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Flashcards in Psych Pharm Deck (253)
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1
Q

What is the preferred drug for alcohol withdrawal?

A

Benzodiazepines

2
Q

What is the preferred treatment for anxiety?

A

SSRIs, SNRIs, buspirone

3
Q

What is the preferred treatment for ADHD?

A

Methylphenidate
Amphetamines
Atomoxetine (non-stimulant: NE selective reuptake inhibitor)

4
Q

What is the preferred drug for bipolar disorder?

A

Lithium
Valproate
Carbamazepine
Atypical antipsychotic

5
Q

What is the preferred drug for bulimia?

A

SSRIs

6
Q

What is the preferred drug for depression?

A

SSRIs, SNRIs, TCAs, buspirone, mirtazapine

7
Q

What is the preferred drug for obsessive compulsive disorder?

A

SSRIs, clomipramine

8
Q

What is the preferred drug for panic disorder?

A

SSRIs, venlafaxine, benzodiazepines

9
Q

What is the preferred drug for PTSD?

A

SSRIs

10
Q

What is the preferred drug for schizophrenia?

A

Antipsychotic

11
Q

What is the preferred drug for social phobias?

A

SSRIs

12
Q

What is the preferred drug for Tourette’s?

A

Antipsychotics - haloperidol, risperidone

13
Q

What are the CNS stimulants?

A

Methylphenidate, dextroamphetamine, meth

14
Q

What is the MOA of CNS stimulants?

A

Increase catecholamines at the synaptic cleft, especially NE and DA

15
Q

What is the clinical use of CNS stimulants?

A

ADHD, narcolepsy, appetite control

16
Q

What are the antipsychotics?

A

Haloperidol, trifluoperazine, fluphenazine, thioridazine, chlorpromazine

17
Q

What is the MOA of antipsychotic?

A

Block D2 receptors (inc. camp)

18
Q

What are the high potency antipsychotics?

A

Trifluoperazine
Fluphenazine
Haloperidol
These have extra pyramidal effects

19
Q

What is the clinical use of antipsychotics?

A

Schizophrenia
Psychosis
Acute mania
Tourette’s

20
Q

What are the low potency antipsychotics?

A

Chlorpromazine
Thioridazine
These cause anticholinergic, antihistamine and alpha 1 blockade effects

21
Q

What is the toxicity of antipsychotics?

A

Slow to be removed from body because lipid soluble.
Extrapyramidal effects - dyskinesia, dystopia, Parkinsonian effects
Endocrine: hyperprolactinemia, galactorrhea
Antimuscarinic: dry mouth, constipation
AntiHistamine receptors: sedation
Neuroepileptic malignant syndrome
Tardive dyskinesia
Alpha 1 blockade: hypotension, vasodilation – reflex tachycardia

22
Q

What is neuroepileptic malignant syndrome?

A

Rigidity, myoglobinuria, autonomic instability, hyperprexia

23
Q

What is the treatment for neuroepileptic malignant syndrome?

A

Dantrolene

d2 agonist - bromocriptine

24
Q

What is tardive dyskinesia?

A

Stereotypic oral-facial movements as a result of long term antipsychotic use
Often irreversible

25
Q

What is the acronym for remembering what happens with NMS?

A
Fever
Encephalopathy 
Vitals unstable
Elevated enzymes
Rigidity of muscles
26
Q

What are the atypical antipsychotics?

A
Olanzapine
Clozapine 
Quetiapine
Risperidone 
Aripiprazole
Ziprasidone
27
Q

What is the MOA of atypical antipsychotics?

A

Varied effects on 5-HT, dopamine, alpha, and histamine receptors

28
Q

What is the clinical use of atypical antipsychotics?

A
Schizophrenia
Bipolar
OCD
Anxiety
Depression
Mania
Tourette's
29
Q

What is the toxicity of olanzapine?

A

Weight gain

30
Q

What is the toxicity of clozapine?

A

Weight gain
Agranulocytosis
Seizure

31
Q

What is the toxicity of ziprasidone?

A

Prolonged QT interval

32
Q

What is the MOA of lithium?

A

Inhibitor of phosphoinositol cascade?

MOA unclear

33
Q

What is the clinical use of lithium?

A

Bipolar disorder

Blocks relapse and acute mania events and SIADH

34
Q

What is the toxicity of lithium?

