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Pharm > Psych > Flashcards

Psych Flashcards

1
Q

drugs that increase dopamine activity

A

amphetamines
methylphenidate
cocaine
cause/worsen psychosis and tourettes

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2
Q

measure of clinical potency of antipsychotics

A

ability to block dopamine D2 receptors
relieve positive symptoms
potency is directly related to risk of extrapyramidal symptoms

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3
Q

effect of 5HT2 blockade

A

relieve positive symptoms

perhaps some relief of negative symptoms

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4
Q

effect of muscarinic blockade w/ antipsychotics

A

confusion, memory impairment, protection against extrapyramidal side effects by blocking increase in DA turnover in basal ganglia

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5
Q

characteristics of atypical antipsychotics

A

Low D2 affinity (low potency)
High 5HT2 affinity
reduced risk of EPS
effective for negative symptoms

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6
Q

effect of a1 blockade

A

autonomic side effects: orthostatic hypotension, tachycardia

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7
Q

characteristics of typical antipsychotics

A

D2 blockers
produce EPS, urticaria/dermatitis
elevate PRL
effective for positive symptoms

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8
Q

phenothiazine with piperazine side chain

A

higher potency and risk of EPS

fluphenazine and perphenazine

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9
Q

phenothiazine with aliphatic side chain

A

low potency and risk of EPS
Chlorpromazine
antimuscarinic effect
causes orthostatic hypotension and sedation, increased risk of seizures, impairs glucose tolerance, decreases insulin resistance, jaundice, urticaria/dermatitis, associated with NM syndrome

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10
Q

phenothiazine with piperidine side chain

A

low potency and risk of EPS
Thiothixine
antimuscarinic effect
causes hypotension and sedation

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11
Q

butyrophenones

A

haloperidol
high potency
associated with NM syndrome

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12
Q

atypical antipsychotics

A 
clozapine
olanzapine
quetiapine
ziprasidone
ripiprazole
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13
Q

risperidone MOA

A

low dose- D2/5HT2 blockade

*approved for use in children and teens

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14
Q

aripiprazole MOA

A

D2 partial agonist
5HT2A antagonist
5HT1 partial agonist
lower incidence of side effects

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15
Q

asenapine MOA

A

D1, D2, 5HT1, 5HT2, a, H1 blockade

low affinity for muscarinic receptors

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16
Q

neuroleptic syndrome

A

behavioral effects produced by antipsychotics
suppression of spontaneous movements and complex behaviors, reduced initiative and interest in environment, decreased emotion (flat affect), psychotic symptoms disappear over time

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17
Q

effect of D2 blockade on limbic system

A

reduction of psychosis and positive symptoms
long term therapy leads to increased synthesis, release, and neuronal activity of dopamine to overcome blockade
antimuscarinics have no effect on antipsychotic-induced increases in DA turnover

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18
Q

effect of D2 blockade on basal ganglia

A

causes EPS
long term therapy leads to increased synthesis, release, and neuronal activity of dopamine to overcome blockade
anticholinergics block antipsychotic-induced increases in DA turnover (block EPS symptoms)

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19
Q

EPS

A

early in therapy:
1) acute dystonia- stiff neck, oculogyric crisis, distorted facial expression
2) akathesia- restlessness, especially in the legs
3) parkinsonian syndrome- akinesia, rigidity, tremor, mask facies
4) neuroleptic malignant syndrome
delayed onset:
5) perioral tremor- rabbit syndrome
6) tardive dyskinesia- choreiform movements of face, eyelids, mouth, tongue

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20
Q

treatment of acute dystonia

A

anticholinergic (antiparkinsonian) agent such as benztropine

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21
Q

treatment of akathesia

A

decrease dose
add antiparkinsonian (anticholinergic) agent
anti-anxiety agent
propanolol

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22
Q

treatment of parkinsonian syndrome

A

anticholinergic parkinsonian agents

amantadine

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23
Q

neuroleptic malignant syndrome

A

develops in 1-3 days
hyperthermia (fever)- D2 blockade in hypothalamus
autonomic dysfunction- D2 blockade on SNS
Muscle rigidity and extrapyramidal tremor- D2 blockade in SN causes increased Ca release from SR (elevated CK, myoglobinemia)

