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Spring '20/ L. Pharm Exam 3 - sympatholytics/mimetics, LAs, antiarrhythmics, vaso > SYMPATHOLYTICS > Flashcards

SYMPATHOLYTICS Flashcards

1
Q

Beta Adrenergic Receptor Antagonists bind where? create what response?

A

beta receptors

interfere with the ability of catecholamines or other sympathomimetics to provide beta responses

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2
Q

Beta Adrenergic Receptor Antagonists- prevents effects of ____ and _____ on the _____ and ______ of the airways and blood vessels.

A

Beta adrenergic blockade prevents the effects of catecholamines and sympathomimetics on the heart and smooth muscles of the airways and blood vessels.

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3
Q

Beta Adrenergic Receptor Antagonists- why must these be give periop?

A

must be maintained periop to maintain effects and avoid sympathetic nervous system hyperactivity with abrupt D/C of these drugs

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4
Q

Beta Adrenergic Receptor Antagonists- what drug is the standard to which all other beta adrenergic antagonist are compared

A

Propranolol

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5
Q

Beta Adrenergic Receptor Antagonists: mao- are they competitive or noncompetitive binders?

A

Exhibit selective affinity for beta adrenergic receptors, where thy act by competitive inhibition.

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6
Q

Beta Adrenergic Receptor Antagonists: mao- because its reversible what does that mean for beta agonist

A

Binding of an antagonists to beta adrenergic receptors is reversible such that the drug can be displaced if enough agonist drugs are available. Sufficiently large doses of an beta agonist may still exert a full pharmacologic effect.

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7
Q

Beta Adrenergic Receptor Antagonists: mao- chronic administration of beta adrenergic antagonist means what for the receptors?

A

up regulation of beta receptors

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8
Q

beta receptors mao- tell me about the G protein on these receptors. If NE or EPI occupy a beta receptor what happens

A

Beta adrenergic receptors are G protein-coupled receptors and their occupancy by agonists (norepinephrine, epinephrine) stimulates G proteins that in turn activate cAMP.

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9
Q

what is the net effect of beta adrenergic agonist stimulation in the heart

A

positive effects of:
Chronotropic - heart rate
Inotropic- contractility
Dromotropic- electrical condition

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10
Q

Beta Adrenergic Receptor Antagonists- net effect of beta adrenergic antagonist blunt what effects

A

chronotropic
inotropic
dromotropic

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11
Q

what percent of beta receptors are beta 1 in the myocardium what percent are beta 2

A

~ 75% of beta receptors in the myocardium are Beta 1 while ~ 20 % are Beta 2

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12
Q

Beta Adrenergic Receptor Antagonists- derivatives of what drug?

A

Beta agonist drug isoproterenol

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13
Q

Beta Adrenergic Receptor Antagonists- what determines the ability of the drug to act as a agonist or antagonist.

A

Substitutions on the benzene ring determine whether the drugs acts as an agonists or antagonist

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14
Q

Beta Adrenergic Receptor Antagonists- which drugs are non selective beta 1 & beta 2

A

Propranolol
Nadolol
Timolol
Pindolol

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15
Q

Cardioselective Beta 1: (6)

A 
Metoprolol
Atenolol
Acebutolol
Betaxolol
Esmolol
Bisoprolol
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16
Q

beta antagonist receptor selectivity is… dependent on what?
what makes it less selective?

A

Beta receptor selectivity is dose dependent and is lost when large doses of the antagonist are administered.

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17
Q

Beta Adrenergic Receptor Antagonists- what are they classified as?

how do they classify that?

A

Beta adrenergic antagonists are also classified as partial or pure antagonists based on the presence or absence of intrinsic sympathomimetic activity.

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18
Q

Beta Adrenergic Receptor Antagonists- which patient population is better suited for cardiac selective beta 1 receptor drugs?

A

Cardiac selective Beta 1 receptor drugs are better suited for administration to patients with asthma and reactive airway disease

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19
Q

what patients are better suited for cardio selective drugs beta 1?

A

Theoretically, cardioselective drugs are better suited for treatment of patients with essential hypertension since these drugs lack inhibition of peripheral Beta 2 receptors that produce vasodilation

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20
Q

beta 1 receptor blockade effects

A

Slows sinus rate
Slows conduction of cardiac impulses through AV node
Decreases inotropy

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21
Q

Beta Adrenergic Receptor Antagonists- when are beta 1 effects greater?

