Pharm: Autonomics

Front 1

parasympathetic neurons originate from

Back 1

midbrain, medulla oblongata or sacral region

Front 2

where do parasym nerves synaspe with post ganglionic neurons?

Back 2

typically close to the effector tissue

Front 3

parasym preganglionic neurons are

Back 3

long

Front 4

sympathetic preganglion neurons are ___. They originate from _______ spinal cord

Back 4

short; thoracolumbar

Front 5

sympathetic neurons synapse with post ganglionic neurons in:

Back 5

ganglia close to the spinal cord

Front 6

symp and parasymp systems typically work in

Back 6

opposition

Front 7

cholinergic neurons

Back 7

NT is Ach. Pregangl: symp and parasymp. Postgangl: parasymp only

Front 8

adrenergic neurons

Back 8

NT is NEpi. Post ganglionic: sympathic only

Front 9

what releases epinephrine

Back 9

adrenal medulla

Front 10

some adrenergic neurons release

Back 10

dopamine

Front 11

NANC neurotransmitter

Back 11

nitroc oxide

Front 12

muscarinic receptors are innervated by

Back 12

post ganglionic parasympathetic nerves

Front 13

nicotinic receptors are innervated by

Back 13

preganglionic sympathetic and parasympathetic nerves

Front 14

a adrenergic receptors are

Back 14

excitatory, except in GI

Front 15

b adrenergic receptors are

Back 15

inhibitory, except in heart

Front 16

dopamine1 receptors

Back 16

selective vasodilation of renal, mesenteric and coronary vessels

Front 17

SNS to the heart

Back 17

(b-1rc)increases rate, force, conduction velocity, automaticity

Front 18

ParaSNS to the heart

Back 18

(musc rc) decreases rate, force, conduction velocity

Front 19

SNS to GI

Back 19

(a-1 rc) smooth m relaxation, contracts sphincters, decrease secretion= overall inhibition

Front 20

ParaSNS to GI

Back 20

(musc rc) smooth m contractions, relaxes sphincters, secretions increasion.

Front 21

parasympathomimetics

Back 21

increase GI motility

Front 22

SNS to vasculature

Back 22

(a rc), generally vasoconstriction

Front 23

ParaSNS to vasculature

Back 23

(musc rc) generally vasodilation

Front 24

selective vasodilation (of renal, mesenteric and coronary vessels) NT=

Back 24

NO (by NANC) fibers

Front 25

SNS to sweat

Back 25

secretions increased. Horse = b adrenergic rc, non horse = sympathetic cholinergic/muscarinic

Front 26

role of parasympathetic in sweating?

Back 26

none

Front 27

SNS / salivation

Back 27

low volume, viscous

Front 28

ParaSNS / salivation

Back 28

high volume, dilute

Front 29

SNS to eye

Back 29

mydriasis, distance vision.

Front 30

ParaSNS to eye

Back 30

miosis, near vision

Front 31

radial m

Back 31

dilates pupil --> mydriasis. SNS

Front 32

constrictor m

Back 32

constricts pupil --> miosis ParaSNS

Front 33

Ciliary mm

Back 33

ParaSNS= Can lead to glaucoma (tx = anticholinergic, carbonic anhydrase inhibitor, prostaglandins). Also SNS- relaxation

Front 34

what does the ciliary mm control

Back 34

lens thickness( para=contract, symp=relax)

Front 35

define glaucoma

Back 35

increased intraocular pressure

Front 36

effect of muscarinic agonists on ciliary mm

Back 36

increase contraction and increase outflow

Front 37

effect of prostaglandins on glaucoma

Back 37

increase outflow through alternate pathway

Front 38

effect of carbonic anhydrase inhibitors on glaucoma

Back 38

decrase aqueous humor production

Front 39

SNS to urinary bladder

Back 39

relax bladder wall (beta3 rc), sphincter contracts (a1 rc)

Front 40

ParaSNS to urinary bladder

Back 40

bladder wall contracts (M3 rc) sphincter relaxes.

Front 41

what nerve carries paraSNS fibers to bladder wall

Back 41

pelvic n (detrussor m)

Front 42

what nerve carries SNS fibers to bladder wall

Back 42

hypogastric n

Front 43

urinary bladder somatic control is via _____ n. it _____ the sphincter

Back 43

pudendal; contracts

Front 44

NT for pelvic nerve

Back 44

ParasNS = ACh

Front 45

NT for hypogastric nerve

Back 45

SNS= NE

Front 46

NT for pudendal nerve

Back 46

somatic - ACh

Front 47

neurotransmitter for relaxation of urethral smooth m

Back 47

nitric oxide

Front 48

receptor type for contraction of urethral smooth m

Back 48

a1 receptor

Front 49

there is ____ innervation to sweat glands but no _____

Back 49

sympathetic ; parasympathetic

Front 50

postganglionic fiber to sweat glands releases _____ and activates _____ rc to increase sweating.

Back 50

acetylcholine; muscarinic

Front 51

the horse has ______ sympathetic fibers that activate ___ receptor to increase sweating

Back 51

adrenergic ; beta

Front 52

the SNS and paraSNS work in _____ and ____ fashion to regulate organ systems

Back 52

coordianted and opposing

Front 53

cholinergic neurons release

Back 53

ACh

Front 54

adrenergic neurons release

Back 54

NEpi

Front 55

autonomic drugs are most intesively used in

Back 55

cardiology, anesthesiology, emergency/crit care medicine

Front 56

how do drugs work in the autonomic nervous system?

Back 56

generally either activate or block neurotransmitter receptors

Front 57

an agonist will

Back 57

activate receptor, therefore increasing signalling through that receptor

Front 58

an agonist mimics the

Back 58

endogenous signal.

Front 59

ACh relaesed by vagus n at sinoatrial node will ____ heart rate. A cholinergic agonist applied at the sinoatrial node will _____ heart rate.

Back 59

decrease ; decrease

Front 60

an antagonist will

Back 60

block the effect of an agonist.

