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Pharmacology > Deja Ch 4 Autonomics > Flashcards

Deja Ch 4 Autonomics Flashcards

1
Q

What are the major subdivisions of the autonomic nervous system?

A

It is divided into the sympathetic and the parasympathetic nervous systems.

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2
Q

What is the major neurotransmitter of the parasympathetic autonomic nervous system?

A

Acetylcholine (ACh). ACh is released into the synaptic clefts from the pre-and the postsynaptic neurons of the parasympathetic nervous system.

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3
Q

In the sympathetic nervous system, what neurotransmitter is released from the preganglionic neuron into the synaptic cleft?

A

ACh. Remember that while the postganglionic neurotransmitters may differ between the sympathetic and parasympathetic branches of the autonomic nervous system, the preganglionic neurotransmitter released into the synaptic cleft is identical—ACh.

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4
Q

Where are sympathetic preganglionic fibers located?

A

In the paravertebral chains on either side of the spinal column or the prevertebral ganglia on the ventral surface of the aorta. Sympathetic preganglionic fibers are short.

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5
Q

Where are parasympathetic preganglionic fibers located?

A

In or near the wall of the organ they innervate. Parasympathetic preganglionic fibers are very long.

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6
Q

Where are nicotinic receptors located?

A

Postsynaptic neurons in ganglia of both the parasympathetic nervous system (PNS) and sympathetic nervous system (SNS); adrenal medulla; neuromuscular junction (NMJ); central nervous system (CNS)

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7
Q

Where are muscarinic receptors located?

A

Organs innervated by the PNS; thermoregulatory sweat glands innervated by the SNS; CNS (cortex, hippocampus)

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8
Q

What does the PNS do to heart rate?

A

It decreases the heart rate. Remember that at rest the heart is constantly under parasympathetic tone to slow the heart rate from the intrinsic rate set by the sinoatrial (SA) node at about 80 beats per minute.

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9
Q

What enzyme catalyzes the reaction between choline and acetyl-CoA to form ACh?

A

Choline acetyltransferase (CAT)

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10
Q

The neuronal release of ACh into the synapse is inhibited by what toxin?

A

Botulinum toxin

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11
Q

What organism produces botulinum toxin?

A

Clostridium botulinum (anaerobic, spore forming, gram-positive rod)

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12
Q

The venom of which spiders result in the release of stored ACh into the synapse?

A

Any spider of the genus Latrodectus (widow spiders) of which the black widow is the most common species found in North America. They produce α-latrotoxin which causes the release of ACh from the preganglionic neuron into the synaptic cleft.

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13
Q

What enzyme degrades ACh?

A

Acetylcholinesterase (AChE)

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14
Q

What are the breakdown products of ACh?

A

Choline and acetate

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15
Q

Where is AChE located in the autonomic nervous system?

A

In the synaptic cleft

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16
Q

What is muscarine?

A

It is an alkaloid found in various poisonous mushrooms.

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17
Q

Where are each of the following types of muscarinic receptors found in the body? M1

A

Nerves; gastric parietal cells

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18
Q

Where are each of the following types of muscarinic receptors found in the body? M2

A

Nerves; cardiac cells; smooth muscle

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19
Q

Where are each of the following types of muscarinic receptors found in the body? M3

A

Smooth muscle; exocrine glands; lungs; gastrointestinal (GI) tract; eye; bladder

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20
Q

Where are each of the following types of muscarinic receptors found in the body? M4

A

CNS

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21
Q

Where are each of the following types of muscarinic receptors found in the body? M5

A

CNS

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22
Q

For each of the following muscarinic receptor types, name the type of G-protein it is coupled to and the second messenger system responsible for execution of its activity upon stimulation: M1

A

Gq coupled; inositol triphosphate (IP3), diacylglycerol (DAG) cascade

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23
Q

For each of the following muscarinic receptor types, name the type of G-protein it is coupled to and the second messenger system responsible for execution of its activity upon stimulation: M2

A

Gi coupled; inhibition of cyclic AMP (cAMP) production, activation of potassium channels

