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2nd Year 2nd Term > MT6314 ANTIPSYCHOTICS AND ANTIDEPRESSANTS > Flashcards

MT6314 ANTIPSYCHOTICS AND ANTIDEPRESSANTS Flashcards

1
Q

Study of the drugs that affect cognition, affect, and behavior of an individual

A

Psychopharmacology

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2
Q

Psychopharmacology includes the study of what drugs?

A

 Antidepressants
 Antipsychotics
 Classic Mood Stabilizers
 Stimulants
 Benzodiazepines

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3
Q

What is psychosis?

A

Inability to distinguish between what is real and what is not real

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4
Q

Psychosis involves?

A

̶ Delusions
̶ Hallucinations
̶ Disorganized thinking with clear sensorium

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5
Q

What is the most common psychotic disorder?

A

Schizophrenia

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6
Q

Schizophrenia is characterized by?

A

̶ Structural and functional changes in the brain
̶ Dysregulated neurotransmitters

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7
Q

Neuronal Networks of Psychosis

A

Dopamine theory
NMDA theory
Serotonin theory

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8
Q

NMDA theory effect on NMDA receptors?

A
  • NMDA receptor hypofunction
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9
Q

What neuronal pathway is the main reason behind Schizophrenia?

A

Dopamine pathway

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10
Q

Serotonin theory is defined as?

A
  • 5-HT2A receptor hyperfunction in the cortex
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11
Q

Purpose of Antipsychotic drugs?

A
  • Improve mood and reduce anxiety
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12
Q

Type of antipsychotic drug with high incidence of EPS

A

Neuroleptic

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13
Q

Classical drugs affinity?

A

D2&raquo_space; 5-HT2 receptors

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14
Q

Atypical / Newer agents affinity?

A

5-HT2&raquo_space; D2 receptors

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15
Q

Classes of older antipsychotics?

A

Phenothiazine
Thioxanthine
Butyrophenone

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16
Q

Antipsychotics are well absorbed when administered ______

A

Orally

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17
Q

Antipsychotics are lipid or water soluble?

A

Lipid

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18
Q

Antipsychotics are extensively bound to?

A

Plasma proteins

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19
Q

Antipsychotics have long or short half lives?

A

Long

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20
Q

Parenteral forms of antipsychotics?

A
  • Fluphenazine
  • Haloperidol
  • Ziprasidone
  • Olanzapine
  • Aripiprazole
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21
Q

Schizophrenia is due to excess of what in where?

A

functional DA in mesocortical tracts in the brain

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22
Q

Types of Dopamine receptors

A

̶ GPCR, D1-D5

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23
Q

Location of D2 receptors?

A

in the caudate, putamen, cortex, hypothalamus – negatively coupled to adenylyl cyclase

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24
Q

Blockade of D2 receptors leads to?

A

EPS (tremor, slurred speech, akathisia, dystonia)

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25
Q

Has affinity for other receptors and less EPS

A
  • Atypical antipsychotics
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26
Q

All antipsychotic drugs block H1 receptor to some degree except?

A

̶ Haloperidol
̶ Iloperidone
̶ Lurasidone

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27
Q

Antagonist for D2 blockade?

A

Clozapine

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28
Q

Weak agonist for D2 blockade?

A

Olanzapine (+)
Quetiapine (+)
Aripiprazole (+)
Brexipiprazole (+)

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29
Q

Agonist for D4 blockade?

A

Haloperidol (+)
Iloperidone (+)
Asenapine (++)
Clozapine (++)
Aripriprazole (+)
Brexipriprazole (+)

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30
Q

Antagonist for alpha1 blockade?

A

Lurasidone
Cariprazine

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31
Q

Antagonists for 5-HT2 blockade?

A

Haloperidol
Molindone

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32
Q

Agonists for M blockade?

