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Pharmocology > SNS antagonists > Flashcards

SNS antagonists Flashcards

1
Q

What are the SNS adrenoceptor subtypes and what do they cause to happen?

A

alpha 1- vasoconstriction, relaxation of GIT
alpha 2 - inhibition of transmitter release, contraction of vascular smooth muscle and CNS actions
beta 1 - increased cardiac rate and force, relaxation of GIT and renin release from kidney
beta 2 - bronchodilation, vasodilation, relaxation of visceral smooth muscle, hepatic glycogenolysis
beta 3 - lipolysis

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2
Q

What can neurotransmitters also act as?

A

-auto receptors on the presynaptic membrane that influence the synthesis and release of neurotransmitter

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3
Q

What adrenoceptors does carvedilol favour?

A
  • totally non-selective

- alpha 1 and beta 2

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4
Q

what adrenoceptor does phentolamine favour?

A
  • alpha 1 and -alpha 2

- non-selective

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5
Q

what adrenoceptor does prazosin favour?

A

-alpha 1

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6
Q

what adrenoceptor does propranolol favour?

A
  • beta 1 and beta 2

- non-selective

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7
Q

what adrenoceptor does atenolol favour?

A

-beta 1

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8
Q

what is hypertension defined as?

A

-BP consistently over 140/90 mmHg

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9
Q

what is the most important risk factor for stroke?

A

-hypertension

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10
Q

what is hypertension a high risk factor for?

A
  • chronic kidney disease

- myocardial infarction

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11
Q

what is the equation for blood pressure?

A

BP=CO x TPR

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12
Q

What are the main contributors towards blood pressure?

A
  • cardiac output
  • blood volume
  • vascular tone
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13
Q

What effect do beta blockers have on adrenoceptors?

A
  • block beta 1 receptors on the heart leading to a reduction in HR and force of contraction, leading to reduced BP
  • blocks beta 1 receptors on the kidney, reducing renin production, reducing angiotensinogen II - decreasing peripheral resistance
  • blockade of beta 1 and beta 2 may block noradrenaline release from sympathetic nerves
  • reduces sympathetic tone in the CNS
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14
Q

What are the side effects of beta blockers?

A
  • bronchoconstriction
  • cardiac failure
  • hypoglycaemia
  • fatigue
  • cold extremities
  • bad dreams
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15
Q

what extra property does carvedilol have?

A

-alpha 1 blockade give additional vasodilator properties

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16
Q

what does nebivolol effect?

A
  • it is a beta 1 blocker

- stimulates NO release

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17
Q

what does sotalol effect?

A
  • blocks both beta1 and beta 2

- inhibits K+ channels, interferes with cell hyperpolarisation

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18
Q

what type of patients do you not want to give beta blockers to?

A
  • asthmatic/COPD
  • cardiac failure (these patients rely on a degree of sympathetic drive to maintain adequate CO)
  • diabetic (beta blockers can mask the symptoms of hypoglycaemia e.g. sweating)
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19
Q

Why do you experience fatigue?

A

-reduced CO and reduced muscle perfusion

20
Q

Why do you suffer from cold extremities?

A

-loss of beta receptor mediated vasodilation of cutaneous vessels

21
Q

What are the advantages of propranolol vs atenolol

A
  • atenolol has a reduction of B2side effects

- asthmetics and diabetics are lesslikely tp respond badly to the drug but it is STILL NOT SAFE

22
Q

What advantage does carvedilol have over atenolol and propranolol?

A

-more powerful hypotensive effect - decreases FOC on the heart through B1, blocked renin release on the kidney through B2 and blocks vasoconstriction on vessels through A1

23
Q

What is the mechanism for A1 receptors and where are they found?

A
  • Gq linked
  • PIP2 - IP3 - Ca2+
  • PIP2 - DAG - PKC
  • postsynaptic on vascular smooth muscle
24
Q

What is the mechanism for A2 receptors and where are they found?

A
  • Gi linked
  • ATP - CAMP -PKA
  • presynaptic autoreceptors inhibiting NA release
25
Q

What is phentolamine used for?

A

-pheochromocytoma- induced hypertension

26
Q

What is prazosin used for?