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24
Q

For each of the following muscarinic receptor types, name the type of G-protein it is coupled to and the second messenger system responsible for execution of its activity upon stimulation: M3

A

Gq coupled; IP3, DAG cascade

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25
Q

For each of the following muscarinic receptor types, name the type of G-protein it is coupled to and the second messenger system responsible for execution of its activity upon stimulation: M4

A

Gi coupled; inhibition of cAMP production

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26
Q

For each of the following muscarinic receptor types, name the type of G-protein it is coupled to and the second messenger system responsible for execution of its activity upon stimulation: M5

A

Gq coupled; IP3, DAG cascade

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27
Q

Does the PNS directly innervate the vasculature?

A

No. Vascular tone is primarily determined by the degree of stimulation of adrenergic receptors of the sympathetic nervous system which directly innervate the vascular smooth muscle cells. However, there are muscarinic receptors located on the vasculature.

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28
Q

How can ACh lower blood pressure?

A

ACh binds to ACh receptors in the vasculature leading to increased synthesis of nitric oxide (NO) via second messenger pathways. An increase in NO leads to vasodilation.

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29
Q

NO is also known as what?

A

Endothelial-derived relaxation factor (EDRF)

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30
Q

What amino acid is a precursor to NO synthesis?

A

Arginine

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31
Q

Does AChE have a high affinity for ACh?

A

Yes

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32
Q

Does ACh increase or decrease the following (in other words, what is the effect of parasympathetic stimulation of the following)? Blood pressure

A

Decreases (both arterial and venous dilation via NO)

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33
Q

Does ACh increase or decrease the following (in other words, what is the effect of parasympathetic stimulation of the following)? Heart rate

A

Decreases (via M2 receptors)

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34
Q

Does ACh increase or decrease the following (in other words, what is the effect of parasympathetic stimulation of the following)? Salivation

A

Increases (via M3 receptors)

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35
Q

Does ACh increase or decrease the following (in other words, what is the effect of parasympathetic stimulation of the following)? Lacrimation

A

Increases (via M3 receptors)

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36
Q

Does ACh increase or decrease the following (in other words, what is the effect of parasympathetic stimulation of the following)? Sweating

A

Increases (via sympathetic stimulation of muscarinic cholinergic receptors)

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37
Q

Does ACh increase or decrease the following (in other words, what is the effect of parasympathetic stimulation of the following)? GI secretions

A

Increases (via M3 receptors)

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38
Q

Does ACh increase or decrease the following (in other words, what is the effect of parasympathetic stimulation of the following)? GI motility

A

Increases (via M3 receptors)

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39
Q

Does ACh increase or decrease the following (in other words, what is the effect of parasympathetic stimulation of the following)? Miosis (constriction of pupil)

A

Increases (via M3 receptors)

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40
Q

Does ACh increase or decrease the following (in other words, what is the effect of parasympathetic stimulation of the following)? Bladder detrusor muscle tone

A

Increases (via M3 receptors)

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41
Q

Does ACh increase or decrease the following (in other words, what is the effect of parasympathetic stimulation of the following)? Bladder sphincter tone

A

Decreases (in combination with increased detrusor tone this leads to increased urination also via M3receptors)

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42
Q

Does ACh increase or decrease the following (in other words, what is the effect of parasympathetic stimulation of the following)? Bronchodilation

A

Decreases (via M3 receptors)

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43
Q

What does ACh do to the ciliary muscle of the eye?

A

Increased contraction which leads to increased accommodation

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44
Q

How does ACh cause miosis?

A

Increased contraction of the circular muscle in the iris

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45
Q

Does bethanechol have muscarinic activity?

A

Yes (agonist)

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46
Q

Does bethanechol have nicotinic activity?

A

No

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47
Q

Does AChE have a high affinity for bethanechol?

A

No (zero affinity). This gives bethanechol a long duration of action.

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48
Q

What is a clinical use for bethanechol?