A

Most phenothiazines and thioxanthenes (+)
Thioridazine (+++)
Molindone (+)
Paliperidone (+)
Clozapine (++)
Olanzapine (++)
Quetiapine (+)

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33
Q

Antagonists for H1 blockade?

A

Haloperidol
Iloperidole
Lurasidone

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34
Q

Effect is dopamine receptor blockade

A

First generation drugs

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35
Q

Underlies antipsychotic effect

A

Mesocortical-mesolimbic path

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36
Q

Antiemetic effect in the Mesocortical-mesolimbic path due to?

A

blockade of the chemoreceptor trigger zone

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37
Q

Common adverse effects in first generation antipsychotics?

A

̶ Extrapyramidal symptoms, hyperprolactinemia (1st Generation)

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38
Q

Clinical use of antipsychotics?

A
  • Treatment of schizophrenia
  • Mania
  • Tourette syndrome
  • Alzheimers and Parkinsonism
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39
Q

How long do effects of antipsychotics take for treating Schizophrenia?

A

Effects take several weeks to develop

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40
Q

lower cost, EPS

A

1st gen

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41
Q

improves negative symptoms (emotional blunting,
social withdrawal, lack of motivation)

A

2nd gen

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42
Q

For treating mania, antipsychotics should be given with?

A

lithium

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43
Q

For treating mania, 2nd generation antipsychotics should be given with?

A

benzodiazepines

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44
Q

Drugs for prevention of manic phase of bipolar disorder

A

o Aripiprazole, olanzapine, asenapine

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45
Q

Drugs for prevention of bioplar depression

A

o Quetiapine, lurasidone, olanzapine, carizapine

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46
Q

Drugs for Tourettes syndrome

A

Molindone

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47
Q

What develops Parkinson-like symptoms?

A

Dose-dependent EPS

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48
Q

Dose-dependent EPS is common with?

A

Common with Haloperidol and more potent piperazine derivatives (Fluphenazine, trifluoperazine)

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49
Q

Dose-dependent EPS is infrequent with?

A

2nd generation drugs, Clozapine

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50
Q

Methods to deal with dose-dependent EPS?

A

 Mx: reduce dose, use of antimuscarinic agents

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51
Q

Other neurologic dysfunction in the toxicity of antipsychotics are seen in?

A

akathisia, dystonias

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52
Q

Instances of akathisia, dystonias respond to?

A

 Also respond to antimuscarinic agents, or diphenhydramine

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53
Q

Why do the autonomic effects of toxicity occur?

A

̶ Due to blockade of peripheral muscarinic and alpha receptors

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54
Q

Order of strength of autonomic effects?

A

Thioridazine»clozapine and atypicals»haloperidol

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55
Q

Atropine like effects are ? and treated by?

A

Dry mouth, constipation, urinary retention – Thioridazine and Chlorpormazine

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56
Q

Caused by alpha blockade

A

Postural Hypotension

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57
Q

Choreoathetoid movements of the lip and buccal muscle

A

Tardive dyskinesia

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58
Q

Is tardive dyskinesia reversible?

A

May be irreversible

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59
Q

What increases severity of the symptoms in tardive dyskinesia?

A

Antimuscarinic drugs that improve EPS

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60
Q

T or F: Switching to Clozapine for treating tardive dyskinesia improves the condition

A

F, does not exacerbate only

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61
Q

How to temporarily improve the condition of tardive dyskinesia?

A

increasing neuroleptic dosage

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62
Q

Endocrine effects in antipsychotic toxicity?

A

Hyperprolactinemia, gynecomastia, infertility due to D2 blockade in pituitary, prominent with Risperidone

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63
Q

Who are prone to NMS?

A

Patients sensitive to the EPS

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64
Q

How to treat NMS?

A

̶ Treat with dantrolene, diazepam, dopamine agonists

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65
Q

Sedation in antipsychotic toxicity is marked in what drug?

A

Chlorpromazine

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66
Q

Least sedating antipsychotics?

