Pharm-Pharmacology Of The Autonomic Nervous System

Front 1

adrenal medulla is most like what neurons?

Back 1

post-ganglionic

Front 2

sweat gland post-ganglionic neurotransmitter and receptor

Back 2

ach; muscarinic

Front 3

somatic motor neurons neurotransmitter and receptor?

Back 3

ach; nicotinic

Front 4

nicotinic receptor locations

Back 4

parasympathetic ganglia; skeletal muscle; sympathetic ganglia

Front 5

nicotinic receptors are what kind of receptors?

Back 5

ligand-gated ion channel

Front 6

muscarinic receptor locations?

Back 6

cardiac m., smooth m., glands

Front 7

muscarinic receptor types?

Back 7

M1-M5

Front 8

which muscarinic receptors activate Gq? where are these located? what are effects?

Back 8

M1, M3, M5; s. muscle and secretory glands

Front 9

which muscarinic receptors activate Gi? where located? effects?

Back 9

M2 and M4; heart; binding decreases activity (increased k permeability causes hyperpolarization, which decreases heart rate)

Front 10

which muscarinic receptors are the primary concerns?

Back 10

M2 and M3

Front 11

all adrenergic receptors are what kind of receptors?

Back 11

g-protein coupled receptors

Front 12

t or f: NE binds well to beta-2 receptors?

Back 12

f

Front 13

how is NE made?

Back 13

tyrosine->dopa->dopamine->vesicle enclosed NE

Front 14

possible fates of NE?

Back 14

1. binds to alpha-1 or beta receptors postsynaptically
2. binds to alpha-2 receptors presynaptically
3. taken back to nerve terminal for reuse (70%)

Front 15

when NE binds to beta receptors, what is downstream effect?

Back 15

depolarization

Front 16

what enzyme degrades NE?

Back 16

MAO or COMT

Front 17

how is EPI made?

Back 17

tyrosine->dopa->dopamine->NE->pnmt->EPI

Front 18

where does EPI bind?

Back 18

alpha or beta receptors

Front 19

what is the downstream effect when EPI binds to beta receptor?

Back 19

depolarization

Front 20

t or f: EPI has high affinity for beta-2 receptors

Back 20

t

Front 21

on blood vessels, what receptors are present? which does EPI prefer?

Back 21

beta-2 and alpha-1

Front 22

low dose of EPI effect on blood vessels? high dose?

Back 22

low dose binds beta-2 and causes vasodilation; high dose binds beta-2 receptors first, then alpha-1 receptors, causing increased PVR

Front 23

how is ach formed?

Back 23

glucose->acetyl coa + choline->CAT used to make vesicle

Front 24

downstream effect of ach binding to m-receptor? n-receptor?

Back 24

opens ion channel; increased na influx and k efflux, depolarizing membrane

Front 25

how is ach degraded?

Back 25

acetylcholinesterase breaks into acetate and choline; choline is recycled

Front 26

what is main mechanism of inactivation of NE? ach?

Back 26

recycling

Front 27

t or f: ach can travel easily

Back 27

f

Front 28

what are g-proteins attached to?

Back 28

7 transmembrane receptors

Front 29

what are the 3 g-proteins? what do they do?

Back 29

Gs-activates adenyl cyclase; Gi-inhibits adenyl cyclase; Gq-activates plc-beta

Front 30

what are the 4 signal transduction mechanisms?

Back 30

ligand regulated ion channels; membrane receptor linked via g-proteins; tyrosine kinase; intracellular receptors

Front 31

what are the 2 possible results of depolarization in ligand regulated ion channels?

Back 31

n-subclass-n increases firing; n-subclass-m increases contraction

Front 32

which receptors work by ligand regulated ion channels?

Back 32

nicotinic

Front 33

which receptors work by membrane receptor linked via g proteins? (hint:3 groups)

Back 33

1. alpha-1, M1, M3, and M5
2. alpha-2, M2, M4
3. beta-1, beta-2, beta-3

Front 34

steps involved in membrane receptor linked via g-proteins for alpha-1, M1, M3, and M5?

Back 34

ligand binds to 7 transmembrane receptor->GDP exchanged for GTP to form Gq-GTP complex->GTP binds to plc-beta->plc-beta cleaves pip2 into dag and ip3->ip3 binds to channels causing ca release->contraction/secretion occurs->ca binds with pkc->dag binds with pkc->phosphorylation of downstream proteins

Front 35

steps involved in membrane receptor linked via g-proteins for alpha-2, M2, and M4 receptors?

Back 35

same steps as for alpha-1, M1, M3, and M5 except that Gi-GTP complex inhibits adenyl cyclase->increased k permeability->decreased neurotransmitter release

Front 36

alpha-2 receptors can also be located where? what is their effect?

Back 36

cholinergic postganglionic neurons; decreased ach release

Front 37

what are the locations and effects of the three beta receptors?

Back 37

1. beta-1 is on the heart, causes increased rate and increased force of contraction
2. beta-2 is on the lungs and causes relaxation; skeletal muscle (causes tremors when EPI binds); and on the liver and causes glucose production
3. beta-3 is located in adipose tissue and causes lipolysis

Front 38

what is the signal transduction for beta receptors?

Back 38

same as alpha-1, M1, M3, M5, alpha-2, M2, and M4 except that the Gs-GTP complex binds to adenylate cyclase->atp converted to camp->pka activation->downstream phosphorylation

Front 39

steps in tyrosine kinase signaling?

Back 39

transmembrane protein is bound to tyrosine kinase->ligand binds to receptor and activates it->cell signaling

Front 40

steps to intracellular receptor signaling?

