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Neuroscience > Adrenergics I > Flashcards

Adrenergics I Flashcards

1
Q

What are the two major subsystems of the Autonomic Nervous System?

A

parasympathetic and sympathetic

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2
Q

True or False: the parasympathetic and sympathetic nervous system can act independently or cooperatively

A

True

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3
Q

what is a predominant tone?

A

that nervous system has a stronger influence on tissue function when the body is at rest

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4
Q

Most organ systems’ predominant tone is which nervous system?

A

parasympathetic

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5
Q

what are the three places where the sympathetic nervous system exerts dominance?

A

vasculature
sweat glands
ventricular myocardium

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6
Q

Both branches of the ANS have a ____ neuron efferent pathway involving what?

A

2

preganglionic nerve that synapses with a postganglionic nerve before innervating the target organ

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7
Q

what is the neurotransmitter in the ganglia of both the parasym and sym NS?

A

acetylcholine

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8
Q

acetylcholine activates what and what is unique about it?

A

ach activates a unique nicotinic ganglionic receptor on the postgang mem that has a different subunit comp compared to nicotinic receptors expressed in the neuromuscular jxn

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9
Q

administration of which drugs will reduce the effects produced by both para and sym NS?
what else will this drug do?

A

ganglionic blocker such as mecamylamine or trimethaphan
it will also reduce or eliminate the effects produced by any baroreceptor mediated reflex changes that normally reg heart rate and blood pressure

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10
Q

what is the sym postgang NT at some sweat glands?

A

ACh NOT norepinephrine

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11
Q

what is the major NT released by postgang sym neurons?

A

norepinephrine

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12
Q

how is the adrenal medulla innervated?

A

directly by preganglionic sym neurons that release ACh which acts on nicotinic receptors of the adrenal gland to stimulate the release of epinephrine into the bloodstream along with small amount of norepinephrine

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13
Q

what is the chemical basis of fight or flight?

A

sympathetic nerves discharge in unison and results in the release of both norepinephrine from nerve terminals, and epinephrine from the adrenal glad

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14
Q

fight or flight responses include increased:

A

bronchodilation in the lung (increased delivery of O2)
vasodilation of skeletal muscle aa. (prod increased blood flow to provide nutrients and O2)
hepatic breakdown of glycogen to glucose and gluconeogenesis
inc hrt rate and cardiac output
inc atrerial blood pressure
mydriasis - widen pupils (inc ability to see in low light cond)
dec peristalsis and secretion of the gut and visceral vasoconstriction (diversion of energy for mm. exertion)

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15
Q

what is a catechol?

A

benzine with 2 hydroxyls (OH)

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16
Q

what is a catecholamine?

A

catechol + ethylamine

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17
Q

what are the alpha and beta carbons?

A

alpha C is closer to the N

beta is closer to the ring

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18
Q

what is the starting product in catecholamine syn?

A

phenylalanine

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19
Q

what is phenylalanine converted into and what does that?

A

Phe—> tyrosine

phenylalanine hydroxylase in liver (add OH to benzene ring)

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20
Q

how is tyrosine transported into neurons?

A

via an aromatic aa transporter that uses the Na+ gradient across the mem to concentrate tyrosine in the cytoplasm
(active transport)

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21
Q

what is tyrosine converted into and what does this?

A

tyrosine —> Dihydroxyphenlyalanine (DOPA)

tyrosine hydroxylase oxidizes tyrosine

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22
Q

what is the rate limiting step in catecholamine syn?

A

tyrosine—> DOPA by tyrosine hydroxylase

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23
Q

what does the rate limiting step mean?

A

inhibitors of tyrosine hydroxylase can shut down all catecholamine syn

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24
Q

what is DOPA converting into and by what?

A

DOPA ___> Dopamine

dopa decarboxylase decarcoxylases DOPA

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25
Q

what else is dopa decarboxylase known as?

A

L-aromatic amino acid decarboxylase b/c it is relatively nonspecific

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26
Q

what is dopa decarboxylase?

A

a pyridoxal-phosphate dependent enzyme

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27
Q

what is dopamine converted into and by what?

A

dopamine —> norepinephrine by dopamine B-hydroxylase

the beta carbon in the side chain is hyroxylated

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28
Q

what can norepinehrine be converted into and how?

A

NEpi —>Epinephrine by adding a methyl group on the ethylamine nitrogen by phenylethanolamine N-methyltranferase (PNMT)

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29
Q

All catecholamine syn enzymes are cytoplasmic except which?

A

dopamine b-hydoxylase

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30
Q

what is the significance of the fact that dopamine b-hydroxylase is not cytoplasmic?

