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Fifth Term > PHARM > Flashcards

PHARM Flashcards

1
Q

Acetylcholine

A

Direct Acting Cholinergic Agonist
Choline Ester

Rapidly Hydrolized

Rapid miosis after cataract surgery

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2
Q

Cromolyn

A

Autacoid
Mast stabilizer

Reduces immunologic degranulation of mast cells

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3
Q

Nedocromil

A

Autacoid
Mast stabilizer

Reduces immunologic degranulation of mast cells

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4
Q

Bethanechol Receptor

A

Muscarinic Only

Direct Cholinergic Action

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5
Q

Bethanechol Structure

A

Ester of choline, not hydrolized by AChE, inactivated by other esterases

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6
Q

Bethanecol Uses

A

GI-Post-op distension, atony, retention, ileus, megacolon, refulx

Neurogenic Atonic Bladder

Xerostomia

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7
Q

Bethanecol Adverse Effects

A

Exaggeration of PSNS (DUBMBELLS)

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8
Q

Carbachol Receptor

A

Muscarinic, Nicotinic

Direct Cholinergic Action

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9
Q

Carbachol Structure

A

Ester of choline, pore substrate for AChE, slow biotransformation

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10
Q

Carbachol Effects

A

Miosis

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11
Q

Carbachol Use

A

Glaucoma-reduces intraocular pressure

Miosis during surgery or post-op

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12
Q

Carbachol AE

A

External only: high potency and long duration

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13
Q

Methacholine Receptor

A

Muscarinic mostly, some nicotinic

Direct Cholinergic Action

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14
Q

Methacholine Structure

A

Ester of Choline, slow hydrolysis by AChE

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15
Q

Methacholine Use

A

Diagnose asthma by bronchial agitation (not commonly used)

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16
Q

Pilopcarpine Receptor

A

Partial Muscarinic

Direct Cholinergic Action

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17
Q

Pilocarpine Structure

A

Natrual Alkaloid-Tertiary Amine, stable to hydrolysis by AChE

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18
Q

Pilocarpine Effects

A

Sweat, salivary, lacrimal, and bronchial gland secretions.

Contracts Iris

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19
Q

Pilocarpine Uses

A

DOC for acute angle glaucoma
2nd choice for open angle (timolol is DOC)

Xerostima/Sjorgen’s Syndrome

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20
Q

Pilocarpine AE

A

CNS Disturbances

Sweating, salivation

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21
Q

Nicotine Receptor

A

Nn, some Nm

Direct Cholinergic Action

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22
Q

Nicotine Structure

A

Natural Alkaloid-Tertiary amine

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23
Q

Nicotine MOA, Low dose

A

ganglion stimulation by depolarization (SNS and PSNS)

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24
Q

Nicotine MOA, High dose

A

Ganglion and neuromuscular blockade

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25
Q

Nicotine Effects

A

CVS: SNS due to catecholamine from andrenergic nerves and adrenal medulla

GI and Urinary: PSNS and initial stimulation of salivary and bronchial secretions

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26
Q

Areocoline Structure

A

Natural Alkaloid (muscarinic), less important clinically

Direct Cholinergic Action

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27
Q

Varenicline Receptor

A

Nn (partial)

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28
Q

Vernicline MOA

A

Ganglion Stimulant

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29
Q

Verincline Use

A

Smoking cessation, orally or transdermally applied

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30
Q

Phenobarbital PK

A

Induces P450

PXR and CAR

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31
Q

Pheyntoin PK

A

Induces P450

CAR

Shows saturation kinetics (zero order) for clearance

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32
Q

Rifampin PK

A

Induces P450

PXR

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33
Q

Carbamazepine PK

A

Induces P450

PXR

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34
Q

Cimetidine PK

A

Inhibits P450

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35
Q

Ketoconazole PK

A

Inhibits P450

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36
Q

Erythromycin PK

A

Inhibits P450

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37
Q

Chloramphenicol PK

A

Inhibits P450

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38
Q

Warfarin PK

A

Induces P450

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39
Q

Acetominophen PK

A

Metablized by CYP2E1

In presence of alcohol, Acetominophen is metabolized into Nacteylcysteine.

Antidoe is NAPQ and cysteine

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40
Q

Endrophonium Receptor

A

Anti-AChE-Amplification of endogenous ACh

Won’t work on epithelial M3

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41
Q

Endrophonium Structure

A

Simple alcohol with quaternary ammonium group-can’t enter CNS

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42
Q

Endrophonium MOA

A

Inhibits AChE and ButylcholinesteEst to increase ACh

Binds reversibly to active site on AChE

Competetive antagonist, short lived

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43
Q

Endrophonium Effects

A

NMJ: Increased contraction in weak muscles

Can reverse blockade after surgery

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44
Q

Endrophonium Indications

A

Diagnosis of Myasthenia-gravis

Reverse Neuromuscular block from non-polarizing muscular blockers

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45
Q

Endrophonium PK

A

Hydrolized by receptor, short duration, not meant for treatment

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46
Q

Neostigmine Receptor

A

Anti-AChE, Amplifies endogenous ACh action

Won’t work on epithelial M3

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47
Q

Neostigmine Structure

A

Carbamate ester of alcohol, quaternary ammonium, no CNS effect

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48
Q

Neostigmine MOA

A

Inhibits AChE and butyrlcholineE to increase ACh

Binds covalenty to active site, longer duration

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49
Q

Neostigmine Effects

A

CNS: EEG Activation

Eye, Respiratory, GI and urinary: PSNS

CVS: negative chronotrope, hypotension and decrease cardiac output

NMJ: Increased contraction in weak muscles

Can reverse blockade after surgery

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50
Q

Neostigmine Indications

A

Stimulates GI, bladder

Antidote for tubocararine, other competitive NMJ blockers

Treats myasthenia gravis

More effect on NMJ than physostigmine

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51
Q

Neostigmine PK

A

Hydrolized by receptor

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52
Q

Neostigmine AE

A

Salivation, flushing, low bp, nausea, abdominal pain, diarrhea, bronchospasm

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53
Q

Phsyostigmine Receptor

A

Anti-AChE, amplifies action of endogenous ACh

Won’t work on epithelial M3

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54
Q

Physostigmine Structure

A

Carbamate Ester of Alcohol, tertiary ammonium, enters CNS

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55
Q

Phsyostigmine MOA

A

Inhibits AChE and butyrlcholineE

Binds covalently to active site, long duration

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56
Q

Physostigmine Effects

A

CNS: EEG Activation

Eye, Respiratory, GI and urinary: PSNS

CVS: negative chronotrope, hypotension and decrease cardiac output

NMJ: Increased contraction in weak muscles

Can reverse blockade after surgery

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57
Q

Physostigmine Indications

A

Intestinal, bladder atony

Treat anticholinergic drug overdose (ie-Atropine overdose)

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58
Q

Physostigmine PK

A

Hydrolized by receptor

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59
Q

Physostigmine AE

A

Convulsions, Flushing, Bradycardia, Accumulation of ACh leading to skeletal muscle paralysis

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60
Q

Physostigmine Contraindications

A

Patients with TCA overdose (aggrevates block and AV node)

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61
Q

Pyridostigmine Receptor

A

Anti-AChE, amplification of endogenous ACh.

