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LCRS 1 - Pharmacology COPY COPY > SNS antagonists > Flashcards

SNS antagonists Flashcards

1
Q

How does methyldopa work?

A
  • Methyldopa takes place of DOPA in NA synthesis
  • Converted to alpha-methyl NA (false transmitter)
  • Less active at a1/b R - less effective at vasoconstriction
  • More active on a2 Rs - autoinhibitory fb mech –> reduces NA release below normal levels
  • Some CNS effects - stimulates vasopressor centre in BS to inhibit symp outflow –> improved blood flow
  • Not metabolised by MAO
  • More likely to accumulate and displace NA in vesicle
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2
Q

What are the clinical uses of methyldopa?

A
  • Anti-hypertensive in pregnant women (no adverse effects on foetus despite crossing blood-placenta barrier)
  • Also in kidney disease and cerebrovascular disease
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3
Q

What are the side effects of methyldopa?

A
  • Dry mouth
  • Sedation
  • Orthostatic hypotension
  • Male sexual dysfunction
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4
Q

What are the main clinical uses of adrenoceptor antagonists and false transmitters?

A
  • Hypertension
  • Cardiac arrhythmias
  • Angina
  • Glaucoma
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5
Q

What are the unwanted effects of alpha adrenoceptor antagonists?

A

Postural hypotension

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6
Q

What are the unwanted effects of beta antagonists?

A

Negative effects from b2 blockade:

  1. Bronchoconstriction - bad for asthma/COPD
  2. Cardiac failure - need some symp drive to heart to maintain adequate CO
  3. Hypoglycaemia - masks symptoms (sweating, palpitations, tremor)
  4. Block b2-mediated glycogenolysis - bad for diabetics
  5. Fatigue - reduced CO and muscle perfusion; impairs exercise
  6. Cold extremities - loss of bR-mediated vasodilation in cutaneous vessels
  7. Bad dreams
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7
Q

What is the mechanism of action of propranolol (non-selective beta antagonist)?

A

Positive effects from b1 blockade:

  • Decrease HR, FoC, CO
  • Heart doesn’t have to work as hard
  • Reduced BP
  • Decrease renin
  • Decrease AngII
  • Less vasoconstriction, less aldosterone
  • Decreased TPR
  • Block positive facilitatory effects of presynaptic b1Rs on NA release
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8
Q

What is the main clinical use of propranolol (non-selective beta antagonist)?

A

Anti-hypertensive (during exercise)

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9
Q

What are the main clinical uses of atenolol (cardioselective b1 antagonist)?

A

Beta blocker for CV diseases: hypertension, angina, acute MI, long QT syndrome, tachycardia

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10
Q

What are main clinical uses of carvediol (mixed B and a antagonist)?

A
  • Mild to severe congestive HF
  • Left ventricular dysfunction following heart attack in otherwise stable patients
  • Anti-hypertensive
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11
Q

What are the 4 different types of SNS antagonists?

A
  1. Non-selective - propranolol
  2. b1-selective - atenolol
  3. Mixed a-b blockers - carvedilol
  4. Other - nebivolol - B1, also potentiates NO, sotalol - B, also inhibits K channels
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12
Q

What is the clinical use of phentolamine (non-selective alpha antagonist)?

A

Phaechromocytoma-induced hypertension

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13
Q

What is the clinical use of prazosin (selective a1 antagonist)?

A

Anti-hypertensive

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14
Q

What are the effects of a1 stimulation?

A

Vasoconstriction

GIT relaxation

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15
Q

What are the effects of a2 stimulation?

A

Inhibition of transmitter release (presynaptic - NA)
Contraction of VSM
CNS actions

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16
Q

What are the effects of b1 stimulation?

A

Inotropic effect
Chronotropic effect
GIT relaxation
Renin release

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17
Q

What are the effects of b2 stimulation?

A

Bronchodilation
Vasodilation
relaxation of visceral SM
Hepatic glycogenolysis

18
Q

What are the effects of b3 stimulation?

A

Lipolysis

19
Q

How does the sympathetic NS control BP?

A 
SNS controls heart via b1Rs
Major controller = symp drive to kidneys controlling rening release (b1)
Renin release
ATII production
Powerful vasoconstrictor
Aldosterone production
Increases BP
20
Q

What tissues do anti-hypertensives target?

A

Kidneys - regulate blood volume and vasoconstriction (renin)
Heart
Arterioles - determine TPR (a1-mediated vasoconstriction)
Symp nerves that release NA (vasoconstrictor)
CNS - determines BP set point

21
Q

Do beta-blockers affect arterioles?

A

No

Do not antagonise a1 receptors

22
Q

What are the side effects of propranolol (non-selective beta antagonist)?