Back 40

agonist is lipid soluble (NO, steroids)->transported to nucleus->activates translation and transcription

Front 41

alpha-1 agonist effects on bp? effect on glands?

Back 41

contraction of blood vessels->increased pvr->increased bp; glands will secrete

Front 42

what happens when you increase k permeability on the cardiac myocyte?

Back 42

hyperpolarization that slows heart rate

Front 43

what are the affinities of EPI and NE for adrenergic receptors?

Back 43

1. EPI: alpha-1=alpha-2; beta-1=beta-2
2. NE: alpha-1=alpha-2; beta-1>beta-2

Front 44

is the iris sphincter parasympathetic or sympathetic innervation?

Back 44

parasympathetic

Front 45

is the iris radial parasympathetic or sympathetic?

Back 45

sympathetic

Front 46

what are the neurotransmitter, receptor, and effect of the iris sphincter?

Back 46

ach binds to M3 receptor to cause contraction and miosis

Front 47

what are the neurotransmitter, receptor, and effect of the iris radial?

Back 47

NE binds to alpha-1 receptor to cause contraction and mydriasis

Front 48

how are lacrimal glands innervated? how are they stimulated?

Back 48

parasympathetics; ach binds to M3 to increase secretion

Front 49

what is the effect of the ciliary muscle relaxing? contracting?

Back 49

far vision; near vision

Front 50

how are the ciliary muscles innervated? how are they stimulated?

Back 50

parasympathetics; ach bind to m-receptors to contract muscle, which will change the lens to short and fat for near vision

Front 51

what causes open angle glaucoma? closed angle glaucoma?

Back 51

1. open-blocked aqueous outflow
2. too little space between cornea and iris

Front 52

what are 2 ways to induce mydriasis?

Back 52

1. give M3 antagonist (blocks m-receptors)
2. give alpha-1 agonist

Front 53

if an m-antagonist is given to dilate pupil, what happens to their vision?

Back 53

m-antagonist decreases near vision by relaxing ciliary muscle

Front 54

will an alpha-1 agonist cause blurry vision?

Back 54

no, because near/far vision is regulated by m-receptors

Front 55

what drugs could you give to help with trouble breathing?

Back 55

1. beta-2 agonist to vasodilate and thus bronchodilate
2. M3 antagonist to block mucus secretion and bronchoconstriction

Front 56

what 3 things do the parasympathetics do to GI tract? which receptor?

Back 56

1. increase secretion, relax sphincters, increase contractions
2. M3

Front 57

what 2 things do the sympathetics do to GI tract? which receptors?

Back 57

1. contract sphincters-alpha-1
2. relaxation-alpha-2 and beta-2

Front 58

if a patient has too much gastric acid secretion, what drug can be given?

Back 58

M3 antagonist

Front 59

what are the parasympathetic receptors on the bladder? what are their effects?

Back 59

1. M receptors
2. Contract the detrusor and relax the trigone

Front 60

what are the sympathetic receptors on the bladder? what are their effects?

Back 60

1. beta-2 receptor relaxes the detrusor
2. alpha-1 receptor contracts the trigone

Front 61

what drug can be given for urinary incontinence?

Back 61

M-blocker because it will relax the detrusor and contract the trigone

Front 62

what are the parasympathetics and sympathetics of erection and ejaculation?

Back 62

1. erection-parasympathetic-M receptors
2. ejaculation-sympathetic-alpha-1 receptors

Front 63

what are the effects of muscarinic receptors on blood vessels?

Back 63

1. activation of M3 receptors on endothelial cells induces NO
2. NO diffuses to vascular smooth muscle and activates guanylyl cyclase
3. guanylyl cyclase increases production of cgmp
4. cgmp causes smooth muscle relaxation and vasodilation

Front 64

how do parasympathetics and administration of a m-agonist differ in their effects on pvr?

Back 64

1. parasympathetics don't change pvr because they don't innervate blood vessels
2. an m-agonist on blood vessels will cause NO release and end up with smooth muscle relaxation and vasodilation (lowers pvr)

Front 65

which blood vessels are innervated by the parasympathetics?

Back 65

salivary glands, GI glands, erectile tissue

Front 66

which receptors are on blood vessels? what are their effects?

Back 66

1. alpha-1 receptors on most blood vessels (vasoconstriction)
2. beta-2 receptors on liver and skeletal muscle (vasodilation)

Front 67

what are the autonomics of the heart?

Back 67

1. parasympathetics- M-receptors (decrease HR, force of contraction, and conduction velocity)
2. sympathetics- beta-1 receptors (do the opposite)

Front 68

stimulation of which receptor will cause greatest increase in CO?

Back 68

beta-1

Front 69

what is a side effect of a m-blocker?

Back 69

dry mouth

Front 70

which glands do the parasympathetics work on? which receptors?

Back 70

1. salivary and nasopharyngeal
2. M3

Front 71

which glands to sympathetics work on? which receptors?

Back 71

1. sweat glands
2. M3 (thermoregulatory) and alpha-1 (palms)

Front 72

what is a possible side effect of beta-blockers on diabetics?

Back 72

blocking beta-2 receptors leads to decreased gluconeogenesis and glycogenolysis

Front 73

describe autonomics to the endocrine glands. what is the predominant effect of EPI on insulin release?

Back 73

1. pancreas- alpha-2 decreases insulin release and beta-2 increases insulin release
2. kidney- beta-2 increases renin release
3. EPI inhibits insulin release

Front 74

what happens to bp when EPI is given in high doses? low doses?

Back 74

1. increased bp->as response wanes->decreased bp
2. little or no effect on bp

Front 75

why is there little or no effect on bp when EPI is given in low doses?

