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Cardiovascular > Autonomic Pharm > Flashcards

Autonomic Pharm Flashcards

1
Q

2 common first line therapies for pregnancy

A

Methyldopa, Labetalol

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2
Q

4 Primary effects of ACh on CV system

A

Vasodilation, Dec HR, Dec AV Node conduction velocity, Dec force of contraction

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3
Q

a2 agonists are a useful adjuntive Rx, especially to block __

A

reflex tachycardia

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4
Q

A2 agonists are particularly useful in what type of patients

A

Diabetics and Asthmatics

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5
Q

a2 agonists have dose-dependent __

A

salt and water retention

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6
Q

A2 agonists that do not penetrate BBB, do not ___

A

decrease blood pressure

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7
Q

ACh acts on what receptors in vascular endothelial cells

A

M3 receptors

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8
Q

Action of a2 adrenergic autoreceptors

A

Limit release of NE from sympathetic nerves and Epi from adrenal chromaffin cells

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9
Q

Action of Clonidine

A

Binds auto-receptors (a2 agonist)

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10
Q

Action of Ephedrine

A

Mixed-actining sympathomimetic: direct agonist of a and b receptors

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11
Q

Action of Isopreterenol

A

Acts on beta in SM –> Vasodilation –> Reduction in Diastolic BP; Also increase HR

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12
Q

Action of Labetolol

A

A and B blocker

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13
Q

Action of Metyrosine

A

In tx of Pheochromocytoma, decreases excessive production of catecholamines by blocking tyrosine hydroxylase

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14
Q

Action of Phentolamine

A

Competitive antagonist at alpha1 and 2 receptors

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15
Q

Activation of alpha2 receptor:

A

Decreases production of cAMP –> Inhibition of further release of NE from Neuron (pre-synaptic)

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16
Q

Activation of beta 2 in skeletal muscle

A

Vasodilation

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17
Q

Activation of M2 Muscarinic Receptors –>

A

Gi/Go inhibit AC, decrease cAMP, activate inward rectifying K channels, inhibit v-gated Ca channels = Hyperpolarization/ inhibition

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18
Q

Activation of M3 Muscarinic Receptors –>

A

Gq/11, Activation of PLC, Increased IP3 and DAG, Increased Ca and PKC –> Depolarization and Excitation

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19
Q

Activation of vascular a2 adrenoreceptors leads to

A

vasoconstriction (when given locally, by rapid IV, or in very high oral doses)

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20
Q

Additional actions of Carvedilol, Acebutolol, Propranolol

A

Block fast Na+ channels (and thus rapid depolarization, phase 0) in non-nodal cardiomyocytes –> Decrease slope of phase 0, decrease amplitude of AP

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21
Q

Advantage of drugs with ISMA

A

Can stimulate resting heart to provide relief from bradycardia, but also inhibit stimulation by sympathetics

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22
Q

Adverse effects of Epi

A

Cerebral hemm; Vent Arrhythmias; Angina

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23
Q

Adverse effects of Ganglionic Blockers

A

Postural Hypotension, Tachycardia, Arrhythmias, etc.

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24
Q

AE’s of Ephedrine

A

Angina, Vent dysfunction/arrhythmias, Fatal arrythmias

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25
Q

AE’s of NE

A

Similar to Epi, but BP increase more prominent

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26
Q

AE’s of Phenoxybenzamine

A

Sinus tach, Nasal Congestion

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27
Q

AE’s of Phentolamine

A

Postural Hypotension, Reflex Tach that precipitates cardiac arrhythmias

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28
Q

After pretreat with alpha-blocker, what is effect of Epi

A

decrease in BP (vasodilation still intact (beta2), vasoconstriction blocked (alpha))

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29
Q

After pretreat with alpha-blocker, what is effect of NE

A

Very minimal rise in BP

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30
Q

After pretreat with beta-blocker, what is effect of Epi

A

Rise in BP (vasodilation blocked (beta2), vasocontriction intact (alpha))

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31
Q

After pretreat with beta-blocker, what is effect of isoproterenol

A

Elimination of drop in BP (beta only, mostly 2)

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32
Q

After pretreat with beta-blocker, what is effect of NE

A

Reletively normal rise in BP

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33
Q

Alfuzosin is used for

A

BPH (alpha-1a blocker)

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34
Q

Alpha blockers prevent ___ effect of NE

A

Vasoconstrictive (increase BP)

