Week 8 - Chapter 18 (Adrenergic Antagonists) Flashcards Preview

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Flashcards in Week 8 - Chapter 18 (Adrenergic Antagonists) Deck (20)
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1
Q

“Cardioselective” beta-adrenergic antagonists

A

[Blank] beta-adrenergic antagonists (drugs that block only beta1 receptors at therapeutic doses).

2
Q

First-Dose Effect

A

[BLANK] Effect -may cause fainting from severe orthostatic hypotension. Forewarn patients about first-dose hypotension and advise them to avoid driving and other hazardous activities for 12 to 24 hours after the initial dose. To minimize risk, advise patients to take the first dose at bedtime.

3
Q

Intrinsic Sympathomimetic Activity

A
  • This term refers to the ability of certain beta blockers—especially pindolol—to act as partial agonists at beta-adrenergic receptors.
  • In contrast to other beta blockers, agents with [BLANK] have very little effect on resting heart rate and cardiac output. When patients are at rest, stimulation of the heart by the sympathetic nervous system is low. If an ordinary beta blocker is given, it will block sympathetic stimulation, causing heart rate and cardiac output to decline. However, if a beta blocker has [BLANK], its own ability to cause limited receptor activation will compensate for blocking receptor activation by the sympathetic nervous system and, consequently, resting heart rate and cardiac output are not reduced.
4
Q

Orthostatic Hypotension

A

[BLANK] (postural) hypotension is the most serious adverse response to alpha-adrenergic blockade. This hypotension can reduce blood flow to the brain, causing dizziness, lightheadedness, and even syncope (fainting).

  • The cause of [BLANK] hypotension is blockade of alpha receptors on veins, which reduces muscle tone in the venous wall. Because of reduced venous tone, blood tends to pool (accumulate) in veins when the patient assumes an erect posture. As a result, return of blood to the heart is reduced, which decreases cardiac output, which in turn causes blood pressure to fall.
  • Patients should be informed about symptoms of [BLANK] hypotension (lightheadedness or dizziness on standing) and be advised to sit or lie down if these occur. In addition, patients should be informed that [BLANK] hypotension can be minimized by avoiding abrupt transitions from a supine or sitting position to an erect posture.
5
Q

Partial Agonist Activity

A
  • It’s another way of saying Intrinsic Sympathomimetic Activity.
  • A [BLANK] agonist is a drug that, when bound to a receptor, produces a limited degree of receptor activation while preventing strong agonists from binding to that receptor to cause full activation.
6
Q

Pheochromocytoma

A

A [BLANK] is a catecholamine-secreting tumor derived from cells of the sympathetic nervous system. These tumors are usually located in the adrenal medulla. If secretion of catecholamines (epinephrine, norepinephrine) is sufficiently great, persistent hypertension can result. The principal cause of hypertension is activation of alpha1 receptors on blood vessels, although activation of beta1 receptors on the heart can also contribute. The preferred treatment is surgical removal of the tumor, but alpha-adrenergic blockers may also be employed.

7
Q

Raynaud’s Disease

A

[BLANK] disease is a peripheral vascular disorder characterized by vasospasm in the toes and fingers. Prominent symptoms are local sensations of pain and cold. Alpha blockers can suppress symptoms by preventing alpha-mediated vasoconstriction. It should be noted, however, that although alpha blockers can relieve symptoms of [BLANK] disease, they are generally ineffective against other peripheral vascular disorders that involve inappropriate vasoconstriction.

8
Q

Rebound Cardiac Excitation

A

Long-term use of beta blockers can sensitize the heart to catecholamines. As a result, if a beta blocker is withdrawn abruptly, anginal pain or ventricular dysrhythmias may develop. This phenomenon of increased cardiac activity in response to abrupt cessation of beta-blocker therapy is referred to as [BLANK} excitation. The risk of [BLANK] excitation can be minimized by withdrawing these drugs gradually (eg, by tapering the dosage over a period of 1 to 2 weeks). If rebound excitation occurs, dosing should be temporarily resumed. Patients should be warned against abrupt cessation of treatment. Also, they should be advised to carry an adequate supply of their beta blocker when traveling.

9
Q

Reflex Tachycardia

A

Alpha-adrenergic antagonists can increase heart rate by triggering the baroreceptor reflex. The mechanism is this: (1) blockade of vascular alpha1 receptors causes vasodilation; (2) vasodilation reduces blood pressure; and (3) baroreceptors sense the reduction in blood pressure and, in an attempt to restore normal pressure, initiate a reflex increase in heart rate via the autonomic nervous system. If necessary, reflex tachycardia can be suppressed with a beta-adrenergic blocking agent.

10
Q

Prazosin

Mechanism of action?

A

Prazosin [Minipress], our prototype, is a competitive antagonist that produces selective blockade of alpha1-adrenergic receptors. The result is dilation of arterioles and veins, and relaxation of smooth muscle in the bladder neck (trigone and sphincter) and prostatic capsule. Prazosin is approved only for hypertension, but it can also benefit men with BPH.

11
Q

Prazosin

Pharmacokinetics?