A
LMNOP:
Movement (tremor). 
Nephrogenic diabetes insipidus
HypOthyroidism
Pregnancy problems (teratogenicity)
35
Q

Where is the lithium excreted?

A

In the kidney

Mostly reabsorbed at the PCT

36
Q

What is the MOA of buspirone?

A

Stimulates 5HT1A receptors

37
Q

What is the clinical use of buspirone?

A

Generalized anxiety disorder
1-2 weeks to take effect
Does not interact with alcohol

38
Q

What is the advantage of buspirone?

A

Does not cause Sedation, addiction, tolerance

39
Q

What are the SSRIs?

A

Fluoxetine, paroxetine, sertraline, citalopram

40
Q

What is the clinical use of SSRIs?

A
Depression
Bulimia
Anxiety disorder
Panic disorder
OCD
Social phobias
PTSD
41
Q

What is the toxicity of SSRIs?

A

GI
Sexual dysfunction
Serotonin syndrome

42
Q

What is serotonin syndrome?

A

Hyperthermia, confusion, myoclonus, CV collapse, flushing, diarrhea, seizures

43
Q

What it the tx for serotonin syndrome?

A

Cyproheptadine - 5HT2 receptor antagonist

44
Q

What are the SNRIs?

A

Venlafaxine

Duloxetine

45
Q

What is the MOA of SNRIs?

A

Inhibit serotonin and NE uptake

46
Q

What is the clinical use of SNRIs?

A

Depression

47
Q

What is the clinical use of venlafaxine?

A

Generalized anxiety and panic disorder

48
Q

What is the clinical use of duloxetine?

A

Diabetic peripheral neuropathy

Has greater effect of NE

49
Q

What is the toxicity of SNRIs?

A

elevated BP
Sedation
Nausea
Stimulant effects

50
Q

What are the TCAs?

A

Amitryptyline, nortriptyline, imipramine, desipramine, doxepin, clomipramine, amoxapine

51
Q

What is the MOA of TCAs?

A

Block reuptake of NE and serotonin

52
Q

What is the clinical use of TCAs?

A

Major depression
Bed wetting (imipramine)
OCD (clomipramine)
Fibromyalgia

53
Q

What is the toxicity of TCAs?

A
Sedation 
Alpha 1 blockade effects
Anticholinergic effects 
Convulsions
Coma
Cardio toxicity
Respiratory depression
Hyperprexia 
In elderly: hallucinations, confusion
54
Q

What is the treatment for cardio toxicity from TCA?

A

NaHCO3

55
Q

What are the MAOi’s?

A

Tranylcypromine
Phenelzine
Isocarboxazid
Selegiline

56
Q

What is the MOA of MAOi’s?

A

Nonselective MAO inhibition

Increase amine NTs (NE, serotonin, dopamine)

57
Q

What is the clinical use of MAOi’s?

A

Atypical depression
Anxiety
Hypochondriasis

58
Q

What is the toxicity of MAOi’s?

A

Hypertensive crisis

CNS stimulation

59
Q

What is contraindicated with the use of MAOi’s?

A
SSRIS 
TCAS
St. John's Wort
Meperidine 
Dextromethorphan
60
Q

What are the atypical antidepressants?

A

Bupropion
Mirtazapine
Maprotiline
Trazodone

61
Q

What is trazadone used for?

A

Insomnia

62
Q

What is the MOA of trazadone?

A

Primarily inhibits serotonin reuptake

63
Q

What is the toxicity of trazadone?

A

Sedation
Nausea
Priapism
Postural hypotension

64
Q

What is the MOA of maprotiline?

A

Blocks NE reuptake

65
Q

What is the toxicity of maprotiline?

A

Sedation

Ortho static hypotension

66
Q

What is the MOA of mirtazapine?

A

Alpha 2 antagonist, potent 5-HT2/3 receptor antagonist

67
Q

What is the toxicity of mirtazapine?

A

Sedation
Increased appetite
Weight gain
Dry mouth

68
Q

What is the MOA of bupropion?

A

Increases NE and DA

69
Q

What is the toxicity of bupropion?

A

Tachycardia
Insomnia
Headache
Seizure

70
Q

What is bupropion used for?

A

Smokin cessation

71
Q

What is the advantage of bupropion?

A

No sexual side effects

72
Q

What is the MOA of memantine?

