Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

PSYCHIATRY > Psych PHARM > Flashcards

Psych PHARM Flashcards

1
Q

MOA: fomepizole

A

inhibitor of alcohol dehydrogenase to prevent conversion of methanol to formic acid and ethylene glycol to oxalic acid (reduce toxicity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

MOA: disulfiram

A

inhibitor of aldehyde dehydrogenase to accumulate acetylaldehyde leading to nausea and flushing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

MOA: naltrexone

A

mu opiod (OP-3) antagonist to decrease feelings of reward with alcohol and decrease craving

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

MOA: acamprosate

A

weak NMDA antagonist and GABAa agonist to decrease feeling of “need” for alcohol (decrease abstinence syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Antidote for alcohol + acetaminophen

A

N-acetylcysteine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What CYP does ETOH stimulate?

A

CYP2E1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Is ETOH metabolized by CYPs?

A

NO! (unless they are a chronic alcoholic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does ETOH do in the brain?

A

reinforces GABA action (hypopolarize), inhibits glutamate (blackouts), increase DA (to VTA and NA to increase reward), increase beta-endorphins, 5-HT and ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Disorder: ataxia, confusion, ocular muscle paralysis

A

Wernicke-Korsakoff

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why do you use lorazepam in an alcoholic in withdrawal instead of diazepam?

A

lorazepam is processed by phase II glucoronidation (so it is not as toxic in patients with hepatic toxicity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

3 things used to treat anxiety (with CBT)?

A
  • Benzodiazepines
  • Buspirone
  • Propranolol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

MOA: benzodiazepines

A

allosteric agonists of GABAa to increase potency of endogenous GABA (increase frequency of Cl- opening)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which benzos are commonly used IV?

A

diazepam

lorazepam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which benzos are NOT metabolized to nordiazepam (long half-life metabolite)?

A

Alprazolam
Oxazepam
Lorazepam

(NORdic said NOT to get on AOL messenger)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Instead of metabolism to nordiazepam, how are Alprazolam, Oxazepam, and Lorazepam processed?

A

rapid conjugation (simple metabolism) and urinary elimination (shorter duration)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Benzo speed of onset determinants?

A

dissolution rate

speed of absorption from GI tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

RAPID ONSET BENZOs

A 
Aprazolam*
Clonazepam*
Diazepam*
Lorazepam*
Midazolam
Flurazepam
Triazolam

(CLAD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

SLOW ONSET BENZOs

A

Oxazepam
Prazepam

(ox’s are slow)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

SHORT ACTING BENZOS

A

Alprazolam
Triazolam
Midazolam

(go to ATM when I am SHORT on money)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Which 3 drugs have the worst withdrawal symptoms (due to rapid decline in serum drug levels with no time for body adjustment)?

A

Alprazolam
Estazolam
Triazolam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

LONG ACTING BENZOs

A 
Chlordiazepoxide*
Clorazepate*
Diazepam*
Flurazepam
Quazepam
Prazepam*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Which benzos are NOT CYP metabolized?

A

Lorazepam
Oxazepam

(OnLy 2 not cyp metabolized)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Toxicities seen in all benzos.

A
  • Category D teratogen

- Avoid with CNS depressants or ETOH (get respiratory depression)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How do you treat benzo-induced respiratory depression?

