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piggy > Pharmacology - Autonomic Drugs Part 2 > Flashcards

Pharmacology - Autonomic Drugs Part 2 Flashcards

1
Q

According to the mnemonic DUMBBELSS, what four major physiologic processes are blocked by atropine?

A

Diarrhea, Urination, Miosis,Bronchospasm, Bradycardia, Excitation of skeletal muscle, Lacrimation, Sweating, and Salivation

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2
Q

True or False? Increased body temperature is a sign of atropine toxicity.

A

True (ie, “hot as a hare”)

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3
Q

True or False? Slower heart rate is a sign of atropine toxicity.

A

False; heart rate would be increased

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4
Q

True or False? Dry mouth is a sign of atropine toxicity.

A

True (ie, “dry as a bone”)

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5
Q

True or False? Dry, flushed skin is a sign of atropine toxicity.

A

True (ie, “dry as a bone, red as a beet”)

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6
Q

True or False? Cycloplegia is a sign of atropine toxicity.

A

True (ie, “blind as a bat”)

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7
Q

True or False? Diarrhea is a sign of atropine toxicity.

A

False; constipation is a sign of atropine toxicity

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8
Q

True or False? Disorientation is a sign of atropine toxicity.

A

True (ie, “mad as a hatter”)

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9
Q

Which two adverse effects of atropine are more common in elderly patients?

A

Urinary retention and acute angle closure glaucoma

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10
Q

True or False? Atropine toxicity can cause urinary incontinence.

A

False; atropine toxicity can cause urinary retention in men with prostatic hypertrophy

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11
Q

True or False? Atropine toxicity can cause fecal incontinence.

A

False; atropine toxicity causes constipation, not fecal incontinence

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12
Q

What type of acetylcholine receptors does hexamethonium antagonize?

A

Nicotinic acetylcholine receptors

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13
Q

What effect does hexamethonium have on heart rate?

A

It can prevent bradycardia in response to increased blood pressure when pressors are given

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14
Q

Name four toxicities of hexamethonium.

A

Severe orthostatic hypotension, blurred vision, constipation, sexual dysfunction

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15
Q

Name 11 drugs that act as direct sympathomimetics.

A

Isoproterenol, dobutamine, phenylephrine, epinephrine, norepinephrine, dopamine, albuterol, terbutaline, ritodrine, metaproterenol, and salmeterol

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16
Q

Which types of receptors are activated by epinephrine?

A

α1-, α2-, β1-, and β2-receptors

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17
Q

Low doses of epinephrine are selective for _____ (α1, α2, β1, β2) adrenergic receptors.

A

β1

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18
Q

Which types of receptors are activated by norepinephrine?

A

α1- and α2-; β1-receptors (with lower affinity)

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19
Q

Does norepinephrine have greater affinity for α-adrenergic receptors or β1-receptors?

A

α-Adrenergic receptors

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20
Q

Isoproterenol is an agonist for which receptors?

A

β1- and β2-receptors equally

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21
Q

Which types of receptors does dopamine activate, and how strongly does it activate them relative to one another?

A

D1 = D2 receptors > β-receptors > α-receptors

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22
Q

Dopamine is an agonist for which receptors?

A

β1- and β2-receptors

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23
Q

Dopamine is _____ (ionotropic/not ionotropic) and _____ (chronotropic/not chronotropic), while dobutamine is _____ (ionotropic/not ionotropic) and _____ (chronotropic/not chronotropic).

A

Ionotropic; chronotropic; ionotropic; not chronotropic

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24
Q

Phenylephrine is an agonist for which receptors?

A

α1-receptors > α2-receptors

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25
Q

Metaproterenol, albuterol, salmeterol, and terbutaline are agonists for which receptors?

A

β2-receptors > β1-receptors

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26
Q

Ritodrine acts on _____ (α1, α2, β1, β2)-adrenergic receptors.

A

β2

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27
Q

What are the clinical applications of epinephrine?

A

Anaphylaxis, open-angle glaucoma, asthma, hypotension

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28
Q

What effect does norepinephrine have on renal perfusion?

A

It decreases renal perfusion

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29
Q

What is the clinical application for isoproterenol?

A

Atrioventricular block

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30
Q

What role does dopamine have in treating shock?

A

Increases blood pressure while maintaining renal perfusion

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31
Q

True or False? Dopamine can be used to treat heart failure.

A

True

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32
Q

What are the clinical applications for dobutamine?

A

Shock, heart failure, cardiac stress testing

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33
Q

What are the clinical applications of phenylephrine?

A

Treats nasal decongestion; causes vasoconstriction; dilates pupils

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34
Q

What is the clinical application for albuterol?

A

Acute asthma

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35
Q

Which sympathomimetics can be used to reduce premature uterine contractions?

A

Terbutaline, salmeterol

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36
Q

Amphetamine, ephedrine, and cocaine are (direct/indirect) sympathomimetics.

