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Y2 - PHARM > SNS Antagonists > Flashcards

SNS Antagonists Flashcards

1
Q

What does the SNS do to the following effectors?

1) Pupil
2) Salivation
3) Bronchi
4) Heart
5) Stomach
6) Liver
7) Kidney
8) Bladder
9) Rectum

A

1) Pupil dilation
2) Inhibits salivation
3) Relaxes bronchi
4) Accelerates heart
5) Inhibits digestive activity - reduces motility and secretions
6) Stimulates glucose release by liver - stimulates glycogenolysis and gluconeogenesis

7)

  • Stimulates secretion of adrenaline and noradrenaline from kidney
  • Stimulates renin release

8) Relaxes bladder
9) Contracts rectum

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2
Q

What does the PNS do to the following effectors?

1) Pupil
2) Salivation
3) Bronchi
4) Heart
5) Stomach
6) Gallbladder
7) Bladder
8) Rectum

A

1) Pupil constriction
2) Stimulates salivation
3) Bronchi constriction
4) Inhibits heart (negative chronotropic and inotropic effect)
5) Stimulates stomach motility and secretions
6) Stimulates gallbladder
7) Contracts bladder - pee
8) Relaxes rectum - poo

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3
Q

5 subtypes of SNS adrenoreceptors?

A
  1. a1
  2. a2
  3. B1
  4. B2
  5. B3
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4
Q

Actions mediated by a1 adrenoreceptors?

A
  • Vasoconstriction
  • Relaxation of GIT
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5
Q

Actions mediated by a2 adrenoreceptors?

A
  • Inhibition of transmitter release
  • Conctraction of vascular smooth muscle
  • CNS actions
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6
Q

Actions mediated by B1 adrenoreceptors?

A
  • Positive chronotropic and inotropic effect on heart
  • GIT relaxation
  • Renin release from kidney
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7
Q

Actions mediated by B2 receptors?

A
  • Bronchodilation
  • Vasodilation
  • Relaxation of visceral SM
  • Hepatic glycogenolysis
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8
Q

Actions mediated by B3 adrenoreceptors?

A

Lipolysis

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9
Q

How do a2 receptors inhibit release of neurotransmitter, and which one in particular?

A
  • Noradrenaline
  • Noradrenaline binds autoreceptors on the presynaptic membrane and these presynaptic a2 adrenoreceptors have a negative impact on the synthesis and release of noradrenaline from the nerve terminal
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10
Q

List 5 adrenoreceptor antagonists and the adrenoreceptor subtypes they work against

A
  1. Carvedilol: a1 + B1
  2. Phentolamine: a1 + a2
  3. Prazosin: a1
  4. Propanolol: B1 + B2
  5. Atenolol: B1
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11
Q

Basic formula for BP?

A

BP = CO x TPR

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12
Q

Over what systolic and diastolic BP is it considered HTN?

A

> 140/90 mmHg

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13
Q

1) What are the associated disease with HTN?
2) Thus what is the ultimate goal of HTN therapy?

A

1)

  • Ischaemic stroke
  • HF
  • MI
  • CKD

2)

  • To reduce the mortality from cardiovascular or renal events
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14
Q

3 main elements that contribute to HTN?

A
  1. Blood volume
  2. CO
  3. Peripheral vascular tone
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15
Q

How does B1 adrenoreceptor mediated action increase BP, and which effect is greater?

A
  • B1 receptors on heart - positive chronotropic and inotropic effect → increases CO → increases BP
  • B1 receptors on kidneys → increases renin release which has effects on RAAS system
  • Increases aldosterone release → increases Na+ and water retention to increase blood volume and CO
  • Increases AT1 → increases AT2 (vasoconstrictor) levels → increases TPR
  • Renal effect > heart effect
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16
Q

4 targets for anti-hypertensives and what these target sites are generally responsible for in relation to HTN?

A
  1. Heart - CO
  2. Kidneys - CO / TPR
  3. SNS nerves - secreting NA (vasoconstrictor)
  4. CNS - BP set point + ANS + other systems regulating BP
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17
Q

What are cardioselective antagonists?

A

B1 antagonists

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18
Q

How do beta-blockers work in general - mention the 4 target sites - the beta-adrenoreceptor subtypes it acts on, and the action it has

A
  1. Heart - blocks B1 - therefore decreases HR and force of contraction - reducing CO and thus BP
  2. Kidneys - blocks B1 - therefore reduces renin release and thus also reduces aldosterone and AT2 production so there’s less sodium and water retention and vasoconstriction - thereby reducing CO and TPR and thus BP
  3. SNS nerves - B1/B2 - prevents release of noradrenaline from SNS nerves (vasoconstrictor) so less vasoconstriction - reduces TPR. Could be via presynaptic B1 adrenoreceptors and dampening there positive facilitative effect on NA release also
  4. CNS - B1/B2 - reduces sympathetic tone and BP set point
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19
Q

What is the physiological effect of presynaptic B1 adrenoreceptors and what effect do Beta-blockers have by acting on these?

