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KLowe Pharm 2 > Lecture 1-Vasoconstrictors > Flashcards

Lecture 1-Vasoconstrictors Flashcards

1
Q

What are the three arms of the autonomic nervous system?—sympathetic innervation of ___; ___ nervous system; ___ nervous system

A
  • Sympathetic innervation of adrenal medulla (causes the release of epinephrine into the blood)
  • Sympathetic nervous system
  • Parasympathetic nervous system
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2
Q

What neurotransmitter kicks off all of the arms of the autonomic nervous system? What receptor does it bind to?

A

Acetylcholine; binds to nicotinic receptors

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3
Q

Catecholamines bind to ___ receptors; acetylcholine binds to ___ and ___ receptors

A

Catecholamines bind to adrenergic receptors; acetylcholine binds to nicotinic and muscarinic receptors

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4
Q

The sympathetic nervous system has thoracolumbar origin from T___-L___

A

T1-L2

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5
Q

Preganglionic neurons of the sympathetic nervous system are near the ___

A

Spinal cord

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6
Q

Postganglionic neurons secrete ___-adrenergic fibers

A

Norepinephrine-adrenergic fibers

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7
Q

How is norepinephrine created?—dopamine ___ converts ___ to ___

A

Dopamine beta hydroxylase converts dopamine to NE

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8
Q

Norepinephrine signal termination—80% of norepi that is released is ___

A

Recycled (via reuptake)

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9
Q

Norepinephrine signal termination—a ___ (small/large) amount of NE dilutes away by diffusion

A

Small amount

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10
Q

Norepinephrine signal termination—20% of NE that is not recycled is metabolized by ___ and ___

A

MAO (monoamine oxidase) and COMT (catechol-o-methyltransferase)

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11
Q

What are the 4 adrenergic receptors?

A
  • Alpha 1
  • Alpha 2
  • Beta 1
  • Beta 2
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12
Q

Alpha 1 receptors are located in the ___

A

Periphery

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13
Q

Alpha 2 receptors are located in the ___ (central/peripheral) nervous system

A

Central

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14
Q

Beta 1 receptors are located in the ___

A

Heart

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15
Q

Beta 2 receptors are located in other ___ muscle

A

Other smooth muscle

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16
Q

What binds to adrenergic receptors?

A

Catecholamines!

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17
Q

When catecholamines bind to beta adrenergic receptors, the result is ___ mediated effects; stimulatory proteins activate ___, causing a change from ATP into cyclic ___; cyclic ___ pulls ___ into the cells (cardiac myocytes, peripheral vasculature, skeletal muscle) to cause contraction of skeletal muscle or dilation in the periphery

A

G-protein mediated effects; stimulatory proteins activate adenylyl cyclase, causing a change from ATP into cyclic AMP; cyclic AMP pulls calcium into the cells to cause contraction of skeletal muscle or dilation in the periphery

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18
Q

Cyclic AMP is metabolized into ___, then ___, which has no further action

A

Phosphodiesterase 3, then AMP

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19
Q

When catecholamines bind to alpha receptors, the reaction is again ___ mediated; a ____ causes increases in calcium, which leads to contraction

A

G-protein mediated; a second messenger causes increases in calcium, which leads to contraction

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20
Q

SNS—alpha 1 postsynaptic receptor—activation ___ (increases/decreases) intracellular calcium; causes smooth muscle ___ (contraction/relaxation); peripheral vaso___ (constriction/dilation); broncho___ (constriction/dilation); ___ (stimulates/inhibits) insulin secretion from beta islet cells of the pancreas; ___ (stimulates/inhibits) glycogenolysis and gluconeogenesis; my___ (driasis/osis); GI ___ (relaxation/contraction)

A

Activation increases intracellular calcium; causes smooth muscle contraction; peripheral vasodilation; bronchoconstriction; inhibits insulin secretion from beta islet cells of the pancreas; stimulates glycogenolysis and gluconeogenesis; mydriasis—opens up the eyes; GI relaxation

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21
Q

SNS—alpha 2 receptors—presynaptic in the ___; postsynaptic in the ___

A

Presynaptic in the PNS; postsynaptic in the CNS

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22
Q

Alpha 2 receptors—presynaptic in the PNS—stimulation of these receptors ___ (increases/decreases) entry of calcium into the cell; limits the release of ___

A

Decreases entry of calcium into the cell; limits the release of norepinephrine

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23
Q

Alpha 2 receptors—postsynaptic in the CNS—stimulation of these receptors causes ___ation; ___ (increased/decreased) sympathetic outflow; ___ (increased/decreased) BP; platelet ___

A

Sedation; decreased sympathetic outflow; decreased BP; platelet aggregation

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24
Q

Two medications that are alpha 2 receptor agonists = ___ and ___

A

Dexmedetomidine (precedex) and clonidine

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25
Q

The agonistic activity at the alpha 2 receptor is technically ___ (agonistic/antagonistic)

