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320 Cards in this Set

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90% of peripheral 5-HT is found where?

enterochromaffin cells (EC) throughout the GI tract

powerful stimulant of GI smooth muscles, increasing tone and facilitating peristalsis?


Overproduction of 5-HT here is associated with diarrhea?

carcinoid tumor, aneoplasm of enterochromaffin cells

how much of the body's 5-HT is found in the brain?


can 5-HT cross the BBB?


where are 5-HT containing neurons found?

near the midline or raphe regions of the pons and upper brain stem

First important step in the synthesis of 5-HT?

uptake of essential amino acid tryptophan

primarily from the diet and elimination from the diet can significantly lower brain serotonin?


facilitates the entry oftryptophan into the brain?

active uptake

open tocompetition from large neutral amino acids?

tryptophan uptake transporter

1st step in the synthetic pathway of tryptophan?

hydroxylationof tryptophan to form 5-hydroxytrptophan (5-HTP)

rate limiting enzymein the synthetic pathway of tryptophan?

tryptophan hydroxylase

tryptophan hydroxylase can be specifically blocked by?


competes directly with tryptophan and binds irreversiblyto the enzyme?


most effective route of metabolism of serotoninis?

deamination by monoamine oxidase (MAO)

which MAO subtype preferentially prefers 5-HT and norepi?


inhibitor of MAOa?


metabolite formed when 5-HT is deaminated by MAO can be oxidized to?


metabolite formed when 5-HT is deaminated by MAO can be reduced to?


how is melatonin synthesized?

5-HT > 5-HT acetylase > N-Acetyl-5-HT > hydroxyindole O-methyltransferase > melatonin

after synthesis, 5-HT is?

stored or rapidly inactivated by MAOa

5-HT is accumulated in secretory granulesby?


action of vesicular released 5-HT fromserotonergic terminals is terminated by?


localized in the membrane of serotonergicaxon terminals?


located on platelets and are responsiblefor platelets acquiring 5-HT?


why is SERT present on platelets?

platelets need 5-HT but they lack theenzymes responsible for the synthesis of 5-HT

largest knownneurotransmitter-receptor family?

5-HT receptor subtypes

expressed at distinct but oftenoverlapping sites and are coupled to different transmembrane- signaling mechanisms?

5-HT receptors subtypes

5-HT1, 5-HT2, and 5-HT4-7 receptor families are members of?


5-HT3 receptor is a?

ligand-gated ion channel that gates Na+and K+

most 5-HT receptors can activate G-protein independently ofagonist, what is this called?

constitutive activity

example of serotonin receptor with constitutive activity?


consist of 5 members, all whichpreferentially couple to Gi/o and inhibit adenylyl cyclase?


receptors that also activate a receptor-operatedK+ channel and inhibit a voltage-gated Ca2+ channel?

5-HT1A, 5-HT1B and 5-HT1D

found in the raphe nuclei of the brainstemwhere it functions as an inhibitory, somatodendriticautoreceptor on cell bodies of serotonergic neurons?


abundantly expressed in the substantia nigra andbasal ganglia and regulate the firing of DA-containing neuronsand the release of DA at axon terminals?

5-HT1B and 5-HT1D

coupled to Gq/G11 proteins and activate phospholipase C (DAG and IP3)?


broadly distributed in the CNS, primarily inserotonergic terminal areas (high densities are found inthe prefrontal, parietal, and somatosensory) and expressed in blood platelets and smoothmuscle cells?


has beenimplicated in the control of CSF (found in the choroid plexus) production and infeeding behavior and mood?


which serotonin receptor responds by causing vasoconstriction when platelets release serotonin?


only monoamine neurotransmitter receptor known tofunction as a ligand-gated ion channel?


activation of this receptor leads to a rapidlydesensitizing depolarization, mediated by the gating ofcations?


located on parasympatheticterminals in the GI tract (including the vagus andsplanchnic afferents)?


receptors in the GI tract and CNS (NTS and areapostrema) that participate in the emetic response?