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24
Q

treatment of neuroleptic malignant syndrome

A

stop antipsychotic
dantrolene for fever/skeletal muscle relaxation
dopamine agonist- bromocriptine competes for dopamine receptors
Lorazepam- reduce psychosis

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25
Q

treatment of perioral tremor

A

antimuscarinic

stop antipsychotic

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26
Q

effect of D2 blockade on cerebral cortex

A

no change in DA metabolism

lower seizure threshold

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27
Q

effect of D2 blockade on brainstem

A

decreased vasomotor reflexes @ low doses

reduced BP

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28
Q

effect of D2 blockade on chemoreceptor trigger zone

A

protection against N/V

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29
Q

effect of D2 blockade on hypothalamus

A

increased PRL

seen mostly w/ typicals and risperidone

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30
Q

symptoms of sustained hyperprolactinemia

A

sexual dysfunction, amenorrhea, gynecomastia, galactorrhea, hypoestrogenism, osteopenia

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31
Q

effect of D2 blockade on CV system

A

QT prolongation

mild orthostatic hypotension

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32
Q

clozapine AE

A

agranulocytosis
weight gain
Use if patient has already failed 2 drugs

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33
Q

atypical antipsychotics AE

A

increase risk for T2DM

weight gain via 5HT1 and H1 blockade, major concern for long term use

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34
Q

antipsychotics ADME

A 
erratic oral absorption
IM increases bioavailibility
lipophilic- protein and membrane bound
accumulates in high blood supply tissues
crosses placenta, enters breast milk
peak plasma conc. 2-4 hrs
metabolism via oxidation
CYP2D6 and 3A4 substrates
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35
Q

antipsychotics with active metabolites

A

7-OH chlorpromazine
N-methylated metabolites of phenothiazines
Paliperidone
dehydroaripirazole

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36
Q

antipsychotics DDI

A

act as CYP2D6 inhibitors- raise levels of TCAs and SSRIs

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37
Q

depot antipsychotics

A

used in noncompliant patients to produce slow drug release

tissue esterases remove fatty acids over a month

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38
Q

serotonin syndrome cause

A

SSRIs, triptans, setrons, MAOIs, TCAs, Li

can be precipitated by use of concurrent CYP2D6/3A4 inhibitors and by withdrawal of current treatment

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39
Q

serotonergic neurons

A

high concentration in GI tract, midline raphe nuclei in brainstem
regulation of noiception, motor tone, vascular tone, and GI motility

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40
Q

clinical presentation of serotonin syndrome

A 
AMS
clonus
tremor 
hyperreflexia
mydriasis
fever >38 deg C
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41
Q

risk factors for neuroleptic malignant syndrome

A 
high dose or potency antipsychotics Associated w/ haloperidol and chlorpromazine
rapid increase in dose
use of depot IM (haloperidol >>>> clozapine)
concurrent predisposing drugs
withdrawal of anti-parkinsonian agents
increased temp, dehydration
catatonia, agitation
previous history
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42
Q

malignant hyperthermia

A 
caused by volatile anesthetics and succinylcholine, develops within 30 min- 24 hrs
uncontrolled release of Ca from SR
dantrolene IV
correct metabolic acidosis
maintain urinary output
decrease temperature
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43
Q

physostigmine AE

A

seizures (contraindicated w/ TCA overdose)

bradyasystole

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44
Q

treatment of serotonin syndrome

A

stop drug

serotonin antagonist- cyproheptadine

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45
Q

metabolism of ethanol

A

takes place in liver, metabolized to acetaldehyde via alcohol dehydrogenase then acetate via aldehyde dehydrogenase (zero order)
chronic alcoholism- substantial CYP2E1 induction

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46
Q

disulfiram MOA

A

inhibits aldehyde dehydrogenase, causing accumulation of acetaldehyde

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47
Q

disulfiram AE

A

nausea and flushing

reinforcement of alcohol seeking behavior in VTA by production of salsolinol

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48
Q

ALDH21/22 heterozygosity

A

aldehyde dehydrogenase polymorphism seen in Asians

more positive feelings after alcohol intoxication

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49
Q

ethanol induction of CYP2E1

A

acetaminophen is converted to NAPQI toxic intermediate by CYP2E1 instead of nontoxic sulfate/glucuronide conjugates
NAPQI accumulation –> hepatotoxicity of acetaminophen