A

Nonobstructive urinary retention as can result from denervation of the urinary sphincter in conditions such as diabetes or spinal cord injury. Bethanechol can also be used for gastroesophageal reflux disease (GERD). As a cholinergic drug, it will increase detrusor tone and GI motility.

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49
Q

Does carbachol have muscarinic activity?

A

Yes, it is a muscarinic agonist.

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50
Q

Does carbachol have nicotinic activity?

A

Yes, it is also a nicotinic agonist.

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51
Q

Does AChE have a high affinity for carbachol?

A

No, the enzyme has zero affinity for carbachol.

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52
Q

What is carbachol used for?

A

It is a miotic agent to reduce intraocular pressure (IOP) in emergency settings of narrow-angle and open- angle glaucoma.

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53
Q

Does pilocarpine have muscarinic activity?

A

Yes, it is a muscarinic agonist.

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54
Q

Does pilocarpine have nicotinic activity?

A

No

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55
Q

Does AChE have a high affinity for pilocarpine?

A

No, the enzyme has zero affinity for pilocarpine.

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56
Q

What is pilocarpine used for?

A

It is the miotic drug of choice to lower IOP in emergency settings of narrow-angle and open-angle glaucoma.

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57
Q

Can pilocarpine cross the blood-brain barrier (BBB)?

A

Yes. Because it is a tertiary, uncharged amine.

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58
Q

Give examples of reversible AChE inhibitors:

A

Neostigmine; pyridostigmine; physostigmine; edrophonium; rivastigmine; donepezil; galantamine; tacrine

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59
Q

What are donepezil, galantamine, rivastigmine, and tacrine used for?

A

Alzheimer-type dementia. They are AChE inhibitors, thereby increasing the levels of ACh in the brain.

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60
Q

What two AChE inhibitors are quaternary ammonium compounds and therefore cannot cross the BBB?

A
  1. Neostigmine 2. Pyridostigmine ; As a result, these drugs will not reverse the central nervous system effects of cholinergic toxicity.
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61
Q

What short-acting AChE inhibitor is used to diagnose myasthenia gravis and is also used to differentiate myasthenic from cholinergic crisis?

A

Edrophonium. The trade name of edrophonium is Tensilon. This test is commonly referred to as the Tensilon test.

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62
Q

Which reversible AChE inhibitor is used as an antidote in atropine overdose?

A

Physostigmine, a tertiary amine, is able to cross the BBB to act on the CNS.

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63
Q

Give examples of irreversible AChE inhibitors:

A

Echothiophate; isoflurophate; sarin; malathion; parathion

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64
Q

Name an irreversible AChE inhibitor that is used as nerve gas:

A

Sarin

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65
Q

Which two AChE inhibitors are used as insecticides?

A
  1. Malathion 2. Parathion
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66
Q

What is another name for the irreversible AChE inhibitors?

A

Organophosphates

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67
Q

How do organophosphates irreversibly inhibit AChE?

A

The phosphate group covalently binds to serine hydroxyl group in the active site of AChE, thereby rendering the enzyme permanently inactive.

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68
Q

What is used to counteract the muscarinic and CNS effects of organophosphate poisoning?

A

Atropine via competitive inhibition. Atropine binds the muscarinic receptors, outcompeting the increased levels of ACh thereby preventing overstimulation.

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69
Q

What agent is used to reactivate inhibited AChE during organophosphate poisoning?

A

Pralidoxime (2-PAM). It is critical to initiate treatment with pralidoxime early along with atropine to prevent the process of aging where AChE is irreversibly inactivated by the organophosphates.

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70
Q

What are the signs and symptoms of organophosphate poisoning?

A

SLUDGE: salivation; lacrimation; urination; diaphoresis; GI motility (diarrhea); emesis. Basically, parasympathetic overstimulation.

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71
Q

Does atropine block nicotinic receptors, muscarinic receptors, or both?

A

It blocks muscarinic receptors.

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72
Q

What are the pharmacologic actions of atropine?

