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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)

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2
Q

MOA: disulfiram

A

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

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3
Q

MOA: naltrexone

A

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

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4
Q

MOA: acamprosate

A

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

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5
Q

Antidote for alcohol + acetaminophen

A

N-acetylcysteine

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6
Q

What CYP does ETOH stimulate?

A

CYP2E1

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7
Q

Is ETOH metabolized by CYPs?

A

NO! (unless they are a chronic alcoholic)

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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

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9
Q

Disorder: ataxia, confusion, ocular muscle paralysis

A

Wernicke-Korsakoff

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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)

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11
Q

3 things used to treat anxiety (with CBT)?

A
  • Benzodiazepines
  • Buspirone
  • Propranolol
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12
Q

MOA: benzodiazepines

A

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

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13
Q

Which benzos are commonly used IV?

A

diazepam

lorazepam

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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)

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15
Q

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

A

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

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16
Q

Benzo speed of onset determinants?

A

dissolution rate

speed of absorption from GI tract

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17
Q

RAPID ONSET BENZOs

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

(CLAD)

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18
Q

SLOW ONSET BENZOs

A

Oxazepam
Prazepam

(ox’s are slow)

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19
Q

SHORT ACTING BENZOS

A

Alprazolam
Triazolam
Midazolam

(go to ATM when I am SHORT on money)

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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

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21
Q

LONG ACTING BENZOs

A 
Chlordiazepoxide*
Clorazepate*
Diazepam*
Flurazepam
Quazepam
Prazepam*
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22
Q

Which benzos are NOT CYP metabolized?

A

Lorazepam
Oxazepam

(OnLy 2 not cyp metabolized)

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23
Q

Toxicities seen in all benzos.

A
  • Category D teratogen

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

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24
Q

How do you treat benzo-induced respiratory depression?

A

Flumazenil

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25
Q

Benzo withdrawal symptoms

A

rebound anxiety, insomnia, autonomic dysfunction (tachycardia, treamor, sweating, dry mouth, HA)

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26
Q

Tolerance rarely if ever develops to what benzodiazepine effect?

A

anxiolytic effect

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27
Q

MOA: Buspirone

A

suppress 5-HT activity and increase NE and DA activity

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28
Q

How do buspirone and benzo’s differ in effect for anxiety?

A

buspirone is just as effective but has a much slower onset (weeks)

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29
Q

MOA: propranolol

A

Beta-blocker that suppresses somatic and autonomic symptoms of anxiety but does NOT alter emotional symptoms (brain)

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30
Q

Propranolol is the DOC for what anxiety condition?

A

stage fright

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31
Q

Only anxiolytic to inhibit monosynaptic reflexes in the spinal cord at clinical doses (muscle relaxant).

A

diazepam

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32
Q

Best drugs to treat anxiety associated with ETOH withdrawal (if liver function is normal).

A

Diazepam

Chlordiazepoxide

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33
Q

BNZ with some anti-depressant activity (similar to TCAs)

A

alprazolam (panic disorder treatment?)

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34
Q

What is the biogenic amine hypothesis of depression?

A

Funcitonal deficit of monoamines (NE and 5-HT) is thought to be involved in pathophysiology of depression

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35
Q

What evidence supports the biogenic amine hypothesis?

A

reserpine (VMAT inhibitor that presents packaging of monoamines into veiscles) causes depression symptoms

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36
Q

What is the therapeutic lag?

A

even though NE and 5-HT levels increase immediately with anti-depressants, it takes around 2-8 weeks to see clinical effect

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37
Q

Why are NSAIDs not good to take in depression?

A

cytokines may cause an anti-depressant effect!

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38
Q

BBW for all antidepressants

A

Increased risk of suicide in children to 24 yos (especially with initial treatment)

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39
Q

Antidepressants that are substrates for MDRI

A

Amitryptyline
Citalopram
Paroxetine
Venlafaxine

(TRIP to the CITy of PARis or VENice)

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40
Q

Antidepressants that are NOT MDRI substrates.

A

Mirtazepine

Fluoxetine

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41
Q

What about the MDRI renders patients resistant to amitryptyline, citalopram, paroxetine, and venlafaxine?

A

if they are “C-carriers” becuase this increases activity of the P-gp pump

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42
Q

Which anti-depressant classes cause decreased libido and sexual dysfunction?