Back 75

increased bp from increased heart rate and increased contractility is countered by tpr decrease from vasodilation that occurs when EPI acts preferentially to beta-2 receptors

Front 76

explain bp pressor and depressor effects of high dose EPI

Back 76

1. pressor-due to increased heart rate, contractility, and vasoconstriction in vascular beds
2. depressor effects due to beta-2 activation, which vasodilates (not seen initially due to alpha-1 vasoconstricting effects)
3. effects of alpha-1 wane, but effects of beta-2 remain

Front 77

what is epinephrine reversal?

Back 77

pretreat person with alpha adrenergic blocker and only the beta-2 vasodilation effects are seen, decreasing tpr and bp

Front 78

which has a lower threshold to activation by low dose EPI, alpha-1 or beta-2 receptors?

Back 78

beta-2 receptors

Front 79

what happens during stage fright? what drug can help this?

Back 79

1. excess EPI binds to beta-2 receptors, causing skeletal muscle contractions
2. beta-2 blocker

Front 80

how does EPI work on a beta-2 receptor? in what condition can this mechanism be advantageous?

Back 80

1. EPI binds to beta-2 receptor, causes k influx into skeletal muscle
2. hyperkalemia

Front 81

generally speaking, what do alpha-1 receptors do? alpha-2 receptors?

Back 81

1. smooth muscle contraction
2. presynaptic regulation of neurotransmitter

Front 82

generally speaking, what do beta-1 receptors do? beta-2 receptors?

Back 82

1. cardiac stimulation
2. smooth muscle bronchodilation and skeletal muscle vasodilation

Front 83

potency rank for alpha-adrenergic receptors?

Back 83

EPI>NE>isoproterenol

Front 84

potency rank for beta-adrenergic receptors beta-1? beta-2?

Back 84

1. iso>EPI=NE
2. iso>EPI>NE

Front 85

what is the formula for bp?

Back 85

SV x HR X TPR

Front 86

NE binds to which receptors?

Back 86

alpha-1=alpha-2; beta-1>beta-2

Front 87

EPI binds to which receptors?

Back 87

alpha-1=alpha-2; beta-1=beta-2

Front 88

isoproterenol binds to which receptors?

Back 88

beta-1=beta-2; beta>alpha

Front 89

effect of low dose EPI, NE, and ISO on bp?

Back 89

1. no change
2. increase
3. decrease

Front 90

effect of low EPI, NE, and ISO on hr?

Back 90

1. increase
2. decrease
3. increase

Front 91

effects of low dose EPI, NE, and ISO on tpr?

Back 91

1. decrease
2. decrease
3.increase

Front 92

how do we calculate mean arterial pressure?

Back 92

map=co x tpr

Front 93

how do we calculate stroke volume?

Back 93

sv=end diastolic volume-end systolic volume

Front 94

activation of what receptors will result in increased tpr?

Back 94

alpha-1

Front 95

activation of what receptors will result in increased co?

Back 95

beta-1

Front 96

how are EPI and NE given?

Back 96

parenterally due to low oral bioavailability

Front 97

why do NE and EPI have low oral bioavailability?

Back 97

high amounts of mao and comt in gut and liver

Front 98

EPI vs. NE in binding to alpha-1, beta-1, and beta-2 receptors?

Back 98

1. E >/= N
2. E=N
3. E>>N

Front 99

what are the overall effects of EPI and which receptors are activated?

Back 99

1. increase systolic pressure via beta-1 on heart
2. vasodilation in vascular bed of skeletal muscle via beta-2
3. vasoconstriction of vascular bed in kidney via alpha
4. increases coronary blood flow
5. increases aqueous humor drainage via alpha
6. dilates the pupil via alpha
7. relaxes bronchial smooth muscle via beta-2

Front 100

what are the overall effects of EPI and which receptors are activated?

Back 100

1. increases tpr and diastolic pressure more than EPI because it can't vasodilate via beta-2 receptors like EPI
2. increases systolic pressure
3. directly stimulates heart

Front 101

what is dipivefrin? what are the effects? how is it given?

Back 101

1. prodrug converted to EPI
2. ophthalmic agent
3. topical

Front 102

what kind of a drug is dopamine? what receptors does it activate? what are its effects on these receptors?

Back 102

1. catecholamine
2. alpha, beta-1, and dopamine
3. increases hr and contractility via beta-1
4. reduces arterial resistance and increases blood flow via dopamine

Front 103

what are the effects of dopamine at low doses? high doses?

Back 103

1. increases systolic pressure
2. vasoconstriction

Front 104

what can be given in treatment of minor hemorrhage? mechanism of action?

Back 104

EPI will activate alpha-1 receptors to vasoconstrict blood vessels in the area

Front 105

what can be given in treatment of anaphyaxis? mechanism of action?

Back 105

1. angioedema-high dose EPI activates alpha-1 to constrict capillaries
2. bronchoconstriction-EPI activates beta-2 to bronchodilate
3. pruritus-activates b-receptors on mast cells to suppress mediator release
4. hypotension-activates alpha-1 and beta-2 receptors to vasoconstrict and raise bp

Front 106

does high dose EPI cause reflex bradycardia?

Back 106

no

Front 107

what can be given to stop premature labor?

Back 107

terbutaline will activate beta-2 receptors, causing uterine smooth muscle relaxation

Front 108

why is NE not drug of choice in anaphylaxis?

Back 108

EPI has better affinity for receptors needed to stop reaction; NE doesn't bind to beta-2 to stop the bronchoconstriction

Front 109

what are the 3 therapeutic effects of phenylephrine?

Back 109

nasal congestion, hemorrhoids, and psvt

Front 110

how does phenylephrine work?

