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YR2 LCRS Pharm > 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 + GIT relaxation
Alpha 2: Inhibition of transmitter release + Contraction of vascular smooth muscle + CNS actions
Beta 1: increased HR + contractility, increased renin release + GIT relaxation
Beta 2: Bronchodilation, Vasodilation, Relaxation of visceral smooth muscle + Hepatic glycogenolysis
Beta 3: Lipolysis

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2
Q

State 5 adrenoceptor antagonists including the receptors that they block.

A 
Carvedilol = alpha 1 + beta 1 
Phentolamine = alpha 1 + alpha 2 
Prazosin = alpha 1 
Propranolol = beta 1 + beta 2  
Atenolol = beta 1
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3
Q

State 4 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 BP > 140/90 mm Hg

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5
Q

State 3 elements that contribute to hypertension.

A

Blood volume
Peripheral vascular tone
Cardiac output

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6
Q

What are the target tissues for hypertensives? What effect do beta blockers have on these?

A

Heart: reduces FOC + HR
Kidney: blocks renin release, blocks production of AII (vasoconstrictor) + aldosterone
CNS: Reduces sympathetic tone
Blockade of facilitatory effects of presynaptic B-adrenoceptors on NA release

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7
Q

Blockade of which receptors cause the positive and 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

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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10
Q

What is the effect of presynaptic beta 1 receptors?

A

positive facilitation effect on the synthesis + release of noradrenaline

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11
Q

State 4 conditions in which you would not give a patient a betablocker. Explain each of them.

A

Asthma: blockade of B2 receptors in the lungs can prevent B2 mediated bronchodilation, can be fatal
Cardiac Failure: these patients rely on a certain degree of sympathetic drive to the heart to maintain adequate CO
COPD: same reason as asthma
Diabetes: B blockade masks the symptoms of hypoglycaemia (tremors, palpitations, sweating) + B2 blockade inhibits hepatic glycogenolysis

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12
Q

State 3 unwanted actions of beta-blockers.

A

Fatigue
Cold extremities
Bad dreams

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13
Q

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

A

Little effect on these parameters at rest

Decreases all of these parameters when exercising

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14
Q

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

A

Selectivity is dependent on concentration

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15
Q

List 4 types of beta blocker

A

Non selective: Propanolol
B1-selective: Atenolol (more selective for B1)
Mixed B-A blockers: Carvedilol (A1 blockade gives additional vasodilator properties)
New: Nebivolol (potentiates NO) + Sotalol (Inhibits K+ channels)

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16
Q

What is the main mediator of total peripheral resistance?

A

Alpha 1 mediated vasoconstriction

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17
Q

What are the effects of alpha blockade?

A

Vasodilation causing a fall in TPR + hence a fall in BP

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18
Q

What reflex will be triggered by alpha blockade?

A

Baroreceptor mediated reflex tachycardia to increase HR + CO

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19
Q

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

A

A1 blockade causes vasodilation + a fall in TPR + BP
But A2 blockade results in removal of the negative feedback effect on the synthesis + release of NA so more NA will be released from the nerve terminal
This enhances the reflex tachycardia
Side effects include increased GIT motility + diarrhoea
Thus, Phentolamine is no longer used

20
Q

What are the effects of prazosin?

A

Highly selective A1 antagonist
Leads to vasodilation + a fall in BP
Less tachycardia than with non-selective alpha blockers because the negative effect of A2 on NA release has not been removed
Hypotensive effect is dramatic, postural hypotension is troublesome

21
Q

Describe the mechanism of action of methyldopa.

A

Methyldopa is taken up by noradrenergic neurones, is decarboxylated + hydroxylated for form alpha-methyl noradrenaline
This is not deaminated by MAO so accumulates > NA in the synapse
Alpha-methyl NA displaces NA from the synaptic vesicles
It is less effective than NA on A1 receptors so does not cause as much vasoconstriction
It is more effective than NA on A2 receptors thus reducing NA release
Also affects the CNS by inhibiting sympathetic outflow

22
Q

State 2 benefits of methyldopa other than its effect as an anti-hypertensive.