10-20% of the population is affected with this condition?


A specific neurological syndrome, the manifestation varieswidely?


most common type of migraine?

without aura

effective, acute anti-migraine agents?


pharmacological effects of triptans appear to be limited to?

5-HT1 (B and D)

how is trigeminal nerve innervation involved in migraines?

trigeminal nerve endingsrelease powerful vasodilator (calcitonin gene-related peptide)

appears to be responsible for the mechanical vascular stretching andactivation of pain nerve endings associated with migraines?

extravasation of plasma and plasma protein into the perivascular space

two hypothesis of how triptans work?

may activate 5-HT1B and 5-HT1D receptors on presynaptic trigeminal nerve terminals toinhibit release of calcitonin gene related peptide

vasoconstrictionaction of direct 5-HT 1B and 5-HT1D may prevent vasodilation and thestretching of the pain endings

believed to reverse the shunting of carotid arterial blood flowby stimulating 5-HT1B and 5-HT1D receptors leading to vasoconstriction?


effective in the acute treatment of migraines (with or withoutaura)?


should triptans be used to prevent a migraine from occuring?


when should migraine treatment with triptans begin?

as soon as possible with the onset ofthe migraine attack

rare but serious cardiac events have beenassociated with administration of?

5-HT1 agonists

triptans are contraindicated in patients with?

uncontrolled hypertension

patientswho have a history of ischemic coronary arterydisease, cerebrovascular or peripheralvasculature disease

produced by Claviceps purpurea, a fungus thatinfects grasses and grains?

ergot alkaloids

synthesizes histamine, acetylcholine,tyramine, and ergot alkaloids?

Claviceps purpurea

affect alpha adrenergic receptors,dopamine receptors, and 5-HT receptors?

ergot alkaloids

characteristic symptoms was gangreneof the feet, legs, hands, and arms and , in extreme cases, mummified limbs separated off without loss ofblood?

ergotism (St. Anthony's Fire)

used in patients with migraine headache or pituitary dysfunction(hyperprolactinemia), occasionally in the postpartum patient?

ergot alkaloids

restricted to patients havingfrequent, moderate migraine or infrequent, severe migraine attacks?

ergot alkaloids

ergot alkaloids available for migraine?

ergotamine (SL tablets)

dihydroergotamin (nasal spray or solution injection)

nausea and vomiting due to ergot alkaloids occurs because of?

direct effect on CNSemetic centers

significantly increase the motor activity of the uterus, used to control bleeding and maintain uterinecontraction in postpartum or after abortion?

ergot alkaloids

ergot alkaloids used as uterine-stimulating agents?


methylergonovine (semisynthetic derivative of ergonovine)

which is more toxic: ergonovine or ergotamine?


synthetic derivative of the natural ergotalkaloids, is used to control hyperprolactinemia?


strong D2 agonist, low affinity for 5-HT and alpha receptors

associated with secretingtumors of the gland and also with the centrally acting dopamineantagonists, especially the D2-blocking anti-psychotics


strong D2 agonist, low affinity for 5-HT and alpha receptors

neither a selective antagonist nor always an antagonist, blocks 5-HT2A and C receptors?


used for prophylactic treatment of migraine and other vascularheadaches, including Horton’s syndrome?


selective partial agonist at 5-HT1A receptors, used forthe treatment of anxiety?


drugs that enhance coordinated GI motility and transit of materials in the GI tract?

prokinetic agents

treats depression in teens, certain indications can have seizures?


serotonin receptors involved with the peristaltic response?


plays an important role in the normal motor andsecretory function of the gut?


rapidly release 5-HT in response tochemicals and mechanical stimulation?

enterchromaffin cells

triggers the peristaltic reflex by stimulating intrinsicsensory neurons in the myenteric plexus?


by which receptors does 5-HT trigger the peristaltic reflex?