A

Flumazenil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Benzo withdrawal symptoms
rebound anxiety, insomnia, autonomic dysfunction (tachycardia, treamor, sweating, dry mouth, HA)
26
Tolerance rarely if ever develops to what benzodiazepine effect?
anxiolytic effect
27
MOA: Buspirone
suppress 5-HT activity and increase NE and DA activity
28
How do buspirone and benzo's differ in effect for anxiety?
buspirone is just as effective but has a much slower onset (weeks)
29
MOA: propranolol
Beta-blocker that suppresses somatic and autonomic symptoms of anxiety but does NOT alter emotional symptoms (brain)
30
Propranolol is the DOC for what anxiety condition?
stage fright
31
Only anxiolytic to inhibit monosynaptic reflexes in the spinal cord at clinical doses (muscle relaxant).
diazepam
32
Best drugs to treat anxiety associated with ETOH withdrawal (if liver function is normal).
Diazepam | Chlordiazepoxide
33
BNZ with some anti-depressant activity (similar to TCAs)
alprazolam (panic disorder treatment?)
34
What is the biogenic amine hypothesis of depression?
Funcitonal deficit of monoamines (NE and 5-HT) is thought to be involved in pathophysiology of depression
35
What evidence supports the biogenic amine hypothesis?
reserpine (VMAT inhibitor that presents packaging of monoamines into veiscles) causes depression symptoms
36
What is the therapeutic lag?
even though NE and 5-HT levels increase immediately with anti-depressants, it takes around 2-8 weeks to see clinical effect
37
Why are NSAIDs not good to take in depression?
cytokines may cause an anti-depressant effect!
38
BBW for all antidepressants
Increased risk of suicide in children to 24 yos (especially with initial treatment)
39
Antidepressants that are substrates for MDRI
Amitryptyline Citalopram Paroxetine Venlafaxine (TRIP to the CITy of PARis or VENice)
40
Antidepressants that are NOT MDRI substrates.
Mirtazepine | Fluoxetine
41
What about the MDRI renders patients resistant to amitryptyline, citalopram, paroxetine, and venlafaxine?
if they are "C-carriers" becuase this increases activity of the P-gp pump
42
Which anti-depressant classes cause decreased libido and sexual dysfunction?
- TCAs - SSRIs - MAOIs
43
Which anti-depressant does NOT cause libido problems?
bupropion
44
Which anti-depressants lead to weight gain?
- TCAs - Mirtazepine - MAOIs
45
Which anti-depressant is safest for bipolar disorder?
bupropion
46
Which anti-depressant has the highest risk of birth defects?
paroxetine
47
Which drugs are used to treat depression in pregnant women?
fluoxetine citalopram sertraline
48
Which anti-depressants have increased risk of seizures?
Maprotiline | Bupropion
49
With which anti-depressant may you see extrapyramidal effects?
amoxamine
50
Which anti-depressant is no longer in common use due to hepatotoxicity?
nefazodone
51
What drug should be avoided in those taking SSRIs for 2 weeks at least?
MAOIs (can lead to serotonin syndrome)
52
TCAs
Amitriptyline Nortryptyline -"pramines" Doxepin
53
SSRIs
``` Citalopram Escitalopram Fluoxetine Sertraline Paroxetine ```
54
MAOIs
tranylcypromine isocarboxazid phenelzine
55
SNRIs
Venlafaxine | Duloxetine
56
SARIs
Trazodone Nefazodone "sari we're NoT -done"
57
SMSs
Vortioxetine | Vilazodone
58
Other than depression, what are 3 interesting things TCAs are used for?
ADHD Nocturnal enuresis anxiety disorders
59
MOA: TCAs
block reuptake of NE and 5-HT | block M, alpha, and histamine receptors
60
MOA: SSRIs
Block SERT | Less block of M, alpha and histamine receptors so increase compliance due to lower side effects)
61
MOA: MAOIs
IRREVERSIBLY BLOCK MAOs to prevent pre-synaptic degradation of NE and 5-HT (MAO-A) or DA (MAO-B) and increase their availablity
62
MOA: SNRIs
inhibit 5-HT and NE reuptake | NO activity at M, alpha, or histamine receptors
63
MOA: SARIs
moderate 5-HT reuptake block 5-HT2a antagonist 5-HT1a partial aognist
64
MOA: SMSs
potent 5-HT1a partial agonist | block SERT
65
MOA: amoxamine
inhibits NET > SERT ~ DAT
66
MOA: bupropion
weak block of NET, DAT and SERT (and metabolite blocks NE reuptake)
67
MOA: maprotiline