A

in the adrenal medulla most of the norepinephrine leaves the chromaffin granules and is methylated by phenylethanolamine N-methyltransferase in the cytoplasm to form epinephrine which then reenters the chromaffin granules via VMAT until released

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31
Q

what % of catecholamines stored in the adrenal medulla is epinephrine and what % is norepinephrine?

A

80% Epi

20% NEpi

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32
Q

what drug is used to stop catecholamine syn?

A

tyrosine hydroxylase inhibitor
metyrosine
which is irreversible and can enter CNS

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33
Q

what is metyrosine used for?

A

short term management of patients prior to removal of a catecholamine producing tumor (pheochromocytoma)
it dec the freq and sev of hypertensive attacks, HA, N, sweating, and tachycadia caused by excess catecholamine production, peripherally and centrally
also used for long term mang of patients with inoperable phenochromocytomas

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34
Q

what are the side effects of metyrosine?

A

metyrosine gets into the CNS
sedation (most common)
extrapyramidal signs (drooling, speech diff, tremor, pseudo-parkinsonism)
anxiety and psychic disturbances (depression, hallucinations, disorientation, confusion)
diarrhea (result from unopposed parasym activity in the GI tract)

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35
Q

what are drug interactions of metyrosine?

A

potentiates extrapyramidal side effects of phenothiazines or haloperidol
potentiates sedative effects of alcohol or other CNS depressants

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36
Q

what is carbidopa?

A

enzyme inhibitor of LAAD (L-DOPA—>dopamine)
carbidopa does not readily cross the blood-brain barrier and does not affect the metabolism of levodopa within the CNS
net effect is to make more levodopa available for transport to the brain

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37
Q

what are indications for use of carbidopa?

A

indicated to use with levodopa, either alone or in a fixed combination as Sinemet, for treatment of the symptoms of parkinson’s disease

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38
Q

what are the contraindications for carbidopa?

A

hypersensitivity to carbidopa
discontinue non-selective MAO inhibitors at least 2 weeks prior to initiating treatment with levodopa
carbidopa-levodopa or levodopa alone can be given concomitantly with selective MAO-A inhibitors like selegiline

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39
Q

what are the side effects for carbidopa?

A

may activate malignant melanoma in susceptible patients

most side effects are attributed to levodopa

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40
Q

what are the pharmacokinetics for carbidopa?

A

reduces the amount of levodopa by ~75%
increases both plasma levels and plasma half life of levodopa
decreases plasma and urinary dopamine
decreased urinary HVA

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41
Q

what are the major drug interactions of carbidopa?

A

postural hypotension which administered with antihypertensive drugs
dopamine D2 receptor anatagonists may reduce therapeutic effects of levodopa

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42
Q

why is storage of catecholamines an important step in their syn?

A

protects the transmitters from catabolic enzymes

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43
Q

what is the most important site for the storage of norepinephrine?

A

granular vesicles which are highly concentrated in the varicosities of the n. terminals

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44
Q

what serves the same storage role in the adrenal medulla as synaptic vesicles in the postgang n. terminals?

A

chromaffin granules

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45
Q

How do catecholamines get into the storage vesicle?

A

by the pump VMAT (Vesicular MonoAmine Transporter)

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46
Q

How does VMAT work?

A

VMAT is an antiporter that uses the proton gradient generated by an H+-ATPase in the vesicular mem to [] DA or NE inside the vesicle
ATPase moves H+into the vesicle
Antiporter moves 2H+ out for each DA or NE moved in

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47
Q

what are the two isoforms of VMAT

A

VMAT2 only: neurons in the CNS and periphery

both VMAT1 & VMAT2: chromaffin cells of the adrenal medulla

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48
Q

How high can [NE] get within the vesicles and what does this cause?

A

100mM which causes high osmotic pressure

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49
Q

How is the high osmotic pressure of storage vesicles stabilized?

A

NE may condense with ATP and chromogranin proteins to form a complex
osmotic pressure inc with particle dissociation and dec as the particle associate

50
Q

what happens upon vesicular exocytosis?

A

there is a co-release of NE, ATP, and chromogranins

51
Q

what is reserpine?

A

antihypertensive
a drug what is a selective inhibitor of VMAT so the patient cannot store catecholamines
produces a depetion of releasable neuronal catecholamine stores
reserpine’s effects produce a reduction in blood pressure due to decreased cardiac output and decreased peripheral vascular resistance

“tranquilization” was first used in 1950s to describe the effects of reserpine on manic psychiatric patients
has been used by ancient Indian physicians for centuries as an herbal tranquilizer

52
Q

what is the reserpine mechanism?