A

No adverse effects on foetus’ despite crossing the placenta
Maintains renal + CNS blood flow so it is used in patients with renal insufficiency or cerebrovascular disease

23
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 interfere with the heart rhythm

24
Q

What controls the pacemaker current in the heart?

A

Sympathetic drive

25
Q

What can precipitate or aggravate arrhythmias?

A

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

26
Q

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

A

AV conductance depends heavily on sympathetic activity

27
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 AVN

It can interfere with AV conduction in atrial tachycardias + slow ventricular rate

28
Q

What class of drugs are beta-blockers?

A

Class II anti-arrhythmics

29
Q

What is propranolol particularly effective at treating?

A

Arrhythmias that occur during exercise or mental stress

Reduces mortality of patients with MI

30
Q

Define angina.

A

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

31
Q

Describe the 3 different types of angina.

A

Stable: Pain on exertion due to a FIXED narrowing e.g. atheroma
Unstable: Pain with less + less exertion culminating with pain at rest. Platelet-fibrin thrombus associated with a ruptured atheromatous plaque without complete occlusion of the vessel. High risk of infarction
Variable: Occurs at rest. Caused by coronary artery spasm. Associated with atheromatous disease

32
Q

Describe how beta-blockers can help prevent angina attacks.

A

Decrease HR + contractility
Reduces oxygen demand of the heart whilst maintaining the same degree of effort
Thus, less likely of getting to a situation where the oxygen supply to the myocardium is insufficient for its needs (angina)

33
Q

State 6 adverse effects of beta-blockers.

A 
Fatigue 
Insomnia 
Dizziness 
Sexual dysfunction 
Bradycardia 
Hypotension
34
Q

State 3 circumstances in which you would not give a beta-blocker.

A

Hypotension
Bradycardia
Uncontrolled heart failure

35
Q

Where is aqueous humour produced?

A

Blood vessels in the ciliary body via the actions of carbonic anhydrase

36
Q

What dictates the amount of aqueous humour produced?

A

Blood flow in the ciliary body (+ BP)

37
Q

Where does the aqueous humour drain?

A

Into the trabecular network in the canals of Schlemm

38
Q

How can adrenaline affect intraocular pressure?

A

Adrenaline can act on A1 receptors to cause vasoconstriction + reduce blood flow through the ciliary body

39
Q

Describe the use of beta antagonists in treating glaucoma.

A

Reduce rate of aqueous humour formation by blocking the receptors on the ciliary body

40
Q

State 3 other uses of beta antagonists.

A 
Anxiety states (to control somatic symptoms associated with sympathetic over reactivity such as palpitations + tremor) 
Migraine prophylaxis: maintain good blood supply within the CNS so reduces the risk of migraines  
Benign essential tremor
41
Q

What is the purpose of alpha 2 receptors?

A

Prevent further release of NA via negative feedback on the pre-synaptic nerve terminal itself.

42
Q

What determines peripheral resistance? How can the effect of beta blockers on renin production affect this?

A

Arterioles.
Decreased renin results in decreased AII + decreased aldosterone.
Aldosterone works to increase blood volume through reabsorption of Na+ + water, thus blood volume is not increased

43
Q

What is the advantage of atenolol over propranolol ?

A

Reduces likelihood of negative side effects (on lungs + liver, as these are B2 mediated)

44
Q

What advantage does carvedilol have over atenolol and propranolol?

A

More powerful hypotensive effect as a dual acting B1 + A1 antagonist
B-mediated effects on heart + kidney, reducing HR + CO
A-mediated vasoconstriction is blocked, thus reducing TPR + BP

45
Q

Describe reflex tachycardia as seen in Alpha blockade

A

If A1 blockers cause vasodilation, BP decreases, baroreceptor firing rate decreases, vagal stimulation is lost + SNS tries to compensate by increasing HR + SV

46
Q

Why is Prazosin becoming more popular as an anti-hypertensive agent?

A

Causes a modest decrease in LDL, + an increase in HDL cholesterol

47
Q

List 4 adverse effects of methyldopa

A 
Dry mouth
Sedation
Postural hypotension
Male sexual dysfunction 
Thus, it is rarely used

YR2 LCRS Pharm (34 decks)

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