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Yr 2 LCRS - Pharm > 9 - SNS Antagonists > Flashcards

9 - SNS Antagonists Flashcards

1
Q

What are the effects of the sympathetic nervous system in the body?

A
  • Dilates pupil
  • Inhibits salivation
  • Relaxes bronchi
  • Accelerates heart
  • Inhibits digestive activity
  • Stimulates glucose release by liver
  • Secretion of epinephrine and norepinephrine from kidney
  • Relaxes bladder
  • Contracts rectum
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2
Q

What subsequent actions are the activation of the different adrenoreceptor subtypes associated with?

A

Alpha-1
= vasoconstriction
= relaxation of GIT

Alpha-2
= inhibition of transmitter release
= contraction of vascular smooth muscle
= CNS actions

Beta-1
= increased cardiac rate and force
= relaxation of GIT
= renin release from kidney

Beta-2
= bronchodilation
= vasodilation
= relaxation of visceral smooth muscle
= hepatic glycogenolysis

Beta-3
= lipolysis

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3
Q

Which adrenoreceptors can be found in large quantities pre-synaptically?

A

Alpha-2 adrenoreceptors

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4
Q

How do alpha-2 adrenoreceptors function?

A
  • Found on pre-synaptic membrane
  • Inhibit sympathetic nerve function
  • Decrease amount of NA released into synapse
  • Work via negative feedback
  • Discrete and quick action
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5
Q

Name an example of each type of adrenoreceptor antagonist

A

Alpha-1 + Beta-1
= Carvedilol
= non-selective adrenoreceptor antagonist
= mixed beta-alpha blocker

Alpha-1 +Alpha-2
= Phentolamine
= non-selective alpha adrenoreceptor antagonist

Alpha-1
= Prazosin

Beta-1 + Beta-2
= Propanolol
= non-selective beta adrenoreceptor antagonist

Beta-1
= Atenolol

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6
Q

What is another name for beta-adrenoreceptor antagonist drugs?

A

Beta-Blockers

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7
Q

What cardiac parameters equate to blood pressure?

A

BP = CO x TPR

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8
Q

What is the main factor that affects blood pressure?

A

Total Peripheral Resistance (TPR)

- e.g. due to atherosclerosis

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9
Q

What blood pressure defines hypertension?

A

Hypertension

= blood pressure consistently above 140/90 mmHg

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10
Q

What condition is hypertension the single biggest risk factor for?

A

Stroke

- it causes about 50% of ischaemic strokes

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11
Q

For what conditions is hypertension a risk factor?

A
  • stroke
  • heart failure
  • myocardial infarction
  • chronic kidney disease
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12
Q

What is the ultimate goal of hypertension therapy?

A

Reduce mortality from cardiovascular or renal events.d

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13
Q

What are the main contributors to blood pressure?

A

Blood volume
Cardiac output
Vascular tone

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14
Q

What are the tissue targets for anti-hypertensives?

A

The Heart
= affects cardiac output and heart rate
= this effect disappears in chronic treatment

Sympathetic nerves
= they release the vasoconstrictor NA

The Kidney
= Blood volume/vasoconstriction
= renin causes increased aldosterone, increased water retention, increased blood volume
= angiotensin II is also a powerful vasoconstrictor

Arterioles
= determine TPR

CNS
= determines blood pressure set point and regulates some systems involved in blood pressure control and autonomic Ns
= reduce sympathetic tone

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15
Q

What beta-adrenoreceptors do beta-blockers act on?

A

Heart = beta-1

Sym nerves that release the vasoconstrictor NA = beta-1/2

Kidney = beta-1

CNS = beta-1/2

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16
Q

By what mechanism do beta-adrenoreceptor antagonists work?

A

Competitive antagonism of beta-1 receptors mainly but also beta-2 receptors to a lesser extent

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17
Q

What type of adrenoreceptor antagonist is Propranolol?