Won’t work on epithelial M3

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62
Q

Pyridostigmine Strucutre

A

Carbamate ester of alcohol, quaternary ammonium, won’t enter CNS

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63
Q

Pyridostigmine MOA

A

Inhibits AChE and ButyrlcholineE

Covalenty binds to active site, long mechanism of action

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64
Q

Pyridostigmine Effects

A

CNS: EEG Activation

Eye, Respiratory, GI and urinary: PSNS

CVS: negative chronotrope, hypotension and decrease cardiac output

NMJ: Increased contraction in weak muscles

Can reverse blockade after surgery

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65
Q

Pyridostigmine Indications

A

Most common drug for Myasthenia Gravis

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66
Q

Pyridostigmine AE

A

CNS toxicity

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67
Q

Echothiophate Receptor

A

AChE, amplifies endogneous ACh

Won’t work on epithelial M3

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68
Q

Malathion Receptor

A

AChE, amplifies endogneous ACh

Won’t work on epithelial M3

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69
Q

Parathion Receptor

A

AChE, amplifies endogneous ACh

Won’t work on epithelial M3

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70
Q

Tabun Receptor

A

AChE, amplifies endogneous ACh

Won’t work on epithelial M3

Nerve Agent

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71
Q

Sarin Receptor

A

AChE, amplifies endogneous ACh

Won’t work on epithelial M3

Nerve Agent

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72
Q

Soman Receptor

A

AChE, amplifies endogneous ACh

Won’t work on epithelial M3

Nerve Agent

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73
Q

Tacrine Receptor

A

AChE, amplifies endogneous ACh

Won’t work on epithelial M3

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74
Q

Donepezil Receptor

A

AChE, amplifies endogneous ACh

Won’t work on epithelial M3

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75
Q

Rivastigmine Receptor

A

AChE, amplifies endogneous ACh

Won’t work on epithelial M3

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76
Q

Galantamine Receptor

A

AChE, amplifies endogneous ACh

Won’t work on epithelial M3

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77
Q

Echothiophate Structure

A

Organophosphate (not lipid soluble)

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78
Q

Echothiophate MOA

A

Inhibits AChE and butrylcholineE

Binds to and hydrolized by enzyme, active site is phosphorylated-extremely stable covalent bond

Phosphorylated enzyme may undergo aging, which strengthens bond.

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79
Q

Echothiophate Indications

A

Gluacoma

-Chronic open angle, subacute or chronic angle closure after surgery or if surgery is not chosen

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80
Q

Echothiophate PK

A

All organophosphates are distributed throughout the entire body, inlcuding CNS

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81
Q

Echothiophate AE

A

Organophosphate overdose or exposure is treated with atropine and pralidoxime

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82
Q

Malathion Structure

A

Organophosphate (Thiophosphate)

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83
Q

Malathion MOA

A

Inhibits AChE and butrylcholineE

Binds to and hydrolized by enzyme, active site is phosphorylated-extremely stable covalent bond

Phosphorylated enzyme may undergo aging, which strengthens bond.

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84
Q

Malathion Indications

A

Insecticide

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85
Q

Malathion PK

A

Acitvated by conversion to oxygen analogs

Rapidly metabolized to inactive products by birds and humans but not in insects.

Less toxic to humans than parathion

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86
Q

Malathion AE

A

CNS toxicity, treated with atropine or pralidozime

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87
Q

Parathion Structure

A

Organosphosphate (Thiophosphate)

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88
Q

Parathion MOA

A

Inhibits AChE and butrylcholineE

Binds to and hydrolized by enzyme, active site is phosphorylated-extremely stable covalent bond

Phosphorylated enzyme may undergo aging, which strengthens bond.

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89
Q

Parathion Indications

A

Insecticide

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90
Q

Parathion PK

A

Activated in body by conversion to oxygen analogs

Not detoxed in vertebrates, very toxic to humans

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91
Q

Parathion AE

A

CNS Toxcity, treated by atropine or pralidoxime

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92
Q

Tabun Structure

A

Organophosphate

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93
Q

Tabun MOA

A

Inhibits AChE and butrylcholineE

Binds to and hydrolized by enzyme, active site is phosphorylated-extremely stable covalent bond

Phosphorylated enzyme may undergo aging, which strengthens bond.

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94
Q

Tabun Effects

A

Extremely potent CNS Toxin

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95
Q

Tabun Indications

A

Terrorism

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96
Q

Tabun AE

A

CNS Toxicity, treated with atropine and pralidozime

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97
Q

Sarin Structure

A

Organophosphate

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98
Q

Sarin MOA

A

Inhibits AChE and butrylcholineE

Binds to and hydrolized by enzyme, active site is phosphorylated-extremely stable covalent bond

Phosphorylated enzyme may undergo aging, which strengthens bond.

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99
Q

Sarin Effects

A

Extremely potent CNS toxin

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100
Q

Sarin Indications

A

Terrorism

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101
Q

Sarin AE

A

CNS Toxicity, treated with atropine and pralidoxime

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102
Q

Soman Structure

A

Organophosphate

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103
Q

Soman MOA

A

Inhibits AChE and butrylcholineE

Binds to and hydrolized by enzyme, active site is phosphorylated-extremely stable covalent bond

Phosphorylated enzyme may undergo aging, which strengthens bond.

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104
Q

Soman Effects

A

Extremely potent CNS toxin

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105
Q

Soman Indications

A

Terrorism

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106
Q

Soman AE

A

CNS toxicity, treated with atropine and pralidoxime

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107
Q

Tacrine MOA

A

Inhibits AChE and butrylcholineE

Binds to and hydrolized by enzyme, active site is phosphorylated-extremely stable covalent bond

Phosphorylated enzyme may undergo aging, which strengthens bond.

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108
Q

Tacrine Use

A

Alzheimer’s

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109
Q

Donepezil MOA

A

Inhibits AChE and butrylcholineE

Binds to and hydrolized by enzyme, active site is phosphorylated-extremely stable covalent bond

Phosphorylated enzyme may undergo aging, which strengthens bond.

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110
Q

Donepezil Use

A

Alzheimer’s

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111
Q

Rivastigmine MOA

A

Inhibits AChE and butrylcholineE

Binds to and hydrolized by enzyme, active site is phosphorylated-extremely stable covalent bond

Phosphorylated enzyme may undergo aging, which strengthens bond.

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112
Q

Rivastigmine Use

A

Alzheimer’s

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113
Q

Galantamine MOA

A

Inhibits AChE and butrylcholineE

Binds to and hydrolized by enzyme, active site is phosphorylated-extremely stable covalent bond

Phosphorylated enzyme may undergo aging, which strengthens bond.

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114
Q

Galantamine Use

A

Alzheimer’s

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115
Q

Pralidoxime Receptor

A

AChE Regenerator

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116
Q

Pralidoxime MOA

A

AChE reactivator outside CNS

will split the phosphate-enzyme bond if aging has not occured-needs early administration

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117
Q

Pralidoxime Uses

A

Early ogranophosphate poisoning

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118
Q

Muscarine Structure

A

Natural Alkaloid

Direct Cholinergic Action

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119
Q

Atropine Receptor

A

Muscarinic Antagonist

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120
Q

Atropine MOA

A

Bines competitively to muscarinic Receptors, central and peripheral

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121
Q

Atropine Effects

A

Eye: Myrdriasis, cyclopegia, unresponsiveness to light

GI: Antispasmodic, HCl not effected

Urinary: Decreased hypermobility of bladder eneuresis

CVS: High dose: Blockade of atrial M2 with tachycardia
Low dose: initial bradycardia (M2 blockade on vagal Post-gang fibers), blocks vasodilation of skeletal muscle and coronary vascular beds

Secretions: inhibition of salivary, sweat, and lacrimal glands, increases body temp