A
  • Positive facilitative effect on release of NA from nerve terminal
  • But if you block this, then there will be less release of NA from the nerve terminals and thus less vasoconstriction
20
Q

Name 1….

1) Non-selective beta antagonist
2) B1 selective beta antagonist
3) Mixed beta and alpha antagonists
4) What effects does the beta blocker Nebivolol have (receptors it acts on / other effect) ?
5) What effect does the beta blocker Sotalol have (receptors it acts on / other effects)?

A

1) Propanolol (B1+B2)
2) Atenolol ( (B1)
3) Carvedilol (B1/B2 + A1)
4) Blocks B1 and potentiates NO (vasodilator)
5) Blocks B1 + B2 and also inhibits K+ channels

21
Q

List 6 unwanted effects of beta-blockers and explain why these occur including which beta adrenoreceptors exactly its mediated by

A
  1. Bronchoconstriction - bad in patients with bronchitis and COPD - prevents B2 mediated bronchodilation
  2. Cardiac failure - Need some SNS drive to the heart to maintain CO so by inhibiting this, you can struggle to maintain CO - prevents B1 mediated positive chronotropic and inotropic effect
  3. Hypoglycaemia - Inhibits hepatic glycogenolysis and blocks symptoms associated with hypoglycaemia (sweating, palpitations and tremor) - as otherwise mediated by B2
  4. Fatigue - lower cardiac output and less muscle perfusion - as otherwise B1 mediated
  5. Cold extremities - loss of B2 adrenoreceptor mediated vasodilation in cutaneous vessels
  6. Bad dreams
22
Q

1) List advantage sof the use of cardioselective (B1 selective) rather than non-selective beta-blockers, and why must you still be careful with certain people?
2) Name one cardioselective and one non-selective beta-blocker

A

1)

  • LESS UNWANTED EFFECTS OF B2 ANTAGONISM
  • Less effect on airways as doesn’t antagonise B2 adrenoreceptors on the bronchial smooth muscle and so doesn’t cause bronchoconstriction, which can be particularly bad for people with lung problems such as bronchitis and asthma
  • Because selectivity is dependent upon concentration, so at higher concentrations, the B1 selective antagonists can still also antagonise B2 adrenoreceptors

2)

  • Cardioselective - atenolol
  • Non-selective - propanolol
23
Q

What advantage does carvedilol have over propanolol and atenolol?

A

It acts centrally on the heart to reduce BP but also antagonises a1 receptors to give a vasodilatory effect so lowers TPR as well as lowering CO

24
Q

What type of hypotension may alpha antagonists cause and what is the physiology behind this normally when uninterfered?

A
  • Postural hypotension
  • When you stand up, there is baroreceptor-SNS mediated tachycardia and blood flow through cutaneous and splanchnic vascular bed increases but effects on vascular smooth muscle are little
  • Alpha antagonists prevent this reflex and so causes postural hypotension
25
Q

What G protein pathway do the alpha adrenoreceptors act through?

A
  • a1 → Gq-linked → PLC 2nd messenger → PIP2 increase → IP3 + Ca2+ or DAG and PKC
  • a2 → Gi linked → Adenylate cyclase 2nd messenger → ↓cAMP → PKA
26
Q

1) What type of adrenoreceptor antagonist is phentolamine
2) What can phentolamine be used to treat?
3) How does phentolamine have its effect?
4) Phentolamine is no longer in clinical use - what side effects can phentolamine have and why do these occur?

A

1) Non-selective alpha antagonist
2) Treats pheochromocytoma-induced HTN (adrenal medulla oversecretes NA thus HTN
3) Causes vasodilation and fall in BP due to blockade of a1 adrenoreceptors
4) a1 normally relaxes GIT, so by antagonising it:

  • Increased GIT motility
  • Diarrhoea
27
Q

3 reasons why Phentolamine has less anti-hypertensive effect / enhances the reflex tachycardia?

A
  1. Concomitant imhibition of a2 adrenoreceptors prevents the prejunctional negative feedback mechanism controlling NA release - so increases NA release - increases vasoconstriction
  2. This increased noradrenaline outcompetes phentolamine acting at the a1 adrenoreceptors so there’s less vasodilation
  3. Decreases BP so arterial baroreceptor firing rate lowers, this increases the SNS activity of the heart, increasing SV and CO
28
Q

1) What type of adrenoreceptor antagonist is Prazosin
2) How is it useful as an anti-hypertensive
3) Why is there better effect as an anti-hypertensive with Prazosin (and other adrenoreceeptor antagonists of the same type as Prasozin - see question 1) than with the other type of alpha antagonists?
4) One side benefit of it?
5) One problem with it?