A

Non-Selective
= equal affinity for beta-1 and beta-2 receptors
= e.g. propranolol

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18
Q

What type of adrenoreceptor antagonist is Atenolol?

A

Beta-1 Selective

= more selective for beta-1 receptors

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19
Q

What type of adrenoreceptor antagonist is Carvediol?

A

Mixed Beta-Alpha Selective

= alpha-1 blockade gives additional vasodilator properties

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20
Q

What type of adrenoreceptor antagonist is Nebivolol?

A

Beta-1 Selective
= also facilitates release NO which is a good vasodilator
= newer drug

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21
Q

What type of adrenoreceptor antagonist is Sotalol?

A 
Beta-1 and Beta-2 Selective
= also inhibits K+ channels, slow HR
= good for hypertension with associated arrhythmia
= prolong ventricular conduction
= prolong time between heart beats
= slower, more rhythmic contraction
= improve CO
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22
Q

What are the major side effects of beta-blockers?

A

Bronchoconstriction
= very life-threatening for asthmatics/people obstructive lung diseases
= even Beta-1 selective drugs may bind to Beta-2 receptors occasionally and cause this effect

Cardiac Failure
= need some sympathetic drive to the heart
= such as people with heart disease may rely on a certain degree of sympathetic drive to maintain adequate CO

Hypoglycaemia
= mask the symptoms of hypoglycaemia (e.g. sweating, palpitations, tremor)
= use of non-selective beta-blockers is even more dangerous in such patients as blocking beta-2 receptors can also inhibit glycogen breakdown

Fatigue
= reduced CO and muscle perfusion

Cold Extremities
= loss of beta-receptor mediated vasodilatation in cutaneous vessels

Bad Dreams

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23
Q

Why are beta-blockers no longer first-line treatment for hypertension?

A

This is because of their high side effect profile.

Alpha and Beta Blockers are now add-on therapies for hypertension, but not first-line.

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24
Q

What drugs are first-line treatment for hypertension?

A
  • ACE Inhibitors
  • Calcium Channel Blockers
  • Diuretics
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25
Q

What is another name used for beta-1 selective adrenoreceptor antagonists?

A

Cardiac-Selective Beta-Blockers

(However, there are still beta-2 receptors in the heart so non-selective beta-blockers may have more on an effect on the heart)

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26
Q

What is the advantage of atenolol over propranolol?

A

Atenolol is just beta-1 selective
= antagonises the effect of NA on the heart
= but also will affect any tissue with beta-1 receptors such as the kidney
= lose all beta-2 effects

Propanolol is a non-selective beta blocker
= has an effect on the airways as well because of the presence of beta-2 receptors in the lungs
= also has an effect on the liver
= however there are beta-2 receptors in the heart so propranolol could have a beneficial effect on those

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27
Q

What measurement is adrenoreceptor antagonist selectivity dependent on?

A

Selectivity is concentration dependent

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28
Q

What advantage does carvediol have over atenolol and propranolol?

A

It is a mixed beta-alpha blocker

Therefore, it gives alpha-1 blockade vasodilator properties.

It lowers blood pressure via a reduction in peripheral resistance.

The beta-selective part of carvedilol also have beneficial effects on the beta-1 receptors in the heart (decrease CO) and kidneys (decrease renin secretion), helping to lower blood pressure

29
Q

What is the function of alpha-1 adrenoreceptors?

A

Alpha-1 Receptors

  • Gq linked
  • generally increase activity in vascular smooth muscle
  • linked to stimulatory G proteins
  • post-synaptic
30
Q

What is the function of alpha-2 adrenoreceptors?

A

Alpha-2 receptors

  • Gi linked
  • Presynaptic autoreceptors inhibiting NE
  • generally reduce/inhibit activity
31
Q

What type of adrenoreceptor antagonist is Phentolamine?

A

Non-Selective Alpha Blocker

32
Q

What is Phentolamine used to treat?

