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ANS Pharm! Flashcards

1
Q

What are some traits about NEO?

A

RBF: decreased
MAP: ^^
Metabolism: MAO
Receptor: alpha 1
Use: hypotension

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2
Q

What are some traits about Clonidine?

A

RBF: no change
MAP: decreased
Metabolism: 50% liver/50% unchanged
Receptor: a2
Use: HTN (rebound HTN with abrupt stop)

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3
Q

What are some traits about dexmedetomidine?

A

RBF: no change
MAP: decreased
Metabolism: CYP liver
Receptor: a2
Use: sedation, analgesia, (may cause bradycardia and hypotension)

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4
Q

What may occur following the administration of phenylephrine?

A

Significant bradycardia

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5
Q

What is the alpha 2: alpha 1 ratio in clonidine?

A

200:1

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6
Q

What is the alpha 2: alpha 1 ratio in precedex?

A

1600:1

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7
Q

What type of action does clonidine have at the alpha 2 receptor?

A

Partial agonist

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8
Q

What type of action does precedex have at the alpha 2 receptor?

A

Full agonist

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9
Q

What aspect of the nervous system do alpha 2 agonist work?

A

Locus coeruleus and dorsal horn

Precedex produces more than clonidine

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10
Q

What does abrupt discontinuation of clonidine cause?

A

Rebound HTN, tachycardia, and arrhythmia

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11
Q

What drug can reduce emergence and agitation in both adults and children?

A

Precedex

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12
Q

What are some traits about epinephrine?

A

RBF: decreased
MAP: ^
Airway resistance: decreased
Metabolism: reuptake; MAO, COMT
Receptor: B1 > B2, a1
Use: shock, anaphylaxis, ACLS

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13
Q

What are some traits about norepinephrine?

A

RBF: decreased (most)
MAP: ^^^ (most)
Airway resistance: no change
Metabolism: reuptake, MAO, COMT
Receptor: a1, B1 >nB2
Use: shock, vasoplegia

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14
Q

What are some traits about dopamine?

A

RBF: ^^^
MAP: ^
Airway resistance: no change
Metabolism: reuptake; MAO and COMT
Receptor: B1 > B2, a1
Use: shock

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15
Q

What are some traits about isoproterenol?

A

RBF: deceased
MAP: ^
Airway resistance: decreased sig.
Metabolism: COMT
Receptor: B1 > B2
Use: drug pacing

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16
Q

What are some traits about dobutamine?

A

RBF: ^^
MAP: ^
Airway resistance: no change
Metabolism: COMT
Receptor: B1 > B2 > a1
Use: cardiogenic shock, stress test

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17
Q

What are some traits about ephedrine?

A

RBF: decreased
MAP: ^^
Airway resistance: decreased
Metabolism: liver (^ % Renally unchanged)
Receptor: a, B, indirect
Use: hypotension

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18
Q

What will organs with a higher incidence of B2 see if epi is administered?

A

Dilation (skeletal muscle)

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19
Q

What will organs with a higher incidence of alpha 1 see if epi is administered?

A

Vasoconstriction
(Mesentery/kidneys)

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20
Q

What does a lower dose of epi favor?

A

Beta stimulation

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21
Q

What does a higher dose of epi stimulate?

A

Alpha effects

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22
Q

What epinephrine reversal?

A

Converts the pressor response (mediated by a receptors) to a depressor response (mediated by B2 receptors)

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23
Q

Which med is a first line therapy in distributive shock that otherwise may be refractory to hypotension?

A

NE

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24
Q

What does low-dose dopamine do?

A

< 3 mcg/kg/min

Stimulates D1 receptors ~ resulting in vasodilation and increased renal and splanchnic flow

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25
Q

What does moderate dose dopamine do?

A

3-8 mcg/kg/min

Stimulates a1 and B1 adrenergic receptors in the heart and periphery, this increasing contractility

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26
Q

What does high dose dopamine do?

A

> 10 mcg/kg/min

Acts as a pure a1 agonist > increased BP

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27
Q

Does dopamine prevent/reverse kidney injury or failure?