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122
Q

Atropine Indications

A

AChE inhibotor or organosphophate poisoning treatment

Mydriasis with cyclopegia

Antispadmotic for atonic bladder

Reverses sinus bradycardia

Given with neostigmine to counter NMJ blockade

Atropine flush at high doses: cutaneous vasodilation

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123
Q

Atropine PK

A

Readily absorbed, partially metabolized by liver, eliminated in urine

half life: 4 hours

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124
Q

Muscarinic Antagonist AE

A

May raise intraocular pressure colose angle glaucoma

Cutaneous vasodilation in upper body

High body temp (no sweat)

Dry mouth, blurred vision, sandy eyes, tachycardia, constipation, urinary retention

Bradycardia (low dose) and tachycardia and CNS effects (high doses)

Tertiary only: confusion, hallucinations, delerium, leading to depression, circulatory and respiratory collapse, leading to death

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125
Q

Muscarinic Antagonist Contraindications

A

Patients with:
Peptic ulcers, old age, close angle glaucoma, prostratic hypertrophy/BPH (risk of decreased detrussor contraction), Fever, Elderly patients

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126
Q

Scopalamine Receptor

A

Muscarinic Antagonist

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127
Q

Scopalamine Structure

A

Belladona alkaloid
Tertiary amine
Greater effects on CNS and longer action than atropine

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128
Q

Atropine Structure

A

Belladonna alkaloid

Tertiary amine

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129
Q

Scopalamine Effects

A

DOC for motion sickness-transdermal

Blocks short term memory, sedation, excitment at high doses

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130
Q

Scopalamine Indications

A

DOC for motion sickness-transdermal

Mydriasis and cyclopegia in diagnostic procedures and treatment of irdocyclitis

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131
Q

Ipratropium Receptor

A

Muscarinic Antagonist

Blocks M3

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132
Q

Ipratropium Structure

A

Quaternary Ammonium, no CNS

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133
Q

Ipratropium MOA

A

Blocks M3, causes bronchodialtaion

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134
Q

Ipratropium Indications

A

COPD for patients unable to take andrenergic agonists

Off label: Asthma

Inhaled

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135
Q

Tiotropium Receptor

A

Muscarinic Antagonist

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136
Q

Tiotropium Structure

A

Quaternary ammonium, no CNS

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137
Q

Tiotropium Effects

A

Bronchodilation

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138
Q

Tiotropium Indications

A

COPD only

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139
Q

Homatropine Structure

A

Tertiary Amine, topical

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140
Q

Homatropine Effects

A

Mydriasis with cyclopegia

Short duration

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141
Q

Homatropine Uses

A

Opthamology

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142
Q

Cyclopentaloate Receptor

A

Muscarinic Antagonist

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143
Q

Cyclopentaloate Structure

A

Tertiary amine, topical

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144
Q

Cyclopentaloate Effects

A

Mydriasis with cyclopegia

Short duration

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145
Q

Cyclopentaloate Uses

A

Opthamology

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146
Q

Tropicamide Receptor

A

Muscarinic Antagonist

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147
Q

Tropicamide Structure

A

Tertiary Amine, topical

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148
Q

Tropicamide Effects

A

Mydriasis with cyclopegia

short duration

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149
Q

Tropicamide Indications

A

Opthamology

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150
Q

Benztropine Receptor

A

Muscarinic Antagonist

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151
Q

Bextropine Structure

A

Tertiary amine

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152
Q

Benztropine Indications

A

Parkinsoniism and extrapyrimidal effects of anti-psychotic drugs

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153
Q

Trihexyphenidyl Receptor

A

Muscarinic Antagonist

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154
Q

Trihenxyphenidyl Structure

A

Tertiary amine

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155
Q

Trihenxyphenidyl Use

A

Parkinsoniism and extrapyrimidal effects of anti-psychotic drugs

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156
Q

Glycopyrrolate Receptor

A

Muscarinic antagonist

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157
Q

Glycopyrrolate Structure

A

Quaternary Ammonium (no CNS)

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158
Q

Glycopyrrolate Uses

A

Oral: Inhibits GI motility

Parental: Prevents bradycardia during surgery

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159
Q

Tolterodine Receptor

A

Muscarinic Antagonist

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160
Q

Tolterodine Structure

A

Tertiary amine

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161
Q

Tolterodine Use

A

Overactive bladder

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162
Q

Tetraethylammonium (TEA) Receptor

A

Nn Ganglion Blocker

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163
Q

Tetraethylammonium (TEA) Structure

A

Quaternary ammonium

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164
Q

Ganglion Blocker MOA

A

Blocks ACh at nicotinic receptors of both PSNS and SNS ganglia by prolonging depolaraization after stimulation of antagonising receptors.

Can also block ion channel gated by the Nn

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165
Q

Tetraethylammonium (TEA) Indications

A

First ganglion blocker, little use

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166
Q

Tetraethylammonium (TEA) PK

A

Very short duration

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167
Q

Ganglion Blocker AE

A

Vaso/venodilation, hypotension, tachycardia, mydriasis, reduced GI/urinary motlilty, xerostima, anyhydrosis.

No longer used for HTN

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168
Q

Hexamethonium Receptor

A

Nn Ganglion Blocker

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169
Q

Hexamethonium Structure

A

Quaternary Ammonium

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170
Q

Hexamethonium Indications

A

Hypertension

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171
Q

Hexamethonium PK

A

Longer duration than other ganglion blockers

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172
Q

Mecamylamine Receptor

A

Nn Ganglion Blocker

Only ganglion blocker in US

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173
Q

Mecamylamine Indications

A

Severe/essential and uncomplicated/malignant HTN

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174
Q

Trimethephan Receptor

A

Nn Ganglion Blocker

One of two ganglion blockers in clinical use

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175
Q

Tubocurarine Receptor

A

Nn Antagonist, NMJ blocker

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176
Q

Tubocurarine Structure

A

From curare, prototype of NMJ blockers

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177
Q

Tubocurarine MOA

A

Nondepolarizing antagonist blocker

Binds Nn to prevent ACh from binding, prevents depolarization of the cell membrane, inhibiting contraction

Competitive Antagonist

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178
Q

Tubocurarine Effects

A

Small, rapidly contracting muscle paralyzed firs (face and eyes), followed by finger, arms, neck and trunk, eventually diaphragm

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179
Q

Tubocurarine Indications

A

Anasthesia adjuvant during surgery to relax skeletal muscle

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180
Q

Tuborcurarine PK

A

needs to be given IV due to poor oral absorption

Poor membrane/BBB permeability

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181
Q

Tubocurarine AE

A

Autonomic: Some agents are moderate blockers of Muscarinic receptors

May cause histamine release

Overcome by increased ACh with AChE inhibitors

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182
Q

Succinylcholine Receptor

A

Nn Antagonist, NMJ blocker

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183
Q

Succinylcholine MOA

A

Depolarizing agonistic blocker

Binds Nn to act like ACh-end plate depolarization

Genearlized disorganized contraction of motor units leading to flaccid paralysis

Receptor desensitizes

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184
Q

Succinylcholine Effects

A

Muscle Paralysis

Repsiratory muscles paralyzed last

Ganglion block at High Doses

Weak Histamine Release

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185
Q

Syccinylcholine Uses

A

Endotracheal intubation

Electroconvulsive therapy

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186
Q

Succinylcholine PK

A

IV by continous infusion

Poorly metabolized at synapse, rapidly hyrdolyzed by plasma cholinesterase

Rapid onset (1-15 min) brief duration (5-10 min)

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187
Q

Succinylcholine AE

A

Malignant Hyperthermia-Massive release of Calcium from SR.