A

Antagonistic—through a positive action at the alpha 2 receptor, you see negative effects

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26
Q

SNS—beta 1 postsynaptic receptor—___ (increases/decreases) HR, conduction velocity, and myocardial contractility

A

Increases HR, conduction velocity, and myocardial contractility

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27
Q

SNS—beta 2 postsynaptic receptor—stimulation leads to smooth muscle ___ (relaxation/contraction); peripheral vaso___ (constriction/dilation); ___ (increases/decreases) BP; broncho___ (constriction/dilation); ___ (increases/decreases) insulin secretion; ___ (increases/decreases) glycogenolysis and gluconeogenesis; ___ (increases/decreases) GI mobility

A

Stimulation leads to smooth muscle relaxation; peripheral vasodilation (improves oxygen exchange); decreases BP; bronchodilation; increases insulin secretion; increases glycogenolysis and gluconeogenesis; decreases GI mobility

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28
Q

Parasympathetic nervous system has a ___ origin (CN ___, ___, ___, ___)

A

Craniosacral origin (CN III, V, VII, X)

Remember SNS has a thoracolumbar origin T1-L2

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29
Q

PNS preganglionic are near ___

A

Organs of innervation

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30
Q

Postganglia of PNS secrete ___, which stimulates ___ fibers

A

Acetylcholine, which stimulates cholinergic fibers

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31
Q

Acetylcholine activates both arms of the ___ nervous system

A

Autonomic nervous system (sympathetic and parasympathetic nervous systems)

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32
Q

___ + ___ = acetylcholine; brought together by ___ ____ase

A

Choline + acetyl coA = acetylcholine; brought together by choline acetyltransferase

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33
Q

Acetylcholine is deactivated by ___esterase; breaks acetylcholine down into ___ + ___

A

Acetylcholinesterase; breaks acetylcholine down into choline + acetate

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34
Q

Acetylcholine ___ receptors = ___ and ___ receptors

A

Acetylcholine cholinergic receptors = nicotinic and muscarinic receptors

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35
Q

Long-term activation of a receptor can cause a change in the receptor field—T/F?

A

True

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36
Q

Effector cell receptors may down or up regulate, depending on exposure to agonists/antagonists—T/F?

A

True

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37
Q

This type of regulation results from extended exposure to agonists; it reduces the number of receptors, but not their response; results in tachyphylaxis

A

Down regulation

When the beta 1 or alpha 1 receptors start realizing they are getting a lot of stimulation, the body will change the amount of receptors available—the body doesn’t want to become over-constricted; cannot change the amount of norepi/epi that is circulating, so the body will change the amount of receptors available; results in tachyphylaxis—can continue to give medication, but you’re not going to get anymore effect; you may also start to see the effects taper off

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38
Q

This type of regulation results from chronic depletion of catecholamines or use of antagonists (blockade of the receptor); increases the number of receptors, but not their sensitivity; may account for withdrawal syndrome with beta blockers

A

Up regulation

The body will create more receptors when it cannot increase the amount of neurotransmitter needed or if it has attempted to with no effect

Beta blocker withdrawal—when you stop a beta blocker without any kind of taper, there is potential for severe tachyarrhythmias because there are so many beta 1 receptors available. Tapering beta blockers allows the receptors to be uncoupled and prevents withdrawal symptoms

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39
Q

Methods of receptor desensitization/down regulation—receptor ___; ___ation; ___ regulation

A

Receptor uncoupling; sequestration; down regulation

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40
Q

This type of receptor desensitization occurs rapidly; causes inability of the receptor to bind G protein and alter the function of the receptor

A

Receptor uncoupling

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41
Q

This type of receptor desensitization occurs more slowly; causes movement of receptors from the cell surface to intracellular compartments

A

Sequestration

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42
Q

This type of receptor desensitization is a prolonged process; causes movement of receptors from the cell surface to intracellular compartments, where they are then destroyed

A

Down regulation

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43
Q

This describes residual basal activity of the autonomic system

A

Tone

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44
Q

This condition results from an uncontrolled release of catecholamines due to an adrenal gland tumor; results in constant SNS stimulation

A

Pheochromocytoma

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45
Q

Catecholamines include both ___ and ___; act on ___ receptors

A

Include both neurotransmitters and hormones; act on adrenergic receptors

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46
Q

___ are compounds that resemble catecholamines (mimic the SNS) except the hydroxyl groups are NOT present in both the 3 and 4 positions of the benzene ring

A

Sympathomimetics

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47
Q

All sympathomimetics are catecholamines—T/F?