Front 61

true or false: antagonists have their own inherent/intrinsic activity

Back 61

FALSE

Front 62

antagonists can have dramatic effect by ____ endogenous signal's activity

Back 62

blocking

Front 63

an antagonist may have no effect on ____ cells but may have big effects "_____"

Back 63

isolated ; "in context"

Front 64

autoreceptors

Back 64

presynaptic receptors for the same transmitter; a receptor located on presynaptic nerve cell membranes and serves as a part of a feedback loop in signal transduction (homeostatic manner)

Front 65

indirect drugs will ____ endogenous signals effect.

Back 65

enhance

Front 66

indirect drugs can affect NT ___, ____ and ____

Back 66

synthesis, breakdown and accumulation

Front 67

NANC stands for

Back 67

non adrenergic, non cholinergic

Front 68

nitric oxide synthasse

Back 68

synthesizes NO from arginine

Front 69

NO is a

Back 69

nonpolar gas that readily crosses cell membranes

Front 70

NO plays a role in:

Back 70

vasodilation, bronchodilation, neuronal control of GIT function

Front 71

autonomic drugs are receptor ______

Back 71

mediated

Front 72

can antagonists block exogenous agonists in addition to endogenous signals?

Back 72

yes

Front 73

describe a cholinergic synapse

Back 73

ACh packaged in synaptic vessel, released with depolarization. Activates musc/nic rc.

Front 74

what degrades ACh

Back 74

AChe

Front 75

describe an adrenergic synpase

Back 75

NEpi packaged in synaptic vessel. Released with depolarization. Activates a/b receptor. Reuptake by MAT. Degraded by MAO, COMT

Front 76

MAT

Back 76

monoamine transmitter

Front 77

MAO

Back 77

monoamine oxidase

Front 78

COMT

Back 78

Catechol-O-methyltransferase

Front 79

what degrades NEpi?

Back 79

MAO, COMT

Front 80

neurotransmission is ____ by activating postsynaptic receptors

Back 80

mediated

Front 81

neurotransmission is ____ by activating presynaptic receptors

Back 81

modulated

Front 82

indirect agonists

Back 82

increase effects of the transmitter by blocking its degradation, reuptake. Can also increase synthesis

Front 83

indirect antagonists

Back 83

decrase effects of transmitter by depleting the NT (ex: blocking vesicular packaging)

Front 84

what activates NT release?

Back 84

depolarization of the terminal region of an axon

Front 85

what is ACh synthesized from?

Back 85

choline and acetyl coenzyme A

Front 86

ACh can also interact with presynaptic cholinergic receptors invovled in ______ of ACh release

Back 86

autoregulation

Front 87

how does AChE work?

Back 87

hydrolyzes ACh to choline and acetate

Front 88

which by product of ACh breakdown is recycled?

Back 88

choline

Front 89

what transports NEpi molecules into vesicles?

Back 89

vesicular monoamine transporter (VMAT)

Front 90

which presynaptic receptors will NEpi typcally activate to inhibit further transmitter release?

Back 90

alpha 2

Front 91

are NEpi molecules degraded?

Back 91

no- taken back up into the terminal as intact NEpi

Front 92

Cholinesterase inhibitors are ___ agonists

Back 92

indirect

Front 93

how can indirect drugs work?

Back 93

block degradation of the transmitter, block reuptake, block or activate synthesis, block uptake into synaptic vesicles

Front 94

what stimulates the activity of nitric oxide synthase?

Back 94

neuronal activity

Front 95

NO diffuses into muscle cells where it activates

Back 95

guanalyl cyclase (forms cGMP)

Front 96

a mimetic will

Back 96

activate

Front 97

a lytic will

Back 97

antagonize

Front 98

parasympathomimetics

Back 98

cholinergic agonists

Front 99

parasympatholytics

Back 99

cholinergic antagonists

Front 100

sympathomimetics

Back 100

adrenergic agonists (except in sweat glands/except in horses)

Front 101

sympatholytics

Back 101

adrenergic anatogonists

Front 102

ganglionic blockers

Back 102

mainly parasympatholytic (parasympathetic tone typically dominant)

Front 103

parasympathomimetics will produce what type of effects?

Back 103

increase GI motility, increased secretions, increased bladder wall contractions, bronchospasm, inhibition of heart force/frequency.

Front 104

what type of receptors will parasympathomimetics activate?

Back 104

muscarininc/ M3

Front 105

how is muscarinic receptor activated?

Back 105

direct stim- drug binds directly to rc and acts as an agonist. Indirect stim- endogenous ACh is mediator. Inhibition of acetylcholinesterase leads to elevated endogenous acetylcholine, which then increases cholinergic receptor activation

Front 106

what is the mediator of indirect stimulation of musc rcs?

Back 106

endogenous ACh

Front 107

two functional types of drug effects in the autonomic system. Drugs will either:

Back 107

mimic the effects of the endogenous signal or counteract the effects of the endogenous signal

Front 108

Mimetic responses in parasympathetic system are elicited

Back 108

by cholinergic agonists

Front 109

Lytic responses in parasympathetic system are elicited by

Back 109

cholinergic antagonists

Front 110

Mimetic responses in sympathetic system are elicited by

Back 110

adrenergic agonists

Front 111

Lytic responses in sympathetic system are elicited by

Back 111

adrenergic antagonists

Front 112

Ganglionic blockers: while they block symp and parasymp activation, the main result is

Back 112

reduction in parasym. due to underlying “tone”

Front 113

ACHe

Back 113

typically rapidly inactivates the ach molecules, with a generally short period of receptor activation.

Front 114

You can block excessive receptor activation (or normal levels of activation) by a

Back 114

directing acting antagonist, such as atropine

Front 115

f a direct acting agonist was being used at the time, e.g., if bethanecol was being used to treat micturition difficulties, co-exposure to an anticholinesterase could elicit much more extensive enhancement

Back 115

of parasympathetic signaling

Front 116

most parasympathomimetics are mediated through M3 receptors with the exception being

Back 116

those involved in cardiac function (primarily M2 receptors)

Front 117

A direct agonist

Back 117

physically interacts with the receptor and elicits the endogenous signal-like response

Front 118

An indirect agonist works through

Back 118

modifying the actions of the endogneous signal molecule, such as when acetylcholinesterase inhibitor increases the time for acetylcholine to survive in the synapse and thus be able to activate those receptors.