A

Uncompetitive NMDA receptor antagonist

Competes with Mg2+ after calcium influx thereby preventing over excitation

73
Q

What is the toxicity of memantine?

A

Dizziness, confusion, hallucinations, constipation, H/A

74
Q

What is the treatment of choice for Alzheimer’s?

A

Anti-acetylcholinesterases

75
Q

What are the anti-acetylcholinesterases?

A

Donezapil
Galantamine
Rivastigmine

76
Q

What is the disadvantage to using rivastigmine?

A

It also inhibits butyrylcholinesterase thereby inhibiting the breakdown of succinylcholine and giving it longer duration of action. Patients on this drug can’t go under surgery.

77
Q

What are the side effects of anti-AchEs?

A

Diarrhea, incontinence, N/V, dizziness, insomnia, miosis

78
Q

What anti-AchE treats all forms of Alzheimer’s?

A

Donezapil

79
Q

What is the toxicity of tacrine?

A

Liver toxicity

80
Q

When are galantamine and rivastigmine used?

A

In mild to moderate Alzheimer’s

81
Q

What is the tx for Lewy Body disease?

A

Low dose anti-AchE and Parkinson drugs

82
Q

What do all anti-psychotics do?

A

Block dopamine receptors

83
Q

Where are the dopamine tracts in the brain?

A

Ventral tegmental area –> nucleus accumbens, prefrontal cortex
Substantia nigra –> striatum
Hypothalamus –> pituitary
Medulla

84
Q

What are the effects of dopamine?

A

Euphoria, psychosis, reinforcement
Voluntary motor activity
Prolactinemia
Eating, hiccups, vom

85
Q

Why do schizophrenics get negative symptoms?

A

From decrease DA in the nucleus accumbens and prefrontal cortex

86
Q

What accounts for the positive sx in schizophrenia?

A

Excess dopamine in the Mesolimbic system

87
Q

What drugs can cause psychotic episodes in normal individuals?

A

Dopaminergic agonists:
Amphetamines
PCP
Cocaine

88
Q

What do the typical antipsychotics do?

A

Block DA receptors, especially D2

These are usually messy and also block histamine, muscarinic and cholinergic receptors –> lots of side effects

89
Q

What are the general effects of antipsychotics?

A

Control bizarre behavior and calm agitation, impulsivity, aggression
Improve the core thought disorders
Tx: Tourette’s, hiccups, and nausea

90
Q

What are the typical psychotics?

A

Phenothiazines: chlorpromazine, prochlorperazine, promethazine
Butyrophenomes: haloperidol

91
Q

What is the prototype typical antipsychotic?

A

Chlorpromazine

92
Q

What are the side effects of chlorpromazine?

A

Urinary retention, dry mouth - from anti muscarinic effects

Ortho static hypotension - from alpha blockade

93
Q

What is the risk of taking haloperidol?

A

Cleaner D2 antagonist so it causes more extra pyramidal side effects: dystonias, Parkinsonism, neuroleptic malignant syndrome

94
Q

What is the tx for the extrapyramidal side effects of haloperidol?

A

Reduce the dose of the antipsychotic

Give anticholinergics

95
Q

What is the tx of neuroleptic malignant syndrome?

A

Stop antipsych and anticholinergics!
Give antipyretic
Give DA agonist

96
Q

What are the general side effects of antipsychotics?

A
Dysphoria,
 hyperprolactinemia: galactorrhea, gynecomastia, menstrual disturbances
Impotence
Sexual dysfunction 
Poikilothermia
Weight gain
Hypotension
97
Q

What is the major long term side effect of antipsychotics?

A

Tardive dyskinesia

98
Q

What is the tx for tardive dyskinesia?

A

Decrease the dose of anti-psychotics –> will get worse initially but then it will be ok

99
Q

What are the atypical antipsychotics?

A
Olanzapine 
Clozapine 
Quetiapine
Risperidone 
Aripiprazole
100
Q

What is the advantage of atypical antipsychotics?

A

Greater efficacy for negative sx

Less likely to cause tardive dyskinesia

101
Q

What are the side effects of olanzapine?

A

Weight gain
Somnolence
Type II diabetes

102
Q

What is the MOA of atypical antipsychotics?

A

Block DA receptors and 5HT2 receptors

103
Q

What is the FDA warning against atypical antipsychotics?