A
  • inhibits vasoconstrictor activity of NA
  • modest BP lowering effects
  • adjunctive treatment
27
Q

How does phentolamine work?

A
  • blocks alpha 1 and alpha 2 (non-selective)
  • reduced negative feedback from alpha 2 leads to increased release of NA
  • this competes with the alpha 1 blockade
  • baroceptors detect dilated blood vessels through decreased vagal activity, sympathetic activity is increased
28
Q

What is an advantage of prazosin over phentolamine?

A
  • less tachycardia occurs as NA release is not increased from the end of nerve terminals
  • CO decreases due to fall in venous pressure and from dilation of capacitance vessels
  • hypotensive effect is dramatic
  • also causes a modest decrease in LDL, increase in HDL
29
Q

Describe how methyldopa works?

A
  • it is taken up by noradrenergic neurons, it is then decarboxylated and hydroxylated to form a false transmitter (a-methyl-noradrenaline) so it cannot be modified by MAO
  • it accumulates in larger quantities than noradrenaline, displacing it from synaptic vessels
30
Q

How is A-methyl-noradrenaline release?

A

the same way as noradrenaline

31
Q

what adrenoceptors does AMN act on?

A
  • less effective than NA on alpha 1 so they are less effective causing vasoconstriction
  • more active on presynaptic alpha 2, reduces NA release below normal
  • stimulates vasopressor centre in the brain to inhibit sympathetic outflow
32
Q

What other benefits are there of methyldopa?

A
  • used in renal insufficiency or cerebrovascular disease

- advised for an antihypertensive in pregnant women as it has no adverse side effects on the foetus

33
Q

What are the side effects of methyldopa?

A

-dry mouth
-sedation
-orthostatic hypotension
male sexual dysfunction

34
Q

What is an arrhythmia and what is its main cause?

A
  • abnormal or irregular heartbeat

- myocardial ischemia

35
Q

What increases the chance of an arrhythmia?

A

exercise

36
Q

What are used for treatment of arrhythmia and why?

A
  • beta blockers
  • -increase the refractory time of AV node, slowing down ventricular rate- beneficial in the case of atrial tachycardia
  • this controls sympathetic drive

-propranolol, particularly successful in ones that occur during exercise or mental stress

37
Q

What is angina?

A

-pain when the oxygen supply to the myocardium is insufficient for its needs

38
Q

What causes angina?

A

-exertion or excitement, mostly by atherosclerosis

39
Q

What are the 3 types of angina?

A
  • stable (pain on exertion)
  • unstable (pain with less and less exertion)
  • variable (at rest)
40
Q

What are used to treat anginas and why?

A
  • beta adrenoceptor antagonists
  • decrease HR, systolic BP and cardiac contractile activity
  • they will reduce oxygen demand whilst maintaining the same degree of effort

-at low dose metoprolol reduces HR and myocardial contractile activity without affecting bronchial smooth muscle

41
Q

What patients are beta blockers not used in to treat angina?

A
  • bradycardic (<55 bpm)
  • Bronchospasm
  • Hypotensive
  • AV block or severe congestive heart failure
42
Q

What is glaucoma?

A

-increase in intraocular pressure

43
Q

How does fluid normal pass through the eye?

A
  • aqueous humour is produced by blood vessels in the ciliary body via carbonic anhydrase
  • the amount of humour produced is directly related to the blood flow in the ciliary body
  • the aqueous humour flows through the posterior chamber, through the pupil and into the anterior chamber
  • drains into the trabecular meshwork in the canal of schlemm
44
Q

What can adrenaline act on in the eye?

A

-alpha 1 receptors to cause vasoconstriction and reduce blood flow through the ciliary body

45
Q

What are used to treat glaucoma?

A
  • non selective or selective antagonists
  • they reduce the rate of aqueous humour formation by blocking receptors on the ciliary body
  • non selective that work: carteolol hydrochloride, levobunolol hydrochloride, timolol maleate
  • selective that work: betaxolol hydrochloride
46
Q

WHat other uses of beta antagonists are there?

A
  • anxiety states e..g palpitations and tremor
  • migraine prophylaxis, maintains a good supply to the CNS
  • benign essential tumour

Pharmocology (16 decks)

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