A
  • TCAs
  • SSRIs
  • MAOIs
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43
Q

Which anti-depressant does NOT cause libido problems?

A

bupropion

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44
Q

Which anti-depressants lead to weight gain?

A
  • TCAs
  • Mirtazepine
  • MAOIs
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45
Q

Which anti-depressant is safest for bipolar disorder?

A

bupropion

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46
Q

Which anti-depressant has the highest risk of birth defects?

A

paroxetine

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47
Q

Which drugs are used to treat depression in pregnant women?

A

fluoxetine
citalopram
sertraline

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48
Q

Which anti-depressants have increased risk of seizures?

A

Maprotiline

Bupropion

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49
Q

With which anti-depressant may you see extrapyramidal effects?

A

amoxamine

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50
Q

Which anti-depressant is no longer in common use due to hepatotoxicity?

A

nefazodone

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51
Q

What drug should be avoided in those taking SSRIs for 2 weeks at least?

A

MAOIs (can lead to serotonin syndrome)

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52
Q

TCAs

A

Amitriptyline
Nortryptyline
-“pramines”
Doxepin

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53
Q

SSRIs

A 
Citalopram
Escitalopram
Fluoxetine
Sertraline
Paroxetine
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54
Q

MAOIs

A

tranylcypromine
isocarboxazid
phenelzine

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55
Q

SNRIs

A

Venlafaxine

Duloxetine

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56
Q

SARIs

A

Trazodone
Nefazodone

“sari we’re NoT -done”

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57
Q

SMSs

A

Vortioxetine

Vilazodone

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58
Q

Other than depression, what are 3 interesting things TCAs are used for?

A

ADHD
Nocturnal enuresis
anxiety disorders

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59
Q

MOA: TCAs

A

block reuptake of NE and 5-HT

block M, alpha, and histamine receptors

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60
Q

MOA: SSRIs

A

Block SERT

Less block of M, alpha and histamine receptors so increase compliance due to lower side effects)

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61
Q

MOA: MAOIs

A

IRREVERSIBLY BLOCK MAOs to prevent pre-synaptic degradation of NE and 5-HT (MAO-A) or DA (MAO-B) and increase their availablity

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62
Q

MOA: SNRIs

A

inhibit 5-HT and NE reuptake

NO activity at M, alpha, or histamine receptors

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63
Q

MOA: SARIs

A

moderate 5-HT reuptake block
5-HT2a antagonist
5-HT1a partial aognist

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64
Q

MOA: SMSs

A

potent 5-HT1a partial agonist

block SERT

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65
Q

MOA: amoxamine

A

inhibits NET > SERT ~ DAT

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66
Q

MOA: bupropion

A

weak block of NET, DAT and SERT (and metabolite blocks NE reuptake)

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67
Q

MOA: maprotiline

A

NRI= blocks NE reuptake

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68
Q

MOA: mirtazepine

A
  • antagonize presynaptic alpha-1 to increase NE and 5-HT release
  • antagonize 5-HT2 receptors
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69
Q

Anti-depressant that can help you quit smoking.

A

bupropion

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70
Q

DOC for depression treatment in psychotic patients.

A

amoxamine

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71
Q

MOA: vortioxetine

A

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

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72
Q

Anti-depressant that inhibits CYP3A4.

A

trazodone

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73
Q

Antidepressent used in anxiety disorders with sleep problems.

A

trazodone

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74
Q

Most potent SNRI

A

duloxetine

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75
Q

How is duloxetine metabolized?

A

CYP2D6 and CYP1A2

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76
Q

TOXICITY: CNS stimulation, agitation, euphoria (2-6 wk), sleep disturbance, orthostatic hypotension, weight gain, sexual dysfunction

A

MAOIs

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77
Q

What happens if you eat cheese and wine with your MAOI and then take a diet pill?

A

HTN crisis due to tyramine and sympathomimetic

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78
Q

What 2 drugs can lead to delirium, hyperpyrexia, convulsions, coma and death if taken with MAOIs?

A

meperidine

dextromethorpham

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79
Q

How are MAOIs metabolized?

A

acetylation

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80
Q

How long does MAOI action last?

A

1-3 weeks

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81
Q

TOXICITY: CNS stimulation, agitation, anxiety (2-6 weeks), rare CV effects, nausea, reduced libido and sexual function

A

SSRIs

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82
Q

What causes serotonin syndrome?