Tx: Dantrolene

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188
Q

Dantrolene Uses

A

Tx for Malignant Hyperthermia

Blocks Calcium release from SR

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189
Q

Hemicholonium Receptor

A

Presynaptic-ACh Transporter

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190
Q

Hemicholonium MOA

A

Blocks choline transporter, prevents choline uptake, and therefore ACh synthesis

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191
Q

Hemicholonium Uses

A

Research

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192
Q

Vesamicol Receptor

A

Presynaptic, ACh-H+ Transporter

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193
Q

Vesamicol MOA

A

Blocks ACh-H+ Transporter used to transport ACh into vesicles, preventing ACh storage

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194
Q

Vesamicol Uses

A

Research

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195
Q

Botulinum Toxin Receptor

A

Presynaptic, synaptobrevin

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196
Q

Botulinum Toxin Structure

A

Bacterial protein from anaerobic C. botulinum

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197
Q

Botulinum Toxin MOA

A

Degrades synaptobrevin, preventing release as ACh containing vesicles into synaptic cleft

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198
Q

Botulinum Toxin Uses

A

Disease with increased muscle tone: torticollis, achalasia, staismus, blepharopsams, etc

Facial wrinkles

Headache and pain syndromes

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199
Q

Epinephrine Receptors

A

a and B Direct Andrenergic agonist

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200
Q

Epinephrine Structure

A

Made from tyrosine in adrenal glange

Polar, doesn’t enter CNS

Similar to hormone

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201
Q

Epinephrine MOA

A

Low dose: B effects

High dose: a effects

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202
Q

Epinephrine Effects

A

Blood pressure: Low dose-increases systolic due to increased heart contractility and decreases diastolic due to vasodilation, little change in mean BP

High dose-increase BP through increase ventricular contraction, vasoconstriction through a (which my cause bradycardia from sinus reflex)

CV: Positive ionotrope, chronotrope, dromotropc, increases O2 demands of heart and CO

Resp: Bronchodilation

Metabolic: Hyperglycemia, insulin inhibition, lypolysis

GI: smooth muscle relaxation, detrusor relaxation, contracts trigone and sphincter

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203
Q

Norepinephrine Receptor

A

a and B1 Direct Andrenergic Agonist

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204
Q

Norepinephrine MOA

A

Mostly a actions at therapeutic doses

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205
Q

Norepinephrine Effects

A

Vasoconstriction, causing reflex bradycardia-doesn’t act as positive ionotrope

Renal-Vasoconstricion of kidneys

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206
Q

Norepinephrine Indications

A

Tx for shock, dopamine is usualy better to maintain renal profusion

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207
Q

Norepinephrine PK

A

Rapid onset, IV admin in emergencies, can also be administered subcutaneously, inhaled, through ET tube, topicalled

Oral admin ineffective

metabolized by COMT and MAO, excreted in urine as VMA

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208
Q

Epinephrine PK

A

Rapid onset, IV admin in emergencies, can also be administered subcutaneously, inhaled, through ET tube, topicalled

Oral admin ineffective

metabolized by COMT and MAO, excreted in urine as VMA

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209
Q

Epinephrine AE

A

CNS: Anxiety, fear, tension, headache, tremor, cerebral hemorrhage, cardia arrythmias (especially if combined with digitalis), pulmonary edema

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210
Q

Enpinephrine Contraindications

A

Enhanced CV actions with hyperthyroidism (increased receptors) and cocaine (inhibited reuptake)

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211
Q

Norepinephrine AE

A

Shut down of kidneys

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212
Q

Norepinephrine Contraindications

A

Cause tachycardia with atropine

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213
Q

Dopamine Receptor

A

D, a, and B Direct andrenergic antagonist

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214
Q

Dopamine MOA

A

D1-Gs

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215
Q

Dopamine Effects

A

Real vasodilation (D1), increases GFR

Positive ionotrope

Release of NE from nerve termina

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216
Q

Dopamine Indications

A

DOC for shock

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217
Q

Dopamine PK

A

Ineffective Orally

218
Q

Dopamine AE

A

Nausea, HTN, arrhythmias

219
Q

Feneldopam Receptors

A

D1 Direct Andrenergic Agonist

220
Q

Feneldopam MOA

A

Vasodilation of selective vascular beds D1, 5 (Gs)

221
Q

Feneldopam Indications

A

In hospital, short-term management of severe HTN

222
Q

Feneldopam PK

A

Given by continuous IV only

223
Q

Isoproterenol Receptor

A

B1 and B2, singnificant a effect, Andrenergic Agonist

224
Q

Isoproterenol MOA

A

Stimulates B1 and B2

Generally stimulates rate and force of heart, vasodilation, bronchodilation

225
Q

Isoproterenol Effects

A

Bronchodilation-B2

Increases systolic BO slightly, greatly decreases mean arterial and diastolic press

Inhibits GI, insulin not blocked so no hyperglycemia, lipolysis

226
Q

Isoproterenol Indications

A

Stimulates Heart in Emergency situations

227
Q

Isoproterenol AE

A

Anxiety, fear, tensions, headache, tremor, cerebral hemorrhage, cardiac arrhythmia, pulmonary edema (Same as Epinephrine)

228
Q

Dobutamine Receptor

A

B Andrenergic Agonist

229
Q

Dobutamine Structure

A

Racemic mixutre of a1/B1 agonist and a1 antagonist/potent B1 agonist. Mixture cancels each other out to get a clinical B1 agonist

230
Q

Dobutamine MOA

A

Stimulates B1, generally generating more force and rate in heart

231
Q

Dobutamine Effects

A

Increase CO with little change in HR. Does not raise O2 demands of myocardium.

232
Q

Dobutamine Indications

A

Acute management of CHF

233
Q

Dobutamine AE

A

Same as Epinephrine: anxiety, fear, tensions, headache, tremor, cerebral hemorrhage, cardiac arrhythmias

234
Q

Terbutaline Receptor

A

B2 Andrenergic Agonist

235
Q

Terbutaline Structure

A

Contains Resorcinol Ring

236
Q

Terbutaline MOA

A

Stimulates B2 effects, causes bronchodilation

237
Q

Terbutaline Effects

A

Bronchodilation, reduces uterine contractions

238
Q

Terbutaline Indications

A

Acute asthma attacks (status athmaticus)

Premature Labor

239
Q

Terbutaline PK

A

Oral inhalation or subcutaneous administration

Not a substrate for COMT

240
Q

Isoprotenerol PK

A

Absorbed sublingually, parenterally, or inhaled

Not a substrate for MAO

241
Q

Albuterol (Salbutamol) Receptor

A

B2 andrenergic agonist

242
Q

Albuterol (Salbutamol) MOA

A

B2 activation stimulates bronchodilation

243
Q

Albuterol (Salbuterol) Effects

A

Fast acting bronchodilator

244
Q

Albuterol (Salbutamol) Uses

A

Acute asthma attacks

245
Q

Albuterol (Salbutamol) PK

A

Oral, inhalation, or SC

246
Q

Salmeterol Receptor

A

B2 andrenergic agonist

247
Q

Salmeterol Structure

A

Long hydrocarbon chain-liposoluble

248
Q

Salmeterol MOA

A

Stimulates B2, bronchodilates

249
Q

Salmeterol Effects

A

B2 stimulation and bronchodilation, long acting

250
Q

Salmeterol Uses

A

Management of Asthma

251
Q

Salmeterol Contraindications

A

Not for prompt releif of asthma

252
Q

Dobutamine Contraindications

A

Increases AV conduction, use in cautino in AF

253
Q

Formoterol Receptor

A

B2 Andrenergic Agonist

254
Q

Formoterol MOA

A

Stimulates B2 for bronchodilation

255
Q

Formoterol Effects

A

Long acting bronchodilator (about 12 hrs.)

