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Pharm > final > Flashcards

final Flashcards

1
Q

Describe the types of beta recepetors

A

B1, B2, B3

GPCR

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2
Q

Difference in beta action when occupied by agonist vs antagonist

A

agonist
• Activates adenylyl cyclase to produce cAMP
• Enhances Ca++ influx
•Chronotropic, inotropic, and dromotropic effects

antagonist:
inhibition of adenylyl cyclase to produce cAMP
chronotropic, inotropic and dromotropic effects

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3
Q

How do beta-antagonist work

A

Selective affinity for b-adrenergic receptors
NOT necessarily specificity
Selectivity dose dependent response

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4
Q

What type of drugs are beta-antagonist

A

Competitive antagonists

Large concentrations of agonist can out-compete and displace the b-antagonist

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5
Q

benefits of beta blockers

A

 May restore receptor responsiveness
• After desensitization from over exposure to catecholamines (tachyphylaxis)
 Protect myocytes from perioperative ischemia and infarction
 decrease arterial vascular tone and reduce afterload
 Decrease CO
 inhibit renin release

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6
Q

Cardiac effects of beta blockers

A
  • Negative inotrope
  • Negative chronotrope
  • Delay conduction speed through AV node
  • Decrease phase 4 depolarization
  • Increase diastolic coronary perfusion time
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7
Q

Indications for beta blockers

A
  • Excessive SNS stimulation
  • Noxious stimuli, acute cocaine ingestion
  • Thyrotoxicosis
  • Cardiac dysrhythmias
  • SCIP
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8
Q

beta blocker scip protocol

A

Beta blockers w/in 24 hrs
Esp for:
Pt at risk for MI
Pt already on beta blocker

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9
Q

Which beta antagonist would be best used in the asthmatic pt

A

selective B1 antagonist

atenolol, metoprolol, esmolol

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10
Q

Examples of B1 selective agents

A

Atenolol

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11
Q

Benefits of B1 antagonists

B1 selectivity

A

Does not cause:
Vasodilation
Bronchoconstriction

Increases diastolic filling time

Selectivity about 75%

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12
Q

Clearance for metoprolol, atenolol and esmolol

A 
metoprolol= hepatic
Atenolol= renal
Esmolol = plasma hydrolysis
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13
Q

Do metoprolol, atenolol, and esmolol have active metabolite

A

No

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14
Q

Metoprolol
E 1/2 time
protein binding
adult iv dose

A

E 1/2 time = 3-4 hrs
protein binding= low
adult iv dose= 1-15 mg

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15
Q

Atenolol
E 1/2 time
protein binding
adult iv dose

A

E 1/2 time= 6-7 hr
protein binding= low
adult iv dose= 5-10 mg

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16
Q

Esmolol
E 1/2 time
protein binding
adult iv dose

A

E 1/2 time = 0.15 hr (9 min)
protein binding= low
adult iv dose= 10-80 mg

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17
Q

Propranolol
REceptor site
Drawbacks

A

Receptor site: B1 = B2 activity

Drawbacks: HR slowing LONGER than negative inotropic effects

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18
Q

How does dosing differ for propranolol

A

Very pt specific
Can have 20-fold difference in plasma concentrations after PO
Dosing ranges from 40-800 mg/day

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19
Q

Propranolol effects on amide LA and opioids

A

decreases clearance

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20
Q

Which drugs’ clearance are affected by the use of propranolol
Considerations for administration of those drugs

A

amid LAs
opioids

May affect redosing of opioids and LAs

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21
Q

What is the beta antagonist of choice that will still maintain B2 funcion

A

Atenolol

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22
Q

Which beta blocker is the most B1 selective

A

Atenolol

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23
Q

Perioperative cardiac effects of atenolol

A

VERY cardio-protective

May decrease cardiac complications from surgery in CAD pts for up to 2 years

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24
Q

Effects of atenolol on blood glucose

A

does not potentiate insulin-induced hypoglycemia

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25
Q

CNS effects of atenolol

A

less entering CNS

so less fatigue

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26
Q

Atenolol dose

A

5 mg q 10 min IV

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27
Q

Metoprolol formulations

What is the action and dosing difference

A

Tartrate:
E1/2 2-3 hrs
bid/qid dosing

Succinate:
E1/2 5-7 hrs
qd dosing

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28
Q

Possible drawbacks to metoprolol succinate

A

May cause withdrawal tachycardia

Could be cause of postop HR increase

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29
Q

Metoprolol dosing

A

1 mg q 5 IV

for total 5 mg

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30
Q

which b-blocker has the most rapid onset and offset

A

Esmolol
Onset = 5 min
Offset = 10-30 min

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31
Q

Which beta blocker would be most useful for rapid blunting of SNS effects from noxious stimuli