A

False—sympathomimetics resemble catecholamines but because they do not have hydroxyl groups present in the 3 and 4 positions of the benzene ring, they are not catecholamines

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48
Q

Catecholamines = ___ + ___ group with ___, ___ OH- groups attached to the benzene ring

A

Catechol + amine group with 3, 4 OH- groups attached to the benzene ring

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49
Q

3 types of sympathomimetics—naturally occurring ___ (i.e.: epi, norepi, dopamine); synthetic ___ (not in our bodies naturally but have the catecholamine structure); synthetic ___ (not in our bodies naturally and don’t have the catecholamine structure)

A

Naturally occurring catecholamines; synthetic catecholamines; synthetic non-catecholamines

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50
Q

All sympathomimetics are derived from ___

A

Beta phenylethylamine

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51
Q

Presence of hydroxyl groups on the ___ and ___ position of the benzene ring of the beta phenylethylamine creates a ___; drugs with this composition are ___

A

Hydroxyl groups on the 3 and 4 position of the benzene ring of the beta phenylethylamine creates a catechol; drugs with this composition are catecholamines

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52
Q

Epinephrine, norepinephrine, dopamine, isoproterenol, and dobutamine are all ___ because they have hydroxyl groups on the 3 and 4 positions of the benzene ring

A

Are all catecholamines

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53
Q

Ephedrine and phenylephrine are synthetic ___

A

Non-catecholamines (because they don’t have hydroxyl groups on the 3 and 4 positions of the benzene ring)

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54
Q

Clinical use of sympathomimetics—most often used as positive inotropes to improve cardiac ___; vasopressor to elevate ___ from unacceptable low levels

A

Most often used as positive inotropes to improve cardiac contractility; vasopressor to elevate blood pressure from unacceptable low levels

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55
Q

Sympathomimetics can also be used clinically for treatment of ___ in the asthmatic patient; management of ___; ___ management; and addition to local anesthetic to ___ (slow/speed up) systemic absorption

A

Treatment of bronchospasm in the asthmatic patient; management of anaphylaxis; arrhythmia management; and addition to local anesthetic to slow systemic absorption (and thus prolong the duration of action of the local)

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56
Q

Metabolism of catecholamines—all drugs containing the 3,4 dihydroxybenzene structure (catecholamines) are rapidly inactivated by what two enzymes?

A
  • MAO—monoamine oxidase

- COMT—catechol-o-transferase

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57
Q

___ (what enzyme?) is present in the liver, kidneys, and GI tract; catalyzes oxidative deamination

A

MAO

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58
Q

___ (what enzyme?) methylates the hydroxyl group of catecholamines

A

COMT

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59
Q

Catecholamines are inactivated by ___ and ___

A

MAO and COMT

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60
Q

Non-catecholamines do not have the catecholamine structure, so they can be broken down by ___ but NOT by ___

A

Can be broken down by MAO but NOT by COMT (because they don’t have the hydroxyl group of catecholamines)

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61
Q

Reuptake of catecholamines—inhibition of this uptake mechanism produces a greater potentiation of effects of epinephrine than does inhibition of either enzyme—T/F?

A

True

Because 80% of catecholamines undergo reuptake; the other 20% are metabolized by MAO/COMT

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62
Q

Metabolism of synthetic non-catecholamines—they lack a ___-hydroxyl group; not metabolized by ___; dependent on ___ for metabolism

A

Non-catecholamines lack a 3-hydroxyl group; not metabolized by COMT; dependent on MAO for metabolism

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63
Q

Metabolism of synthetic non-catecholamines is often ___ (slower/faster) than that of catecholamines

A

Slower

Because they are not being taken up/stored away and they only have one enzyme responsible for their metabolism

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64
Q

Metabolism of synthetic non-catecholamines—inhibition of MAO may ___ (shorten/prolong) their duration of action

A

Prolong their duration of action (because they are only metabolized by MAO)

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65
Q

Metabolism of synthetic non-catecholamines—patients on MAO inhibitors may manifest exaggerated responses when treated with synthetic non-catecholamines—T/F?

A

True

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66
Q

Sulfoconjugation reactions—genetic polymorphism of single nucleotides (SNPs) may affect the metabolism of catecholamines and phenylephrine—T/F?

A

True

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67
Q

Sulfoconjugation reactions—SULT1A___ and SULT1A___ polymorphisms primarily affect ___ metabolism by making its metabolism even slower

A

SULT1A3 and SULT1A4 polymorphisms primarily affect phenylephrine metabolism by making its metabolism even slower

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68
Q

What class of vasoconstrictors undergo reuptake?

A

Catecholamines—epi, norepi, dopamine

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69
Q

Sympathomimetics like ephedrine and phenylephrine undergo reuptake—T/F?

A

False—sympathomimetics like ephedrine and phenylephrine do NOT undergo reuptake—they are metabolized by MAO

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70
Q

Ephedrine and phenylephrine are metabolized by COMT—T/F?

A

False—they are only metabolized by MAO because they do not have the hydroxyl groups in the 3,4 positions of the benzene ring

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71
Q

The structure of catecholamines is unique because they have a hydroxyl group on the 3,4 position of the benzene ring—T/F?

A

True

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72
Q

Catecholamines are metabolized by COMT only—T/F?

