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Anesthesia Pharm > Sympathomimetics and Sympatholytics > Flashcards

Sympathomimetics and Sympatholytics Flashcards

1
Q

Which branches of the nervous system have ganglions?

A

Both the parasympathetic and the sympathetic

BUT NOT the somatic. All motor neurons are one long neuron

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2
Q

The peripheral nervous system employs three neurotransmitters:

A

Acetylcholine

Norepinephrine

Epinephrine

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3
Q

What are cholinergic receptors?

A

Regulate responses to Acetylcholine

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4
Q

What are adrenergic receptors?

A

mediate response to epinephrine and norepinephrine

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5
Q

Where are NM Receptors located?

A
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6
Q

Where are Muscarinic Receptors located?

A
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7
Q

Where are NN receptors located?

A
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8
Q

What are the muscarinic target organs?

A

Eye (miosis)

Heart (decreased HR)

Lung (Bronchial constriction)

Bladder and Bowels

Sweat Glands

Sex organs (erection)

Blood vessels (vasodilation)

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9
Q

Does parasympathetic stimulation cause vasodilation?

A

NO! Even though there are muscarinic receptors on blood vessels, there are NO ParaSNS nerves that terminate on blood vessels

These receptors only matter when we’re using drugs

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10
Q

Epinephrine is specific to what receptors?

A

Alpha 1

Alpha 2

Beta 1

Beta 2

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11
Q

Dopamine is specific to what receptors?

A

Alpha 1

Beta 1

Dopamine

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12
Q

Norepinephrine is specific to which receptors?

A

Alpha 1

Alpha 2

Beta 1

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13
Q

Where are alpha 1 receptors found?

A

Eyes (dilation)

Arterioles (vasoconstriction in the skin, viscera, and mucous membranes)

Sex organs (ejaculation)

Prostate and bladder

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14
Q

Where are alpha 2 receptors found?

A

Presynaptic nerve terminals

Inhibit transmitter release

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15
Q

Where are Beta 1 receptors located?

A

Heart (increased rate, contractility, and conduction)

Kidney (release of renin, which increases BP)

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16
Q

Where are beta 2 receptors located?

A

Arterioles (dilation of arterioles in the heart, lungs, and skeletal muscles)

Bronchodilation

Uterus (relaxation)

Liver (glycogenolysis)

Skeletal muscle (contraction, glycogenolysis)

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17
Q

Where are dopamine receptors located?

A

Kidney (dilate kidney vasculature)

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18
Q

Which neurotransmitters act on Beta 2 receptors?

A

ONLY EPINEPHRINE

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19
Q

Where is epinephrine released from?

A

The adrenal medulla, NOT neurons

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20
Q

What are the naturally occurring catecholamines?

A

Epinephrine

Norepinephrine

Dopamine

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21
Q

What cerebral effects does epinephrine cause?

A

NONE

it isn’t lipid soluble, so it doesn’t cross the BBB

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22
Q

Which two adrenergic receptors effect the heart?

A

Alpha 1

Beta 1

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23
Q

What determines epinephrine’s specificity for alpha or beta receptors?

A

The dose

beta receptors are more sensitive to lower epinephrine doses (inotropy dose)

Alpha 1 receptors are more sensitive to higher doses (pressor dose)

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24
Q

A patient who takes a beta blocker develops a bronchospasm and you give them epinephrine. What will happen?

A

It will get worse.

Epinephrine causes bronchodilation via beta 2 receptors BUT it also stimulates bronchial alpha 1 receptors

If they’re on a beta blocker, you’ll get unopposed alpha 1 bronchoconstriction

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25
Q

What electrolyte changes does Epinephrine cause?

A

Beta 2 stimulation leads to increased transfer of potassium into cells, decreasing serum potassium

This is why a lot of patients with high pre-op anxiety come in with low K

BUT epinephrine also stimulates potassium release from the liver, so offsets most of the effect

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26
Q

Norepinephrine is a derivative of _______

and is the precursor of _______

A

dopamine

epinephrine

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27
Q

Which endogenous catecholamine exerts the strongest effect on BP and SVR?