A

NO!! Data does not support that.

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28
Q

What is isoproterenol derived from?

A

Dopamine!

Potent B1 and B2 activity (2-3 x the potency of epi)

***no alpha activity

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29
Q

What does isoproterenol tend to precipitate?

A

Supra ventricular and ventricular arrhythmias (hence why it is given in EP lab for SVT)

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30
Q

What is dobutamine derived from?

A

Isoproterenol!

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31
Q

What does dobutamine act as?

A

“Pharmacological stress test”

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32
Q

Why is dobutamine sometimes used in patient with pulmonary HTN?

A

Increase inotropy as it decreases pulmonary arterial pressures and PVR through its B2 stimulation

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33
Q

How does ephedrine elicit it’s indirect effect?

A

Results from the endo utopia of ephedrine into the adrenergic presynaptic terminals ~ displaying NE from secretory vesicles

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34
Q

What is seen with repeat administrations of ephedrine?

A

Tachyphylaxis

This results from depletion of the presynaptic norepinephrine

***this is why it is NOT given as an infusion

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35
Q

Does ephedrine cross the BBB?

A

Yes. ~ mild stimulating effects which may lead to misuse

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36
Q

What are B2 agonists commonly used for?

A

Airway dx!

COPD, asthma, airway reactivity

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37
Q

What are considered short acting B2 agonists?

A

Albuterol, terbutaline, LR albuterol

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38
Q

What are considered long acting B2 agonist drugs?

A

Salmeterol and formoterol

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39
Q

What are some side effects of B2 stimulation?

A

Tremor, anxiety, restlessness

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40
Q

What happens with escalated dosing of B2 agonists?

A

B2 selectivity wanes and B1 effects (tachycardia and arrhythmias) become more apparent

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41
Q

How does B2 agonists work?

A

^cAMP (BUT in this region) increased cAMP reduced Ca levels leading to smooth muscle relaxation

***happens in uterine musc too!

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42
Q

What is the black box warning to longer-acting B2 selective agents?

A

Due to a risk of asthma-related deaths.

***could be noted hyperresponsivenss after continuous use.

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43
Q

What are examples of two nonselective alpha 1 and alpha 2 antagonists?

A

Phenoxybenzamine

Phentolamine

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44
Q

Which alpha antagonist is a NONcompetitive antagonist?

A

Phenoxybenzamine

The bonding of this receptor is irreversible!!

**oral administration

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45
Q

What is phenoxybenzamine exclusively used for?

A

Preoperative management of pheochromocytoma ~ prevents episodic HTN and normalizes BP

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46
Q

What is the BEST treatment for phenoxybenzamine-induced severe hypotension?

A

Vasopressin and fluids! (NE and Neo will be useless)

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47
Q

What is phentolamine?

A

COMPETITIVE nonselective alpha receptor antagonist

**it can be overcome by Neo and NE

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48
Q

How is Phentolamine administered?

A

Potent, rapid acting vasodilator. It can cause baroreceptor-mediated bradycardia!!!

***use in extreme caution with patients with flow-limited CAD

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49
Q

Can Phentolamine be given as a local injection?

A

Yes! Especially after extravasation of a vasoconstrictor like NE or Epi.

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50
Q

What other receptor does phentolamine have an affinity for?

A

5-HT ~ this will stimulate stomach acid secretion

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51
Q

What is prazosin?

A

Highly selective alpha 1 receptor antagonist

1000:1 (alpha 1 vs alpha 2)

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52
Q

What are the side effects to prazosin?

A

Postural/orthostatic hypotension

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53
Q

What is Terazosin?

A

Less potent and longer acting than prazosin.

It’s main use is in treating prostate hypertrophy! (There are a large number of alpha 1 receptors there) ~ Anesthetic-induced hypotension may be exacerbated.

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54
Q

What is Yohimbe?