A

These effects are relatively greater during activity than during rest

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22
Q

Beta Adrenergic Receptor Antagonists

beta 1 effects on the 02 demand during exercise

A

Decreases myocardial O2 demand with subsequent decrease in occurrence of myocardial ischemia during exercise.

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23
Q

Beta Adrenergic Receptor Antagonists- beta 1 effects on diastolic function

A

increases diastolic perfusion time which may enhance myocardial perfusion

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24
Q

Beta Adrenergic Receptor Antagonists- beta 2 receptor blockade- have increased risk of

A

bronchospasm in patients with restrictive airway disease and can worsen symptoms of PVD

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25
Q

Beta Adrenergic Receptor Antagonists half time for esmolol vs other drugs

A

Principle difference in pharmacokinetics b/t all the beta adrenergic receptor antagonists is the elimination half-time range from:
Brief: esmolol ~ 10 minutes
Other drugs that can be hours

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26
Q

Beta Adrenergic Receptor Antagonists- how is propranolol plasma protein bound?

A

Among the beta adrenergic receptor antagonists only Propranolol is highly plasma protein bound 90-95%

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27
Q

Beta Adrenergic Receptor Antagonists- what is the volume distribution

A

Volume of distribution of beta adrenergic receptor antagonists is high and are rapidly distributed following IV administration

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28
Q

Beta Adrenergic Receptor Antagonists- MI what should they receive

A

It is recommended that all patients who experience an acute MI receive IV beta adrenergic antagonists unless contraindicated

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29
Q

Beta Adrenergic Receptor Antagonists- MI and reperfusion therapy?

A

They should receive IV beta blocker therapy whether or not they receive reperfusion therapy

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30
Q

Beta Adrenergic Receptor Antagonists- contraindications

A

Severe bradycardia

Unstable LV failure

AV heart block

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31
Q

Beta Adrenergic Receptor Antagonists- relative contraindications? (4)

A

Asthma

Reactive airway disease

Mental depression

PVD

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32
Q

Beta Adrenergic Receptor Antagonists- what are the diabetic considerations

A

DM is not a contraindication to the use of beta adrenergic receptor antagonists but can mask signs hypoglycemia

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33
Q

Beta Adrenergic Receptor Antagonists- which produce cardio protective effect

A

Cardio protective effect is present with both cardioselective and nonselective beta antagonists

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34
Q

periop- beta blockade is recommended for patients considered at risk for myocardial ischemia name 4 disease risk factors

high risk surgeries include (4)

A

CAD
Positive Preop Stress Test
DM using insulin
LV hypertrophy

Vascular
Thoracic
Intraperitoneal surgery
Anticipation of large blood loss

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35
Q

Beta Adrenergic Receptor Antagonists- goal of preop resting HR

A

Goal of preop therapy is resting HR of 65-80 bpm

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36
Q

benefits of beta adrenergic receptor antagonist?

A

All beta adrenergic receptor antagonists except those with intrinsic SNS activity, decrease mortality

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37
Q

Beta Adrenergic Receptor Antagonists-name the most important potentially reversible risk factor for mortality and cardiovascular complications after noncardiac surgery

A

Periop myocardial ischemia

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38
Q

Beta Adrenergic Receptor Antagonists- benefits of atenolol for 7 days before and after non cardiac surgery in patients at risk for CAD does what

A

decrease mortality and incidence of CV complications for as long as 2 years after surgery

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39
Q

beta blocker- Preop. PO can be initiated with either:
drug 1 dose?
drug 2 dose?
drug 3 dose?

A

Atenolol 50 mg

Bisoprolol 5-10 mg

Metoprolol 25-50 mg

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40
Q

Beta Adrenergic Receptor Antagonists- morning of surgery what 2 drugs can we titrate? and what are their doses?

A

atenolol 5-10 mg

or

metoprolol 5-10 mg can be titrated.

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41
Q

Beta Adrenergic Receptor Antagonists- what drug is used during surgery and post op ICU

A

Esmolol is acceptable drug to achieve beta blockade during surgery and postop in ICU

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42
Q

Beta Adrenergic Receptor Antagonists- which drugs can be given IV until patient can take PO

A

IV atenolol or metoprolol can be administered until pt can take PO atenolol or bisoprolol

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43
Q

Labetalol- which receptors?

A

Exhibits selective alpha 1 and nonselective Beta 1 and 2 antagonists

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44
Q

Labetalol- what about alpha 2 receptors

A

Presynaptic alpha 2 receptors are spared by labetalol such that released norepinephrine can continue to inhibit further release of catecholamines via the negative feedback mechanism resulting from stimulation of alpha 2 receptors.