A

Mydriasis; cycloplegia; tachycardia; sedation; urinary retention; constipation; dry mouth; dry eyes; decreased sweating; hallucinations; sedation; hyperthermia; delirium; blurred vision; coma (high doses). Basically, anticholinergic/sympathetic overstimulation.

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73
Q

What class of drugs can be used to counteract atropine overdose?

A

AChE inhibitors

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74
Q

Name three drug classes that may cause antimuscarinic adverse effects:

A
  1. Sedating/first-generation antihistamines (diphenhydramine) 2. Tricyclic antidepressants (TCAs) 3. Phenothiazines
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75
Q

Low-dose (less than 0.5-1 mg) atropine does what to heart rate?

A

Decreases heart rate (unknown paradoxical vagalmimetic effect)

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76
Q

High-dose (>0.5-1 mg) atropine does what to heart rate?

A

Increases heart rate (parasympatholytic effect)

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77
Q

What is belladonna?

A

A perennial plant also known as “deadly nightshade” due to the toxic effects of its foliage and berries from which atropine is derived. Other toxins include scopolamine and hyoscyamine. The name belladonna derives from the cosmetic enhancing effects of dilated pupils, blushing of the cheeks, and reddening of the lips for which the plant was originally used.

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78
Q

How does scopolamine differ from atropine?

A

Scopolamine has a longer duration of action, more potent CNS effects, and is able to block short-term memory.

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79
Q

What is the main therapeutic indication of scopolamine?

A

Motion sickness

80
Q

Giving drugs with anticholinergic activity can precipitate an emergent situation in patients with what medical condition?

A

Patients with narrow-angle glaucoma

81
Q

What are the signs and symptoms of acute-angle-closure glaucoma?

A

General distress; pain; headache; red eye; photophobia; increased IOP; visual changes; malaise; nausea; vomiting

82
Q

What two anticholinergic agents are quaternary ammonium compounds and used for the treatment of asthma and chronic obstructive pulmonary disease (COPD)?

A
  1. Ipratropium 2. Tiotropium ; Tiotropium has a longer half-life compared to ipratropium.
83
Q

Does ipratropium effect airway secretions?

A

No (unlike atropine, which decreases airway secretions)

84
Q

Name three ganglionic blocking agents:

A
  1. Hexamethonium 2. Mecamylamine 3. Trimethaphan
85
Q

What are ganglionic blocking agents primarily used for?

A

Lowering blood pressure; blocking autonomic nervous system reflexes; smoking cessation due to blockade of central nicotine receptors

86
Q

Why can ganglionic blockers cause a marked postural hypotension?

A

Since sympathetic tone to the blood vessels is blocked, both arterial and venous dilation occur, lowering blood pressure. Moreover, the ganglionic blockers prevent the sympathetically mediated baroreceptor response to a sudden decrease in blood pressure, such as that occurs with a rapid change in position from sitting to standing.

87
Q

Neuromuscular blocking agents (NMBs) can be grouped into what two general categories?

A
  1. Depolarizing 2. Nondepolarizing
88
Q

Do NMBs work at muscarinic or nicotinic receptors?

A

Nicotinic receptors (remember the NMJ has nicotinic receptors).

89
Q

How many subunits is the nicotinic receptor made of?

A

Five subunits. Two α:- and three β-subunits make up this transmembrane ligand-gated ion channel

90
Q

Which subunit of the nicotinic receptor does ACh bind to?

A

Between the two α-subunits

91
Q

Binding of ACh to the nicotinic receptor at the NMJ is required to open which type of ion channel?

A

Sodium channel

92
Q

What is the most commonly used NMB?

A

Succinylcholine, the only depolarizing NMB. This is an ideal drug for endotracheal intubation due to its fast onset of action and short duration of action.

93
Q

How does succinylcholine work at the NMJ?

A

It behaves as a cholinergic agonist that remains bound to the ACh receptor for a prolonged period.

94
Q

What happens during each of the following phases of succinylcholine activity at the NMJ? Phase I

A

The receptor becomes depolarized and transient fasciculations are observed as various motor units depolarize.

