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CV Module Pharm > Beta Blockers > Flashcards

Beta Blockers Flashcards

1
Q

What are β-blockers (BB’s)?

A

They are antagonists of β-adrenergic receptors in the SNS. They have widespread use in the tx of CV conditions.

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2
Q

When we think about the actions of BB’s that affect the CV system, what are the two main locations involved?

A
  1. Actions on the heart itself

2. A secondary site: action on the juxtaglomerular apparatus (JGA) in the kidney, interrupting the release of renin.

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3
Q

What do the names of all the BB’s end in?

A

OLOL (or just LOL if they have extended pharmacologic actions on other receptor systems)

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4
Q

What are the two main subclasses of β-R’s and where are they located?

A

A. β1 primarily (and also β2 to a lesser extent) are found directly within the cardiac tissue, where they increase HR (SA node and ectopic pacemakers) and increase contractility
B. β2’s are located in skel m blood vessels where they play an important role in relaxing/vasodilating the vasculature.

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5
Q

Why does tx with β1 agonists cause an increase in the release of renin? What does this mean in regards to the effects of BB’s?

A

B/c there B1-R’s (linked to Gs→increase cAMP) on JGA cells in the kidneys, which respond to β1-agonists and cause an increase in the release of renin, which modulates renal function.
Therefore, BB’s, as a secondary action, will BLOCK the release of RENIN from the JGA in the kidney.

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6
Q

How does pre-tx w/ a BB, affect the influence on BP of a) NE b) E and c) Isoproterenol?

A

a) Pre-tx w/ BB does not do anything to the increase in BP produced by NE, as it is primarily alpha-R-mediated vasoconstriction.
b) The effects of E on BP are also relatively unchanged in the face of pre-tx w/ a BB. E has activity on α1 and α2-R’s, causing vasoconstriction and an increase in BP.
c) Isoproterenol is a synthetic agonist of both β1 and β2-R’s, so the decrease in BP produced by isoproterenol alone via β2-mediated vasodilation is almost completely ablates by the presence of a BB (an alpha-blocker would have no effect on the decrease in BP by isoproterenol as it acts exclusively on β-R’s)

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7
Q

How are the BB’s categorized into subclasses? What are the three classes and some examples?

A

Although there is no absolute specificity, in the clinical context, they are categorized based on their relative receptor specificities.

  1. β1-specific: (BE A MAN) Metropolol, Acebutolol, Atenolol, Betaxolol, Esmolol, Nebivolol
  2. Nonspecific (β1=β2): Propanolol, Carteolol, Penbutolol, Pindolol, Timolol
  3. β2-specific: experimental only
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8
Q

What is the prototype BB to which all others are compared? What are the characterisitics of this BB?

A

Propanolol: it is a competitive nonspecific BB

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9
Q

What are the important parameters that can be used to distinguish the various BB’s (β antagonists)? Why are they important?

A
  1. Relative affinity for β1 and β2-R’s
  2. Intrinsic Sympathomimetic Activity (ISA)
  3. Blockade of α-receptors
  4. Differences in lipid solubility
  5. Capacity to induce vasodilation
  6. PK parameters
    Some of these have clinical significance and help guide the appropriate choice of BB for an individual patient.
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10
Q

What are the different generations of BB’s?

A

A. 1st Generation: nonselective BB’s
B. 2nd Generation: β1-selective
C. 3rd Generation: can be nonselective or β1-selective but with ADDITIONAL ACTIONS (end in LOL but not OLOL)

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11
Q

What are the first generation BB’s?

A

Nadal Terrorizes Professional Pinball Players

1. Nadolol 2. Timolol 3. Propanolol 4. Penbutolol 5. Pindolol

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12
Q

What are the 2nd generation BB’s?

A

Ask A Busy Eskimo Man

  1. Acebutolol 2. Bisoprolol 3. Esmolol
  2. Atenolol 5. Metropolol
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13
Q

What are the 3rd generation BB’s?

A 
A. Nonselective
Carver Labels Cartographers
1. Carteolol 2. Carvedilol 3. Labetalol
B. β1-selective
you Better Never
1. Betaxolol 2. Nebivolol
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14
Q

Which BB has an extremely short half-life? Why is this important?

A

Esmolol
By virtue of its short life, rather than being given orally like the other BB’s, esmolol has to be given by IV infusion to hospitalized patients. The short half-life provides the ability to have very close hour-by-hour control of drug levels based on the rate of administration and the rate of dissolution.

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15
Q

Which three BB’s are most commonly associated with membrane-stabilizing activity (MSA) at therapeutic concentrations? As a result, what are they categorized as?

A

PAC: Propanolol, Acebutolol, Carvedilol

As a result of this MSA, they are categorized as Class I Antiarrhythmics

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16
Q

How do propanolol, acebutolol, and carvedilol have MSA? In what type of cells?

