Pharm I: Autonomic Drugs

Front 1

Non-selective adrenergic agonists (3)

Back 1

Epinephrine, norepinephrine, dopamine

Front 2

Non-selective beta adrenergic agonists (1)

Back 2

Isoproterenol

Front 3

Selective alpha-1 adrenergic agonists (1)

Back 3

Phenylephrine

Front 4

Selective alpha-2 adrenergic agonists (1)

Back 4

Clonidine

Front 5

Selective beta-1 adrenergic agonists (1)

Back 5

Dobutamine

Front 6

Selective beta-2 adrenergic agonists (1)

Back 6

Albuterol

Front 7

Indirect adrenergic agonists (4)

Back 7

Ephedrine, amphetamine, tyramine, cocaine

Front 8

Non-selective alpha adrenergic anatagonists (2)

Back 8

Phentolamine (reversible), phenoxybenzamine (irreversible)

Front 9

Selective alpha-1 adrenergic antagonists (1)

Back 9

Prazosin

Front 10

Non-selective beta adrenergic antagonists (4)

Back 10

Propranolol, timolol, pindolol, sotalol

Front 11

Selective beta-1 adrenergic antagonist (2)

Back 11

Metoprolol, atenolol

Front 12

Non-selective beta adrenergic and selective alpha-1 adrenergic antagonists (2)

Back 12

Labetolol, carvedilol

Front 13

These are the clinical findings in cholinergic (muscarinic) syndrome

Back 13

Drop in blood pressure
Bradycardia (SA node activation)
Diarrhea (incr. gut motility)
Urination (contraction of detrusor)
Bronchorrhea (incr. secretions) and bronchoconstriction (wheezing)
Emesis (incr. stomach and GI tone)
Lacrimation
Sweating (sympathetic-cholinergic)

Front 14

These are the clinical findings in atropine poisoning (opposite of cholinergic syndrome)

Back 14

Mad as a hatter (delirium, hallucinations)
Blind as a bat (mydriasis, photophobia, cycloplegia)
Dry as a bone (dry mouth, block of sweating)
Red as a beet (PG's, fever, anhidrosis)
Hot as a hare (anhidrosis)
**You're removing parasympathetic effects**

Front 15

This receptor, when stimulated,causes constriction of blood vessels

Back 15

Alpha-1 adrenergic receptor

Front 16

This receptor, when stimulated, inhibits NE release (feeback receptor; located on pre-synaptic cells)

Back 16

Alpha-2 adrenergic receptor

Front 17

This receptor, when activated, increases heart rate and contractility

Back 17

Beta-1 adrenergic receptor

Front 18

This receptor, when stimlated, relaxes smooth muscles of airways, vessels and uterus

Back 18

Beta-2 adrenergic receptor

Front 19

Receptors at the postganglionic terminus of parasympathetic fibers

Back 19

Muscarinic cholinergic receptor

Front 20

Receptor found at the NMJ (muscle contraction)

Back 20

Nicotinic cholinergic receptor

Front 21

This drug is a seldom-used non-selective alpha AR agonist

Back 21

Phentolamine

Front 22

This adrenergic antagonist is notable for being irreversible

Back 22

Phenoxybenzamine

Front 23

This drug is used to suppress peripheral vasospasm

Back 23

Phenoxybenzamine
(it blocks the constrictive effects of alpha-1 receptors)

Front 24

This drug is an alpha-1 adrenergic antagonist that is used to treat hypertension

Back 24

Prazosin

Front 25

T/F: Prazosin is reversible

Back 25

True.

Front 26

T/F: Phentolamine is reversible

Back 26

True.

Front 27

T/F: Phenoxybenzamine is reversible

Back 27

False.