A

potent and irreversible inhibitor of VMAT
n. terminals and adrenal chromaffin cells cant store catecholamines
catecholamines leak into the cytoplasm and are destroyed by MAO in the mitochondria
central and peripheral neurons gradually become depleted of NE, Epi, DA, and 5-Ht. eventually little or no active transmitter is left to be released from n. ending or medulla
effects last for days or weeks until new vesicles are synthesized by cell body and transported to axon terminals

53
Q

what is the differences btwn the depletion of catecholamines by reserpine and metyrosine?

A

metyrosine induces depletion results from inhibition of tyrosine hydroxylase and inability to synthesize DA

reserpine induced depletion results from inhibition of VMAT and inability to store DA in synaptic vesicles

54
Q

what are the indication for reserpine usage?

A

hypertension- not used for treating hypertension in the US excepts when cost prohibits use of other safer alternatives

55
Q

what are the pharmacokinetics of reserpine?

A

reserpine readily crosses the blood-brain barrier and depletes cerebral catecholamine stores. This can cause CNS side effects

56
Q

what are side effects of reserpine?

A

sedation
depression (suicidal tendencies)
parkinsonism symptoms

57
Q

explain reserpine induced supersensitivity?

A

loss of receptor stimulation by cessation of endogenous NT release causes a time dependent increase in tissue sensitivity to agonist
this is due to up regulation in expression of mem receptor of agonist (induced by lack of tonic stimulation by NE)

58
Q

how does exocytotic transmitter release happen?

A

an action potential is generated by ganglionic cell body (caused by entery of NA+ and Ca2+ into the cytoplasm)
as a consequence of increased intaneuronal [Ca2+] the granular vesicles migrate toward and fuse with the neuronal cell membrane and empty their Ne into synaptic cleft
exocytotic release also releases ATP, chromogranin, and dopamine B hydroxylase
a similar mech of release occurs for Epi and NEpi in the adrenal medulla but they are released directly into circulation

59
Q

what is synaptic vesicle recycling?

A 
filling
storage
release
endocytosis
refilling
60
Q

what are the actions of the released transmitter?

A

once released, NE diffuses away from sympathetic nerve endings, crosses the synaptic cleft and activated postsynaptic adrenergic receptors
adrenergic receptors are also located on presynaptic nerve terminals to provide an autoreg mech to modulate the amount of NE release

61
Q

how are NE effects terminated?

A

after NE interacts with postsynpatic receptors its response is terminated by rapid and efficient reputake into the presynaptic nerve terminal by NE Transporter (NET) = Uptake 1

62
Q

about what % of NE released from postgang sym n. terminals id rapidly taken back up into the presynaptic axon terminals by uptake 1?

A

75-90%

63
Q

what is the major mechanism for terminating the effects of released adrenergic transmitters?

A

reuptake into the n. terminal

64
Q

what is uptake 2 and when do you see this?

A

catecholamines taken up into parechymal cells of the effector tissue (extraneuronal uptake)
under normal conditions uptake 2 does NOT play a sig role in term of action pot, but may become imp if uptake 1 is blocked

65
Q

in addition to limiting the duration of postsynaptic response what else does uptake 1 do?

A

recycling of transmitter
after re uptake into neuronal cytoplasm NE and other catecholamines can be transported back into synaptic vesicles by VMAT

66
Q

the pool of transmitter available for release comes from:

A

molecules newly syn by tyrosine

mol that are recycled via neuronal reuptake

67
Q

what enzymes are involved in catecholamine metabolism?

A 
monoamine oxidase (MAO)
catechol-O-Methyl Transferase (COMT)
68
Q

where is MAO found?

A

most = liver

also localized to outer surface of mitochondria within catecholaminergic nerve terminals

69
Q

MAO in GI tract breaks down what?

A

ingested catecholamines

70
Q

what breaks down catecholamines in the cytoplasm?

A

mitochondrial MAO in neurons

catecholamines with synaptic vesicles are protected

71
Q

what are the two isoforms of MAO and what does each degrade?

A

MAO-A: degrades serotonin, NE, dopamine
resp for detoxyfying bioactive monoamines in food and drink
MAO-B: degrades dopamine faster than serotonin and NE

72
Q

what does MAO do?

A

MAO oxidizes the terminal amino groups (removes it) to form aldehyde intermediates that can be further oxidized by aldehyde dehydrogenase to
EPI and NE —> DihydroOxyMandelic Acid
DA —-> DihydrOxyPhenlyACetic acid)

the aldehyde intermediate arising from NE and EPI may also be reduced by aldehyde reductase to Dihydroxyphenylethylglycol

73
Q

what does COMT do?

