Psych Flashcards
(196 cards)
1
Q
drugs that increase dopamine activity
A
amphetamines
methylphenidate
cocaine
cause/worsen psychosis and tourettes
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
3
Q
effect of 5HT2 blockade
A
relieve positive symptoms
perhaps some relief of negative symptoms
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
5
Q
characteristics of atypical antipsychotics
A
Low D2 affinity (low potency)
High 5HT2 affinity
reduced risk of EPS
effective for negative symptoms
6
Q
effect of a1 blockade
A
autonomic side effects: orthostatic hypotension, tachycardia
7
Q
characteristics of typical antipsychotics
A
D2 blockers
produce EPS, urticaria/dermatitis
elevate PRL
effective for positive symptoms
8
Q
phenothiazine with piperazine side chain
A
higher potency and risk of EPS
fluphenazine and perphenazine
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
10
Q
phenothiazine with piperidine side chain
A
low potency and risk of EPS
Thiothixine
antimuscarinic effect
causes hypotension and sedation
11
Q
butyrophenones
A
haloperidol
high potency
associated with NM syndrome
12
Q
atypical antipsychotics
A
clozapine olanzapine quetiapine ziprasidone ripiprazole
13
Q
risperidone MOA
A
low dose- D2/5HT2 blockade
*approved for use in children and teens
14
Q
aripiprazole MOA
A
D2 partial agonist
5HT2A antagonist
5HT1 partial agonist
lower incidence of side effects
15
Q
asenapine MOA
A
D1, D2, 5HT1, 5HT2, a, H1 blockade
low affinity for muscarinic receptors
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
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
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)
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
20
Q
treatment of acute dystonia
A
anticholinergic (antiparkinsonian) agent such as benztropine
21
Q
treatment of akathesia
A
decrease dose
add antiparkinsonian (anticholinergic) agent
anti-anxiety agent
propanolol
22
Q
treatment of parkinsonian syndrome
A
anticholinergic parkinsonian agents
amantadine
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)
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
25
treatment of perioral tremor
antimuscarinic
| stop antipsychotic
26
effect of D2 blockade on cerebral cortex
no change in DA metabolism
| lower seizure threshold
27
effect of D2 blockade on brainstem
decreased vasomotor reflexes @ low doses
| reduced BP
28
effect of D2 blockade on chemoreceptor trigger zone
protection against N/V
29
effect of D2 blockade on hypothalamus
increased PRL
| seen mostly w/ typicals and risperidone
30
symptoms of sustained hyperprolactinemia
sexual dysfunction, amenorrhea, gynecomastia, galactorrhea, hypoestrogenism, osteopenia
31
effect of D2 blockade on CV system
QT prolongation
| mild orthostatic hypotension
32
clozapine AE
agranulocytosis
weight gain
Use if patient has already failed 2 drugs
33
atypical antipsychotics AE
increase risk for T2DM
| weight gain via 5HT1 and H1 blockade, major concern for long term use
34
antipsychotics ADME
```
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
```
35
antipsychotics with active metabolites
7-OH chlorpromazine
N-methylated metabolites of phenothiazines
Paliperidone
dehydroaripirazole
36
antipsychotics DDI
act as CYP2D6 inhibitors- raise levels of TCAs and SSRIs
37
depot antipsychotics
used in noncompliant patients to produce slow drug release
| tissue esterases remove fatty acids over a month
38
serotonin syndrome cause
SSRIs, triptans, setrons, MAOIs, TCAs, Li
| can be precipitated by use of concurrent CYP2D6/3A4 inhibitors and by withdrawal of current treatment
39
serotonergic neurons
high concentration in GI tract, midline raphe nuclei in brainstem
regulation of noiception, motor tone, vascular tone, and GI motility
40
clinical presentation of serotonin syndrome
```
AMS
clonus
tremor
hyperreflexia
mydriasis
fever >38 deg C
```
41
risk factors for neuroleptic malignant syndrome
```
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
```
42
malignant hyperthermia
```
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
```
43