Front 119

two direct cholinergic agonists

Back 119

bethanecol and pilocarpine

Front 120

bethanechol mechanism

Back 120

similar to acetylcholine but metabolized slowly
Principally muscarinic agonist

Front 121

Bethanecol has some degree of selectivity for _____ over nicotinic receptors.

Back 121

muscarinic

Front 122

bethanecol metabolism

Back 122

slower than ACh

Front 123

why is ACh not suitable to be used as a drug?

Back 123

because of its rapid metabolism

Front 124

bethanechol effects?

Back 124

It will increase GI motility, gut secretions, and . It will increase bladder contractions and facilitate urination.

Front 125

bethanechol primary drug utility

Back 125

to increase urination, stimulate bladder contractions

Front 126

adverse effects of bethanechol?

Back 126

diarrhea or bronchospasms

Front 127

pilocarpine has a ________ ____ action

Back 127

dominant muscarinic

Front 128

pilocarpine effects

Back 128

GI activity, elicits negative chronotropy, and causes miosis.

Front 129

pilocarpine adverse effects

Back 129

diarrhea or increased secretions

Front 130

pilocarpine can be used as a ___ agent

Back 130

miotic agent

Front 131

pilocarpine can be used as a cholingergic agonist to decrease

Back 131

intraocular pressure

Front 132

two general types of cholinesterase inhibitors

Back 132

carbamates and organophosphate

Front 133

difference between carbamates and organophosphates

Back 133

carbamates are relatively short acting inhibitors; organophosphates typically inhibit for much longer times. Carbamates "reversibly" inhibit, organophosphates are irreversible

Front 134

both carbamates and organophosphates cause

Back 134

acetylcholine accumulation and prolonged/excessive stimulation of muscarinic and nicotinic receptors

Front 135

carbamates and organophosphates principally act on the

Back 135

peripheral nervous system

Front 136

two carbamate anticholinesterases

Back 136

neostimine and pyridostigmine

Front 137

do neostigmine and pyridostigmine enter the CNS?

Back 137

no, not readily

Front 138

neostigmine and pyridostigmine cause typical signs of ___ of the ParaSNS

Back 138

overactivity (incrased GI motility, increased secretios, miosis, etc)

Front 139

Why would you want to use either neostigmine or pyridostigmine?

Back 139

1)To reverse a neuromuscular blockade with drug such as tubocurarine 2)To increase smooth mm tone (e.g., after surgery) 3)To increase skeletal mm control (e.g., in mm diseases involving cholinergic signaling)

Front 140

edrophonium

Back 140

has very similar effects as neostigmine and pyridostigmine, but its action is incredibly fast (IV lasts only a few minutes)

Front 141

when is edophonium useful?

Back 141

when diagnosing myasthenia gravis- it increases mm tone for a brief period of time

Front 142

organophosphates are cholinesterase inhibitors that ______________________. Thus, the inhibition of ____ lasts much longer

Back 142

phosphorylate the active site of the enzyme; ACHe

Front 143

two indirect parasympathomimetics

Back 143

cisaparide, metaclopromide

Front 144

cisapride and metaclopromide are NOT __________ but it is thought that they increase __________________________

Back 144

cholinesterase inhibitors; ACh release in the myenteric plexus through activating serotonergic receptors.

Front 145

primary effect of cisapride and metaclopromide is ______. Primary adverse effect would be ________

Back 145

increase GI motility; too much increase leading to ab pain, diarrhea

Front 146

why are metoclopramide and cisapride used?

Back 146

To increase GI motility, i.e., to treat constipation, gastric stasis. (promotility/prokinetic agent)

Front 147

dopaminergic and serotonergic agonists/antagonists can influence GI

Back 147

motility

Front 148

enteric nervous system consists of

Back 148

interactions between serotonin, dopamine, NO, ACh in contraction and secretions.

Front 149

Excitatory (EM) and inhibitory (IM) motor neurons control motility and are found in the _______ throughout the GI tract

Back 149

circular and longitudinal muscle

Front 150

____ control transmission in the enteric nervous system

Back 150

interneurons

Front 151

Ascending interneurons

Back 151

contribute to local motility reflexes

Front 152

descending interneurons participate in

Back 152

migrating myoelectric complexes (MMCs), secretomotor reflexes (REFLEX), as well as local motility reflexes.

Front 153

Secretomotor neurons (SM) have both _________ functions

Back 153

secretory and vasodilator

Front 154

Intrinsic primary afferent nerves (IPAN) respond to

Back 154

chemical stimuli or distension in the gut, thereby exerting actions on blood flow and secretion.

Front 155

___________ of the GI tract conveys information from the enteric nervous system to the brain and vice versa

Back 155

extrinsic innervation

Front 156

examples of resident and infiltrating immune cells that are found largely in the mucosa in physiological states and during states of inflammation

Back 156

mast cells and macrophages

Front 157

Immune cells express cannabinoid receptors and release ________ as chemical mediators, potentially altering gut function.

Back 157

endocannabinoids

Front 158

eCB receptors are found in

Back 158

CNS, PNS, immune cells

Front 159

antinociceptive effecs of cannabinoids are mediated, in part, at the

Back 159

spinal level

Front 160

_____ is the prototype parasympatholytic

Back 160

atropine

Front 161

atropine directly binds to all subtypes of

Back 161

muscarinic receptors

Front 162

atropine has some higher selectivity for ____ salivation and bronchial secretions and sweating (Except in horses)

Back 162

decreasing

Front 163

atropine can be used as a ___ agent and to temporariliy paralyze the ______ m.

Back 163

mydriatic; ciliary

Front 164

atropine effects

Back 164

increase heart rate, decrease GI motility,

Front 165

atropine can cross the _____ and block ____ receptor signalling in the CNS

Back 165

BBB; muscarinic

Front 166

why does atropine need to be used with extreme caution in horses?