A

COMT methylates the hydroxyl group on the catechol ring that is meta to the ethylamine side chain to form:
metanephrine from EPI
Normetanephrine from NE
3-methoxytyramine from DA

74
Q

what are the effects of both MAO and COMT?

A

NE and EPI= VMA (3-methoxy-4-hydroxymandelic acid)
DA=HVA (homovanillic acid)

as with DOPEG from EPI and NE a portion of metanephrines may be reduced to MOPEG (3-methoxy-4-hydroxyphenylglycol)

75
Q

what is the major matabolite found in urine?

A

VMA (from both EPI and NE)

76
Q

what can VMA be used for?

A

detect neuroblastoma and other tumors of neural crest origin in children

77
Q

what is phenelzine?

A

a antidepressant- MAO inhibitor

78
Q

what is the mechanism of action of phenelzine?

A

MAO inhibitor that prevents MAO from metabolizing biogenic amines

79
Q

what are the indications for phenelzine?

A

atypical depression- patient is depressed but sleeps and eats excessively
investigational- alone or as an adjunct to treat bulimia nervosa, agoraphobia with panic attacks, globus hystericus syn, chronic HA

80
Q

what are the contraindications for phenelzine?

A

pheochromocytoma
CHF
Liver disease (abnormal liver fxn test)
avoid use with other sympathomimetic drugs due to the possibility of hypertensive crisis

81
Q

what are the side effects of phenelzine?

A 
dizziness
HA
drowsiness
sleep disturbances (insomnia, hypersomnia)
fatigue
weakness
tremors
convulsions
slight anticholinergic, sedative, and orthostatic hypotensive effects
82
Q

what are the pharmacokinetics of phenelzine?

A

onset: beneficial effects at doses of 60 mg/day may not be seen for at lease 4 weeks
clinical effects of the drug may be observed for up to 2 weeks after termination of the therapy (MAO is irreversibly inhibited, and it takes time for biosyn of new MAO)

83
Q

what are the major drug interaction of phenelzine?

A

co-administration with other serotoninergic agents (prozac, fluoxetine…) may produce serious, sometime fatal, rxns (serotonin syndrome)
consumption of tyramine-rich foods (can produce a hypertensive crisis
use with caution in combo with antihypertensive drugs, such as thiazide diuretics or beta blockers, due to the possibility of severe hypotensive effects

84
Q

what is selegiline?

A

Inhibitor of MAO type B

85
Q

what is the mech of action of selegiline?

A

irreversible inhibitor of MAO. It is activated by MAO to a product that bnds covalently to the active site of the enzyme
has greater affinity for MAO-B than for MAO-A. Can be considered a selective MAO-B inhibitor provided dose is not exceeded

86
Q

what are the indications for selegiline?

A

used as an adjunct to levodopa/carbidopa in parkinson’s disease treatment, selegiline can inhibit catabolism of dopamine and potentially increase he net amount of dopamine available to nigrostriatal neurons

87
Q

what are the contraindications of selegiline?

A

hypersensitivity to selegiline

concomitant use of meperidine

88
Q

what are the side effects of selegiline?

A

many of the adverse rxns seen with selegiline appear to be symp of dopamine excess

89
Q

what are the major drug interactions of selegiline?

A

use with meperidine may cause stupur, muscular rigidity, severe agitation and elevated temperature
use with serotonin reuptake inhibitors may cause serious, sometime fatal rxns

90
Q

what is entacapone?

A

inhibitor of COMT

91
Q

what is the mech of action of entacapone?

A

selective and reversivle inhibition of catechol-O-methyl transferase. physiological substrates of COMT include dopa, dopamine, NE, and EPI and their hydroxylated metabolites
in the presence of an aromatic aa decarboxylase inhibitor (carbidopa) COMT becomes the major metabolizing enzyme for levodopa, catalyzing the metabolism to (3-OMD) in the brain and periphery
After COMT inhibition, plasma levels of levodopa are greater and more sustained and result in more constant dopaminergic stimulation in the brain

92
Q

what are the indication for entacapone?

A

used as an adjunct to levopopa/carbidopa to treat patients with idiopathic parkinson’s disease

93
Q

what are the contraindication for entacapone?

A

hypersensitivity to entacapone

94
Q

what are the side effects of entacapone?

A

dyskinesia/hyperkinesia, N, urine discoloration, D, and abd pain

95
Q

what are the major drug interaction of entacapone?