A

They cause hyperglycemia, type II diabetes

104
Q

What atypical antipsychotic is more efficacious than other antipsychotics?

A

Clozapine

105
Q

What are the advantages to clozapine?

A

Better efficacy

No extrapyramidal side effects

106
Q

What is the major side effect of clozapine?

A

Agranulocytosis

107
Q

What are the other side effects of clozapine?

A

Strong Sedation
Anticholinergic effects: urinary retention
Hypotension

108
Q

What is the most prescribed atypical antipsychotic?

A

Quetiapine

109
Q

What other disorder is quetiapine used for?

A

Bipolar disorder

110
Q

Why do you give quetiapine at night?

A

Because it is slightly more sedative

111
Q

What is the disadvantage of risperidone?

A

It has a higher affinity for D2 receptors so it is more likely to cause tardive dyskinesia and extrapyramidal sx

112
Q

What are the side effects of risperidone?

A
Anxiety
Somnolence
Extrapyramidal sx
Dizziness
Type II diabetes
113
Q

What is the MOA of aripiprazole?

A

Partial DA agonist and partial 5HT1 agonist

5HT2 antagonist.

114
Q

What is the aripiprazole?

A

Used for depression and schizophrenia

115
Q

What are the advantages of aripiprazole?

A

Causes less weight gain than olanzapine
No incidence of Type II diabetes
And can be used for schizophrenia and depression

116
Q

How can aripiprazole be used for schizophrenia when it’s a dopamine agonist?

A

As a weak partial agonist it inhibits the full agonist

117
Q

What drugs may cause depression by lowering bio genic amines?

A
Reserpine
Propranolol
Methyldopa and clonidine
Amphetamines
OCs
Drugs of abuse
118
Q

What is the MOA of TCAs?

A

Block mono amine reuptake with more effect on 5HT

Down regulate norepinephrine and/or 5HT receptor

119
Q

What are the side effects of TCAs?

A
Anti muscarinic: blurred vision, dry mouth, constipation, confusion
Weight gain
Sexual disturbance
Tremor
Insomnia
Ortho static hypotension 
Arrhythmias
120
Q

What is the danger of TCAs?

A

Patients OD easily

121
Q

What other conditions are TCAs used for?

A

Chronic pain and panic disorder

122
Q

What’s the drug of choice for chronic pain?

A

Amitryptiline

123
Q

Which TCA has the most sedative and strongest anti muscarinic side effects?

A

Amitryptiline

124
Q

What are the TCAs?

A

All the -pramines, amitryptiline, nortriptyline, doxepin, protripyline

125
Q

What are the second generation antidepressants?

A
Venlafaxine 
Bupropion
Trazadone
Duloxetine 
Mirtazapine
126
Q

What is the MOA of venlafaxine?

A

SSNRI a selective serotonin and NE reuptake inhibitor

More potent at 5ht

127
Q

What are the side effects of venlafaxine?

A

HTN

Tachycardia

128
Q

What are th disadvantages of venlafaxine compared to SSRIs?

A

More intense withdrawal

Greater toxicity in OD

129
Q

What second generation is used for physical pain symptoms of depression and diabetic neuropathic pain?

A

Duloxetine

130
Q

What is the MOA of bupropion?

A

Occupies 25% of DA uptake sites

131
Q

What is the advantage of bupropion?

A

Causes little to no sexual dysfunction

132
Q

What is bupropion used for?

A

Smoking cessation

133
Q

What is the contraindication to using bupropion?

A

Seizure disorder

134
Q

What is the MOA of trazadone?

A

5HT-2 antagonist

Weak selective 5HT reuptake inhibitor

135
Q

What are the side effects of trazodone.?

A

Priapism

Sedation

136
Q

What is the advantage to trazodone?

A

Less toxic in OD

137
Q

What is the MOA of mirtazapine?

A

Selective stimulation of 5Ht1 receptors due to blockade of 5HT2/3
Increase 5HT cell firing due to increase in NE and blockade of alpha2 adrenergic receptors.

138
Q

What are the side effects of mirtazapine?

A

Significant sedation
Increased appetite
Weight gain

139
Q

Why are SSRIs the first choice for depression?

A

Much safer in OD

140
Q

What is another advantage of SSRIs?

A

Little action at other receptors so little side effects

Longer half life

141
Q

What is the most common side effect of SSRIs?