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35
Q

Alpha vs Beta blockers: prevent vasoconstrictive effect of NE

A

Just alpha

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36
Q

Alpha-1a receptors represent 70% of alpha receptors in

A

prostate

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37
Q

Alpha-1b and Alpha-1d receptors are in

A

vasculature

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38
Q

Alpha-blockers DTP have much higher affinity for which subtype

A

Alpha 1

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39
Q

Alpha: Post-synaptic, down-stream signaling

A

Alpha 1

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40
Q

Alpha: Pre-synaptic, auto-receptors

A

Alpha 2

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41
Q

Alpha1 receptor antagonism would prevent

A

reflex vasoconstrictive effect produced by beta blockers

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42
Q

Alpha2 agonist prodrug

A

methyldopa

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43
Q

Alpha2 agonists

A

Clonidine, Guanabenz, Guanfacine

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44
Q

At low conc., DA acts predominantly

A

on DA receptors in renal vasculature

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45
Q

Atropine with higher dose

A

Progressive tachycardia: Blockade of M2 receptors on SA nodal pacemaker cells (vagal tone antagonized)

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46
Q

Atropine with low dose

A

Blockade of presynaptic M1 receptors –> Increased ACh release

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47
Q

Autonomic control of resting heart is primarily

A

Parasympathetic

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48
Q

BB’s with __ tend to have less effect on TG’s and HDLs

A

ISMA OR Cardio-selectivity

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49
Q

BB’s with ___ tend to reduce total cholesterols and LDLs

A

BOTH ISMA AND Cardio-selectivity

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50
Q

BB’s with Membrane Stabilizing Activity

A

Carvedilol, Acebutolol, Propranolol

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51
Q

beta 2 receptor role in glucose regulation

A

Normally stimulate hepatic glycogen breakdown and pancreatic glucagon release (increase plasma glucose)

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52
Q

Block fast Na+ channels (and thus rapid depolarization, phase 0) in non-nodal cardiomyocytes –> Decrease slope of phase 0, decrease amplitude of AP

A

Additional actions of Carvedilol, Acebutolol, Propranolol

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53
Q

Blockade of alpha-1a in bladder neck and prostate can

A

improve urine flow and reduce symptomes of BPH

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54
Q

Cat. B a2 agonists

A

Methyldopa and Guanafacine

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55
Q

Cholinergic innervation in skeletal muscle

A

none

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56
Q

Clinical use of Dobutamine

A

Short-term tx of cardiac decompensation; After cardiac surgery, CHF, or Acute MI

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57
Q

Clinical use of Ephedrine

A

Hypotension

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58
Q

Clinical use of Phenylephrine

A

Control of Hypotension

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59
Q

CNS depression can occur with what type of BB drugs

A

Lipophilic

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60
Q

CNS effects of BB’s

A

Mental disorders, fatigue, vivid dreams

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61
Q

Concentration-dependent receptor effects of DA:

A

D1 –> B1 –> A

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62
Q

Correlation b/t serum levels of a2 agonists and duration of central effect

A

Poor

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63
Q

Difference b/t NE and Epi action

A

Epi also activates beta2 in skeletal muscle vessels –> Vasodilation and decline in BP

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64
Q

Direct cardiac effects of ACh are mediated primarily by

A

M2 receptors

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65
Q

Direct cardiac effects of ACh mediated primarily by M2 receptors

A

Activation of K-ACh channels; Inhibition of L-type Ca channels

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66
Q

Drugs that prevent Ca entry can cause

A

vasodilation of smooth muscle

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67
Q

Duration of Phenoxybenzamine vs Phentolamine

A

Phenoxy is longer duration

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68
Q

Effect of BB’s on Plasma Glucose

A

Hypoglycemia

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69
Q

Effect of beta-blockers on renin-angiotensin pathway

A

Blocks renin release from JGA of kidney

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70
Q

Effect of DA on CV system

A

Increased CO (contractility&raquo_space; HR), D1 vasodilation; At high doses: Inc PVR and Renal vasoconstriction (alpha-agonism predominates)

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71
Q

Effect of Epi on Coronary BF

A

Increased (decreased systole duration)

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72
Q

Effect of Epi on Lungs

A

Inc Pulmonary pressures

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73
Q

Effect of Epi on Pulse Pressure

A

Inc in Systolic > Diastolic –> Increase in PP

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74
Q

Effect of Epi on Pulse Rate

A

Increase

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75
Q

Effect of Epi on TPR

A

Decrease

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76
Q

Effect of ganglionic blockade in Arterioles

A

Vasodilation; Increased Peripheral Blood Flow; Hypotension

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77
Q

Effect of ganglionic blockade in Veins

A

Dilation; Peripheral pooling of blood, Decreased venous return, Decreased cardiac output