5-HT4 (intrinsic sensory neurons in the myenteric plexus)

5-HT3 (extrinsic vagal and spinal sensoryneurons)

which 5-HT receptors are also found on other neurons of theenteric nervous system (stimulatory)?

5-HT3 and 4

which 5-HT receptors are also found on other neurons of the enteric nervous system (inhibitory)?


stimulation of excitatory motor neurons that have this receptor enhancesAch release at the neuromuscular junction?


a specific 5-HT4 receptor agonist thatfacilitates cholinergic neurotransmission, increases oral-cecaltransit and colonic transit?



used in patients withchronic idiopathic constipation to improve colonic transit and stoolfrequency?



potent 5-HT3 receptor antagonist for thetreatment of diarrhea-predominant IBS in women?


which gender has a high incidence of ischemic colitis associated with IBS?


5-HT3 antagonists widely used for chemotherapy-induced emesis?

Ondansetron, granisetron, dolasetron, palonosetron, andtropistron

5-HT2A and 5-HT2C antagonists with reduced incidence of extrapyramidal side effects and also have dopamine D2 receptor blocking effects (lower)?

clozapine, risperidone, olanzapine, quetiapine

5-HT is N-acetylated and methoxylated to produce?


where is melatonin found?

pineal gland

what kind of receptors are MT1 and MT2?


where are melatonin receptors found?

centrally and peripherally

Binding of melatonin to MT1 and MT2 leads to?

inhibition of adenylyl cyclase

found on neurons in thesuprachiasmatic nucleus of the hypothalamus,an area associated with circadian rhythm?

MT1 and MT2

Activation of MT1 results in?


promoted commercially as a sleep aid?


selective MT1 and MT2 agonist thatis approved for medical treatment of insomnia?


characterized by a combination of symptoms that interferewith a person's ability to work, sleep, study, eat, and enjoyonce-pleasurable activities?

major depressive disorder (MDD)

disabling andprevents a person from functioning normally and some peoplemay experience only a single episode within their lifetime, butmore often a person may have multiple episode?


occurs when a person has severedepression plus some form of psychosis, such as having disturbingfalse beliefs or a break with reality (delusions), or hearing orseeing upsetting things that others cannot hear or see(hallucinations)?

psychotic depression

much more serious than the "baby blues"that many women experience after giving birth, it is estimated that10 to 15 percent of women experience this aftergiving birth?

postpartum depression

characterized by the onset ofdepression during the winter months, when there is less naturalsunlight, generally lifts during spring and summer?

seasonal affective disorder (SAD)

individual alternates between periods ofdepression and mania?

bipolar depression

depression is most likely caused by?

a combination ofgenetic, biological, environmental, and psychologicalfactors

what have MRIs of people with depression shown?

brains of people who have depression look differentthan those of people without depression, the parts ofthe brain involved in mood, thinking, sleep, appetite,and behavior appear different

can depression run in families?

yes, some types

can depression occur in people without family histories of depression?


symptoms of depression?

lots of them

most common mentaldisorders in the United States?


what percent of US adults experience MDD yearly?


which gender is more likely to experience depression during their lifetime?

women (70% more likely)

average onset of age for depression?


3.3% of 13 to 18 year olds have experienced?

aseriously debilitating depressive disorder

the idea that depression is related to a deficiency in the amount of orfunction of cortical and limbic serotonin (5-HT),norepinephrine (NE), and dopamine (DA) is known as?

monoamine hypothesis of depression

associated with depression in a subset of individuals?

reserpine treatment (depletes monoamines)

which patients rapidly sufferfrom relapse when given diets free of tryptophan?

those who respond to treatment with fluoxetine (SSRI)

administration of an inhibitor of norepinephrine synthesis isalso associated with a rapid return of depressive symptomsin patients that?

respond to noradrenergic antidepressants (but not necessarilyserotonergic antidepressants)

all classes of antidepressants appear to enhance the synapticavailability of?