Back 110

activates alpha-1 to vasoconstrict blood vessels, increasing bp->activates baroreceptors->increased parasympathetics to heart->activation of m-receptors on av node, slowing it->stops arrythmia

Front 111

what are side effeccts of phenylephrine?

Back 111

shrinks mucosa when not needed

Front 112

what would be used for av block?

Back 112

beta-1 agonist to increase av conduction (EPI or ISO)

Front 113

compare phenyleprhine, xylometazoline, oxymetazoline, ephedrine, and pseudoephedrine in the treatment of nasal congestion

Back 113

1. phenyleprhine-short duration (topical, oral)
2. xylometazoline-long duration (topical)
3. oxymetazoline-long duration (topical)
4. ephedrine-indirect effect through release of NE; has NO REBOUND EFFECT
5. pseudoephedrine-indirect effect through release of NE; less side effects than ephedrine

Front 114

what is the problem with chronic activation of alpha-1 receptor in nasal mucosa?

Back 114

downregulation of receptor->once stopped, insufficient NE to activate receptors (rebound nasal congestion)

Front 115

compare beta-2 agonists, ephedrine, atropine, and ipratropium bromide in treatment of asthma and copd

Back 115

1. short and long-acting beta-2 agonists cause bronchodilation
2. ephedrine-seldom used for this due to cardiac and cns
3. atropine-blocks M3, which reverses bronchoconstriction and secretion
4. ipratropium bromide is short acting, inhaled, works like atropine, which is how copd is reversed (less side effects than beta-agonists)

Front 116

which beta-2 agonists are short acting?

Back 116

1. albuterol
2. metaproterenol
3. bitolterol
4. pirbuterol
5. terbutaline

Front 117

which beta-2 agonists are long acting (at least 15 minutes)

Back 117

1. salmeterol
2. formoterol
3. arformoterol

Front 118

compare treating asthma with ipratropium vs. beta-2 agonist

Back 118

asthma may have minimal bronchoconstriction caused by parasympathetics, which means beta-2 agonist works better

Front 119

compare treating copd with ipratropium vs. beta-2 agonist

Back 119

copd may have significant bronchoconstriction caused by parasympathetics, which means that ipratropium works just as well as beta-2 agonists

Front 120

what is the advantage of giving albuterol vs. EPI/isoproterenol to treat asthma?

Back 120

albuterol only targets beta-2 receptor, EPI/ISO also affects beta-1 receptors

Front 121

compare phenylephrine, atropine, scopolamine, and tropicamide in dilatint the pupil

Back 121

1. phenylephrine-alpha-1 agonist on iris radial smooth muscle->contracts iris radial smooth muscle, dilating pupil without cycloplegia
2. atropine-blocks m-receptors on iris sphincter smooth muscle (long-acting)
3. scopolamine-same as atropine
4. tropicamide-same mechanism as atropine, but is short-acting

Front 122

what is cycloplegia?

Back 122

paralysis of the ciliary muscle

Front 123

what are side effects of adrenomimetics on alpha-1 receptors? beta-1 receptors? beta-2 receptors?

Back 123

1. alpha-1 effects on blood vessels->vasoconstriction->cv problems/ischemia at site
2. alpha-1 effects on nasal mucosa->rebound nasal congestion
3. alpha-1 effects on pupils->photophobia or narrow angle glaucoma
4. beta-1 effects on heart->increased heart rate->heart problems
5. beta-2 effects on liver->hyperglycemia
6. beta-2 effects on skeletal muscle->tremors

Front 124

contraindications of adrenomimetics?

Back 124

1. cv disease (alpha-1 effects)
2. hyperthyroidism (heart is sensitive to catecholamines in hyperthyroidism patients->exaggerated effect)
3. diabetes (beta-2 effects)

Front 125

what is the action of mao inhibitors?

Back 125

blocks mao->indirect acting adrenomimetics are not metabolized->buildup leads to increased NE release

Front 126

what is the interaction between mao inhibitor and tyramine?

Back 126

1. tyramine comes from gut bacteria
2. if not metabolized->tyramine travels to synaptic nerve terminal->buildup leads to increased NE release

Front 127

what is the effect of an mao inhibitor on a patient who eats a lot of cheese and drinks a lot of beer?

Back 127

hypertensive reaction due to buildup of tyramine, which increases NE release

Front 128

describe ephedrine and pseudoephedrine mixed effects

Back 128

1. ephedrine-acts directly on alpha and beta receptors; indirectly releases NE
2. pseudoephedrine-acts directly on alpha and to a lesser extent beta receptors; indirectly releases NE

Front 129

t or f: ephedrine crosses the bbb?

Back 129

t

Front 130

what receptors does ephedrine act on in the cns?

Back 130

alpha and beta receptors

Front 131

what are the therapeutic effects of ephedrine?

Back 131

asthma and copd (beta-2), and nasal congestion (alpha-1)

Front 132

does ephedrine show rebound effect on alpha-1 receptors when used in treating nasal congestion?

Back 132

no

Front 133

what is the route of administration for ephedrine and pseudoephedrine?

Back 133

1. oral
2. nasal

Front 134

what drug has replace pseudoephedrine? why?

Back 134

phenylephrine; pseudoephedrine was used in meth labs

Front 135

why is ephedrine seldom used for asthma?

Back 135

cv and cns adverse effects

Front 136

what class of drugs can be used to treat nasal congestion in general?

Back 136

alpha-1 selective agonists

Front 137

what are the therapeutic uses of the alpha-1 selective, reversible antagonists?

Back 137

1. prazosin-htn, bph, raynaud's disease
2. teazosin-htn/bph
3. doxazosin-htn/bph
4. tansulosin-bph
5. alfuzosin-bph

Front 138

what is the mechanism of action in alpha-1 blockers?