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50
Q

treatment of NAPQ1 hepatotoxicity

A

N-acetylcysteine

provides fresh conjugate substrate for NAPQI to be converted into nontoxic cysteine/ mercapturic acid conjugates

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51
Q

BAL less than 50

A

limited muscular incoordination

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52
Q

BAL 50-100

A

pronounced incoordination

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53
Q

BAL 100-150

A

mood and personality changes

intoxication over legal limit

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54
Q

BAL 150-400

A

N/V, ataxia, amnesia, dysarthria

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55
Q

BAL >400

A

coma, respiratory insufficiency, death

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56
Q

ethanol effect on GABA

A 
increased GABA release
increased GABA (a) receptor density
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57
Q

ethanol effect on NMDA

A

inhibition of postsynaptic NMDA receptors

up regulation of receptors with chronic use

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58
Q

ethanol effect on DA

A

increased synaptic DA

increased reward effects in VTA/nucleus accumbens

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59
Q

ethanol effect on ACTH

A

increased CNS and blood levels of ACTH

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60
Q

ethanol effect on opiod receptors

A

increased release of B endorphins

activation of mu receptors

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61
Q

ethanol effect on 5HT

A

increased synaptic serotonin

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62
Q

ethanol effect on cannabinoid system

A

increased CB1 activity increases DA, GABA, and glutamate activity

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63
Q

mechanism of alcoholic blackout

A

inhibition of the stimulatory actions of glutamate

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64
Q

acute effects of ethanol

A

CV depression
relaxes vascular smooth muscle (vasodilation, hypothermia, increased gastric bloodflow)
relaxes uterine smooth muscle

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65
Q

contributing factors to BAL

A

More weight= low BAL
More fat = high BAL
More lean muscle weight = low BAL
females= high BAL (higher % fat)

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66
Q

chronic effects of ethanol

A 
decreased gluconeogenesis, hypoglycemia, fatty liver, GI bleeding/scarring, nutritional deficiencies, peripheral neuropathy, Wernicke Korsakoff syndrome, gynecomastia, testicular atrophy, HTN, arrhythmias, cardiomyopathy, increased HDL, GI cancer, infections PNA, teratogen, increased acetaminophen toxicity, increased risk of bleeding w/ NSAIDs
delirium tremens (visual hallucinations w/ withdrawal)
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67
Q

clinical presentation Wernicke Korsakoff syndrome

A 
ataxia (cerebellar dysfunction)
confusion (AMS)
ocular muscle paralysis
treat w/ thiamine
thiamine deficiency causes decreased biosynthesis of AA and proteins
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68
Q

clinical presentation fetal alcohol syndrome

A 
alcohol triggers apoptosis and incorrect cell migration during development
intrauterine growth retardation
microcephaly
poor coordination
flattened face
minor joint anomalies
congenital heart defects
neurological deficits
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69
Q

treatment of acute ethanol intoxication

A

ABCs, dextrose, thiamine, electrolytes

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70
Q

treatment of ethanol withdrawal

A

BNZ

lorazepam preferred due to glucuronidation metabolism

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71
Q

drugs that have a disulfram-like effect

A

increase acetaldehyde concentration

sulfonylureas, cefotetan, ketoconazole, procarbazine

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72
Q

naltrexone MOA

A

mu opiod antagonist
decreases feelings of reward and cravings w/ alcohol use
long acting injectable

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73
Q

acamprosate MOA

A

GABA (a) agonist
weak NMDA antagonist
promotes abstinence

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74
Q

treatment of ethylene glycol/methanol toxicity

A

fomepizole- competitive alcohol dehydrogenase inhibitor
ethanol- acts as a substrate for alcohol dehydrogenase
used to prevent initial metabolic conversion of ethylene glycol and methanol into toxic metabolites oxalic acid and formaldehyde
Promotes renal elimination without metabolism

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75
Q

core syndrome of depression

A

sad mood, hopelessness, physical symptoms

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76
Q

vital signs of depression

A

difficulty concentrating, anhedonia, fatigue, insomnia, restlessness, irritability

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77
Q

reactive (secondary) depression

A

associated with loss, physical illness, drugs, psychiatric disorders
consists of core depressive syndrome

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78
Q

major depressive disorder (endogenous)