Back 166

decrease in gut motility results in colic

Front 167

atropine side effects

Back 167

photophobia, xerostomia, and hyperthermia

Front 168

when is atropine indicated?

Back 168

useful preanesthetic, first like of defense with OP intoxication, treat bronchoconstriction, increase heart rate

Front 169

why is atropine useful as a preanesthetic?

Back 169

decreases respiratory secretions, reduces movement in bowels, bladder

Front 170

four other antimucsarinic drugs

Back 170

aminopentamide, Propantheline, glycopyrrolate, and tropicamide

Front 171

aminopentamide has some selectivity for the ____ system

Back 171

GI

Front 172

tropicamide is used more in

Back 172

opthamology

Front 173

aminopentamide, Propantheline, glycopyrrolate, and tropicamide all act like ____, but cannot __________

Back 173

atropine; cross the BBB

Front 174

there is a ____ ____ of symp and parasymp activity

Back 174

resting tone

Front 175

the dominant resting tone for vasculature is

Back 175

sympathetic

Front 176

the dominant tone for essentially all other autonomic functions is

Back 176

parasympathetic

Front 177

if autonomic ganglia stimulation is blocked, what will be observed is a NET decrease in parasympathetic function in

Back 177

almost all tissues except the blood vessels

Front 178

effects of a ganglionic blocker

Back 178

heart rate (a net reduction in parasympathetic function), decrease GI motility, decrease bladder function, increase eye pupil opening, reduce ciliary mm function, decrease salivation and other secretions (e.g., bronchial).

Front 179

hexamethonium is a competitive blocker of

Back 179

nicotinic r

Front 180

dysautonomia

Back 180

Degeneration of neurons in the autonomic ganglia with associated failure of sympathetic and parasympathetic functions.

Front 181

common signs of dysautonomia include

Back 181

urinary retention, thick nasal discharge, photophobia (mydriasis), anorexia, weight loss

Front 182

canine dysautonomia primariliy is a net reduction in

Back 182

parasympathetic functions (functions under predominant parasymp tone)

Front 183

three therapies of dysautonomia

Back 183

bethanechol (improvement in secretions/urination), pilocarpine (eye drops to reduce photophobia), metoclopramide/cisapride (incraese GI motility)

Front 184

effects of hexamethonium

Back 184

tachycardia, decreased GI motility, mydriasis, urinary retention, dry mouth. Vasodilation/hypotension due to blocking dominant vascular symp tone

Front 185

dysautonomia is a lesion of

Back 185

cell bodies in autonomic ganglia

Front 186

phenylpropanolamine is a mixed sympathomimetic. it is sometimes used topically to treat nasal congestion. Why is it appropriate for this purpose?
A) it can activate B2 receptors in the nasal vasculature leading to vasodilation
B) it can activate B1 receptors in the nasal vasculature leading to vasoconstriction
C) it can activate alpha receptors in the nasal vasculature leading to vasoconstriction
D) it can activate nicotinic receptors at the autonomic ganglia leading to vasoconstriction

Back 186

C) it can activate alpha receptors in the nasal vasculature leading to vasoconstriction

Front 187

medetomidine is an a2 receptor agonist that has sedative and analgesic properties. aside from these useful traits of anesthesia, what is an important propety of this drug?
a) it activates b2 receptors in the vessel of the kidney
b) it typically increases the amount of anesthesia needed
c) it typically decreases the amount of volatile anesthesia needed
d) it activates nicotinic receptors at autonomic ganglia

Back 187

c) it typically decreases the amount of volatile anesthetic needed

Front 188

metoclopramide is a prokinetic agent. why would you use this type of drug?
a) if you needed to increase the RBC concentration in the blood
b) if the patient had a distended urinary bladder
c) if the patient had megacolon
d) none of the above

Back 188

c) if the patient had megacolon

Front 189

what would happen to heart rate following systemic administration of isoproterenol?
a) increase because of direct b1 receptor activation
b) increase because of indirect b1 receptor activation
c) increase because of direct b2 receptor activation
d) increase because of indirect B2 receptor activation

Back 189

a) increase because of direct b1 receptor activation

Front 190

propantheline is
a) an antimuscarinic useful as a preanesthetic agent
b) an antimuscarinic useful for treating tachycardia
c) an antimuscarinic that readily crosses the BBB
d) all of the above

Back 190

c) an antimuscarinic that readily crosses the BBB

Front 191

terbutaline is a direct b2 agonist and effective bronchodilator. if you injected this drug intradermally, what response might you anticipate?
a) reduction in local sweating if the patient is a horse
b) increase in local sweating if the pateitnt is a horse
c) reduction in local swearint if the pateint is a dog
d) increase in local sweating if the patient is a dog

Back 191

b) increase in local sweating if the patient is a horse

Front 192

the ileal muscle can sometimes lose tone (atony) following sx procedures. which of the following drugs might be useful to treat this condition?
a) aminopentamide
b) propanolol
c) clenbuterol
d) neostigmine

Back 192

d) neostigmine

Front 193

dopamine is effective for treating shock because
a) it increases NEpi release to enhance cardiac b1 receptor activation and icnrease cardiac output
b) it increases renal blood flow through direct activation of dopamine D1
c) both a and b are true
d) neither a or b are true

Back 193

c) both a and b are true

Front 194

bethanecol is a drug that can be used to treat dysautonomia, why is it useful?
a) it increases GI motility by activating M3 rc
b) it increases heart rate by activating b1 rc
c) it incraeses urinary output by activating m3 rc at the detrusor m
d) bethanecol should not be used in dysautonomia

Back 194

c) it increases urinary output by activating m3 receptors at the detrusor muscle

Front 195

pheochromocytoma is a tumor of the adrenal gland associated with elevation of serum catecholamines. which of the following drugs might be useful for treating this tumor?
a) phenoxybenzamine
b) phenylephrine
c) dobutamine
d) medeomidine
e) none of the above