Back 138

blocking the alpha-1 receptor prevents binding of EPI/NE

Front 139

how do alpha-1 blockers treat raynaud's disease? which is drug of choice? which would not be used?

Back 139

1. alpha-1 blockers prevent vasospasm in digits
2. prazosin
3. tamsulosin

Front 140

what are the actions of muscarinic agonists?

Back 140

parasympathetic effects: decreased hr, vasodilation via NO, ciliary contraction, miosis, increased gi activity, and micturition

Front 141

why are muscarinics used often?

Back 141

many side effects

Front 142

what are some problems with ach usage?

Back 142

very non-specific and is metabolized quickly by gi enzymes

Front 143

what disease can be treated with muscarinic agonists?

Back 143

sjogren's syndrome

Front 144

describe moa of pilocarpine and cevimeline in treating sjogren's syndrome

Back 144

1. oral->m-receptors->salivation
2. more selective for salivary glands only; longer lasting; fewer side effects than pilocarpine

Front 145

which m-receptor is found on salivary glands?

Back 145

M3

Front 146

compare moa of bethanechol, neostigmine, alpha-1 antagonists, and muscarinic antagonists in treating urinary retention or incontinence

Back 146

1. treats non-obstructive urinary retention->m-agonist->stimulates bladder (used for post-op)->given orally or sc
2. treats urinary retention->indirect psns->inhibits ache->increases ach->stimulates bladder
3. treats urinary retention->blocks alpha-1 trigone contraction->relaxes trigone->stimulates bladder
4. treats urinary incontinence->relaxes ureter and bladder->constricts urinary sphincter->sedates bladder

Front 147

can bethanecol be used to treat bph?

Back 147

no, because bph is a form of urinary obstruction and bethanecol can only be used to treat non-obstructive urinary retention

Front 148

what is the drug of choice in treating bph? why? moa?

Back 148

1. tamsulosin
2. greater affinity for the alpha-1-a receptors in the prostate
3. blocks alpha-1-a receptor->relaxes smooth muscle in base of bladder and prostate->improved urine flow

Front 149

where are alpha-1-b receptors located?

Back 149

vascular smooth muscle

Front 150

what are side effects of muscarinic agonists?

Back 150

1. excessive salivation
2. excessive sweating
3. intestinal cramps, nvd, increased gastric acid production
4. vasodilation via M3 receptors->increased hr and force of contraction
5. bradycardia (common) via m2 receptors, reflex tachycardia
6. bronchoconstriction, dyspnea, asthma attack
7. contracts ciliary muscle and iris sphincter

Front 151

describe the effects of baroceptor reflex vs. drug action

Back 151

if a drug causes a change in pvr, but also works directly on the heart, the reflex reaction wins over the direct heart effect

Front 152

poisoning by mushrooms can have effects similar to which drug class?

Back 152

muscarinic agonists

Front 153

what is the advantage of using ipratropium bromide instead of atropine?

Back 153

atropine crosses bbb and causes cns side effects; ipratropium bromide does not cross the bbb

Front 154

what is the advantage of using a muscarinic blocker prior to surgery?

Back 154

they help to reduce secretions, create amnesia, and induce sedation

Front 155

why does atropine have no effect on ventricular arrythmias?

Back 155

1. because it only works on muscarinic receptors in the atria (m-receptors normally decrease hr)
2. beta-2 receptors are in the atria and ventricles (b-2 normally increases hr)

Front 156

would atropine work better on asthma or copd? why?

Back 156

1. atropine is an m-blocker, and would work better on copd because it is caused mostly by psns problems; asthma is not usually caused by psns problems
2. atropine->blocks bronchoconstriction and mucus secretion

Front 157

why can an m-blocker be used for acute rhinitis?

Back 157

because it blocks m-receptors on nasopharyngeal glands to reduce mucus secretion

Front 158

what are the thereapeutic uses of m-blockers?

Back 158

1. hyperactive carotid sinus syndrome
2. vagal-induced heart block (prevents av block and bradycardia)
3. gi tract-gi spasm
4. motion sickness-vestibular apparatus signals to vomit center can be blocked
5. urinary incontinence-ach is blocked from activating bladder

Front 159

what are dicyclomine and hyoscyamine used for?

Back 159

gi spasm

Front 160

can m-blockers be used in ulcers? ibs?

Back 160

1. too many side effects
2. questionable efficacy

Front 161

what drug treats motion sickness?

Back 161

scopolamine

Front 162

which m-blockers can be used to treat urinary incontinence?

Back 162

1. tolterodine
2. oxybutynin chloride
3. darifenacin
4. solifenacin
5. trospium chloride

Front 163

what are some adverse effects of m-antagonists?

Back 163

cns effects

Front 164

rate the side effects for scopolamine, atropine, and ipratropium

Back 164

scopolamine>atropine>>ipratropium

Front 165

contraindications for m-antagonist?

Back 165

narrow angle glaucoma

Front 166

what is nicotine? what does it do?

Back 166

1. ganglionic stimulant
2. stimulates cns, autonomic ganglia, adrenal medulla, and neuromuscular junction

Front 167

what are some ganglionic blockers? what is their moa?

Back 167

1. trimethaphan
2. mecamylamine
3. moa-nicotinic receptor antagonist

Front 168

physostigmine, neostigmine, pyridostigmine, and organophosphates: which crosses bbb

Back 168

physostigmine and organophosphates

Front 169

which alpha-1 antagonists treat htn?

Back 169

prazosin, terazosin, doxazosin

Front 170

what 3 drugs treat pheochromocytoma?