A 
recurrent
core syndrome + vital signs
peak onset 20-40 y/o, W>M
\+ FHx
precipitating life event not adequate for the severity
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79
Q

Bipolar II

A

manic depression

alternating episodes of depression and mania

80
Q

biogenic amine hypothesis for depression

A

functional deficit of monoamines (NE, 5HT)

81
Q

St. John’s wort AE

A

DDI- HIV treatment, heart disease, seizures, cancers, organ transplant rejection, serotonin syndrome

82
Q

MDR1 (P-gp, ABCB1) substrates

A 
citalopram
venlafazine
paroxetine
amitriptyline
less accumulation in CNS due to efflux
83
Q

C carriers of MDR1 allele

A

higher rate of MDR1 activity

less effective therapy with drugs that are substrates of MDR1 due to less accumulation

84
Q

TCAs MOA

A

“pramines” and “triptylines”
inhibit reuptake of serotonin and NE into presynaptic terminals
block muscarinic, histamine, and alpha receptors = side effects

85
Q

TCAs AE

A

a1 block- orthostatic hypotension
mAch block- anticholinergic effects
H1 block- sedation
weight gain, sexual disturbances

86
Q

TCA overdose

A

arrhythmias, myocardial depression, CHF worsening, acidosis, delirium, seizures

87
Q

TCAs ADME

A

high first pass metabolism
lipophilic, protein bound
oxidation by CYP2D6 and conjugation
DDI- potentiation of alcohol and other sedatives, block effects of clonidine

88
Q

SSRIs MOA

A

“prams” and “xetines” + fluvoxamine and sertraline
first line therapy in major depression
selective inhibition of SERT, potentiates and prolongs effect of 5HT
greater therapeutic index than TCAs

89
Q

SSRIs AE

A

Nausea, decreased libido, sexual dysfunction, birth defects w/ Paroxetine, suicidal ideation
contraindicated w/ MOAIs
serotonin syndrome

90
Q

SSRIs ADME

A

moderate bioavailbility
high protein binding
CYP 2D6/2C19 substrates and inhibitors

91
Q

Venlafaxine MOA/AE

A

SNRI

HTN, diaphoresis, nausea, anxiety

92
Q

Duloxetine MOA/AE

A

most potent SNRI

CYP2D6/1A2 substrate

93
Q

Amoxamine MOA/AE

A

Mixed inhibitor NET>SERT~DA

DA antagonism- EPS

94
Q

Bupropion MOA/AE

A

Weak inhibitor DAT, SERT, NET
NE reuptake blocker
agitation, anxiety, restlessness, seizure
smoking cessation tx

95
Q

Maprotiline MOA/AE

A

NRI

seizures

96
Q

Mirtazepine MOA/AE

A

antagonizes presynaptic a2 receptors, increasing release of 5HT and NE
antihistamine- sedation
weight gain
less GI/sexual side effects than SSRIs

97
Q

Trazodone MOA/AE

A

5HT2a antagonist
5HT1a partial agonist
serotonin reuptake inhibitor
CYP3A4 inhibitor

98
Q

Nefazodone MOA/AE

A

5HT2a antagonist
serotonin reuptake inhibitor
hepatotoxicity

99
Q

Vilazodone MOA

A

potent 5HT1a partial agonist and SSRI

100
Q

Vortioxetine MOA

A

serotonin modulator and stimulator

101
Q

tranylcypromine MOA

A

MOAI
irreversibly inhibits oxidative metabolism of monoamines
MAO-A= NE, 5HT, tyramine
MAO-B= DA

102
Q

isocarboxazid MOA

A

MOAI
irreversibly inhibits oxidative metabolism of monoamines
MAO-A= NE, 5HT, tyramine
MAO-B= DA

103
Q

phenelzine MOA

A

MOAI
irreversibly inhibits oxidative metabolism of monoamines
MAO-A= NE, 5HT, tyramine
MAO-B= DA

104
Q

MAOIs AE

A

sleep disturbances, orthostatic hypotension, weight gain, sexual dysfunction, DDI w/ tyramine (cheese), HTN w/ sympathomimetcs,, contraindicated w/ SSRIs

105
Q

MAOIs ADME

A

high bioavailability
inactivated by acetylation
drug effect persists 1-3 weeks

106
Q

Lithium MOA

A

maintenance of manic depression
First line treatment for bipolar disorder
inhibits inositol phosphate signaling, inhibits AC