95
Q

What happens during each of the following phases of succinylcholine activity at the NMJ? Phase II

A

The receptor becomes resistant to depolarization and a flaccid paralysis ensues.

96
Q

What are the two main uses of succinylcholine?

A
  1. It is used for facilitation of endotracheal intubation via relaxation of pharyngeal and laryngeal muscles. 2. It is used as an adjunct during electroconvulsive shock therapy to prevent prolonged full body convulsions which would result in muscle breakdown. A tourniquet is placed on a lower extremity to prevent the drug from reaching this location so that the seizure is visible in a localized area and the rest of the body is spared.
97
Q

Is succinylcholine short or long acting?

A

It is short acting with a duration of 4-8 minutes because of rapid hydrolysis by plasma cholinesterase.

98
Q

What are the adverse effects of succinylcholine?

A

Malignant hyperthermia; apnea; hypertension; hyperkalemia

99
Q

What are the signs and symptoms of malignant hyperthermia?

A

Muscular rigidity; increased oxygen consumption; increased carbon dioxide production (usually the first sign detected during surgery); tachycardia; hyperthermia is a late finding

100
Q

How is malignant hyperthermia treated?

A

With dantrolene

101
Q

What is the mechanism of action of dantrolene?

A

It inhibits calcium release from the sarcoplasmic reticulum of muscle cells, thereby relaxing muscle tone and reducing heat production.

102
Q

Succinylcholine may have a prolonged half-life in what type of patients?

A

Patients with a genetic deficiency or altered form of plasma cholinesterase

103
Q

What is the mechanism of action of nondepolarizing NMBs?

A

Competitive antagonists of ACh at the NMJ

104
Q

Which drug is the prototype of the nondepolarizing NMBs?

A

Tubocurarine

105
Q

What antidote is used in tubocurarine overdose?

A

AChE inhibitor (increases ACh concentration which competes with tubocurarine at ACh receptors at the NMJ)

106
Q

List in order, from first to last, the muscles that are paralyzed by nondepolarizing NMBs:

A
  1. Small muscles of the face and eye 2. Fingers 3. Limbs, neck, trunk 4. Intercostals 5. Diaphragm
107
Q

Which antimicrobial class of drugs may act in synergy with nondepolarizing NMBs by inhibiting release of ACh from nerve endings by competing with calcium ions, thereby increasing neuromuscular blockade?

A

Aminoglycosides (most likely to occur with high doses; patients with hypocalcemia, hypomagnesemia, or neuromuscular disorders)

108
Q

Give examples of nondepolarizing NMBs:

A

Tubocurarine; atracurium; mivacurium; rocuronium; vecuronium; pancuronium; pipercuronium

109
Q

What is the only nondepolarizing NMB that does not require dosage reduction in patients with renal failure?

A

Atracurium, which excreted in bile, not in urine

110
Q

What nondepolarizing NMB has the most rapid onset of action?

A

Rocuronium. Think: ROcuronium—Rapid Onset

111
Q

In what situations are nondepolarizing NMBs used?

A

Adjunct to general anesthesia to facilitate endotracheal intubation and to relax skeletal muscles during surgery; to facilitate mechanical ventilation in ICU patients

112
Q

What are the major neurotransmitters of the SNS?

A

Epinephrine; norepinephrine; dopamine

113
Q

What amino acid is the precursor to dopamine, epinephrine, and norepinephrine?

A

Tyrosine

114
Q

What are the steps, in order, to the synthesis of epinephrine starting from tyrosine?

A

Tyrosine is converted into DOPA by tyrosine hydroxylase (rate-limiting step); DOPA is converted into dopamine by DOPA decarboxylase; dopamine is converted into norepinephrine by dopamine β-hydroxylase; norepinephrine is converted into epinephrine by methylation in the adrenal medulla.

115
Q

What two enzymes metabolize norepinephrine?

A
  1. Monoamine oxidase (MAO) 2. Catechol-O-methyltransferase (COMT)
116
Q

What is the mechanism of action of reserpine?