A

fluphenazine and haloperidol; aripiprazole and lurasidone

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67
Q

Visual toxicities for antipsychotics?

A

̶ Visual: retinal deposits with thioridazine

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68
Q

Cardiac effects of antipsychotic toxicity?

A

̶ Cardiac rhythm abnormalities: thioridazine, quetiapine, ziprasidone

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69
Q

What causes agranulocytosis and seizure a high doses?

A

Clozapine

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70
Q

Commonly used for manic phase of bipolar disorder

A

Lithium

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71
Q

Why is important to monitor levels of lithium in the plasma?

A

to establish effective and safe dosage

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72
Q

MOA of lithium?

A
  • inhibits enzymes for recycling neuronal membrane phosphoinositides
  • depletion of PIP2 , IP3, DAGs
  • prevents amine neurotransmission
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73
Q

Antiseizure drugs include?

A

̶ Valproic acid
̶ Carbamazepine and lamotrigine

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74
Q

Valproic acid prolongs inactivation of?

A

voltage gated Na channels, GABAA agonist

75
Q

Used for antimanic effects when failed to respond to lithium

A

̶ Valproic acid

76
Q

Prolongs inactivation of voltage gated Na channels

A

̶ Carbamazepine and lamotrigine

77
Q

Carbamazepine and lamotrigine are used for?

A

 for mania and prophylaxis of depressive phase

78
Q

Half life of lithium?

A

20hrs

79
Q

How is lithium distributed?

A

Body water

80
Q

Therapeutic dosage of lithium?

A

0.6-1/4 mEq/L

81
Q

Increases renal clearance

A

Theophylline

82
Q

Treatment for increased lithium at toxic levels

A

Thiazide diuretics

83
Q

Why is lithium required at the initiation of treatment?

A

Slow onset of action

84
Q

Lithium can increase what anomaly?

A

Ebstein’s anomaly (congenital cardiac anomaly)

85
Q

What drugs are under phenothiazines?

A

Chlorpromazines
Fluphenazine
Thioridazine

86
Q

Phenothiazines block what receptors?

A

alpha
M
H1

87
Q

What drug is under butyrophenones?

A

Haloperidol

88
Q

MOA of butyrophenones?

A

Blocks D2 > 5-HT2 receptors

89
Q

What receptors to butyrophenones block?

A

Some for alpha
Less for M

90
Q

Antipsychotic drug class used in Huntington chorea and Tourettes

A

Butyrophenones

91
Q

MOA of second generation antipsychotics

A

Block 5-HT2 > D2

92
Q

Feelings of sadness and or loss of interest in normally
pleasurable activities, leading to emotional and physical problems, with resulting impairment in social, occupational and other areas of functioning for 2 weeks

A

depression

93
Q

Hypotheses for antidepressants?

A

Monoamine hypothesis
Neurotrophic hypothesis
Neuroendocrine hypothesis

94
Q

TCAs are related to?

A

phenothiazine antipsychotics

95
Q

TCAs route of administration

A

Orally
has 1st pass effect

96
Q

What kind of metabolism required for TCAs?

A
  • Excessive hepatic metabolism required
97
Q

Short or long half life for TCAs?

A

Long

98
Q

Fluoxetine long or short half life?

A

Long (1 dose/ week)

99
Q

Heterocyclics have Pharmacokinetics similar to ?