107
Q

Lithium ADME

A

very narrow therapeutic window
rapid and complete absorption
distributes to total body water
no metabolism

108
Q

Lithium AE

A

tremor, ataxia, hyperreactivity, edema, mild hypothyroidism, nephrogenic diabetes insipidus, bradycardia-tachycardia, acne, folliculitis, worsening psoriasis
DDIs- NSAIDs and diuretics

109
Q

valproate MOA

A

alternative bipolar tx
inhibits voltage gated Na channels by stabilizing inactivated state
Blocks T-type Ca channels
Potentiates GABA

110
Q

valproate AE

A

inhibits its own metabolism via CYP2D6

nausea, abdominal pain, heartburn, sedation, hepatotoxicity

111
Q

carbamazepine MOA

A

alternative bipolar tx

inhibits voltage gated Na channels- prolongs recovery from inactivation

112
Q

carbamazepine AE

A

CYP2C/3A inducer
UGT inducer
diplopia, ataxia, GI upset, rash, aplastic anemia

113
Q

BNZ MOA

A

increase affinity of GABA for receptor (increased efficacy)
Ceiling effect reached unless combined with another CNS depressant (ethanol, morphine, barbituates)
Allosteric agonist

114
Q

Flumazenil MOA

A

competitive antagonist, blocks effects of BNZ
treat BNZ overdose/respiratory depression
can cause seizures and agitation (from withdrawal)

115
Q

Nordiazepam

A

common metabolic product of BNZ w/ long half lives (clorazepate, diazepam, chlordiazepoxide, prazepam, halazepam)

116
Q

BNZ w/ rapid conjugation/elimination in urine

A

lorazepam, alprazolam, oxazepam

117
Q

BNZ that are not CYP substrates

A

lorazepam and oxazepam

118
Q

BNZ AE

A

pregnancy category D
withdrawal reactions w/ abrupt discontinuation
excessive sedation- resp depression
nausea, xerostomia, HA

119
Q

alprazolam indications

A

panic attacks (antidepressant effect)

120
Q

diazepam indications

A

inhibits monosynaptic reflexes in spinal cord to cause muscle relaxation

121
Q

BNZ tolerance

A

1) sedative/hypnotic effects
2) anticonvulsant
Rarely to anxiolytic effects
Mechanism: receptor down regulation, glutamate up regulation, GPCR cross talk

122
Q

Buspirone MOA

A

supresses 5HT

slow onset compared to BNZ

123
Q

propanolol MOA

A

B receptor agonist suppresses somatic and autonomic symptoms of anxiety (stage fright)

124
Q

physical drug dependence

A

physiologic response to repeated drug exposure
adaptation produced by resetting homeostatic mechanisms in response to repeated drug use
withdrawal is evidence

125
Q

substance dependence

A

compulsive drug use

126
Q

tolerance

A

1) need for increased amounts of substance to reach desired effect
2) diminished effect with continued use of the same amount of substance

127
Q

withdrawal

A

1) withdrawal syndrome occurs

2) closely related substance is taken to relieve or avoid withdrawal symptoms

128
Q

loss of control over drug use

A

1) substance is often taken in larger amounts or over a longer period than was intended
2) persistent desire or unsuccessful efforts to cut down or control substance use

129
Q

preoccupation with drug use

A

great deal of time is spent in activities necessary to obtain, use, or recover from the substance

130
Q

continued use despite adverse consequences

A

1) important social, occupational, or recreational activities are sacrificed
2) use is continued despite knowledge that a persistent or recurrent physical or psychological problem is likely to have been caused or exacerbated by the substance

131
Q

drug use reinforcement

A

activation of dopamine pathways VTA-> NA

modulation by frontal cortex is weakened by repeated drug exposure

132
Q

sensitization

A

opposite of tolerance

causes cravings and relapse

133
Q

psychoactive THC isoforms

A

delta 9 (most prevalent) and delta 8

134
Q

synthetic (medical) marijuana

A

dronabinol and nabilone

135
Q

indications for medical marijuana

A

antiemetic (cancer)
AIDS wasting syndrome
intractable epilepsy

136
Q

opiate overdose antidote

A

naloxone

137
Q

BNZ overdose antidote

A

flumazenil

138
Q

drugs that cause miosis

A

cholinergic agonists, opiods, nicotine

139
Q

drugs that cause mydriasis

A

sympathomimetics, amphetamines, cocaine, LSD

140
Q

drugs that cause horizontal nystagmus

A

barbituates, ethanol, carbamazapine, phenytoin, scorpion venom

141
Q

drugs that cause horizontal, vertical, or rotary nystagmus

A

phencyclidine (PCP)