A

They bind and block fast Na+ channels responsible for rapid depolarization (phase 0) of fast-response cardiac action potentials in non-nodal cardiomyocytes (atrial, ventricular, purkinje). (Thus, they slow the rate of depolarization and decrease the amplitude of the action potential)

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17
Q

Why do BB’s normally have minimal activity on the resting heart?

A

Autonomic control of the heart is primarily mediated thru the PSNS, w/ vagal control of the HR predominating under resting conditions.

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18
Q

When does the effect of BB’s on the heart come into play?

A

The activity of BB’s on the heart only comes into force when the heart begins to be stimulated by the SNS

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19
Q

What does it mean for a BB to have intrinsic sympathomimetic activity?

A

They have a partial agonist effect on the heart and can stimulate the resting heart in the absence of catecholamines via partially activated β1 receptors. When the SNS to the heart is stimulated, the residence of these drugs on the β-R’s means that they are now functioning as antagonists (competitive) of the stimulated heart.

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20
Q

In what kind of patients would BB’s with intrinsic sympathomimetic activity be a better option than a BB w/out ISA activity? Why?

A

Patients who experience profound bradycardia or negative inotropy in the resting heart. The partial agonist effect due to ISA can stimulate the resting heart to provide relief from the profound bradycardia/negative inotropy normally produced.

21
Q

What are some drugs with ISA activity?

A
  1. PINDOLOL 2. ACEBUTOLOL 3. Labetalol (also carteolol) (PAPA: Pindolol and Acebutolol and Partial Agonists)
    NOT PROPANOLOL b/c it’s a pure antagonist
22
Q

In addition to being antagonists and partial agonists, other BB’s are actually what type of drug?

A

Inverse Agonists: they bind to inactive receptors and shift the equilibrium toward the inactive conformation (behave like competitive antagonists in systems that are not constitutively active)

23
Q

What does it mean when we say that 3rd generation BB’s have extended/additional actions?

A

It means they have pharmacological effects upon other receptor systems in the body, over and above their effects on the β-R’s.

24
Q

What are the five potential mechanisms of extended action of BB’s?

A
  1. Nitric oxide (NO) Production: NO is a potent vasodilator (Carteolol, Nebivolol)
  2. β2-R Agonism (Carteolol)
  3. α1-R Antagonism (Carvedilol, Labetabol)
  4. Ca2+ Entry Blockade (Carvedilol, Betaxolol)
  5. Antioxidant Activity (Carvedilol)
    These all protect against reflexive vasoconstriction in the first few doses of BB’s.
25
Q

What is the result of 3rd generation with the extended action of α1-R antagonism?

A

This prevents the reflex vasoconstrictive effect mediated thru α1-R’s. When the first few doses of BB are used clinically in order to reduce BP, there tends to be reflexive/homeostatic vasoconstrictive response, which increases BP in order to compensate for the reduced cardiac function. α1-antagonism blocks this reflex, and allows the BB to better reduce BP.

26
Q

What is the result of 3rd generation with the extended action of Ca2+ entry blockade?

A

Since Ca2+ is involved in smooth m contraction, BB’s that prevent Ca2+ entry can also have utility in causing VASODILATION of sm m, which can compensate for any reflexive vasoconstriction that might occur with the first few doses of BB.

27
Q

What is the result of 3rd generation with the extended action of NO production and β2-agonism?

A

These also result in vasodilation to counter reflexive vasoconstriction.

28
Q

Despite the fact that BB’s enjoy widespread use in the management of HTN (decrease BP) and other CV conditions, what do we still not know about them?

A

We still don’t know how they work in the long-term to reduce BP.

29
Q

How does the use of BB effect the BP in normotensive patients?

A

It has no effect (it does not lower their BP)

30
Q

a) Which BB is effective with little or no effect upon plasma renin levels?
b) Which BB is most effective in patients with high plasma renin levels (most effective in lowering plasma renin)?

A

a) Pindolol

b) Propanolol

31
Q

What is the result of long-term administration of a BB?

A

A reduction in peripheral vascular resistance via an unknown mechanism

32
Q

As a class, what are the adverse effects of BB’s?

A
  1. CHF in susceptible patients
  2. Bradycardia/Bradyarrhythmias
  3. Cold extremities (uncommonly symptoms of peripheral vascular ds may worsen)
  4. Abrupt discontinuation can be bad
33
Q

Use of BB can lead to CHF in what types of patients?

A

Suscpetible patients: those w/ compensated HF, acute MI, or cardiomegaly. This is b/c these patients are relying on SNS stimulation of their declining CV activity to maintain CO. When administered BB’s that prevent this SNS stimulation, their CHF worsens.

But, chronic therapy w/ BB prolongs life in selected CHF patients

34
Q

Why do BB’s cause bradycardia as an adverse effect? In what type of patients? What increases this risk and should be avoided?

A

BB’s cause bradyarrhythmias in pts w/ partial/complete AV conduction defects.
This is b/c these drugs prevent AV conduction and produce AV block.
The risk of bradycardia/bradyarrhythmia is especially increased when BB is used in combination with other drugs that impair SA node function or AV conduction, such as VERAPAMIL or anti-arrhythmic agents.