physostigmine AE
seizures (contraindicated w/ TCA overdose)
| bradyasystole
44
treatment of serotonin syndrome
stop drug
| serotonin antagonist- cyproheptadine
45
metabolism of ethanol
takes place in liver, metabolized to acetaldehyde via alcohol dehydrogenase then acetate via aldehyde dehydrogenase (zero order)
chronic alcoholism- substantial CYP2E1 induction
46
disulfiram MOA
inhibits aldehyde dehydrogenase, causing accumulation of acetaldehyde
47
disulfiram AE
nausea and flushing
| reinforcement of alcohol seeking behavior in VTA by production of salsolinol
48
ALDH2*1/2*2 heterozygosity
aldehyde dehydrogenase polymorphism seen in Asians
| more positive feelings after alcohol intoxication
49
ethanol induction of CYP2E1
acetaminophen is converted to NAPQI toxic intermediate by CYP2E1 instead of nontoxic sulfate/glucuronide conjugates
NAPQI accumulation --> hepatotoxicity of acetaminophen
50
treatment of NAPQ1 hepatotoxicity
N-acetylcysteine
| provides fresh conjugate substrate for NAPQI to be converted into nontoxic cysteine/ mercapturic acid conjugates
51
BAL less than 50
limited muscular incoordination
52
BAL 50-100
pronounced incoordination
53
BAL 100-150
mood and personality changes
| intoxication over legal limit
54
BAL 150-400
N/V, ataxia, amnesia, dysarthria
55
BAL >400
coma, respiratory insufficiency, death
56
ethanol effect on GABA
```
increased GABA release
increased GABA (a) receptor density
```
57
ethanol effect on NMDA
inhibition of postsynaptic NMDA receptors
| up regulation of receptors with chronic use
58
ethanol effect on DA
increased synaptic DA
| increased reward effects in VTA/nucleus accumbens
59
ethanol effect on ACTH
increased CNS and blood levels of ACTH
60
ethanol effect on opiod receptors
increased release of B endorphins
| activation of mu receptors
61
ethanol effect on 5HT
increased synaptic serotonin
62
ethanol effect on cannabinoid system
increased CB1 activity increases DA, GABA, and glutamate activity
63
mechanism of alcoholic blackout
inhibition of the stimulatory actions of glutamate
64
acute effects of ethanol
CV depression
relaxes vascular smooth muscle (vasodilation, hypothermia, increased gastric bloodflow)
relaxes uterine smooth muscle
65
contributing factors to BAL
More weight= low BAL
More fat = high BAL
More lean muscle weight = low BAL
females= high BAL (higher % fat)
66
chronic effects of ethanol
```
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)
```
67
clinical presentation Wernicke Korsakoff syndrome
```
ataxia (cerebellar dysfunction)
confusion (AMS)
ocular muscle paralysis
treat w/ thiamine
thiamine deficiency causes decreased biosynthesis of AA and proteins
```
68
clinical presentation fetal alcohol syndrome
```
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
```
69
treatment of acute ethanol intoxication
ABCs, dextrose, thiamine, electrolytes
70
treatment of ethanol withdrawal
BNZ
| lorazepam preferred due to glucuronidation metabolism
71
drugs that have a disulfram-like effect
increase acetaldehyde concentration
| sulfonylureas, cefotetan, ketoconazole, procarbazine
72
naltrexone MOA
mu opiod antagonist
decreases feelings of reward and cravings w/ alcohol use
long acting injectable
73
acamprosate MOA
GABA (a) agonist
weak NMDA antagonist
promotes abstinence
74
treatment of ethylene glycol/methanol toxicity
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
75
core syndrome of depression
sad mood, hopelessness, physical symptoms
76
vital signs of depression
difficulty concentrating, anhedonia, fatigue, insomnia, restlessness, irritability
77
reactive (secondary) depression
associated with loss, physical illness, drugs, psychiatric disorders
consists of core depressive syndrome
78
major depressive disorder (endogenous)
```
recurrent
core syndrome + vital signs
peak onset 20-40 y/o, W>M
+ FHx
precipitating life event not adequate for the severity
```
79
Bipolar II
manic depression
| alternating episodes of depression and mania
80
biogenic amine hypothesis for depression
functional deficit of monoamines (NE, 5HT)
81
St. John's wort AE