Front 28

This drug is known for causing a "1st dose" effect of postural hypotension

Back 28

Prazosin

Front 29

These are the clinical indications of Metoprolol

Back 29

Hypertension and ischemic heart disease

Front 30

These are the general side effects of beta-blockers

Back 30

Bronchconstriction, bradyarrhythmias, bradycardia

Front 31

Metabolism of Metoprolol

Back 31

Hepatic

Front 32

This drug is used to treat pheochromocytoma

Back 32

Labetolol

Front 33

This beta-blocker has as its major side effect postural hypotension

Back 33

Labetotol

Front 34

Excretion of Atenolol

Back 34

Renal

Front 35

This non-selective beta blocker is used to treat atrial and ventricular tachycardias

Back 35

Sotalol

Front 36

This non-selective beta blocker prolongs cardiac action potentials by blocking potassium channels

Back 36

Sotalol

Front 37

This drug has anti-oxidant effects, and has been shown to improve survival in CHF

Back 37

Carvedilol

Front 38

This drug has low lipophilicity

Back 38

Timolol

Front 39

This drug is used to treat open-angle glaucoma

Back 39

Timolol

Front 40

This drug is extremely lipophilic and therefore enters the CNS readily

Back 40

Propranolol

Front 41

This drug has a "membrane stabilizing effect" at high concentrations

Back 41

Propranolol

Front 42

This drug is given intravenously to treat life-threatening arrhythmias

Back 42

Propranolol

Front 43

This drug is notable for being a partial agonist

Back 43

Pindolol

Front 44

This drug produces smaller reductions in resting heart rate than other drugs in its family

Back 44

Pindolol

Front 45

Beta-1 blockade has these two main effects

Back 45

Slows down the heart, and inhibits the RAAS

Front 46

Between beta-1 and beta-2 blockades, this has a more systemic effect

Back 46

Beta-2 blockade

Front 47

Tmax (peak concentration) of beta blockers

Back 47

medium (1-3 h)

Front 48

Half life of beta blockers

Back 48

short (3-10 h) due to extensive 1st pass metabolism in the liver

Front 49

Beta blockers should be tapered when discontinuing for this reason

Back 49

Receptor upregulation

Front 50

Beta blockers should not be given with this drug

Back 50

Verapamil

Front 51

These are contraindications for beta blockers

Back 51

Airway disease, diabetes, acute CHF

Front 52

These are the adrenergic agonists that target either alpha or beta AR's specifically

Back 52

Clonidine, Phenylephrine, Isoproterenol, Dobutamine, Albuterol

Front 53

This is the role of MAO

Back 53

MAO (monamine oxidase) metabolizes catecholamines, along with COMT

Front 54

This is the role of COMT

Back 54

COMT (catechol-o-amine methyl transferase) metabolizes catecholamines, along with MAO

Front 55

This drug has its effect by inhibiting MAO

Back 55

Trancyclopromine

Front 56

This drug is an adrenergic agonist that works by blocking reuptake

Back 56

Cocaine

Front 57

This drug is an adrenergic agonist that works by promoting release of catecholamines

Back 57

Amphetamine

Front 58

This is the route of synthesis for catecholamines

Back 58

Tyrosine --> DOPA --> dopamine --> NE --> E

Front 59

This is the form in which catecholamines are stored in the cell

Back 59

Dopamine

Front 60

This catecholamine has very little effect on the beta-2 receptor

Back 60

NE

Front 61

Metabolism of Catecholamines

Back 61

Metabolized in liver by MAO and COMT, excreted in urine with sulfate and glucuronates

Front 62

Episodic hypertension is a presentation of this disease

Back 62

Pheochromocytoma

Front 63

This drug is used in the treatment of cardiogenic shock

Back 63

Dobutamine (it has beta affects but no alpha effects, therefore it raises the HR without raising the BP)

Front 64

This drug dilates renal and mesenteric vessels

Back 64

Dobutamine

Front 65

Administratino of Dobutamine

Back 65

Intravenous

Front 66

These are the side effects of Dobutamine

Back 66

Ectopic activity, tachycardia, HTN, hypotension (hyper-reactive heart)

Front 67

This drug is a non-selective beta agonist

Back 67

Isoproterenol

Front 68

This drug is useful for treating people with bradycardia

Back 68

Isoproterenol

Front 69

This drug is an extremely potent drug with side effects of arrthythmias

Back 69

Isoproterenol

Front 70

This drug is found in fermented foods, such as cheese

Back 70

Tyramine

Front 71

This drug is an indirect AR agonsit that has its effect by releasing biogenic amines from storage

Back 71

Tyramine

Front 72

Metabolism of Tyramine

Back 72

Hepatic, by MAO

Front 73

T/F: Cocaine has a shorter effect than amphetamine

Back 73

True

Front 74

This is the difference in BP and HR that is observed between Isoproterenol and Phenylephrine

