Phar 443 Final

Front 1

90% of peripheral 5-HT is found where?

Back 1

enterochromaffin cells (EC) throughout the GI tract

Front 2

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

Back 2

5-HT

Front 3

Overproduction of 5-HT here is associated with diarrhea?

Back 3

carcinoid tumor, aneoplasm of enterochromaffin cells

Front 4

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

Back 4

1-2%

Front 5

can 5-HT cross the BBB?

Back 5

no

Front 6

where are 5-HT containing neurons found?

Back 6

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

Front 7

First important step in the synthesis of 5-HT?

Back 7

uptake of essential amino acid tryptophan

Front 8

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

Back 8

tryptophan

Front 9

facilitates the entry oftryptophan into the brain?

Back 9

active uptake

Front 10

open tocompetition from large neutral amino acids?

Back 10

tryptophan uptake transporter

Front 11

1st step in the synthetic pathway of tryptophan?

Back 11

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

Front 12

rate limiting enzymein the synthetic pathway of tryptophan?

Back 12

tryptophan hydroxylase

Front 13

tryptophan hydroxylase can be specifically blocked by?

Back 13

p-chlorophenylalanine

Front 14

competes directly with tryptophan and binds irreversiblyto the enzyme?

Back 14

p-chlorophenylalanine

Front 15

most effective route of metabolism of serotoninis?

Back 15

deamination by monoamine oxidase (MAO)

Front 16

which MAO subtype preferentially prefers 5-HT and norepi?

Back 16

MAOa

Front 17

inhibitor of MAOa?

Back 17

clorgyline

Front 18

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

Back 18

5-HIAA

Front 19

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

Back 19

5-hydroxytryptophol

Front 20

how is melatonin synthesized?

Back 20

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

Front 21

after synthesis, 5-HT is?

Back 21

stored or rapidly inactivated by MAOa

Front 22

5-HT is accumulated in secretory granulesby?

Back 22

VMAT2

Front 23

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

Back 23

SERT

Front 24

localized in the membrane of serotonergicaxon terminals?

Back 24

SERT

Front 25

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

Back 25

SERT

Front 26

why is SERT present on platelets?

Back 26

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

Front 27

largest knownneurotransmitter-receptor family?

Back 27

5-HT receptor subtypes

Front 28

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

Back 28

5-HT receptors subtypes

Front 29

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

Back 29

GPCRs

Front 30

5-HT3 receptor is a?

Back 30

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

Front 31

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

Back 31

constitutive activity

Front 32

example of serotonin receptor with constitutive activity?

Back 32

5-HT2C

Front 33

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

Back 33

5-HT1s

Front 34

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

Back 34

5-HT1A, 5-HT1B and 5-HT1D

Front 35

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

Back 35

5-HT1A

Front 36

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

Back 36

5-HT1B and 5-HT1D

Front 37

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

Back 37

5-HT2s

Front 38

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?

Back 38

5-HT2A

Front 39

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

Back 39

5-HT2C

Front 40

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

Back 40

5-HT2A

Front 41

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

Back 41

5-HT3

Front 42

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

Back 42

5-HT3

Front 43

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

Back 43

5-HT3

Front 44

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

Back 44

5-HT3

Front 45

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

Back 45

migraines

Front 46

A specific neurological syndrome, the manifestation varieswidely?

Back 46

migraine

Front 47

most common type of migraine?

Back 47

without aura

Front 48

effective, acute anti-migraine agents?

Back 48

triptans

Front 49

pharmacological effects of triptans appear to be limited to?

Back 49

5-HT1 (B and D)

Front 50

how is trigeminal nerve innervation involved in migraines?

Back 50

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

Front 51

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

Back 51

extravasation of plasma and plasma protein into the perivascular space

Front 52

two hypothesis of how triptans work?

Back 52

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

Front 53

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

Back 53

triptans

Front 54

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

Back 54

triptans

Front 55

should triptans be used to prevent a migraine from occuring?

Back 55

no

Front 56

when should migraine treatment with triptans begin?

Back 56

as soon as possible with the onset ofthe migraine attack

Front 57

rare but serious cardiac events have beenassociated with administration of?

Back 57

5-HT1 agonists

Front 58

triptans are contraindicated in patients with?

Back 58

uncontrolled hypertension

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

Front 59

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

Back 59

ergot alkaloids

Front 60

synthesizes histamine, acetylcholine,tyramine, and ergot alkaloids?