256
Q

Formoterol Uses

A

Management of asthma, not acute treatment

257
Q

Phenylephrine Receptor

A

a1 Andrenergic Agonist

258
Q

Phenylephrine Chemical Structure

A

Not a catechol derivative

259
Q

Phenylephrine MOA

A

Peripheral Vasoconstriction

260
Q

Phenylephrine Effects

A

No direct effect on heart

Causes vasoconstriction, induces reflex bradycardia

261
Q

Phenylephrine Indications

A

Nasal decongestant (topical)

Mydriasis without cyclopegia

Supraventricular tachycardia, shock (increases bp)

262
Q

Phenylephrine PK

A

Not a substrate for COMT

Combined with H1-histamine for oral nasal decongestant

263
Q

Phenylephrine AE

A

Hypertensive headaches

Cardiac Irregulataries

264
Q

Clonidine Receptor

A

Partial a2 Andrenergic Agonist, centrally acting

265
Q

Clonidine MOA

A

Activation of a2 in the CV control centers in the CNS

266
Q

Clonidine Effects

A

Centrally acting anti-hypertensive

Suppresses sympathetic outflow from brain

267
Q

Clonidine Indications

A

Hypertension

268
Q

Clonidine AE

A

Transient vasoconstriction leading to prolonged hypotensive response (seen only with IV administration)

Sedation, mental lassitude, impaired concentration, lethargyy, zerostima

269
Q

Clonidine Contraindications

A

Not to be taken with yohimbine (a2 antagonist), will reverse HTN effects

270
Q

Methyldopa Receptor

A

a2 Andrenergic agonist

271
Q

Methyldopa MOA

A

Taken up by norandrenergic neurons and metabolized to a-methylnorepinephrine, activates a2

272
Q

Methyldopa Effects

A

Reduces sympathetic outflow, decreases, bp

273
Q

Methyldopa Indications

A

DOC for hypertension during pregnancy

274
Q

Methyldopa AE

A

Sedation, mental lassitude, impaired concentration

275
Q

Bromidine Receptor

A

Highly selective a2 Andrenergic Agonist

276
Q

Bromidine MOA

A

Vasoconstriction of ciliary body blood vessels

277
Q

Bromidine Effects

A

Reduces aqueous humor production (not through canal of schlemm) to lower intraocular pressure

278
Q

Bromidine Uses

A

Glaucoma

279
Q

Amphetamine MOA

A

Releases Exogenous Catecholamines from vesicles, weak inhibitor of MAO

280
Q

Amphetamine Effects

A

Increase alertness, decrease fatigue, appetite suppression, insomnia, increase bp by a action on vasculature, B stimulatory effects on heart

281
Q

Amphetamine Indications

A

Narcolepsy, depression, appetite suppression

282
Q

Amphetamine AE

A

Fatigue and depression following central stimulation, withdrawl

283
Q

Methylphenidate Structure

A

Analogue of amphetamine

284
Q

Methylphenadate MOA

A

Releases NE from vesicles, weak inhibitor of MAO (same as amphetamine)

285
Q

Methylphenidate Indications

A

ADHD in Children

286
Q

Tyramine Structure

A

Product of Tyrosine metabolism

Not clinically useful

287
Q

Tyramine MOA

A

Acts on storage vesicles

Displaces, releases stored NE

288
Q

Tyramine PK

A

Found in fermented foods such as cheese and wine, normally oidized by MAO

289
Q

Tyramine Contraindications

A

Persons taking MAO Inhibitors

290
Q

Ephedrine Receptor

A

a and B Andrenergic Agonist, also works on storage vesicles

291
Q

Ephedrine Structure

A

Plant alkaloid, not a catecholamine, poor substrate for MAO and COMT, long duration

292
Q

Ephedrine MOA

A

Induces release of NE and activates andrenergic receptors

293
Q

Ephedrine Effects

A

Increases systolic and diastolic bp, bronchodilation, mild stimulation of CNS (alertness and decreases fatigue, therefore increases athletic performance)

294
Q

Ephedrine Indications

A

Chronic asthma prohylaxis, nasal decongestant, performance improving

295
Q

Ephedrine PK

A

Excellent absorption orally, Penetrates CNS, Long Duration, eliminated unchanged in urine

296
Q

Ephedrine AE

A

Life threatening CV reactions

Banned by FDA for supplements

297
Q

Pseudoephedrine Receptor

A

a, B andrenergic agonist, also acts on vesicles

298
Q

Psuedoephedrine Structure

A

One of 4 enantiomers

299
Q

Pseudoephedrine MOA

A

Induces release of NE and activates adnrenergic receptors

300
Q

Psuedoephedrine Indications

A

Nasal decongestant

301
Q

Pseudoephedrine PK

A

Combined with H1-histamine as oral nasal decongestant

302
Q

Phenoxybenzamine Receptor

A

a1 Andrenergic antagonist

Also H1, M, Serotonin-R, NE reuptake

303
Q

Phenoxybenzamine Structure

A

Haloalkylamine

304
Q

Phenoxybenzamine MOA

A

Alyklates-> Irreversibly blocks a receptors by forming covalent bonds

305
Q

Phenoxybenzamine Effects

A

Prevents vasoconstriction of peripheral blood vessels and causes reflex tachycardia

a2 blockage in the heart can increase CO

306
Q

Phenoxybenzamine Indications

A

Pheochromocytoma, 14 days prior to tumor removal or as long term treatment if surgery isn’t an option

307
Q

Phenoxybenzamine AE

A

Postural Hypotension, nasal stiffness, nausea, vomiting, inhibits ejaculation

308
Q

Phenoxybenzamine Contraindications

A

Patients with decreased perfusion

B blockers should not be given before as they could cause bp elevation to due increased vasoconstricion

309
Q

Phentolamine Receptors

A

a andrenergic antagonist

Serotonin, M, H1, H2

310
Q

Phentolamine MOA

A

Reversibly blocks a1 and a2

311
Q

Phentolamine Indications

A

Diagnosis of pheochromocytoma though phentolamine blocking test

Hypertensive crisis die to stimulant overdose, or sympathetic anti-HTN withdrawl

Prevent dermal necrosis after NE extravasation

312
Q

Phentolamine AE

A

Postural hypotension, reflex cardiac stimulation, arrhythmias, anginal pain

313
Q

Phentolamine Contraindications

A

Patients with decreased coronary perfusion

314
Q

Prazosin Receptors

A

a1 Andrenergic Antagonist

315
Q

Prazosin MOA

A

Lowers arterial bp-no reflex tachycardia

Suppresses SNS from CNS

Decreases LDL and Tag, increases HDL

Inmproves urinary flow

316
Q

Prazosin Indications

A

Hypertension

BPH

317
Q

Prazosin PK

A

1st dose must be small to avoid rapid hypotension or syncope (1/3 to 1/4)

318
Q

Prazosin AE

A

Dizziness, lack of energy, nasal decongestion, headache, drowsiness, orthostatic hypotension, sodium and fluid retention

319
Q

Terazosin Receptor

A

a1 andrenergic antagoinst

320
Q

Terazosin Structure

A

Prazosin analog with longer half life

321
Q

Terazosin Indications

A

HTN

BPH Symptom Releif

322
Q

Terazosin and Doxasin AE

A

Dizziness, lack of energy, nasal decongestion, headache, drowsiness, orthostatic hypotension, sodium and fluid retention