Back 170

phentolamine, phenoxybenzamine, and propranolol

Front 171

what should be used in conjunction with an alpha-blocker in the treatment of htn due to pheochromocytoma?

Back 171

beta-antagonist

Front 172

how does propranolol affect pheochromocytoma?

Back 172

beta-blocker blocks beta-1 on kidneys->decreases blood pressure

Front 173

what happens if beta-blocker is given without an alpha blocker in treatment of pheochromocytoma?

Back 173

1. beta-blocker will also block beta-2 on smooth muscle->vasoconstriction->htn
2. the alpha-blocker will block the vasoconstrictive effects on the blood vessels to lower bp

Front 174

what are adverse reactions in alpha-antagonists?

Back 174

1. orthostatic hypotension- 1st dose effect
2. reflex tachycardia- alpha-1 blockers decrease pvr->baroreceptor increases hr
3. nasal congestion
4. salt and water retention- decrease in bp will reduce kidney perfusion
5. inhibition of ejaculation- blocks alpha-1 on prostate, seminal vesicles, and vas deferens
6. h/a, weakness, vertigo- due to bp increase

Front 175

baroreceptor reflex?

Back 175

1. inhibitory signals to m-receptors on heart->increase hr/force
2. excitatory signals to beta-1 receptors on heart->increase hr/force
3. excitatory to alpha-1 on blood vessels->vasoconstrict

Front 176

why is venoconstriction important in baroreceptor reflex?

Back 176

blood would only pool in veins and never make it to heart to increase co

Front 177

what is the s-isomer of betaxolol?

Back 177

levobetaxolol

Front 178

how can you remember beta-1 selective, competititive, reversible antagonists?

Back 178

all begin with b, e, a, or m (take levo out of levobetaxolol)

Front 179

therapeutic uses of beta-blocker for cv disease?

Back 179

1. htn
2. ischemia
3. arrythmia
4. mi
5. heart failure

Front 180

how are beta-blockers used in migraines?

Back 180

prophylaxis only

Front 181

2 theories of beta-blocker effects on migraines?

Back 181

1. if migraines are from dilated blood vessels, then beta-blocker will block beta-2, which will vasoconstrict vessels
2. beta blockers block beta-1 on kidneys->inhibit renin->decrease arachidonic acid and prostaglandins->might affect serotonin

Front 182

how do essential tremors and parkinson's tremors differ?

Back 182

essential occurs in action; parkinson's occurs at rest

Front 183

can beta-blockers work on parkinson's tremors?

Back 183

no

Front 184

how do beta-blockers affect essential tremors?

Back 184

bind to beta-2 on red, slow-contracting skeletal muscle fibers->stops tremor

Front 185

what causes esophageal varices?

Back 185

1. portal hypertension
2. cirrhosis->portal htn

Front 186

how can a non-selective beta-blocker prevent variceal bleeding? should you try to block beta-1 or beta-2?

Back 186

1. reduction of blood into esophageal veins
2. you should try to block both beta-1 (to lower hr) and beta-2 (to vasoconstrict)

Front 187

what are adverse effects of beta-blockers?

Back 187

1. cardiac- bradycardia, av block, decrease contractility
2. cns- nightmares, depression, insomnia (if this occurs, switch to non-lipid soluble form)
3. nvd
4. sexual dysfunction (placebo)
5. increases tg and lowers hdl
6. rebound htn- chronic therapy upregulates beta-receptors (withdrawal will cause rebound htn)

Front 188

what is an adverse effect of propranolol?

Back 188

decreases hr/force->decreases co->decreases sv->hypotension

Front 189

contraindications for beta-blockers?

Back 189

1. diabetes- beta-blocker stops beta-1 on heart from increasing hr in hypoglycemia, which is a warning sign to eat
2. liver- beta-blocker stops beta-2 receptor from activating gluconeogenesis/glycogenolysis to increase glucose levels
3. bronchospasm- beta-blockers block beta-2->bronchoconstriction
4. atherosclerosis- beta-blockers cause unopposed vasoconstriction

Front 190

how does propranolol affect exercise?

Back 190

1. normally, hr increases in exercise
2. patient on propranolol won't have hr increase->fatigue->exercise intolerance

Front 191

non-selective and beta-1 selective blockers are contraindicated in what disease? why?

Back 191

1. asthma
2. high doses can block beta-2 receptors as well as beta-1 receptors

Front 192

tetraethyl pyrophosphate is used for what?

Back 192

insecticide

Front 193

how are reversible ache inhibitors hydrolyzed?

Back 193

they bind to ache and are slowly hydrolyzed->impairs ability of ache to hydrolyze ach (30 minutes-6 hours, but clinical effects last 2.5-4 hours)

Front 194

what happens to ach in presence of neostigmine?

Back 194

neostigmine binds to ache and is slowly hydrolyzed->impairs ability of ache to hydrolyze ach->ach stays in synapse longer->increased ach activity

Front 195

what are therapeutic uses of neostigmine?

Back 195

1. lipid soluble->crosses bbb
2. miotic (topical)
3. glaucoma (topical)
4. reverses antimuscarinic effects from m-blocking plants and drugs

Front 196

what non-selective, competitive, reversible beta-antagonists can treat migraines? what selective, competitive, reversible beta-antagonists can treat migraines?

Back 196

1. propranolol, nadolol, timolol
2. metoprolol and atenolol

Front 197

what non-selective, competitive, reversible beta-antagonists can treat oag? what selective, competitive, reversible beta-antagonists can treat oag?

Back 197

1. timolol, carteolol, and levobunolol
2. betaxolol an levobetaxolol

Front 198

what happens with irreversible ache inhibitors that makes them dangerous?