Back 195

a) phenoxybenzamine

Front 196

if you injected turbutaline by ID route and detected a drop in systemic blood pressure, what might have happened
a) it may have gained access to the systemic circulation and blocked cardiac b1 rc
b) it may have gained access to the systemic circulation and blocked vascular b2 rc
c) it may have gained access to the systemic circulation and activated cardiac b1 rc
d) it may have gained access to the systemic circulation and activated vascular b2 rc

Back 196

d) it may have gained access to the systemic circulation and activated vascular b2 rc

Front 197

we discussed how NEpi adminstered systemically can lead to a reflex bradycardia. Why does this happen?
a) NEpi markedly increases blood pressure which then activates the baroreceptor reflex to decrease heart rate
b) NEpi activates b2 rc which decreases blood pressure and in turn decreases heart rate
c) NEpi causes an increase in the release of Epi from the adrenal gland when then leads to reflex reduction in heart rate
d) none of the above

Back 197

a) NEpi markedly increases blood pressure which then activates the baroreceptor reflex to decrease heart rate

Front 198

activation of this rather short, postganglionic neuron leads to NO release, which in turn relaxes the urethral sphincter. Where is the location of the cell bodies of the preganglionic neurons which innervate the ganglia of this type of postganglionic neuron?
a) midbrain
b) thoracic cord
c) lumbar cord
d) sacral cord
e) none of these

Back 198

d) sacral cord

Front 199

cisapride and metoclopramide are both indirect parasympathomimetics that can be used as prokinetic agents. how do they work?
a) they block acetylcholine release in the myenteric plexus
b) they enhance ACh release in the myenteric plexus
c) they block NEpi release in the mytenteric plexus
d) they enhance NEpi release in the myenteric plexus

Back 199

b) they enhance ACh release in the myenteric plexus

Front 200

the catecholamines epi, nepi, and isoproterenol can differentially affect blood flow thru the muscles (eg, femoral blood flow). based on their receptor selectivity (a and b as well as subtypes) the following relative femoral blood flow responses are seen with IV administration of
Epi: NEpi : ISO
a) intermediate blood flow : highest blood flow : lowest blood flow
b) lowest : intermediate : highest
c) highest : intermediate : lowest
d) intermediate : lowest : highest

Back 200

d) intermediate : lowest : highest

Front 201

metoprolol is a b1 antagonist. what condition would this be best suited for treating?
a) photophobia
b) xerostomia
c) reversal of medetomidine sedation
d) cardiac tachy arrhythmia

Back 201

d) cardia tachy arrhythmia

Front 202

nephrosplenic ligament entrapment in horses is the physical consitriction of a the large colon by the left kidney and spleen, such that congestion in both spleen and colon occur. a direct a1 agonist can contract the spleen and sometimes rectify this problem. which of the following drugs might be used?
a) clenbuterol
b) cisapride
c) propantheline
d) phenylephrine
e) terbutaline

Back 202

d) phenylephrine

Front 203

which of the following is an inappropriate use of a compounded drug?
a) purchanse of a compounded drug for use in a horse. the drug is no longer manufacturedL it was removed from the human marked due to severe adverse effects in humans
b) purchase of a manufactured human injectable drug compounded for topical use in a cat
c) purchanse of a manufactured cattle antibiotic compounded at a lower concentration for use in a dog with chronic urinary tract infection
d) purchase of a compounded alternative for Clomicalm

Back 203

d) purchase of a compounded alternative for clomicalm

Front 204

which of the following statements cmoparing manufactured drugs and compounded drugs is true?
a) compounded drugs in the us must be formulated from FDA approved bulk chemicals
b) generic manufactured drugs are not quality controlled by the FDA
c) all legal risk incurred when a vet prescribes a compounded drug to a patient is assumed by the compounding pharmacy
d) expiration dates on compounded drugs may not be based on satbility testing and therefore may not be correct

Back 204

d) expiration dates on compounded drugs may not be based on satbility testing and therefore may not be correct

Front 205

which of the following properties of a drug is likely to be associated with hyperpolarization?
a) drug facilitates Cl channel opening
b) drug blocks NEpi reuptake transport
c) drug inhibits monoamine oxidase A
d) drug is an agonist at NMDA glutaminergic ionotropic rc

Back 205

a) drug facilitates Cl channel opening

Front 206

in most species, sympathetic neurons innervating this particular effector release Ach to activate cholinergic rc on the effector cells. what is the end organ innervated by these sympathetic cholinergic neurons?
a) sweat gland
b) salivary gland
c) ocular radial m
d) renal blood vessel

Back 206

a) sweat gland

Front 207

activation of alpha receptors in the sympathetic system is typically stimulatory in nature except for those residing in the
a) heart
b) lungs
c) GI tract
d) blood vessels

Back 207

GI tract

Front 208

isoproterenol is used to treat bronchospasm due to its ability to
a) activate a-adrenergic rc
b) activate b-adrenergic rc
c) block a- adrenergic rc
d) block b-adrenergic rc

Back 208

b) activate beta adrenergic rc

Front 209

pilocarpine is a direct muscarinic agonist. if instilled into the eye:
a) contraction of the radial m will follow
b) contraction of the ocular sphincter m will occur
c) contraction of the ciliary m will result
d) both b and c are true

Back 209

b) contraction of the ocular sphincter muscle will occur

Front 210

at low dosages (<10ug/kg iv in dogs) dopamine will
a) activate b1 receptors in cardiac m
b) increase nepi release in symp fibers innervating the heart
c) increase renal blood flow thru activation of dopamine receptora
d) activate a1 rc in peripheral vessels
e) all except D

Back 210

a) activate beta 1 rc in cardiac muscles

Front 211

epi causes an increase in blood pressure following systemic administration. coexposure to an alpha blocker causes
a) hypotension because of net increased activation of b2 receptors by epi
b) no effect becaues epi has no action at a rc
c) no effect because epi has no action at b rc

Back 211

a) hypotension becaues of net increased activation of beta 2 rc by epi

Front 212

ephedrine is a mixed adrenergic agonist that can work by both increasing Nepi release from symp neurons and by directly activating both a and b rc. it could be used to
a) dilate bronchioles
b) treat urianry incontinence
c) treat nasal congestion
d) all of the above