Back 60

Claviceps purpurea

Front 61

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

Back 61

ergot alkaloids

Front 62

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

Back 62

ergotism (St. Anthony's Fire)

Front 63

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

Back 63

ergot alkaloids

Front 64

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

Back 64

ergot alkaloids

Front 65

ergot alkaloids available for migraine?

Back 65

ergotamine (SL tablets)

dihydroergotamin (nasal spray or solution injection)

Front 66

nausea and vomiting due to ergot alkaloids occurs because of?

Back 66

direct effect on CNSemetic centers

Front 67

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

Back 67

ergot alkaloids

Front 68

ergot alkaloids used as uterine-stimulating agents?

Back 68

ergonovine

methylergonovine (semisynthetic derivative of ergonovine)

Front 69

which is more toxic: ergonovine or ergotamine?

Back 69

ergotamine

Front 70

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

Back 70

bromocriptine

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

Front 71

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

Back 71

bromocriptine

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

Front 72

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

Back 72

methysergide

Front 73

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

Back 73

methysergide

Front 74

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

Back 74

buspirone

Front 75

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

Back 75

prokinetic agents

Front 76

treats depression in teens, certain indications can have seizures?

Back 76

buspirone

Front 77

serotonin receptors involved with the peristaltic response?

Back 77

5-HT4

Front 78

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

Back 78

5-HT

Front 79

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

Back 79

enterchromaffin cells

Front 80

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

Back 80

5-HT

Front 81

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

Back 81

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

5-HT3 (extrinsic vagal and spinal sensoryneurons)

Front 82

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

Back 82

5-HT3 and 4

Front 83

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

Back 83

5-HT1A

Front 84

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

Back 84

5-HT4

Front 85

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

Back 85

prucalopride

prokinetic

Front 86

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

Back 86

prucalopride

prokinetic

Front 87

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

Back 87

alosetron

Front 88

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

Back 88

women

Front 89

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

Back 89

Ondansetron, granisetron, dolasetron, palonosetron, andtropistron

Front 90

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

Back 90

clozapine, risperidone, olanzapine, quetiapine

Front 91

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

Back 91

melatonin

Front 92

where is melatonin found?

Back 92

pineal gland

Front 93

what kind of receptors are MT1 and MT2?

Back 93

GPCRs

Front 94

where are melatonin receptors found?

Back 94

centrally and peripherally

Front 95

Binding of melatonin to MT1 and MT2 leads to?

Back 95

inhibition of adenylyl cyclase

Front 96

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

Back 96

MT1 and MT2

Front 97

Activation of MT1 results in?

Back 97

sleepiness

Front 98

promoted commercially as a sleep aid?

Back 98

melatonin

Front 99

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

Back 99

ramelteon

Front 100

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

Back 100

major depressive disorder (MDD)

Front 101

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?

Back 101

MDD

Front 102

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)?

Back 102

psychotic depression

Front 103

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?

Back 103

postpartum depression

Front 104

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

Back 104

seasonal affective disorder (SAD)

Front 105

individual alternates between periods ofdepression and mania?

Back 105

bipolar depression

Front 106

depression is most likely caused by?

Back 106

a combination ofgenetic, biological, environmental, and psychologicalfactors

Front 107

what have MRIs of people with depression shown?

Back 107

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

Front 108

can depression run in families?

Back 108

yes, some types

Front 109

can depression occur in people without family histories of depression?

Back 109

yes

Front 110

symptoms of depression?

Back 110

lots of them

Front 111

most common mentaldisorders in the United States?

Back 111

MDD

Front 112

what percent of US adults experience MDD yearly?

Back 112

6.7%

Front 113

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

Back 113

women (70% more likely)

Front 114

average onset of age for depression?

Back 114

32

Front 115

3.3% of 13 to 18 year olds have experienced?

Back 115

aseriously debilitating depressive disorder

Front 116

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?

Back 116

monoamine hypothesis of depression

Front 117

associated with depression in a subset of individuals?

Back 117

reserpine treatment (depletes monoamines)

Front 118

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

Back 118

those who respond to treatment with fluoxetine (SSRI)

Front 119

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

Back 119

respond to noradrenergic antidepressants (but not necessarilyserotonergic antidepressants)

Front 120

all classes of antidepressants appear to enhance the synapticavailability of?

Back 120

5-HT, NE, or DA

Front 121

is the monoamine hypothesis of depression complete?

Back 121

no

Front 122

corticosteroids are?

Back 122

stress hormones

Front 123

actions of corticosteroids in stressful situations are?

Back 123

homeostatic (allostatic)

Front 124

prolonged exposure to what is pathological?