Back 198

covalently change ache->perpetuating ach effects

Front 199

what are possible problems with physostigmine?

Back 199

1. sites of action are all cholinergic synapses->many side effects
2. asystole, respiratory problems, seizures

Front 200

neostigmine and pyridostigmine act directly on which receptors?

Back 200

n-subclass-m receptors

Front 201

what are therapeutic uses of neostigmine and pyridostigmine?

Back 201

1. neostigmine treats post-op urinary retention and abdominal distension
2. neostigmine and pyridostigmine treat myasthenia gravis

Front 202

how can muscle strength be increased in myasthenia gravis patients?

Back 202

inhibit ache->increase ach concentration in neuromuscular junction

Front 203

how does a reversible ache inhibitor work on myasthenia gravis?

Back 203

1. myasthenia gravis-antibodies to n-subclass-m receptors cause down regulation of receptor
2. this impaires action of ach on skeletal muscle->weakness
3. inhibiting ache in neuromuscular junction prolongs ach effect in junction

Front 204

compare neostigmine, pyridostigmine, and edrophonium in treatment of myasthenia gravis

Back 204

1. 2-4 hour duration (oral)
2. 3-6 hour duration (oral); 12 hour duration (time-release)
3. 3-4 minute duration (iv); less potent; used to determine if problem is myasthenic or cholinergic crisis and to test adequacy of treatment dose

Front 205

explain myasthenic crisis and cholinergic crisis in patient with myasthenia gravis?

Back 205

1. disease flares up->shortness of breath and weakness
2. overexposure to med->overstimulation of ach->stimulation followed by depression of autonomics and skeletal muscle

Front 206

how can too much neostigmine produce muscle weakness?

Back 206

depolarization blcokade- insufficicent repolarization time

Front 207

toxicity potential and uses of echothiphate, dfp, parathion, malathion, and sarin gas

Back 207

1. echothiphate-last resort drug for miotic pupils and glaucoma; will not cross bbb; not volatile
2. dfp- volatile, lipid soluble, highly toxic
3. parathion- insecticide easily absorbed that is major problem in accidental poisoning; more toxis than malathion
4. malathion- treats lice; low dermal absorption
5. sarin gas- nerve gas; irreversibly phosphorylates ache; very toxic; very volatile
sarin>parathion>malathion

Front 208

adverse effects of ache inhibitors:

Back 208

1. lens opacity
2. chronic neurotoxicity

Front 209

symptoms of cholinergic overstimulation/crisis:

Back 209

1. stimulate m-receptors at effector organs
2. stimulate cholinergic receptors in cns
3. both 1 and 2 are followed by depression/paralysis of autonomics and skeletal muscle
4. miosis, salivation, bronchoconstriction, nvd, bradycardia, hypotension, urgency

Front 210

what is the difference between neostigmine, physostigmine, and organophosphates?

Back 210

1. neostigmine-reversible, does not cross bbb
2. physostigmine-reversible, crosses bbb
3. organophosphates-irreversible, most cross bbb (except echothiphate)

Front 211

what is treatment for sarin gas exposure?

Back 211

1. m-blocker (atropine) will prevent bronchoconstriction
2. cholinesterase reactivator (pralidoxime) will break bond between phosphate and oxygen->then ach can be broken down

Front 212

compare atropine and pralidoxime in cholinergic crisis

Back 212

1. atropine- m-blocker; has central and peripheral effector sites; used for reversible/irreversible ache inhibitors
2. pralidoxime- works in neuromuscular junction and autonomic ganglia; only peripheral sites; used only in organophosphate poisoning

Front 213

what effect will pralidoxime have on neostigmine overdose?

Back 213

none because it will not break the carbon-oxygen bond between neostigmine and ach

Front 214

compare effects of m-agonists, ache inhibitors, and m-antagonists on cv system

Back 214

1. m-agonists- hypotension, bradycardia, reflex tachycardia
2. ache inhibitors- bradycardia and hypotension
3. m-agonists- tachycardia and hypertension

Front 215

what are therapeutic uses for nm-blockers?

Back 215

1. relax skeletal muscles for surgery or intubation
2. prevent fractures associated with ect
3. control muscle spasms of tetanus
4. sustained nm blockade in critically ill patients

Front 216

compare moa of non-depolarizing and depolarizing nm blockers in causing muscular paralysis

Back 216

non-depolarizing- competitively inhibit the effect of ACh at the postjunctional membrane nicotinic receptor of the neuromuscular junction (prevent depolarization and AP propagation)
2. depolarizing- nicotinic receptor agonist that acts at the motor endplate of the neuromuscular junction to produce persistent stimulation and depolarization of the muscle, thus preventing stimulation of contraction by ACh

Front 217

what is the order of flaccid paralysis due to nondepolarizing agents?

Back 217

1. eyes and face
2. limbs
3. abdomen
4. intercostals
5. diaphragm
6. reversed in recovery

Front 218

how can you reverse the effects of pancuronium?

Back 218

ache inhibitor

Front 219

compare phase I and phase II (desensitizing) block in succinylcholine

Back 219

phase I- depolarizes membrane by opening channel (same as ach)->succinylcholine binds to channel->na influx->resistance to ache allows longer duration->brief period of repetitive excitation may cause fasciculations->depolariztion block of neuromuscular transmission->flaccid paralysis
phase II- occurs with higher doses or continuous exposure; initial depolarization followed by gradual repolarization; this is like receptor desensitization; ache inhibtors may reverse

Front 220

will neostigmine reverse the phase I block effecs of succinylcholine?

Back 220

no, it acts in the same manner and will enhance phase I blocking

Front 221

will neostigmine reverse phase II block of succinylcholine?

