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GT BSN/CNL PHARM > Psychotherapeutics > Flashcards

Psychotherapeutics Flashcards

1
Q

Do first or second generation antipsychotics work better in the treatment of schizophrenia?

A

They work the same

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2
Q

Pros and cons of first gen antipsychotics

A

Pros = cheaper
Cons = EPS

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3
Q

Pros and cons of second gen antipsychotics

A

Pros = no EPS
cons = more expensive, metabolic effects that put the patient at risk for CV events and death

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4
Q

Which receptors do 1st gen antipsychotics work on?

A

D2

Also can interact with ACh, histamine, and NE receptors

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5
Q

Which receptors do 2nd gen antipsychotics work on?

A

D1, D2, D4, 5-HT

Also can interact with a1, histamine, and M receptors

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6
Q

How long does it take for schizophrenia symptom improvement upon initiation of pharmacological therapy?

A

2-4 weeks
Full effect: months

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7
Q

Adverse effects of FGAs

A

EPS!!!
neuroleptic malignant syndrome
Anti cholinergic effects
Orthostatic hypotension
Hyperprolactinemia
Seizures
Sexual dysfunction
Dysrhythmias

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8
Q

What are EPS?

A

Movement disorders due to drug effects on the extrapyramidal motor system

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9
Q

List 4 types of EPS

A

pseudoparkinsonism
Acute dystopia
Akathisia
Tardive dyskinesia

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10
Q

Which category of EPS does not have a treatment?

A

Tardive dyskinesias

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11
Q

How are 3/4 of EPS treated?

A

Anticholinergics
Amantadine
Beta blockers
Benzodiazepines

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12
Q

Mechanism of neuroleptic malignant syndrome?

A

DA receptor blockade from antipsychotic medications

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13
Q

S/s neuroleptic malignant syndrome

A

Rigidity
Sudden high fever
Sweating
ANS instability —> BP changes/dysrhythmias
Seizures, coma

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14
Q

Treatment for neuroleptic malignant syndrome

A

Withdraw antipsychotic med
Possibly switch to SGA
Supportive care (resp, hemodynamics)

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15
Q

What can NMS also look like?

A

Serotonin syndrome (from drugs that increase 5-HT)

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16
Q

Major adverse of haloperidol?

A

Earlier EPS
QT prolongation

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17
Q

What is the potency of haloperidol?

A

High

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18
Q

What are the major adverse effects of phenothiazine?

A

Sedation
Orthostatic hypotension
Anticholinergic effects
QT prolongation
Lower incidence of EPS

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19
Q

What are the three metabolic adverse effects of SGA that can result in CV events?

A

DM
Weight gain
HLD

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20
Q

Schizophrenia relapse while on pharmacological therapy is most likely to occur because of ______.

A

Nonadherence

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21
Q

How long is the pharmacological treatment of schizophrenia?

A

Indefinite

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22
Q

Neurotransmitters hypothesized to be involved in depression?

A

Norepi
Serotonin

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23
Q

When initiating antidepressant therapy, how long until drug effects are at plateau?

A

Up to 3m

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24
Q

Pharmacological antidepressant therapy should be combined with:

A

Psychotherapy

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25
Q

Antidepressants have a black box warning because:

A

Early in treatment, depression/suicidal ideation can increase

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26
Q

List 4 classes of antidepressants

A

SSRIs
SNRIs
TCAs
MAOIs

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27
Q

Mechanism of SSRIs

A

Inhibit reputake of 5-HT = increased concentration in neuronal synapse

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28
Q

Which is the safest antidepressant class?

A

SSRIs

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29
Q

List some SSRIs

A

Fluoxetine
Citalopram
Escitalopram
Paroxetine
Sertaline
(Others)

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30
Q

Adverse effects of SSRIs

A

Nausea
Agitation/insomnia
Sexual dysfunction
Weight gain
Serotonin syndrome

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31
Q

Major drug interactions with SSRIs

A

Other drugs that increase serotonin (MAOIs, SNRIs, TCAs, analgesics, triptans) = serotonin syndrome

Other drugs that inhibit platelet aggregation (antiplatelets) = increased bleeding risk

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32
Q

Mechanism of SNRIs

A

Inhibit reuptake of 5-HT and NE = increased concentration on neuronal synapse

33
Q

Adverse effects of SNRIs

A

Same as SSRIs
+ HTN

34
Q

List some SNRIs

A

Venlafaxine
Duloxetine
(Others)

35
Q

Mechanism of TCAs:

A

As an antidepressant, they inhibit 5-HT and NE reuptake = increased concentration in neuronal synapse

Not selective tho, so also impact H, M, and various other receptors

36
Q

List some TCAs

A

Amitriptyline
Clomioramine
(Others)

37
Q

Adverse effects of TCAs

A

Commonly due to H & M receptor interaction
- orthostatic hypotension
- anticholinergic effects
- sedation
- cardiac toxicity (dyrhythmias, HB)
- seizures
- SI

38
Q

Major reasons for drug interactions with TCAS:

A
  1. HTN risk (MAOIs, sympathomimetics)
  2. CNS depression (additive with other agents)
39
Q

Mechanism of MAOIs

A

Inhibit monoamine oxidase = decreased metabolism of NE, 5-HT, DA, tyramine

Antidepressant = increased NE and 5-HT availability

40
Q

Duration of effect of MAOIs

A

2 weeks

(Since irreversible inhibition of MAO)

41
Q

List some MAOI inhibitors used for depression

A

Isocarboxazid
Phenelzine
Tranycypromine

42
Q

Are nonselective MAOI or MAO-B inhibitors used for treatment of depression?

A

Nonselective

43
Q

Adverse effects of MAOIs

A

CNS stim
Orthostatic hypotension
Others same as SSRIs

44
Q

Major causes of drug interactions with MAOIs

A
  1. Severe HTN with any other drug that increases NE or causes hypertension
  2. Serotonin syndrome risk with any other drug that increases 5-HT
45
Q

Food element that should be avoided while on MAOIs

A

Tyramine

46
Q

What is the risk with tyramine when on a MAOI

A

Excessive NE release = HTN, HA, tachycardia/MI
Can be deadly

47
Q

List some tyramine containing foods

A

Aged cheeses
Cured meats
Processed meats
Fermented or pickled foods
Some sauces (soy sauce)
Fava beans
Alcoholic beverages
(Others)

48
Q

List some atypical antidepressants

A

Bupropion
Mirtazapine
Esketamine
(Others)

49
Q

List mood stabilizers used in the treatment of bipolar disorder

A

Lithium
Valproate
Carbamazepine

50
Q

Which antipsychotics are used in bipolar disorder

A

Second gen

51
Q

Specific PK considerations with lithium

A
  • rapid 1/2 life = multiple doses per day
  • narrow therapeutic index = drug levels must be monitored
52
Q

S/s mild lithium toxicity (to educate patients)

A

Fine tremor
GI disturbances
Polyuria & polydipsia
Agitation
Confusion/delirium

53
Q

S/s severe lithium toxicity

A

Tremors
Delirium
Seizures
QT prolongation
Renal failure
Coma
Death

54
Q

Goal range in lithium treatment

A

0.4-1mEq/L

55
Q

Mechanism of action of benzodiazepines

A

Potentiation of GABA
(I.e. utilizes the GABA that the body has)

56
Q

Why does ceiling effect occur with benzodiazepines?

A

Because they potentiate endogenous GABA, they don’t agonize the receptor on their own

57
Q

Adverse effects of benzodiazepines

A

CNS depression
Anterograde amnesia
Teratogenic

58
Q

Mechanism of action of benzodiazepine like drugs

A

Agonize GABA receptor

59
Q

List some benzodiazepine like drugs

A

Zolpidem
Zaleplon
Eszipiclone

60
Q

What is the difference between zalpeplon and zolpidem

A

Zaleplon has a rapid onset but short duration, so only helpful for falling asleep

Zolpidem has a longer duration so helpful also for staying asleep

61
Q

How does ramelteon work

A

Agonizes melatonin receptor (15x more potent than melatonin itself)

62
Q

Which sleep aid isn’t a controlled substance

A

Ramelteon (melatonin agonist)

63
Q

How does suvorexant work?

A

Antagonizes the effects of orexin, resulting in decreased wakefulness

64
Q

Major difference between barbiturates and benzodiazepines

A

Barbiturates agonize GABA receptor directly, thus there is no ceiling effect to CNS and respiratory depression

65
Q

Adverse effects of barbiturates

A

Severe resp depression (death)
Sedation (can be used as a general anesthetic)
CYP450 induction
Tolerance & physical dependence

66
Q

Drugs used in anxiety

A

SSRIs
SNRIs
Buspirone
Benzodiazepines

67
Q

Mechanism of action of buspirone

A

Not we’ll known, but likely binds 5-HT receptors

68
Q

Adverse effects of buspirone

A

Minimal
Dizziness
Nausea
HA

69
Q

First line drugs for ADHD

A

CNS stimulants

70
Q

Adverse effect of all CNS stimulants

A

Seizures

71
Q

Types of CNS stimulants

A

Amphetamines
Methylphenidate/dexmethylphenidate
Methylxanthines
Modafinil

72
Q

Mechanism of action of amphetamines

A

Stimulate release of NE & DA, inhibit some of their reuptake

73
Q

Adverse effects of amphetamines

A

Insomnia, restlessness, euphoria
Appetite suppression
Tachycardia, vasocontriction (can lead to dysrhythmias, HTN)

74
Q

How do methylxanthines work

A

Block adenosine receptor = cAMP accumulation

75
Q

Which schedule drug is methylphenidate

A

II

76
Q

Adverse effects of methylxanthines

A

Decreased fatigue
Tremors, insomnia
Cardiac stimulation
CNS vasoconstriction
Bronchodilation

77
Q

How does modafinil work

A

Unclear
Influences sleep/wake cycles

78
Q

Adverse effects of modafinil

A

Minimal, just avoid in pregnancy

GT BSN/CNL PHARM (26 decks)

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