NRI= blocks NE reuptake
68
MOA: mirtazepine
- antagonize presynaptic alpha-1 to increase NE and 5-HT release - antagonize 5-HT2 receptors
69
Anti-depressant that can help you quit smoking.
bupropion
70
DOC for depression treatment in psychotic patients.
amoxamine
71
MOA: vortioxetine
SMS moa (potent 5-HT1a partial agonist + block SERT) as well as 5-HT1b partial agonist Antagonist of NET, beta-1, 5-HT1d, 3a, 7
72
Anti-depressant that inhibits CYP3A4.
trazodone
73
Antidepressent used in anxiety disorders with sleep problems.
trazodone
74
Most potent SNRI
duloxetine
75
How is duloxetine metabolized?
CYP2D6 and CYP1A2
76
TOXICITY: CNS stimulation, agitation, euphoria (2-6 wk), sleep disturbance, orthostatic hypotension, weight gain, sexual dysfunction
MAOIs
77
What happens if you eat cheese and wine with your MAOI and then take a diet pill?
HTN crisis due to tyramine and sympathomimetic
78
What 2 drugs can lead to delirium, hyperpyrexia, convulsions, coma and death if taken with MAOIs?
meperidine | dextromethorpham
79
How are MAOIs metabolized?
acetylation
80
How long does MAOI action last?
1-3 weeks
81
TOXICITY: CNS stimulation, agitation, anxiety (2-6 weeks), rare CV effects, nausea, reduced libido and sexual function
SSRIs
82
What causes serotonin syndrome?
overstimulation of 5-HT1a in central gray area and medulla
83
What is the active metabolite of fluoxetine?
norfluoxetine (7-9 day half-life)
84
How are SSRIs metabolized?
CYP2D6, CYP2C19, CYP3A4
85
True or false: SSRIs are highly protein bound
true! so are TCAs
86
What CYPs are inhibited by SSRIs?
CYP2D6 and CYP2C19
87
TOXCICITY: drowsy, anxious, decreased cognition (2-8 wk), orthostatic hypotension, tachycardia, dry mouth, weight gain, decreased libido and sexual function
TCAs
88
Why do you have to be especially careful with TCAs?
very narrow therapeutic window (can get arrhythmia, worsened CHF, or seizures with an overdose)
89
DDIs of TCAs?
``` ETOH Sedatives Anti-parkinsonism agents Antipscyhotics Biogenic amines (compete for protein binding) Clonidine (TCAs block its effect) ```
90
Which has better bioavailability TCAs or SSRIs?
SSRIs (TCAs have incomplete absorption)
91
Describe TCA metabolism.
tertiary amines are demethylated to secondary (active) amines which are oxygenated and conjugated to CYP2D6
92
What should you always check for BEFORE giving an antidepressant?
that the patient actually doesn't have bipolar disorder with hidden mania
93
How do you treat bipolar?
mood stabilizers (ex. lithium, anti-convulsants)
94
True or false: mood stabilizers take away mania
FALSE (they prevent cycling from mania to depression)
95
What drugs may help acute mania?
antipsychotics | benzos
96
First line for bipolar
lithium
97
MOA: lithium
poorly understood (possibly inhibits inositol phosphate signaling and NT-stimulated adenylyl cyclase
98
TOXICITY: lithium
very narrow therapeutic window (nephrogenic DI (ADH antagonist), mild hypothyroidism, sick sinus, acne, folliculitis, psoriasis, ataxia, tremor, aphasia, sedation
99
What is sick sinus?
brady-tachy cardia dur to block of Na/K ATPase in cardiac tissue
100
CONTRAINDICATIONS of lithium
diabetes | heart disease
101
DDIs of lithium
diuretics | NSAIDs
102
How is lithium metabolized?
trick question, it isn't--distributes to total body water (and bone) and is cleared in urine
103
What are the benefits of anticonvulsants in bipolar?
quicker response | larger therapeutic index
104
MOA: valproate
stabilizes inactive state of Na channels (inhibition), blocks T-type Ca2+ channels, stimulates GABA release
105
Toxicity: valproate
Hepatotoxic (check LFTs), Sedation, heart burn, abdominal pain, nausea
106
Metabolism of valproate
CYP2C metabolized and inhibitor (scale down dose over time)
107
MOA: carbamazepine
inhibits Na channels (prolongs recovery from inactivation
108
Toxicity of carbamazepine
RARE aplastic anemia, diplopia, ataxia, rash (uncommon), mild GI upset, drowsy
109
Metabolism of carbamazepine
CYP3A4 metabolism to active metabolite (induces 3A4 so speeds up own metabolism)
110
What type of agents worsen psychosis?
agents that increase DA activity