Back 124

corticosteroids

Front 125

normal biorhythm is for cortisol?

Back 125

peak very early in the morning and then decline

Front 126

how is the behavior of cortisol levels different in depression?

Back 126

the early morning peak is not followed by asubstantial decline

Front 127

exogenous glucocorticoids and endogenous elevation ofcortisol are associated with?

Back 127

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

Front 128

reported in approximately 25% of depressed patients?

Back 128

thyroid dysfunction

Front 129

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

Back 129

estrogen deficiency states (postpartum and postmenopausal periods)

Front 130

does cortisol associated pathology impact serotonergic transmission?

Back 130

under investigation

Front 131

TCAs are?

Back 131

tricyclic antidepressants

Front 132

an example of an atypical antidepressant is?

Back 132

trazodone

Front 133

an example of a norepi-serotonin reuptake inhibitor is?

Back 133

venlafaxine

Front 134

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

Back 134

less SERT receptors

Front 135

which classes of antidepressants inhibit NET?

Back 135

TCAs

SNRIs

Front 136

which classes of antidepressants inhibit SERT

Back 136

SSRIs

TCAs

SNRIs

Front 137

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

Back 137

lithium

Front 138

common combination used in the treatment of depression?

Back 138

antidepressant + antipsychotic

Front 139

how long before a therapeutic response is evident with antidepressants?

Back 139

3-4 weeks

Front 140

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

Back 140

8 week antidepressant trials

Front 141

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

Back 141

single antidepressant

Front 142

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

Back 142

switch to another antidepressant with adifferent mechanism of action

Front 143

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

Back 143

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

Front 144

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

Back 144

TCAs

Front 145

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

Back 145

TCAs

Front 146

how many TCAs are available in the US now?

Back 146

9

Front 147

TCAs MOA?

Back 147

block NE/5-HT reuptake

Front 148

highly anti-muscarinic TCA?

Back 148

imipramine

Front 149

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

Back 149

anti-muscarinic effects of TCAs like imipramine

Front 150

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

Back 150

TCAs

Front 151

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

Back 151

TCAs

Front 152

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

Back 152

TCAs

Front 153

TCAs PK?

Back 153

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

Front 154

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

Back 154

TCAs

Front 155

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

Back 155

selective serotonin reuptake inhibitors (SSRIs)

Front 156

first line antidepressants?

Back 156

SSRIs

Front 157

SSRI MOA?

Back 157

inhibition of the serotonin transporter

Front 158

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

Back 158

fluoxetine

Front 159

how many SSRIs currently available?

Back 159

7

Front 160

effective in treating major depression?

Back 160

SSRIs

Front 161

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

Back 161

SSRIs

Front 162

SSRI with mild anti-muscarinic effects?

Back 162

paroxetine

Front 163

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

Back 163

adverse effects of SSRIs

Front 164

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

Back 164

GI effects which include nausea but also include diarrhea and emesis

Front 165

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

Back 165

SSRIs

Front 166

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

Back 166

sudden withdrawal of SSRIs

Front 167

what are trazodone and nefazodone?

Back 167

atypical antidepressants (5-HT2 antagonists)

Front 168

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

Back 168

blockade of the 5-HT2A receptor

Front 169

inhibition of the 5-HT2A receptor is associated with?

Back 169

substantial anti-anxiety, antipsychotic, and antidepressant effects

Front 170

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

Back 170

nefazodone

Front 171

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

Back 171

trazodone

Front 172

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?

Back 172

trazodone

Front 173

weaker 5-HT2 receptor antagonist?

Back 173

mirtazapine

Front 174

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

Back 174

mirtazapine

Front 175

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

Back 175

tetracyclic antidepressants

Front 176

what kind of drug is bupropion?

Back 176

a unicyclic antidepressant

Front 177

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

Back 177

bupropion

Front 178

has modest-moderate inhibition on DAT andNET?

Back 178

bupropion

Front 179

has virtually no effects on the serotonin system?

Back 179

bupropion

Front 180

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

Back 180

bupropion

Front 181

may improve systems of attention deficithyperactivity disorder (ADHD)?

Back 181

bupropion

Front 182

used in combination with SSRIantidepressants?

Back 182

bupropion

Front 183

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

Back 183

mirtazapine

Front 184

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

Back 184

mirtazapine

Front 185

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

Back 185

mirtazapine

Front 186

actions resembles that ofthe TCA desipramine?

Back 186

amoxapine and maprotiline

Front 187

both are potent NET inhibitorsand less potent SERT inhibitors?