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78
Q

Effect of ganglionic blockade on Heart

A

Tachycardia

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79
Q

Effect of Isoproterenol on Pulse

A

Increase

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80
Q

Effect of Isoproterenol on TPR

A

Decrease

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81
Q

Effect of M2 receptors on Peripheral Nerves

A

Inhibition via auto- and heter-receptors = Decreased ganglionic transmission

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82
Q

Effect of M2 receptors on SA node

A

Slowed, spontaneous depolarization; Hyperpolarization, decreased HR

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83
Q

Effect of M2 receptors on SM

A

Contraction

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84
Q

Effect of NE infusion

A

Predominantly activates a-adrenergic –> Raises BP –> Increased MAP and TPR –> Reflexive decrease in HR

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85
Q

Effect of NE on CO, TPR, SV

A

Down, Up, Up

86
Q

Effect of NE on Coronary BF

A

Up

87
Q

Effect of NE on Pulse Rate

A

Decrease (reflexive)

88
Q

Effect of NE on TPR

A

Increase

89
Q

Effect of SC Epi on BP

A

Inc in SBP secondary to inotropic effect (inc CO); Dec DBP (b2-mediated dec. TPR)

90
Q

Effects of BB’s on Total cholesterol, LDL, HDL, TG

A

Little effect on Total, LDL; Increased TG’s and decreased HDL

91
Q

Effects of Dobutamine on CV system

A

Inc CO, SV w/o effect on HR

92
Q

Effects of Ephedrine on CV system

A

Inc HR and CO; Inc TPR (BP)

93
Q

Effects of Epi on Kidneys

A

Inc Renal Vascular Resistance; Dec Renal BF; GFR unchanged; Increase Renin secretion (b-1); Dec excretion of Na, K, Cl

94
Q

Effects of Isoproteronol on CO, BP, TPR

A

Inc CO, Dec Diastolic BP, Dec TPR

95
Q

Effects of NE on CV emanate predominantly from

A

Alpha-1-mediated action = Vasoconstriction

96
Q

Effects of Phenylephrine on CV system

A

Alpha: systemic arterial vasoconstriction –> Inc BP (reflex HR and CO)

97
Q

Effects of Reserpine on response to Mixed-Acting CV stims

A

blunted, but not abolished

98
Q

Epi acts on what receptors

A

Alpha1, 2, Beta1, 2

99
Q

Epinephrine is agonist except at

A

Sweat glands and facial arteries

100
Q

For whom is Reserpine contraindicated

A

Depression, PUD, Ulcerative Colitis, Pregnancy/Breastfeeding

101
Q

General clinical utility of Atropine

A

Inhibit temporary overactivity of vagal tone on heart; Abolish effects of para-sympathomimetic drugs in circulation

102
Q

Half life of Dobutamine

A

Very short

103
Q

In atria, ACh causes

A

hyperpolarization and a dec. AP duration by increasing Ik-ACh (also dec. cAMP formation -> dec. NE release)

104
Q

In AV node, ACh ___

A

decreases conduction and inc. refractory period by inhibiting Ica-L (responsible for drug-induced complete heart block)

105
Q

In high doses, what is effect of Atropine on blood vessels

A

Dilate cutaneous vessels (Atropine Flush)

106
Q

In larger doses of Phentolamine, what effect predominates

A

Peripheral vascular vasodilation –> Decrease BP

107
Q

In smaller doses of Phentolamine, what effect predominates

A

Positive inotropic effect –> Increase BP

108
Q

In the SA node, ACh dec HR primarily by

A

Decreasing the rate of spontaneous depolarization

109
Q

In which alpha blocker is Orthostatic Hypotension most prominent

A

Prazosin

110
Q

Indirect cardiac effects of ACh

A

Opposition of B-1-mediated increase in cAMP; Inhibition of NE from sympathetic nerve terminals

111
Q

Indirect-acting CV stimulants ultimately increase

A

availability of NE or Epi

112
Q

Inhibits vesicular catecholamine transporter: VMAT2

A

MOA of Reserpine

113
Q

Intracellular actions of Epi are mediated by

A

cAMP

114
Q

Isoproterenol acts on which receptors

A

Beta1 and 2

115
Q

IV formulation available to treat hypertensive emergencies in pregnancy

A

Hydralazine, Labetolol

116
Q

Locations of nAChR’s

A

Paravertebral chain, Parasympathetics

117
Q

Long-term administration of BB’s leads to fall in

A

peripheral vascular resistance

118
Q

M3 Muscarinic receptor activation leads to synthesis of

A

NO

119
Q

Main effect of alpha 1

A

Smooth muscle contraction

120
Q

Main effect of Atropine is to

A

alter HR

121
Q

Mecamylamine is used for

A

Tourette’s (orphan)

