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Pharmacology RDT Autumn term > SNS antagonists > Flashcards

SNS antagonists Flashcards

1
Q

Name some sympathetic effects

A
  • Pupil dilation
  • Bronchi relaxation
  • heart acceleration
  • Stimulation of HGO
  • Secretion of adrenaline and NA from kidney
  • Contracts rectum
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2
Q

What do alpha 1 receptors do?

A

Alpha 1 receptors are present on blood vessels and when NA/ A binds to them, they cause vasoconstriction and relaxation of GIT.

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3
Q

What do alpha 2 receptors do?

A

Inhibition of transmitter release, contraction of vascular smooth muscle, CNS actions- suppress sympathetic activity.

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4
Q

What do beta 1 receptors do?

A

They are present in the heart.

They cause increased cardiac rate and force, relaxation of GIT, renin release from kidney.

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5
Q

What do beta 2 receptors do?

A

They are present in the lungs.

Causes bronchodilation, vasodilation, relaxation of visceral smooth muscle, hepatic glycogenolysis- drives the sympathetic effect in the liver.

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6
Q

Describe the negative feedback mechanism of the alpha 2 adrenoreceptor

A

NA produced from tyrosine (upstream), packaged into vesicles and leaves pre-synapse into the synaptic cleft. NA activates the receptor on the post synapse (alpha 1). Alpha 2 switches off this effect and stops NA being released.

NA release is fast in response to stimulus, but you don’t want a prolonged response. Swift response but quickly switched off too.

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7
Q

Name a non-selective SNS antagonist

A

Carvedilol

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8
Q

Name an alpha-1 and alpha-2 selective SNS antagonist

A

Phentolamine

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9
Q

Name an alpha-1 selective antagonist

A

Prazosin

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10
Q

Name an SNS antagonist which is selective to beta 1 and beta 2 over alpha receptors?

A

Propanolol

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11
Q

Name a beta-1 selective antagonist?

A

Atenolol

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12
Q

What do you need to think about if someone has hypertension?

A

You’re probably thinking that there is something wrong with the physiology in mechanisms to control BP.

Think CO X TPR = MAP

CO- there is probably something wrong with the heart (and the brains control of it)

TPR- to do with the blood vessels and the kidney’s ability to produce renin

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13
Q

Above which BP is considered hypertensive?

A

140/90

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14
Q

What are the main physiological contributors to BP?

A
  • Blood volume
  • cardiac output
  • vascular tone
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15
Q

What are the tissue targets for anti-hypertensives?

A
  • The heart- CO
  • Arterioles- controls and determines TPR
  • Kidneys- blood volume and vasoconstriction
  • Sympathetic nerves that release NA (vasoconstrictor)- the CNS determines BP set point and regulate some systems involved in Bp control and autonomic nervous system.
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16
Q

how to spot a beta-blocker from the name?

A

They end in “olol”

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17
Q

What are the 2 main effects of beta blockers?

A

Beta-blockers will act on the heart (beta 1), on the kidney (beta 1) and sympathetic nerves that release the vasoconstrictor NA (beta1 and 2).

There are some beta receptors in the brain which regulate BP and to reduce sympathetic tone. Arterioles do not have beta-adrenoreceptors so will not be affected (vessels have alpha 1 receptors).

18
Q

Action of beta-blockers specifically to reduce HR and BP

A

Decrease in HR & FOC and a decrease in cardiac output

The heart does not have to work as hard - reduced blood pressure. Reduction in cell activity.

Decrease in renin and therefore angiotensin II (Ang II) release-

lost vasoconstricting effect (positive TPR effect) and reduce aldosterone production.

Ang II - potent vasoconstrictor & increased aldosterone production. There are a number of stimuli for renin production (sympathetic nerves, sodium plasma level).

Blockade of the facilitatory effects of presynaptic β-adrenoceptors on noradrenaline release may also contribute to the antihypertensive effect.

Minor effect: Adrenaline increases the ability to create NA in the pre-synaptic neuron.

19
Q

What does Nebivolol bind to? and why is it special?

A

Beta-1 adrenoreceptors and it also potentiates NO release.

NO is a vasodilator

20
Q

What does sotalol do?

A

It binds to both beta-adrenoreceptors and it also inhibits potassium channels

21
Q

what are the unwanted side effects of beta-blockers?

A
  1. Bronchoconstriction- should not be given to people with asthma/COPD
  2. Cardiac failure- should not be given to heart failure patients if you slow CO down too much, the heart cannot keep up with demand and worsen heart failure
  3. Hypoglycaemia- the symptoms are masked. There is usually a sympathetic response to hypoglycaemia, so you won’t notice it. Glucose is released from the liver it is stimulated via the beta 2 receptors.
  4. Fatigue - Reduced cardiac output and muscle perfusion
  5. Cold extremities- they are the vasodilating receptors and are present on muscles. Sympathetic nervous system activates the beta 2 receptors but if they are blocked, then the muscles will not get blood- leading to fatigue and cold extremities (limited capacity to dilate blood flow to the skin).
  6. Bad dreams
22
Q

Why do you have to be careful when using propranolol?