Back 187

amoxapine and maprotiline

Front 188

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

Back 188

amoxapine

Front 189

considered a last resort treatment for depression?

Back 189

monamine oxidase inhibitors (MAOs)

Front 190

first class of antidepressants, were introduced in the1950s?

Back 190

MAOis

Front 191

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

Back 191

MAOis

Front 192

phenelzine, isocarboxazid,tranylcypromine, selegiline are all?

Back 192

MAOis?

Front 193

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

Back 193

phenelzine, isocarboxazid, tranylcypromine

Front 194

is a reversible and selective MAO-Binhibitor?

Back 194

selegiline

Front 195

one of the life-threatening toxicitiesassociated with MAOIs?

Back 195

hypertensive crisis resulting from food or druginteraction

Front 196

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

Back 196

SNRIs

Front 197

used for treatment of depression, anxietydisorders?

Back 197

SNRIs

Front 198

current approved SNRIs for depression?

Back 198

venlafaxine, desvenlafaxine, and duloxetine

Front 199

enhances serotonergic and noradrenergicneurotransmission via inhibiting NET and SERT?

Back 199

SNRIs

Front 200

have desirable safety effects over TCAs?

Back 200

SNRIs

Front 201

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

Back 201

SNRIs

Front 202

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

Back 202

one with D2 blocking

Front 203

do some antidepressants have analgesic activity?

Back 203

yes

Front 204

heterogeneous symptom complex is associated with?

Back 204

epilepsy

Front 205

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

Back 205

epilepsy

Front 206

types of seizures?

Back 206

non-epileptic and epileptic

Front 207

drugs used clinically to inhibit seizures?

Back 207

anticonvulsants

Front 208

what is epileptogenesis?

Back 208

the development of epilepsy

Front 209

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

Back 209

focal seizures (partial)

Front 210

how many types of partial focal seizures are there?

Back 210

3

Front 211

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

Back 211

focal seizure without dyscognitive features

Front 212

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?

Back 212

focal seizure without dyscognitive features

Front 213

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?

Back 213

focal seizure with dyscognitive features

Front 214

tonic-clonic seizure aka?

Back 214

grand mal seizure

Front 215

sustained muscular contractions?

Back 215

tonic

Front 216

muscle relaxation?

Back 216

clonic

Front 217

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

Back 217

focal seizure with secondarilygeneralized tonic-clonic seizure

Front 218

types of general seizures?

Back 218

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

Front 219

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?

Back 219

absence (petit mal) seizures

Front 220

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

Back 220

myoclonic seizure

Front 221

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?

Back 221

atonic seizures

Front 222

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?

Back 222

infantile spasms

Front 223

what are the most common forms of epileptic seizures?

Back 223

partial and secondarily generalized tonic-clonic

Front 224

what are the three mechanisms by which anticonvulsants work?

Back 224

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)

Front 225

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

Back 225

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

Front 226

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

Back 226

anti-seizure drugs

Front 227

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

Back 227

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

Front 228

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

Back 228

enhance GABA mediated synaptic inhibition

Front 229

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

Back 229

vigabatrin, valproate

Front 230

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

Back 230

valproate

Front 231

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

Back 231

tiagabine

Front 232

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

Back 232

barbiturates and benzos

Front 233

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

Back 233

valproate, ethosuximide

Front 234

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

Back 234

carbamazepine, phenytoin, valproate

Front 235

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

Back 235

gabapentin, lacosamide, lamotrigine, levetiracetam, topiramate

Front 236

first synthesize in 1908, anticonvulsant activity discovered in 1938?

Back 236

phenytoin

Front 237

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

Back 237

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

Front 238

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

Back 238

phenytoin

Front 239

diplopia and ataxia are the most common toxicities associated with?

Back 239

phenytoin

Front 240

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

Back 240

carbamazepine

Front 241

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?

Back 241

carbamazepine

Front 242

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?

Back 242

valproic acid

Front 243

inhibits the metabolism of drugs that are substratesfor CYP2C9?

Back 243

valproic acid

Front 244

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?

Back 244

valproic acid

Front 245

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?

Back 245

gabapentin

Front 246

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

Back 246

gabapentin

Front 247

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

Back 247

gabapentin

Front 248

similar target to gabapentin?

Back 248

pregabalin

Front 249

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?

Back 249

lamotrigine

Front 250

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

Back 250

lamotrigine

Front 251

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

Back 251

lamotrigine

Front 252

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?

Back 252

lacosamide

Front 253

does lacosamide induce or inhibit CYP enzymes?

Back 253

no

Front 254

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?