A

overstimulation of 5-HT1a in central gray area and medulla

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83
Q

What is the active metabolite of fluoxetine?

A

norfluoxetine (7-9 day half-life)

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84
Q

How are SSRIs metabolized?

A

CYP2D6, CYP2C19, CYP3A4

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85
Q

True or false: SSRIs are highly protein bound

A

true! so are TCAs

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86
Q

What CYPs are inhibited by SSRIs?

A

CYP2D6 and CYP2C19

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87
Q

TOXCICITY: drowsy, anxious, decreased cognition (2-8 wk), orthostatic hypotension, tachycardia, dry mouth, weight gain, decreased libido and sexual function

A

TCAs

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88
Q

Why do you have to be especially careful with TCAs?

A

very narrow therapeutic window (can get arrhythmia, worsened CHF, or seizures with an overdose)

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89
Q

DDIs of TCAs?

A 
ETOH
Sedatives
Anti-parkinsonism agents
Antipscyhotics
Biogenic amines (compete for protein binding)
Clonidine (TCAs block its effect)
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90
Q

Which has better bioavailability TCAs or SSRIs?

A

SSRIs (TCAs have incomplete absorption)

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91
Q

Describe TCA metabolism.

A

tertiary amines are demethylated to secondary (active) amines which are oxygenated and conjugated to CYP2D6

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92
Q

What should you always check for BEFORE giving an antidepressant?

A

that the patient actually doesn’t have bipolar disorder with hidden mania

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93
Q

How do you treat bipolar?

A

mood stabilizers (ex. lithium, anti-convulsants)

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94
Q

True or false: mood stabilizers take away mania

A

FALSE (they prevent cycling from mania to depression)

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95
Q

What drugs may help acute mania?

A

antipsychotics

benzos

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96
Q

First line for bipolar

A

lithium

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97
Q

MOA: lithium

A

poorly understood (possibly inhibits inositol phosphate signaling and NT-stimulated adenylyl cyclase

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98
Q

TOXICITY: lithium

A

very narrow therapeutic window (nephrogenic DI (ADH antagonist), mild hypothyroidism, sick sinus, acne, folliculitis, psoriasis, ataxia, tremor, aphasia, sedation

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99
Q

What is sick sinus?

A

brady-tachy cardia dur to block of Na/K ATPase in cardiac tissue

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100
Q

CONTRAINDICATIONS of lithium

A

diabetes

heart disease

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101
Q

DDIs of lithium

A

diuretics

NSAIDs

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102
Q

How is lithium metabolized?

A

trick question, it isn’t–distributes to total body water (and bone) and is cleared in urine

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103
Q

What are the benefits of anticonvulsants in bipolar?

A

quicker response

larger therapeutic index

104
Q

MOA: valproate

A

stabilizes inactive state of Na channels (inhibition), blocks T-type Ca2+ channels, stimulates GABA release

105
Q

Toxicity: valproate

A

Hepatotoxic (check LFTs), Sedation, heart burn, abdominal pain, nausea

106
Q

Metabolism of valproate

A

CYP2C metabolized and inhibitor (scale down dose over time)

107
Q

MOA: carbamazepine

A

inhibits Na channels (prolongs recovery from inactivation

108
Q

Toxicity of carbamazepine

A

RARE aplastic anemia, diplopia, ataxia, rash (uncommon), mild GI upset, drowsy

109
Q

Metabolism of carbamazepine

A

CYP3A4 metabolism to active metabolite (induces 3A4 so speeds up own metabolism)

110
Q

What type of agents worsen psychosis?

A

agents that increase DA activity

111
Q

What agents reduce the positive symptoms of psychosis?

A

D2 receptor antagonists

112
Q

What agents reduce the negative symptoms of psychosis?

A

NONE (but at one time, 5-HT block was thought to help)

113
Q

What determines potency of an anti-psychotic?

A

in vitro inhibition of D2 receptor binding

114
Q

What determines level of extrapyramidal toxicity?

A

tends to occur with more potent drugs (with less muscarinic blockage)

115
Q

How does the MOA of typical and atypical antipsychotics differ?