323
Q

Doxazosin Receptor

A

a1 andrenergic antagonist

324
Q

Doxazosin Structure

A

Prazosin analog with longer half life

325
Q

Doxazosin Indications

A

HTN

BPH Symtpom Releif

326
Q

Tamsulosin Structure

A

a1A (Genitourinary) Andrenergic antagonist

327
Q

Tamsulosin Effects

A

Relexes genitourinary smooth muscle

328
Q

Tamsulosin Indications

A

Only approved for symptomatic relief of BPH

Little effect on blood pressure

329
Q

Tamsulosin AE

A

Less likely to cause hypotension than other a1 antagonists

330
Q

Yohimbine Receptor

A

a2 andrenergic antagonist

331
Q

Yohimbine MOA

A

Blocks a2, acts as indirect andrenergic agonist

332
Q

Yohimbine Effects

A

Increase NE Release

333
Q

Yohimbine Indications

A

Increases BP

334
Q

Yohimbine PK

A

Treats erectile dysfunction, replaced by P5 inhibitors (sildenifil)

335
Q

Yohimbine AE

A

Not to be taken with Clonidine!

336
Q

Yohimbine Contraindications

A

Can reverse antihypertensice effects of a2 agonist actions of clonidine

337
Q

Labetalol Receptor

A

mixed a1 and B Antagonist

338
Q

Labetalol MOA

A

Competetive antagonist

More potent at B antagonism, antioxidant

339
Q

Labetalol Effects

A

Decreases HTN

340
Q

Labetalol Indications

A

HTN for pheochromocytoma and HTN emergencies

Stimulant drug overdose

341
Q

Labetalol AE

A

Orthostatic hypotension, dizziness, hepatic injury

342
Q

Labetalol Contraindications

A

For HTN with bradycardia, use pure a blocker to maintain B2 vasodilation

343
Q

Carvedilol Receptor

A

a1 and B antagonist

344
Q

Carvedilol Indications

A

HTN, Congestive Heart Failure

345
Q

Pindolol Receptor

A

Partial B antagonist

346
Q

Pindolol MOA

A

Smaller reductions in resting HR and BP

Less metabolic effects

347
Q

Pindolol Effects

A

B-antagonist with intrinsic SNS activity

348
Q

Pindolol Indications

A

HTN with diminished cardiac reserve or propensity to bradycardia (diabetics)

349
Q

Pindolol Contraindications

A

Clinical significance of ISA uncertain

350
Q

Propanolol Receptor

A

non-selective B Blocker

351
Q

Propanolol Structure

A

Lipophillic

352
Q

Propanolol MOA

A

Inhibits cardiac B1 and CNS Sympathetics, decreases myocardial contractility

353
Q

Propanolol Effects

A

Lowers HTN by decreasing CO

Increases glucagon release, lowers glycogenolysis

354
Q

Propanolol Indications

A

Hypertension

Prophylaxis for Migraine

Post MI

Prophylaxis for Performance Anxiety

355
Q

B Blocker AE

A

Bronchconstriction, masks hyperglycemic tachycardia associated with diabetes

356
Q

B Blocker Contraindications

A

Asthmatics, Variental Angina

Diabetics use with caution

357
Q

Timolol Receptor

A

Non-selective B blocker

358
Q

Timolol Uses

A

HTN

Open Angle Glaucoma

Migraine Prophylaxis

359
Q

Nadolol Receptor

A

Non-selective B blocker

360
Q

Nadolol Uses

A

Long term management of angina

Management of HTN

361
Q

Atenolol Receptor

A

B1 cardioselective antagonist

362
Q

Atenolol Effects

A

Decreases HTN

Increases exercise tolerance in angina

363
Q

Atenolol Indications

A

HTN in patients with impaired pulmonary funcion

Diabetic HTN recieving oral treatment

364
Q

Metoprolol Receptor

A

B1 Cardioselective Antagonist

365
Q

Metoprolol Effects

A

Decreases HTN

Increases exercise tolerance in angina

366
Q

Metorpolol Uses

A

HTN in patients with pulmonary impairment or diabetes

367
Q

Esmolol Receptor

A

B1 cardioselective Antagonist

368
Q

Esmolol Structure

A

Ester Bond

369
Q

Esmolol MOA

A

Ultra short acting, half life about 10 minutes

Anti-emetic

370
Q

Esmolol Effects

A

Decreases HTN

Increases exercise tolerance in angina

371
Q

Esmolol Indications

A

Supraventricular Arrhythmias

372
Q

Esmolol PK

A

Rapidly broken down by esterases in RBCs

373
Q

Metyrosine Receptor

A

Tyrosine Hydroxylase

Indirect Andrenergic Antagonist

374
Q

Metyrosine MOA

A

Competitive Inhibitor of tyrosine hydroxylase, interferes with DA synthesis, decrease NE and Epinephrine secretion

375
Q

Metyrosine Effects

A

Inhibits NE Synthesis

376
Q

Metyrosine Indications

A

Given with phenoxybenzamine to manage malignant pheochormocytoma and preop

377
Q

Reserpine Receptor

A

Irreversible VMAT damage

Indirect Andrenergic Antagonist

378
Q

Reserpine MOA

A

Irreversibly damages VMAT, vesicles lose ability to concentrate and store NE and DA, NE broken down by MAO in cytoplasm and depleted

379
Q

Resperpine Effects

A

Depletes NE stores

380
Q

Resperpine Indications

A

Slow, gradual decrease in bp, previously used for HTN

381
Q

Reserpine PK

A

long duration of action

382
Q

Guanethidine Structure

A

Transported into SNS nerve by NET, no CNS actions

383
Q

Guanethidine MOA

A

Displaces NE from vesicles, disrupts process by which action potentials release stored NE from terminals

384
Q

Guanethidine Effects

A

Depletes NE stores and prevents NE release

385
Q

Guanethidine Indicatinos

A

PSNS no altered (Distinguished from ganglion blockers)

386
Q

Guanethidine AE

A

Orthostatic Hypotension, Male Sexual dysfunction, Supersensitivity to NE

387
Q

Cocaine Receptor

A

DAT, SET, NET, Sodium Channels

Indirect Andrenergic Antagonist

388
Q

Cocaine MOA

A

Blcoks monoamine reuptake, monoamines accumulate in synaptic space

389
Q

Cocaine Effects

A

Increase/prolonged monoamine singaling, especially dopamine in the limbic pleasure centers

390
Q

Cocaine Uses

A

Local anesthetic

391
Q

Epinephrine H1 effect

A

Physiological Antagonist

392
Q

Choloremphenicol

A

First Generation H1 Antagonist

393
Q

Diphenhydramine (Benadryl) Receptor

A

H1 Antagonist, First Generation

394
Q

Dimenhydrinate Receptor

A

First Generation H1 Antagonist

395
Q

Doxylamine Receptor

A

First Generation H1 Antagonist

396
Q

Hydroxyzine Receptor

A

First Generation H1 Antagonist

397
Q

Meclizine Receptor

A

First Generation H1 Receptor Antagonist

398
Q

Promethazine Receptor

A

First Generation H1 Antagonist

399
Q

First Generation H1 Antagonist Effects

A

Sedative (penetrates BBB), more likely to block ANS receptors

400
Q

First Generation H1 antagonist MOA

A

Actually inverse agonist of H1

Also block cholinergic, a andrenergic, and Na receptors (Local anesthetic)

