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Y2 Pharmacology and Therapeutics > SNS Antagonists > Flashcards

SNS Antagonists Flashcards

1
Q

What are alpha1 receptors involved in

A

Vasconstriction

Relaxation of the GIT

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2
Q

What are alpha2 receptors involved in

A

Inhibition of transmitter release
Contraction of vascular smooth muscle
CNS actions

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3
Q

What are beta1 receptors involved in

A

Increased cardiac rate and force
Relaxation of GIT
Renin release from the kidney

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4
Q

What are beta2 receptors involved in

A

Bronchodilation
Vasodilation
Relaxation of visceral smooth muscle
Hepatic glycogenolysis

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5
Q

What are beta3 receptors involved

A

Lipolysis

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6
Q

What is the mechanism of SNS synaptic transmission

A
  1. norepinephrine
  2. Release of norepinephrine into synaptic cleft
  3. alpha1 receptor stimulation
  4. alpha2-mediated negative feedback
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7
Q

Describe carvedilol targets

A

Mixed alpha1 and beta1 - non-selective

alpha1 blockade gives additional vasodilator properties

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8
Q

Which receptors does phentolamine target

A

alpha1 and alpha2

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9
Q

Which receptors does prazosin target

A

alpha1

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10
Q

Which receptors does propanalol target

A

non-selective
beta1 and beta2 receptors
equal affinity for both

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11
Q

Which receptors does atenolol target

A

beta1 selective

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12
Q

How is blood pressure calculated

A

BP = cardiac output x total peripheral resistance

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13
Q

What is hypertension defined as

A

Blood pressure is consistently above 140/90

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14
Q

Describe the pathophysiology of hypertension

A

Important risk factor for stroke, causes about 50% of ischaemic strokes
Accounts for 25% of heart failure cases, increasing to ~70%
Major risk factor for MI and chronic kidney disease
The goal of therapy is to reduce mortality from cardiovascular or renal events

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15
Q

What are the main contributors to blood pressure

A

Blood volume
Cardiac output
Vascular tone

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16
Q

What are the targets for anti hypertensives

A 
The heart (cardiac output)
Sympathetic nerves (release the vasoconstrictor noradrenaline)
Kidney (blood volume/vasoconstriction)
Arterioles (determine peripheral resistance)
CNS (determines blood pressure set point and regulates some systems involved in Blood pressure control & autonomic NS)
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17
Q

What are the targets of beta blockers

A

heart - b1 (reduce rate and CO)
Sympathetic nerves - b1 + b2
Kidney - b1 (reduce renin production)
CNS - b1/b2 (reduce sympathetic tone)

18
Q

Why can beta blockers be used to treat hypertension

A

Reduction in heart rate and - , leading to a reduction in CO
The heart does not have to work as hard and the BP decreases

Reduction in renin and angiotensin II release - vasodilation

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

19
Q

What are the targets and effects of nebivolol

A

beta1

Potentiates NO

20
Q

What are the targets and effects of sotalol

A

beta1 and beta2

Inhibits potassium channels

21
Q

What are the unwanted effects of beta blockers

A

Bronchoconstriction (bad for asthma/COPD)
Cardiac failure
Hypoglycaemia (masks symptoms of hypoglycaemia and inhibit glycogen breakdown)
Fatigue (due to reduction in CO and muscle perfusion)
Cold extremities (loss of beta receptor mediated vasodilation in cutaneous vessels)
Bad dreams

22
Q

What is the advantage of atenolol over propanolol

A

Atenolol is b1 selective, avoiding some unwanted side effects
Less effects on the airways

23
Q

What is the advantage of carvedilol over atenolol and propranolol

A

Beta-mediated effects on the heart and kidney but also vasodilation from blockage of vasoconstriction in arterioles

24
Q

Compare alpha1 to alpha2 receptors

A

a1 - Gq linked (stim), pathway involves DAG and IP3, postsynaptic on vascular smooth muscle

a2 - Gi linked, pathway involves cAMP and PKA, presynaptic auto receptors inhibiting NE release

25
Q

Describe phentolamine

A

Non-selective alpha-blocker

Used to treat phaechromocytoma-induced hypertension

26
Q

Describe prazosin

A

alpha1 specific blocker
Inhibits the vasoconstrictor activity of NE
Have modest blood pressure lowering effects
Only used as adjunctive treatment

27
Q

How do non-selective alpha blockers lower blood pressure

A

Vasodilation to reduce arterial pressure

28
Q

What are the unwanted effects of non-selective alpha blockers

A

Postural hypotension
CO and heart rate increases as a reflex to low arterial pressure
Increased blood flow through cutaneous and splanchnic beds
Blockade of alpha2 increases NA release, enhancing the reflex tachycardia
Increased GIT motility -> diarrhoea

29
Q

Compares phentolamine to prazosin

A

Less tachycardia from prazosin than non-selective antagonists since they do not increase noradrenaline release from nerve terminals (no a2 actions)
Baroreceptor firing rate decreases -> increases sympathetic activity

30
Q

Describe methyldopa

A

Antihypertensive

  1. Taken up by noradrenergic neurons
  2. Decarboxylated and hydroxylated to form the false transmitter a-methyl-noradrenaline
  3. Taken into the pre-synaptic neurone
  4. Not de-aminated by MAO
  5. Accumulates in larger quantities and displaces NA from synaptic vesicles
31
Q

What are the effects of methyldopa

A

Improved blood flow
Anti-hypertensive
Stimulates vasopressor center in the brainstem to inhibit sympathetic outflow

32
Q

What are the side effects of methyldopa

A

Dry mouth
Sedation
Orthostatic hypotension
Male sexual dysfunction

33
Q

Why are SNS antagonists used for treating arrhythmias

A

An increase in sympathetic drive to the heart via b1 can precipitate or aggravate arrhythmias
After MI there is an increase in sympathetic tone
AV conductance also depends on sympathetic activity
Refractory period of the AV node is increased by beta-adrenoceptor antagonists. interfering with AV conduction in tachycardias and slowing ventricular rate

34
Q

How may propranolol be used for arrhythmias

A

non-selective b-antagonists so reduces mortality of patients with MI
Particularly successful in arrhythmias that occur during exercise or mental stress

35
Q

What is stable angina

A

Stable-pain on exertion. Increased demand on the heart and is due to fixed narrowing of the coronary vessels e.g. atheroma

36
Q

What is unstable angina

A

Unstable-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.

37
Q

What is variable angina

A

Occurs at rest
caused by coronary artery spasm
Associated with atheromatous disease

38
Q

What is angina

A

Pain that occurs when the oxygen supply to the myocardium is insufficient for its needs.
Pain distribution - chest, arm , neck.
Brought on by exertion or excitement.

39
Q

How is angina treated using SNS antagonists

A

Metoprolol (b-selective) at low doses will reduce heart rate and myocardial contractile activity without affecting bronchial smooth muscle
Reduces oxygen demand whilst maintaining the same degree of effort

40
Q

What is glaucoma

A

Characterised by an increase in intraocular pressure
Caused by poor drainage of the aqueous humour
If untreated, it permanently damages the optic nerve, blindness

41
Q

Describe intraocular fluid drainage

A

Produced by blood vessels in ciliary body via the actions of carbonic anhydrase.
Flows into posterior chamber, through the pupil to anterior chamber.
Drains into trabecular network and into the veins and canal of Schlemm.

Y2 Pharmacology and Therapeutics (34 decks)

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