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Exam prep tutorials (Pharmacology) > Adrenoceptor Antagonists > Flashcards

Adrenoceptor Antagonists Flashcards

1
Q

Is esmolol cardioselective?

A

Yes

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2
Q

How does esmolol affect airways resistance?

A

It increases airway resistance

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3
Q

What does stimulation of alpha-adrenoceptors cause?

A

α1-receptor stimulation causes:

  • vasoconstriction
  • mydriasis
  • smooth muscle contraction

α2-receptor stimulation causes:

  • platelet aggregation
  • reduced release of noradrenaline from nerve endings
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4
Q

What is the autonomic nervous system?

A

Part of the peripheral nervous system. It controls the involuntary regulation of most body organ systems and homeostatic mechanisms

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5
Q

What kind of receptor are adrenergic receptors?

A

G protein coupled membrane receptors activated by the catecholamines adrenaline and noradrenaline.

Stimulation causes a sympathetic response

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6
Q

What are the different types of adrenoceptor?

A

Alpha-adrenergic

  • alpha 1 causes smooth muscle contraction and glycogenolysis
  • alpha 2 causes inhibition of noradrenaline release and smooth muscle contraction

Beta-adrenergic

  • contraction of cardiac muscle
  • smooth muscle relaxation
  • glycogenolysis
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7
Q

What is the MOA of alpha 1 adrenoceptors?

A

Gq protein coupled

Activation increases intracellular Phospholipase C causing an increase in intracellular calcium ions to have their action

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8
Q

What does stimulation of alpha 1 adrenoreceptors do?

A
  • Vascular smooth muscle contraction
  • Bladder and iris muscle contraction
  • Intestinal relaxation
  • Glycogenolysis
  • Decreased secretion of insulin and glucagon
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9
Q

What is the MOA of alpha 2 receptors?

A

Mainly presynaptic Gi protein coupled

Activation inhibits adenylate cyclase causing a decrease in intracellular calcium ions to have their effects

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10
Q

What does stimulation of alpha 2 receptors cause?

A
  • Reduced release of noradrenaline
  • Vasodilatation of arterioles
  • Vasoconstriction of veins and coronary arteries
  • Platelet aggregation
  • Intestinal relaxation
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11
Q

How do beta-adrenoceptors work?

A

They are all Gs protein coupled causing an increase in intracellular adenylate cyclase which increases cyclic adenosine monophosphate (cAMP) and therefore intracellular calcium ions to have their effects.

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12
Q

What are the 3 subtypes of beta-adrenergic receptors?

A

Beta1

  • increase HR and positive inotropy
  • increased renin secretion
  • lipolysis

Beta2

  • smooth muscle relaxation invluding vascular, bronchiolar and intestinal
  • glycogenolysis and increased insulin and glucgon secretion

Beta3

  • lipolysis and thermogenesis
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13
Q

What do B1 blockers do?

A
  • ↓Heart rate
  • ↓Myocardial contractility
  • ↓Myocardial excitability by ↓atrio-ventricular node conduction
  • ↓Renin release
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14
Q

What do B2 blockers do?

A
  • Vasoconstriction
  • ↓Heart rate
  • ↓Myocardial contractility
  • ↓Noradrenaline release
  • Bronchoconstriction
  • Bladder/uterine contraction
  • Inhibition glycogenolysis
  • ↓Insulin secretion
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15
Q

What do alpha 1 blockers do?

A
  • Vasodilatation
  • ↑Intestinal motility
  • Bladder/uterine relaxation
  • Iris relaxation
  • Inhibition glycogenolysis
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16
Q

What are the selective alpha-adrenoceptor antagonists?

A
  • prazosin
  • doxazosin
  • terazosin
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17
Q

What are the selective alpha 1 adrenoceptor antagonists used for?

A
  • essential HTN
  • phaeochromocytoma
  • congestive cardiac failure
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18
Q

How do selective alpha1 antagonists work?

A

Prevent vasoconstrictive effects of noradrenaline, causing a reduction in SVR without a reflex tachycardia

CO may increase due to reduced afterload.