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45
Q

Labetalol- metabolism by what?

how much unchanged in the urine

A

Metabolism is by conjugation of glucuronic acid

5% unchanged in the urine

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46
Q

Labetalol- elimination half time?

elimination prolonged in ?

elimination is unchanged by what?

A

Elimination half time is 5-8 hours
Elimination is prolonged in liver disease
Elimination is unchanged by renal dysfunction.

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47
Q

Labetalol- oral dose? how often?

iv dose?

A

Oral (100-600 mg BID) and IV doses available

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48
Q

Labetalol- how does it lower BP

A

Labetalol lower systemic BP by decreasing SVR (alpha 1 blockade) and reflex tachycardia triggered by vasodilation is attenuated by simultaneous beta blockade.

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49
Q

Labetalol- CO

A

CO unchanged

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50
Q

Labetalol- how does it vasodilate?

A

Vasodilation is by alpha 1 blockade and maybe by vasodilation mediated by beta 2 agonist activity as well

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51
Q

Labetalol- IV dose? how fast does it work?

A

Max systemic BP lower effect of an IV dose of 0.1 – 0.5 mg/kg is present in 5-10 minutes

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52
Q

Labetalol- can it be used in hypertensive emergencies

A

Safe to use in hypertensive emergencies

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53
Q

Labetalol- how is this used with EPI overdose

A

Has been used to control severe hptn associated with epinephrine overdose

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54
Q

Labetalol- large dose may do what? what is a large dose? what is an appropriate dose

A

Large doses 2 mg/kg IV may over treat and have excessive decreases in BP. Smaller doses 20 – 80 mg IV are less likely to produce undesirable decreases in BP

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55
Q

Labetalol the appropriate dose can be repeated how often

A

Repeated doses of 20 – 80 mg every 10 minutes until desired therapeutic response if achieved.

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56
Q

Labetalol- how is it used with pheochromocytoma? how is it used in clonodine withdrawal?

A

Rebound hptn after withdrawal of clonidine therapy and hypertensive responses in patients with pheochromocytoma can be effectively treated with labetalol.

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57
Q

Labetalol- how is it used for angina

A

Effective in angina pectoris

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58
Q

Labetalol- what dose is best used for surgical stimulation increased HR and BP

A

Can be used (0.1 to 0.5 mg/kg IV) when increase in surgical stimulation cause increases in HR and BP

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59
Q

Labetalol- side effects

prolonged used will cause ?

A

Orthostatic hypotension: most common
Bronchospasm is possible
Prolonged chronic therapy causes fluid retention and a diuretic is given with for prevention.

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60
Q

CCB- what is this also called?

A

Also called calcium entry blockers and calcium antagonists

61
Q

ccb- where does it interfere with calcium movement across what two places

A

Selectively interferes with inward calcium ion movement across myocardial and vascular smooth muscle cells.

62
Q

ccb-Classified based on chemical structure:

Phenylalkylamines:

Dihydropyridines:

Benzothiazepines:

A

Phenylalkylamines: selective for atrioventricular node

Dihydropyridines: selective for arteriolar beds

Benzothiazepines: selective for atrioventricular node

63
Q

ccb- common side effects (4)

A

Hypotension

Peripheral edema

Flushing

Headache

64
Q

CCBs produce:

A

Decreased myocardial contractility
Decreased HR
Decreased activity of the SA node
Decreased rate of conduction of cardiac impulses through AV node
Vascular smooth muscle relaxation with associated vasodilation
Decreases in systemic BP

65
Q

What were the results of the POISE trial

what were the criticisms of the trial

A

increased mortality by increase in cerebrovascular events

aggressive BB dosing, without considering patient baseline hemodynamics- leads to cerebrovascular hypo perfusion.

patients had BP reduction >30% below preoperative levels

practitioners now start low dose BB preop- or wait until post op

66
Q

CCB- which are effective for treatment for coronary artery spasms

A

All CCBs are effective for treatment of coronary artery spasms

67
Q

CCB

A

Decreases vascular smooth muscle contractility
peripheral vasodilation with reduction in systemic vascular resistance
systemic blood pressure

68
Q

CCB- possess what type of ischemic effects

A

Possess anti-ischemic effects

69
Q

CCB- coronary arteries effect?

what drug complements ccb

A

Dilates coronary arteries via a different mechanism than nitrates thus these two classes complement each other in tx of coronary spasms.

