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eLCRS - 팜 > PHARM 9: SNS Antagonists > Flashcards

PHARM 9: SNS Antagonists Flashcards

1
Q

What are the main subtypes of adrenoceptor subtypes?

A

a1
a2
B1
B2

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2
Q

stimulation of a1 adrenoceptor subtype causes –>

A

a1

  • vasoconstriction
  • relaxation of GIT
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3
Q

stimulation of a2 adrenoceptor subtype causes –>

A

a2

  • causes inhibition of transmitter release
  • causes contraction of vascular smooth muscle
  • causes CNS actions
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4
Q

stimulation of B1 adrenoceptor subtype causes –>

A

B1

  • causes increase in cardiac rate + force
  • causes relaxation of GIT
  • causes renin release from kidney
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5
Q

stimulation of B2 adrenoceptor subtype causes –>

A

B2

  • causes bronchodilator
  • causes vasodilation
  • causes relaxation of visceral smooth muscle
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6
Q

What are the 5 main adrenoceptor antagonists?

A
  • Labetalol –> a1 + B1
  • Phentolamine –> a1 + a2
  • Prazosin –> a1
  • Propranolol –> B1 + B2
  • Atenolol –> B1
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7
Q

What are the main clinical uses of SNS antagonists + false transmitters?

A
  • hypertension
  • cardiac arrhythmias
  • angina
  • glaucoma
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8
Q

What is considered as hypertension?

A

NICE guideline = 140/90 mmHg or higher

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9
Q

What are 3 main elements that contribute to hypertension?

A
  • blood volume
  • cardiac output
  • vascular tone
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10
Q

Where are the tissue targets for anti-hypertensives ?

A

a) Heart (B1)
b) sympathetic nerves (B1/2)
c) Kidney (B1)
d) arterioles (B1)

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11
Q

Describe the mechanism of how beta adrenoceptors antagonists act as anti hypertensives

A
  • they act on the CNS –> to reduce sympathetic tone
  • they act on B1 receptors on the heart
  • -> reduces HR + CO
  • they act on B1 receptors on the kidney
  • -> reduces Renin production
  • -> reducing ATII
  • -> which causes reduction in TPR
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12
Q

What are the 4 different categories/ types of beta blockers?

A
  1. non selective
  2. B1 - selective
  3. Mixed blockers
  4. other
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13
Q

give examples of each type of beta blockers

  1. non selective
  2. B1 - selective
  3. Mixed blockers
  4. other
A
  1. non selective
    e. g propranolol
  2. B1 - selective
    e. g atenolol
  3. Mixed blockers
    e. g carvedilol
  4. other
    e. g nebivolol, sotalol
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14
Q

How do the 4 types of beta blockers differ?

  1. non selective
  2. B1 - selective
  3. Mixed blockers
  4. other
A
  1. non selective
    - -> has equal affinity for B1 + B2 receptors
  2. B1 - selective
    - -> more selective for B1 receptors
  3. Mixed B-a blockers
    - -> a1 blockade give additional vasodilator properties
  4. other
    - -> Nebivolol potentiates NO
    - -> Sotalol Inhibits K+ channels
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15
Q

List some unwanted effects of beta antagonists

A
  • beta blockers can mask symptoms of hypoglycemia
  • dangerous for diabetics –> because it also blocks B2 mediated glycogen breakdown.
  • fatigue
  • cold extremities
  • bad dreams
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16
Q

If you have what condition - would you not give a non selective beta blocker?

A
  • asthma
  • COPD
  • Cardiac Failure
  • Diabetes
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17
Q

What is Propranolol?

A
  • it is a non selective beta antagonist.
  • at rest: little effect on HR/CO
  • exercise: has effect
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18
Q

What is atenolol

A
  • it is a B1 selective beta blocker
  • mainly antagonists effect of NA on the heart
  • but also acts on other tissues with B1 receptors
  • not safe with asthmatic patients
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19
Q

note: selectivity depends on conc

A

-

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20
Q

What is the advantage of atenolol over propranolol?

A

Atenolol = B1 selective

  • so effects are predominantly on the heart
  • so there is for e.g less effects on the lung such as bronchoconstrction
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21
Q

What is Carvedilol?

A
  • mixed B-a blocker
  • has dual acting b1 + a1 antagonists
  • at ratio 4:1
  • lower BP through reduction in TPR
22
Q

What advantage does carvedilol have over atenolol + propranolol ?

A

carvedilol also acts on alpha 1 receptor –> which causes vasodilation of blood vessels

  • which would decrease TPR and causes decrease in BP
23
Q

What is the difference between a1 vs a2 adrenoceptor?

A

a1

  • Gq linked
  • postsynaptic on vascular smooth muscle

a2

  • Gi linked
  • presynaptic autoreceptors inhibiting NE release
24
Q

Give an example of a non selective a-blocker

A

phentolamine

25
Q

give an example of an a1 specific blocker

A

prazosin

26
Q

what is phentolamine used for?

A
  • used to treat phhaechromocytoma-induced hypertension

–> has dramatic hypotensive effect

27
Q

what is prazosin used for?

A
  • used to inhibit vasoconstrictor activity of NE

- -> leads to vasodilation + decrease in BP

28
Q

What is the effect of a1 antagonists on cholesterol?

