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LCRS - pharma > SNS antagonists > Flashcards

SNS antagonists Flashcards

1
Q

Diagram outlining effects of PSNS and SNS

A
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2
Q

What are the effects of agonisation of a1, a2, b1, b2 nad b3 adrenocreceptors?

A

a1- Vasoconstriction, Relaxation of GIT.

a2- Inhibition of transmitter release, contraction of vascular smooth muscle, CNS actions.

b1- Increased cardiac rate and force, relaxation of GIT, renin release from kidney.

b2- Brochodilation, vasodilation, relaxation of visceral smooth muscle, hepatic glycogenolysis

b3- Lipolysis

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3
Q

alpha 2 receptor action diagram. Why does alpha 2 act in this way?

A

too allow for a swift response that isn’t prolonged.

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4
Q

Give examples of a non-selective (a1 and b1), an a1 + a2, an a1 selective, a b1 + b2 and a b1 selective antagonist

A

Non-selective:(a1+ b1) Carvedilol - a1 blockage gives vasodilator properties.

a1+ a2: Phentolamine

a1: Prazosin

b1 + b2: Propranolol

b1: Atenolol

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5
Q

What systems should be considered when trying to treat hypertension?

A

cardiovascular - blood vessels + heart.

renal - total blood volume, RAAS system.

CNS.

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6
Q

Define hypertension.

A

BP consistently above 140/90mmHg when sitting/lying down for average 30 year old man.

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7
Q

What conditions does hypertension contribute to?

A

Stroke - causing 50% of ischaemic strokes.

25% HF cases. 70% in elderly.

Risk factor for MI and chronic kidney disease.

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8
Q

What are the main contributors to hypertension?

A

Blood volume

Cardiac output

Vascular tone

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9
Q

What are the tissue targets for anti-hypertensives and why?

A

The heart - reduce CO

sympathetic nerves that release NA - vasoconstrictor

Kidney - blood volume/vasconstriction via RAAS.

Arterioles - determine TPR.

CNS - determine BP set point + regulates some systems involved in BP + ANS control.

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10
Q

What receptors are present on the heart, kidney, CNS, sympathetic nerves and arterioles?

A

Heart - B1

Kidney - B1

sympathetic nerves - B1/B2

CNS - B1/B2

arterioles - A2

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11
Q

What effect do beta blockers have in the heart?

A

Reduce HR and FOC –> reduce CO. Heart works less hard, BP drops.

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12
Q

Diagram to show G protein receptor activated by B receptor agonisation.

A
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13
Q

What effect do beta blockers have on the kidney?

A

Reduced renin secretion –> reduced AngII release.

Ang II = powerful vasoconstrictor + increases aldosterone production.

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14
Q

How might beta blockers reduce hypertension due to beta receptors on SNS nerves?

A

Beta receptors on nerves increase SNS nerves’ ability to secrete NA for fight or flight response.

Blocking this reduces that, contributing to antihypertensive effect.

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15
Q

What is nebivolol used for?

A

Cardioselective beta blocker that also stimulates NO release.

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16
Q

What is sotalol used for?

A

non selective beta blocker, also inhibits K+ channels.

17
Q

Outline the important side effects of administering beta blockers and why they arise or are concerning.

A

Bronchoconstriction - Asthma/COPD

Cardiac failure - some SNS drive needed

Hypoglycaemia - symptoms of hypoglycaemia masked. glycogen breakdown inhibited.

Fatigue - reduced CO and muscle perfusion

Cold extremities - loss of b2 receptor mediated vasodilation in cutaneous vessels.

Bad dreams.

18
Q

what is the advantage of atenolol over propanolol?

A

Atenolol = b1 selective, doesn’t stimulate b2 airway and liver receptors, minimising bad side effects compared to non-selective propanolol.

(relative since selectivity is not total).

19
Q

What advantage does carvedilol have over atenolol and propranolol?

A

More powerful hypotensive effect due to blocking of a2 receptor mediated vasoconstriction of arterioles on top of beta mediated effects.

However, side effects more severe.

20
Q

How do a1 and a2 receptors differ?

A

A1 - coupled to stimulatory G protein, PLC and Ca2+ influx.

A2 - coupled to inhibitory G protein - reduce cAMP.

21
Q

What might non-selective a blockers be used for?

A

phentolamine (non-selective) to treat phaechromocytoma-induced hypertension.

prazosin (a1 specific) inhibit vasoconstrictor activity of NE - modest effects.

22
Q

What are the side effects of alpha blockers?

A

increased gastrointestinal function (SNS reduced motility effect blocked)

23
Q

Why do a2 and baroreceptors reduce phentolamine effectiveness?

A

a2 - phentolamine = non selective. Block a1 and a2 receptor. a2 receptor blocked –> reduced negative feedback –> more NA release into synapse. All that is done is set up a competing reaction between phentolamine and NA at a1 receptor in synapse.

baroreceptors - blood vessels dilated by alpha blocking, BP drops, barorecptor firing rate decreased –> sympathetic activity increased –> compensation with increased HR and SV.

24
Q

Outline the method of action of methyldopa.

A

1 & 2 – Methyldopa converted to false

transmitter (alphamethylnoradrenaline)

3 – Less active at Beta/Alpha 1 receptor

4 – Not metabolised by MAO

5 – Concentration gradient reduced across presynaptic membrane for reabsorption, so it lingers around the synapse.

High affinity for a2 means inhibition of further NA release increased.

25
Q

What is methyldopa used for?

A

Anti-hypertensive - specifically relative to kidney/cerebrovascular disease.

26
Q

What are the side effects of methyldopa?

A

Extremely profound hypotension - very powerful.

Dry mouth

27
Q

Define arrhythmia. What is the most common cause?

A

Abnormal/irregular heartbeat.
Myocardial ischaemia.

28
Q

How does sympathetic activity relate to arrhythmias?

A

AV conductance dependent on sympathetic activity. Increased sympathetic drive to heart can precipitate arrhythnmias.

So beta blockers used to slow heart down and restore normal rhythm, normally propanolol.

29
Q

What normally causes angina?

A

artherosclerosis.

30
Q

Compare stable, unstable and variable angina.

A

Stable - pain on exertion. ok at rest.

unstable - pain at rest or with less exertion. risk of infarction. thrombus formation.

variable - at rest, caused by coronary artery spasm.

31
Q

How can angina be treated?

A

Increase O2 supply to tissue, or reduce workload of heart.

Aim is to match blood flow to tissue demand.

b1 blockers can reduce HR and contractility to reduce workload (metoprolol).

32
Q

What produces the aqueous humour?

A

ciliary body

33
Q

How can beta blockers be used to treat glaucoma?

A

Aqueous humour production linked to carbonic anhydrase - HCO3- leaving ciliary body with Na+ to create osmotic gradient.

B1 receptors linked to carbonic anhydrase - blocking this reduces aqueous humour formation.

LCRS - pharma (12 decks)

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