5-HT, NE, or DA

is the monoamine hypothesis of depression complete?


corticosteroids are?

stress hormones

actions of corticosteroids in stressful situations are?

homeostatic (allostatic)

prolonged exposure to what is pathological?


normal biorhythm is for cortisol?

peak very early in the morning and then decline

how is the behavior of cortisol levels different in depression?

the early morning peak is not followed by asubstantial decline

exogenous glucocorticoids and endogenous elevation ofcortisol are associated with?

mood symptoms and cognitivedeficits similar to those seen in major depressive disorder

reported in approximately 25% of depressed patients?

thyroid dysfunction

are thought to play a role in theetiology of depression in some women?

estrogen deficiency states (postpartum and postmenopausal periods)

does cortisol associated pathology impact serotonergic transmission?

under investigation

TCAs are?

tricyclic antidepressants

an example of an atypical antidepressant is?


an example of a norepi-serotonin reuptake inhibitor is?


what was found in the brains of those who had depression and committed suicide?

less SERT receptors

which classes of antidepressants inhibit NET?



which classes of antidepressants inhibit SERT




inhibits the depolarization provoked and Ca dependent release of NE, DA, and not 5-HT?


common combination used in the treatment of depression?

antidepressant + antipsychotic

how long before a therapeutic response is evident with antidepressants?

3-4 weeks

two-thirds of depressed patients will show a 50% decrease indepressive symptoms over the course of?

8 week antidepressant trials

one-third of depressed patients will experience a complete remission with?

single antidepressant

if a patient is not responding to a given antidepressant after 8weeks, what should be done?

switch to another antidepressant with adifferent mechanism of action

after successful initial treatment phase for depression, what is done?

a 6-12 monthmaintenance treatment phase is typical, after which the drugis gradually withdrawn

imipramine, amitriptyline, doxepin, desipramine, nortriptyline, clomipramine, trimipramine, and protriptyline are all?


dominant class of antidepressants until theintroduction of the selective serotonin uptake inhibitors(SSRIs) in the 1980s and 1990s?


how many TCAs are available in the US now?



block NE/5-HT reuptake

highly anti-muscarinic TCA?


dry mouth, cognitive dulling, and constipation are symptoms of?

anti-muscarinic effects of TCAs like imipramine

also tend to be potent antagonists of the histamine H1 receptor, leading to sedation?


also tend to have blockade effects of α1adrenoreceptors that contributes to orthostatichypotension?


primarily used in depression thatis unresponsive to more commonly usedantidepressants such as SSRIs and serotonin/norepinephrine reuptake inhibitors (SNRIs)?



steady-states concentrations occurwithin several days to several weeks for the beginningof treatment

can be used also for enuresis, anxiety, attention deficithyperactivity disorder (ADHD)?


fluoxetine, fluvoxamine, paroxetine, citalopram, escitalopram, and sertraline are?

selective serotonin reuptake inhibitors (SSRIs)

first line antidepressants?



inhibition of the serotonin transporter

introduced in the US in 1988 became themost commonly prescribed medication in medicalpractice?


how many SSRIs currently available?


effective in treating major depression?


also are anxiolytics with efficacy in the treatment of generalized anxiety, panic, society anxiety, and obsessive-compulsive disorders?


SSRI with mild anti-muscarinic effects?


excessivestimulation of brain 5-HT2 receptors that mayresult in insomnia, increased anxiety, irritability,decreased libido are all?

adverse effects of SSRIs

Stimulation of 5-HT3 receptors in the CNS andperiphery by SSRIs contributes to?