122
Q

Mechanism of signaling for Alpha 1

A

Formation of IP3 and DAG –> Inc. Ca

123
Q

Mechanism of signaling for Alpha 2

A

Inhibition of AC –> Decrease cAMP

124
Q

Mechanism of signaling for Beta 1

A

Stimulation of AC –> Increase cAMP

125
Q

Mechanism of signaling for Beta 2

A

Stimulation of AC –> Increase cAMP; Activates cardiac Gi under some conditions

126
Q

Mechanism of signaling for D1, D5

A

Stimulation of AC –> Increase cAMP

127
Q

Mechanism of signaling for D2

A

Inhibition of AC; Increase K+ conductance

128
Q

Membrane Stabilizing Activity

A

Block fast Na+ channels (and thus rapid depolarization, phase 0) in non-nodal cardiomyocytes –> Decrease slope of phase 0, decrease amplitude of AP

129
Q

Methyldopa interferes with

A

catecholamine quantitation

130
Q

Methyldopa is relatively contraindicated in

A

Pheochromocytoma

131
Q

MOA of Ganglionic Blockers

A

Compete with ACh for nicotinic receptor sites, or block the channel –> Initial EPSP is blocked –> Ganglionic transmission inhbited

132
Q

MOA of Hydralazine

A

Peripheral Vasodilator

133
Q

MOA of Phenoxybenzamine

A

Non-competitive (covalent) alpha1 and 2 antagonist

134
Q

MOA of Reserpine

A

Inhibits vesicular catecholamine transporter: VMAT2

135
Q

More important receptor subtypes activated by A2 agonists

A

Hetero-receptors –> Vagal activation

136
Q

Most beta blockers are specific for which subtype

A

beta1

137
Q

Most common anti-hypertensive classes

A

ACEi, ARBs > B-Blockers > Diuretics

138
Q

Most common reason for prescription in US

A

HTN

139
Q

Most prominent AE of alpha blockers

A

First Dose Orthostatic Hypotension

140
Q

Most significant CNS Toxicities of Reserpine

A

Sedation, Inability to concentrate, Psychosis

141
Q

NE acts on what receptors

A

Alpha1, 2, Beta1

142
Q

NE storage depletion drug

A

Reserpine

143
Q

Notable AE for Prazosin

A

First Dose Orthostatic Hypotension

144
Q

NT’s affected by Reserpine

A

NE and DA

145
Q

Off Target Lipid Profile effects of BB’s

A

Alpha1, beta1,2,3 mediate lipolysis

146
Q

Off Target Pulmonary Effects of BB’s

A

Blockade of bronchial SM beta2 receptors –> bronchodilation

147
Q

Onset and duration of Phenoxybenzamine

A

Slow onset and long duration (3-4 days)

148
Q

Other AE’s for alpha blockers

A

Sinus-tach, syncope, vertigo

149
Q

Plasmin renin activity when taking a2 agonists

A

Decreased

150
Q

Predominant tone in Arterioles

A

Sympathetic

151
Q

Predominant tone in Heart

A

Parasympathetic

152
Q

Predominant tone in Veins

A

Sympathetic

153
Q

Primary CV conditions for BB tx

A

HTN, Acute MI

154
Q

Primary sympathetic receptor in skin and splanchnic vessels

A

Alpha

155
Q

Principal alpha blockers for essential HTN

A

Doxazosin, Terazosin, Prazosin

156
Q

Propanolol is most effective in patients with

A

Elevated plasma renin

157
Q

Receptor affinity of Phenoxyenzamine

A

A1 > A2

158
Q

Receptor affinity of Phentolamine

A

A1 = A2

159
Q

Receptor specificity of Dobutamine

A

Increase BP via alpha; Increase HR, CO via beta

160
Q

Receptor specificity of Ephedrine

A

Increase BP via alpha; Increase HR, CO via beta

161
Q

Receptor specificity of epi

A

Vasoconstrictor locally via alpha; Increase HR and CO via beta

162
Q

Receptor specificity of Isoproterenol

A

No alpha; Increase HR, CO via beta receptors

163
Q

Receptor specificity of NE

A

Increase BP via alpha receptors

164
Q

Receptor specificity of Phenylephrine

A

Increase BP via alpha; No beta

165
Q

Responses to ACh may be obscured by

A

CV reflexive effects

166
Q

Rise in BP not as pronounced with ___ (epi vs ne)