DDI- HIV treatment, heart disease, seizures, cancers, organ transplant rejection, serotonin syndrome
82
MDR1 (P-gp, ABCB1) substrates
```
citalopram
venlafazine
paroxetine
amitriptyline
less accumulation in CNS due to efflux
```
83
C carriers of MDR1 allele
higher rate of MDR1 activity
| less effective therapy with drugs that are substrates of MDR1 due to less accumulation
84
TCAs MOA
"pramines" and "triptylines"
inhibit reuptake of serotonin and NE into presynaptic terminals
block muscarinic, histamine, and alpha receptors = side effects
85
TCAs AE
a1 block- orthostatic hypotension
mAch block- anticholinergic effects
H1 block- sedation
weight gain, sexual disturbances
86
TCA overdose
arrhythmias, myocardial depression, CHF worsening, acidosis, delirium, seizures
87
TCAs ADME
high first pass metabolism
lipophilic, protein bound
oxidation by CYP2D6 and conjugation
DDI- potentiation of alcohol and other sedatives, block effects of clonidine
88
SSRIs MOA
"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
SSRIs AE
Nausea, decreased libido, sexual dysfunction, birth defects w/ Paroxetine, suicidal ideation
contraindicated w/ MOAIs
serotonin syndrome
90
SSRIs ADME
moderate bioavailbility
high protein binding
CYP 2D6/2C19 substrates and inhibitors
91
Venlafaxine MOA/AE
SNRI
| HTN, diaphoresis, nausea, anxiety
92
Duloxetine MOA/AE
most potent SNRI
| CYP2D6/1A2 substrate
93
Amoxamine MOA/AE
Mixed inhibitor NET>SERT~DA
| DA antagonism- EPS
94
Bupropion MOA/AE
Weak inhibitor DAT, SERT, NET
NE reuptake blocker
agitation, anxiety, restlessness, seizure
smoking cessation tx
95
Maprotiline MOA/AE
NRI
| seizures
96
Mirtazepine MOA/AE
antagonizes presynaptic a2 receptors, increasing release of 5HT and NE
antihistamine- sedation
weight gain
less GI/sexual side effects than SSRIs
97
Trazodone MOA/AE
5HT2a antagonist
5HT1a partial agonist
serotonin reuptake inhibitor
CYP3A4 inhibitor
98
Nefazodone MOA/AE
5HT2a antagonist
serotonin reuptake inhibitor
hepatotoxicity
99
Vilazodone MOA
potent 5HT1a partial agonist and SSRI
100
Vortioxetine MOA
serotonin modulator and stimulator
101
tranylcypromine MOA
MOAI
irreversibly inhibits oxidative metabolism of monoamines
MAO-A= NE, 5HT, tyramine
MAO-B= DA
102
isocarboxazid MOA
MOAI
irreversibly inhibits oxidative metabolism of monoamines
MAO-A= NE, 5HT, tyramine
MAO-B= DA
103
phenelzine MOA
MOAI
irreversibly inhibits oxidative metabolism of monoamines
MAO-A= NE, 5HT, tyramine
MAO-B= DA
104
MAOIs AE
sleep disturbances, orthostatic hypotension, weight gain, sexual dysfunction, DDI w/ tyramine (cheese), HTN w/ sympathomimetcs,, contraindicated w/ SSRIs
105
MAOIs ADME
high bioavailability
inactivated by acetylation
drug effect persists 1-3 weeks
106
Lithium MOA
maintenance of manic depression
First line treatment for bipolar disorder
inhibits inositol phosphate signaling, inhibits AC
107
Lithium ADME
very narrow therapeutic window
rapid and complete absorption
distributes to total body water
no metabolism
108
Lithium AE
tremor, ataxia, hyperreactivity, edema, mild hypothyroidism, nephrogenic diabetes insipidus, bradycardia-tachycardia, acne, folliculitis, worsening psoriasis
DDIs- NSAIDs and diuretics
109
valproate MOA
alternative bipolar tx
inhibits voltage gated Na channels by stabilizing inactivated state
Blocks T-type Ca channels
Potentiates GABA
110
valproate AE
inhibits its own metabolism via CYP2D6
| nausea, abdominal pain, heartburn, sedation, hepatotoxicity
111
carbamazepine MOA
alternative bipolar tx
| inhibits voltage gated Na channels- prolongs recovery from inactivation
112
carbamazepine AE
CYP2C/3A inducer
UGT inducer
diplopia, ataxia, GI upset, rash, aplastic anemia
113
BNZ MOA
increase affinity of GABA for receptor (increased efficacy)
Ceiling effect reached unless combined with another CNS depressant (ethanol, morphine, barbituates)
Allosteric agonist
114
Flumazenil MOA
competitive antagonist, blocks effects of BNZ
treat BNZ overdose/respiratory depression
can cause seizures and agitation (from withdrawal)
115
Nordiazepam