GI effects which include nausea but also include diarrhea and emesis

some patients report a dullness of intellectual abilities and concentration with?


dizziness, headache,nervousness, nausea, and insomnia are symptoms of?

sudden withdrawal of SSRIs

what are trazodone and nefazodone?

atypical antidepressants (5-HT2 antagonists)

principle action of both nefazodone (generic forms are stillused) and trazodone appears to be?

blockade of the 5-HT2A receptor

inhibition of the 5-HT2A receptor is associated with?

substantial anti-anxiety, antipsychotic, and antidepressant effects

atypical antidepressant that is a weak inhibitor of both SERT and NET?


atypical antidepressant that is a weak but selective inhibitor of SERT with little effects on NET?


atypical antidepressant that also has weak-to-moderate presynaptic alpha adrenergic blocking properties (alpha-2 adrenergic receptors) and isa modest antagonist of the H1 receptor?


weaker 5-HT2 receptor antagonist?


choice antidepressant to use in depressed patients with insomnia because of its sedating effects (H1 receptor antagonist)?


what kind of drugs are amoxapine, maprotiline, and mirtazapine?

tetracyclic antidepressants

what kind of drug is bupropion?

a unicyclic antidepressant

enhances both noradrenergic and dopaminergicneurotransmission via reuptake presynaptic release ofcatecholamines (VMAT2 effects)?


has modest-moderate inhibition on DAT andNET?


has virtually no effects on the serotonin system?


is indicated for the treatment of depression,prevention of seasonal depressive disorder and as a smokingcessation treatment?


may improve systems of attention deficithyperactivity disorder (ADHD)?


used in combination with SSRIantidepressants?


is an antagonist of the presynaptic α2autoreceptor and enhances the release of bothnorepinephrine and serotonin?


is an antagonist of 5-HT2 and 5-HT3receptors?


is a potent H1 receptor antagonist, which isassociated with the drugs sedative effects?


actions resembles that ofthe TCA desipramine?

amoxapine and maprotiline

both are potent NET inhibitorsand less potent SERT inhibitors?

amoxapine and maprotiline

unlike other TCAs and antidepressants, isa moderate inhibitor of the postsynaptic D2 receptor(some antipsychotic properties)?


considered a last resort treatment for depression?

monamine oxidase inhibitors (MAOs)

first class of antidepressants, were introduced in the1950s?


primary use now is in the treatment of depressionunresponsive to other antidepressants?


phenelzine, isocarboxazid,tranylcypromine, selegiline are all?


bindirreversible and non-selectively with MAO-A andMAO-B?

phenelzine, isocarboxazid, tranylcypromine

is a reversible and selective MAO-Binhibitor?


one of the life-threatening toxicitiesassociated with MAOIs?

hypertensive crisis resulting from food or druginteraction

non-tricyclic structure that inhibit the reuptake of both5-HT and norepinephrine (NE)?


used for treatment of depression, anxietydisorders?


current approved SNRIs for depression?

venlafaxine, desvenlafaxine, and duloxetine

enhances serotonergic and noradrenergicneurotransmission via inhibiting NET and SERT?


have desirable safety effects over TCAs?


adverse side effects are similar to that of SSRIs,including nausea, constipation, insomnia, headaches,and sexual dysfunction?


what kind of antidepressant would be used in someone also having hallucinations?

one with D2 blocking

do some antidepressants have analgesic activity?


heterogeneous symptom complex is associated with?


a chronic disorder characterized by the periodic andunpredictable occurrences of seizures (approximately 40distinct types of seizures)?


types of seizures?

non-epileptic and epileptic

drugs used clinically to inhibit seizures?


what is epileptogenesis?

the development of epilepsy

abnormal discharge isinitiated in a specific locus in the brain in?

focal seizures (partial)

how many types of partial focal seizures are there?


minimal spread of the abnormal discharge, noloss of consciousness or awareness is characteristic of?

focal seizure without dyscognitive features

patient may display sudden clonic jerkingof an extremity lasting 60-90 seconds, esidualweakness will follow that may last 15-30minutes after the attack, what kind of seizure is this?

focal seizure without dyscognitive features

localized onset, abnormal discharge becomes more widespread (usuallybilateral) and almost always involves the limbic system, temporal lobe usually involved (hypoxia or infection), alteration of consciousness, duration 10-45 seconds, develop automatism which the patient has no memory, examples of automatism: lip smacking, swallowing,fumbling, scratching?