A
  • Used to treat phaechromocytoma-induced hypertension
  • This is a tumour which releases lots of adrenaline
  • Rarely used, as its effect is limited
33
Q

What is the effect of beta-blockers acting on beta-1 receptors?

A

Heart
= reduce HR and CO
= this effect disappears in chronic treatment

Kidney
= reduce renin production
= long-term feature is to reduce peripheral resistance

34
Q

Why is it useful for beta blockers to have an effect on the CNS?

A

Beta 1 and Beta receptors

CNS

  • determines blood pressure set point
  • regulates some systems involved in blood pressure control and autonomic NS
35
Q

Why is it useful for beta blockers to have an effect on sympathetic nerves?

A

beta-1 and beta-2 receptors

Sympathetic nerves can release the vasoconstrictor NA

36
Q

Despite all its benefits as a non-selective beta blocker, what disadvantage does carvediol have over atenolol and propranolol?

A

Because it is less selective, it has a larger side effect profile than the other two drugs.

37
Q

What type of adrenoreceptor antagonist is Prazosin?

A

alpha-1 selective Alpha Blocker

38
Q

What is the mechanism of action of Prazosin?

A

It inhibits the vasoconstrictor activity of NE

- have more widespread use in hypertension treatment

39
Q

What is one potential benefit and one drawback of alpha-blockers as opposed to beta-blockers for hypertension treatment?

A

BENEFIT
- fewer side effects

DRAWBACK
- slightly less effective as hypertension treatment

40
Q

What are the side effects of Phentolamine?

A

GastroIntestinal

  • constipation
  • not absorbing food as well
  • bloating
41
Q

Why do alpha 2 receptors and baroreceptors reduce the effectiveness of Phentolamine?

A

Phentolamine blocks alpha-1 and alpha-2 receptors

Alpha-1

  • by blocking this, you prevent vasoconstriction
  • this is ideal

Alpha-2

  • by blocking this, you lose negative feedback
  • therefore more NA is released into synapse
  • therefore, phentolamine and NA are competing for alpha-1 receptors
  • NA will outcompete because it’s in high concentration

Baroreceptors

  • alpha-1 blockade causes vasodilation
  • arterial pressure falls
  • this causes reduced baroreceptor firing
  • therefore, in rebound, sympathetic activity increases
  • CO goes up despite TPR going down
  • this is especially bad if the hypertension is associated with cardiac problems
42
Q

Compare Phentolamine to Prazosin

A

Prazosin

  • because it only affects alpha-1 receptors, no alpha-2 loss of negative feedback
  • as a result, it is more effective at reducing blood pressure than phentolamine
43
Q

What drugs can treat hypertension?

A
  • ACE Inhibitors
  • Calcium Channel Blockers
  • Diuretics
  • Beta-Blockers
  • Alpha-Blockers
  • False Transmitters
44
Q

What are False Transmitters?

A

These are drugs that replace endogenous neurotransmitters

45
Q

What kind of hypertensive treatment is Methyldopa?

A

A False Transmitter

46
Q

What is the mechanism of action of Methyldopa?

A

Methyldopa administered

Converted to false transmitter

  • a version of noradrenaline called Alphamethylnoradrenaline
  • via the same enzymes as DOPA would use)

Less active at Beta/Alpha 1 receptor

  • not a good agonist
  • not good at stimulating the receptors

Not well metabolised by MAO like NA is

More likely to accumulate in synapse

Displaces and outcompetes NA

47
Q

Which receptor is Methyldopa a better agonist for than Noradrenaline?

A

In its form Alphamethynoradrenaline

  • better agonist for Alpha-2
  • worst agonist for Beta-1 and Alpha-1
48
Q

What are the benefits of Methyldopa’s affinity for alpha-2 receptors as treatment?