A

1) a1-selective antagonist

2)

  • Reduces TPR - inhibits NA vasoconstrictor activity via a1 adrenoreceptors
  • Reduces CO - due to fall in venous pressure as a result of dilation of capacitance vessel

3)

  • Does NOT simultaneously increase NA release from nerve terminals as no a2 actions

4)

  • Causes decrease in LDL and an increase in HDL cholesterol - improves lipid profile

5)

  • Troublesome postural hypotension
29
Q

1) Outline the process by which methyldopa works as an anti-hypertensive by being a false transmitter
2) Give 2 other mechanisms by which it acts as an anti-hypertensive

A

1)

  • Methyldopa taken up by noradranergic neurones
  • Decarboxylated and hydroxylated to form methylnoradrenaline
  • Less active at B1 and a1 receptors
  • Not metabolised (de-aminated) by MAO in neurone
  • So accumulates and displaces NA in the vesicle

2)

  1. More powerful effect on presynaptic a2 receptors so inhibits release of NA more - so less vasoconstriction
  2. Stimulates vasopressor centre in the brain stem to inhibit SNS outflow
30
Q

3 HTN conditions methyldopa (an anti-hypertensive) is used to treat?

A
  1. Renal - CKD
  2. CNS - cerebrovascular disease
  3. HTN in pregnancy
31
Q

List some adverse effects of methyldopa use

A
  • Dry mouth
  • Orthostatic HOTN
  • Male sexual dysfunction
  • Sedation
32
Q

What is arrythmia?

A

Abnormal or irregular heart beats

33
Q

Main cause of arrythmia?

A

MI

34
Q

Give 2 ways in which SNS activity is related to arrythmias

A
  • Increase in sympathetic drive to the heart via B1 as seen following MI where there is an increase in sympathetic tone, can precipitate or aggravate arrythmias
    1. AV conductance is dependent upon sympathetic activity, the refractory period of the AV node is increased by beta-antagonists (blockers) - e.g. slows AV conduction in atrial tachycardias and slows down ventricular rate. This is also useful as, even if you have a re-entry type electrial activity in damaged myocardium, it wont stimulate extra heart beats as the refractory period is prolonged
35
Q

1) What type of drugs are class 2 anti-arrythmics usually?
2) Give an example class 2 anti-arrythmic
3) What are class 2 anti-arrythmics used to treat?

A

1) B1 adrenoreceptor antagonists
2) Propanolol

3)

  • Reduce mortality following MI
  • Arrythmia following exercise
  • Arrythmia following mental stress
36
Q

Define Angina

A

‘Pain that occurs when the oxygen supply to the myocardium is insufficient for its needs’

37
Q

What is the pain distribution of angina?

A
  • Chest
  • Arm
  • Neck
38
Q

List the 3 types of angina

A
  1. Stable
  2. Unstable
  3. Variable
39
Q

Describe stable angina, including the pain onset pattern and the cause, and any other details

A
  • Pain on exertion
  • Due to fixed narrowing of the coronary vessels e.g. atheroma
  • Increased demand on the heart
40
Q

Describe unstable angina, including the pain onset pattern and the cause, and any other details

A
  • Pain with less and less exertion - which culminates with pain at rest
  • The atheromatous plaque is starting to rupture - you get a platelet-fibrin thrombus associated with the ruptured atheromatous plaque but without complete occlusion of the vessel
  • High risk of infarction
41
Q

Describe variable angina, including the pain onset pattern and the cause, and any other details

A
  • Occurs at rest
  • Caused by coronary artery spasm
  • Associated with atheromatous disease
42
Q

List factors that increase myocardial oxygen supply and demand respectively

A

SUPPLY

  • Coronary blood flow - high
  • Arterial O2 content - high

DEMAND

  • HR - high
  • Contractility - high
  • Preload - high
  • Afterload - high
43
Q

Why might exercise induce angina and what kind of drugs (including a specific drug named example) work to prevent this, and how?

A
  • The HR and force of contracility increases with exercise so the metabolic demand of the myocardium increases. If this increased demand is not met by the supply to the myocardium, exercise can induce angina
  • B1 specific antagonists e.g. metoprolol reduce HR and force of contractility of the heart without affecting bronchial smooth muscle - thereby reducing oxygen demand whilst maintaining the same degree of effort. This lower myocardial oxygen demand means it is less likely for the supply to not meet the demand and lead to angina
44
Q

Where is aqueous humour formed and what is its circulation route?

A
  • Blood vessels in the ciliary body via the actions of carbonic annhydrase
  • Flows into the posterior chamber, through the pupil into the anterior chamber
  • It drains into the trabecular meshwork in the canal of Schlemm
45
Q

The production of aqueous humour is linked to….?

A

… BP and blood flow in the ciliary body

46
Q

How does adrenaline use treat glaucoma?

A

Adrenaline acts on a1 receptors to cause vasoconstriction and reduce blood flow through the ciliary body - thereby reducing aqueous humour production and reduce intraocular pressure in glaucoma

47
Q

How do beta-antagonists treat glaucoma?

A
  • B1 adrenoreceptors are coupled with the carbonic annhydrase (CA)
  • CA forms bicarbonate - a constituent of aqueous humour (=bicarbonate + Na+ + water)
  • So beta-blockers prevent aqueous humour formation by inhibiting CA

Y2 - PHARM (27 decks)

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