases, such as neostigmine and atropine)

123
Q

What are the pharmacokinetics of tubocurarine?

A

Admin = IV, doesn’t cross BBB or placenta, duration of paralysis = 40-60min, not metabolised and excreted 70% urine and 30% bile (which is important in renal/hepatic impairment)

124
Q

What are the unwanted effects of tubocurarine?

A

Ganglion block, histamine release -> Hypotension (due to ganglion blockade causing decrease TPR and histamine release from mast cells), tachycardia (may affect arrhythmias, due to reflex action from blockade of vagal ganglia), bronchospasm and excessive secretions (bronchial and salivary) (due to histamine release), apnoea so resp assist always necessary

125
Q

The clinical use of neuromuscular blocking drugs will most likely involve interference with which of following physiological processes?A: Kidney functionB: ConsciousnessC: Body temperature regulationD: Pain sensationE: Respiration

A

E

126
Q

Which of the following effects would be observed with a non-depolarising neuromuscular block?A: Initial muscle fasciculationsB: Irreversible nAChR blockadeC: The block would be enhanced by anti-cholinesterase drugsD: A flaccid paralysisE: Increased arterial pressure

A

D

127
Q

Where is the NMJ located?

A

It is located in the somatic NS not the autonomic -> with motor neurone releasing ACh onto the skeletal muscle

128
Q

What is the process of action potential transmission across the NMJ and which drugs act on the different parts of the transmission?

A

NB: alpha is the subunit in the nicotinic receptors (slightly different than the ganglionic receptors as they are the muscular type, and have different pharmacologies)

129
Q

Which points of the transmission of the action potential is acted upon by drugs?

A

ACh release (reduce it), potentiating transmission, NM blocking drugs

130
Q

Which drugs reduce ACh release?

A

Hemicholinium, botulinum toxin, aminoglycosides, Mg/Co ions

131
Q

Which drugs potentiate transmission of AP?

A

Anticholinesterases - Pyridostigmine, neostigmine, edrophonium, distigmine, physostigmine

132
Q

Which drugs block the NM (act on channel)?

A

COMPETITIVE: Tubocurarine, gallamine, pancuronium, alcuronium, atracurium, vecuronium;DEPOLARIZING: suxamethonium

133
Q

What does the nAChR look like?

A

Span the membrane with significant EC and IC domain (pentameric -> 5 different, 2A, 1B, 1G, 1D in the muscular)

Pharm (11 decks)

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