Back 74

Phenylephrine, an alpha-1 agonist, will raise BP but have no effect on HR; Isoproterenol decreases BP because of its beta-2 relaxing effect on vessel smooth muscle, but increases HR because of its beta-1 effects

Front 75

This drug is a plant alkaloid

Back 75

Ephedrine

Front 76

This drug increases NE release

Back 76

Ephedrine

Front 77

This indirect adrenergic receptor agonist drug is used as a nasal decongestant

Back 77

Ephedrine

Front 78

This drug has as its side effects insomnia and tachyphylaxis

Back 78

Ephedrine

Front 79

This drug is used in the treatment of nasal congestion, but is also a CNS stimulant

Back 79

Ephedrine

Front 80

These three adrenergic agonists are used in the treatment of cardiogenic shock

Back 80

Dopamine, Dobutamine, Norepinephrine

Front 81

This drug works by reducing NE release via activation of the alpha-2 receptor

Back 81

Clonidine

Front 82

Clonidine is used to treat these conditions

Back 82

Migraines, hypertension, menopausal flushing

Front 83

This drug has as its side effects dry mouth, sedation and contact dermatitis

Back 83

Clonidine

Front 84

Given orally, this drug has a prolonged hypotensive response

Back 84

Clonidine

Front 85

This drug causes an acute hypertensive response following by hypotension when given intravenously

Back 85

Clonidine

Front 86

This drug is given to patients in cardiac arrest

Back 86

Epinephrine

Front 87

This drug is given to patients in acute anaphylaxis

Back 87

Epinephrine

Front 88

These are the mechanisms by which Epinephrine alleviates asthma

Back 88

It stimulates beta-2 receptors to cause bronchodilation, and stimulates alpha-1 receptors to cause vasoconstriction which, in the lungs, decreases airway resistance

Front 89

Direct muscarinic agonists

Back 89

Bethanechol, methacholine, pilocarpine

Front 90

Direct cholinergic agonist

Back 90

Nicotine

Front 91

Indirect cholinergic agonists (6)

Back 91

Edrophonium, neostigmine, physostigmine, organophosphates (sarin, soman, parathion, malathion), echothiophate, pralidoxime

Front 92

Muscarinic antagonists (3)

Back 92

Atropine, scopolamine, benztropine

Front 93

Depolarizing NMJ blocker

Back 93

Succinylcholine

Front 94

Nondepolarizing NMJ blocker

Back 94

d-Tubocurarine

Front 95

Competitive nondepolarizing NMJ blockers (5)

Back 95

Pancuronium, vercuronium, rocuronium, cisatracurium, curare

Front 96

Competitive nondepolarizing ganglionic blocker

Back 96

Trimethaphan

Front 97

Indirect muscarinic antagonist

Back 97

Botulinum toxin

Front 98

These are where acetylcholine has its action and transmission

Back 98

CNS
Autonomic ganglia
NMJ (somatic motor nerves)
Postganglionic terminus of parasympathetic fibers
Postganglionic terminus of sympathetic cholinergic fibers (sweat glands)
Adrenal medulla (specialized sympathetic ganglion)

Front 99

This drug has little to no effect on the CNS when injected due to poor penetration of the BBB

Back 99

Acetylcholine

Front 100

This neurotransmitter acts on the non-innervated receptors of vascular smooth muscles

Back 100

Acetylcholine

Front 101

This is the hierarchy of effects that cholinergics have

Back 101

#1 Vascular smooth muscle
#2 Parasympathetic postganglionic sites
#3 NMJ
#4 Ganglia
#5 CNS

Front 102

T/F: Urination is a sympathetic phenomenon

Back 102

False. It is parasympathetic: cholinergic stimulation contracts the bladder and relaxes the sphincter

Front 103

This drug is used to treat narrow-angle glaucoma

Back 103

Pilocarpine

Front 104

These cholinergic agonists have their effect by blocking degredation of ACh

Back 104

Organophosphates, Echothiophate, Neostigmine, Edrophonium, Physostigmine

Front 105

This is the general type of drug class that Parthion and Malathion belong to

Back 105

Organophosphates

Front 106

These drugs bind cholinesterase for hundreds of hours, sometimes irreversibly

Back 106

Organophosphates

Front 107

This drug cures cholinesterase inhibitor poisons (sarin, etc.) by reactivating cholinesterase