A

use with caution when drugs known to interdere with biliary excretion, glucuronidation, and intestinal beta-glucuronidase are given concurrently with entacapone, as these could increase entacapone plasma levels. interacting drugs include probenecid, cholestyramine, and some antibiotics

96
Q

what is cardiac output? (CO)

A

the flow of blood from the ventricles to the arterial circulation

97
Q

what is stroke volume? (SV)

A

the volume of blood pumped out of the ventricles with each contraction

98
Q

what is contractility?

A

a measure of the contractile force generated by the cardiac mm. for a given degree of stretch
increased contractility caused increased SV
increases in SV and heart rate increases CO

CO= HR x SV

99
Q

what is total peripheral resistance? (TPR)

A

resistance of flow of blood caused by constriction of the arterioles

100
Q

what is mean arterial pressure? (MAP)

A

is affected by flow and resistance

MAP= CO x TPR

101
Q

what is diastolic pressure? (DP)

A

affected by arteriolar vasoconstriction
increased TPR increases DP
decreased TPR decreased DP

102
Q

what is pulse pressure? (PP)

A

the difference btwn systolic pressure and diastolic pressure

PP is a measure of SV

103
Q

what is systolic pressure? (SP)

A

SP = DP + PP

SP is affected by both vasoconstriction (which alters TPR) and contractliity (which alters SV)

104
Q

What is Mean Pressure? (MAP)

A 
MAP= DP + PP/3
MAP = (SP + 2DP)/3
105
Q

what is arterial pressure sensed by?

A

stretch receptors (barorecptors) in the carotid sinus and aortic arch

106
Q

what is the afferent pathway for the carotid sinus reflex?

A

carotid sinus n. which then joins the glossopharyngeal trunk (CN IX)

107
Q

what is the afferent pathway for the aortic arch reflex?

A

sensory fibers in the depressor br. of the vagus n. (CN X)

108
Q

if arterial pressure rises what happens to afferent nerve activity?

A

increases

109
Q

if arterial pressure falls what happens to afferent nerve activity?

A

decreases

110
Q

where do afferent fibers from the baroreceptors project?

A

to the nucleus tractus solitarii (NTS) located bilaterally in the dorsal medulla

111
Q

inhibitory interneurons project from the NTS onto where?

A

onto the vasomotor area in the caudal ventrolateral medulla

112
Q

stimulation of the NTS inhibits the tonic excitatory activity of the vasomotor area and ___?

A

decreases excitation of the neurons in the rostral ventrolateral medulla

113
Q

what does decrease excitation of the neurons in the rostral ventrolateral medulla do?

A

turn off input to the sympathetic preganglionic cell bodies in the intermediolateral horn of the spinal cord

114
Q

responses to decreased sympathetic activity are what?

A

decreased heart rate and cardiac mm. contractility, and vasodilation of resistance arterioles

115
Q

excitatory neurons project from the NTS onto what?

A

a cardioinhibitory area

116
Q

the cardioinhibitory area includes the what?

A

nucleus ambiguus (NA) and the dorsal motor nucleus of the vagus

117
Q

stimulation of cardioinhibitory area increases what?

A

vagus n. efferent activity to cells in the sinoatrial node of the heart

118
Q

the primary response to the increased vagal activity is what?

A

bradycardia (slowing of HR)

119
Q

baroreflex response to increased arterial pressure?

A 
Increased arterial pressure stretches 
the baroreceptors which respond by 
increasing their firing rate 
• The increase in firing frequency 
stimulates neurons in the NTS 
• The NTS responds by inhibiting the 
cardioacceleratory and vasomotor 
centers, thus decreasing 
sympathetic stimulation of the heart 
and vasculature 
• Simultaneously, cardioinhibitory 
centers are stimulated, thus 
increasing parasympathetic 
stimulation to the heart 
• Responses are slowing of heart rate, 
decreased cardiac output 
• These changes will help lower blood 
pressure back to normal
120
Q

baroreflex response to decreaed arterial pressure?

A 
• If pressure falls, such as when 
transitioning from a supine to a 
standing posture, afferent nerve 
activity to the NTS in the medulla 
decreases 
• Decreases in the activity of neurons in 
the NTS results in less inhibition (i.e. 
greater activity) of the vasomotor and 
cardioacceleratory centers, so 
sympathetic nerve activity to the heart 
and vessels increases 
• At the same time, NTS inhibition of 
the vagal cardioinhibitory centers 
causes parasympathetic nerve activity 
to the SA node to decrease 
• Taken together, these changes result 
in increased heart rate and cardiac 
output, and increased arteriolar 
resistance, which help elevate pressure 
back to normal levels

Neuroscience (1 decks)

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