A

Sexual dysfunction

142
Q

What is discontinuation syndrome?

A

Flu like syndrome from stopping SSRIs abruptly
Most pronounced with paroxetine
Sx: agitation, anxiety, anorexia, insomnia, sweating, tremor, vom

143
Q

Why don’t you ever give an SSRIS with an MAOi?

A

Can cause serotonin syndrome

144
Q

What are the sx of serotonin syndrome?

A

Altered mental status, fever, agitation, sweating, myoclonus, tremor, hyperprexia, ataxia, GI

145
Q

What are the SSRIs?

A
Fluoxetine
Sertraline
Paroxetine
Citalopram 
Fluvoxamine
146
Q

Which SSRI has the longest half life?

A

Fluoxetine

147
Q

What are the side effects of fluoxetine?

A
Nausea 
Insomnia
Weight loss
Agitation 
Sexual dysfunction
148
Q

Which SSRIs have the potential for drug interactions because they inhibit CYP2D6?

A

Fluoxetine

Paroxetine

149
Q

Which SSRI is most likely to cause a discontinuation syndrome?

A

Paroxetine

150
Q

Which SSRI is most likely to cause GI upset as a side effect?

A

Sertraline

151
Q

Which SSRI causes the most sexual dysfunction?

A

Paroxetine

152
Q

Which SSRI is less likely to produce mania?

A

Citalopram

153
Q

What disorder is fluvoxamine usually prescribed for?

A

Obsessive compulsive disorder

154
Q

Which SSRI is the most selective?

A

Citalopram

155
Q

What is the mechanism of action of MAOi’s?

A

Block the deamination of tyramine which results in increased norepinephrine release and therefore a deadly increase in bp

156
Q

What foods contain tyramine?

A
Aged cheese
Wine
Beer
Pickled herring
Liver
Yeast extract
Fava beans
157
Q

What are the MAOi’s?

A

Phenelzine

Tranylcypromine

158
Q

Which MAOi is irreversible?

A

Phenelzine

159
Q

What are antipsychotics useful for in the treatment of bipolar disorder?

A

Acute mania
Not good for depressive episodes
Use for rapid correction of a manic episode then add a mood stabilizer

160
Q

What is the tx for lithium OD?

A

Dialysis

161
Q

What are the side effects of lithium?

A
Most common = tremor
Decreased thyroid fxn
Mild cognitive impairment
Acne eruptions
Leukocytosis
Polydipsia/polyuria
Chronic interstitial nephritis
Minimal change glomerulopathy
GI 
Edema
Weight gain
162
Q

What condition is a contraindication to using lithium?

A

Sick sinus syndrome because lithium suppresses the sinus node

163
Q

Why do patients get polydipsia/polyuria on lithium?

A

Lithium makes the collecting tubule unresponsive to ADH

164
Q

What is the MOA of lithium?

A

Substitutes for Na in generating action potentials and in the Na/K pump (causes seizures)
Also decreased PIP2 therefore decreasing the responsiveness to synaptic transmission (decreased calcium influx)

165
Q

Is lithium contraindicated in pregnancy?

A

N

166
Q

What is th leading cause of death in bipolar disorder if left untreated?

A

Suicide

167
Q

How long does it take before lithium effects are seen?

A

2-3 weeks

168
Q

What can cause the concentration of lithium to go up in the body?

A

NSAIDs

Diuretics

169
Q

What are the mood stabilizing drugs?

A
Lithium
Valproate 
Lamotrigine
Carbamazepine 
Oxycarbazepine
170
Q

What is the advantage to using valproate over lithium?

A

Faster onset (4-5 days)

171
Q

What are the side effects of valproate?

A
GI upset
 Hepatotoxicity
Neural tube defects
Alopecia
Increases appetite and weight gain
172
Q

What is the MOA of carbamazepine?

A

Blocking of voltage gated sodium channels

173
Q

What are the side effects of carbamazepine?

A
Agranulocytosis -stop if you see a rash
Diplopia
Ataxia
GI upset
Sedation
Weight gain
174
Q

What is lamotrigine not effective for?

A

Acute mania

175
Q

What is the MOA of lamotrigine?

A

Blocks sodium and calcium channels

176
Q

What is the side effect of lamotrigine?

A

Steven-Johnson syndrome

Raise levels very slowly

177
Q

When are atypical antipsychotics or benzodiazepines used?