35
Q

What is the result of abrupt discontinuation of BB after long-term treatment (KNOW THIS)? Why? How do you avoid this?

A

Abrupt discontinuation of BB after long-term therapy can exacerbate angina and increase the risk of sudden cardiac death. This is b/c antagonism of β-R’s over a long period of time results in upregulation of β-R’s by the cells, so there is enhanced responsiveness, leading to a sudden and dramatic increase in SNS activity if the BB is discontinued abruptly.
To avoid this, gradually taper down doses and restrict exercise during this period.

36
Q

What are the four main areas where BB’s have off-target effects? Why?

A

They have off-target effects (outside of the CV system) on:
1. Pulmonary
2. CNS
3. Glucose Levels
4. Lipid Profile
These are locations outside of the CV system in which β-R’s play an important role.

37
Q

Why do BB’s cause off-target pulmonary effects? As a result, in what kinds of patients should BB’s not be given?

A

BB’s block the bronchial smooth muscle β2-R’s that promote bronchodilation in patients with bronchospastic disease.
Patients with ASTHMA and COPD, who rely on this β2-mediated bronchodilation to breath, should not be given BB’s, as they will induce bronchospasm, preventing the bronchodilation and causing a life-threatening increase in airway resistance.

38
Q

What type of BB is worse for patients with Asthma (COPD)? Can another type be used instead?

A

Nonspecific BB’s should not ever be given. β1-selective BB’s or those with ISA are less likely to induce bronchospasm. However, the selectivity of current BB’s is not absolute, so there is still risk and they should be avoided if possible in Asthmatics. But, there are some individual cases where the benefits of using a β1 antagonists outweighs the risk.
IF YOU HAVE TO USE ONE IN AN ASTHMATIC USE A β1 BB, BUT AVOID IF POSSIBLE.

39
Q

What are the off-target effects of BB’s on the CNS? Which BB’s are more likely to cause CNS problems? Why?

A

CNS depression occur, resulting in mental disorders, fatigue, and in some cases, VIVID DREAMS.
These CNS effects are more commonly associated with LIPOPHILIC BB’s than hydrophilic BBs, b/c the lipophilic ones can more easily cross the BBB and enter the CNS.

40
Q

What effect do BB’s have on plasma glucose levels? Why?

A

β2-R’s normally stimulate hepatic glycogen breakdown (glycogenolysis) and pancreatic glucagon release, which together cause an increase in plasma glucose. However, BB’s prevent these actions, leading to HYPOGLYCEMIA.

41
Q

Why should you use BB’s cautiously in diabetics?

A

β1-blockers MASK/BLOCK the TACHYCARDIA , which normally serves as a warning sign in diabetics for insulin-induced hypoglycemia, telling them to consume something to fix this.
So, diabetics taking a BB are at increased risk of insulin-induced hypoglycemia.

42
Q

Why do BB’s have lipid profile effects? What are these effects of BB’s in general?

A

α1, and β1,2,3-R’s normally mediate LIPOLYSIS.
So, BB’s cause: a) little effect on total cholesterol and plasma LDLs b) increased triglycerides and decreased plasma HDLs

43
Q

More specifically, how do BB’s w/ wither ISA or cardioselectivity (β1-selectivity), or both affect lipid profiles?

A

BB’s with either ISA or cardioselectivity tend to have less effect on triglycerides and HDLs.
BB’s with BOTH ISA and cardioselectivity tend to reduce total cholesterol and LDLs.

44
Q

What are the two situations in which acute BB toxicity occurs?

A
  1. In children accessing adult medications.

2. In adults as a result of a suicide attempt or accidental overdose (OD).

45
Q

What are the symptoms of acute BB toxicity?

A
  1. Bradycardia 2. Hyptension 3. Arrhythmias (1,2 &3 are issues on the heart/CV itself)
  2. Hypothermia 5. Hypoglycemia 6.Seizures(more common w/ lipophilic ones)
46
Q

a) What situation causes a worse prognosis of BB toxicity?

b) What situation places a patient at increased risk for BB toxicity?

A

a) Co-ingestion of BB with cardio-active or psychotropic (CNS) drugs markedly worsens the prognosis for BB toxicity.
b) Underlying CV or pulmonary disease places pt at increased risk for toxic effects of BB’s.

47
Q

What are the primary CV conditions for which BB’s are used clinically?

A
  1. HTN

2. Acute MI (in combo w/ other agents): BB has beneficial effect on mortality when used post-MI.

48
Q

What are some of the non-CV applications of BB’s?

A
  1. Essential tremor
  2. Thyrotoxicosis
  3. Anxiety
  4. Prophylaxis of migraine headaches
  5. Prevention of bleeding associated with esophageal varices
  6. Treatment of glaucoma (topical application)

CV Module Pharm (13 decks)

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