common metabolic product of BNZ w/ long half lives (clorazepate, diazepam, chlordiazepoxide, prazepam, halazepam)
116
BNZ w/ rapid conjugation/elimination in urine
lorazepam, alprazolam, oxazepam
117
BNZ that are not CYP substrates
lorazepam and oxazepam
118
BNZ AE
pregnancy category D
withdrawal reactions w/ abrupt discontinuation
excessive sedation- resp depression
nausea, xerostomia, HA
119
alprazolam indications
panic attacks (antidepressant effect)
120
diazepam indications
inhibits monosynaptic reflexes in spinal cord to cause muscle relaxation
121
BNZ tolerance
1) sedative/hypnotic effects
2) anticonvulsant
Rarely to anxiolytic effects
Mechanism: receptor down regulation, glutamate up regulation, GPCR cross talk
122
Buspirone MOA
supresses 5HT
| slow onset compared to BNZ
123
propanolol MOA
B receptor agonist suppresses somatic and autonomic symptoms of anxiety (stage fright)
124
physical drug dependence
physiologic response to repeated drug exposure
adaptation produced by resetting homeostatic mechanisms in response to repeated drug use
withdrawal is evidence
125
substance dependence
compulsive drug use
126
tolerance
1) need for increased amounts of substance to reach desired effect
2) diminished effect with continued use of the same amount of substance
127
withdrawal
1) withdrawal syndrome occurs
| 2) closely related substance is taken to relieve or avoid withdrawal symptoms
128
loss of control over drug use
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
preoccupation with drug use
great deal of time is spent in activities necessary to obtain, use, or recover from the substance
130
continued use despite adverse consequences
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
drug use reinforcement
activation of dopamine pathways VTA-> NA
| modulation by frontal cortex is weakened by repeated drug exposure
132
sensitization
opposite of tolerance
| causes cravings and relapse
133
psychoactive THC isoforms
delta 9 (most prevalent) and delta 8
134
synthetic (medical) marijuana
dronabinol and nabilone
135
indications for medical marijuana
antiemetic (cancer)
AIDS wasting syndrome
intractable epilepsy
136
opiate overdose antidote
naloxone
137
BNZ overdose antidote
flumazenil
138
drugs that cause miosis
cholinergic agonists, opiods, nicotine
139
drugs that cause mydriasis
sympathomimetics, amphetamines, cocaine, LSD
140
drugs that cause horizontal nystagmus
barbituates, ethanol, carbamazapine, phenytoin, scorpion venom
141
drugs that cause horizontal, vertical, or rotary nystagmus
phencyclidine (PCP)
142
nicotine AE
stimulates nicotinic receptors on autonomic ganglia and in the CNS
abdominal cramps, agitation, rapid HR, seizures, nausea
143
treatment of nicotine intoxication
drugs to control symptoms
gastric lavage
activated charcoal
mecamylamine- ganglionic blocker, contraindicated if vomiting, convulsing, or hypotensive
144
effect of heroin use
euphoria rush then alternating wakeful and drowsy states ("on the nod")
145
methods of oxycodone abuse
snorting powder, chewing the pill, injection of the powder + water
146
opiates with short duration of action
heroin and fentanyl
147
acute opiate intoxication triad
pinpoint pupils, respiratory depression, and coma
148
treatment of acute opiod intoxication
goal is to reverse respiratory depression, not precipitate acute withdrawal
Naloxone
Flumazenil if BNZ use also suspected because naloxone response was inadequate
149
BNZ intoxication
allosteric agonist at GABA receptor, increasing GABA binding efficiency to receptor
150
ultra short acting BNZ
midazolam
| triazolam
151
short acting BNZ
alprazolam
| lorazepam
152
long acting BNZ
chlordiazepoxide
| diazepam
153
barbituate intoxication
alkaline diuresis
154
marijuana intoxication
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
endocannabinoids
anandamide and 2-arachidonoylglycerol bind to CB1 or CB2 receptors to regulate release of glutamate and GABA for homeostasis
156
marijuana MOA
binding to CB1 receptors prevents GABA/glutamate release
| disinhibition of DA neurons in the VTA = euphoria
157
treatment of MJ + hallucinogen intoxication