Back 107

Pralidoxime

Front 108

Pralidoxime cannot be used to cure this type of cholinesterase poisoning

Back 108

Carbamate

Front 109

This drug was formerly used to treat glaucoma but is no longer used

Back 109

Echothiophate

Front 110

This is the only direct-acting nicotinic agonist in use today

Back 110

Nicotine

Front 111

Flaccid paralysis is a worry when using this drug

Back 111

Nicotine

Front 112

This is the cause of flaccid paralysis

Back 112

There is a depolarization-desensitization block at the cholinergic receptor site

Front 113

This is a muscarinic agonist used in the diagnosis of asthma

Back 113

Methacholine

Front 114

Bethanecol has been replaced by this drug in the treatment of GI dysmotility

Back 114

Metoclopramide

Front 115

This drug has a quaternary ammonium group that prevents it from entering the CNS

Back 115

Neostigmine

Front 116

This drug is used to reverse paralysis

Back 116

Neostigmine

Front 117

This drug cannot be used to reverse succinylcholine paralysis

Back 117

Neostigmine

Front 118

This drug can cause myasthenic crisis and small concentrations, and cholinergic crisis at high concentrations

Back 118

Neostigmine

Front 119

This is how to treat OD of Neostigmine

Back 119

Muscarinic antagonists (block muscarinic effect)

Front 120

This is the main side effect of Pilocarpine

Back 120

Blury vision, due to impedment of accomodation of the lens, which also has muscarinic receptors

Hint 120

Pilocarpine is used to treat narrow-angle glaucoma

Front 121

This cholinesterase inhibitor is highly charged

Back 121

Edrophonium

Front 122

This drug is used in the diagnosis of myasthenia gravis

Back 122

Edrophonium

Front 123

This is how myasthenia gravis is diagnosed

Back 123

Patient is given Edrophonium, a very short-acting cholinesterase inhibitor, thereby increasing cholinergic stimulation at the NMJ, and patients report a very rapid increase in muscle strength

Front 124

This drug is used to distinguish between myasthenic and cholinergic crisis in Neostigmine administratino

Back 124

Edrophonium

Front 125

This is the pathophysiology of myasthenia gravis

Back 125

Auto-Ab's bind nicotinic receptors at the motor end plate, causing muscle weakness and rapid fatigue

Front 126

This cholinesterase inhibitor can cross the BBB

Back 126

Physostigmine

Front 127

This drug is used to reverse the CNS effects of muscarinic blockers

Back 127

Physostigmine (it increases concentrations of acetylcholine in the CNS by inhibiting its degredation)

Front 128

T/F: All cholinergic receptors are G-protein coupled receptors

Back 128

False. Muscarinic receptors are GPCR's, but Nicotinic receptors are Na/K ion channels

Front 129

This class of muscarinic receptor is found in the heart

Back 129

M2

Front 130

This class of muscarinic receptor is found in the glands

Back 130

M3

Front 131

This class of muscarinic receptor is found in the stomach

Back 131

M2

Front 132

This class of muscarinic receptor is found only in nerves and the CNS

Back 132

M1, M4, M5

Front 133

These classes of muscarinic receptors are linked to phospholipase C (PLC)

Back 133

Odd-numbered (M1, M3, M5)

Front 134

These classes of muscarinic receptors are linked to, and inhibit, adenylyl cyclase, and decrease cAMP levels

Back 134

Even-numbered (M2, M4)

Front 135

This class of muscarinic receptor also activates potassium channels

Back 135

M2

Front 136

This class of drugs is notable for the lack of selectivity for any one subtype or group of subtypes

Back 136

Muscarinic agonists

Front 137

These are the two subtypes of nicotinic receptors

Back 137

Muscle type (NM) and neuronal type (NN)

Front 138

This nicotinic receptor is a pentamer

Back 138

Muscle type (NM)

Front 139

This nicotinic receptor is a dimer

Back 139

Neuronal type (NN)

Front 140

Definition of cycloplegia

Back 140

Paralysis of the ciliary muscle, which leads to blurred vision

Front 141

Atropine vs. Cholinergic Poisoning

Back 141

Atropine poisoning blocks cholinergic effect (ie, enhanced sympathetic effect), and cholinergic poisoning is enhanced parasympathetic effect