Back 212

d) all of the above

Front 213

following sx including insertion of a urinary bladder catheter, the bladder smooth muscle may become immobile. which drug might you use to increase bladder detrusor muscle motility?
a) atropine
b) hexamethonium
c) neostigmine
d) aminopentamide

Back 213

c) neostigmine

Front 214

a cat is brought into a clinic presenting with excessive secretions (tearing, salivation, urination). Skeletal muscle fasciculations are present. Upon ocular exam, miosis is observed. Pulmonary auscultation indicates labored breathing with probably obstructive secretions in the upper airways. Atropine is administered and all signs except muscle fasciculations improve. What is the most likely explanation?
a) the cat got into some atropa belladonna
b) the cat ate muscarine containing mushrooms
c) the cat was exposed to an AChE-inhibiting insecticide
d) the cat has dysautonomia

Back 214

c) the cat was exposed to an AChE-inhibiting insecticide

Front 215

metoclopramide is a prokinetic agent (will increase transit thru the GI tract). it is acting as a parasympathomimetic in this setting. it elicits this response by
a) directly acvtivating muscarinic rc in gi smooth m
b) directly activating beta2 rc in Gi smooth m
c) directly activating serotonin rc in GI smooth m
d) directly activating dopamine rc in GI smooth m

Back 215

c) directly acvitvating serotonin rc in gi smooth m

Front 216

colic in a horse is a possible consquence with ocular administration of this agent
a) atropine
b) isoproterenol
c) propantheline
d) phentolamine
e) propanol

Back 216

a) atropine

Front 217

aminopentamide has a relative selectivity for blocking musc rc in the
A) heart
b) airways
c) GI smooth m
D) CNS

Back 217

c) GI smooth M

Front 218

canine dysautonomia involves loss of neurons in autonomic ganglia from an unknown etiology. this leads to subsequent loss of innervation to both symp and parasymp end organs. three common signs in this condition: 1) thick, viscous nasal secretions, 2) dilated pupils, 3) distended bladder, suggest that either the parasymp or symp system is predominantly affected. Which branch of the autonomic nervous system appears most affected in canine dysautonomia?
a) symp
b) parasymp

Back 218

b) parasympathetic

Front 219

what might you expect if a cow was exposed to botulinum toxin?
a) excitation of musc rc in the heart
b) exictation of the nicotinic rc in the somatic m
c) excitation of nicotinic rc in the autonomic ganglia
d) none of the above

Back 219

b) excitation of nicotinic rc in the somatic m

Front 220

sodium nitroprusside is a drug that releases NO when given systemically. knowing what you know about the effects of NO, what would you expect to occur
a) increased GI tract motility
b) incraesed cardiac muscle contraction
c) increased vasodilation
d) increased blood pressure

Back 220

increased vasodilation

Front 221

the pevlic n originates from the sacral cord to innervate the bladder smooth m to contract. this nerve is a
a) symp n that releases nepi
b) parasymp n that releases nepi
c) symp n that relases dopamine
d) parasymp n that releases ACh
e) parasymp n that releases NO

Back 221

d) parasymp n that releases ACh

Front 222

an a2 adrenergic rc is often located on the presynaptic noradrenergic neuron termincal region where it typically:
a) stimulates nepi release
b) inhibits nepi release
c) inhibits epi release
d) inhibits ACh release

Back 222

b) inhibits Nepi release

Front 223

clenbuterol is a selective b 2 rc agonist. you would consider using this when
a) increased cardiac contractile force is needed
b) selective vasodilation
c) decreased nepi release from adrenergic neurons would be advantageous
d) decreased bronchial smooth m contractions is needed

Back 223

d) decreased bronchial smooth m contractions is needed

Front 224

which drug would be expected to incraese nepi release by blockign adrenergic autoreceptors on symp nerve terminals?
a) yohimbine
b) atenolol
c) propanolol
d) clonidine
e) isoproterenol

Back 224

d) clonidine

Front 225

megacolon is a chronic dz that causes ieleus of the colon and requires long term therapy. which one of the following drugs is potentially usefin in treating a cat with megacolon?
a) metaclopramide
b) cisapride
c) apomorphine
d) lidocaine by CRI
e) diazepam

Back 225

b) cisapride

Front 226

which of the following promotes termination of effects induced by sympathetic postganglionic neurons?
a) MAO activity
b) catechol-O-methyltransferase activity
c) reuptake of Nepi into the postganglionic neuron
d) a and b
e) all of the above

Back 226

e) all of the above

Front 227

which of the following agents can be used in combo with neostigmine for reversal of competitive neuromuscular blocking agents to prevent the muscarinic effects of neostigmine?
a) bethanecol
b) pilocarpine
c) glycopyrrolate
d) edrophonium
e) atenolol

Back 227

c) glycopyrrolate

Front 228

which of the following tissues/organs is predominantly under the control of the symp nervous system
a) GI smooth m
b) arterioles and veins
c) myocardium
d) eye
e) b and c

Back 228

b) arterioles and veins

Front 229

which of the following is most likely to cause bronchospasm as an adverse effect?
a) atropine
b) propantheline
c) propanolol
d) phenyoxybenzamine
e) clenbuteral

Back 229

c) propranolol

Front 230

which of the following is most likely to cause hypertension as an adverse effect?
a) phenyephrine
b) isoproterenol
c) yohimbine
d) phenoxyybenzamine
e) terbutaline

Back 230

a) phenylephrine

Front 231

which of the following species is most sensitve to the depressent effects of atropine of GI motility
a) rabbit
b) dog
c) cattle
d) horse
e) cat

Back 231

d) horse

Front 232

which of the following agents is the safest to use a bronchdilator in an animal with cardiac dz?
a) clenbuterol
b) isoproterenol
c) propanolol
d) epi
e) atenolol

Back 232

a) clenbuterol

Front 233

which of the following effects is most likley to be observed after administration of hexamethonium?
a) tachycardia
b) hypertension
c) miosis
d) incraesed peristalsis
e) increased salivation