A

TCA

100
Q

Heterocyclics that have short half lives

A

Nefazodone and trazodone

101
Q

Related to amphetamines and orally active

A

Monoamine oxidase inhibitor

102
Q

metabolizes NE, Epinephrine, Serotonin

A

MAOI-A

103
Q

metabolizes Dopamine, Tyramine

A

MAOI-B

104
Q

MAOI with fastest onset, short duration of action

A

Tranylcypromine

105
Q

What class drug: Phenelzine, Selegiline, Tranylcypromine

A

MAOIs

106
Q

What class drug: Amoxapine, Bupropion, mirtazapine

A

Heterocyclic antidepressants

107
Q

WHAT CLASS DRUG: Duloxetine, venlafaxine

A

5-HT-NE reuptake inhibitors

108
Q

WHAT CLASS DRUG: Nefazodone, Trazodone

A

5-HT antagonists

109
Q

WHAT CLASS DRUG: Escitalopram, Fluoxetine, Fluvoxamine, Paroxetine, Sertraline

A

Selective Serotonin reuptake inhibitors

110
Q

WHAT CLASS DRUG: Amitryiptyline, Clomipramine, imipramine

A

TCA

111
Q

Neuroendocrinic factors include?

A

ACTH
Sex steroids
Thyroid hormone

112
Q

During depressed states, what happens with the thyroid hormone?

A

Blunting of response of thyrotropin and thyrotropin-releasing hormones, elevations in thyroxine

113
Q

ACTH effect in depression

A

Nonsupression of ACTH in the dexamethasone suppression test

114
Q

Other drugs with antidepressant action

A

Ketamine
Brexanolone

115
Q

NMDA antagonist

A

Ketamine

116
Q

Nasal spray version of ketamine

A

Esketamine

117
Q

modulator of GABA A receptors

A

Brexanolone

118
Q

Use of brexanolone

A

PPD

119
Q

Inhibit SERT

A

SSRIs

120
Q

6 major SSRIs

A

Fluoxetine
Sertraline
CItalopram
Paroxetine
Fluvoxamine
Escitalopram

121
Q

S enantiomer of citalopram

A

Escitalopram

122
Q

Not optically active

A

Paroxetine
Fluvoxamine

123
Q

Indications of SSRIs

A

GAD
PTSD
OCD
Panic disorder
PMDD

124
Q

Half life of SSRIs

A

18-24hrs

125
Q

SSRIs have minimal inhibitory effects on?

A

NE

126
Q

Bind to transporters for both serotonin and NE

A

SNRI

127
Q

TCA MOA?

A

Inhibit the reuptake transporters that terminate the
actions of NE and 5-HT and blocks H receptors and α-adrenoceptors

128
Q

blocks 5HT2A receptor in the neocortex

A

Nefazodone and trazodone

129
Q

MAOI MOA?

A

Increase brain amine levels, interfering with metabolism –> increase in vesicular stores of NE and 5-HT

130
Q

Fluoxetine are inhibitors of?

A

CYPD2D

131
Q

Fluvoxamine inhibitor of?

A

CYPD3A4

132
Q

Citalopram, Escitalopram and Sertraline have what kind of interactions with CYP?

A

Modest interactions with CYP

133
Q

increase amine release by antagonism of α-2 receptors

A

Mirtazapine

134
Q

Anti-anxiety and anti-depressant

A

5-HT2 Receptor Antagonist

135
Q

no effect on 5-HT or NE amine transporters

A

Bupropion

136
Q

Pharmacologic effects of antidepressants

A

Amine uptake blockade
Sedation
Muscarinic blockade
Cardiovascular effects
Seizures

137
Q

Sympathomimetic effects in the amine uptake blockade include?

A

increase NE in nerve endings; inhibit reuptake of NE in nerve endings

138
Q

Chronic use of antidepressants for amine uptake blockade leads to?

A

Low BP

139
Q

Sedation with the use of antidepressants are common in?

A

Common in TCA and heterocyclic (mirtazapine) and 5-HT2 blockers (nefazodone and trazodone)

140
Q

Muscarinic blockade occurs in?

A

Occurs with all TCA esp. amitryptaline and doxepine; also with nefazedone, amoxapine, amprotiline

141
Q

Atropine like effects are minimal with?

A

SSRI and bupropion

142
Q

Cardiovascular effects are common with? and this causes?

A

TCA causing hypotension, arrhythmias

143
Q

Cardiotoxicity is caused by?