A

Propranolol is non-selective Beta 1 and Beta 2. In a subject at rest causes very little effect but during exercise, can reduce HR, CO and ABP. As it is non-selective, it produces all the typical adverse effects.

23
Q

why would you use atenolol over propranolol?

A

Atenolol is b1-Selective, antagonises the effects of noradrenaline on the heart but will affect any tissue with b1 receptors e.g. Kidney.

Less effect on airways than non-selective drugs, but still not safe with asthmatic patients. Selectivity is concentration-dependent.

Reduce the side effects that are beta 2 mediated. Given to asthmatics and diabetics to reduce the negative side effects.

24
Q

Why use carvedilol over atenolol or propranolol?

A

There are beta mediated effects with carvedilol but there is blocking of vasoconstriction of arterioles (due to the alpha 1 selectivity). It is a more powerful anti-hypertensive but can have more potent side effects.

25
Q

What is the main effect seen in alpha-blockers?

A

There is a fall in arterial pressure (e.g. problem with postural hypotension)- as there is a fall in TPR, you get reflex tachycardia. Blood flow increases.

26
Q

Describe the alpha 1 receptor structure

A
  • Gq-linked
  • Postsynaptic on vascular smooth muscle
27
Q

Describe the alpha 2 structure

A
  • Gi-linked
  • Presynaptic autoreceptors inhibiting NE release
28
Q

What are the clinical effects of alpha-blockers?

A
  • Non-selective a-blocker: phentolamine - used to treat phaeochromocytoma-induced hypertension
  • a1 specific blocker: prazosin inhibit the vasoconstrictor activity of NE
  • Have modest blood pressure lowering effects
  • Only used as adjunctive treatment

Blocking alpha-1 receptors will lead to arterial vasodilation

Phentolamine is a more potent anti-hypertensive as opposed to prazosin. However, it has a lot of side effects so it is no longer clinically used.

29
Q

How do alpha-blockers increase BP?

A

They dilate the blood vessels, changing the pressure system.

Baroreceptor firing rate will change to the pressure change- if high BP, the firing rate is high and there is a parasympathetic drive.

If baroreceptor firing slows, there is a loss in vagal stimulus and there will be an increased sympathetic drive, increasing CO and stroke volume.

30
Q

Describe the effects of prazosin

A

Highly selective for a1-receptors.

Vasodilatation and fall in arterial pressure.

Less tachycardia than non-selective antagonists since they do not increase noradrenaline release from nerve terminals (no a2 actions)

Cardiac output decreases, due to fall in venous pressure as a result of dilation of capacitance vessels.

Hypotensive effect is dramatic.

Does not affect cardiac function appreciably, although postural hypotension is troublesome.

Unlike other anti-hypertensive agents, a1-antagonists cause a modest decrease in LDL, and an increase in HDL cholesterol. Starting to become more popular again as anti-hypertensive agents.

31
Q

What is methyl DOPA?

A

is a false transmitter- instead of NA, you get alpha-methyl NA. Will end up in the vesicles like normal but is more selective to alpha 2- therefore main effect is negative feedback.

The alpha-methyl NA is not oxidised by MAO. This is important because usually MAO provides the concentration gradient and provides the drive for NA to be reabsorbed. Alpha methyl NA is not broken down. Therefore, uptake is a lot slower as the concentration gradient is a lot less. There is heavier alpha 2 stimulation and less NA is released.

32
Q

What is methyl-DOPA used for?

A

It improves blood flow and can be used as an anti-hypertensive.

Not usually used but used when renal disease and CNS issues.

33
Q

What are the unwanted side effects of methyldopa?

A

Methyl-NA is more sensitive to alpha-2 so negative feedback is the main effect here.

BUT, this can cause so much hypotension that it is limiting and it causes dry mouth (dries the sympathetically drive saliva production)

34
Q

Beta-blockers in the treatment of arrhythmias

A

If you increase the sympathetic drive, it will lead to arrhythmia. The AV conductance is dependent on sympathetic activity.

Beta 1 drives heart rate and contraction, therefore, use beta-blockers to treat and to restore a normal rhythm in order to have better blood flow to the heart.

35
Q

What is angina?

A

Not enough blood flow to the heart to match tissue demand. Usually due to atherosclerosis in major vessels.

36
Q

What are the three different types of angina?

A
  1. Stable angina
  2. Unstable angina
  3. Variable angina
37
Q

What is stable angina?

A

there’s enough blood flow but pain on exertion. Increased blood flow cannot be met due to atherosclerosis blocking blood flow.

38
Q

What is unstable angina?

A

pain with less and less exertion, culminating with pain at rest. Platelet-fibrin thrombus associated with a ruptured atheromatous plaque, but without complete occlusion of the vessel. Risk of infarction.

39
Q

What is variable angina?

A

occurs at rest, caused by coronary artery spasm, associated with atheromatous disease

40
Q

how do you approach the treatment of angina?

A

You can try and increase blood flow to tissue or you can try and make the heart work less hard. Beta-blockers will impede your ability to exercise because all you are doing is letting the heart work less hard.

41
Q

What is the ABCD of antihypertensive medication?

A

A- ACE inhibitors

B- Beta-blockers

C- calcium channel blockers

D-diuretics

Pharmacology RDT Autumn term (10 decks)

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