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Pharmacology > SNS Antagonists > Flashcards

SNS Antagonists Flashcards

1
Q 
Describe the effects of each type of adrenoceptor. 
Alpha 1
Alpha 2
Beta 1
Beta 2
Beta 3
A 
Alpha 1
 Vasoconstriction 
 GI tract relaxation 
Alpha 2
 Inhibition of transmitter release 
 Contraction of vascular smooth muscle  
 CNS actions  
Beta 1
 Heart – increased heart rate + contractility 
 Kidneys – increased renin release 
 GI tract relaxation  
Beta 2
 Bronchodilation 
 Vasodilation 
 Relaxation of visceral smooth muscle  
 Hepatic glycogenolysis  
Beta 3
 Lipolysis
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2
Q

State five adrenoceptor antagonists including the receptors that they block.

A 
Labetalol = alpha 1 + beta 1 (more beta 1 (4:1)) 
Phentolamine = alpha 1 + alpha 2 
Prazosin = alpha 1 
Propranolol = beta 1 + beta 2  
Atenolol = beta 1
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3
Q

State four main clinical uses of SNS antagonists and false transmitters.

A

Hypertension
Angina
Arrhythmia
Glaucoma

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4
Q

What is defined as hypertension?

A

Sustained diastolic blood pressure greater than 90 mm Hg

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5
Q

State three elements that contribute to hypertension.

A

Blood volume
Peripheral vascular tone
Cardiac output

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6
Q

What is the main control of blood pressure?

A

Sympathetic drive to the kidneys via beta 1 receptors

This triggers renin release from the kidneys (leads to an increase in angiotensin II and aldosterone)

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7
Q

Blockade of which receptors cause the positive effects and thenegative effects of beta-blockers?

A

Beta 1 blockade = positive effects

Beta 2 blockade = negative effects

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8
Q

What are beta-1 selective blockers called?

A

Cardioselective Beta-blockers

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9
Q

What effect is responsible for most of the anti-hypertensive effect of beta-blockers?

A

Beta 1 blockade in the kidneys – this reduces renin release from the kidneys

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10
Q

What effect does beta-1 blockade have on the heart?

A

Decrease in heart rate

Decrease in cardiac output

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11
Q

How does the effect of beta-blockers on the heart change?

A

The effect of beta blockade on the heart disappears with chronic treatment as the heart begins to reset itself

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12
Q

What is the effect of presynaptic beta 1 receptors?

A

They have a positive facilitation effect on the synthesis and release of neurotransmitter

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13
Q

State four conditions in which you would not give a patient a betablocker. Explain each of them.

A

Asthma – blockade of beta 2 receptors in the lungs can take away the beta 2 mediated bronchodilation, which can be fatal in asthmatics
Cardiac Failure – these patients rely on a certain degree of sympathetic drive to the heart to maintain adequate cardiac output
COPD – same reason as asthma
Diabetes – beta blockade masks the symptoms of hypoglycaemia (e.g. tremors, palpitations, sweating) and beta 2 blockade also inhibits hepatic glycogenolysis

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14
Q

State some other unwanted actions of beta-blockers.

A

Fatigue

Cold extremities

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15
Q

What effect does propranolol have on heart rate, cardiac output and blood pressure?

A

It has little effect on these parameters at rest

It decreases all of these parameters when exercising

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16
Q

Why would you still not give a cardioselective beta-blocker to anasthmatic patient?

A

Selectivity is dependent on concentration

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17
Q

What are the effects of labetalol?

A

Acts more on beta 1 than alpha 1
It lowers blood pressure by reducing total peripheral resistance and it induces a change in heart rate and cardiac output (beta 1 mediated)

18
Q

What is the main mediator of total peripheral resistance?

A

Alpha 1 mediated vasoconstriction

19
Q

What are the effects of alpha blockade?

A

Vasodilation causing a fall in TPR and hence a fall in blood pressure
NOTE: blocking the sympathetic drive can cause postural hypotension

20
Q

What reflex will be triggered by alpha blockade?

A

It triggers a baroreceptor mediated reflex tachycardia to increase heart rate and cardiac output

21
Q

State some of the problems with non-selective alpha blockers (e.g. phentolamine).

A

Alpha 1 blockade will cause vasodilation and a fall in TPR and blood pressure
But the alpha 2 blockade will mean that you take away the negative effect of alpha 2 on the synthesis and release of noradrenaline so more noradrenaline will be released from the nerve terminal
This enhances the reflex tachycardia
Side effects include increased GIT motility and diarrhoea
Phentolamine is no longer used

22
Q

What are the effects of prazosin?