A

Epi, due to vasodilation in skeletal muscle

167
Q

Route of Isoproterenol

A

Parenteral or by Aerosol

168
Q

Special AE’s of Phenylephrine

A

CNS: Hallucinations, Psychosis

169
Q

Stimluation of postsynaptic alpha 2 by epi leads to

A

Arteriolar Vasoconstriction

170
Q

Stimulation of alpha 1 by Epi leads to

A

Arteriolar Vasoconstriction

171
Q

Stimulation of beta1 by epi induces

A

positive chronotropic and inotropic response

172
Q

Stimulation of beta2 by epi leads to

A

Arteriolar Vasoconstriction, Bronchial SM relaxation, Increased Glycogenolysis

173
Q

Stimulation of M3, 5 receptors in endothelium does what

A

Synthesis and release of EDRF –> Vasodilation

174
Q

Stimulation of presynaptic alpha 2 by epi leads to

A

inhibition of NE release

175
Q

T/F: BB’s will reduce BP in all patients

A

False, just patients with hypertension

176
Q

The production of cAMP is augmented by __, and attenuated by ____

A

Beta stim; Alpha stimulation

177
Q

Top Adverse Event in alpha 2 agonists

A

Drowsiness

178
Q

Tx Utility of Epi

A

Restoring cardiac rhythm in patients with cardiac arrest

179
Q

Use of ACE inhibitors or ARBs in pregnancy

A

Contraindicated

180
Q

Uses for Phentolamine

A

Pheochromocytoma and Hypertensive emergency

181
Q

Vascular effects of a2 receptors are normally obscured by

A

Central inhibition of sympathetic tone and decreased BP

182
Q

Very low doses of Epi will

A

decrease BP, activation Beta-2 in absence of action on alpha-1

183
Q

What dose of Phentolamine would you want to give to decrease BP

A

Larger –> Peripheral vascular vasodilation predominates

184
Q

What is advantage of Esmolol

A

BB with extremely short half life, given IV, precise and regulated drug levels

185
Q

What patients decline after admin of BB

A

Relying on sympathetic stimulation to compensate for CHF

186
Q

When given alone, how does Atropine affect vessels

A

Inconsistently, not significant

187
Q

When is ISMA indicated

A

Low resting heart rate

188
Q

When is Isoproterenol used

A

Emergencies to stimulate HR in pts w/ bradycardia or heart block; particularly in anticipation of inserting an artificial cardiac pacemaker, or torsades de pointes

189
Q

When is Phenoxybenzamine Rx’d

A

Sympathetic excess secondary to pheochromocytoma, Raynaud’s, frostbite, and acrocyanosis

190
Q

Where is beta 2 mostly located

A

Skeletal Muscle, Lungs

191
Q

Where is DA synthesized and released

A

Proximal tubule

192
Q

Which BB has alpha-1 receptor antagonism

A

Carvedilol, Labetalol

193
Q

Which BB has beta-2 receptor agonism

A

Carteolol

194
Q

Which BB has NO production activity

A

Carteolol, Nebivolol

195
Q

Which beta blockers are beta-1-specific

A

A-N, after that, non-specific

196
Q

Which CV stimulant acts only of Beta

A

Isoproterenol

197
Q

Which CV stimulant acts only on Alpha

A

NE, Phenylephrine

198
Q

Which drugs have ISMA

A

Pindolol, Acebutolol

199
Q

Which effect of Epi is greater: Systolic vs Diastolic BP

A

Systolic –> Increase in MAP and widening of pulse pressure

200
Q

Which muscarinic receptor couples by Gi/Go

A

M2

201
Q

Which muscarinic receptor couples by Gq/11

A

M3

202
Q

Which receptors are more sensitive to the effects of Epi

A

Beta 2 > Alpha

203
Q

Which responses are reduced by prior treatment with Reserpine: Direct or Indirect

A

Indirectly-Acting

204
Q

Which SNS receptors decrease cAMP

A

Alpha2, D2

205
Q

Which SNS receptors increase cAMP

A

Beta1, Beta2, Beta3, D1, D5

206
Q

Who shouldn’t receive non-specific beta blockers because of pulmonary effects

A

COPD, Asthma (need sympathetic bronchodilation)

207
Q

Why are BB’s dangerous in Diabetics

A

Beta-1 blockers mask tachycardia which serves as a warning sign for insulin-induced hypoglycemia

208
Q

Why give precursor instead of Dopamine

A

DA does not cross BBB

209
Q

Why is action of Phenoxybenzamine longer than Phentolamine

A

Covalent binding (noncompetitive)

210
Q

Why is rise in BP not as pronounced with Epi compared to NE

A

Vasodilation in skeletal muscle with epi

211
Q

With increasing concentrations, DA acts

A

on Beta-1-adrenergic receptors, then alpha at higher

Cardiovascular (18 decks)

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