70
Q

patient has chronic stable angina with fixed obstructive coronary artery lesions. what medication is effective for this

A

ccb

71
Q

ccb- which two drugs exert negative inotropic effects

A

All CCBs exert negative inotropic effects which are most significant with:
verapamil
diltiazem

72
Q

Phenylalkylamines
verapamil synthetic derivative of ?

supplied how?

A

Verapamil:

Synthetic derivative of papverine supplied in a racemic mixture

73
Q

Phenylalkylamines

verapamil side effects- AV node effect

A

Verapamil Side Effects:

Major depressant of the AV node

74
Q

Phenylalkylamines

Verapamil Clinical Uses:

A

Effective in tx of SVT

vasospastic angina pectoris

hptn

As effective as beta blockers in relieving angina pectoris

symptomatic hypertrophic cardiomyopathy with or without LV outflow obstruction

Should not be routinely given for acute MI as a post infarction mortality is not decreased

75
Q

Verapamil Clinical Uses: fetal and maternal

A

Useful in tx of maternal and fetal tachy dysrhythmias and premature labor
It prolongs atrioventricular conduction of the fetus despite limited placental transport of the drug.
Fetal hepatic extraction of verapamil is substantial
May decrease uterine blood flow
Use with caution in the parturient with impaired uteroplacental perfusion

76
Q

Verapamil: protein bound?

elimination half time

A

90% protein bound

Elimination half time 6-12 hours

77
Q

Nicardipine (Cardene): mechanism of action

A

Lacks effects on SA and AV nodes with minimal myocardial depressant effect

78
Q

Nicardipine

elimination half time

how many hours should elapse before increasing the oral dose

metabolized in the ___

% protein bound?

A

3-5hr
~72 hours should elapse before increasing oral dosage
Metabolized in the liver
Highly protein bound 95%

79
Q

Nicardipine Uses: for labor

A

Tocolytic drug with similar effects as salbutamol but with fewer side effects
It binds to the inside of myometrial L-type voltage-dependent calcium ion channels causing them to remain closed and thus inhibits uterine contractility.

80
Q

Nicardipine Uses: as a tocolytic with salbutamol?

A

Pulmonary edema associated with salbutamol used as a tocolytic has also been reported in a parturient treated with nicardipine

81
Q

Diltiazem does it interact with beta blockers?

A

Unlikely to interact with beta blockers to decrease myocardial contractility.

82
Q

Diltiazem Uses:

IV bolus dose

iv drip dose

A

Similar to those of verapamil
PO and IV
Manages angina pectoris: IV 0.25 - 0.35 mg/kg over 2 minutes repeated in 15 minutes if needed
After initial IV dose can be given continuous IV ~ 10 mg/hr up to 24 hours

83
Q

Pharmacokinetics: diltiazem

po onset & peak

% protein bound

% excreted bile
% excreted urine

A

PO: excellent absorption: onset of 15 minutes peak of 30 minutes
70-80% protein bound
Excreted in bile ~ 60% Urine ~35%

84
Q

Diltiazem Pharmacokinetics:
elimination half time
elimination half time metabolites

liver disease effects?

A

Elimination half time 4-6 hours for parent drug and 20 hours for metabolites
Liver disease may necessitate decreasing dosage.

85
Q

Drug Interactions verapamil and diltiazem- cardiac effects?

A

Verapamil and diltiazem have depressant effects on the generation of cardiac action potentials at the SA node and slows movement of the cardiac impulses through the AV node

86
Q

what can result in a patient with cardiac conduction abnormalities and concurrent administration of beta blockers or digoxin?

A

greater degrees of AV heart block

87
Q

Drug Interactions- ccb and volatile anesthetics

A

Myocardial depression and peripheral vasodilation produced by volatile anesthetics could be exaggerated by similar actions of CCBs (ppt)

Per page 496- no evidence that patients being treated chronically with CCB are at increased risk for anesthesia.

Yet, it also says patients with decreased ventricular function under anesthesia show further decrease with administration of CCB.

88
Q

what is the effect of calcium channel blockers in the hypovolemic patient

A

Exaggerated systemic hypotension if given in hypovolemic patients

89
Q

can calcium channel blockers be continued until the time of surgery?

A

Treatment with CCBs can be continued until the time of surgery without risk of significant drug interactions, especially with respect to conduction of cardiac impulses

90
Q

How do we treat overdoses of CCB

A

IV administration of calcium or dopamine.