A

typical is majorly D2 block

atypical is D2 block and 5-HT2a block

116
Q

Typical antipsychotics

A

Chlorpromazine
Fluphenazine
Haloperidol
(also perphenazine, thiothixene, butyrophenones)

117
Q

Atypical antipsychotics

A 
Clozapine
Risperidone
Olanzapine
Aripiprazole
(and quetiapine, ziprasidone, and paliperidone)
118
Q

How do you improve bioavailability of an antipsychotic?

A

IM injection increases by 4-10X (erratic oral absorption)

119
Q

How long are the biological effects of antipscyhotics?

A

24 hours (so give entire dose at one time per day)

120
Q

True or false: antipsychotics can cross the placenta but not enter breast milk

A

FALSE: they can cross placenta AND enter breast milk because they are highly lipophillic

121
Q

How are antipsychotics metabolized?

A

hepatic oxidation (and typicals are metabolized by CYP2D6 and 3A4) with conjugation

122
Q

Which antipsychotics have active metabolites?

A

chlorpromazine
risperidone
aripirazole
phenothiazines

123
Q

Which antipsychotics are available in depot form (drug + decanoid acid)?

A

prolixin decanote
haldol decanote
risperidal consta

124
Q

True or false: antipsychotics are not addicting

A

TRUE (but they do cause physcial dependence and will cause malaise and difficulty sleeping if they are abruptly stopped)

125
Q

Antipsychotics are first line for what disorder?

A

schizophrenia

126
Q

Antipsychotic block of what receptor causes EPS and hyperprolactinemia

127
Q

Antipsychotic block of what receptor causes orthostatic hypotension

128
Q

Antipsychotic block of what receptor causes sedation

129
Q

Antipsychotic block of what receptor causes confusion, decreased memory, constipation, orthostatic hypotension, blurred vision, dry mouth

130
Q

Antipsychotic block of what receptor causes sexual side effects

A

5-HT, Ach, NE, D2 (via affects on PRL)

131
Q

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)

A

neuroleptic syndrome

132
Q

Antichollinergics can block increased DA turnover in what brain area?

A

BG (not in limbic system)

133
Q

What is the consequence of long term anti-pyschotic treatment on the limbic system?

A

presynaptic increase in DA synthesis, relesase and activity

134
Q

What antipsychotic decreases the seizure threshold?

135
Q

Due to increased PRL, such antipsychotics should be avoided in which patients?

A

breast cancer patients

136
Q

What causes extrapyramidal effects?

A

D2 blockage in BG (worse with potent antipsychotics)

137
Q

List the EPSs.

A 
Acute dystonia
Akathesia
Parkinsonian syndrome
Neuroleptic malignant syndrome
Perioral tremor
Tardive Dyskinesia
138
Q

What is acute dystonia and when would it present?

A

Muscle spasm (facial grimace, etc.) in days 1-5 of treatment

139
Q

How do you treat acute dystonia?

A

IV benzotropine (anticholinergic)

140
Q

What is akathesia and when would it present?

A

“ants in pants” occurring 5-60 days after treatment onset

141
Q

How do you treat akathesia?

A

lower dose

142
Q

When does parkinsonian syndrome occur in antipsychotic treatment?

A

1st month of treatment

143
Q

What drugs are used to treat parkinsonian syndrome (due to antipsychotics)?

A

Benzotropine
Amantidine
(DO NOT USE L-DOPA OR BROMOCRIPTINE)

144
Q

What is neuroleptic malignant syndrome and when does it present?

A

WEEKS after starting treatment –>fever, parkinsonism + catatonia,fluctuations in coarse tremor intensity, atuonomic instability, increased serum creatinine, myoglobinemia, 10% mortality

145
Q

How do you treat neuroleptic malignant syndrome?

A
  • stop agent
  • Supportive care
  • Dantrolene (fever)
  • Bromocriptine (DA competition)
146
Q

What is perioroal tremor and when does it develop?

A

“rabbit syndrome” occuring months to years into therapy onset

147
Q

Why does tardive dyskinesia occur?

A

thought to result from compensatory increases in BP dopamine function

148
Q

What are the 3 classes of typical antipsychotics?