A

Norepinephrine exerts a much stronger effect than epinephrine

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28
Q

What are the metabolic effects of norepinephrine?

A

Unlike epinephrine, there really aren’t that many

Doesn’t usually cause hyperglycemia

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29
Q

Is norepinephrine an inotrope?

A

yes and no

it acts on Beta 1 receptors to increase HR, contractility and conduction BUT it’s alpha 1 action is so strong that the increased afterload may decrease CO

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30
Q

Does dopamine cross the BBB?

A

No. It’s very polar.

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31
Q

What Dopamine dose rate stimulates D1 and D2 receptors?

A

0.5-3 mcg/kg/min

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32
Q

What happens when D1 and D2 receptors are stimulated?

A

Decreased BP

vasodilation

increased renal and splanchnic flow

Diuresis

Natriuresis

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33
Q

What dopamine dose rate stimulates Beta 1 receptors and alpha 1 receptors?

A

3-10 mcg/kg/min

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34
Q

What dopamine dose rate stimulates primarily alpha 1 receptors?

A

> 10 mcg/kg/min

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35
Q

Which hormones does Dopamine inhibit?

A

anterior pituitary hormones:

Prolactin (which causes immune problems)

GH (impaired anabolism)

central hypothyroidism

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36
Q

How does dopamine impact ventilation?

A

low dose dopamine interferes with pulmonary hypoxic vasoconstriction and raises the CO2 threshold

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37
Q

Name the synthetic catecholamines:

A

Isoproterenol

Dobutamine

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38
Q

ISOPROTERENOL

CLASSIFICATION & MOA

A

Synthetic catecholamine

Beta 1 and Beta 2 selective agonist

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39
Q

Which causes more reflex tachycardia: dobutamine or isoproterenol?

A

isoproterenol

both because of direct beta 2 effects and because it causes more vasodilation, causing reflexive increase from decreased vascular tone

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40
Q

DOBUTAMINE

CLASSIFICATION AND MOA

A

Synthetic Catecholamine

Racemic mixture derived from isoproterenol

Potent Beta 1 effects

Weak Beta 2 effects

Some alpha effects at high dose

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41
Q

What makes dobutamine an inotrope?

A

It increases cAMP, increasing Ca release from the SR and increasing contractility

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42
Q

Is blood pressure effected by dobutamine?

A

It usually isn’t, because one enantiomer stimulates alpha 1, but the other antagonizes it

So usually the two equal out

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43
Q

How does dopamine impact pulmonary vasculature?

A

It does dilate, but not as much as phosphodiesterase inhibitors

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44
Q

Which is more dysrhythmogenic: dobutamine or dopamine?

A

Dopamine

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45
Q

Why does epinephrine results in increased lactate levels?

A

Decreased splanchnic flow means decreased lactate metabolism

46
Q

There are two synthetic noncatecholamine sympathomimetics:

A

Ephedrine

Phenylephrine

47
Q

EPHEDRINE

CLASSIFICATION & MOA

A

synthetic noncatecholamine sympathomimetic

DIRECTLY stimulates alpha and beta receptors

INDIRECTLY stimulates alpha and beta receptors by increased NE release

48
Q

What are the clinical uses of ephedrine?

A

Increase BP

Decrease nausea (IM)

49
Q

What is the PRINCIPAL reason that ephedrine increases BP?

A

increased contractility from Beta 1 activation

If beta blockers are on board, ephedrine will only cause vasoconstriction

50
Q

How do the cardiovascular effects of ephedrine differ from those of epinephrine?

A

they’re less intense and longer lasting

51
Q

Phenylephrine mimics the effects of ______

A

norepinephrine

52
Q

PHENYLEPHRINE

CLASSIFICATION & MOA

A

Synthetic noncatecholamine sympathomimetic

Mimcs the action of NE mostly at alpha 1 receptors

53
Q

Which one raises the heart rate: ephedrine or phenylephrine?

A

Ephedrine

54
Q

Does phenylephrine cause venoconstriction or vasoconstriction?

A

mostly venoconstriction

55
Q

What happens to cardiac output when phenylephrine is given?