91
Q

Anesthetic Drugs CCB caution for what patients

A

CCB must be administered with caution to patients with impaired LV function or hypovolemia

92
Q

Anesthetic Drugs- patients treated with beta blockers and nifedipine tolerate what?

A

Patients treated with beta blockers and nifedipine tolerate high dose fentanyl anesthesia and do not show evidence of additive depression of cardiac function when verapamil is infused.

93
Q

Anesthetic Drugs verapamil and anesthetized patients with preexisting lv dysfunction is associated with

A

Conversely in anesthetized pts with preexisting LV dysfunction administration of verapamil is associated with myocardia depression and decreased CO.

94
Q

Anesthetic Drugs verapamil or diltiazem during open chest surgery in patients with depressed ventricular function may be associated with …

A

IV administration of verapamil or diltiazem during open chest surgery in patients with depressed ventricular function and anesthetized with a volatile anesthetic may be associated with further decreases in ventricular function

95
Q

treating cardiac dysrhythmias with CCB’s in anesthetized patients results in what type of blood pressure?

what does it do to the PR interval?

A

Treatment of cardiac dysrhythmias with CCBs in anesthetized patients produces only transient decreases in systemic blood pressure and infrequent prolongation of PR interval

96
Q

Anesthetic Drugs- verapamil and digitalis or beta blockers caution. why?

A

Verapamil should be used cautiously in patients being treated with digitalis or beta blockers b/c of the tendency to produce AV heart block.

97
Q

with chronic use of CCB and Beta blockers do you see cardiac conduction abnormalities in the periop period

A

no

98
Q

beta agonist do what to the calcium channels in the myocardial cell membrane

A

Beta agonists increase the number of functioning slow calcium channels in myocardial cell membrane through a cAMP mechanism and readily counter the effects of CCBs

99
Q

what is a patient risk for anesthesia if they are chronically treated with ccb

A

NOT at increase risk for anesthesia

100
Q

What is the concern with CCB and neuromuscular blocking drugs.

A

CCBs potentiate the effects of depolarizing and non depolarizing NMBD.
Local anesthetic effects of verapamil and diltiazem reflecting inhibition of sodium ion flux via fast sodium channels may also contribute to the potentiation of NMBD.

101
Q

explain why ccb affect ACH release..how does this affect NMBD

A

Antagonism of NMBD may be impaired b/c of diminished presynaptic release of acetylcholine in the presence of a CCB- because you have less calcium.

102
Q

local anesthetics risk with CCB

A

verapamil & diltiazem have potent LA activity.

This may increase the risk of LAST when regional anesthesia is administered to patients being treated with these CCB

103
Q

What is the concern with CCB & potassium infusion?

A

CCB’s slow inward movement of K+. hyperkalemia in pts treated with verapamil may occur after small amounts of exogenous potassium infusion.

104
Q

SYMPATHOLYTICS - side effects of alpha adrenergic blockade (3)

A

orthostatic hypotension
baroreceptor mediated reflex tachycardia
impotence

105
Q

if you dont have beta adrenergic blockade what happens to cardiac stimulation from norepinephrine

A

maximim expression of cardiac stimulation from norepinephrine: leads to tachycardia (typically)

106
Q

what does the dextroisomer of verapamil show its activity?

A

The dextroisomer of verapamil has no activity at slow calcium channels and instead act on fast sodium channels accounting for local anesthetic effects of verapamil

107
Q

the fast acting dextroisomer of verapamil on sodium channels means this drug is good for what

A

local anesthetic

108
Q

how much more potent is verapamil than procaine

A

1.6 times as potent as procaine

109
Q

what is the levoisomer of verapamil responsible for

A

The levoisomer of verapamil is specific for slow calcium channels and accounts for the classification as a calcium blocking drug

110
Q

verapamil side effects

sa node

A

Negative chronotropic effect on SA node

111
Q

verapamil side effects

effect on cardiac muscle

A

Negative inotropic effect on cardiac muscle: exaggerated in pts with preexisting LV dysfunction

112
Q

verapamil side effects - coronary and systemic arteries

A

Moderate vasodilating effect on coronary and systemic arteries

113
Q 
verapamil should not be administered to 
1
2
3
4
A

heart failure

severe bradycardia

sinus node dysfunction

atrioventricular nodal block

114
Q

verapamil what effects may be enhanced in the presence of concomitant treatment with beta adrenergic antagonist.

A

Negative inotropic and chronotropic effects may be enhanced in the presence of concomitant tx with beta adrenergic antagonists.