Back 221

it can reverse the block in some circumstances

Front 222

ache inhibitor effects in reversing non-depolarizing and depolarizing nm-blockers

Back 222

1. enhances initial phase I block by succinylcholine, but can reverse phase II block
2. ache inhibitors are administered for pharmacologic antagonism to reverse residual postsurgical muscarinic receptor blockade and avoid inadvertent hypoxia or apnea

Front 223

compare ability of ache in neuromuscular junction and butyrylcholinesterase in plasma and liver to metabolize succinylcholine

Back 223

1. metabolizes succinylcholine more slowly than ach because of resistance to hydrolysis
2. rapidly metabolizes succinylcholine in plasma and liver (some genetics can prolong its effects causing poisoning and death)

Front 224

what is succinylcholine?

Back 224

2 ach molecules together

Front 225

what is important about all nm-blockers?

Back 225

1. don't enter cns
2. don't affect sensory organs
3. not anesthetic or analgesic

Front 226

duration of action for succinylcholine and pancuronium?

Back 226

1. (depolarizing) 5 minutes and eliminated in plasma
2. (non-depolarizing) 120-180 minutes and eliminated in kidney

Front 227

do we get depolarization blockade on cardiac muscle?

Back 227

no, M2 receptors are not ligand-gated channels

Front 228

what are side effects of non-depolarizing nm-blockers and cv effects?

Back 228

1. posoperative muscle pain in high doses, hyperkalemia, malignant hyperthermia, prolonged paralysis
2. bradycardia, stimulates histamine release->vasodilation and bronchoconstriction

Front 229

what effect can a ganglionic blockade have on the cv system?

Back 229

only one part of cv innervated by ans: blood vessels by sns->blocking this->vasodilation and tachycardia (from lack of psns regulation of resting tone)

Front 230

what effect can muscarinic blockade have on cv system?

Back 230

tachycardia

Front 231

how can succinylcholine cause malignant hyperthemia nad hyperkalemia in some patients?

Back 231

1. malignant hyperthermia- disorder of skeletal muscle->excessive calcium release->rapid hyperthermia and metabolic acidosis, tachycardia, muscle rigidity, accelerated muscle metabolism
2. hyperkalemia- loss of tissue potassium during depolarization->sodium influx->excitatory postsynaptic potential (risk high in burns, muscle trauma, and spinal cord transections)->can result in cardiac arrest or circulatory collapse

Front 232

what patients are contraindicated from receiving succinylcholine?

Back 232

heart failure patients on digoxin or diuretics

Front 233

what is drug to treat malignant hyperthermia?

Back 233

dantrolene

Front 234

atropine vs. ipratropium, which can pass through bbb?

Back 234

atropine

Front 235

compare use of atropine and scopolamine as pre-op med

Back 235

both induce sedation, amnesia, and less oral secretions, but scopolamine is more potent than atropine

Front 236

moa and use of atropine in cardiac disorders

Back 236

1. blocks M2 on heart to prevent overstimulation
2. used for hyperactive carotid sinus syndrome and vagal induced heart block

Front 237

which anticholinergics are used to treat urinary incontinence?

Back 237

1. tolterodine
2. oxybitynin chloride
3. darifenacin
4. solifenacin
5. trospium chloride

Front 238

m antagonist side effects

Back 238

1. cns
2. dry mucus membranes
3. mydriasis, can't constrict pupil, cycloplegia
4. increased hr
5. decreased gut motility and acid secretion
6. can't micturate

Front 239

scopolamine can do what in therapeutic doses?

Back 239

cns depression

Front 240

rank in potency: scopolamine, atropine, and ipratropium

Back 240

scopolamine>atropine>ipratropium

Front 241

what are cns effects of scopolamine?

Back 241

1. sedation or excitement
2. cns depression
3. cns problems

Front 242

why are adremomimetics and cholinolytics contraindicated in glaucoma?

Back 242

in nag, these will cause dilation of the eye; this leads to increased intraocular pressure, which causes a nag attack

Front 243

what is the moa and efficacy of beta-blockes, EPI, and alpha-2 agonists on oag?

Back 243

1. beta-blockers and alpha-2 agonists decrease aqueous humor production by ciliary body->decrases introcular pressure
2. EPI is given as dipivefrin->increases aqueous humor outflow
3. beta-blockers>alpha-2 agonists>EPI

Front 244

moa of cholinomimetics in treatment of oag and nag?

Back 244

1. oag-contracts ciliary muscle to open trabecular meshwork
2. nag-contracts iris sphincter muscle->moves iris->aqueous humor can flow out of tm

Front 245

compare use of pilocarpine, physostigmine, and echothiphate in treating glaucoma

Back 245

1. pilocarpine (drug of choice)- contracts ciliary muscle->opens holes
2. physostigmine given 2nd
3. echothiphate given 3rd (more side effects)

Front 246

what are the alternative drugs for oag treatment?

Back 246

1. alpha-2 agonists
2. EP
3. cholinomimetics

Front 247

why do you get blurred vision with pilocarpine but not betaxolol?

Back 247

1. pilocarpine is m-agonist->activates m-receptors on iris sphincter muscle and ciliary muscle causing contraction
2. betaxolol is beta-1 selective blocker->blocks beta-1 receptors on eye muscles->prevents contraction

Front 248

describe moa of pilocarpine in treating nag

Back 248

contracts iris sphincter muscle->induces miosis->pulls iris away from tm->increases aqueous humor outflow->decreases intra-ocular pressure

Front 249

identify the drugs used to treat oag

Back 249

1. non-selective beta-blockers: timolol, carteolol, levobunolol
2. beta-1 selective beta-blockers: betaxolol and levobetaxolol