A

It decreases

Maybe from increased afterload, but more likely from reflex bradycardia from baroreceptor response to the sudden increase in BP

56
Q

Name two beta two agonists

A

albuterol

terbutaline

57
Q

What is the primary side effect of using beta 2 agonists?

A

Muscle tremors because of B2 receptors in skeletal muscle

58
Q

DIGOXIN

CLASSIFICATION & MOA

A

Cardia Glycoside

Inhibit the Na-K sodium pump in the sarcolemma

Bind to the alpha subunit on the ATPase enzyme and stop it from transporting sodium ions out

The increased sodium ion concentration blocks the Na-Ca pump, so calcium builds up inside the cell

having more calcium inside the cell = stronger contraction

59
Q

What electrolyte imbalance may cause dig toxicity?

A

Hypokalemia

Hypomagnesemia

Hypoxemia

60
Q

How are potassium and digoxin related?

A

Potassium interferes with the binding of digitalis on cardiac muscle

61
Q

Which phosphodiesterase inhibitors impact cardiac cells?

A

PDE III

62
Q

In the myocardium, increased intracellular cAMP concentration results in:

A

stimulation of protein kinases that phosphorylate the sarcoplasmic reticulum → increased inward calcium current → increased intracellular calcium → increased contractility

63
Q

In vascular smooth muscle, increased cAMP results in:

A

facilitates uptake of calcium by the sarcoplasmic reticulum → decreased intracellular calcium → vasodilation and smooth mm relaxation

64
Q

Milrinone improves cardiac output by:

A

improving contractility (increased ca in myocardium)

Decreasing preload and afterload (reduced ca in vasculature)

65
Q

What are the three invariable side effects of all alpha blockers?

A

Orthostatic hypotension (can’t shunt blood)

Baroreceptor mediated reflex tachycardia

Impotence

66
Q

PHENTOLAMINE

CLASSIFICATION & MOA

A

Non selective, competitive Alpha blocker

Alpha 1: peripheral vasodilation and decreased BP

Alpha 2: increased release of NE from the brain leads to increased HR and CO

67
Q

What is the primary use for phentolamine?

A

acute hypertensive emergencies from pheochromocytoma manipulation or ANS hyperreflexia

68
Q

PHENOXYBENZAMINE

CLASSIFICATION & MOA

A

Nonselective, irreversible alpha blocker

Blockade at both receptors, but primarily alpha 2

69
Q

What is the primary use of phenoxybenzamine?

A

chronic alpha blockade for patients awaiting pheochromocytoma resection

70
Q

Any drug ending in “-osin” belongs to what class?

A

Alpha blockers

71
Q

Which beta blockers are preferred for patients with asthma and reactive airway disease?

A

Cardioselective beta blockers (beta 1 selective)

72
Q

What are the effects of beta 2 blockade?

A

Bronchospasm

peripheral vascular insufficiency

73
Q

Which beta blocker has the shortest half-life?

A

Esmolol

74
Q

Which beta blocker has the longest half life?

A

Betaxolol and/or Nebivolol

75
Q

How does propranolol impact clearance of LAs and opioids?

A

LAs: decrease clearance of amides because it decreases hepatic blood flow and inhibits metabolism

Opioids: decreases the first pass uptake of fentanyl. 2-4x as much drug enters the systemic circulation after injection

76
Q

A patient with asthma is receiving metoprolol, but needs increasingly large doses. Eventually they develop wheezing. What should be given?

A

A Beta 2 agonist (terbutaline)

77
Q

A patient with severe coronary artery disease should receive which beta blocker?

A

One that is as beta selective as possible BECAUSE beta 2 blockade will prevent coronary artery dilation

Atenolol is the current favorite for pre-treating cardiac patients undergoing noncardiac surgery

78
Q

What does it mean if a beta blocker has intrinsic sympathomimetic activity?

A

It means that in addition to blocking certain beta receptors, it also agonizes others

79
Q

If a patient cannot tolerate tachycardia due to intubation, which meds should be given?

A

Interestingly, lidocaine or fentanyl will reduce the BP response, but they will NOT stop the tachycardic response. Esmolol is a great choice for those patients.

80
Q

How does esmolol interact with propofol?