Relaxes bladder muscle so can help in management of benign prostatic hypertrophy.

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19
Q

What are the SEs of alpha 1 adrenoceptor antagonists?

A
  • Severe postural hypotension can occur following first doses
  • Syncope
  • vertigo
  • dizziness
  • increased frequency of micturition
  • drowsiness
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20
Q

What are the SEs of non-selective adrenoceptor antagonists?

A

They will also block alpha2 adrenoceptors

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21
Q

What is phentolamine?

A
  • short acting competitive antagonist of alpha 1 and alpha 2 receptors, 3 x more affinity for alpha 1
  • given IV
  • used for hypertensive crises due to excessive sympathetic activity, monoamine oxidates inhibitor (MAOI) reactions or intra-op phaeochromocytoma removal
  • α1 causes vasodilatation and therefore reduction in systemic vascular resistance
  • α2 causes increased heart rate and increased cardiac output due to the increased noradrenaline release
22
Q

What are the SEs of phentolamine?

A
  • Nasal congestion due to vasodilatation of nasal blood vessels
  • Sulphites in the preparation can cause bronchospasm in some asthmatics
  • Hypoglycaemia due to raised insulin levels
23
Q

What is phenoxybenzamine?

A
  • longer acting alpha-adrenoceptor antagonist with more affinity for alpha1 receptors
  • given orally or IV
  • used to treat phaeochromocytoma and hypertensive crises
  • irreversible blockade of alpha-receptors and inhibits catecholamine uptake into neurones
  • half life is 24hrs and effects last until new receptors are produced
24
Q

What are the SEs of phenoxybenzamine?

A
  • Reflex tachycardia due to the alpha2 effects
  • miosis
  • sedation
25
Q

What are the non-selective beta blockers?

A
  • carvedilol
  • labetalol
  • pindolol
  • propranolol
  • timolol
26
Q

What are the selective B1-receptor antagonists?

A
  • atenolol
  • metoprolol
  • esmolol
  • nebivolol
27
Q

What are the 1st generation beta blockers?

A
  • non-selective beta adrenoceptor antagonists
  • propranolol, sotalol and timolol
28
Q

What are the 2nd generation beta blockers?

A
  • relatively selective for beta1 - cardioselective
  • bisoprolol, atenolol, metoprolol and esmolol
29
Q

What are the 3rd generation beta blockers?

A
  • some are cardioselective but all possess vasodilatory action via alpha1-antagonism or causing nitric oxide release
  • carvedilol, celiprolol and dilevalol are non-cardioselective
  • nebivolol is cardioselective
30
Q

What is the MOA of beta blockers?

A

By blocking beta receptors:

  • negative inotropy and chronotropy
  • reduces SA node automaticity
  • increases AV node conduction
  • increases time in diastole increasing oxygen supply to myocardium
31
Q

What are the indications for beta blockers?

A
  • ischaemic heart disease- angina and post myocardial infarction
  • arrhythmias
  • congestive heart failure
  • phaeochromocytoma management in conjunction with alpha-antagonist
  • thyrotoxicosis (propranolol)
  • anxiety
  • migraine prophylaxis
  • glaucoma
32
Q

What are the SEs of beta blockers?

A
  • reduced peripheral circulation and cool extremities
  • bronchospasm in susceptible individuals
  • masks hypoglycaemic symptoms
  • some cross BBB causing hallucinations, nightmares, depression
  • urinary retention
  • increased uterine tone
33
Q

How do beta blockers act if endogenous catecholamine levels are low?

A

They act as a sympathomimetic at the β-adrenoceptor

34
Q

Which beta blockers are less likely to cause a bradycardia?

A
  • Acebutolol
  • oxprenolol
  • pindolol
  • timolol
35
Q

Which β-blockers have been shown to reduce hospital admissions, prevent disease progression and even improve long term survival in chronic congestive cardiac failure? What is the mechanism?

A
  • bisoprolol
  • metoprolol
  • carvedilol

The mechanism is thought to be due to

  • reduction in harmful cardiac remodelling by blocking excessive chronic sympathetic stimulation of the heart
  • reduction in renin secretion reduces heart O2 demand by lowering extracellular volume
36
Q

What are the indications for a trial of β-blockers?

