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Farmer > SNS Antagonists > Flashcards

SNS Antagonists Flashcards

1
Q

Describe the effects of each type of adrenoceptor.

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

Block Alpha:
Phentolamine = alpha 1 + alpha 2
Prazosin = alpha 1 (Note: Prazosin is actually an inverse agonist and also causes a rise in HDL)

Block Beta:
Propranolol = beta 1 + beta 2
Atenolol = beta 1

Block both selectively:
Carvediol = alpha 1 + 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

Sustained systolic blood pressure greater than 140 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 the negative 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

COPD – same reason as asthma

Cardiac Failure – these patients rely on a certain degree of sympathetic drive to the heart to maintain adequate cardiac output

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?

A

Selectivity is dependent on concentration - will still act on Beta 2 at sufficient 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 causes vasodilation and fall in TPR and blood pressure, but alpha 2 blockade means you inhibit negative effect of alpha 2 on noradrenaline synthesis and release - so more noradrenaline released from nerve terminal, enhancing 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 to 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 (used for gestational hypertension)

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 only used for specific subsets of patients

25
Q

What are arrhythmias usually caused by and why?

A

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

What effect do beta antagonists have on the refractory period of the AV node? How does this help in dealing with arrhythmia?

A

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

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.

A

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

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 diseases

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 the oxygen 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 
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

Adrenaine 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 over reactivity such as palpitations and tremor)

Migraine prophylaxis – maintain good blood supply within the CNS so reduces the risk of migraines

Benign essential tumour

Farmer (33 decks)

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