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(J2) Pharm > Antiadrenergics > Flashcards

Antiadrenergics Flashcards

1
Q

What is phentolamine?

Which receptors it selective for?

What is its effect on the receptor?

A

Non-selective, competitive α antagonist

  • short acting
  • does not covalently bind
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2
Q

What are the expected effects of phentolamine?

A

Vasculature:

  • vasodilation (-α1) -> desceased BP -> reflex tachycardia
  • orthostatic hypotension

Nerves/Heart:

-decreased modulation of NE release (-α2) -> NE stimulation of β1 -> tachycardia

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3
Q

What is phenoxybenzamine?

Which receptors is it selective for?

What is its effect on the receptor?

A

Non-competitive α antagonist

  • long acting
  • covalently binds receptor
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4
Q

What are the expected effects of phenoxybenzamine?

A

Vasculature:

  • vasodilation (-α1) -> desceased BP -> reflex tachycardia
  • orthostatic hypotension

Nerves/Heart:

-decreased modulation of NE release (-α2) -> NE stimulation of β1 -> tachycardia

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5
Q

What is a common suffix for alpha-1 blockers?

A

“-osin”

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6
Q

What is prazosin?

Which receptors is it selective for?

What is its effect on the receptor?

A

Selective α1 antagonist

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7
Q

What are the expected effects of prazosin?

A

Vasculature:

  • vasodilation (-α1) -> decreased BP
  • less risk for tachycardia due to α1 selectivity

GU:

-relaxation of prostate smooth muscle (-α1) -> decreased urethral resistance -> increased urine flow

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8
Q

What is tamsulosin?

Which receptors is it selective for?

What is its effect on the receptor?

A

Selective α1 antagonist

(specifically a subtype predominatley found in the prostate)

*trade name is flomax

*BPH

*kidney stones

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9
Q

What are the expected effects of tamsulosin?

A

GU:

-relaxation of prostate smooth muscle (-α1) -> decreased urethral resistance -> increased urine flow

Vasculature:

-less low BP effect due to specificity for subtype of α1 found in prostate

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10
Q

What is doxazosin?

Which receptors is it selective for?

What is its effect on the receptor?

A

Selective α1 antagonist

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11
Q

What are the expected effects of doxazosin?

A

Vasculature:

  • vasodilation (-α1) -> decreased BP
  • less risk for tachycardia due to α1 selectivity

GU:

-relaxation of prostate smooth muscle (-α1) -> decreased urethral resistance -> increased urine flow

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12
Q

What is a common suffix for beta-blockers?

A

“-olol”

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13
Q

What is labetalol?

Which receptors is it selective for?

What is its effect on the receptor?

A

Non-selective, partial β agonist/selective α1 antagonist

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14
Q

What is carvediolol?

Which receptors is it selective for?

What is its effect on the receptor?

A

Competitive, non-selective β/selective α1 antagonist

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15
Q

What is propanolol?

Which receptors is it selective for?

What is its effect on the receptor?

A

Non-selective β antagonist (beta-blocker)

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16
Q

What is pindolol?

Which receptors is it selective for?

What is its effect on the receptor?

A

Non-selective β partial agonist (beta-blocker)

17
Q

What is nadolol?

Which receptors is it selective for?

What is its effect on the receptor?

A

Non-selective β antagonist (beta-blocker)

18
Q

What is metoprolol?

Which receptors is it selective for?

What is its effect on the receptor?

A

Selective β1 inverse agonist (beta-blocker)

19
Q

What is betaxolol?

Which receptors is it selective for?

What is its effect on the receptor?

A

Selective β1 inverse agonist (beta-blocker)

20
Q

What is acebutolol?

Which receptors is it selective for?

What is its effect on the receptor?

A

Selective β1 partial agonist (beta-blocker)

21
Q

What is atenolol?

Which receptors is it selective for?

What is its effect on the receptor?

A

Selective β1 antagonist (beta-blocker)

22
Q

Which beta-blockers are non-selective?

A
  • propanolol
  • pindolol
  • nadolol
23
Q

Which beta-blockers are β1 selective?

A
  • metoprolol
  • betaxolol
  • acebutolol
  • atenolol
24
Q

What are the expected effects of non-specific beta-blockers?

A

Cardiovascular:

  • decreased force and rate of contraction (decreased cardiac work and oxygen demand, -β1)
  • decreased AV conduction velocity (decreased arrhythmia risk, -β1)
  • initial elevation of BP (vasoconstriction, -β2), eventual decreased BP (decreased renin, -β1)

Lungs:

-increased airway resistance (-β2​)

Metabolic:

  • inhibit lipolysis (-β2)
  • inhibit gluconeogenesis/glycogenolysis (-β2​) -> hypoglycemia

Eyes:

-decreased aqueous humor production (-β2​)

25
Q

What are the expected effects of selective β1 beta-blockers?

A

Cardiovascular:

  • decreased force and rate of contraction (decreased cardiac work and oxygen demand, -β1)
  • decreased AV conduction velocity (decreased arrhythmia risk, -β1)
  • eventual decreased BP (decreased renin, -β1)
26
Q

Which beta-blockers are antagonists?

A

PAN

  • propranolol (β non-selective)
  • atenolol (β1 selective)
  • nadolol (β non-selective)
27
Q

Which beta-blockers are partial agonists?

A

PAL

  • pindolol (β non-selective)
  • acebutolol (β1 selective)
  • labetolol (β non-selective/α1 selective)
28
Q

Which beta-blockers are inverse agonists?

A
  • metroprolol (β1 selective)
  • betaxolol (β1 selective)
29
Q

What is the signicifant difference between antagonisitic, partially agonistic, and inversely agonistic beta-blockers?

A

In order, partial agonists, antagonists, and inverse agonists have:

  • increased risk for bradycardia
  • increased VLDL/HDL ratio
30
Q

What is the risk of abrupt discontiunation of beta-blockers?

A

Long-term beta-blocker use upregulates β receptor expression. When beta-blocker use is discontinued, endogenous agonists have increased receptors available leading to exagerated response resulting in tachycardia and possible arrhythmia.

31
Q

What advantages do selective β1 blockers have over non-selective beta-blockers?

A

Loss of the potentially harmful effects from blockade of the β2 receptor such as:

  • risk of bronchospasm/asthma exacerbation due from bronchoconstriction
  • risk of hypoglycemia from inhibition of gluconeogenesis and glycogenolysis
32
Q

What does quanethidine do?

A

NE release inhibitor -> indirect antiadrenergic

33
Q

What does metyrosine do?

A

inhibits tyrosine hydroxylase, preventing dopamine synthesis -> antiadrenergic effect

34
Q

What antiadrenergics would be most effective in treating pheochromocytoma?

A

Pheochromocytoma - adrenal tumor producing large amounts of catecholamines

  • phentolamine (non-specific α antagonist)
  • phenoxybenzamine (non-specific α antagonist)
  • metyrosine (indirect antiadrenergic)
35
Q

What antiadrenergics would be most effective in treating chronic hypertension?

A

selective α1 antagonists

  • prazosin
  • doxazosin
36
Q

What antiadrenergics would be most effective in treating PBH?

A

-tamsulosin (increased specificity for smooth muscle of prostate)

37
Q

What antiadrenergics would be most effective in treating heart failure?

A
  • metoprolol
  • carvedilol
38
Q

What antiadrenergics would be most effective in treating glaucoma?

A

-betaxolol

39
Q

What antiadrenergics would be most effective in treating side effects of hyperthyroidism?

A

-propanolol

(J2) Pharm (9 decks)

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