111
What agents reduce the positive symptoms of psychosis?
D2 receptor antagonists
112
What agents reduce the negative symptoms of psychosis?
NONE (but at one time, 5-HT block was thought to help)
113
What determines potency of an anti-psychotic?
in vitro inhibition of D2 receptor binding
114
What determines level of extrapyramidal toxicity?
tends to occur with more potent drugs (with less muscarinic blockage)
115
How does the MOA of typical and atypical antipsychotics differ?
typical is majorly D2 block | atypical is D2 block and 5-HT2a block
116
Typical antipsychotics
Chlorpromazine Fluphenazine Haloperidol (also perphenazine, thiothixene, butyrophenones)
117
Atypical antipsychotics
``` Clozapine Risperidone Olanzapine Aripiprazole (and quetiapine, ziprasidone, and paliperidone) ```
118
How do you improve bioavailability of an antipsychotic?
IM injection increases by 4-10X (erratic oral absorption)
119
How long are the biological effects of antipscyhotics?
24 hours (so give entire dose at one time per day)
120
True or false: antipsychotics can cross the placenta but not enter breast milk
FALSE: they can cross placenta AND enter breast milk because they are highly lipophillic
121
How are antipsychotics metabolized?
hepatic oxidation (and typicals are metabolized by CYP2D6 and 3A4) with conjugation
122
Which antipsychotics have active metabolites?
chlorpromazine risperidone aripirazole phenothiazines
123
Which antipsychotics are available in depot form (drug + decanoid acid)?
prolixin decanote haldol decanote risperidal consta
124
True or false: antipsychotics are not addicting
TRUE (but they do cause physcial dependence and will cause malaise and difficulty sleeping if they are abruptly stopped)
125
Antipsychotics are first line for what disorder?
schizophrenia
126
Antipsychotic block of what receptor causes EPS and hyperprolactinemia
D2
127
Antipsychotic block of what receptor causes orthostatic hypotension
alpha
128
Antipsychotic block of what receptor causes sedation
histamine
129
Antipsychotic block of what receptor causes confusion, decreased memory, constipation, orthostatic hypotension, blurred vision, dry mouth
Ach
130
Antipsychotic block of what receptor causes sexual side effects
5-HT, Ach, NE, D2 (via affects on PRL)
131
Definition: suprress spontaneous movements and complex behaviors with decreased initiative and interest in the environment with decreased manifestations of emotion or affect (with psychotic symptoms like hallucinations, delusions, and disorganized thinking that go away in days)
neuroleptic syndrome
132
Antichollinergics can block increased DA turnover in what brain area?
BG (not in limbic system)
133
What is the consequence of long term anti-pyschotic treatment on the limbic system?
presynaptic increase in DA synthesis, relesase and activity
134
What antipsychotic decreases the seizure threshold?
clozapine
135
Due to increased PRL, such antipsychotics should be avoided in which patients?
breast cancer patients
136
What causes extrapyramidal effects?
D2 blockage in BG (worse with potent antipsychotics)
137
List the EPSs.
``` Acute dystonia Akathesia Parkinsonian syndrome Neuroleptic malignant syndrome Perioral tremor Tardive Dyskinesia ```
138
What is acute dystonia and when would it present?
Muscle spasm (facial grimace, etc.) in days 1-5 of treatment
139
How do you treat acute dystonia?
IV benzotropine (anticholinergic)
140
What is akathesia and when would it present?
"ants in pants" occurring 5-60 days after treatment onset
141
How do you treat akathesia?
lower dose
142
When does parkinsonian syndrome occur in antipsychotic treatment?
1st month of treatment
143
What drugs are used to treat parkinsonian syndrome (due to antipsychotics)?
Benzotropine Amantidine (DO NOT USE L-DOPA OR BROMOCRIPTINE)
144
What is neuroleptic malignant syndrome and when does it present?
WEEKS after starting treatment -->fever, parkinsonism + catatonia,fluctuations in coarse tremor intensity, atuonomic instability, increased serum creatinine, myoglobinemia, 10% mortality
145
How do you treat neuroleptic malignant syndrome?
