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85 Cards in this Set

  • Front
  • Back
what is Dale's principle?
all terminals of the same neuron release the same neurotransmitter
which NT's are amines? Amino acids?
ACH, dopa, NE, serotonin. Glu, gly, GABA, asp
how is ACH made? Degraded?
choline plus acetyl choline via acetyltransferase. Degraded by acetylcholinesterase
what precursor of choline is found in cell membranes?
phosphatidyl choline which is made from phosphatidyl ethanolamine
what chemical is a potent inhibitor of the release of ACH?
botulinus toxin
what are some ACH antagonists?
curarine, atropine, carbachol
what is are two anticholinesterases?
DFP, physostigmine
what prevents choline uptake?
what is the pathway for catecholamine synthesis?
phenylalanine [phenylalanine or tyrosine hydroxylase] tyrosine [tyrosine hydroxylase] DOPA [aromatic amino acid decarboxylase] dopamine [hydroxylase] NE [PMNT] epi
what do MAO's do? Which one is protective in the gut by destroying molecules that may raise blood pressure?
oxidizes amines, main degratory pathway for catecholamines. MAO-A.
what drugs are MAOI for MAO-A? MAO-B?
clorygyline, moclobemide. Selegilene
aside from MAO what enzyme can break down catecholamines via what cofactor?
catechol-O-methyltransferase, SAM
what are the major dopamine catabolites?
homovanillic acid, DOPAC, 3-Methoxytyramine
what are the major NE catabolites?
normetanephrine, DHPG, MHPG, and vanillylmandelic acid
what is the catabolite of epi and why is there only one?
metanephrine bc MAO cannot break it down
distinguish between uptake I Of NT's and uptake II
uptake I is re-uptake, it is very specefic, needs Na, very efficient, and only found in neurons releasing the NT that is being taken up. Uptake II is backup/overflow, it has a high capacity, found in neurons and glia, no Na needed
what does metyrosine do?
inhibits tyrosine hydroxylase thus inhibits formation of DOPA
what does carbidopa do?
inhibits the decarboxylation step in dopamine synth (from DOPA to dopamine) (used to inhibit peripheral effects of L DOPA bc it does not cross the BBB thus limiting vomitting and nausea)
this drug blocks the storage of DA, NE, epi, 5HT, and histamine in synaptic vesicles.
haloperidol and other antipsychotics do what in terms of DA transmission?
block DA receptors
what is cocaines mechanism of action?
prevents DA reuptake
what drug inhibits dopamine beta hydroxylase thus inhibiting production of NE?
diethyldithiocarbamate AKA DDC
this drug inhibits NE release.
amitriptyline and desipramine are used as anti depressants bc?
they block NE re-uptake
as the dose of amphetamine is increased, what are its mechanisms of action?
displaces catecholamines from the synaptice vessels releasing them, inhibits transporters and thus re-uptake, inhibits MAO, alpha receptor agonist.
what is the synthesis pathway for serotonin?
tryptophan [tryptophan hydroxylase] 5-hydroxytryptophan [L aromatic aminoacid decarboxylase] 5-hydroxytryptophan AKA serotonin
what is the metabolic pathway of serotonin degradation via MAO?
serotonin [MAO] to some other crap and then 5-HIAA which is the major metabolite of serotonin
what important hormone is serotonin a precursor for and what compounds and enzymes are needed to make this?
melatonin. Ac CoA and SAM
this drug inhibits the conversion of tryptophan to 5-HTP.
LSD is an agonist to what?
serotonin receptors
what is methylsergides mechanism of action?
blocks serotonin receptors
what drug has amphetamine like activities on serotonergic neurons?
what are the illegal drugs of serotonin mechanisms?
5-hydroxytryptamine, bufotenine, LSD, psilocybin and psilocin (shrooms), dimethyltryptamine
how is histamine made and inactivated?
decarboxylated to histamine from the essential amino acid histidine. It is inactivated by methylation via SAM and the major product that is excreted is methylimidazoleacetic acid
how is GABA made?
glutamate is decarboxylated via pyridoxal phosphate to GABA
how is GABA inactivated?