142
Q

nicotine AE

A

stimulates nicotinic receptors on autonomic ganglia and in the CNS
abdominal cramps, agitation, rapid HR, seizures, nausea

143
Q

treatment of nicotine intoxication

A

drugs to control symptoms
gastric lavage
activated charcoal
mecamylamine- ganglionic blocker, contraindicated if vomiting, convulsing, or hypotensive

144
Q

effect of heroin use

A

euphoria rush then alternating wakeful and drowsy states (“on the nod”)

145
Q

methods of oxycodone abuse

A

snorting powder, chewing the pill, injection of the powder + water

146
Q

opiates with short duration of action

A

heroin and fentanyl

147
Q

acute opiate intoxication triad

A

pinpoint pupils, respiratory depression, and coma

148
Q

treatment of acute opiod intoxication

A

goal is to reverse respiratory depression, not precipitate acute withdrawal
Naloxone
Flumazenil if BNZ use also suspected because naloxone response was inadequate

149
Q

BNZ intoxication

A

allosteric agonist at GABA receptor, increasing GABA binding efficiency to receptor

150
Q

ultra short acting BNZ

A

midazolam

triazolam

151
Q

short acting BNZ

A

alprazolam

lorazepam

152
Q

long acting BNZ

A

chlordiazepoxide

diazepam

153
Q

barbituate intoxication

A

alkaline diuresis

154
Q

marijuana intoxication

A

hasish potency > MJ
cognitive dysfunction, depersonalization, sharpened vision, changes in perception, reaction time impairment, conjunctival injection, paranoia/psychosis with new use or patients w/ preexisting psych conditions

155
Q

endocannabinoids

A

anandamide and 2-arachidonoylglycerol bind to CB1 or CB2 receptors to regulate release of glutamate and GABA for homeostasis

156
Q

marijuana MOA

A

binding to CB1 receptors prevents GABA/glutamate release

disinhibition of DA neurons in the VTA = euphoria

157
Q

treatment of MJ + hallucinogen intoxication

A

BNZ- sedation

B-blockers to control sinus tach

158
Q

drugs that cause rhabdomyolysis

A 
excessive muscular hyperactivity, rigidity, or seizures -> release of myoglobin from damaged muscle -> renal failure
amphetamines
clozapine
olanzapine
cocaine
Li
MAOIs
phencyclidine (PCP)
159
Q

treatment of rhabdomyolysis

A

hydration

alkalinize urine w/ bicarb

160
Q

cocaine MOA

A

inhibits presynaptic dopamine transporter, decreasing DA clearance (reuptake) from the synaptic cleft

161
Q

amphetamine MOA

A

amphetamine is a dopamine transporter substrate, competitively inhibiting reuptake of DA from the synaptic cleft
once inside the cell, amphetamine
inhibits vesicular monoamine transporter (VMAT) so vesicles aren’t filled with DA in the presynaptic terminal. The concentration of DA rises in the presynaptic terminal, causing the transporter to reverse direction and release non-vesicular DA into the synaptic cleft

162
Q

sympathomimetic effects of cocaine and amphetamine

A

dose dependent increase HR and BP
increased arousal, alertness
dilated pupils, diaphoresis, agitation

163
Q

treatment of cocaine/amphetamine intoxication

A 
BNZ- seizures and anxiety
adenosine- SVtach
lidocaine- ventricular arrhythmia
nitro or phentolamine- HTN
alkalinize urine
external cooling
164
Q

MDMA AE

A

hyponatremia

165
Q

ketamine/PCP MOA

A

NDMA binding- prevents glutamate signaling
MAO degradation- elevated sympathetic activity (CV effects)
sigma receptor binding- lethargy, coma