A

During an acute manic episode

178
Q

What are the first choice drugs for treating anxiety?

A

SSRI
Venlafaxine
TCAs

179
Q

Why are these the first drugs of choice for anxiety?

A

Because they have no potential for abuse/dependence

180
Q

What is the timing of onset for the first choice drugs for anxiety?

A

Slow - 2-4 weeks which is considered a negative for the patient

181
Q

How many subunits make up the GABA receptor complex?

A

5

182
Q

Which unit binds GABA?

A

Alpha

183
Q

What is the binding site for BZD?

A

Alpha/beta

184
Q

What subunit must be present for BZDs to modulate GABA?

A

Gamma

185
Q

What happens when GABA binds the receptor complex?

A

The channel opens up to chloride ions causing the cell to become more negative inside making it harder to depolarize - decreased neural firing

186
Q

What is the endpoint of the using the GABA receptor?

A

Coma and death

187
Q

What do inverse agonists of BZDs do?

A

They decrease chloride conductance by inhibiting GABA in a non-competitive way

188
Q

What are the overall effects of BZDs?

A
Anxiolytix
Hypnotic
Anticonvulsant
Amnestic
Produce confusion
DO NOT produce coma
189
Q

What is the major problem with BZDs?

A

Dependency
Don’t use more than 3 days at a time
Shorter half-lives have worse withdrawal effects
Longer half-lives have less severe withdrawal effects but they effects are longer

190
Q

How can death ensue with BZDs and anoth CNS depressant?

A

Respiratory depression

191
Q

What are the uses of diazepam?

A
Anxiolytic
Hypnotic
Muscle relaxant
Amnestic
Pre-anesthetic 
Terminates status epilepticus 
Block convulsions of withdrawal from BZD or EtOH
192
Q

What is the half-life of diazepam?

A

50+ hours

193
Q

What is the half life of alprazolam?

A

12-15 hours

More rapid oral absorption

194
Q

What are the advantages to alprazolam?

A

Shorter half life
Faster absorption
Less sedative

195
Q

What is the BZD of choice for anxiety?

A

Alprazolam

196
Q

What is a potential side effect of alprazolam ?

A

Early morning wakening

197
Q

Which BZD has a longer duration of action then diazepam?

A

Lorazepam

198
Q

What is oxazepam used for?

A

Anxiolytic

Sleep induction

199
Q

Who do you give oxazepam to?

A

The elderly because of more reliable pharmacokinetics

200
Q

What are the properties of midolazam?

A

Very short acting

Water soluble

201
Q

What is midolazam used for?

A

Pre-op anesthesia
Anxiolytics and muscle relaxant
Amnestic

202
Q

What is flumazenil?

A

It is an antagonist of BZD receptor.

No action without BZD in the system

203
Q

What is flumazenil used for?

A

Post anesthesia

BZD overdose

204
Q

What is the thing you should watch out for with flumazenil?

A

Precipitated withdrawal from the BZD – seizures!

205
Q

What do inverse agonist?

A

Anxiety then seizures

206
Q

What drugs can cause lethality if combined with a BZD?

A
EtOH
Opioids
Antipsychotics
TCAs
Antihistamines
207
Q

What is the action of cimetidine?

A

Inhibits liver oxidase so prolonged the action of BZDs.

208
Q

What BZDs would you prescribe for someone on cimetidine?

A

Alprazolam
Lorazepam
Oxazepam
Because of shorter duration of action

209
Q

What are the signs of BZD withdrawal?

A

Tremors

Seizures

210
Q

What are the sx of withdrawal sx?

A

Anxiety
Insomnia
Nausea
Malaise

211
Q

What is the MOA of 5-HT1a agonists?

A

Increase K conductance via same channels as GABAb receptors

212
Q

What is the MOA of buspirone?

A

5-HT1a agonist

213
Q

What is the advantage to using buspirone over a BZD?

A

No sedation

No motor impairment

214
Q

What is the use of buspirone?

A

Anxiety

215
Q

What are the disadvantages to buspirone?

A

Takes 3-6 weeks to work

Can cause anxiety

216
Q

What are the side effects of buspirone?

A

Dizziness, nausea, vomiting
No dependence or tolerance
No cross tolerance with BZDs
Does not alleviate BZD or EtOH withdrawal

217
Q

What are the drug interactions of buspirone?