focal seizure with dyscognitive features

tonic-clonic seizure aka?

grand mal seizure

sustained muscular contractions?


muscle relaxation?


seizure involving loss of conciousness, tonic-clonic behavior, lasts 1 to 2 minutes?

focal seizure with secondarilygeneralized tonic-clonic seizure

types of general seizures?

tonic-clonic, absence (petit mal), myoclonic, atonic, infantile spasm

characterized by sudden onset and abrupt cessation ofconsciousness, consciousness is altered, seizure may also be associated with mild clonic jerking ofthe eye lids or extremities, attacks begin in childhood or adolescence, and may occur ahundred times a day, typically lasting about 30 seconds?

absence (petit mal) seizures

brief shock-like contraction of muscles, may be restricted to parts of one extremity or may be generalized?

myoclonic seizure

sudden loss of postural tone, individual my fall if standing, ifseated, head or torso may drop forward, often seen with children not usually in adults?

atonic seizures

epileptic syndrome, recurrent myoclonic jerks of the body with sudden flexion orextension of the body and limbs, first attack before the age of one, many of the patients are intellectually delayed?

infantile spasms

what are the most common forms of epileptic seizures?

partial and secondarily generalized tonic-clonic

what are the three mechanisms by which anticonvulsants work?

promote inactivation of voltage-gated Na channels

enhance pre- or post-synaptic GABA inhibition

inhibit voltage-gated CA channels responsible for T-type Ca current (absence seizures)

which mechanism of action of anticonvulsants is specific to treating absence seizures?

inhibition of voltage-gated CA channels responsible for T-type Ca current

prolong the inactivation of the Na+ channels, thereforereducing the ability of neurons to fire at high frequencies?

anti-seizure drugs

how do the anti-seizure drugs carbamazepine, phenytoin, topiramate, lamotrigine, valproate, and zonisamide work?

prolong the inactivation of the Na+ channels, thereforereducing the ability of neurons to fire at high frequencies

how do the anti-seizure drugs benzos, barbiturates, vigabatrin, valproate, and tiagabine work?

enhance GABA mediated synaptic inhibition

which anti-seizure drug(s) enhance GABA mediated synaptic inhibition by inhibiting GABA-T?

vigabatrin, valproate

which anti-seizure drug(s) enhance GABA mediated synaptic inhibition by inhibiting succinic semialdehyde dehydrogenase?


which anti-seizure drug(s) enhance GABA mediated synaptic inhibition by inhibiting reuptake by GAT-1?


which anti-seizure drug(s) enhance GABA mediated synaptic inhibition by enhancing the activity of the GABA receptor?

barbiturates and benzos

which anti-seizure drug(s) enhance GABA mediated synaptic inhibition by inhibiting voltage-gated T-type Ca channels?

valproate, ethosuximide

what are the conventional anti-seizure drugs for partial seizures?

carbamazepine, phenytoin, valproate

what are the recently developed anti-seizure drugs for partial seizures?

gabapentin, lacosamide, lamotrigine, levetiracetam, topiramate

first synthesize in 1908, anticonvulsant activity discovered in 1938?


limits the repetitive firing of actionpotentials, effect is mediated by a slowing of the rate ofrecovery of the voltage-activated Na+ channels frominactivation?

phenytoin, carbamazepine, and valproic acid (has more MOAs as well)

can be displaced by other highly protein bounddrugs, such as sulfonamides (antimicrobial)?


diplopia and ataxia are the most common toxicities associated with?


drug interactions related to the drug’s enzyme inducingproperties (example: Increased rate ofmetabolism of phenytoin and valproic acid)?


acute intoxication can result in stupor orcoma, hyperirritability, and respiratory depression, diplopia, blurred vision, and ataxia are the mostcommon side effects with long-term therapy with?