A

venlafaxine

144
Q

What lowers convulsion threshold?

A

TCA and MAOI

145
Q

Overdose of what antidepressants causes seizures?

A

Maprotiline and SSRI’s

146
Q

T or F: Newer drugs more tolerable side effects

A

T

147
Q

most useful if with psychomotor retardation, sleep disturbances, poor appetite, wt. loss

A

TCA

148
Q

for significant anxiety, phobia, hypochondriasis

A

MAOIs

149
Q

increase suicidal risk

A

SSRI, SNRI

150
Q

What do TCAs have that SNRIs don’t?

A

antihistamine, alpha blocking, and anticholinergic
effects

151
Q

Antidepressant for Neuropathic pain

A

Duloxetine, venlafaxine

152
Q

Antidepressant for OCD

A

Clomipramine and SSRI

153
Q

Antidepressant for Stress incontinence and vasomotor menopausal symptoms

A

SNRI

154
Q

Antidepressant for for patients withdrawing from nicotine dependence

A

Bupropion

155
Q

Causes serotonin syndrome

A

SSRI

156
Q

Serotonin syndrome is characterized by?

A

interaction of fluoxetine and MAOI

157
Q

Why is fluoxetine not recommended to be used with MAOIs?

A

Fluoxetine has long half life

158
Q

Serotonin syndrome drugs include?

A

MAOIs
TCAs
Meperidine
MDMA
Antiseizure drugs
Management drugs
Muscle relaxants
Blockers of 5-HT

159
Q

Causes a dose dependent increase in BP

A

Venlafaxine

160
Q

Causes weight gain

A

Mirtazapine and Trazodone

161
Q

Causes seizures and cardiotoxicity

A

Amoxapine, amrotilline

162
Q

Hypertensive crisis in patients taking MAOIs and high ____ in diet

A

Tyramine

163
Q

Causes hepatic microsomal enzyme inhibition

A

SNRI, 5-HT2 antagonists, and heterocyclic drugs

164
Q

Venlafaxine is metabolized where to form?

A

In liver
Desvenlaxafine

165
Q

Lowest protein binding amongst all antidepressants

A

Venlafaxine

166
Q

Well absorbed
Half life of 12hrs
Tightly bound to proteins

A

Duloxetine

167
Q

MOA of Venlafaxine?

A

Inhibits NE transporters

168
Q

Most SNRIs have a great affinity for SERT or NET?

A

SERT

169
Q

TCA plasma half life?

A

8-36hrs

170
Q

MOA is the Potentiation of NTA actions at post synaptic receptors

A

TCA

171
Q

Antagonism of muscarinic receptors in TCAs are marked with?

A

Amitryptyline

172
Q

What GCPR is distributed around the cortex?

A

5-HT2A

173
Q

Weak inhibitor of SERT and NET but potent against 5-HT2A

A

Nefazodone

174
Q

Selective inhibitor for SERT with little effect on NET

A

Trazodone

175
Q

Trazodone metabolic which is a potent 5-HT2A antagonist

A

M-CPP

176
Q

Weak-Moderate presynaptic adrenergic blocking properties
Modest antagonist of H1

A

Trazodone

177
Q

Resembles amphetamine and has CNS activating structures

A

Buproprion

178
Q

Biphasic elimination phase of Buproprion

A

1st - 1hr
2nd - 14hrs

179
Q

New antidepressant with no sexual side effects
Piperazino-azepine group

A

Mitrazapine

180
Q

Mitrazepine enhances the release of?

A

5-HT2 and 5-HT3

181
Q

Similar properties with Maprotiline
Rapidly absorbed

A

Amoxapine

182
Q

Used in Parkinson’s
Inhibits MAO-B

A

Selegiline

183
Q

BDNF affects what parts of the brain?

A

Hippocampus
Anterior cingulate gyrus
Medial frontal cortex

2nd Year 2nd Term (38 decks)

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