A

It inhibits the transport of norepinephrine from the neuronal cytoplasm into the synaptic vesicles.

117
Q

What are the common side effects of reserpine?

A

Depression; sedation

118
Q

What breakdown products of norepinephrine are excreted in the urine and can be measured to help diagnose pheochromocytoma?

A

Vanillylmandelic acid (VMA); metanephrine; normetanephrine

119
Q

What are the two major classes of adrenergic receptors?

A
  1. α-Receptors 2. β-Receptors
120
Q

What neurotransmitters are metabolized by MAO type A?

A

Norepinephrine; epinephrine; serotonin; tyramine; dopamine

121
Q

What neurotransmitters does MAO type B metabolize?

A

Dopamine. Dopamine is metabolized by both the A and B type of the enzyme.

122
Q

How does cocaine increase norepinephrine levels in the synaptic cleft?

A

It inhibits the reuptake of neurotransmitter back into the presynaptic neuron.

123
Q

How do amphetamine, ephedrine, and tyramine increase norepinephrine levels?

A

They act as indirect sympathomimetic agents by entering the presynaptic neuron releasing stored norepinephrine into the synaptic cleft.

124
Q

Where are α1-receptors found?

A

Vascular smooth muscle; papillary dilator muscle; pilomotor smooth muscle; prostate; heart

125
Q

Where are α2-receptors found?

A

Postsynaptic CNS adrenoceptors; pancreatic β-cells; platelets; adrenergic and cholinergic nerve terminals; vascular smooth muscle; fat cells

126
Q

Where are β1-receptors found?

A

Heart; juxtaglomerular cells

127
Q

Where are β2-receptors found?

A

Respiratory, uterine, and vascular smooth muscle; skeletal muscle; liver

128
Q

Where are D1-receptors found?

A

Smooth muscle

129
Q

Where are D2-receptors found?

A

Nerve endings

130
Q

Compare and contrast the local versus the systemic effects of α2-receptor activation.

A

Local infusion of an α2-agonist will activate the α2-receptors in the vasculature, causing vasoconstriction. Systemic administration will activate the central α2-receptors in the locus ceruleus which inhibits norepinephrine release and sympathetic activation. The central effects overwhelm the local effects leading to decreased blood pressure.

131
Q

Give examples of α2-receptor agonists:

A

Clonidine; α-methyldopa; guanabenz; guanfacine; dexmedetomidine

132
Q

What are the therapeutic indications of clonidine?

A

Hypertension; severe pain; heroin withdrawal; nicotine withdrawal; ethanol dependence; clozapine-induced sialorrhea; prevention of migraines

133
Q

What is dexmedetomidine used for?

A

Sedation of intubated and mechanically ventilated patients; prolongation of spinal anesthesia

134
Q

With drugs that activate both α- and β-receptors, which receptors are generally activated first (which receptors are more sensitive)?

A

β-Receptors

135
Q

Activation of what receptor type in the eye will lead to contraction of the radial muscle and subsequently lead to mydriasis?

A

α1-Receptor

136
Q

For each of the following receptor types, name the type of G-protein it is coupled to: α1

A

Gq

137
Q

For each of the following receptor types, name the type of G-protein it is coupled to: α2

A

Gi

138
Q

For each of the following receptor types, name the type of G-protein it is coupled to: β1,β2,D1

A

Gs

139
Q

Name the major effects mediated by each of the following receptor types: α1

A

Mydriasis; vasoconstriction → increased blood pressure; decreased urination; increased glycogenolysis; decreased renin release; ejaculation

140
Q

Name the major effects mediated by each of the following receptor types: α2

A

Inhibition of norepinephrine release (central effect); inhibition of insulin release; platelet aggregation

141
Q

Name the major effects mediated by each of the following receptor types: β1

A

Increased heart rate; increased conduction velocity; increased force of heart contraction; increased renin release

142
Q

Name the major effects mediated by each of the following receptor types: β2

A

Vasodilation; bronchodilation; relaxation of uterine, respiratory, and vascular smooth muscle; increased insulin secretion; increased potassium uptake; increased glycogenolysis

143
Q

Name the major effects mediated by each of the following receptor types: Peripheral

A

Vasodilation of coronary, renal, and mesenteric vasculature; increased glomerular filtration rate (GFR); increased renal blood flow (RBF); increased sodium excretion

144
Q

Will α2-receptor activation in the pancreas cause insulin secretion to increase or decrease?