A

Increase bp with MAOi

Better effects against obsessive-compulsive behavior with SSRI

218
Q

What are the signs of TCA toxicity?

A
QRS prolongation 
Anticholinergic effects
Agitation
Seizures
Coma
219
Q

Why should you wait 2 weeks to switch a patient from an MAOi to an SSRI?

A

Because it takes up to 2 weeks to resynthesize MAO and without normal levels, catecholamines will not be degraded. Add an SSRI and we have even more catecholamines in the synapse –> serotonin syndrome

220
Q

What should people on levodopa avoid?

A

Vitamin B6 because it catalyzes peripheral metabolism of levidopa and decreases its effectiveness

221
Q

What is infused with IV lorazepam to reduce recurrence of seizures?

A

Phenytoin

222
Q

What is the MOA of phenytoin?

A

Increase sodium channel inactivation in cortical neurons

223
Q

What is infused if status epilepticus does not stop with lorazepam?

A

Phenobarbital

224
Q

Why is methadone effective in treating heroin addiction?

A

It is a mu agonist with a long half life so it allows for continuous suppression of withdrawal sx

225
Q

What are the high potency antipsychotics?

A

Haloperidol
Fluphenazine
Pimozide

226
Q

What are the high potency antipsychotics more likely to cause?

A

Extrapyramidal sx - increased skeletal muscle tone

227
Q

What are the higher potency antipsychotics less likely to cause?

A

Anticholinergic and antihistamine effects

228
Q

What are the lower potency typical antipsychotics?

A

Chlorpromazine and thioridazine

229
Q

What antipsychotic causes retinitis pigmentosa?

A

Thioridazine - typical, low potency

230
Q

What is chlorpromazine associated with?

A

Corneal deposits

231
Q

What is ziprasidone associated with?

A

Prolonged QT interval

232
Q

What is the MOA of varenicline?

A

Partial agonist at nicotine receptor - competes with nicotine for binding.
Causes limited downstream dopamine release resulting in less stimulation of the reward pathway.
Decreases withdrawal sx, reduces craving and reduces pleasure from other tobacco products

233
Q

What is the MOA of reserpine?

A

Inhibits dopamine entry into synaptic vesicles - reduces heart rate and bp

234
Q

What are beta blockers used for?

A

Performance anxiety

Use where sympathetic outflow is high and serves no purpose

235
Q

Treat alcoholism in someone that needs a deterrent?

A

Disulfiram

causes aldehyde syndrome = hangover

236
Q

What do you treat the initial phases of DTs with?

A

benzodiazepines

*just supportive care if already enter true DT’s

237
Q

What is the treatment for SSRI toxicity?

A

Cyproheptadine

5-HT2 receptor antagonist

238
Q

What are the common SNRI’s?

A

Venlafaxine & Duloxetine

239
Q

MOA of SNRI’S?

A

Inhibits serotonin and NE reuptake

240
Q

Use of Venlafaxine?

A

Depression

Generalized anxiety and panic disorder

241
Q

Use of Duloxetine?

A

Depression

Diabetic peripheral neuropathy

242
Q

How do you treat TCA toxicity?

A

NaHCO3

Treats cardiotoxicity/ arrhythmia

243
Q

Use of Imipramine?

A

Sleep enuresis

244
Q

DOC for sleep enuresis?

A

DDAVP (desmopressin)

2DOC- Imipramine (TCA)

245
Q

What to you treat night terrors and sleep walking with?

A

Benzodiazepines

246
Q

What do you treat narcolepsy with?

A

Aronodafinil & Modafinil
Amphetamines
(day-time stimulants)
and night time Sodium oxybate (GHB)

247
Q

What do you treat restless leg syndrome with?

A

Dopamine agonists (Ropinirole & Gabapentin)

248
Q

What do you treat REM-behavioral disorder with?

A

Clonazepam

249
Q

What do you treat acute insomnia with?

A

BZD’s- short term

250
Q

What do you treat chronic insomnia with?

A

CBT w/ pyschophysiologic treatment

sleep hygiene

251
Q

What drug may cause an exaggerated response to ADH?

A

Carbamazepine

252
Q

What does an exaggerated response to ADH cause?

A

Hyponatremia because of increased volume - dilution

253
Q

What is primidone?

A

An anti epileptic drug that is metabolized to phenobarbital