- stop agent - Supportive care - Dantrolene (fever) - Bromocriptine (DA competition)
146
What is perioroal tremor and when does it develop?
"rabbit syndrome" occuring months to years into therapy onset
147
Why does tardive dyskinesia occur?
thought to result from compensatory increases in BP dopamine function
148
What are the 3 classes of typical antipsychotics?
- Phenothiazines - Thioxanthenes - Butyrophenones
149
List the low potency typicals
Chlorpromazine (phenothiazine) | Thiothixene (thioxanthene)
150
List the high potency typicals
Fluphenazine | Haloperidol
151
Typical with aliphatic side chain
chlorproamzine
152
Typical with piperidine ring in side chain
thiothixene
153
Typical with piperazine group in side chain
fluphenazine
154
Toxicity of chlorpromazine
- PROLONGED QT (direct and indirect) - JAUNDICE (wk 2-4 due to hypersenstivity) - URTICARIA (in first 8 weeks) - Impaired glucose tolerance and decreased insulin release - Mild orthostatic hypotension that decreases over time
155
Toxicity of thiothixene
prlonged QT, increased risk of hypotension and sedation
156
Toxicity of fluphenazine and haloperidol
increased risk of ESP
157
True or false: ALL typicals increase PRL levels
TRUE (lead to sexual dysfunction, amenorrhea, gynecomastia, etc)
158
Which typical is safe to use in patients with alzheimers?
fluphenazine (less CV concerns)
159
MOA: partial agonist of D2 with 5-HT2a antagonism and 5-HT1a partial agonism
aripiprazole
160
Which atypicals act like atypicals at low doses and typicals at high doses?
Risperidone | possibly palperidone and ziprasidone
161
What is interesting about aripiprazole?
it may actually decrease PRL levels
162
What is unique about risperidone?
it is the ONLY approved antipsychotic in children and teens
163
Toxicity: risperidone
PRL secretion, somewhat likely to increase weight gain and T2DM ALWAYS increase weight in children
164
What is palperidone?
active metabolite of risperidone
165
Toxciity of ziprasidone.
QT prolong? | slight increase in PRL
166
What is the drug of last resort (must use at least 2 other antipsychotics that have failed before you try it)?
clozapine
167
What are the major side effects of clozapine?
AGRANULOCYTOSIS (need weekly WBC counts) Increased risk of weight gain (2X increase in CV death) Increased risk of T2DM
168
What are the major side effects of olanzapine?
increased risk of weight gain | increased risk of T2DM
169
Does quetiapine increase PRL?
NO! (aripiprazole and quetiapine only drugs not to really affect it)
170
Atypical antipsychotics have what effect in elderly?
CV effects
171
What are the 5 most common adverse effects of stimulants?
- Appetite suppression - Delayed sleep onset - "wearing off" phenomenon - Tics - Social Withdrawal (zombie)
172
What are the 4 aspects of ADHD treatment?
- Counseling - Titration - Maintenance - Potential termination
173
What does it mean to titrate a stimulant?
You want to decrease dose over time and shift from a short-acting drug to a sustained release drug
174
Why do you need to go to your physician to get a stimulant refill?
it is a schedule II drug
175
What stimulant is NOT safe in children under 6?
Atomoxetine
176
ADHD Stimulants
``` Amphetamines Atomoxetine Clonidine Dexmethylphenidate Guanfacine Haloperidol Methylphenidate ```
177
True or fasle: most stimulants have long half lives.
FALSE- most have short half lives (rapidly cleared from body)
178
True or false: there is little correlation between serum drug levels and adequacy of response
TRUE
179
What drug is absolutely contraindicated with stimulants?
MAOIs
180
What conditions are contraindicated with stimulants?
``` Psychosis H/O stimulant dependence Liver Disease Narrow angle glaucoma Underlying cardiac conditions ```
181
What is the most common comorbid condition with tics and Tourette's?
ADHD
182
What is first line treatment for tics?
Antipsychotics
183
What is the first line treatment for tics + ADHD?
Clonidine Guanfacine (alpha 2 agonists)
184
What stimulant may you combine with alpha 2 agonists?
methylphenidate
185