A

All typical adverse effects due to b2 antagonism

23
Q

What is the mechanism of action of atenolol (cardioselective b1 antagonist)?

A
  • Mainly antagonises effect of NA in heart - reduces HR, BP, CO
  • Also affects any tissue with b1R, e.g. kidneys
24
Q

What are the side effects of atenolol (cardioselective b1 antagonist)?

A
  • Typical adverse effects due to b2 antagonism
  • Less effect on airways than non-selective drugs, but still not safe for asthmatics
  • Higher T2DM risk
25
Q

What is the mechanism of action of phentolamine (non-selective alpha antagonist)?

A
  • Vasodilation and reduced BP due to a1 blockade
  • a2 blockade removes inhibitory effect of a2Rs on NA release –> increased NA release –> more NA in synapse to compete with drug
26
Q

What are the side effects of phentolamine (non-selective alpha antagonist)?

A
  • Increased GIT motility - diarrhoea

- Reflex tachycardia

27
Q

What is the mechanism of action of prazosin (selective a1 antagonist)?

A
  • Inhibits vasoconstrictor activity of NA –> vasodilation and reduced BP
  • Decreases LDL, increases HDL cholesterol
  • Decreases CO due to fall in venous pressure as a result of dilation of capacitance vessels
28
Q

What are the side effects of prazosin (selective a1 antagonist)?

A
  • Reflex tachycardia

- Postural hypotension

29
Q

What is an arrhythmia?

A

Irregular heart beat

30
Q

What is the main cause of death from an arrhythmia?

A

Myocardial ischaemia

31
Q

Why are beta blockers a good way of controlling arrhythmias?

A
  • Beta blockers modulate sympathetic drive
  • Sympathetic drive controls pacemaker current and atrioventricular conductance
  • Increase in sympathetic drive to heart via B1 can precipitate or aggravate arrhythmias
  • Beta blockers INCREASE AVN REFRACTORY PERIOD
  • Interferes w/AV conduction in atrial tachycardias and slows down ventricular rate
  • Re-entry type electrical activity won’t stimulate another heart beat bc still in refractory period
32
Q

Which class of SNS antagonist may be used as an anti-arrhythmic?

A
  • Propranolol - non-selective beta antagonist
  • Positive effects mainly from B1 antagonism
  • Reduces mortality of MI patients
  • Particularly successful in arrhythmias that occur during exercise or mental stress
33
Q

What is angina?

A

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

  • Pain in chest, arm, neck
  • Tends to be brought on by exertion or excitement
34
Q

What are the types of angina and what causes them?

A
  1. Stable - pain on exertion due to a fixed narrowing of the coronary vessels (e.g. atheroma) leading to an increased demand on the heart
  2. Unstable - pain w/less and less exertion; culminates w/pain at rest; atheromatous plaque starting to rupture; platelet-fibrin thrombus forms but w/o complete occlusion of vessel; high risk of infarction
  3. Variable - occurs at rest; caused by coronary artery spasm; associated w/atheromatous disease
35
Q

What class of SNS antagonist may be used to treat angina?

A

Beta 1 antagonist

36
Q

Why are b1 antagonists used to treat angina?

A
  • At low doses, they reduce myocardial oxygen demand by decreasing HR, SBP and cardiac contractile activity without affecting bronchial smooth muscle
  • Match oxygen demand to amount of work required
  • Beta blocker + exercise –> can do same level of work at much lower HR –> heart has to work less hard –> decreased myocardial oxygen demand
37
Q

What are the adverse effects of using a beta blocker in angina?

A
  • Fatigue
  • Insomnia
  • Dizziness
  • Sexual dysfunction
  • Bronchospasm
  • Bradycardia
  • Heart block
  • Hypotension
  • Decreased myocardial contractility
38
Q

When should beta blockers not be used in angina?

A
  • Bradycardia (<55) bc you risk further compromising symp drive to heart
  • Bronchospasm
  • Hypotension (SBP<90)
  • AV block or severe congestive HF - risk MI
39
Q

How do selective and non-selective beta antagonists help treat glaucoma?

A
  • Aqueous humour is produced by blood vessels in ciliary body via actions of carbonic anhydrase
  • Reduce rate of AH formation by blocking B1 receptors on ciliary body –> reduced CA activity producing bicarbonate
40
Q

Why do a1-selective antagonists cause less tachycardia than non-selective a antagonists?

A
  • a1-selective have no a2 effect
  • tf don’t remove inhibitory (-ve fb) effect of a2Rs on NA release on presynaptic membrane
  • Decrease NA release
  • Less tachycardia

LCRS 1 - Pharmacology COPY COPY (33 decks)

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