A

esmolol

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32
Q

How is esmolol metabolized

A

Plasma esterases (distinct from plasma cholinesterases)

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33
Q

Esmolol dosing

A

20-30 mg IV

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34
Q

Beta blocker drug interactions

A

Cimetidine
Concurrent CCB use
Potentiates insulin effects
Anesthetic

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35
Q

How are beta blockers affected by cimetidine

A

Metoprolol has decreased 1st pass metabolism

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36
Q

Risk of concurrent use of CCBs and b-blockers

A

bradyarrhythmias

HF

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37
Q

What effects do b-blockers have on insulin and blood glucose

A

Potentiates insulin effects

prevents glycogenolysis (specific to B2-antag activity)
May cause hypoglycemia
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38
Q

Possible anesthetic interactions with beta antagonist

A
  • Potential additive(?) myocardial depression
  • Greatest with enflurane, least with isoflurane
  • Not significant between 1-2 MAC
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39
Q

Which patients would most benefit from b1 selective antagonists

A

Asthma

Diabetic

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40
Q

Example of mixed beta/alpha antagonist

A

Labetolol

Carvedilol

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41
Q

Which selective receptors are affected by labetolol administration

A

Selective alpha1

non-selective B1 and B2 antagonist effect

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42
Q

Which receptor effect is greater with labetolol use

A

Beta to alpha
7:1

beta effect 7x greater than alpha

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43
Q

Labetolol MOA

A

•Lowers systemic BP by ↓ SVR (alpha1 antagonist and beta2 agonist effects)

NO reflexive tachycardia effects from decreased SVR compensation

44
Q

Which drug may be appropriate for a pt w/ mixed SBP and DBP HTN

A

Labteolol

45
Q

Labetolol
Dose
Maximum effect time

A

Dose: 2/5-5 mg IV (up to 10 mg)

Max effect time: 5-10 min IV

46
Q

Use of sympathomimetics

A
  • Increase myocardial contractility

* Increase systemic blood pressure

47
Q

Sympathomimetics that lack B1 specificity may have what effects

A
  • Cause intense vasoconstriction

* Reflex-mediated bradycardia

48
Q

Sympathomimetic MOA

A
  • Activate directly or indirectly beta or alpha adrenergic GPCR
  • cAMP enhance Ca influx to increase concentrations
  • Actin and myosin interact more forcefully
49
Q

What are the differences in direct and non-direct sympathomimetics

A

Direct:
• Directly activate adrenergic receptors

Indirect:
• Evoke the release of norepi from postganglionic sympathetic nerve endings

50
Q

Examples of direct and indirect sympathomimetics

A

Direct: Epi, norepi, phenylephrine, dopamine

Indirect: Ephedrine, phenylephrine (sometimes)

51
Q

Which receptors does epinephrine act on

A

Alpha, beta1 and beta2

Beta effects greater than alpha

52
Q

Which receptors dose phenylephrine act on

A

alpha receptors

53
Q

Comparative CO effects of epinephrine, ephedrine, phenylephrine and vasopressin.

A

Epi, ephedrine, vaso = INCREASE CO

Phenylephrine has no effect on CO

54
Q

Comparative HR effects of epi, ephedrine, phenylephrine and vaso

A

Epi and ephedrine = INCREASE HR

Phenyleph and vaso = no HR effect

55
Q

Comparative PVR effects of epi, ephedrine, phenyleph, and vaso

A 
Phenylehp = MOST effective on PVR
Vaso = mid-range effect on PVR
Epi/ephedrine = less effect on PVR
56
Q

Receptor effects of epi

A

Alpha 1 and 2= cutaneous, splanchnic and renal bed vasoconstriction
Beta 1 = increased HR and CO
Beta2= skeletal muscle vasodilation, bronchodilation