Back 233

a) tachycardia

Front 234

which of the following is unlikley to be a toxic symptomarising from excessivei nhibition of AChE?
a) salivation
b) miosis
c) tachycardia
d) urination
e) defecation

Back 234

c) tachycardia

Front 235

which of the following has the shortest duration of action?
a) atropine
b) pyridostigmine
c) dopamine
d) propranolol
e) atenolol

Back 235

c) dopamine

Front 236

edrophonium is useful in diagnosis and pyridostigmine useful in tx of myasthenia gravis because:

Back 236

both edrophonium and pyridostigmine are indirect cholindergic agonists that can stimulate cholinergic rcs in the muscles. edrophonium's action is much shorte than pyridostigmine

Front 237

epi is a more potent a agonist than nepi, but if both are injected IV at equivalent dosages, nepi causes greater blood pressure increase. this is because
a) nepi induces the release of dopamine at dopaminergic nerve terminals mediating vasoconstriction
b) nepi is a more potent agonist at b1 rc leading to more pronounced positive ionotropic response
c) epi is a more potent agonist at b1 rc in vessel beds mediating vasodilation
d) epi is a more potent agonist at b2 rc in vessel veds mediating vasodilation

Back 237

d) epi is a more potent agonist at b2 rc in vessel beds mediating vasodilation

Front 238

when using a local anesthetic agent to perform a nerve block, the duration of action can be prolonged by
a) coadministration of epi to activate b2 rc, thus leading to vasoconstriction and lesser systemic absorption of the anesthetic
b) coadministration of epi to activate a1 rc, thus leading to vasonconstriction and lesser system absorption of the anesthetic
c) coadministration of nepi to activate b2 rc, thus leading to vasodilation and lesster systemic absorption of the anesthetic
d) coadministration of nepi to acviate a1 rc, thus leading to vasoconstriction and greater system absorption of the anesthetic

Back 238

b)coadministration of epi to activate a1 rc, thus leading to vasonconstriction and lesser system absorption of the anesthetic

Front 239

dobutamine is a b1 agonist. it is useful for
a) short term tx of heart failure
b) short term tx of bronchospasm
c) short term tx of cardiac arrhythmia
d) short term tx of urinary incontience

Back 239

a) short term tx of heart failure

Front 240

atenolol is a b1 antagonist. based on receptor selectivity, what condition would this be best suited for treating
a) bronchospasm
b) cardiac arrhythmia
c) urinary incontinence
d) reversal of xylazine anesthesia

Back 240

b) cardia arrhythmia

Front 241

binding of an agonist to b2 rc is associated primarily with which of the following effects?
a) tachycardia
B) incrased salivation
c) mydriasis
d) bronchodilation
e) incrased GI motility

Back 241

d) bronchodilation

Front 242

which of the following agents is the safest to use a bronchdilator in an animal with cardiac dz?
a) terbutaline
b) isoproterenol
c) propanolol
d) dobutamine
e) atenolol

Back 242

a) terbutaline

Front 243

which of the following is most likley to cause vasodilation in m, vasoconstriction of cutaneous vessels, and positive chronotropic and inotropic effects on the heart?
a) isoproteerenol
b) nepi
c) ach
d) epi
e) dopamine

Back 243

d) epi

Front 244

if propranolol is administered, followed by epi, what effects of epi will be observed?
a) increased heart rate
b) bronchodilation
c) mydriasis
d) a and b
e) all ofthe above

Back 244

c) mydriasis

Front 245

at low to moderate doses, dopamine has a following pharm effects?
a) vasodilation of coronary vasculature
b) positive inotripic effect
c) vasodilation of mesenteric vasculature
d) a and b
e) all of the above

Back 245

e) all of the above

Front 246

which of the following agents can be used to reverse the effects of a2 agonists such as xylazine?
a) glycopyrrolate
b) neostigmine
c) yohimbine
d) prazosin
e) a and b

Back 246

c) yohimbine

Front 247

which of the following adrenergic agonists will cause in an increase in both heart rate and peripheral resistance?
a) nepi
b) epi
c) isoproterenol
d) low to mod dose of dopamine
e) clenbuterol

Back 247

b) epi

Front 248

which of the following agents would be most appropriate for blocking adrenergic rc in the heart of an asthmatic patient?
a) phenoxybenzamine
b) propranolol
c) prazosin
d) yohimbine
e) atenolol

Back 248

e) atenolol

Front 249

which of the following rc or nt produces biological effects by means of an ion channel?
a) nicotinic
b) muscarinic
c) GABA
d) a and C
e) all off the above

Back 249

d) a and c

Front 250

which of the following drugs would be most effective at reversing the effects of xylazine or clonidine (a2 receptor agonists)
a) glycopyrollate
b) yohimbine
c) aminopentamide
d) terbutaline
e) prazosin

Back 250

b) yohimbine

Front 251

dysautonomia is assocated with a loss of neurons in the autonomic ganglia. If ganglionic neurons are lost nonselectively, this could potentially reduce activation of both sympathetic and parasymp systems. in dysautonomia, however, there is a general reduction in parasym control, leading to mydriasis, thick nasal secretions, photophobia and difficulting urinating with a distended urinary bladder. why is this?
a) parasym tone is predominant over symp tone regulating pupillary constriction, airway secretions and urination
b) symp tone is predominant over parasymp tone regulating pupillary constriction, airway secretions and urination
c) relative predominance of symp/parasymp tone has nothing to do with it

Back 251

a) parasymp tone is is predominant over symp tone regulating pupillary constriction, airway secretions and urination

Front 252

if a cat had excessive spasmodic GI movements and diarrhea, which of these drugs would be reasonable to use?
a) neostigmine
b) bethanecol
c) pilocarpine
d) aminopentamide
e) metoclopramide

Back 252

d) aminopentamide

Front 253

for which of the following conditions would the nonselective b agonist isoproterenol be best suited to treat
a) hypotension
b) urinary incontience
c) bronchospasm
d) reversal of xylazine anesthesia