GABA and alpha ketoglutarate make succinic semialdehyde and glutamate via GABA transaminase and pyroxidal phosphate
GABA synthesis is a shunt in what metabolic pathway? What are the consequences of this?
shunt in the TCA from alpha ketoglutarate to succinate, you get one less ATP, but brain does this so often bc it needs GABA
what are the effects of AOAA and H2NOH?
inhibit both synthesis and degradation of GABA
what is the mechanism of action of tetanus toxin?
inhibits GABA release from synaptic vesicles causing seizures and over stimulation of the CNS, note it can also affect glycine
what do bicuculline and picrotoxin do?
give excitatory effect by blocking GABA receptors
strychnine is a selective antagonist of what?
glycine receptors
where is NE synthesized in the brain? Where is sent? What is its purpose?
the LC and the lateral tegmental area. LC sends it dorsally to the cortex, thalamus, cerebellum, as well as down the brain stem. The tegmental area sends it to the hypothal and down the brain stem. NE is the sympathetic system in the brain basically. It makes us focus on a stressor. The tegmental area NE regulates the HPA axis and thus corticoid levels in the body which are related to stress
where is DA made in the brain and where does it travel? What does it do?
in the SN pars compacta will go to the striatum, putamen, caudate, GP and is involved with movement. In the ventral tegmental area to striatum, amy, septum (mesolimbic which is involved in reward and locomotor activity) and to the prefrontal and cingulate cortices (mesocortical - involved in cognitive function). The tuberoinfundibular DA center goes from hypothal arcuate nu to posterior pit gland and inhibits the release of prolactin (this is why DA antagonists used to treat psychotic patients may get gynecomastia).
where is serotonin made in the brain and where does it go and what does it do?
it is made in the dorsal raphe nu (goes to most of brain except descending tracts) and the caudal raphe nu which sends it down the brainstem and to the cerebellum. It prefers some areas over others, like hippo over the cortex. Its functions are not too clear, growth factor (Hippo growth) and hleps get rid of depression, also endocrine function
where is Ach made and released in the brain and what is its function?
from basal nucleus, nu of diagonal band, and medial septal nu and it sends it throughout the cortex to function in memory, theory of decreased Ach and alzheimers….
what are the clinical uses of benzos?
treat anxiety, insomnia, muscle spasticity, convulsive disorders, anesthesia adjuncts, and alcohol detox
in terms of metabolism and abuse potential how do benzos compare to barbituates?
benzo's do not activate liver enzymes and they have less potential for abuse
due to the autonomic effects of anxiety, what drugs can be given with or without benzo's?
beta blockers like propranolol
what are the drugs used for panic attacks and describe them.
imipramine is a tricyclic that works on panic attacks through a mechanism distinct from the antidepressant activity. Alprazolam is a benzo that is also used
how do you treat chronic anxiety caused by depression?
with a sedating antidepressant such as amitriptyline and a possible low does benzo
what is a cause of anxiety that is medically based on abnormal pathology, thus no benzo should be used?
what is a good treatment for anxiety caused by chronic stress?
benzo's as well as therapy or teaching the person to deal with stress
how should you treat PTSD?
with a benzo and again teach them to cope with the stress
molecularly, how do benzo's work?
they bind to GABA receptors thus enhancing the binding ability for GABA, they are benzodiazepine receptor agonists
how should you treat someone who has OD-ed on Benzos?
with a benzo receptor antagonist like flumazenil (note OD's usually only happen when combined with alcohol).
what is an example of a benzo receptor inverse agonist and what is its affect?
beta carbolines, they bind to the benzo receptor but inhibit the opening of chloride channel via GABA, thus they are anxiogenics
how do benzos affect insomnia?>
they increase total sleep tipe with only a mild effect on REM sleep
what benzo's are usually used for repeated seizures and status epilepticus? What anticonvulsant are they commonly used in adjunct with?
diazepam (valium) and lorazepam (ativan). Phenytoin
what benzos are used for drug withdrawal and for what specefic drugs? Why? What must you be careful of when doing this?
chlordiazepoxide (librium) is used for alcohol and helps with the seizures. IV diazepam can be used to treat seizures and sympathetic discharge along with propranolol resulting from cocain withdrawal. The benzo's depress the CNS like alcohol does…
describe the effects of long half life benzos and give an example.