A

False—catecholamines are metabolized by MAO and COMT

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73
Q

Vasoconstrictors—hemodynamic effects—___ (increase/decrease) arterial resistance and afterload; ___ (increase/decrease) SVR and MAP; ___ (increase/decrease) venous return; ___ (increase/decrease) preload and CO

A

Increase arterial resistance and afterload; increase SVR and MAP; increase venous return; increase preload and CO

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74
Q

Vasoconstrictors—reflex changes—___ (increased/decreased) heart rate; ___ (increased/decreased) conduction; occasionally, ___ (increased/decreased) contractility

A

Decreased heart rate; decreased conduction; occasionally, decreased contractility

May see these reflexive changes in response to the vasoconstriction (alpha 1 effect) that occurs with vasoconstrictors

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75
Q

Vasoconstrictors—non-cardiac effects—broncho___ (dilation/constriction); glyco__ (genolysis or genesis); ___ (release/inhibition) of insulin, renin, pituitary hormone; CNS ___ (stimulation/inhibition)

A

Bronchodilation; glycogenolysis; release of insulin, renin, pituitary hormone; CNS stimulation

76
Q

Risk of end organ damage and mortality from hypotension increases with time—T/F?

A

True

MAP < 65 mm Hg for 13-28 minutes; MAP < 50 mm Hg for 1 minute

77
Q

Contraindications/complications of vasoconstrictors—can worsen ___ failure; can exacerbate ___ failure; can ___ (increase/decrease) renal blood flow; can mask ___volemia

A

Can worsen LV failure; can exacerbate RV failure; can decrease renal blood flow; can mask hypovolemia

78
Q

What are (3) natural catecholamines?

A
  • Epi
  • Norepi
  • Dopamine

Dopamine is broken down to NE; NE is broken down to epi; all are structurally related and can be recycled

79
Q

Epinephrine is a ___ (natural/synthetic) catecholamine; stimulates ___, ___, and ___ receptors

A

Natural catecholamine; stimulates alpha 1, beta 1, and beta 2 receptors

80
Q

Epinephrine is the most potent activator of ___ receptors; ___-___x more potent than NE

A

Alpha 1 receptors

2-10x more potent than NE

81
Q

Epinephrine uses—___ma; ___laxis; cardiac ___; ___ing; to prolong ___ anesthesia; decrease ___ absorption of local anesthetics

A

Asthma; anaphylaxis; cardiac arrest; bleeding; to prolong regional anesthesia; decrease systemic absorption of local anesthetics

82
Q

Epinephrine is first line for ___ and ___

A

Cardiac arrest and anaphylaxis

83
Q

Epi ___ (increases/decreases) lipolysis, glycogenolysis; ___ (stimulates/inhibits) secretion of insulin; ___ (increases/decreases) blood sugar

A

Increases lipolysis, glycogenolysis; inhibits secretion of insulin; increases blood sugar

84
Q

Epi ___ (increases/decreases) renal blood flow, even in the absence of changes in systemic BP; it is a potent renal vaso___ d/t its ___ effects; stimulates ___ release (indirect effect)

A

Decreases renal blood flow, even in the absence of changes in systemic BP; it is a potent renal vasoconstrictor d/t its alpha 1 effects; stimulates renin release (indirect effect)

85
Q

Epinephrine has dose-specific effects—T/F?

A

True

86
Q

Low doses of epi (1-2 mcg/min) = ___ effects in peripheral vasculature predominate; the net effect is ___ (increased/decreased) SVR and distribution of blood to ___; MAP essentially remains ___

A

Beta 2 effects in peripheral vasculature predominate; the net effect is decreased SVR and distribution of blood to skeletal muscle (which improves oxygen exchange in the peripheral vasculature); MAP essentially remains the same

87
Q

Intermediate doses of epi (4 mcg/min) = ___ effects; ___ (increased/decreased) heart rate, contractility, and CO; ___ (increased/decreased) automaticity may lead to dysrhythmias

A

Beta 1 effects; increased heart rate, contractility, and CO; increased automaticity may lead to dysrhythmias

88
Q

High doses of epi (> 10 mcg/min) = ___ effects; potent vaso___ including cutaneous, splanchnic, and renal vascular beds; no significant effect on ___ arterioles; used to maintain myocardial and cerebral ___; reflex ___cardia can occur

A

Alpha 1 effects; potent vasoconstrictor including cutaneous, splanchnic, and renal vascular beds; no significant effect on cerebral arterioles; used to maintain myocardial and cerebral perfusion; reflex bradycardia can occur

89
Q

You can lose the effects of lower dose epi when higher doses are given—T/F?

A

True

90
Q

Reflex bradycardia can occur at higher doses of epi in response to the massive increase in SVR that you get from alpha-1 effects of high dose epi—T/F?