A

It will cause insulin secretion to decrease.

145
Q

Will β2-receptor activation in the pancreas cause insulin secretion to increase or decrease?

A

It will cause insulin secretion to increase.

146
Q

Which receptor type does epinephrine preferentially bind to at low doses?

A

β-Receptors (vasodilation in vasculature)

147
Q

Which receptor type does epinephrine preferentially bind to at high doses?

A

α-Receptors (vasoconstriction in vasculature)

148
Q

What is the drug of choice in patients with type 1 (immediate) hypersensitivity reactions?

A

Epinephrine

149
Q

What is the dose of epinephrine given for anaphylaxis?

A

0.1-0.5 mg. Note: The EpiPen (epinephrine auto-injector) that many patients with a history of anaphylaxis carry is 0.3 mg.

150
Q

What is the concentration of epinephrine used for anaphylaxis?

A

0.736111111

151
Q

What is the concentration of epinephrine used for advanced cardiac life support (ACLS) protocol?

A

1:10,000

152
Q

Why is epinephrine often given in combination with local anesthetics?

A

Epinephrine causes a vasoconstriction, thereby inhibiting the local anesthetics redistribution away from its site of action, so it increases the duration of local anesthesia.

153
Q

What is the concentration of epinephrine when given in combination with local anesthetics?

A

1:100,000

154
Q

State whether each of the following cardiovascular effects increases or decreases with low-dose epinephrine: Peripheral vascular resistance

A

Decreases

155
Q

State whether each of the following cardiovascular effects increases or decreases with low-dose epinephrine: Systolic blood pressure

A

Increases

156
Q

State whether each of the following cardiovascular effects increases or decreases with low-dose epinephrine: Diastolic blood pressure

A

Decreases

157
Q

State whether each of the following cardiovascular effects increases or decreases with low-dose epinephrine: Pulse pressure

A

Increases

158
Q

What receptors are activated by isoproterenol?

A

β1 = β2

159
Q

What receptors are activated by dopamine?

A

D>β>α

160
Q

What receptors are activated by dobutamine?

A

β1 > β2

161
Q

What receptors are activated by phenylephrine?

A

α1 > α2

162
Q

Does norepinephrine activate β2-receptors?

A

No

163
Q

Activation of dopamine receptors will cause what type of response in the mesenteric and renal vasculature?

A

Vasodilation

164
Q

What is dopamine metabolized to?

A

Homovanillic acid (HVA)

165
Q

What is dobutamine used for?

A

Increases cardiac output in congestive heart failure (CHF) without affecting RBF (unlike dopamine)

166
Q

Tyramine is a breakdown product of which amino acid?

A

Tyrosine

167
Q

Where is tyramine found?

A

Examples of foods and beverages which contain tyramine include: beer, ale, robust red wines, chianti, vermouth, homemade breads, cheese, sour cream, bananas, red plums, figs, raisins, avocados, fava beans, Italian broad beans, green bean pods, eggplant, pickled herring, liver, dry sausages, canned meats, salami, yogurt, soup cubes, commercial gravies, chocolate, and soy sauce.

168
Q

What enzyme is responsible for the breakdown of tyramine?

A

MAO type A

169
Q

What can potentially happen if a patient on a monoamine oxidase inhibitor (MAOI) consumes large amount of fermented cheese?

A

Hypertensive crisis due to tyramine in the cheese which leads to the release of norepinephrine from storage vesicles in presynaptic neurons

170
Q

What is phenylephrine and pseudoephedrine used to treat?

A

Nasal congestion

171
Q

What are mixed action adrenergic agonists?