OVERDOSE: mild toxicity (drowsy, agitated, hyperactive, GI upset, tremor, hyperreflexia, tachycardia, HTN, seizure)
Atomoxetine
186
OVERDOSE: mixed picture depending on the central/peripheral effects (initial drowsy + lethargy + dry mouth + sweating --> CV effects like hypotension or HTN
Guanfacine
187
OVERDOSE: toxicity is primarily neuro/ psych (ex. dilated pupils, tremor, agitation, hyperreflexia, combative behavior, confusion, delirium, anxiety, paranoia, movement disorders, seizures) and CV effects (but can effect other organ systems)
Amphetamines | Methylphenidate
188
How do you treat amphetamine overdose?
supportive treatment | judicious use of benzos
189
OVERDOSE: may produce short term HTN (but usually causes low BP)
Nitroprusside for hypertension | Atropine and DA pressors for hypotension
190
MOA: Amphetamines
release NE and DA
191
MOA: atomoxetine
selective NE reuptake inhibitor centrally and peripherally
192
MOA: methylphenidate and dexmethylphenidate
block DE and NE reuptake
193
MOA: guanfacine
post-synaptic alpha-2 receptor agonist effects on prefrontal cortex
194
MOA: clonidine
alpha 2 agonist through to release NE from locus cereuleus
195
MOA: haloperidol
post-synaptic D2 receptor blocker (antipsychotic)
196
TOXICITY: HA, insomnia, decreased appetite (patch), N/V, abdominal pain
Methylphenidate | Dexmethylphenidate
197
TOXICITY: skin reaction (patch), dry mouth, somnolence, HA, fatigue, drowsy, dizzy, anxiety, abdominal pain
Guanfacine | Clonidine
198
TOXICITY: dry mouth, HA, insomnia, abdominal pain, decreased appetite, cough, somnolence, vomiting
Atomoxetine
199
TOXICITY: abdominal pain, appetite, HA, insomnia > anxiety, meotional lability, increased HR, weight loss
Amphetamines
200
Which drug used for ADHD/tics has a DDI with cyclosporine?
Clonidine (clonidine increases levels of cyclosporine)
201
Which drug used for ADHD/tics does NOT have CYP issues?
clonidine and guanfacine
202
Which CYPS are responsible for metabolism of haloperidol?
CYP2D6 | CYP3A4
203
What happens if haloperidol concentrations increase?
potential QT prolongation
204
Which drug used for AHDH has a DDI with albuterol?
atomoxetine (increase CV adverse effects)
205
Which drug used to treat ADHD has a DDI with ergotamine/pseudophedrine?
Amoxetine (exascerbates BP effects) Methylphenidate Dexmethylphenidate
206
All stimulants have DDI with inducers/inhibitors of what CYP?
CYP2D6
207
Which drug used to treat ADHD has a DDI with acetazolamine or Na Bicarb?
Amphetamines (alkalinization of urine increases reuptake to increase drug levels)
208
Which drug used to treat ADHD has a DDI with ETOH?
Methylphenidate Dexmethylphenidate (increase toxic metabolite with the ability to concentrate)
209
Which drug used to treat ADHD has a DDI with phenytoin?
Methylphenidate Dexmethylphenidate (increases blood levels of phenytoin)
210
Which drug used to treat ADHD has a DDI with digoxin?
Amphetamines -->arrhythmia
211
Why is there a DDI with amphetamines and ammonium chloride?
Acidic urine increases elimination so there are decreased drug level sof amphetamines
212
Which drug used to treat ADHD/tics has a DDI with bupropion?
Guanfacine (leads to grand mal seixures)
213
Which drug used to treat ADHD has a DDI with epinephrine?
Amoxetine (incresase BP)
214
Which drug used to treat ADHD has a DDI with chlorpromazine or haloperidol?
amphetamines (because DA blockers diminish their effects)
215
What do you see if a person on amphetamines takes a cough suppressant like dextromethorphan?
increased impairment of judgement | erratic euphoria
216
How long should you wait between an MAOI and a stimulant?
2 weeks
217
What are the problems with short-acting amphetamines?
BID and TID dosing
218
What are the problems with long-acting amphetamines?
appetite and sleep disturbances (worse toxicity)
219
Syndrome seen 1-3 days after DA antagonist (ex. any antipsychotic, haloperidol > chlorpromazine OR mixing with lithium, antidepressant, or anti-Ach OR withdrawal of anti-parkinsonian agent)
Neuroleptic Malignant Syndrome
220
Syndrome seen 30 minutes to 24 hours after succinylcholine or volatile anesthetic
malignant hyperthermia
221