A
  • causes a decrease in LDL

- causes an increase in HDL cholesterol

29
Q

Why do a2 receptors + baroreceptors reduce the effectiveness of phentolamine?

A

with phentolamine, you would be blocking a1 + a2 receptors.

  • if you block a2 receptors, then you lose the negative feedback effect –> and you get an increase in NA release
  • so NA outcompetes phentolamine so there is reduced effect of the drugs
  • also when you block a1 –> it causes dilation
  • which reduces arteriole pressure
  • -> but it is also associated with a decrease in baroreceptors firing
  • so there is increases in sympathy effect
  • HR goes up
  • therefore reducing effect of phentolamine
30
Q

How does Methyldopa act as an anti hypertensive? describe its mechanism of action.

A

methyldopa = taken up by noradrenergic neurons
- then it is converted to a false transmitter (a-methyl-NA)
- which is less active on b1 + a1 receptors
- it is also more active on presynaptic a2 receptors
which causes less release of NA
- ALSO –> it is not metabolized by MAO so displaces NA from vesicles

31
Q

What processes does Methyldopa undergo to form the final false transmitter?

A

Methyldopa –> decarboxylated –> hydroxylated –> to form alpha-methyl noradrenaline

32
Q

How does the false transmitter alpha-methyl NA work?

A
  • false transmitter = not metabolized by MAO
  • accumulates in larger quantities than NA
  • then it displaces NA from synaptic vesicles
  • false transmitter = less active than NA on a1 receptors
  • so has less effect on vasoconstriction

(it is more active on a2 receptors)

  • has -ve feedback mechanism
  • and reduces NA release –> to below normal levels
33
Q

What effect does the false transmitter alpha-methyl NA have on the CNS?

A
  • stimulates vasomotor centre in the brainstem –> to inhibit sypathetic outflow
34
Q

What re some benefits of methyldopa?

A

renal/CNS blood flow = well maintained
–> widely used in patients with renal insufficiency / cerebrovascular disease

  • recommended for pregnant women
35
Q

What are some negative side effects of methyl dopa?

A
  • causes dry mouth
  • sedation
  • orthostatic hypotension
  • causes male sexual dysfunction
36
Q

What is an arrhythmia?

A

arrhythmia = abnormal or irregular heart beats

37
Q

What is the main cause of an arrhythmia?

A
  • main cause = myocardial ischemia

damage to heart muscle –> causes re-entry of impulses, which messes up heart rhythm

38
Q

an increase in sympathetic drive to the heart via the ____ receptor can aggravate arrhythmias.

A

an increase in sympathetic drive to the heart via the B1 receptor can aggravate arrhythmias.

39
Q

AV conductance = also dependent on _______ _______

A

AV conductance = also dependent on sympathetic activity.

40
Q

Give an example of an antagonist which works to avoid / reduce arrhythmia

A

Propranolol

–> reduces mortality of patients with MI

41
Q

Define angina

A

angina = pain that occurs whe the oxygen supply to the myocardium is insufficient for its needs.

–> which tends to be brought on by exertion/excitement

42
Q

pain distribution of angina = usually :

A

pain distribution of angina = usually : chest, arm , neck

43
Q

What are the 3 different types of angina?

A
  1. stable angina
  2. unstable angina
  3. variable angina
44
Q

How do the 3 different types of angina vary?

A
  1. Stable angina
    - -> pain on exertion
    - -> due to fixed narrowing of coronary vessel
    - -> increased demand on heart
  2. Unstable angina
    - -> pain w less + less exertion culminates with pain at rest
    - -> atheromatous plaque = starting to rupture
    - -> but it isn’t a complete occlusion of vessel
  3. Variable angina
    - -> occurs at rest
    - -> due to coronary artery spasm
    - -> linked with atheromatous disease
45
Q

How do B1 selective agents such as metoprolol help with angina?

A
  • at low does
  • they reduce HR + myocardial contractile activity
  • -> but doesn’t affect the bronchial smooth muscle

so it reduced o2 demand, whilst maintaining same degree of effort

46
Q

What is glaucoma characterized by?

A

increased in intraocular pressure

47
Q

what is glaucoma caused by?

A
  • caused by poor drainage of aq humour
48
Q

what happens if glaucoma is left untreated?

A
  • it permanently damaged the optic nerve

- -> results in blindness

49
Q

The amount of humour produced - directly related to the ________

A

The amount of humour produced - directly related to the BLOOD FLOW IN THE CILIARY BODY

50
Q

What effect might adrenaline have on blood flow through the ciliary body ?

A
  • A can act on a1 receptors
  • to cause vasoconstriction
  • which causes reduction in blood flow through the ciliary body
51
Q

How can Beta antagonists help in glaucoma?

give examples

A
  • beta antagonists (selective + non selective)
  • -> reduce formation of aq humour formation by blocking the receptors on the ciliary body

ciliary body B1 receptors are coupled with carbonic anhydrase which forms bicarbonate ions
–> blockage of this causes reduction in formation of aq humour

non selective e.g: carteolol hydrochloride / levobunolol hydrochloride / timolol hydrochloride

selective e.g betaxolol hydrochloride

eLCRS - 팜 (36 decks)

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