Back 254

levetiracetam

Front 255

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

Back 255

levetiracetam

Front 256

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

Back 256

levetiracetam

Front 257

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?

Back 257

topiramate

Front 258

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

Back 258

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

Front 259

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

Back 259

topiramate

Front 260

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

Back 260

false

Front 261

conventional anti-seizure drugs used for absence seizures?

Back 261

ethosuximide, valproate, clonazepam

Front 262

conventional anti-seizure drugs used for myoclonic seizures?

Back 262

valproate, clonazepam

Front 263

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

Back 263

carbamazepine, phenytoin, primidone, valproate

Front 264

recently developed anti-seizure drugs used for absence seizures?

Back 264

lamotrigine

Front 265

recently developed anti-seizure drugs used for myoclonic seizures?

Back 265

levetiracetam

Front 266

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

Back 266

lamotrigine, levetiracetam, topiramate

Front 267

do gabapentin and pregabalin work by mimicking GABA?

Back 267

HECK TO THE NO

Front 268

treats depression by preventing the availability of inositol?

Back 268

lithium

Front 269

metabolized to phenobarbital?

Back 269

primidone

Front 270

where do seizures occur?

Back 270

in the cortex

Front 271

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

Back 271

ethosuximide

Front 272

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

Back 272

T-type Ca currents

Front 273

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

Back 273

ethosuximide

Front 274

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

Back 274

ethosuximide

Front 275

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?

Back 275

clonazepam

Front 276

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

Back 276

clonazepam

Front 277

drowsiness and lethargy are toxicities associated with?

Back 277

clonazepam

Front 278

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)?

Back 278

primidone

Front 279

cross tolerance between alcohol and which anti-convulsant?

Back 279

clonazepam

Front 280

can deposit in bone, especially in young people?

Back 280

lead

Front 281

can be acute while much of it is chronic?

Back 281

lead toxicity

Front 282

prominent chronic lead toxicities?

Back 282

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

Front 283

great solvent?

Back 283

benzene

Front 284

examples of environmental toxicity?

Back 284

harpoon champ, death camas, castor beans/ricin

Front 285

toxin that is a ribosomal inhibitor?

Back 285

ricin

Front 286

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

Back 286

ricin

Front 287

which portion of the ricin heterodimer is the binding portion?

Back 287

ricin A

Front 288

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

Back 288

GAGA

Front 289

more active against animal than plant ribosomes and bacterial ribosomes?

Back 289

ricin

Front 290

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

Back 290

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

Front 291

what is the antidote for ricin?

Back 291

no known antidote

Front 292

decreases in blood lead values have been associated with?

Back 292

the growing prevalence of unleaded gas

Front 293

where does cyanide exert its effects?

Back 293

multiple sites of action

Front 294

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

Back 294

no

Front 295

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

Back 295

combinations of contaminants in aggregate may be harmful

Front 296

used in the linings of cans to give durability characteristics?

Back 296

bisphenol A (BPA)

Front 297

defined as an unusual type of dose response?

Back 297

hormesis

Front 298

what is an example of hormesis?

Back 298

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

Front 299

what is the target receptor type of most poisons?

Back 299

GPCRs

Front 300

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

Back 300

threshold limit value (TLV) for chemical substances

Front 301

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

Back 301

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

Front 302

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

Back 302

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

Front 303

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

Back 303

threshold limit value - ceiling (TLV-C)

Front 304

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

Back 304

lead, mercury, arsenic, iron

Front 305

other metals that bear watching for toxicity?

Back 305

copper, cadmium, nickel

Front 306

lead is chelated by?

Back 306

EDTA

Front 307

mercury is chelated by?

Back 307

dimercaprol

Front 308

arsenic is chelated by?

Back 308

dimercaprol

Front 309

iron is chelated by?

Back 309

deferoxamine

Front 310

copper is chelated by?

Back 310

penicillamine

Front 311

cadmium is chelated by?

Back 311

dimercaprol

Front 312

nickel is chelated by?

Back 312

dimercaprol

Front 313

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

Back 313

EDTA

Front 314

most common form of EDTA?

Back 314

tetrasodium EDTA

Front 315

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

Back 315

calcium disodium salt of EDTA

Front 316

known as British anti-Lewisite?

Back 316

dimercaprol

Front 317

old arsenic based chemical warfare agent?

Back 317

Lewisite

Front 318

inactivates lipoic acid?

Back 318

Lewisite

Front 319

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

Back 319

lipoic acid

Front 320

a bit toxic in its own right?

Back 320

British anti-Lewisite (BAL)