A

Indirect

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37
Q

By what mechanism does amphetamine exert its sympathomimetic effect?

A

It stimulates the release of stored catecholamines

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38
Q

By what mechanism does ephedrine exert its sympathomimetic effect?

A

It stimulates the release of stored catecholamines

39
Q

By what mechanism does cocaine exert its sympathomimetic effect?

A

It inhibits catecholamine uptake in the nerve terminal

40
Q

What are the clinical indications for use of amphetamines?

A

Narcolepsy, obesity, attention deficit hyperactivity disorder

41
Q

What are three clinical applications of ephedrine?

A

To treat nasal congestion, urinary incontinence, and hypotension

42
Q

True or False? Phenylephrine can be used to treat nasal congestion.

A

True

43
Q

What are the effects of cocaine when used topically?

A

Vasoconstriction and local anesthesia

44
Q

Is the effect of epinephrine on β-receptors greater than, equal to, or less than its effect on α-receptors?

A

Equal to, except at low doses, at which epinephrine is selective for β1

45
Q

Is the effect of isoproterenol on β-receptors greater than, equal to, or less than its effect on α-receptors?

A

Greater than

46
Q

What are the effects of norepinephrine on heart rate, systolic and diastolic blood pressure, and pulse pressure?

A

It increases systolic and diastolic blood pressure, slightly increases pulse pressure (systolic increases more than diastolic), and reduces heart rate by causing reflex bradycardia

47
Q

What are the effects of epinephrine on heart rate, systolic and diastolic blood pressure, and pulse pressure?

A

It increases systolic blood pressure, decreases diastolic blood pressure, greatly increases pulse pressure, and increases heart rate

48
Q

Why does norepinephrine administration result in reflex bradycardia?

A

Norepinephrine raises blood pressure, causing a vagal response that leads to reflex bradycardia via increased parasympathetic input to the heart

49
Q

Epinephrine causes an increase in heart rate via which receptor subtype?

A

β1 receptors; although epinephrine exhibits affinity for both β subtypes, it is selective for β1 at low doses, leading to tachycardia

50
Q

What effect does isoproterenol have on pulse pressure and heart rate?

A

Increases pulse pressure and heart rate

51
Q

What is the effect of clonidine on central adrenergic outflow? Which receptor does it act on?

A

It is an α2-agonist and decreases central adrenergic outflow; remember that the α2-receptor is responsible for negative feedback

52
Q

What are the clinical applications of clonidine?

A

Hypertension, especially with renal disease, because it does not decrease blood flow to the kidneys

53
Q

What is the effect of α-methyldopa on central adrenergic outflow? Which receptor does it act on?

A

It is an α2-agonist and decreases central adrenergic outflow

54
Q

What are the clinical applications of α-methyldopa?

A

Hypertension, especially with renal disease, because it does not decrease blood flow to the kidneys

55
Q

What are two patient populations for which α-methyldopa is indicated (as an antihypertensive)?

A

Renal failure patients, pregnant patients

56
Q

What is the clinical application and mechanism of action of phenoxybenzamine?

A

Phenoxybenzamine is a nonselective α-blocker that is used to treat pheochromocytoma

57
Q

Would you use phenoxybenzamine or phentolamine before removal of a pheochromocytoma? Why?

A

Phenoxybenzamine, because it is irreversible. Phentolamine is reversible, so the high levels of catecholamines released during surgery would overcome the α-block

58
Q

What is the clinical application and mechanism of action of phentolamine?

A

Phentolamine is a nonselective α-blocker that is used to treat pheochromocytoma

59
Q

What are two adverse effects of nonselective α-blockers?

A

Orthostatic hypotension and reflex tachycardia

60
Q

What are the clinical applications and mechanisms of action of prazosin, doxazosin, and terazosin?

A

They are each an α1-selective blocker used to treat hypertension and urinary retention in benign prostatic hyperplasia

61
Q

What are three effects of α1-selective blocker toxicity?

A

Orthostatic hypotension (first dose only), dizziness, headache

62
Q

What is the clinical application and mechanism of action of mirtazapine?

A

Mirtazapine is an α2-selective blocker used to treat depression

63
Q

What are three effects of α2-selective blocker toxicity?

A

Sedation, increased serum cholesterol, increased appetite

64
Q

What is the net effect of epinephrine on blood pressure before and after nonselective α-blockade? Why?

A

Before α-blockade, epinephrine increases blood pressure; after α-blockade, it decreases blood pressure. This is because epinephrine also activates β2, which lowers blood pressure and is not blocked

65
Q

What is the net effect of phenylephrine on blood pressure before and after nonselective α-blockade? Why?

A

Before α-blockade, phenylephrine increases blood pressure; after α-blockade, it has little effect on blood pressure. This is because phenylephrine is specific for α and does not activate ß2, so it is completely negated by α-blockade

66
Q

Why does epinephrine, a pressor, cause hypotension if a patient is pretreated with an α-blocker?