A

Improved blood flood
- vasodilation due to alpha-2 stimulation

Anti-hypertensive

  • decreased sympathetic nerve release of NA
  • enhances negative feedback effect of alpha-2 receptors

Renal

  • improve kidney disease
  • increase blood flow to kidneys

CNS

  • improve cerebrovascular disease
  • increase blood flow to brain
49
Q

What are the side effects of Methyldopa?

A

Not a large side effect profile due to low affinity for alpha-1, beta-1 and beta-2 receptors

Alpha-2 Side effects

  • effect on salivary glands (dry mouth)
  • postural hypotension (due to their effectiveness at decreasing blood pressure)
50
Q

What is the main cause of arrhythmias?

A

Myocardial Ischaemia

51
Q

How many deaths in the US are caused by arrhythmias per year?

A

350,000 deaths

52
Q

What is arrhythmia?

A

Abnormal or Irregular Heart Beats

  • this causes sub-optimal blood flow as the heart is not beating rhythmically
  • diminished CO
53
Q

How can beta-blockers treat arrhythmias?

A

Sympathetic nervous system doesn’t cause arrhythmias, but it does exacerbate them

Beta-1 Effects

  • Increased sympathetic drive to heart
  • Precipitates arrhythmias
  • AV conductance dependent on sympathetic activity

These effects are blocked

  • slow heart rate
  • more time for heart to fill
  • improve cardiac output
54
Q

What class of anti-arrhythmics are beta-blockers?

A

Class 2

55
Q

What is main drug used as an anti-arrhythmic?

A

Propanolol

56
Q

What is angina?

A

Chest pain/pressure

57
Q

What is stable angina?

A

Pain on exertion.

Increased demand on the heart and is due to fixed narrowing of the coronary vessels (e.g. atheroma)

Can get enough blood flow to the heart for normal activity but not for exertion

58
Q

What is unstable angina?

A

Pain with less and less exertion, culminating in pain at rest.

Platelet-fibrin thrombus associated with a ruptured atheromatous plaque, but without complete occlusion of the vessel.

Risk of infarction

Thrombus means that pain can come on at any time.

Much more dangerous than stable angina.

59
Q

What is variable angina?

A

Occurs at rest

Caused by coronary artery spasm, associated with atheromatous disease.

Not to do with atherosclerosis narrowing coronary vessels, but instead the vessels constrict themselves during spasm which reduces blood flow.

60
Q

How does angina start?

A

Atherosclerosis narrowing coronary vessels

Blood flow through these vessels is reduced

61
Q

What is typically the first presenting form of angina?

A

Stable Angina

62
Q

What are the 3 forms of angina?

A

Stable

Unstable

Variable

63
Q

How do beta-blockers help to treat angina?

A

Don’t treat the atherosclerosis

At low does, beta-1 selective agents reduce heart rate and myocardial contractile activity without affecting bronchial smooth muscle

Reduce the oxygen demand (and work) of the heart whilst maintaining the same degree of effort

64
Q

What is glaucoma?

A

Characterised by increase in intraocular pressure

Caused by poor drainage of aqueous humour

65
Q

What can happen if glaucoma is left untreated?

A

It can permanently damage the optic nerve

This can cause blindness

66
Q

What is aqueous humour and where is it produced?

A

Fluid that bathes and protects the eye

It is produced in the ciliary body which suspends the lens

It drains through venous drainage channels

67
Q

How can beta-blockers treat glaucoma?

A

There are beta-1 receptors in the ciliary epithelium of the ciliary body

These receptors drive aqueous humour formation by causing bicarbonate formation via carbonic anhydrase

By blocking these receptors, less aqueous humour is produced which reduces intra-ocular pressure

68
Q

How is aqueous humour formed?

A

Beta-1 receptor on ciliary epithelium

This receptor is coupled to carbonic anhydrase

Carbonic anhydrase produces bicarbonate ions

Bicarbonate with sodium and water makes up the majority of aqueous humour

Yr 2 LCRS - Pharm (44 decks)

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