A
  • Phenothiazines
  • Thioxanthenes
  • Butyrophenones
149
Q

List the low potency typicals

A

Chlorpromazine (phenothiazine)

Thiothixene (thioxanthene)

150
Q

List the high potency typicals

A

Fluphenazine

Haloperidol

151
Q

Typical with aliphatic side chain

A

chlorproamzine

152
Q

Typical with piperidine ring in side chain

A

thiothixene

153
Q

Typical with piperazine group in side chain

A

fluphenazine

154
Q

Toxicity of chlorpromazine

A
  • 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
Q

Toxicity of thiothixene

A

prlonged QT, increased risk of hypotension and sedation

156
Q

Toxicity of fluphenazine and haloperidol

A

increased risk of ESP

157
Q

True or false: ALL typicals increase PRL levels

A

TRUE (lead to sexual dysfunction, amenorrhea, gynecomastia, etc)

158
Q

Which typical is safe to use in patients with alzheimers?

A

fluphenazine (less CV concerns)

159
Q

MOA: partial agonist of D2 with 5-HT2a antagonism and 5-HT1a partial agonism

A

aripiprazole

160
Q

Which atypicals act like atypicals at low doses and typicals at high doses?

A

Risperidone

possibly palperidone and ziprasidone

161
Q

What is interesting about aripiprazole?

A

it may actually decrease PRL levels

162
Q

What is unique about risperidone?

A

it is the ONLY approved antipsychotic in children and teens

163
Q

Toxicity: risperidone

A

PRL secretion, somewhat likely to increase weight gain and T2DM

ALWAYS increase weight in children

164
Q

What is palperidone?

A

active metabolite of risperidone

165
Q

Toxciity of ziprasidone.

A

QT prolong?

slight increase in PRL

166
Q

What is the drug of last resort (must use at least 2 other antipsychotics that have failed before you try it)?

167
Q

What are the major side effects of clozapine?

A

AGRANULOCYTOSIS (need weekly WBC counts)
Increased risk of weight gain (2X increase in CV death)
Increased risk of T2DM

168
Q

What are the major side effects of olanzapine?

A

increased risk of weight gain

increased risk of T2DM

169
Q

Does quetiapine increase PRL?

A

NO! (aripiprazole and quetiapine only drugs not to really affect it)

170
Q

Atypical antipsychotics have what effect in elderly?

A

CV effects

171
Q

What are the 5 most common adverse effects of stimulants?

A
  • Appetite suppression
  • Delayed sleep onset
  • “wearing off” phenomenon
  • Tics
  • Social Withdrawal (zombie)
172
Q

What are the 4 aspects of ADHD treatment?

A
  • Counseling
  • Titration
  • Maintenance
  • Potential termination
173
Q

What does it mean to titrate a stimulant?

A

You want to decrease dose over time and shift from a short-acting drug to a sustained release drug

174
Q

Why do you need to go to your physician to get a stimulant refill?

A

it is a schedule II drug

175
Q

What stimulant is NOT safe in children under 6?

A

Atomoxetine

176
Q

ADHD Stimulants

A 
Amphetamines
Atomoxetine
Clonidine
Dexmethylphenidate
Guanfacine
Haloperidol
Methylphenidate
177
Q

True or fasle: most stimulants have long half lives.

A

FALSE- most have short half lives (rapidly cleared from body)

178
Q

True or false: there is little correlation between serum drug levels and adequacy of response

179
Q

What drug is absolutely contraindicated with stimulants?

180
Q

What conditions are contraindicated with stimulants?

A 
Psychosis
H/O stimulant dependence
Liver Disease
Narrow angle glaucoma
Underlying cardiac conditions
181
Q

What is the most common comorbid condition with tics and Tourette’s?

182
Q

What is first line treatment for tics?

A

Antipsychotics

183
Q

What is the first line treatment for tics + ADHD?

A

Clonidine
Guanfacine
(alpha 2 agonists)

184
Q

What stimulant may you combine with alpha 2 agonists?

A

methylphenidate

185
Q

OVERDOSE: mild toxicity (drowsy, agitated, hyperactive, GI upset, tremor, hyperreflexia, tachycardia, HTN, seizure)

A

Atomoxetine

186
Q

OVERDOSE: mixed picture depending on the central/peripheral effects (initial drowsy + lethargy + dry mouth + sweating –> CV effects like hypotension or HTN

A

Guanfacine

187
Q

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)

A

Amphetamines

Methylphenidate

188
Q

How do you treat amphetamine overdose?