A

Prazosin is administered orally. Antihypertensive effects peak in 1 to 3 hours and persist for 10 hours. The drug undergoes extensive hepatic metabolism followed by excretion in the bile. Only 10% is eliminated in the urine. The half-life is 2 to 3 hours.

12
Q

Prazosin

Adverse effects?

A

Blockade of alpha1 receptors can cause orthostatic hypotension, reflex tachycardia, and nasal congestion. The most serious of these is hypotension. Patients should be educated about the symptoms of orthostatic hypotension and be advised to sit or lie down if they occur. Also, patients should be informed that orthostatic hypotension can be minimized by moving slowly when changing from a supine or sitting position to an upright position.

13
Q

Propranolol

What is it and what is it’s therapeutic use?

A

-First-generation (nonselective) beta blockers, which block beta1 and beta2 receptors.

Therapeutic Uses:
Practically all of the applications of propranolol are based on blockade of beta1 receptors in the heart. The most important indications are hypertension, angina pectoris, cardiac dysrhythmias, and myocardial infarction. The role of propranolol and other beta blockers in these disorders is discussed in Chapters 47, 49, 51, and 53. Additional indications include prevention of migraine headache and “stage fright.”

14
Q

Propranolol

Mechanism of action?

A

-By blocking cardiac beta1 receptors, propranolol can reduce heart rate, decrease the force of ventricular contraction, and suppress impulse conduction through the AV node. The net effect is a reduction in cardiac output.
By blocking renal beta1 receptors, propranolol can suppress secretion of renin.
By blocking beta2 receptors, propranolol can produce three major effects: (1) bronchoconstriction (through beta2 blockade in the lungs), (2) vasoconstriction (through beta2 blockade on certain blood vessels), and (3) reduced glycogenolysis (through beta2 blockade in skeletal muscle and liver).

15
Q

Propranolol

Pharmacokinetics?

A

Propranolol is highly lipid soluble and therefore can readily cross membranes. The drug is well absorbed following oral administration, but, because of extensive metabolism on its first pass through the liver, less than 30% of each dose reaches the systemic circulation. Because of its ability to cross membranes, propranolol is widely distributed to all tissues and organs, including the central nervous system (CNS). Propranolol undergoes hepatic metabolism followed by excretion in the urine.

16
Q

Propranolol

Adverse effects?

A

The most serious adverse effects result from blockade of beta1 receptors in the heart and blockade of beta2 receptors in the lungs.
–Bradycardia.

–AV Heart Block (due to the slowing conduction of impulses through the AV node, thus causing AV heart block.

–Heart Failure (due to suppression of myocardial contractility) Early signs of HF are shortness of breath on mild exertion or when lying supine, night coughs, swelling of the extremities, weight gain from fluid retention)

–Rebound Cardiac Excitation.

–Bronchoconstriction (increased airway resistance is hazardous only to patients with asthma and other obstructive pulmonary disorders.)

–Inhibition of Glycogenolysis. (This effect can be dangerous for people with diabetes).

–CNS Effects.
Because of its lipid solubility, propranolol can readily cross the blood-brain barrier, and hence has ready access sites in the CNS. However, although propranolol is reputed to cause a variety of CNS reactions—depression, insomnia, nightmares, and hallucinations—these reactions are, in fact, very rare. Because of the possible risk of depression, prudence dictates avoiding propranolol in patients who already have this disorder.

–Effects in Neonates.
Propranolol crosses the placental barrier putting the neonate at risk of bradycardia, respiratory distress, and hypoglycemia.

17
Q

Metoprolol

What is it and what is its therapeutic use?

A

Second-generation (cardioselective) beta blockers, which produce selective blockade of beta1 receptors (at usual doses).
Therapeutic Uses:
The primary indication for metoprolol is hypertension. The drug is also approved for angina pectoris, heart failure, and myocardial infarction.

18
Q

Metoprolol

Mechanism of action?

A

By blocking cardiac beta1 receptors, metoprolol has the same impact on the heart as propranolol: it reduces heart rate, force of contraction, and conduction velocity through the AV node. Also like propranolol, metoprolol reduces secretion of renin by the kidney. In contrast to propranolol, metoprolol does not block bronchial beta2 receptors at usual doses, and therefore does not increase airway resistance.

19
Q

Metoprolol

Pharmacokinetics?

A

Metoprolol is very lipid soluble and well absorbed following oral administration. Like propranolol, metoprolol undergoes extensive metabolism on its first pass through the liver. As a result, only 40% of an oral dose reaches the systemic circulation. Elimination is by hepatic metabolism and renal excretion.

20
Q

Metoprolol

Adverse effects?

A

Major adverse effects involve the heart. Like propranolol, metoprolol can cause bradycardia, reduced cardiac output, AV heart block, and rebound cardiac excitation following abrupt withdrawal. Also, even though metoprolol is approved for treating heart failure, it can cause heart failure if used incautiously. In contrast to propranolol, metoprolol causes minimal bronchoconstriction and does not interfere with beta2-mediated glycogenolysis.

Decks in NURS 572 Pharmacology - Vocab Class (35):