limits the repetitive firing of actionpotentials, effect is mediated by a slowing of the rate of recovery ofthe voltage-activated Na+ channels from inactivation, also reducesT-types Ca2+ currents, and effect GABA metabolism by increasingactivity of GABA synthetic enzyme glutamic acid decarboxylaseand inhibit GABA degradative enzyme succinic semialdehydedehydrogenase?

valproic acid

inhibits the metabolism of drugs that are substratesfor CYP2C9?

valproic acid

GI symptoms that include anorexia, nausea, and vomiting(seen approximately 16% of patients), CNS effects include sedation,ataxia, and tremors, several effects on hepatic function are toxicities associated with?

valproic acid

binds to alpha-2-beta-1 subunit ofvoltage-activated Ca2+ channels to decrease Ca2+entry on presynaptic N-type channels, the decreasein glutamate release provides the antiepileptic effect?


antiepileptic that does not induce hepaticenzymes, and is not bound to plasma proteins?


somnolence, dizziness, ataxia, and fatigue are toxicities associated with?


similar target to gabapentin?


limits the repetitive firing of actionpotentials, effect is mediated by a slowing of the rate ofrecovery of the voltage-activated Na+ channels frominactivation, also inhibits voltage-activated Ca2+ channelsto decrease Ca2+ entry on presynaptic N-type channels, theinhibition of Ca2+ entry into N-type channels may beresponsible for the decrease in synaptic release ofglutamate?


administration of phenytoin, orcarbamazepine reduces the half-life and plasmaconcentration of?


dizziness, ataxia, blurred or double vision(diplopia), nausea, and vomiting are toxicities associated with?


enhances slowinactivation of voltage-gated Na+ channels, italso binds to the collapsin-response mediatorprotein, CRMP-2, blocking the effects ofneurotrophic factors such as BDNF and NT3on axonal and dendritic growth?


does lacosamide induce or inhibit CYP enzymes?


binds selectively to thesynaptic vesicular protein SV2A, it is speculatedthat the anticonvulsant mechanism may involvemodifying the synaptic release of glutamate andGABA through the action on vesicular function?


does not induce or is asubstrate for CYP enzymes, is not bound toplasma proteins?


well tolerated, with some adverse effectsuch as somnolence, asthenia, and dizziness are toxicities of?


blocking of voltage-gated Na+channels, activates a hyperpolarizing K+ current, enhancespostsynaptic GABAA-receptor currents, and limits activationof the AMPA-kainate subtypes of glutamate ionotropicreceptors?


what is a key PK consideration with co-admin of topiramate and OCs?

higher doses of OCs due to decreased estradiol plasma conc's

well tolerated, most common side effect issomnolence, fatigue, weight loss, and nervousness are toxicities associated with?


T/F: it is recommended that valproic acid be taken with food?


conventional anti-seizure drugs used for absence seizures?

ethosuximide, valproate, clonazepam

conventional anti-seizure drugs used for myoclonic seizures?

valproate, clonazepam

conventional anti-seizure drugs used for tonic-clonic seizures?

carbamazepine, phenytoin, primidone, valproate

recently developed anti-seizure drugs used for absence seizures?


recently developed anti-seizure drugs used for myoclonic seizures?


recently developed anti-seizure drugs used for tonic-clonic seizures?

lamotrigine, levetiracetam, topiramate

do gabapentin and pregabalin work by mimicking GABA?


treats depression by preventing the availability of inositol?


metabolized to phenobarbital?


where do seizures occur?

in the cortex

Reduces low threshold Ca2+currents (T-type currents), atclinical concentrations inhibits the T-typecurrents?


thought to provide a pacemaker current in thalamic neurons responsible for generating the rhythmic cortical discharge of an absence seizure attack?