Front 142

This drug blocks both sympathetic and parasympathetic autonomic ganglia

Back 142

Trimethaphan

Front 143

Clearance of Trimethaphan

Back 143

Liver (within minutes)

Front 144

This drug is used to induce amnesia

Back 144

Scopolamine

Front 145

This drug is applied as transdermal patches for motion sickness

Back 145

Scopolamine

Front 146

This is the main depolarizing nicotinic antagonist

Back 146

Succinylcholine

Front 147

These are two non-selective muscarinic antagonists

Back 147

Atropine, Scopolamine

Front 148

This drug reduces bronchial secretions

Back 148

Scopolamine (and other muscarinic antagonists; M3 receptors are found in glands)

Front 149

This drug is a benzoisoquinolinium

Back 149

Cisatracurium

Front 150

Clearance of Cisatracurium

Back 150

Liver and plasma esterases

Front 151

This NMJ blocker is notable for being safe to use in patients with liver and renal diseae

Back 151

Cisatracurium

Front 152

These NMJ blockers effect small muscles before large muscles

Back 152

Pancuronium, vercuronium, rocuronium, cisatracurium

Front 153

This NMJ blocker effects large muscles before small muscles

Back 153

Succinylcholine

Front 154

These NMJ blockers have drug interactions (synergy) with inhaled anesthetics and aminoglycosides

Back 154

NMJ blockers. These include competitive depolarizing (Succinylcholine) and nondepolarizing (Pancuronium, Vercuronium, Rocuronium, Cisatracurium) NMJ blockers.

Front 155

This is the mechanism of action of botulinum toxin

Back 155

Blocks neuronal release of ACh: it interferes with docking of vessicles, interrupting somatic nerve transmission leading to flaccid paralysis

Front 156

This is the strongest toxin known to man

Back 156

Botulinum toxin

Front 157

These NMJ blockers are aminosterols

Back 157

Pancuronium, vercuronium, rocuronium

Front 158

This NMJ blocker is cleared by the kidney

Back 158

Pancuronium

Front 159

These NMJ blockers are cleared by the liver

Back 159

Vercuronium, Rocuronium

Front 160

This NMJ blocker is a depolarizing antagonist

Back 160

Succinylcholine

Front 161

This nicotinic antagonist is the only depolarizing blocker at the NMJ site in clinical use

Back 161

Succinylcholine

Front 162

This drug is two conjoined acetylcholine molecules

Back 162

Succinylcholine

Front 163

Adminstration of Succinylcholine

Back 163

IV drip

Front 164

Pharmacokinetics of Succinylcholine

Back 164

"Fast acting, short lasting" (onset 1 min, duration 5-7 min)

Front 165

This is the mechanism of action of Succinylcholine

Back 165

Phase I block: persistent occupation of receceptor causes prolonged depolarization; Phase II block: receptor is desensitized to agonists, but will respond to other stimuli
*Depolarization-desensitization block*

Front 166

Patients who lack cholinesterase (ChE) are paralyzed for many hours when given this drug

Back 166

Succinylcholine

Front 167

A patient's large muscles of chest and abdomen fasciculate and then go flaccid when given this drug

Back 167

Succinylcholine

Front 168

This drug, in RARE cases, can cause hyperthermia due to calcium ion release from the SR

Back 168

Succinylcholine

Front 169

This general class of drugs can cause histamine release, leading to vasodilation and warmth

Back 169

Muscarinic antagonists (Succiylcholine, Cisatracurium, Pancuronium, Rocuronium, Vercuronium)

Front 170

This is the prototypical muscarinic blocker

Back 170

Atropine

Front 171

This is the prototypical nicotinic blocker

Back 171

Succinylcholine (muscle type), also: Pancuronium, Rocuronium, Vercuronium, Cisatracurium

Front 172

This nondepolarizing nicotinic blocker has no CNS or analgesic effects, but was used early on in surgery

Back 172

Curare

Front 173

This drug is found in the common plant, Jimson weed

Back 173

Atropine

Front 174

This drug is notable for having inherent sympathomimetic activity.

Back 174

Pindolol