A

True

91
Q

Racemic epinephrine = mixture of levo- and dextrorotatory isomers that ___ (constrict/dilate) edematous mucosa; used to treat severe ___ and post-extubation or traumatic airway ___

A

Mixture of levo- and dextrorotatory isomers that constrict edematous mucosa; used to treat severe croup and post-extubation or traumatic airway edema

92
Q

Racemic epi treatment lasts ___-___ minutes

A

30-60 minutes

93
Q

Racemic epi—observe for ___ hours after treatment to monitor for ___arrhythmias

A

Observe for 2 hours after treatment to monitor for tachyarrhythmias—great risk of this because you can get systemic absorption, even though it is being administered via inhalation

94
Q

Side effects of epinephrine—no ___ effects (see more of this with norepinephrine)

A

No CNS effects

95
Q

Side effects of epinephrine—___glycemia; my___ (driasis/osis); platelet ___; ___ing; ___ache; ___or; ___ea; ___arrhythmias

A

Hyperglycemia; mydriasis; platelet aggregation; sweating; headache; tremor; nausea; tachyarrhythmias

Monitor BG, RR, O2 sat, HR, BP

96
Q

Norepinephrine is an ___ (endogenous/exogenous) catecholamine; responsible for maintaining BP by adjusting ___; ___ (increases/decreases) systolic, diastolic, and mean arterial pressure

A

Endogenous catecholamine; responsible for maintaining BP by adjusting SVR; increases systolic, diastolic, and mean arterial pressure

97
Q

Norepinephrine is the first line choice for ___ because it does not significantly increase ___

A

First line choice for sepsis because it does not significantly increase the heart rate (like epi does)

98
Q

If someone is tachycardic and hypotensive, you don’t want to give a medication that has strong ___ effects, because the heart rate will increase even more; want to pick a drug that is more ___ based

A

You don’t want to give a medication that has strong beta 1 effects, because the heart rate will increase even more; want to pick a drug that is more alpha based

99
Q

Norepinephrine is a potent vasoconstrictor of ___, ___, and ___ vascular beds; may ___ (increase/decrease) renal blood flow and cause ___uria; may lead to ___ infarct; peripheral ___perfusion can lead to ___ of digits

A

Renal, mesenteric, and cutaneous vascular beds; may decrease renal blood flow and cause oliguria; may lead to mesenteric infarct; peripheral hypoperfusion can lead to gangrene of digits

100
Q

Norepinephrine is primarily a/an ___ agonist

A

Alpha 1 agonist

101
Q

___ effects of norepinephrine are overshadowed by alpha 1 effects

A

Beta 1 effects

102
Q

Norepinephrine has beta 2 effects—T/F?

A

False—no beta 2 effects

103
Q

Norepinephrine—cardiac output may ___ (increase/decrease) at low doses; higher doses may cause cardiac output to ___ (increase/decrease) because of ___ (increased/decreased) afterload and baroreceptor-mediated reflex ___cardia

A

Cardiac output may increase at low doses; higher doses may cause cardiac output to decrease because of increased afterload and baroreceptor-mediated reflex bradycardia

104
Q

Norepinephrine may cause refractory ___tension

A

Refractory hypotension

105
Q

Norepinephrine has ___ (more/less) metabolic effects than epinephrine because it has no ___ effects

A

Less metabolic effects than epinephrine because it has no beta 2 effects (only at larger doses)

106
Q

Norepinephrine is used during ___ and ___ pathways after volume corrections are made

A

Sepsis and shock pathways

107
Q

Epi vs. norepi cardiac effects—___ increases HR; ___ keeps HR neutral, may cause reflex bradycardia at higher doses

A

Epi increases HR; norepi keeps HR neutral, may cause reflex bradycardia at higher doses

108
Q

Epi vs. norepi cardiac effects—___ significantly increases CO; ___ keeps CO neutral or may decrease it at higher doses

A

Epi significantly increases CO; norepi keeps CO neutral or may decrease it at higher doses (d/t increased afterload and baroreceptor-mediated reflex bradycardia)

109
Q

Epi vs. norepi cardiac effects—___ can cause tachyarrhythmias; ___ can cause bradyarrhythmias

A

Epi can cause tachyarrhythmias; norepi can cause bradyarrhythmias

110
Q

Epi vs. norepi BP effects—___ has a greater effect on mean arterial and diastolic pressures

A

Norepi

111
Q

Epi vs. norepi circulation—epi ___ (increases/decreases) total peripheral resistance; norepi ___ (increases/decreases) total peripheral resistance

A

Epi decreases total peripheral resistance; norepi increases total peripheral resistance

112
Q

Epi vs. norepi circulation—epi ___ (increases/decreases) cerebral blood flow; norepi ___ (increases/decreases) cerebral blood flow

A

Epi increases cerebral blood flow; norepi decreases cerebral blood flow

113
Q

Epi vs. norepi circulation—epi ___ (increases/decreases) muscle blood flow; norepi ___ (increases/decreases) muscle blood flow

A

Epi increases muscle blood flow; norepi decreases muscle blood flow (because no beta 2 effects)