A

supportive treatment

judicious use of benzos

189
Q

OVERDOSE: may produce short term HTN (but usually causes low BP)

A

Nitroprusside for hypertension

Atropine and DA pressors for hypotension

190
Q

MOA: Amphetamines

A

release NE and DA

191
Q

MOA: atomoxetine

A

selective NE reuptake inhibitor centrally and peripherally

192
Q

MOA: methylphenidate and dexmethylphenidate

A

block DE and NE reuptake

193
Q

MOA: guanfacine

A

post-synaptic alpha-2 receptor agonist effects on prefrontal cortex

194
Q

MOA: clonidine

A

alpha 2 agonist through to release NE from locus cereuleus

195
Q

MOA: haloperidol

A

post-synaptic D2 receptor blocker (antipsychotic)

196
Q

TOXICITY: HA, insomnia, decreased appetite (patch), N/V, abdominal pain

A

Methylphenidate

Dexmethylphenidate

197
Q

TOXICITY: skin reaction (patch), dry mouth, somnolence, HA, fatigue, drowsy, dizzy, anxiety, abdominal pain

A

Guanfacine

Clonidine

198
Q

TOXICITY: dry mouth, HA, insomnia, abdominal pain, decreased appetite, cough, somnolence, vomiting

A

Atomoxetine

199
Q

TOXICITY: abdominal pain, appetite, HA, insomnia > anxiety, meotional lability, increased HR, weight loss

A

Amphetamines

200
Q

Which drug used for ADHD/tics has a DDI with cyclosporine?

A

Clonidine (clonidine increases levels of cyclosporine)

201
Q

Which drug used for ADHD/tics does NOT have CYP issues?

A

clonidine and guanfacine

202
Q

Which CYPS are responsible for metabolism of haloperidol?

A

CYP2D6

CYP3A4

203
Q

What happens if haloperidol concentrations increase?

A

potential QT prolongation

204
Q

Which drug used for AHDH has a DDI with albuterol?

A

atomoxetine (increase CV adverse effects)

205
Q

Which drug used to treat ADHD has a DDI with ergotamine/pseudophedrine?

A

Amoxetine (exascerbates BP effects)
Methylphenidate
Dexmethylphenidate

206
Q

All stimulants have DDI with inducers/inhibitors of what CYP?

207
Q

Which drug used to treat ADHD has a DDI with acetazolamine or Na Bicarb?

A

Amphetamines (alkalinization of urine increases reuptake to increase drug levels)

208
Q

Which drug used to treat ADHD has a DDI with ETOH?

A

Methylphenidate
Dexmethylphenidate
(increase toxic metabolite with the ability to concentrate)

209
Q

Which drug used to treat ADHD has a DDI with phenytoin?

A

Methylphenidate
Dexmethylphenidate
(increases blood levels of phenytoin)

210
Q

Which drug used to treat ADHD has a DDI with digoxin?

A

Amphetamines –>arrhythmia

211
Q

Why is there a DDI with amphetamines and ammonium chloride?

A

Acidic urine increases elimination so there are decreased drug level sof amphetamines

212
Q

Which drug used to treat ADHD/tics has a DDI with bupropion?

A

Guanfacine (leads to grand mal seixures)

213
Q

Which drug used to treat ADHD has a DDI with epinephrine?

A

Amoxetine (incresase BP)

214
Q

Which drug used to treat ADHD has a DDI with chlorpromazine or haloperidol?

A

amphetamines (because DA blockers diminish their effects)

215
Q

What do you see if a person on amphetamines takes a cough suppressant like dextromethorphan?

A

increased impairment of judgement

erratic euphoria

216
Q

How long should you wait between an MAOI and a stimulant?

217
Q

What are the problems with short-acting amphetamines?

A

BID and TID dosing

218
Q

What are the problems with long-acting amphetamines?

A

appetite and sleep disturbances (worse toxicity)

219
Q

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)

A

Neuroleptic Malignant Syndrome

220
Q

Syndrome seen 30 minutes to 24 hours after succinylcholine or volatile anesthetic

A

malignant hyperthermia

221
Q

Syndrome seen <12 hours after pro 5-HT drug (ex. SSRI, MAOI, AED, Anti-depressant, etc)

A

serotonin syndrome

222
Q

Syndrome seen < 12 hours after anti-cholinergic

A

Anticholinergic posioning

223
Q

Syndrome with AKATHISIA, tremor, hyperactive bowels, mydriasis, sialorrhea, diaphroesis, altered mental state, CLONUS, hyper-reflexia, muscular HYPERTONICITY