usually metabolized to active metabolites, increase the risk of cumulative effects like sedation, increased development of tolerance, prolonged washout period. Flurazepam
describe the effects of the short half life benzo's and give an example.
less likely to produce daytime sedation, quick washout period which can result in withdrawal effects, usually for insomnia. Triazolam
what are drug interactions with benzos and what are these interactions?
cimetidine (acid blocker) decreases the metabolism of long acting benzos thus increasing the half life of these benzos. Estrogen oral contraceptives increase the half life of long acting benzos
what are side effects of benzos (besides the obvious)?
idiosyncratic rage, relapse in recovering drug addicts (especially alcohol bc benzos give the same feeling)
how should doses of benzos be initially prescribed?
give lowest effective does first and then add if necessary
generally a patient is at risk for what withdrawal symptoms of benzos after how much time of use?
abrupt return of severe anxiety and possible seizures, usually 3 months of use
what is the mechanism of action of the anxiolytic buspirone and compare it to benzos.
serotonin 1A agonist, used for generalized anxiety disorders, potency comparable to diazepam with less psychomotor impairment, but it has a lag time of 1 to 2 weeks but after 4 wks it is equally effective. Pt's do not feel this drug like benzos (think it is a sugar pill), no interactions with ethanol
what is ondansetron's mechanism of action?
antagonist to 5HT3 receptors, used for generalized anxiety DO's
mania is associated with what physiological basis? Depression?
increased catecholamines; decreased catecholamines
what are some arguments against the catecholamine hypothesis for mood elevation and depression?
the effects of reserpine do not truly mimic depression, depression is associated with increased catecholaminergic activity, and mania is not associated with increased NE activity
what are some biological markers for depression?
elevated plasma cortisol, escape from dexamethasone suppression, elevated CSF MHPG, low plasma tryptophan.
what are the treatments for bipolar disorder?
lithium, valproic acid and carbamazepine
what is ECT used to treat?
list the common TCA's.
amitriptyline, clomipramine, doxepin, imipramine, nortriptyline, protriptyline, trimipramine
what are the therapeutic actions of the TCA's physiologically? Side effects?
inhibition of NE and serotonin reuptake. Animuscarinic (dry mouth, blurred vision, constipation, urinary retention, mild tachycardia, confusion), antihistaminergic (sedation), anti alpha 1 adrenergic (postural hypotension, sedation), and cardiovascular toxicity.
what are the therapeutic effects of the TCA's?
mood elevation, rectification of sleep disturbances, improvement of cognitive function, increased energy
describe the metabolism of the TCA's.
long half lives, high plasma protein binding, production of active catabolites, oxidized by hepatic enzymes
list the common SSRI's.
fluoxetine, fluvoxamine, paroxetine, sertraline, citalopram, escitalopram
what are the side effects of SSRI's?
SEXUAL DYSFUNCTION, insomnia, moderate weight loss, nervousness/anxiety
descrube the metabolism and possible drug interactions of SSRI's.
long half lives, high plasma binding; serotonin syndrome (esp with MAOI's) characterized by tremor, agitation, hyperthermia, CV collapse
what are the atypical antidepressants and what is the mechanism of action for the important ones?
amoxapine, buproprion (DA reuptake), maprotiline, trazodone, nefazodone, venlafaxine (SNRI), mirtazapine (increases NE and serotonin release)
what are the MAOI's?
isocarboxazid, phenelzine, tranylcypromine, moclobemide (reversible inhibitor of MAO AKA RIMA)
what is an alternative/additional theory of depression?
depression is caused by hypersecretion of CRF from neurons in the brain
in depressed patients there is a significant correlation between depressed patients and what in the CSF? What in the urine?
cortisol. MHPG (NE metabolite)
what is lithium's mechanism of action?
inhibits IP3 preventing recycling of inositol and thus inhibiting neurotransmitter-stimulated adenylyl cyclase. Note its low therapeutic index. (therapeutic range is from 0.5 to 1.0 mM while toxic is greater than 1.5 mM). It has renal clearance and is sensitive to diuretics and anti-inflammatory drugs
what is the anti-depressant that causes little if any sexual dysfunction?