114
Q

Epi vs. norepi circulation—epi ___ (increases/decreases) splanchnic blood flow; norepi ___ (increases/decreases/has little to no effect) splanchnic blood flow

A

Epi increases splanchnic blood flow; norepi has little to no effect on splanchnic blood flow (may slightly increase it)

115
Q

Epi metabolic effects—___ (increases/decreases) O2 consumption; ___ (increases/decreases) blood glucose; ___ (increases/decreases) blood lactic acid; ___ (increases/decreases) eosinophilic response

A

Increases O2 consumption; increases blood glucose; increases blood lactic acid; increases eosinophilic response

116
Q

Epi causes ___ (more/less) O2 consumption than norepi because it increases HR and CO

A

More O2 consumption than norepi

117
Q

Norepi and epi both increase the amount of blood pumped per beat, but epi increases CO more than norepi d/t increases in HR—T/F?

A

True

118
Q

___ is a parent catecholamine

A

Dopamine

119
Q

Dopamine has a tiered response to dosing just like epinephrine—T/F?

A

True

120
Q

Ephedrine is a synthetic ___

A

Noncatecholamine

121
Q

Ephedrine has direct and indirect actions; principle effect is ___

A

Indirect

122
Q

Ephedrine works at ___ and ___ receptors

A

Alpha 1 and beta receptors

123
Q

Beta stimulation from ephedrine may evoke ___, particularly in sensitized myocardium

A

Arrhythmias

124
Q

Ephedrine causes ___ (increased/decreased) myocardial contractility; venoconstriction is ___ (greater/less than) arteriolar constriction, which ___ (increases/decreases) preload; with ___ (increased/decreased) heart rate and myocardial contractility, it ___ (increases/decreases) cardiac output; ___ (increases/decreases) systolic and diastolic BP as a result

A

Increased myocardial contractility; venoconstriction is greater than arteriolar constriction, which increases preload; with increased heart rate and myocardial contractility, it increases cardiac output (beta 1 receptor action); increases systolic and diastolic BP as a result

125
Q

With ephedrine, ___ can occur; for this reason, ephedrine is typically given as ___, not as a ___

A

Tachyphylaxis—can lose total effect after a few days; for this reason, ephedrine is typically given as intermittent blouses, not as a continuous infusion

126
Q

Ephedrine preserves or increases ___ blood flow; causes bronchial smooth muscle ___ (relaxation/contraction)

A

Preserves or increases uterine blood flow; causes bronchial smooth muscle relaxation

127
Q

Ephedrine and phenylephrine have a rapid onset with a ___ (shorter/longer) duration of action than epi/norepi; may get peak effect within ___-___ minutes and can last for ___-___ minutes; can give in bolus doses and get more of a sustained effect than you will get with epi/norepi

A

Rapid onset with a longer duration of action than epi/norepi; may get peak effect within 10-15 minutes and can last for 20-25 minutes; can give in bolus doses and get more of a sustained effect than you will get with epi/norepi

128
Q

Ephedrine is like epi—alpha 1 effects ___ (are/are not) as strong as epi; ___ (more/less) intense; lasts ___ (shorter/longer) than epi

A

Alpha 1 effects are not as strong as epi; less intense; lasts longer than epi

129
Q

Side effects of ephedrine—___tension; ___omnia; urinary ___; ___ache; ___ness; ___or; ___tations; ___osis

A

Hypertension; insomnia; urinary retention; headache; weakness; tremor; palpitations; psychosis

130
Q

Ephedrine can have drug interactions with ___ d/t reuptake blockade and ___ may exaggerate HTN or cause significant arrhythmias

A

Drug interactions with cocaine d/t reuptake blockade and amphetamines may exaggerate HTN or cause significant arrhythmias

131
Q

Phenylephrine is a synthetic ___

A

Non-catecholamine

132
Q

Phenylephrine is a direct ___ agonist; increases ___load > ___load; small ___ effect

A

Direct alpha 1 agonist; increases preload > afterload; small beta 1 effect

133
Q

Phenylephrine ___ (increases/decreases) peripheral vascular resistance when CO is adequate; will see reflex ___cardia in response to ___ (increase/decrease) in SVR

A

Increases peripheral vascular resistance when CO is adequate; will see reflex bradycardia in response to increase in SVR

134
Q

Phenylephrine may be used to improve coronary perfusion pressure without chronotropic side effects—T/F?

A

True

135
Q

Phenylephrine is not safe to use in pregnant patients—T/F?

A

False—OK to use in pregnant patients

136
Q

Net effect of phenylephrine is increased pressure and flow without changing CO in normal individuals—T/F?

A

True

137
Q

Phenylephrine may decrease cardiac output in patients with ischemic heart disease; for this reason, may need to use NTG or IABP to decrease ischemic injury—T/F?

A

True

138
Q

Ephedrine is often used in OB because it preserves uterine blood flow—T/F?