A

It significantly decreases the plasma concentration of propofol required to prevent patient movement

81
Q

How would giving a beta blocker impact blood sugar?

A

May cause hypoglycemia AND may mask the s/s of hypoglycemia

82
Q

What’s the difference between membrane stabilization and blockade?

A

Most beta blockers act by removing SNS innervation to the heart. BUT at high doses they will also hyperpolarize the cardiac resting membrane potential

83
Q

Name two beta blockers that are partial beta agonists

A

pindolol

acebutolol

84
Q

What is the initial drug if a beta blocker overdose is suspected?

A

Atropine

A beta selective agonist (like isoproterenol)

Glucagon

85
Q

Why is glucagon given in beta blocker overdoses?

A

It increases intracellular cAMP independent of Beta adrenergic receptors

86
Q

How do beta blockers impact metabolism?

A

Ordinarily when BG is low epinephrine is released. Beta blockers prevent it from binding in the liver and initiating glycogenolysis

87
Q

How do beta blockers influence potassium levels?

A

Beta 2 receptors facilitate movement of potassium INTRACELLULARLY

beta blockade inhibits the uptake of potassium into skeletal muscles, increasing plasma levels

88
Q

How do beta blockers and volatile anesthetics interact with one another?

A

They generally don’t have much of an additive effect as far as myocardial depression goes

Sevo and Des have the least additive effect. Iso has a little.

89
Q

How is the cardiovascular response to fentanyl altered by beta blockers?

A

It isn’t!

Even with high doses, the CV response isn’t altered

90
Q

What impact do beta blockers have on the CNS?

A

fatigue and lethargy, but not well documented

91
Q

Fetuses exposed to beta blockers are likely to be born with three symptoms:

A

bradycardia

hypotension

hypoglycemia

92
Q

There are two combined alpha and beta receptor antagonists:

A

Labetalol

Carvedilol

93
Q

Which receptors is labetalol selective for?

A

Selective Alpha 1

Nonselective Beta (1 and 2)

Alpha 2 is spared

94
Q

Which calcium channel blockers are selective for the AV node?

A

Verapamil and Diltiazem

95
Q

Which calcium channel blockers are selective for the arteriolar beds?

A

All the dihydropyridines:

Clevidipine, Nifedipine, Nicardipine, Nimodipine, Amlodipine

96
Q

What are common side effects of calcium channel blockers?

A

hypotension

peripheral edema

flushing

headache

97
Q

All calcium channel blockers bind to the same subunit of slow calcium channels:

A

the alpha 1 subunit

98
Q

Which calcium channel blockers are effective in treating coronary artery spasm?

A

All of them

99
Q

Which calcium channel blockers exert negative inotropic effects?

A

All of them, but verapamil and diltiazem are the most significant

100
Q

Which patients should not receive verapamil?

A

Patients in heart failure or who have any kind of heart block

101
Q

Verapamil may precipitate ventricular dysrhythmias in patients with what disease?

A

WPW

102
Q

What is special about nimodipine?

A

It favors cerebral vessels

103
Q

Are the dihydropyridines vasodilators or venodilators?

A

Almost exclusively arterial

104
Q

What should you be on the lookout for anytime you begin a dihydropyridine?

A

reflex tachycardia

You’re decreasing BP but not blunting the heart

105
Q

Why is nifedipine used as a tocolytic?

A

It prevents calcium from moving into the uterine cells, which decreases contractile strength

106
Q

What is special about nicardipine?

A

It can be given IV. All the other dihydropyridines have to be given PO.

107
Q

How do calcium channel blockers impact NMBAs?

A

They potentiate the effects of ALL NMBAs

108
Q

Which calcium channel blockers have a local anesthetic effect?

A

verapamil and dilt

109
Q

Do calcium channel blockers have effects at the NMJ?

A

Not in healthy patients, but in patients with muscular dystrophy they seem to cause pretty profound skeletal muscle weakness that isn’t consistent with just decreased neurotransmitter release

110
Q

How do calcium channel blockers impact potassium movement across the cell membrane?

A

the slow the inward movement of potassium, which increases the risk for hyperkalemia

Anesthesia Pharm (12 decks)

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