166
Q

ketamine/PCP intoxication

A

ketamine- less agitation/violence
lethargy, hallicinations, violence, bizarre behavior, hyper secretions, vertical nystagmus, rapidly fluctuating behavior, miosis, analgesic

167
Q

LSD psychosis treatment

A

haloperidol

168
Q

inhaled hydrocarbons MOA

A

displacement of O2
sensitization of myocardium to catecholamines can cause arrhythmia (avoid a/b agonists)
dermatitis, nystagmus, cerebellar ataxia
hippuric acid + UA

169
Q

ADHD pathogenesis

A

delay in the maturation of the brain, especially in the outer layer of the cortex, compared to chronological age

170
Q

ADHD management phases

A

1) counseling
2) titration
3) maintenance
4) potentiation termination

171
Q

ADHD stimulant AE

A

appetite suppression, delayed sleep onset, “wearing off” phenomenon, tics, depression, social withdrawal

172
Q

amphetamine MOA

A

releases DA and NE

173
Q

atomoxetine MOA

A

selective NE reuptake inhibitor centrally and peripherally

174
Q

dexmethylphenidate MOA

A

block reuptake of DA and NE

175
Q

methylphenidate MOA

A

block reuptake of DA and NE

176
Q

clonidine MOA

A

post synaptic a-2 agonism in the PFC

177
Q

guanfacine MOA

A

post synaptic a-2 agonism in the PFC

178
Q

haloperidol MOA

A

blocks post synaptic D2 receptors

179
Q

short acting amphetamines indication

A

initial treatment in small children for ADHD

bid-tif dosing to control symptoms throughout the day

180
Q

long acting amphetamines indication

A

ADHD
more convenient w/ greater adherence
more AE w/ appetite and sleep

181
Q

amphetamine DDI

A

acetazolamide, bicarb- alkaline urine favors drug reuptake
ammonium cl- acidic urine favors drug elimination
chlorpromazine, haloperidol- DA blockers reduce amphetamine effect
dextromethorphan- impaired judgement
digoxin- pro-arrythmogenic
MAOIs- increased serum drug levels and AE
CYP2D6 inducers- decreased serum drug levels
CYP2D6 inhibitors- increased serum drug levels

182
Q

amphetamine AE

A

abdominal pain, HA, insomnia, loss of appetite, increased BP

183
Q

drug of choice in somatization

A

SSRIs

no anti-cholinergic effects

184
Q

citalopram AE

A

GI discomfort
sexual dysfunction
seizures w/ OD
contraindicated w/ lactation

185
Q

second line therapy for ADHD

A

atomoxetine
bupropion
TCAs

186
Q

atomoxetine/methylphenidate DDI

A

albuterol- increased CV effects
epi- increased BP
MAOIs- increased toxicity
alcohol- increased production of toxic metabolite
phenytoin- increased drug concentration
ergotamine/pseudoepi- increased pressor effect on BP
CYP2D6 inducers- decreased serum drug levels
CYP2D6 inhibitors- increased serum drug levels

187
Q

atomoxetine AE

A

dry mouth, HA, abdominal pain, decreased appetite, cough, somnolence, vomiting, insomnia, mania
BBW for increased risk of suicidality

188
Q

methylphenidate AE

A

HA, insomnia, decreased appetite, N/V, abdominal pain

189
Q

contraindications to stimulant use

A 
MAOIs
psychosis
glaucome
underlying cardiac conditions
liver disorders
history of stimulant drug dependence
190
Q

tourette syndrome treatment

A

1) a2 agonist- treats tics + ADHD
2) stimulants- treat ADHD
3) methylphenidate + a2 agonist

191
Q

haloperidol AE

A

QT prolongation, CYPS

192
Q

a2 agonist AE

A 
major CYP DDI
skin reactions
dry mouth
somnolence
HA
fatigue
dizziness
anxiety 
abdominal pain
193
Q

clonidine toxicity treatment

A

HTN- nitroprusside

hypotension- atropine, DA

194
Q

buprenorphine

A

opiod receptor partial agonist
long acting
formulated w/ naloxone to prevent abuse by injection
treat heroin addiction

195
Q

treatment of anticholinergic poisoning

A

condition develops less than 12 hrs
BNZ for agitation
physostigmine for tachydysrhythmias

196
Q

benefit to using clozapine

A

anti-suicidal effect

Pharm (3 decks)

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