A

If α-receptors are blocked, the β-agonist properties of epinephrine predominate and lower blood pressure

67
Q

Name six clinical applications for β-blockers.

A

Hypertension, angina pectoris, myocardial infarction, supraventricular tachycardia, congestive heart failure, glaucoma

68
Q

Which two β-blockers are used to treat supraventricular tachycardia?

A

Propranolol, esmolol

69
Q

What β-blocker is frequently used to treat glaucoma?

A

Timolol

70
Q

How do β-blockers work in the setting of angina pectoris?

A

Decrease heart rate and contractility; decrease myocardial oxygen consumption

71
Q

A 63-year-old patient is referred to you from the emergency room for long-term care after his first myocardial infarction. Is a β-blocker suggested or contraindicated for this patient?

A

Suggested; after myocardial infarction, patients should receive β-blockers to decrease risk of mortality

72
Q

What is the mechanism of β-blockers in the treatment of supraventricular tachycardia?

A

They decrease atrioventricular conduction velocity

73
Q

To which class of antiarrhythmic agents do β-blockers belong?

A

Class II; drugs that slow atrioventricular conduction

74
Q

How does the use of β-blockers affect the progression of congestive heart failure?

A

Slows progression of heart failure; β-blockers reduce cardiac output but have proven benefit in congestive heart failure

75
Q

What is the mechanism of β-blockers in the treatment of glaucoma?

A

They reduce the secretion of aqueous humor, reducing intraocular pressure

76
Q

Why should β-blockers be used with caution in diabetic patients?

A

β-Blockers should be used with caution in diabetic patients because they can block initial warning signs of hypoglycemia such as increased heart rate and diaphoresis

77
Q

Name five nonselective β-blockers.

A

Propranolol, timolol, nadolol, pindolol, and labetalol

78
Q

Name five β1-selective antagonists.

A

Acebutolol, Betaxolol, Esmolol, Atenolol, Metoprolol (remember: A BEAM of β1-blockers)

79
Q

Which β-blocker is the shortest acting?

A

Esmolol

80
Q

What β-blockers have partial agonist activity?

A

Pindolol, Acebutolol (remember: Partial Agonist)

81
Q

What are two nonselective α- and β-antagonists?

A

Carvedilol, labetalol

82
Q

A patient with a history of Graves’ disease (hyperthyroidism) presents with chest pain. Her resting heart rate is 128 beats per minute, her blood pressure is 120/80 mmHg, and her respiratory rate is 18 breaths per minute. You order thyroid-stimulating hormone and thyroxine tests. What class of drugs would address her cardiac problems while you await the lab results?

A

ß-Blockers, such as propranolol, will reduce heart rate and consequently reduce angina

83
Q

What is the mechanism of β-blockers in treatment of hypertension?

A

Decreasing cardiac output and decreasing renin secretion

84
Q

What are some effects of β-blocker toxicity?

A

Bradycardia, atrioventricular block, congestive heart failure (reduced cardiac output), sedation, sleep alteration, impotence, exacerbation of asthma

85
Q

What symptoms indicate cholinesterase inhibitor poisoning?

A

DUMBBELSS: Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of the skeletal muscle and the central nervous system, Lacrimation, Sweating, and Salivation

86
Q

What mechanism underlies the symptoms of acetylcholinesterase inhibitor poisoning?

A

Inhibition of acetylcholinesterase leads to overactivity of the body’s cholinergic systems

87
Q

The symptoms of parathion poisoning are caused by the inhibition of what enzyme?

A

Acetylcholinesterase

88
Q

The symptoms of organophosphate poisoning are caused by the inhibition of what enzyme?

A

Acetylcholinesterase

89
Q

A child ingests insecticide and presents with diarrhea, abdominal pain, wheezing, pinpoint pupils, and copious tears and salivation. What medication should he be given?

A

Atropine and pralidoxime

90
Q

What antidote can be given to a patient who presents with diarrhea, urinary incontinence, miosis, bronchospasm, bradycardia, lacrimation, sweating, and salivation?

A

Atropine and pralidoxime

91
Q

Why is it important to give pralidoxime as well as atropine in organophosphate poisoning?

A

Because organophosphates are irreversible inhibitors of acetylcholinesterase and pralidoxime helps to regenerate functional acetylcholinesterase

92
Q

Atropine is used as an antidote for what kind of poisoning? By what mechanism does it accomplish this?

A

Organophosphate/anticholinesterase inhibitor poisoning; it inhibits muscarinic acetylcholine receptors

93
Q

Pralidoxime is used as an antidote for what kind of poisoning? By what mechanism does it accomplish this?

A

Organophosphate/cholinesterase inhibitor poisoning; it regenerates active acetylcholinesterase

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