A

Substances that release stored norepinephrine from nerve terminals and also directly stimulate α- and β- receptors

172
Q

What are some examples of mixed action adrenergic agonists?

A

Ephedrine; pseudoephedrine; metaraminol

173
Q

Which drug is a nonselective, competitive antagonist at both α1- and α2-receptors?

A

Phentolamine

174
Q

Which drug is a nonselective, irreversible antagonist at both α1- and α2-receptors?

A

Phenoxybenzamine

175
Q

What are phentolamine and phenoxybenzamine mainly used for?

A

To achieve α-receptor blockade before surgical removal of pheochromocytoma, to achieve perioperative blood pressure control, and to prevent intraoperative hypertension from release of catecholamines during surgical manipulation

176
Q

What is the mechanism of action of prazosin?

A

Selective α1-antagonist

177
Q

What are prazosin, terazosin, and doxazosin used to treat?

A

Benign prostatic hyperplasia (BPH); hypertension

178
Q

Does the “H” in BPH stand for hypertrophy or hyperplasia?

A

Hyperplasia, though hypertrophy is still sometimes erroneously used. There is an actual increase in the number of prostatic cells in BPH. The cells do not simply increase in volume as do, for example, skeletal or cardiac muscle cells in response to increased used.

179
Q

This drug is a selective α1A-receptor antagonist, used in the treatment of BPH, and has less cardiovascular side effects versus traditional α1-antagonists.

A

Tamsulosin

180
Q

What advantages do selective α1-antagonists have over nonselective α-antagonists?

A

Less reflex tachycardia

181
Q

What CNS prejunctional α2-receptor antagonist is used to treat postural hypotension and erectile dysfunction
(impotence)?

A

Yohimbine

182
Q

What CNS prejunctional α2-receptor antagonist is used to treat depression?

A

Mirtazapine

183
Q

Give examples of β1-selective antagonists:

A

Acebutolol; atenolol; bisoprolol; betaxolol; esmolol; metoprolol

184
Q

Give examples of nonselective β-antagonists:

A

Propranolol; timolol; pindolol; nadolol

185
Q

What is the name of a β-antagonist that also blocks potassium channels and is used as an antiarrhythmic?

A

Sotalol

186
Q

What is intrinsic sympathomimetic activity (ISA)?

A

Drugs act as partial agonists and only work when there is increased sympathetic drive such as with exercise; less bradycardia; less effects on lipid metabolism

187
Q

Which two β-antagonists have ISA?

A
  1. Acebutolol 2. Pindolol
188
Q

What happens to exercise tolerance in patients being treated with β-blockers?

A

Decreased exercise tolerance

189
Q

What are the main therapeutic indications of β-blockers?

A

Angina; arrhythmias; hypertension; CHF (not all β-blockers); thyrotoxicosis; glaucoma (ophthalmic formulations)

190
Q

What are some noncardiovascular uses of propranolol?

A

Migraine prophylaxis; performance anxiety “stage fright”

191
Q

β-Blockers can inhibit the majority of effects caused by thyrotoxicosis except for what sign?

A

Diaphoresis. Remember that sweat glands have muscarinic receptors and are cholinergic rather than adrenergic.

192
Q

β-Blockers can inhibit the majority of effects caused by hypoglycemia except for what sign?

A

Diaphoresis. β-Blockers are contraindicated in diabetic patients treated with oral hypoglycemics for this reason.

193
Q

What does propranolol do to serum triglycerides?

A

Increases serum triglycerides

194
Q

What does propranolol do to serum low-density lipoprotein (LDL)?

A

Increases serum LDL

195
Q

Why does propranolol cause vivid dreams?

A

Crosses the BBB

196
Q

Why should β-blockers be tapered down instead of abruptly discontinued?

A

Chronic therapy leads to upregulation of β-receptors; therefore, abrupt discontinuation may lead to life- threatening cardiovascular rebound effects (tachycardia; hypertension; arrhythmias; death)

Pharmacology (25 decks)

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