57
Q

Epi effects on renal vessels compared to norepi

A

Epi has 2-10x greater effect than norepi

58
Q

Dosing and DOA for epi

A

Single dose = 2-8 mcg

DOA = 1-5 min

59
Q

Infusion dosing and receptor effects of epi

A

1-2 mcg/min = beta 2 effects
4 mcg/min = beta 1 effects
10-20 mcg/min = mostly alpha effects (decreased peripheral perfusion**)

60
Q

Indications for use of ephedrine

A

Commonly used in sympathetic depression caused by inhaled or injected anesthetics

61
Q

BP effects of ephedrine

A

-BP response much less intense (10x

62
Q

Drawback of ephedrine

A

Increased used leads to tachyphylaxis d/t DEPLETED NOREPI stores

63
Q

Why does ephedrine lead to tachyphylaxis

A

D/t depleted norepi stores from indirect action of ephedrine to increase availability of norepi
Ephedrine effects are dependent on norepi availability

64
Q

Ephedrine use in pregnancy

A

Generally, the preferred sympathomimetic for hypotension d/t SAB

Does not affect uterine blood flow

65
Q

Effects of phenylephrine on parturient patients

A

Equal BP response to ephedrine

Phenyleph increases neonate umbilical pH (so baby is less acidic)

May be more beneficial for neonate

66
Q

Vascular effects of phenyleph

A

Venoconstriction > arterial constriction

67
Q

MOA of phenyleph

A

DIRECT:
Mostly stimulates alpha1 receptors
Indirect:
releases small amounts of norepi

68
Q

How does phenyleph compare to norepi

A

Clinically mimics norepi

  • less potent
  • longer acting
69
Q

Uses for phenyleph

A

To treat hypotension d/t
SNS blockade by regional
Inhaled/injected anesthetics
CAD and AS pts

70
Q

Why is phenyleph most useful in AS pateitns?

A

It maintains afterload

Does not increase heartrate

71
Q

Common phenyleph administration

A

IVP and IV gtt

72
Q

Drawbacks to phenyleph use?

A

Reflex bradycardia

73
Q

MOA of vasopressin

A
  • Stimulates vascular V1 receptors to cause arterial vasoconstriction
  • Increases renal-collecting duct permeability so water is reabsorbed
74
Q

Vasopressin uses

A
  • effective in reversing catecholamine-resistant hypotension

* ACE-I resistant hypotension

75
Q

Side effects of Vaso (CV, GI, hem)

A 
CV= coronary artery vasoconstriction
GI = stimulates GI smooth muscle (abd pain, N/V)
Hem= decreased platelet counts and antibody formation
76
Q

Which drugs are more effective at venodilation (minoxidil, SNP, NTG, hydralazine)

A

Nitrates(NTG) > SNP > Minoxidil > hydralazine

77
Q

Which drugs are more effective at arterial dilation (minoxidil, SNP, NTG, hydralazine)

A

Hydralazine > minoxidil > SNP > nitrates(NTG)

78
Q

Basic MOA of NO

A

A chemical messenger that affects cGMP and decreases intracellular Ca ions which relaxes vessels

79
Q

Physiologic actions of NO

A 
CV tone relaxation
Platelet regulation
CNS NT
GI smooth muscle relaxation
Immune modulation
Effector molecule for volatile anesthetic
Pulm artery vasodilation
80
Q

MOA of SNP

A

Causes relaxation of arterial and venous vascular smooth muscle
More potent arterial dilator

81
Q

Administration considerations for SNP

A

Immediate onset and offset
Requires continuous administration
Requires invasive arterial monitoring
Can lead to Cyanide toxicity

82
Q

Adverse effects of SNP and why it occurs

A

SNP dissociates immediately upon contact oxyhgb
methemoglobin
releases cyanide and NO
Cyanide can build up with prolong use

83
Q

Uses of SNP

A 
When rapid HTN treatment:
Aortic surgery
pheochromocytoma
Spine surgery
Hypertensive emergencies with carotid surgeries
84
Q

When may cyanide toxicity be a concern with SNP administration

A

With prolong use of high doses

Causes accumulation of cyanide d/t sulfur donors

85
Q

What are some suspicions of cyanid toxicity with SNP use

A

 Increasing doses SNP
 Increased mixed-venous sats….tissues aren’t using oxygen
 Metabolic acidosis
 CNS dysfunction/change in LOC occurs