A

Highly selective alpha-1 antagonist
Leads to vasodilation and a fall in blood pressure
You get less tachycardia than with non-selective alpha blockers because the negative effect of alpha 2 on noradrenaline release has not been removed
NOTE: postural hypotension is troublesome
Prazosin also increases HDL and decreases LDL so is becoming more popular as an anti-hypertensive

23
Q

Describe the mechanism of action of methyldopa.

A

Methyldopa is taken up by noradrenergic neurones and is decarboxylated and hydroxylated for form alpha-methyl noradrenaline
This is not deaminated by MAO so accumulates more than noradrenaline in the synapse
Alpha-methyl noradrenaline displaces NA from the synaptic vesicles
It is less effective than NA on alpha 1 receptors so does not cause as much vasoconstriction
It is more effective than NA on alpha 2 receptors thus reducing noradrenaline release
It also affects the CNS by inhibiting sympathetic outflow

24
Q

State some other benefits of methyldopa other than its effect as an anti-hypertensive.

A

It does not have any adverse effects on foetus’ despite crossing the placenta
It maintains renal and CNS blood flow so it is used in patients with renal insufficiency or cerebrovascular disease
Adverse effects: dry mouth, sedation, postural hypotension, male sexual dysfunction
It is RARELY used

25
Q

What are arrhythmias, what are they usually caused by and why?

A

= Irregular or abnormal heart beat

Myocardial ischaemia – damage to the heart muscle can result in re-entry of impulses that messes up the heart rhythm

26
Q

What controls the pacemaker current in the heart?

A

Sympathetic drive

27
Q

What can precipitate or aggravate arrhythmias?

A

An increase in sympathetic drive to the heart via beta 1 receptors

28
Q

What part of the heart’s electrical circuit depends heavily on sympathetic activity?

A

AV conductance depends heavily on sympathetic activity

29
Q

relationships between beta antagonists and arrhythmias

A

Beta-blockers INCREASE the refractory period of the AV node
It can interfere with AV conduction in atrial tachycardias and slow downventricular rate
prevent aggravation of arrhythmias

30
Q

What class of drugs are beta-blockers?

A

Class II anti-arrhythmics

31
Q

What is propranolol particularly effective at treating?

A

It is particularly successful in arrhythmias that occur during exercise or mental stress

32
Q

Define angina.

describe the pain distribution

A

Chest pain that occurs when the oxygen supply to the myocardium is insufficient for its needs

Pain is in chest, arm, neck

33
Q

Describe the three different types of angina.

A

Stable
 Pain on exertion due to a FIXED narrowing
Unstable
 Pain with less and less exertion culminating with pain at rest
 Atheromatous plaque begins to rupture
 Platelet-fibrin thrombus associated with the ruptured plaque without complete occlusion of the vessel
 High risk of infarction
Variable
 Occurs at rest
 Caused by coronary artery spasm
 Associated with atheromatous disease

34
Q

Describe how beta-blockers can help prevent angina attacks.

A

They decrease heart rate, decrease contractility and decrease systolic blood pressure meaning that it will reduce the oxygen demand of the heart whilst maintaining the same degree of effort
This means that you are less likely of getting to a situation where theoxygen supply to the myocardium is insufficient for its needs (angina)

35
Q

State some adverse effects of beta-blockers.

A 
Fatigue 
Insomnia 
Dizziness 
Sexual dysfunction 
Bronchospasm 
Bradycardia 
Heart block  
Hypotension  
Decreased myocardial contractility
36
Q

State some other circumstances in which you would not give a beta-blocker.

A

Hypotension
Bradycardia
Bronchospasm
AV block or severe congestive heart failure

37
Q

Where is aqueous humour produced?

A

They are produced by the blood vessels in the ciliary body via the actions of carbonic anhydrase

38
Q

What dictates the amount of aqueous humour produced?

A

Blood flow in the ciliary body (and blood pressure)

39
Q

Where does the aqueous humour drain?

A

It drains into the trabecular meshwork in the canals of Schlemm

40
Q

How can adrenaline affect intraocular pressure?

A

Adrenaline can act on alpha-1 receptors to cause vasoconstriction and reduce blood flow through the ciliary body

41
Q

Describe the use of beta antagonists in treating glaucoma.

A

They reduce the rate of aqueous humour formation by blocking the receptors on the ciliary body
Examples: carteolol hydrochloride, levobunolol hydrochloride, timilol maleate

42
Q

State some other uses of beta antagonists.

A

Anxiety states
(to control somatic symptoms associated with sympathetic ove reactivity such as palpitations and tremor)
Migraine prophylaxis
– maintain good blood supply within the CNS so reduces the risk of migraines
Benign essential tumour

Pharmacology (32 decks)

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