A

True

139
Q

Phenylephrine may be used in pregnant patients and is associated with better fetal acid-base status; however, there is a higher risk of maternal bradycardia with phenylephrine than with ephedrine that is responsive to atropine—T/F?

A

True

140
Q

Other uses of phenylephrine—drug induced ___; ___ agent; nasal ___

A

Drug induced priapism; mydriatic agent; nasal decongestant

141
Q

Phenylephrine causes reflex ___cardia; ___ (increases/decreases) renal and splanchnic blood flow; ___ (increases/decreases) pulmonary artery resistance and pressure

A

Reflex bradycardia; decreases renal and splanchnic blood flow; increases pulmonary artery resistance and pressure

142
Q

Phenylephrine has no risk of tachyarrhythmias but can still cause bradyarrhythmias—T/F?

A

True

143
Q

Phenylephrine is like norepinephrine because it has significant ___ effects without any significant ___ effects; it is ___ (more/less) potent than norepinephrine and has a ___ (shorter/longer) duration of action

A

It has significant alpha 1 effects without any significant beta effects; it is less potent than norepinephrine and has a longer duration of action

144
Q

Epi and norepi are ___; they have a ___ (slower/faster) onset with a ___ (longer/shorter) duration of action than synthetic non-catecholamines

A

Natural catecholamines; they have a faster onset with a shorter duration of action than synthetic non-catecholamines

145
Q

Ephedrine and phenylephrine are ___; they have a slightly ___ (slower/faster) onset with a ___ (shorter/longer) duration of action than natural catecholamines

A

Ephedrine and phenylephrine are synthetic non-catecholamines; they have a slightly slower onset with a longer duration of action than natural catecholamines

146
Q

(3) posterior pituitary hormones

A
  • Vasopressin (ADH)
  • DDAVP—synthetic ADH
  • Oxytocin
147
Q

Vasopressin has potent ___/___ effects to increase BP

A

Antidiuretic/vasopressor effects to increase BP

100:100

148
Q

Oxytocin ___ (does/does not) have any antidiuretic/vasopressor effects

A

Does not

1:1

149
Q

DDAVP has more ___ effect than ___ effect

A

More antidiuretic effect than vasopressor effect

1200:0.39

150
Q

Vasopressin is used to preserve cardiocirculatory homeostasis in patients with advanced vasodilatory shock—T/F?

A

True

151
Q

Vasopressin can be used in patients who have failed or are resistant to conventional vasopressor therapy; patients who experience adverse effects of conventional vasopressor therapy—T/F?

A

True

152
Q

Unlike catecholamines, effects of vasopressin are preserved during ___ia and severe ___osis

A

Preserved during hypoxia and severe acidosis

153
Q

Vasopressin has ___ effects, as well as ___ effects

A

Vasopressor effects, as well as antidiuretic effects

154
Q

Binding of vasopressin to ___ receptors causes intense arterial vasoconstriction

A

V1 receptors

155
Q

Binding of vasopressin to ___ receptors in the renal collecting ducts increases the permeability of the cell membranes, resulting in the passive reabsorption of water

A

V2 receptors

156
Q

Advantages of vasopressin over epi—epi ___ (increases/decreases) myocardial oxygen consumption, which can contribute to risk of developing post-resuscitation MI and arrhythmias; vasopressin has no direct effect on ___, thus reducing myocardial ___ use

A

Epi increases myocardial oxygen consumption, which can contribute to risk of developing post-resuscitation MI and arrhythmias; vasopressin has no direct effect on heart rate, thus reducing myocardial oxygen use

157
Q

Advantages of vasopressin over epi—catecholamines may not work well in an ___ environment associated with CPR

A

Acidic

158
Q

Vasopressin is at least as effective as epi, may have fewer adverse effects than epi, and therefore is a reasonable alternative to epi in the treatment of cardiac arrest—T/F?

A

True

159
Q

Adverse effects of vasoconstrictors—cardiac ___; pure alpha agonists can activate ___ reflex-mediated ___cardia and possibly ___ (increase/decrease) CO

A

Cardiac dysrhythmias; pure alpha agonists can activate baroreceptor reflex-mediated bradycardia and possibly decrease CO

160
Q

Vasoconstrictors drug interactions—antihypertensives may ___ (increase/decrease) the pressor response to indirect acting drugs or ___ (inhibit/enhance) the response to direct acting drugs

A

Decrease the pressor response to indirect acting drugs or enhance the response to direct acting drugs

I.e.: if patient is on a beta blocker, patient may be hypersensitive to vasoconstrictors d/t up regulation of the beta receptors on the cardiomyocytes—could result in a very severe tachyarrhythmia d/t beta 1 stimulation of an up regulated field

161
Q

Vasoconstrictors and drug interactions—tricyclic antidepressants and MAO inhibitors increase the availability of endogenous ___; results in an exaggerated response with ___ (direct/indirect) acting agents; worse in the first ___-___ days of therapy, then a ___ (up/down) regulation of receptors occurs

A

Increase the availability of endogenous norepinephrine; results in an exaggerated response with indirect acting agents (i.e.: ephedrine, phenylephrine); worse in the first 14-21 days of therapy, then a down regulation of receptors occurs

162
Q

It is okay to continue TCAs and MAOIs in the perioperative period—T/F?