401
Q

H1 Antagonist Uses

A

First and Second Generation:
Allergic Rhinitis, Motion Sickness and nausea,

First generation only: insomnia

402
Q

First Generation H1 Antagonist AE

A 
Sedation
Dry Mouth (especially in elderly patients)
403
Q

Fecofenadine Receptor

A

Second Generation H1 Receptor Antagonist

404
Q

Loratadine (Claritin) Receptor

A

Second Generation H1 Receptor Antagonist

405
Q

Cetirizine Receptor

A

Second Generation H1 Receptor Antagonist

406
Q

Second Generation H1 Receptor Effects

A

Less sedating than first generation, less liposoluble

Substrate of P-glycoprotein, so they are pumped out of the brain

407
Q

Second Generation H1 Antagonist PK

A

Ventricular arrhythmias in patients taking CYP3A4 inhibitors, blocks cardiac K channels

408
Q

Second Generation H1 Antagonist AE

A

Dry Mouth

409
Q

Cimitidine Receptor

A

H2 Receptor Antagonist

410
Q

Ranitidine (Zantac) Receptor

A

H2 Receptor Antagonist

411
Q

Famotidine (Pepcid) Receptor

A

H2 Receptor Antagonist

412
Q

Nizatidine (Axid) Receptor

A

H2 Receptor Antagonist

413
Q

H2 Receptor Antagonist Use

A

Inhibits gastric acid secretion

414
Q

H2 Receptor Antagonist MOA

A

Competitively blocks H2 receptors and decreases gastric acid

415
Q

H2 Receptor Antagonist Indications

A

Peptic Ulcers, acute stress ulcers, GERD

416
Q

H2 Receptor Antagonist AE

A

Very safe drugs

Cimitidine inhibits Cytochrome P450, will slow metabolism of drugs (WARFARIN!!!)

Binds androgen receptors and has antiandrogenic effect-gynecomastia, decreased sperm count, galactorrhea in women

418
Q

Sumatriptan Uses

A

DOC for acute severe migraine attacks

419
Q

Metoclopramide Receptor

A

5-HT4 Receptor Agonist

420
Q

Cisapride Receptor

A

5-HT4 Receptor Agonist

421
Q

Metoclopramide MOA

A

Prokinetic Agent, promotes and organizes peristalsis of the gut

422
Q

Metoclopramide USes

A

Lazy Gut and anti-emetic

423
Q

Cisapride AE

A

Serious cardiac side effects-no longer used

424
Q

Cyproheptadine Receptor

A

5-HT2 Receptor Antagonist

Also blocks H1

425
Q

Cyproheptadine Uses

A

Allergic/vasomotor rhinitis
Cold urticaria, dermatographism, treatment of smooth muscle effects of carcinoid tumor, serotonin syndrome (too much antidepressants)

426
Q

Ondasetron Receptor

A

5-HT3 Antagonist

Most powerful anti-emetic

427
Q

Ondasetron MOA

A

Blocks ligand gated ion channel

428
Q

Ondasteron Indications

A

Severe nauseau and vomiting with cancer therapyq

429
Q

Ergotamine Receptor

A

5-HT Antagonist

Ergot Alkaloid

430
Q

Dihydroergotamine Receptor

A

5-HT antagonist

Ergot Alkaloid

431
Q

Bromocriptine Receptor

A

5-HT Antagonist

Ergot Alkaloid

432
Q

Cabergoline Receptor

A

5-HT Antagonist

Ergot Alkaloid

433
Q

Methylergonovine Receptor

A

5-HT Receptor

Ergot Alkaloid

434
Q

Ergonovine Receptor

A

5-HT Antagonist

Ergot Alkaloid

435
Q

Ergot Alkaloid MOA

A

Non selective agonst/antagonists for a adrenergic, 5-HT, and CNS dopamine

436
Q

Ergotamine/Dihydroergotamine USes

A

Migraines (Triptans preferred)

437
Q

Bromocriptine/Cabergoline Uses

A

Hyperprolactinemia (pituiatary tumor)

438
Q

Methylergonovine/Ergovine Uses

A

Post-partum hemorrhage (oxytocin 1st line)

Ergovine IV used to provoke variant angina

449
Q

Sumatriptan Receptor

A

5-HT (1D/1B) Agonist

450
Q

Dinosprostone Class

A

Eicosanoid-PGE2

451
Q

Eiconsanoid MOA

A

Act in autocrine and paracrine fashion, binds G protein receptor on cell surface.

Gs-activates adenylyl cyclase
Gi-inhibits adenylyl cyclase
Gq-activates PLC

Contractile effects on smooth muscle by releasing Calcium, relaxing effects by cAMP

452
Q

Dinosprostone Indicationss

A

Ripens cervix at term prior to induction of labor with oxytocin

453
Q

Carboprost tromethamine Class

A

Eicosanoid, 15-methyl-PGFa

454
Q

Carboporst tomethamine Indications

A

Induces abortion

455
Q

Misoprostol Drug Class

A

Eiconsanoid, Derivative of PGE1

456
Q

Misoprostol Use

A

Ripens cervix to induce labor before oxytocin administration

457
Q

Alprostadil Class

A

Eicosanoid, PEG1

458
Q

Alprostadil Use

A

Maintains patent ductus arteriosus

459
Q

Prostacyclin/Epoprostenol CCClass

A

Eicosanoid, PGI2

460
Q

Prostacyclin/Epoprostenol Use

A

Severe Pulmonary HTN

Prevents platelet aggregation in dialysis machine

461
Q

Latanoprost Class

A

Eicosanoid, PGF2a derivative

462
Q

Latanoprost Use

A

Glaucoma-GOLD standard

463
Q

Zileuton Class

A

Eicosanoid Inhbitor

464
Q

Zileuton MOA

A

Inhibits 5-LOX

465
Q

Zileuton Uses

A

Asthma attack

466
Q

Zafrilukast Class

A

Eicosanoid Antagonist

467
Q

Mantelukast Class

A

Eicosanoid Antagonist

468
Q

Zafrilukast MOA

A

Inhibits binding of LTD4 to receptoor

469
Q

Montelukast MOA

A

Inhibits binding of LTD4 to receptor

470
Q

Eicosanoid Antagonist Use

A

Asthma attacks

471
Q

Hydrochlorothiazide Class

A

Thiazide Diuretic

472
Q

Chlorthalidone Class

A

Thiazide Diuretic

473
Q

Metoalazone Class

A

Thiazide Diuretic

474
Q

Thiazide Diuretics Effects

A

Decrease peripheral vascular resistance, decrease BP even after vloume recovery

475
Q

Thiazide Diuretic MOA

A

Blocks Na/Cl transport in distal convoluted tubule

“ceiling” diuretic, saturates at low dose

476
Q

Thiazide Diuretics Indications

A

HTN
Heart Failure
Hypercalcuria
Diabetes Insipidus

477
Q

Thiazide Diuretics effect on Urine Composition

A

Increases Na, K, Cl,
Increases Mg
Decrease Ca

478
Q

Thiazide Diuretic PK

A

Oral

half life 40 hrs, takes 1-3 weeks for stable effects

479
Q

Thiaziade AE

A 
Hyokalemia
Hyponatremia
Hyperuricemia
Hypersensitivity
Hyperglycemia (insulin)
Loop effect causing volume depletion
480
Q