Syndrome seen <12 hours after pro 5-HT drug (ex. SSRI, MAOI, AED, Anti-depressant, etc)
serotonin syndrome
222
Syndrome seen < 12 hours after anti-cholinergic
Anticholinergic posioning
223
Syndrome with AKATHISIA, tremor, hyperactive bowels, mydriasis, sialorrhea, diaphroesis, altered mental state, CLONUS, hyper-reflexia, muscular HYPERTONICITY
Serotonin syndrome
224
Syndrome with mydriasis, skin hot/dry, decreased or absent bowel sounds, agitation, delirium
Anticholinergic poisoning
225
Syndrome with temp (<46), mottled skin, diaphoresis, RIGOR-MORTIS LIKE RIGIDITY, HYPOREFLEXIA
malignant hyperthermia
226
Syndrome with fever, pallor, diaphoresis, LEAD PIPE RIGIDITY, EXTRAPYRAMIDAL TREMOR, HYPOREFLEXIA, stupor, alert mutism or coma
Neuroleptic malignant syndrome
227
Symptoms seen in every "syndrome"
HTN, hyperthermia, tachycardia, tachypnea,
228
What are risk factors seen in neuroleptic malignant syndrome?
- H/O NMS - Affective disorders or physical brain disorders that decrease mental funciton - Increased ambient temp or dehydration - Catatonia or agitation
229
What causes the hyperthermia of NMS?
block D2 receptor in hypothalamus
230
What causes the autononic dysfunciton in NMS?
BLock inhibitory actions of DA in SNS
231
What is are some complications that should be avoided in NMS?
- Rhabdomyolysis - Renal failure - Respiratory failure
232
How do you treat NMS?
Dantrolene Lorazepam Bromocriptine (DA agonist)
233
Why does malignant hyperthermia occur?
uncontrolled Ca2+ release from SR (leading to skeletal muscle contraction and metabolic acidosis)
234
How do you treat malignant hyperthermia?
- Dantrolene IV - Treat acidosis (monitor serum K+) - Cool body to <38 - Maintain urinary output (fluids, furosemide, mannitol)
235
What is the rostral midline raphe nuelci responsible for?
wakefulness, behavior, food intake, thermoregulation, emesis, sexual behavior
236
What is the caudal midline raphe nuelci responsible for?
nociception and motor tone
237
What causes serotonin syndrome?
too high of 5-HT levels impact receptors in GI, vascular system and brainstem (midline raphe nuclei)
238
How do you treat serotonin syndrome?
- Stop agent - Administer CYPROHEPTADINE (5-HT agnatonist) - Supportive
239
Why does anticholinergic poisoning occur?
-decreased parasympathetic activity and CV changes due to unopposed sympathetic stimulation
240
What drug do you use to treat an anticholinergic poisoning where the patient is in a self-harming psychosis or is in hemodynamic dysfunciton secondary to tachydysrhythmias?
PHYSOSTIGMINE
241
In which patients is physostigmine contraindicated?
TCA overdose (due to increased seizure risk)
242
Drugs cause activation of ___ pathways in the VTA that project to the ____
Dopamine | Nucleus accumbens
243
How do DA signals from VTA to NA lead to substance abuse?
respond to natural rewards (usurping other things like food and sex)
244
If an overdosed patient has respiratory depression, what should you think?
- Barbiturates - Opiates - ETOH - GHB - Sedative hypnotics
245
If an overdosed patient has mydriasis, what should you think?
Sympathomimetics Amphetamines Cocaine LSD
246
If an overdosed patient has miosis, what should you think?
Sympatholytic agents Opiates Nicotine
247
If an overdosed patient has horizontal nystagmus, what should you think?
- Barbiturates | - ETOH
248
If an overdosed patient has vertical or mixed nystagmus, what should you think?
PCP
249
If an overdosed patient has rhabdomyolysis, what should you think?
AMphetamines Cocaine PCP
250
How to you treat rhabdomyolysis
Alkalinize urine with NaCl to stop myoglobin deposition
251
How would you get nicotine poisoning?
- Multiple patches | - Smokeless E cigarette overuse
252
How do you treat a nicotine overdose?
Mecamylamine (nicotine antagonist)
253
What drug is used to control HTN in a patient who is on cocaine?
Labetalol
254
What drug is used to control ventricular arrhythmia in a patient on cocaine?
Lidocaine
255
What drug is used to control SV-tach in a patient on cocaine?
adenosine

PSYCHIATRY (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions