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Pharm > Week 4 (Quiz 3) (Antidepressants, antipsychotics, antiepileptic, headaches) > Flashcards

Week 4 (Quiz 3) (Antidepressants, antipsychotics, antiepileptic, headaches) Flashcards

1
Q

Monoamine Theory

A

deficiency of serotonin, NE, and dopamine at key sites in brain which control mood and emotions

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2
Q

Major Depressive Disorder Criteria

A 
Sleep 
Interest 
Guilt/Worthlessness 
Energy 
Concentration 
Appetite change 
Psychomotor retardation 
Suicide/Sex
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3
Q

imipramine, desipramine, amitriptyline, nortriptyline, doxepin, clomipramine, amoxapine (Type)

A

Tricyclic Antidepressants

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4
Q

fluoxetine, paroxetine, sertraline, citalopram, escitalopram, fluvoxamine (Types)

A

SSRIs

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5
Q

venlafaxine, desvenlafaxine, duloxetine (Type)

A

SNRIs

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6
Q

isocarboxazid, tranylcypromine, phenelzine, selegiline (Type)

A

Monoamine Oxidase Inhibitors (MAOIs)

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7
Q

mirtazapine, bupropion, trazadone, nefazodone (Type)

A

Atypical Antidepressants

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8
Q

Antidepressants metabolized by CYP2D6

A

All TCAs
All SSRIs
SNRIs (Except desvenlafaxine)

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9
Q

Discontinuation syndrome (especially with SSRIs and SNRIs)

A

Abrupt discontinuation or reduction in dosage can result in:

anxiety, irritability, general malaise (flu-like), headache, insomnia, crying

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10
Q

Reduce symptoms of discontinuation syndrome by:

A
  1. Tapering drugs over weeks or months

2. Switching to an SSRI with a longer half-life for a few weeks before discontinuing medication.

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11
Q

Biopolar disorder drugs

A

Lithium (Main)

Anticonvulsants, Antipsychotics, Benzodiazepines

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12
Q

Lithium mechanism

A

Unknown

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13
Q

Lithium side effects (LMNOP)

A

Movement (tremor); Nephrogenic diabetes insipidus; HypOthyroidism; Pregnancy problems (Class D drug)

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14
Q

TCAs that target 5-HT and NE (3 amine)

A

imipramine, doxepin, amitriptyline

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15
Q

TCAs that target NE only

A

nortriptyline, desipramine, clomipramine, amoxapine

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16
Q

TCA mechanism

A

Inhibits Uptake 1 (NE) and SERT (5-HT)

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17
Q

TCA end effect

A

↑ neurotransmitter in synapse

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18
Q

TCA use

A

Depression (all), nocturnal enuresis/bedwetting (imipramine), OCD (clomipramine), fibromyalgia/pain disorders

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19
Q

What is imipramine specifically used for?

A

nocturnal enuresis/bedwetting

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20
Q

What is comipramine specifically used for?

A

OCD

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21
Q

Side effects of TCAs

A

anticholinergic (muscarinic) = block parasympathetics, delirium in elderly; blockade of α-adrenergic receptors = orthostatic hypotension, ↑HR; sedation; sexual SE, cardiac arrhythmias

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22
Q

TCA Toxicity (3 Cs)

A

Convulsions
Coma
Cardiotoxic

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23
Q

TCA Toxicity Treatment

A

Sodium bicarbonate

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24
Q

Examples of SSRIs

A

fluoxetine [Prozac], paroxetine [Paxil], sertraline [Zoloft], citalopram [Celexa], escitalopram [Lexapro], fluvoxamine [Luvox]

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25
Q

Mechanism of SSRIs

A

inhibits SERT (5-HT)

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26
Q

SSRI use

A

Depression, panic disorder, generalized anxiety disorder, OCD, social phobia, PTSD, bulimia (fluoxetine), PMDD

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27
Q

SSRI side effects

A

headache, GI, sexual dysfunction (from receptors in spinal cord; most common reason for discontinuation), anxiety, insomnia, poss. increased bleed risk?

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28
Q

What is serotonin syndrome associated with SSRIs?

A

Anxiety, agitation –> delirium; autonomic hyperactivity (vital sign changes, ↑BP, HR, temp); tremor/hyperreflexia –> rigidity/hypertonicity

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29
Q

Toxicity treatment for SSRIs

A

remove offending agent, control side effects, administer Cyproheptadine

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30
Q

SNRIs examples

A

venlafaxine, desvenlafaxine, duloxetine

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31
Q

Mechanism

A

inhibits SERT; inhibits NET (uptake-1) at higher doses

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32
Q

SNRIs use

A

depression, generalized anxiety disorder, panic disorder, social phobia, diabetic neuropathy, fibromyalgia

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33
Q

SE of SNRIs

A

same as SSRIs + sexual dysfunction, sedation (typically more than SSRIs), anorexia/weight loss, hypertension at higher doses

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34
Q

Examples of MAOIs

A

Isocarboxazid, tranylcypromine, phenelzine, selegiline

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35
Q

How can MAOIs be given to avoid rxns with tyramine?

A

transdermally

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36
Q

Mechanism of MAOIs

A

prevents neurotransmitter degradation inside neuron

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37
Q

MAO-A metabolizes:

A

5-HT and NE

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38
Q

MAO-B metabolizes:

A

Dopamine

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39
Q

End effect of MAOIs

A

increases amount of available neurotransmitter for release

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40
Q

Use of MAOIs

A

Depression

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41
Q

Off label uses of MAOIs

A

agoraphobia, bulimia, panic disorder, social phobia in conjunction with phenelzine

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42
Q

SE of MAOIs

A

orthostatic hypotension (displaces NE from synaptic vesicles); HA; GI problems; hepatic necrosis with phenelzine (rare); hypertension with tyramine

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43
Q

Mirtazapine mechanism

A

serotonin/NE disinhibitor; α2 receptor ANTAGONIST –> promotes release of NE and 5-HT (α2 receptor INHIBITS release of NE and 5-HT)

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44
Q

Mirtazapine use

A

major depressive disorder

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45
Q

Off label use of Mirazapine

A

due to weigh gain SE = cancer pts

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46
Q

SE of mirtazapine

A

weight gain, sedation, no significant sexual side effects

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47
Q

Bupropion mechanism

A

NE/DA reuptake inhibitor

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48
Q

Bupropion use

A

depression, smoking cessation

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49
Q

SE Bupropion

A

risk of seizures (contraindicated in pts with seizures); jitteriness; no weight gain; no significant sexual side effects

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50
Q

Toxicity of Bupropion

A

Seizure, psychosis

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51
Q

Trazadone/Nefazodone mechanism

A

5-HT antagonist/reuptake inhibitor

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52
Q

Trazadone/Nefazodone use

A

sedation, nausea, constipation, orthostatic hypotension, priapism

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53
Q

Trazadone/Nefazodone toxicity

A

ventricular arrhythmias, prolonged QT; nefazodone highly hepatotoxic

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54
Q

Positive symptoms

A

delusions, hallucinations, disorganized thought

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55
Q

Negative symptoms

A

withdrawl, flattening of emotional response

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56
Q

Cognitive impairments

A

pts lose on average of 10 IQ points during course of illness

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57
Q

Affective disturbance

A

affect is how you present your internal mood - schizophrenic patients are not very good at conveying their mood; depression after a psychotic episode

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58
Q

Four symptoms clusters

A

Positive, negative, cognitive, affective disturbances.

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59
Q

If pt. has high ration of + symptoms to - symptoms, then:

A

better prognosis

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60
Q

4 dopaminergic pathways in brain

A
  1. mesolimbic
  2. mesocortical
  3. nigrostriatal
  4. tuberohypophyseal
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61
Q

Too much dopamine in areas of brain:

A

positive symptoms

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62
Q

Too little dopamine in other parts of the brain:

A

negative symptoms

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63
Q

DOPAMINERGIC

Mesolimbic is associated with what type of symptoms?

A

positive

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64
Q

DOPAMINERGIC

Location of mesolimbic

A

Midbrain ventral tegmental area (VTA) to Nucleus accumbens (NA)

65
Q

DOPAMINERGIC

Pathophys of mesolimbic

A

↑ DA = auditory hallucinations, positive symptoms

66
Q

DOPAMINERGIC

Effects of treatment in mesolimbic

A

↓ positive symptoms

67
Q

DOPAMINERGIC

The limbic system is in charge of:

A

fear, anxiety, reward

68
Q

DOPAMINERGIC

Mesocortical is associated with what type of symptoms?

A

negative symptoms

69
Q

DOPAMINERGIC

Location of mesocortical

A

Midbrain VTA to limbic cortex (dorsolateral prefrontal cortex = DL PFC)

70
Q

DOPAMINERGIC

Pathophys of mesocortical

A

cognitive deficits; + 5 As

71
Q

DOPAMINERGIC

5As of mesocortical

A
  • flat Affect
  • Avolition (apathy)
  • Alogia (lack words)
  • Anhedonia (lack of enjoyment)
  • Attention impairment
72
Q

DOPAMINERGIC

Effects of treatment of mesocortical

A

↑ symptoms = “zombification”

73
Q

DOPAMINERGIC

Where is 75% of the DA in the brain?

A

Basal ganglia from substantia nigra to striatum

74
Q

DOPAMINERGIC

Where is the Nigostriatial impacting?

A

extrapyramidal side effects

75
Q

DOPAMINERGIC

Location of Nigostriatal

A

Basal ganglia from substantia nigra to striatum (extrapyramidal nervous system)

76
Q

DOPAMINERGIC

Pathophys of nigostriatal

A

no major deficits

77
Q

DOPAMINERGIC

Effects of treatment (nigostriatal)

A

↑ break on motor cortex

78
Q

DOPAMINERGIC

4 hrs treatment ns

A

dystonia (sustained muscle contractions, esp. in young males, potentially lethal) [treat with anti-H or anti mACh]

79
Q

DOPAMINERGIC

4 days treatment ns

A

Parkinsonism (more common in elderly)

80
Q

DOPAMINERGIC

4 weeks treatment ns

A

akathisia (feeling of inner restlessness, dose related)

81
Q

DOPAMINERGIC

4 months treatment ns

A 
tardive dyskinesia (potentially
irreversible, women and elderly; delayed onset,
involuntary/repetitive body movements)
82
Q

DOPAMINERGIC

Tuberohypophyseal ( location)

A

hypothalamus to anterior pituitary (tonic DA INHIBITS prolactin release)

83
Q

DOPAMINERGIC

Tuberohypophyseal pathophys

A

no major deficits

84
Q

DOPAMINERGIC

Tuberohypophyseal effects of treatment

A

↓DA = ↑ prolactin = galactorrhea (nipple discharge); amenorrhea; ↓ libido

85
Q

4 seratonergic pathways in brain

A
  1. mesolimbic
  2. mesocortical
  3. nigrostriatal
  4. tuberohypophyseal
86
Q

SEROTONERGIC

Mesolimbic location

A

Raphe (brain stem) to VTA

87
Q

SEROTONERGIC

Mesolimbic effects of treatment

A

5HT blockade less robust than DA (DA blockade wins) = ↓ of positive symptoms preserved

88
Q

SEROTONERGIC

Mesocortical location

A

raphe to DL PFC

89
Q

SEROTONERGIC

Mesocortical effects of treatment

A

5HT blockade wins = relief of negative symptoms; blockade ↑ local DA levels

90
Q

SEROTONERGIC

Nigrostriatial location

A

raphe to SN and striatum

91
Q

SEROTONERGIC

Nicrostriatal effects of treatment

A

5HT block wins = reverses D2 block = ↓EPS

92
Q

SEROTONERGIC

Tuberohypophyseal location

A

raphe to pituitary gland

93
Q

SEROTONERGIC

Tuberohypophyseal pathophys

A

↑ 5HT inhibits prolactin

94
Q

SEROTONERGIC

Tuberohypophyseal effects of treatment

A

DA blockade wins over 5HT = ↑ prolactin levels persist

95
Q

Neuroleptics and antipsychotics absorption

A

oral at 30-90%

96
Q

Neuroleptics and antipsychotics distribution

A

highly protein bound

97
Q

Neuroleptics and antipsychotics metabolism

A

hepatic via CYP2D6 and CYP3A4

98
Q

Neuroleptics and antipsychotics elimination

A

kidney and feces

99
Q

Neuroleptics and antipsychotics site of action

A

D2, 5-HT2A, mACh, α-adrenergics

100
Q

Neuroleptics and antipsychotics SE

A

2-fold increase in risk of sudden death

101
Q

Neuroleptics and antipsychotics mACh off-target effects

A

dry mouth, blurred vision, constipation, urinary retention, cognitive blunting (anti-SLUDGE-y)

102
Q

Neuroleptics and antipsychotics histaminergic off-target effects

A

weight gain, sedation

103
Q

Neuroleptics and antipsychotics α1-adrenergic off-target effects

A

orthostatic hypotension, sedation also QT prolongation (esp. caused by Haloperidol)

104
Q

Neuroleptics

A

Block D2 receptors, preferentially

105
Q

Chlorpromazine

D2 ___ 5-HT

106
Q

SE of Chlorpromazine

A

obstructive jaundice

107
Q

Haloperidol

D2 ___ 5-HT

A

> > > > > >

108
Q

SE of Haloperidol

A

QT prolongation

109
Q

Clozapine

5-HT2A ___ D2

110
Q

What symptoms does clozapine treat?

A

+ and - (efficacious in treatment resistant pts)

111
Q

Metabolism of clozapine

A

CYP1A2 (some 2D6 and 3A4)

112
Q

CYP1A2*1F and clozapine… associated with what?

A

rapid drug metabolism, decreased efficacy

113
Q

Smokers with 1F/1F and clozapine

A

ultrarapid metabolizers

114
Q

Omeprazole and Clozapine

A

omeprazole induces CYP1A2*1C and *1F, even more decreased drug efficacy

115
Q

Clozapine SE

A

weight gain, agranulocytosis risk for those with HLA-DQB1 genotype

116
Q

Risperidone

5-HT ___ D2

117
Q

SE of Risperidone

A

Weight gain, hypotension, EPS with high dose

118
Q

Aripiprazole

D2 ____ 5-Ht

119
Q

SE of Aripiprazole

A

Some sedation, low SE profile may be due to partial DA agonism

120
Q

Metabolism of chlorpromazine

121
Q

Metabolism of haloperidol

122
Q

Metabolism of clozapine

A

1A2, 2D6, 3A4

123
Q

Metabolism of risperidone

124
Q

Metabolism of ariprazole

125
Q

Epilepsy co-morbidities

A

memory loss; depression/anxiety; psychosocial debilitation; ↑ risk of morbidity and mortality

126
Q

Two causes of epilepsy

A

Idiopathic v. symptomatic

127
Q

Idiopathic epilepsy

A

no specific anatomic cause - may result from inherited abnormality in CNS, patients are treated chronically; accounts
for most cases of epilepsy

128
Q

Symptomatic epilepsy

A

due to illicit drug use, tumors, trauma, infection, etc.; may or may not require therapy

129
Q

Partial epilepsy

A

Simple or complex

only involve one portion of the brain; consciousness is usually preserved; may progress to tonic-clonic

130
Q

Simple partial epilepsy

A

a group of hyperactive neurons with abnormal activity –> single locus in brain (usually involves one musclegroup)

131
Q

Complex partial epilepsy

A

complex sensory hallucination, mental distortion, LOC; altered consciousness

132
Q

Generalized epilepsy

A

abnormal electrical discharges in both hemispheres of brain

133
Q

Tonic-clonic generalized epilepsy

A

LOC; continuous contraction followed by rapid contraction/relaxation (clonic)

134
Q

Absence generalized epilepsy

A

brief, abrupt, self-limiting LOC (generally in children)

135
Q

Myoclonic generalized epilepsy

A

short episodes of muscle contractions (begin around puberty)

136
Q

Febrile generalized epilepsy

A

seizures as a result of high fever (tonic-clonic)

137
Q

Status epilepticus

A

two or more seizures occur without full recovery of consciousness between them; prolonged period
of seizures; life-threatening; requires emergency treatment

138
Q

Three classifications of epilepsy

A
  1. Partial
  2. Generalized
  3. Focal
139
Q

Carbamazepine
Phenytoin
Oxcarbazepine
Lamotrigine

Type of drug? (epilepsy)

A

Sodium channel blocker

140
Q

Toxicity of carbamazepine

A

metabolic bone disease (↓ vitamin D); diplopia, leukopenia

141
Q

Toxicity of phenytoin

A

metabolic bone disease (↓ vitamin D);

hirsutism, neuropathy, ataxia, gingival hyperplasia

142
Q

Toxicity of oxcarbazepine

A

low NA, neurotoxicity, drug interactions, rash

143
Q

Toxicity of lamotrigine

A

rash, drug interactions, headache

144
Q

Benzodiazepines
Barbiturates (penobarbital)

What type of drug? (epilepsy)

A

GABA receptor agonists

145
Q

Toxicity of barbiturates

A

metabolic bone disease; cognitive decline, sedation

146
Q

What two drugs block excitatory synaptic binding of glutamate receptor?

A

Felbamate

Tiagabine

147
Q

What does Felbamate target?

A

Targets NMDA

148
Q

What does Tiagabine target?

A

kainate receptors

149
Q

T calcium current suppressor

A

Ethosuximide

150
Q

Gabapentin
Pregabalin

What do they do? (Epilepsy)

A

Bind alpha-2-delta subunit of voltage-gated Ca++ channels

151
Q

Gabapentin toxicity

A

weight changes, neurotoxicity

152
Q

Pregabalin toxicity

A

weight gain, mild neurotoxicity

153
Q

Which drug works on the presynaptic protein on synaptic vesicles?

A

Levetiracetam

154
Q

Mechanism of Topiramate (epilepsy)

A

sodium blocker, GABA agonist

155
Q

Toxicity of Topiramate

A

weight loss, kidney stones, glaucoma

156
Q

Mechanism of Propofol (epilepsy)

A

sodium blocker, GABA agonist

157
Q

Propofol-infusion syndrome

A

prolonged infusion; hyperlipemia, metabolic acidosis, rhabdomyolysis; renal/heart failure

158
Q

Toxicity of propofol

A

apnea, hypotension, bradycardia

Pharm (9 decks)

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