Furosimide Class

A

Loop Diuretic, most common

481
Q

Torsemide Class

A

Loop Diuretic

482
Q

Loop Diuretic Effects

A

Produces a lot of urine, most effective diuretic

483
Q

Loop Diuretic MOA

A

Blocks Na/Cl/K transporter in ascending loop of Henle

484
Q

Loop Diuretics Indications

A

Acute pulmonary edema
Heart Failure
Hypercalcemia
Hyperkalemia

485
Q

Ethacrynic Acid

A

non-sulfa drug used for sulfa allergies

486
Q

Loop Diuretics Effect on urine Composition

A

Increase Ca, Na, K, Mg

487
Q

Loop Diuretic PK

A

Oral, half life 2-4 hours

488
Q

Loop Diuretics AE

A 
Ototoxicity
Hyperuricemia (competition for transport)
Acute hypovolemia
K depletion
Hypomagnesemia
Allergic Reactions-sulfonamides
489
Q

Spironolactone Receptor

A

Potassium sparing, Aldosterone Receptor

490
Q

Eplerenone Receptor

A

Potassium Sparing, Aldosterone Receptor

491
Q

K Sparing-Aldosterone-R MOA

A

Antagonist to aldosterone at cytoplasmic receptors (prevents translocation), acting at collecting duct

492
Q

K-Sparing-Aldosterone Receptor Indications

A

Heart Failure
2’ Hyperaldosteronism
Hepatic Cirrhosis

493
Q

K-Sparing Diuretics Effect on Urine Composition

A

Increase Na

Decrease K

494
Q

K-Sparing-Aldosterone-R PK

A

Oral, strongly protein bound
Active metabolite of sprionolactone is canrenone

Induces CYP450

half life is 2-3 days

495
Q

K-Sparing-Aldosterone-R AE

A

GI upset, peptic ulcers
Endocrine effects (resemble steroids)
Hyperkalemia, lethargy, mental confusion

496
Q

Triamterene Receptor

A

Potassium Sparing, ENaC

497
Q

Amiloride Receptor

A

Potassium Sparing, ENaC

498
Q

K-Sparing-ENaC MOA

A

Blocks Na Transport, lowers Na/K echange

Acts on collecting duct

499
Q

K-Sparing-ENaC Indications

A

Heart Failure

1’Hyperaldosteronism

500
Q

K-Sparing-ENaC AE

A

Resembles sex steroid-endocrine effects

Increase BUN, uric acid and K retention

501
Q

Acetazolamide Class

A

Carbonic Anhydrase Inhibitor (Intracellular)

502
Q

Acetazolamide MOA

A

Acts mainly in the Proximal Tubule

Prevents formation of H+ needed for transport of Na reabsorption in PT

503
Q

Acetazolamide Indications

A

Glaucoma
Mountain Sickness/Metabloc Alkalosis (prophylaxis)
Epilepsy

504
Q

Acetazolamide Effects on Urine

A

Increase Na, K, HCO3-

505
Q

Azetazolamide PK

A

Oral

Increases Urine pH, alters solubulity of other drugs (elminates weak acids)

506
Q

Azetazolamide AE

A

Metabolic Acidosis
K Depletion
Crystalluria
Don’t use with Hepatic cirrhosis-decreased NH4 excretion

507
Q

Mannitol Class

A

Osmotic Diuretic

508
Q

Mannitol MOA

A

Freely filters into glomerulus and draws water into tubular fluid.
Does not effect Na Secretion

Effects everywhere

509
Q

Mannitol Indications

A

Acute Renal Failure
Drug toxicity-excretion
Trauma-maintains urine
Increases intracranial pressure

510
Q

Mannitol PK

A

IV only

511
Q

Mannitol AE

A

Extracellular water expansion
Dehydration
Hypo- or hypernatremia
Osmotic diahrrea if given orally

512
Q

Conivaptan Class

A

ADH Antagonist

513
Q

Conivaptan Effects

A

Renders convoluted tubules impermeable to water, dilutes urine

514
Q

Conivaptan MOA

A

Inhibits effects of ADH by decrasing aquaporins in collecting duct

515
Q

Conivaptan Indications

A

SAIDH

Elevated ADH

516
Q

Conivaptan Effects on Urine

A

increases plasma Na

decreases water reabsorption

517
Q

Conivaptan PK

A

IV only

half life 5-10 hrs

Metabolized by and inhibits CYP3A4

518
Q

Conivaptan AE

A

Nephrogenic Diabetes Insipidus
Renal Failure
Thirst
Atrial Fibrillation

519
Q

Conivaptan Contraindications

A

Renal Failure
Hypovolemic
hyponatremia

520
Q

Captopril Class

A

ACE Inhibito

521
Q

Enalapril Class

A

ACE Inhibito

522
Q

Lisinopril Class

A

ACE Inhibito

523
Q

ACE Inhibitor Effects

A

Decrease bp by decreasing peripheral vascular resistance

524
Q

ACE Inhibitor MOA

A

Decreases Na and water retention via decreased aldosterone action

Blocks enzyme, slow effect

Increases bradykinin levels

Does not refleively decrease CO, hr, or contractility

525
Q

ACE Inhibitors Indications

A

HTN-first line
Chronic Heart Failure
Not as effective as older, black-same effectiveness when used with diuretic
Spares kidney, spares GFR

526
Q

Captopril Use

A

DOC treatment 24 hours post MI

527
Q

Enalapril PK

A

Oral pro-drug, can give IV

528
Q

ACE Inhibitors AE

A

Dry cough, Angioedema

Rash, fever, hypotension, hyperkalemia (from aldosterone), reversible renal failure

529
Q

ACE Inhibitor Contraindications

A

Pregnancy-Category X

530
Q

Valsartan Class

A

ARB

531
Q

Losartan Class

A

ARB

532
Q

ARB Effects

A

Blocks Angiotensin II Receptor (AT1), lowers blood pressure by lowering peripheral vascular resistance, also spares GFR

533
Q

ARB Indications

A

HTN
Least effective in elderly, black, can be given with diuretic
Chronic Heart Failure

534
Q

ARB Uses

A

DOC in HTN in Diabetics

535
Q

ARB AE

A

Angioedema
No cough, no bradykinin levels

Hypotension, hypokalemia

536
Q

Drug Induced Lupus

A

Butterfuly malar rash, ANA and antihistone antibodies, can be caused by Hydralazine

Discontinue drug and symptoms disappear

537
Q

Aliskrien Class

A

Renin Inhibitor

538
Q

Aliskrien MOA

A

Inhibits activity of the enzyme Renin, decreases angiotensin I, II, and aldosterone

Slow effect

539
Q

Aliskrien Uses

A

HTN

540
Q

Aliskrien AE

A

Hyperkalemia, renal impairment, potential teratogenic

541
Q

Amlodipine Class

A

Dihydropyridine CCB

542
Q

Nifidipine Class

A

Dihydropyridinne CCB

543
Q

Dihydropyridine CCB MOA

A

Blocks calcium channels in vascular smooth muscle

Not used for cardiac arrhythmias

544
Q

Dihydropyridine Use

A

First Line for HTN in patients with contraindications or intolerant to ACER, ARBs.

545
Q

Dihydropyridine AE

A

Dizziness, headache, fatigue, ankle edema, reflex tachycardia

546
Q

Drug Induced SLE caused by;

A 
Sulfasulazine
Hydralazine
Isoniazid
Procainimide
Phenytoin
547
Q

Gingival Hypertrophy Caused by:

A

Pheyntoin

Nifidipine

548
Q

Pulmonary Fibrosis Caused By:

A

Amiodarone

Bleomycin

549
Q

Class IA Antiarrhythmics

A

Quinidine
Procainamide
Disopyramide

550
Q

Class IB Antiarrhythmics

A

Lidocaine
Mexiletine
Tocainide

551
Q

Class IC Antiarrythmice

A

Flecainide

Propafenone

Fifth Term (1 decks)

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