T-type Ca currents

not protein bound, drug is completely metabolized to inactive metabolites?


most common side effects is gastrointestinal(nausea, vomiting, and anorexia) and CNS (drowsiness,lethargy, euphoria, dizziness, headache, and hiccough) with?


enhance GABA-mediated synapticinhibition, at therapeutic concentrations, binds tobenzodiazepine receptor site on the GABAa receptor andincrease the frequency of opening at GABA-activated Cl channels, at higher concentrations can reduce high frequencyfiring of neurons, similar to phenytoin?


long-acting drug, the half life inplasma is about 23 hrs, less than 1% of the drug isrecovered unchanged?


drowsiness and lethargy are toxicities associated with?


exact mechanism unknown, but inhibitoryand attenuation of excitatory transmission probably contributes toit’s anti-convulsant activities, like phenytoin, limits the repetitivefiring of action potentials, effect is mediated by a slowing of the rateof recovery of the voltage-activated Na+ channels from inactivation,but only at high concentrations, at high concentrations, blocks L-typeand N-type Ca2+ currents, phenobarbital binds to allosteric siteson the GABAa receptor to enhance the GABA receptor mediatedopening of the Cl- channel, decrease glutamate release (N-type Ca2+ inhibition)?


cross tolerance between alcohol and which anti-convulsant?


can deposit in bone, especially in young people?


can be acute while much of it is chronic?

lead toxicity

prominent chronic lead toxicities?

cancer, blood, nervous system, CV system, renal GI

great solvent?


examples of environmental toxicity?

harpoon champ, death camas, castor beans/ricin

toxin that is a ribosomal inhibitor?


binds and depurinates a specific adenine of the 28s rRNA?


which portion of the ricin heterodimer is the binding portion?

ricin A

the ricin target adenine in the 28S rRNA has which unusual, tetranucleotide loop?


more active against animal than plant ribosomes and bacterial ribosomes?


how does the depurination of the adenine of the 28S rRNA by ricin occur?

adenine ring of the ribosome becomes sandwiched between two tyrosine rings in the catalytic cleft of the enzyme and is hydrolyzed by the enzyme's N-glycosidase action

what is the antidote for ricin?

no known antidote

decreases in blood lead values have been associated with?

the growing prevalence of unleaded gas

where does cyanide exert its effects?

multiple sites of action

do all ages and species react the same way to poisons?


individual drug components that contaminate the environment are usually found in sub-threshold amounts so why is there concern about their presence?

combinations of contaminants in aggregate may be harmful

used in the linings of cans to give durability characteristics?

bisphenol A (BPA)

defined as an unusual type of dose response?


what is an example of hormesis?

beneficial effect from low dose exposure to an otherwise adverse substance like low level radiation

what is the target receptor type of most poisons?


defined as a concentration in air,typically for inhalation or skin exposure?

threshold limit value (TLV) for chemical substances

average exposure on the basis of a 8h/day, 40h/week work schedule?

threshold limit value - time weighted average (TLV-TWA)

spot exposure for a duration shorter than 15 minutes, that cannot be repeatedmore than 4 times per day?

threshold limit value - short term exposure limit (TLV-STEL)

absolute exposure limit that should not be exceeded at any time?

threshold limit value - ceiling (TLV-C)

4 metals that have historically been important acute and chronic toxins?

lead, mercury, arsenic, iron

other metals that bear watching for toxicity?

copper, cadmium, nickel

lead is chelated by?


mercury is chelated by?


arsenic is chelated by?


iron is chelated by?


copper is chelated by?


cadmium is chelated by?


nickel is chelated by?


strong complexing and chelating agent that reacts with many metallic ions to form soluble chelates?


most common form of EDTA?

tetrasodium EDTA

used in pharmaceuticals to prevent calcium depletion of the body during therapy?

calcium disodium salt of EDTA

known as British anti-Lewisite?


old arsenic based chemical warfare agent?


inactivates lipoic acid?


is an antioxidant as well as a component of the mitochondrial pyruvate dehydrogenase complex?

lipoic acid

a bit toxic in its own right?

British anti-Lewisite (BAL)