BNZ- sedation
| B-blockers to control sinus tach
158
drugs that cause rhabdomyolysis
```
excessive muscular hyperactivity, rigidity, or seizures -> release of myoglobin from damaged muscle -> renal failure
amphetamines
clozapine
olanzapine
cocaine
Li
MAOIs
phencyclidine (PCP)
```
159
treatment of rhabdomyolysis
hydration
| alkalinize urine w/ bicarb
160
cocaine MOA
inhibits presynaptic dopamine transporter, decreasing DA clearance (reuptake) from the synaptic cleft
161
amphetamine MOA
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
sympathomimetic effects of cocaine and amphetamine
dose dependent increase HR and BP
increased arousal, alertness
dilated pupils, diaphoresis, agitation
163
treatment of cocaine/amphetamine intoxication
```
BNZ- seizures and anxiety
adenosine- SVtach
lidocaine- ventricular arrhythmia
nitro or phentolamine- HTN
alkalinize urine
external cooling
```
164
MDMA AE
hyponatremia
165
ketamine/PCP MOA
NDMA binding- prevents glutamate signaling
MAO degradation- elevated sympathetic activity (CV effects)
sigma receptor binding- lethargy, coma
166
ketamine/PCP intoxication
ketamine- less agitation/violence
lethargy, hallicinations, violence, bizarre behavior, hyper secretions, vertical nystagmus, rapidly fluctuating behavior, miosis, analgesic
167
LSD psychosis treatment
haloperidol
168
inhaled hydrocarbons MOA
displacement of O2
sensitization of myocardium to catecholamines can cause arrhythmia (avoid a/b agonists)
dermatitis, nystagmus, cerebellar ataxia
hippuric acid + UA
169
ADHD pathogenesis
delay in the maturation of the brain, especially in the outer layer of the cortex, compared to chronological age
170
ADHD management phases
1) counseling
2) titration
3) maintenance
4) potentiation termination
171
ADHD stimulant AE
appetite suppression, delayed sleep onset, "wearing off" phenomenon, tics, depression, social withdrawal
172
amphetamine MOA
releases DA and NE
173
atomoxetine MOA
selective NE reuptake inhibitor centrally and peripherally
174
dexmethylphenidate MOA
block reuptake of DA and NE
175
methylphenidate MOA
block reuptake of DA and NE
176
clonidine MOA
post synaptic a-2 agonism in the PFC
177
guanfacine MOA
post synaptic a-2 agonism in the PFC
178
haloperidol MOA
blocks post synaptic D2 receptors
179
short acting amphetamines indication
initial treatment in small children for ADHD
| bid-tif dosing to control symptoms throughout the day
180
long acting amphetamines indication
ADHD
more convenient w/ greater adherence
more AE w/ appetite and sleep
181
amphetamine DDI
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
amphetamine AE
abdominal pain, HA, insomnia, loss of appetite, increased BP
183
drug of choice in somatization
SSRIs
| no anti-cholinergic effects
184
citalopram AE
GI discomfort
sexual dysfunction
seizures w/ OD
contraindicated w/ lactation
185
second line therapy for ADHD
atomoxetine
bupropion
TCAs
186
atomoxetine/methylphenidate DDI
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
atomoxetine AE
dry mouth, HA, abdominal pain, decreased appetite, cough, somnolence, vomiting, insomnia, mania
BBW for increased risk of suicidality
188
methylphenidate AE
HA, insomnia, decreased appetite, N/V, abdominal pain
189
contraindications to stimulant use
```
MAOIs
psychosis
glaucome
underlying cardiac conditions
liver disorders
history of stimulant drug dependence
```
190
tourette syndrome treatment
1) a2 agonist- treats tics + ADHD
2) stimulants- treat ADHD
3) methylphenidate + a2 agonist
191
haloperidol AE
QT prolongation, CYPS
192
a2 agonist AE
```
major CYP DDI
skin reactions
dry mouth
somnolence
HA
fatigue
dizziness
anxiety
abdominal pain
```
193
clonidine toxicity treatment
HTN- nitroprusside
| hypotension- atropine, DA
194
buprenorphine
opiod receptor partial agonist
long acting
formulated w/ naloxone to prevent abuse by injection
treat heroin addiction
195
treatment of anticholinergic poisoning
condition develops less than 12 hrs
BNZ for agitation
physostigmine for tachydysrhythmias
196
benefit to using clozapine
anti-suicidal effect