A

True

163
Q

If a patient is on a TCA or MAOI, you should use a/an ___ (increased/decreased) dose of direct acting drugs

A

A decreased dose

164
Q

Vasoconstrictor drug interaction with cocaine—cocaine interferes with ___ of catecholamines; both exogenous and endogenous catecholamines exhibit enhanced effects

A

Interferes with reuptake of catecholamines

165
Q

Cocaine + vasoconstrictors produces central and peripheral sympathetic stimulation, resulting in vaso___, ___cardia, and potentially, ___

A

Vasoconstriction, tachycardia, and potentially, arrhythmias

166
Q

Vasoconstrictors will have a ___ (shorter/longer) duration of action in cocaine users because cocaine blocks the reuptake of catecholamines

A

Longer duration of action in cocaine users

167
Q

Acute cocaine toxicity may best be managed with ___ blockade

A

Adrenergic blockade—alpha AND beta blockade

168
Q

Acute cocaine toxicity—never want to use just a ___ blocker

A

Just a beta blocker—i.e.: propranolol, metoprolol, atenolol

169
Q

Acute cocaine toxicity—if you only pick an alpha or beta blocker, you will see unopposed stimulation of the other side that is not being blocked which can cause ischemia—T/F?

A

True

170
Q

___ and ___ are better choices for acute cocaine toxicity because they provide both alpha and beta blockade

A

Labetalol and carvedilol

171
Q

Vasoconstrictors and drug interactions—natural weight loss products that contain ephedra (ephedrine, pseudoephedrine)—long-term use results in ___ from depletion of endogenous catecholamine stores and may contribute to perioperative hemodynamic ___ and cardiovascular ___; stop product at least ___ hours before surgery to prevent

A

Long-term use results in tachyphylaxis from depletion of endogenous catecholamine stores and may contribute to perioperative hemodynamic instability and cardiovascular collapse; stop product at least 24 hours before surgery to prevent

172
Q

Treat extravasation of vasoconstrictors with ___

A

Phentolamine

173
Q

Phentolamine is an ___; peripheral vaso___; treats skin ___ secondary to norepinephrine, dopamine, and epinephrine; 5-10 mg injected around the site of extravasation

A

Phentolamine is an alpha 1 and 2 antagonist; peripheral vasodilator; treats skin necrosis secondary to norepi, dopamine, and epi; 5-10 mg injected around the site of extravasation

174
Q

Goal of treatment of extravasation is peripheral vaso___; want to combat vaso___/alpha ___ effects

A

Peripheral vasodilation; want to combat vasoconstriction/alpha 1 effects

175
Q

Can also use ___, ___ as alternatives to phentolamine for treatment of extravasation

A

Nitroglycerin, terbutaline (cause beta 2 dilation to combat alpha 1 constriction)

If < 2 years old, apply NTG ointment to extravasated area; if persists, administer diluted terbutaline

If > 2 years old, administer terbutaline subcutaneously and apply NTG ointment; can re-administer terbutaline 15 mins later if no improvement is seen and continue with NTG ointment

176
Q

Ephedrine can be given as a continuous infusion—T/F?

A

False—not recommended for continuous infusion d/t risk of tachyphylaxis—body recognizes that there is too much NE and negative feedback mechanisms kick in

177
Q

Giapreza is AKA ___

A

Angiotensin II

178
Q

In studies, giapreza effectively increased blood pressure when added to conventional treatments used to raise blood pressure—T/F?

A

True

179
Q

Giapreza is dosed in nanograms/kg/min—T/F?

A

True

180
Q

Giapreza/angiotensin II causes vaso___ and increases ___ release

A

Vasoconstriction and increases aldosterone release

181
Q

Giapreza peak effect = ___ minutes

A

5 minutes

182
Q

Half-life of giapreza = ___

A

< 1 minute

183
Q

Giapreza is metabolized by ___ and ___

A

ACE and aminopeptidases

184
Q

Giapreza has drug interactions with ___ and ___

A

ACEIs and ARBs

ARBs—angiotensin II cannot bind to its receptor

ACEIs—prevent conversion of angiotensin I to angiotensin II

185
Q

Giapreza possible concerning side effect = ___ and ___; prophylactic treatment for ___ should be used; package insert states risk > ___%

A

Deep venous and arterial thrombosis; prophylactic treatment for blood clots should be used; package insert states risk > 10%

186
Q

Other side effects of giapreza include ___cardia, ___ium, thrombo___

A

Tachycardia, delirium, thrombocytopenia

KLowe Pharm 2 (10 decks)

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