115
Q

verpamile & patients with WPW concerns

A

My precipitate dysrhythmias in pts with WPW

116
Q

what drug may be useful to increase HR in presence of drug induced heart block.

A

Isoproterenol may be useful to increase HR in presence of drug induced heart block

117
Q

metoprolol- what receptor?

A

beta 1 antagonist

118
Q

metroprolol prevents what responses

A

inotropic & chronotropic

119
Q

what is the concern with large doses of metoprolol

A

large doses become nonselective betas exerting antagonist effects at b2 receptors as well as beta 1 receptors.

120
Q

what medication is used to reverse metoprolol’s beta 2 affects of increase in airway resistance

A

TERBUTALINE! (beta 2 agonist)

121
Q

protein binding of metoprolol

A

10% of the drug- low

122
Q

what does the beta 2 antagonist effects of propranolol do

A

increase peripheral vascular resistance

123
Q

how does propranolol affect clearance of local anesthetics

A

it decreases clearance of amide LA by decreasing hepatic blood flow and inhibiting metabolism in the liver.

124
Q

how does propranolol affect fentanyl

A

patients on chronic propranolol have decreased first pass uptake of fentanyl - 2-4x’s as much injected fentanyl enters the systemic circulation in the time period after injection

125
Q

why is nadolol unique

A

due to its long duration of action it is only administered 1/daily

126
Q

how is timolol effective in the treatment of glaucoma?

A

decreases intraocular pressure by decreasing production of aqueous humor

127
Q

describe the protein binding of timolol

A

not extensive

128
Q

timolol elimination half time

A

half time elimination is 4 hours

129
Q

what are the systemic issues of timolol

A

systemic absorption causes resting bradycardia and hypotension refractory to atropine

130
Q

how does betaxolol compare with timolol in bronchoconstriction?

A

betaxolol is cardioselective- less risk of airway hyperreactivity. safer to treat open angle glaucoma if patient at risk for bronchoconstriction.

131
Q

What is the prominent pharmacologic effect of bisoprolol

A

negative chronotropic effect- treats hypertension and improves survival in patients with mild to moderate HF

132
Q

What is the prominent pharmacologic effect of nebivolol

A

very potent and 3.5 more selective beta 1 than bisoprolol

133
Q

esmolol why is this useful for intubation

A

beta 1 when administered prior to intubation proves reliable protection against increases in HR and BP

134
Q

atenolol- which receptors

A

most selective beta 1 adrenergic antagonists

135
Q

why do we give atenolol

A

patients at risk for CAD who must have non cardiac surgery decreases their mortality if administered preop

136
Q

carvedilol indication for treatment

A

mild to moderate CHF & HTN

137
Q

carvedilol which receptors

A

nonselective b-adrenergic receptor antagonist and alpha 1 blocking

138
Q

calcium channel blocker MOA

A

binds to L type channel diminishing entry of calcium ions into cells.

139
Q

classification of CCB phenyalkylamine

A

verapamil

140
Q

classification of CCB benzothiazepine

A

diltiazem

141
Q

classification of CCB dihydropyridines

A 
nifedipine
nicardipine
nimodipine
isradipine
felodipine
amlodipine
142
Q

nicardipine dose for ECT. why do we use it for ECT therapy?

A

40 mcg/kg IV immediately before electroconvulsive therapy is effective in blunting acute hemodynamic responses to the treatment.

143
Q

name three drugs that can increase VERAPAMIL unbound pharmacological effect

A

Lidocaine, diazepam, propranolol can increase pharmacologically active, unbound portion of the drug

144
Q

what drug is first line to treat SVT

A

adenosine

145
Q

in addition to SVT what else does diltiazem treat

A

essential HTN

146
Q

mechanism of action of diltiazem

A

Blocks predominantly calcium channels of the AV node

Intermediate effects on the SA and AV nodes and vasodilating properties.

147
Q

which drug has the greatest vasodilation effect of all CCB

A

nicardipine

148
Q

where is vasodilation prominent with nicardipine

A

Vasodilation is prominent in the coronary arteries

149
Q

nicardipine..

A

Of all antianginal drugs, dihyropyridine calcium channel blockers produce the greatest dilation of the peripheral arterioles
Nicardipine and nifedipine may be particularly useful in pts who have residual hyptn despite beta adrenergic blockade
IV and PO preparations

Spring '20/ L. Pharm Exam 3 - sympatholytics/mimetics, LAs, antiarrhythmics, vaso (17 decks)

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