A

Primary a drug for males. ~ selective alpha 2 antagonist wildly used for sterile dysfunction, athletic performance, weight loss, HTN, etc…

**illegal in US

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55
Q

What are the main indications for Beta blocker use?

A

HTN
SVT
Afib
blunting of a Hemodynamic response
Reducing myocardial O2 consumption

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56
Q

Which two B-blockers have membrane stabilizing activity?

A

Propranolol and acebutolol

(These have MSA ~ inhibits or abolishes action propagation across the cell membrane)

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57
Q

Which B-blockers possess intrinsic sympathomimetic activity?

A

Pindolol, labetalol, and acebutolol

Exert a partial stimulating (agonist) action at the B receptor

58
Q

What is the prototypical NONselective B-blocker?

A

Propranolol

59
Q

What are some side effects of Propranolol?

A

Can produce bronchoconstriction (d/t it’s nonselectivity)

May aggravate Raynaud’s

60
Q

What are some other examples of NONselective B-Blockers?

A

Carvedilol, nadolol, pindolol, sotalol, and timolol

61
Q

What are some examples of CARDIOSELECTIVE B-Blockers?

A

Metoprolol
Atenolol
Acebutolol
Esmolol
Bisoprolol

62
Q

Which BB is metabolized by the kidney?

A

Atenolol

63
Q

What is the first-line drug for rapid perioperative control of HR and BP?

A

Esmolol

64
Q

How is esmolol metabolized?

A

Nonspecific esterases in the red blood cell

65
Q

What are the two main NONselective adrenergic antagonists?

A

Labetalol and Carvedilol

66
Q

What is the ratio of B to alpha block with labetaolol

A

7:1

67
Q

What is labetolol primarily used for?

A

Acute HTN

68
Q

Which BB has both antioxidant and anti-inflammatory properties?

A

Carvedilol

69
Q

What is a common self-administered cholinergic?

A

Nicotine!

70
Q

Which ganglia are activated with nicotine?

A

Both SNS and PNS!!! POSTganglionic neurons are activated by ACh released from PREganglionic receptors

71
Q

Why is Nicotine a concern in the cardiovascular system?

A

Nicotine’s effects will be unopposed because there is insignificant PNS regulation

72
Q

What medication is used to provoke bronchoconstriction, increased airway secretions, and peak expiratory flow rate?

A

Methacholine!

It’s used to identify reactive airway disease in those who do not have apparent signs of asthma.

73
Q

What medication is used to treat nonobstructive urinary retention in the postoperative period?

A

Bethanachol

74
Q

Which two cholinergic agonists produce miosis and have applications in treat glaucoma?

A

Carbamylcholine
Pilocarpine

75
Q

What are some traits about atropine?

A

HR: ^^^ (most)
Smooth musc relax: ^^
Sedation: ^^
Mydriasis: ^
Antisialagogue: ^
Prevent Motion sickness: ^
Decrease gastric secretion: ^
Structure: tertiary amine
BBB: yes

76
Q

What are some traits about scopolamine?

A

HR: ^
Smooth musc relax: ^
Sedation: ^^^
Mydriasis: ^^^
Antisialagogue: ^^^
Prevent Motion sickness: ^^^
Decrease gastric secretion: ^
Structure: tertiary amine
BBB: yes

(Remember MAPS ~ things scopolamine is best at ~ Mydriasis, Antisialagogue, Prevention of motion sickness, and Sedation)

77
Q

What are some traits about Glyco?

A

HR: ^^
Smooth musc relax: ^^
Sedation: 0
Mydriasis: 0
Antisialagogue: ^^
Motion sickness: 0
Decrease gastric secretion: ^
Structure: quaternary Amine
BBB: no

78
Q

What two antimuscarinics are considered belladonna alkaloids?

A

Atropine
Scopolamine

79
Q

What can low-dose atropine cause?

A

Bradycardia! This happens by blocking M1 receptors on preganglionic parasympathetic fibers

80
Q

What is the catchy phrase about anticholinergic syndrome?

A

Dry as a bone
Red as a beet
Blind as a rat
Hot as a hare
Mad as a hatter!