Back 253

c) bronchospasm

Front 254

glycopyrollate is
a) an antimuscarinic useful as a preanesthetic agent
b) an antimuscarinic useful for treating bradycardia
c) an antimuscarinic with little cns effect
d) all of the above

Back 254

d) all of the above

Front 255

epi given IV can increase blood pressure due to both activation of cardiac b1 rc leading to increased heart contraction and activation of a1 rc leading to vasoconstriction. in the presence of which of the following types of drugs would you get epi reversal (ie, drop in blood pressure following epi dosing)
a) a rc blocker
b) b rc blocker
c) a agonist
d) b agonist

Back 255

a) a rc blocker

Front 256

ephedrine is a mixed adrenergic agonist (Acts directly and thru increased release of nepi). it is sometimes used to treat urinary incontinence in small animals. why is it effective for this purprose?
a) ephedrine can activate b3 rc on the bladder wall to decrase detrusor m contractions
b) in can activate b3 rc in the internal sphincter m to cause net relaxation of the sphincter
c) in can activate a receptors in the internal sphincter m to cause net contraction of the sphincter
d) it can activate nicotinic rc to increase sphincter m contraction

Back 256

c) it can activate a rc in the internal sphincter m to cause net contraction of the sphincter

Front 257

A dog shows bradycardia, excessive urination, diarrhea, and airway secretions. which drug could be used?
a) glycopyrrolate
b) bethanecol
c) metoclopramide
d) none of the above

Back 257

a) glycopyrrolate

Front 258

where is the anatomical site of action of nicotine and nicotine like drugs?
a) at symp ganglia
b) at parasymp ganglia
c) at neither ganglia
d) at both ganglia

Back 258

d) at both ganglia

Front 259

sympathomimetic agents that affect SNS

Back 259

NEpi, Epi, Isoproterenol, dopamine

Front 260

sympatholytic agents that affect SNS

Back 260

phentolamine, phenoxybenzamine, propranolol

Front 261

sympathomimetics (a rc)

Back 261

produce peripheral excitation, vasoconstriction of cutaneous, mucosal, splanchnic and renal vessels

Front 262

sympathomimetics (b rc)

Back 262

peripheral inhibition (relaxation of bronchial and GIT smooth m), vasodialuation of skel vasculature, cardiac excitatoy action (inotropic/chronotropic), metabolic (glyocogenolysis, mobilization of fatty acids)

Front 263

catacholamine MOA

Back 263

direct agonism (a and b)

Front 264

cocaine MOA

Back 264

inhibit reuptake of NEpi in presynaptic terminal

Front 265

amphetamine MOA

Back 265

increased release of NE --> mixed effects

Front 266

MAO inhibitor effects

Back 266

indirect agonism, leads to accumulation of NEpi (mostly central) and EPI (antidepressants)

Front 267

how can drug effects be modified in vivo?

Back 267

reflex compensation

Front 268

which agonists are most effective on a rc? Where are they?

Back 268

Epi > Ne >>>> Iso, in blood vessels (vasoconstriction)

Front 269

which agonists are most effective on B1 rc? Where are they?

Back 269

iso > epi >>= NE; heart

Front 270

which agonists are most effective on B2 rc? Where are they?

Back 270

Iso > epi >>>>> NE; blood vessels (vasodilation)

Front 271

what rc will NE act on?

Back 271

a1, a2, b1 (direct)

Front 272

which rc will EPI act on?

Back 272

a1, a2, b1, b2 (direct acting)

Front 273

which rc will DA act on?

Back 273

a1, a2, b1, D (mixed acting, also incrases Nepi release)

Front 274

which rc will ISO act on?

Back 274

b1, b2 (direct acting)

Front 275

do catecholamines easily cross the BBB?

Back 275

no

Front 276

how are catecholamines eliminated?

Back 276

rapid inactivation, involves diffusion, reuptake, and MAO/COMT metabolism

Front 277

most Nepi effects are in the ____ system

Back 277

cardiovascular

Front 278

EPI effects

Back 278

relaxation of GI smooth muscle/contraction of sphincters, urianry retention, bronchodilation, mydriasis, splenic contraction

Front 279

ISO effects

Back 279

bronchodilation and GI smooth muscle relaxation

Front 280

therapeutic indications of NE

Back 280

limited use

Front 281

therapeutic indications of EPI

Back 281

bronchospasm, cardiac rescusc, hypersens rxns/anaphylactoid shock, vasoconstriction due to prolonged effects of local anesthetics, localized hemorrhage

Front 282

thereapeutic indications of ISO

Back 282

cardiac stim in heart block, bronchospasm

Front 283

DA therapeutic indications

Back 283

hypotension, shock (part with oliguria in conjunct with fluid replacement) acute heart failure

Front 284

how do indirect agonists work?

Back 284

inhibit reuptake, increase release, inhibit breakdown

Front 285

why is Da a mixed acting agonist?

Back 285

also increases Nepi release

Front 286

why is DA useful in shock, only at low doses?

Back 286

low doses cause increase NE release in the heart, activation of B1 rc and overall excitation. Also causes vasodilation of renal and mesenteric vessels via D1. BUT high doses cause system vasoconstriction via a receptors

Front 287

how are catecholamiens generally given?

Back 287

IV

Front 288

phenylephrine

Back 288

a1 agonist

Front 289

dobutamine

Back 289

b1 agonist

Front 290

clonidine, xylazine, medetomidine

Back 290

a2 agonists

Front 291

terbutaline, clenbuterol, albuterol

Back 291

b2 agonists

Front 292

ephedrine

Back 292

mixed, indirect mimetic with some direct a1 and b action)

Front 293

phenylpropanolamine

Back 293

mixed indirect mimetic with some direct a1 action

Front 294

phenoxybenzamine

Back 294

a antagonist

Front 295

prazosin

Back 295

a1 blocker

Front 296

yohimbine, tolazoline, atipamezole

Back 296

a2 antagonists, competitive

Front 297

propranolol

Back 297

non selective b blocker

Front 298

atenolol, metoprolol, esmolol

Back 298

b1 antagonist