86
Q

MOA of NTG

A

Acts on venous capacitance vessels and large coronary arteries with dilatory effects

Leads to
venous pooling
relaxation of arterial vascular smooth muscle (high dose)

87
Q

Problems with prolong use of NTG

A

Can lead to tachyphylaxis which is
Dose and duration dependent
Limits vasodilation
Requires drug free interval (12-15 hrs)

88
Q

SNP dosing

A

0.3 mcg/kg/min to 10 mcg/kg/min

89
Q

Dosing of NTG

A

0.5-1 mcg/kg/min or IVP

90
Q

Uses of NTG

A

AMI
Acute HTN
Controlled hypotension
Sphincter of Oddi spasm

91
Q

How does NTG aid in treating AMI

A

relieves pulm congestion
decreases O2 requirements
Limits MI size

92
Q

How does NTG used in controlled hypotension situations

A

Less potent than SNP

Relates to intravascular fluid volume d/t venous dilation

93
Q

How does NTG aid w/ sphincter of Oddi spasm

A

Help determine whether it is chole or opioid related.

94
Q

MOA of hydralazine

Dosing

A

 Direct, systemic arterial vasodilator
• Decreases ITP, ↓ Ca++ release

Initial dose = 2.5 mg IV

95
Q

Side-effects of hydralazine

A

Extreme hypotension

Rebound tachycardia

96
Q

Drawback to hydralazine use

A

Onset = takes about 1 hour to reach peak plasma concentration

97
Q

What are the types of CCBs and the difference in each.

A
  • Phenylalkylamines: selective for AV node
  • Benzothiazepines: selective for AV node
  • Dihydropyrimidines: selective for arteriolar beds
98
Q

MOA of CCBs

A
  • Bind to receptors on VG calcium ion channels (L-type; main pathway)
  • Decrease calcium influx
  • inhibits excitation-contraction coupling
99
Q

Effects of CCBs (4)

A

-Decrease vascular smooth muscle contractility which leads to:
+peripheral vasodilation
+decrease SVR and SBP

  • Increase coronary blood flow
  • Decreases speed of conduction through AV node
100
Q

Use of nicardipine
Dosing
MAX

A

Short-term control of HTN

Dose:
• 5mg/hr (50 ml/hr)
• Increase 2.5 mg/hr (25 ml/hr) x 4 to max of 15mg/hr (150 ml/hr)
• Decrease to 3mg/hr (30ml/hr)

50% drug decrease 30 minutes after D/C

Max = 15 mg/hr

101
Q 
Nicardipine effects on:
HR
Myocardial depression
SA node depressoin
AV node conduction
Coronary artery dilation
Peripheral artery dilation
A 
HR = Inc or NC
Myocardial depression = slight
SA node depression = 0
AV node conduction= 0
Coronary artery dilation= greatest 
Peripheral artery dilation= Marked
102
Q

Comparative HR effects of verapamil, nifedipine, nicardipine, diltiazem

A 
Slows = verapamil, diltiazem
Inc/NC = nifedipine, nicardipine
103
Q

Comparative Myocardial depression effects of verapamil, nifedipine, nicardipine, diltiazem

A 
Moderate = verapamil, nifedipine, diltiazem
Slight= Nicardipine
104
Q

Comparative SA node depression effects of verapamil, nifedipine, nicardipine, diltiazem

A 
Moderate= verapamil
None= nifedipine, nicardipine
slight = diltiazem
105
Q

Comparative AV node conduction effects of verapamil, nifedipine, nicardipine, diltiazem

A 
Marked= verapamil
Moderate= diltiazem
none= nifedipine, nicardipine
106
Q

Comparative coronary artery dilation effects of verapamil, nifedipine, nicardipine, diltiazem

A 
Greatest = Nicardipine
Marked= nifedipine
Moderate= verapamil, diltiazem
107
Q

Comparative peripheral artery dilation effects of verapamil, nifedipine, nicardipine, diltiazem

A 
Marked= nicardipine, nifedipine
Moderated= Verapamil, diltiazem

Pharm (4 decks)

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