81
Q

What medication reverses anticholinergic syndrome?

A

Physostigmine!! 1-2 mg

Ir also crosses the BBB cometitively reversing the effect

82
Q

Which calcium receptor/channel do CCB target?

A

L type Ca channels

83
Q

What are the 3 types of CCB?

A

Dihydropyridines
Benzothiazepines
Phenylalkylamines

84
Q

What are examples of dihydropyridines?

A

Nifedipine, Nimodipine, nicardipine, and clevidipine

85
Q

What is an example of a benzothiazepines?

A

Diltiazem!

The both have Zs in their name!

86
Q

What is an example of a phenylalkylamine?

A

Verapamil

87
Q

Which two CCB are better for controlled HR or contractility?

A

Verapamil and diltiazem

88
Q

In what order do CCBs IMPAIR contractility?

A

Verapamil > nifedipine > diltiazem > nicardipine

89
Q

In a patient with reduced EF, what medication would be best to preserve contractility while reduced HR?

A

Diltiazem

90
Q

What medications are best used for treatment of HTN from elevated SVR?

A

Nifedipine and nicardipine

91
Q

What is the only CCB that is proven to reduce M&M from cerebral vasospasm?

A

Nimodipine

92
Q

Which CCB is also useful as a coronary antispasmodic?

A

Nicardipine

93
Q

Do CCB produce great arterial or venous relaxation?

A

Arterial!!!

**they preserve preload while decreasing afterload

94
Q

What is useful in treating angina/MI in those who may be unable to tolerate B1 antagonists?

A

Verapamil

95
Q

Which CCB is highly selective for arterial smooth muscle with negative chronotropic or inotropy effects?

A

Clevidipine

96
Q

What drug is useful in treating acute HTN, even in the setting of pheochromocytoma and intracerebral hemorrhage?

A

Clevidipine

97
Q

Which drug does not improve or maybe even worsen mortality in those with acute MI?

A

Nifedipine

98
Q

What drug is often prescribed for Raynaud’s?

A

Nifedipine

99
Q

Which CCB is best with CHRONIC HTN?

A

Nicardipine

100
Q

Which vasodilator dilates stenotic coronary arteries?

A

Nitroglycerin

101
Q

Which vasodilator produces coronary steal?

A

Nitroprusside

102
Q

Which vasodilator activates K-ATP channels?

A

Hydralazine

103
Q

Which vasodilator causes hypertrichosis?

A

Minoxidil

104
Q

What are some traits about nitroglycerin?

A

Action: venodilator with reduced afterload
Dose: 5-100 mcg/min
Onset: 2-5 mins
Duration: 5-10 mins
Notes: large coronary arteries may dilate; liver metabolism

105
Q

What are some traits about Nitroprusside?

A

Action: reduces AFTERLOAD and PRELOAD
Dose: 0.3-10 mcg/kg/min
Onset: seconds
Duration: < 5 mins
Notes: potential for cyanide toxicity; liver metabolism

106
Q

What are some traits about hydralazine?

A

Action: arterial smooth muscle dilator
Dose: 2.5-20 mg
Onset: 2-20 mins
Duration: up to 12 hrs!
Notes: patience with dosing d/t slow onset AND offset. Don’t burn yourself; liver metabolism

107
Q

What was nitroglycerin first used for?

A

Dynamite!

108
Q

The vasodilators effect of nitroglycerin is greater on what?

A

Venues!

109
Q

How does NTG exert its action?

A

Liberation if nitric oxide

110
Q

How does NTG improve the balance of O2 supply?

A

Direct coronary vasodilator and system effects (lowers preload)

111
Q

What med is an excellent first-line treatment for cardiac ischemia?

A

NTG ~ dilates even stenotic vessels, preventing vasospasm

112
Q

Why isn’t Nitroprusside used in MI tx?

A

It can produce coronary steal! Redistributing blood away from ischemic sites

113
Q

Is reflex tachycardia worse with Nitroprusside or NTG?