A

Patients with clinically stable NYHA functional class II or III heart failure. Patients should be stabilised on an ACEI prior to β-blocker treatment

37
Q

What is the dose of esmolol?

A

Fast onset and offset

25-100mg boluses

Can be given as infusion: 50-100 micrograms/kg/min

38
Q

What is the dose of propranolol to manage perioperative hypertension and SVTs?

A

1mg over 1 minute and repeated as necessary

39
Q

What is the MOA of labetalol?

A
  • selectively antagonises α1- and β- adrenoceptors
    • 1:3 α:β when used orally
    • 1:7 α:β when given intravenously
  • Made up of four isomers
  • Significant first pass effect
  • 50% plasma protein bound
  • Metabolized in liver

Causes a reduction in BP by decreasing HR (CO and SVR).

40
Q

What effect does labetalol have on airways or cerebral perfusion?

A

No significant effect

41
Q

What are the indications for labetalol?

A
  • Used as an antihypertensive particularly in pregnancy-induced hypertension
  • Management of phaeochromocytomas
  • Deliberate perioperative hypotension
42
Q

What are the SEs of labetalol?

A

Same as other β-blockers but can also cause jaundice

43
Q

What is phaeochromocytoma?

A

A rare tumour of chromaffin cells in the adrenal medulla or in other paraganglia of the sympathetic nervous system.

Commonly produces either:

  • noradrenaline, causing severe HTN often refractory to Rx
  • adrenaline or dopamine, causing episodic symptoms including palpitations or panic attacks
44
Q

What is the treatment of Phaemochromocytoma?

A

Surgery but good preop pharmacological control is essential. Aims are:

  • good BP control
  • Rx of significant dysrrhythmias
  • restoration of circulating blood volume
45
Q

How do you start pharmacological treatment for phaemochromocytoma?

A
  • start with an alpha-adrenoceptor antagonist prior to β-blockade
    • non-selective α-adrenoceptors antagonist e.g. Phenoxybenzamine or
    • Selective α1-adrenoceptor antagonist e.g. Doxazosin
  • this prevents the risk of increasing peripheral vasoconstriction and causing a hypertensive crisis because beta blockade removes the protective effect of beta peripheral vasodilation
  • β-adrenoceptor antagonists are often needed following alpha-adrenoceptor antagonist introduction to control the side effect of tachycardia or if the tumour predominately secretes adrenaline or dopamine
46
Q

What are the advantages of phenoxybenzamine?

A
  • can be given orally
  • long duration due to forming covalent bonds with the alpha-adrenoceptors which helps to prevent catecholamine surge preop
  • effects wear off as new receptors are made with a half life of 24hrs
47
Q

What are the disadvantages of phenoxybenzamine?

A
  • blocks alpha 2 adrenoreceptors which are part of the negative feedback loop, regulating the release of noradrenaline, causing tachycardias via disinhibition of sympathetic fibres
  • beta-blocker may be needed to control tachycardias
  • Rx is stopped 24 - 48hrs before surgery but there can be residual blockade by phenoxybenzamine
  • once the tumour is gone, catecholamine levels return to normal, but patients can be unresponsive to alpha-agonists
  • other SEs: postural hypotension, sedation, nasal stuffiness
48
Q

What are the advantages of doxazosin?

A
  • selective competitive inhibitor of α1-adrenoceptors
  • not associated with tachycardias
  • given once daily orally and has long duration of action
  • does not cross BBB so less likely to cause sedation
  • as α2-adrenoceptors aren’t affected, no need for β-blockade unless the tumour secrets adrenaline or dopamine
49
Q

What are the disadvantages of doxazosin?

A

Postural hypotension can be severe at the start of Rx.

Massive catecholamine surges during surgery can displace the drug from the receptor.

50
Q

What does β1 receptor stimulation cause?

A
  • increased rate and force of myocardial contraction (positive inotropy)
  • breakdown of triglycerides into fatty acids
  • increased renin secretion.
51
Q
A

Exam prep tutorials (Pharmacology) (8 decks)

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