A

Serotonin syndrome

224
Q

Syndrome with mydriasis, skin hot/dry, decreased or absent bowel sounds, agitation, delirium

A

Anticholinergic poisoning

225
Q

Syndrome with temp (<46), mottled skin, diaphoresis, RIGOR-MORTIS LIKE RIGIDITY, HYPOREFLEXIA

A

malignant hyperthermia

226
Q

Syndrome with fever, pallor, diaphoresis, LEAD PIPE RIGIDITY, EXTRAPYRAMIDAL TREMOR, HYPOREFLEXIA, stupor, alert mutism or coma

A

Neuroleptic malignant syndrome

227
Q

Symptoms seen in every “syndrome”

A

HTN, hyperthermia, tachycardia, tachypnea,

228
Q

What are risk factors seen in neuroleptic malignant syndrome?

A
  • H/O NMS
  • Affective disorders or physical brain disorders that decrease mental funciton
  • Increased ambient temp or dehydration
  • Catatonia or agitation
229
Q

What causes the hyperthermia of NMS?

A

block D2 receptor in hypothalamus

230
Q

What causes the autononic dysfunciton in NMS?

A

BLock inhibitory actions of DA in SNS

231
Q

What is are some complications that should be avoided in NMS?

A
  • Rhabdomyolysis
  • Renal failure
  • Respiratory failure
232
Q

How do you treat NMS?

A

Dantrolene
Lorazepam
Bromocriptine (DA agonist)

233
Q

Why does malignant hyperthermia occur?

A

uncontrolled Ca2+ release from SR (leading to skeletal muscle contraction and metabolic acidosis)

234
Q

How do you treat malignant hyperthermia?

A
  • Dantrolene IV
  • Treat acidosis (monitor serum K+)
  • Cool body to <38
  • Maintain urinary output (fluids, furosemide, mannitol)
235
Q

What is the rostral midline raphe nuelci responsible for?

A

wakefulness, behavior, food intake, thermoregulation, emesis, sexual behavior

236
Q

What is the caudal midline raphe nuelci responsible for?

A

nociception and motor tone

237
Q

What causes serotonin syndrome?

A

too high of 5-HT levels impact receptors in GI, vascular system and brainstem (midline raphe nuclei)

238
Q

How do you treat serotonin syndrome?

A
  • Stop agent
  • Administer CYPROHEPTADINE (5-HT agnatonist)
  • Supportive
239
Q

Why does anticholinergic poisoning occur?

A

-decreased parasympathetic activity and CV changes due to unopposed sympathetic stimulation

240
Q

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?

A

PHYSOSTIGMINE

241
Q

In which patients is physostigmine contraindicated?

A

TCA overdose (due to increased seizure risk)

242
Q

Drugs cause activation of ___ pathways in the VTA that project to the ____

A

Dopamine

Nucleus accumbens

243
Q

How do DA signals from VTA to NA lead to substance abuse?

A

respond to natural rewards (usurping other things like food and sex)

244
Q

If an overdosed patient has respiratory depression, what should you think?

A
  • Barbiturates
  • Opiates
  • ETOH
  • GHB
  • Sedative hypnotics
245
Q

If an overdosed patient has mydriasis, what should you think?

A

Sympathomimetics
Amphetamines
Cocaine
LSD

246
Q

If an overdosed patient has miosis, what should you think?

A

Sympatholytic agents
Opiates
Nicotine

247
Q

If an overdosed patient has horizontal nystagmus, what should you think?

A
  • Barbiturates

- ETOH

248
Q

If an overdosed patient has vertical or mixed nystagmus, what should you think?

249
Q

If an overdosed patient has rhabdomyolysis, what should you think?

A

AMphetamines
Cocaine
PCP

250
Q

How to you treat rhabdomyolysis

A

Alkalinize urine with NaCl to stop myoglobin deposition

251
Q

How would you get nicotine poisoning?

A
  • Multiple patches

- Smokeless E cigarette overuse

252
Q

How do you treat a nicotine overdose?

A

Mecamylamine (nicotine antagonist)

253
Q

What drug is used to control HTN in a patient who is on cocaine?

254
Q

What drug is used to control ventricular arrhythmia in a patient on cocaine?

255
Q

What drug is used to control SV-tach in a patient on cocaine?

PSYCHIATRY (9 decks)

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