A

nitroprusside ~ it’s a great arterial dilator

114
Q

What is produced in SNP metabolism?

A

Cyanide

This inhibits aerobic metabolism

**Also bonds with hemoglobin to form methemoglobin and binding to sulfur to form thiocynate

115
Q

What is the action of hydralazine?

A

Activation of K(ATP) channels ~ reducing intracellular Ca.

116
Q

Which medication is now used for topical hair loss?

A

Minoxidil

117
Q

What are the PDE5 inhibitors?

A

Sildenafil
Tadalafil
Vardenafil

118
Q

How do PDE5 inhibitors work?

A

Increase levels of cGMP ~ this enhances nitric oxide vasodilation

**esp in the lungs and penis
Great to promote pulmonary vasodilation and decrease pHTN

119
Q

What are examples of PDE4 inhibitors?

A

Roflumast, apremilast, ibudilast

120
Q

How do PDE4 inhibitors work?

A

They increase levels of cAMP ~ this causes airway smooth muscle relaxation in those hyperactive airways .

(Also work for treating inflammatory states)

121
Q

What is an example of a PDE3 inhibitor?

A

MILRINONE and cilostazol

122
Q

How does PDE3 inhibitors work?

A

They increase levels of cAMP and cGMP ~ this increases inotropy in the heart and relaxation of vascular and airway smooth muscle.

Also called inodilators

123
Q

how do PDE5 inhibitors affect platelet function?

A

They prevent platelet aggregation

124
Q

What are vasopressin’s endogenous roles?

A

Water, osmolar, and BP homeostasis

125
Q

What are ACEi best suited for?

A

HTN r/t increased renin production

***first lien therapy for HTN, CHF, mitral regurge, and LV dysfunction

126
Q

What is the main side effects of acei?

A

> Dry cough ~ blocked degradation of bradykinin (which is a pulmonary inflammatory mediator)

> Angioedema > blocked degradation of bradykinin

> profound Hypotension that is refractory to neo, NE, or ephedrine

127
Q

What are ARBs?

A

Angiotensin receptor blockers
Have a greater affinity for AT1 receptors

***ACE inhibitors work on both AT1 and AT2 receptors

128
Q

Which medications provide renal protection for patients with DM?

A

ARBs

129
Q

How do volatile anesthetics affect the EKG waveform?

A

They all prolong the QT interval d/t inhibition of K+ efflux that normally causes repolarization

130
Q

What type of antiarrhythmic is lidocaine?

A

1B

131
Q

What enzyme converts angiotensinogen to angiotensin 1?

A

Renin

132
Q

What determines the HR of a transplanted heart?

A

Intrinsic rate of the SA node (100-120)

133
Q

What type of drugs must be given in a patient with a transplanted heart?

A

Medications that DIRECTLY stimulate the SA node

(Epi, isuprel, glucagon)

134
Q

Do carotid massages or the valsalva maneuver have any effect on the denervated heart?

A

No!

135
Q

What are Paragangliomas?

A

Neuro endocrine tumors that arise from neural crest cells.

(Similar to pheochromocytoma, BUT exist outside of the adrenal gland)

**location determines S&S

136
Q

Although paragangliomas rarely secrete vasoactive substances, if they did, what is the most common?

A

NE

137
Q

What medication is used to treat carcinoid-like syndrome?

A

Octreotide

138
Q

What is multiple system atrophy?

A

Degeneration and dysfunction of diverse central system structures (such as basal ganglia, cerebella’s cortex, locus coeruleus, pyramidal tracts)

**this was formally called shy-drager syndrome

139
Q

What are S&S of multiple system atrophy? Aka Shy-Drager syndrome?

A

Urinary retention
Bowel dysfunction
Impotence
Postural hypotension
Failure of baroreceptors to produce an increase in HR or vasoconstriction in response to hypotension

140
Q

When does death from cerebral ischemia (associated with prolonged hypotension) occur?

A

Within 8 years

141
Q

Which antiemetics have anticholinergic properties?

A

Benadryl
Promethazine

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