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Psychiatry > Antipsychotics and Sedative Hypnotics > Flashcards

Antipsychotics and Sedative Hypnotics Flashcards

1
Q

How does the mechanism of action of typical vs atypical antipsychotics explain their efficacy in treating the symptoms of schizophrenia?

A

Typical antipsychotics - Strong D2 antagonists -> block dopamine increase in the nucleus accumbens / basal ganglia which mediates the positive symptoms of schizophrenia, while not helping the negative symptoms in the PFC where dopamine is low

Atypical antipsychotics - D2 and 5HT2A antagonists -> serotonin antagonism is thought to mediate improvement in negative symptoms as well

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2
Q

Describe the effects of strong dopamine blockade in each of the following brain regions:

  1. (Acute) Nigrostriatal tract
  2. (Chronic) Nigrostriatal tract
  3. Tuberoinfundibular tract

What class of drugs is more likely to cause these?

A
  1. (Acute) Nigrostriatal tract - extrapyramidal symptoms
  2. (Chronic) Nigrostriatal tract - tardive dyskinesia
  3. Tuberoinfundibular tract - increased prolactin levels (dopamine is PIH from the hypothalamus)

More likely in typical antipsychotics

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3
Q

What are the extrapyramidal symptoms associated with D2 blockade? Describe them.

A
  1. Parkinsoninism - bradykinesia, cogwheel rigidity, masked facies, and RESTING tremor (resting on a park bench)
  2. Dystonia - abnormal muscle tone / spasm
  3. Akathisia - internal sense of restlessness
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4
Q

How is drug-induced parkinsonism treated?

A

Benztropine - anticholinergic

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5
Q

How is acute dystonia treated?

A

Anticholinergics once stable, following anticholinergic antihistamine: diphenhydramine

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6
Q

How is akathisia treated?

A

Beta blockers, benzos, and anticholinergics (all EPS is treated with anticholinergics)

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7
Q

What are the consequences of prolactinemia caused by dopamine blockade going to the infundibulum?

A
  1. Galactorrhea - lactation, even in males
  2. Amenorrhea, fertility problems, and sexual dysfunction due to inhibition of FSH / LH
  3. Osteoporosis, especially in post-menopausal women
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8
Q

How does tardive dyskinesia occur?

A

Chronic dopamine blockade in the striatum coming from the nigrostriatal pathway leads to upregulation of D2 receptors in the striatum -> increased sensitivity to dopamine.

Choreoathetoid movements will result, and the only way to treat is further D2 antagonist drugs.

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9
Q

What movements are associated with tardive dyskinesia?

A

Mouth and tongue movements, and irregular movements in the upper limbs

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10
Q

Who is at increased risk of TD, other than just being on typical antipsychotics?

A
  1. Those who develop EPS in early treatment

2. Elderly patients -> 25% chance in first year of exposure

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11
Q

How is TD diagnosed?

A
  1. A 2 measure brief screen - hands out and wiggle the fingers while checking for mouth movements
  2. AIMS scale - abnormal involuntary movement
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12
Q

How is TD best managed?

A

Decrease dose or discontinue the precipitating antipsychotic

Use Valbenazine - a VMAT2 inhibitor preventing the packaging of dopamine in nigrostriatal neurons

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13
Q

Other than EPS and TD, what other side effects are associated with typical antipsychotics?

A
  1. Neuroleptic malignant syndrome
  2. Cholinergic (M), adrenergic (a1), and histaminergic (H1) antagonism
  3. Lowered seizure threshold
  4. QT prolongation in low potency (guy shaking with seizures holding onto the ECG tape)
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14
Q

How do high potency typical antipsychotics differ from low potency with respect to their side effects?

A

High potency - more D2 blockade, more likely to cause EPS / TD

Low Potency - more anti-M1,H1,and a1 effects, higher seizure risk / cardiotoxicity (QT prolongation)

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15
Q

What features characterize neuroleptic malignant syndrome (NMS)? What labs go with it?

A

Life-threatening reaction to D2 antagonism

  • > Severe muscle rigidity (“Lead pipe rigidity”)
  • > Hyperthermia (guys face is bright red)
  • > autonomic instability - tachycardia, confusion, diaphoresis, labile blood pressure

Lab findings - Increased CPK and myoglobin due to rhabdomyolysis

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16
Q

What are the treatments for NMS?

A
  1. Dantrolene - muscle relaxant blocking SR-mediated calcium release
  2. Bromocriptine - dopamine agonist
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17
Q

What are the high potency typical antipsychotics?

A

Think of the guy in sketchy flapping his wings on the roof
FLUphenazine
TriFLUoperazine
Haloperidol

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18
Q

What are the low potency typical antipsychotics?

A

Color pro paints = Chlorpromazine

Color theory = Thioridazine

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19
Q

What is the ending of most typical antipsychotic drug names?

A

-Azine

Think starry g’azing’

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20
Q

What side effect is associated with thioridazine?

A

Irreversible pigmentatino of retina which may lead to blindness -> think of retina next to color theory color wheel

21
Q

What side effects are particularly associated with chlorpromazine?

A

Photosensitivity

Also weight gain and dyslipidemia / DM like atypicals

22
Q

What are the results of the anti-histaminergic and anti-adrenergic effects of typical antipsychotics?

A 
Anti-H1 = Sedation, weight gain
Anti-a1 = orthostatic hypotension
23
Q

What three endings are common to atypical antipsychotics?

A
  • apine (olanzapine)
  • peridone (risperidone)
  • idone (ziprasidone = zipperazidone)
24
Q

What is the mechanism of action of aripiprazole / brexiprazole / cariprazine? What is the side effect associated with them?

A 
D2 partial agonist (blocks dopamine if there's alot)
5HT2A antagonism (accounts for effects)
5HT1A  partial agonist -> like buspirone

More activating than other antipsychotics

25
Q

What metabolic side effects are associated with atypical antipsychotics? What drugs in the class are most associated with this?

A

Weight gain and diabetes, dyslipidemia - stick of butter abstract art in sketchy

Olanzapine and clozapine

26
Q

What drugs are associated with increased chance of QT prolongation within the atypical antipsychotics?

A

Iloperidone, Ziprasidone (zipper, next to the line with QT prolongation in sketchy)

27
Q

Which atypical is thought to have a pro-cognitive effect due to 5HT7 antagonism (like vortioxetine)?

A

Lurasidone

28
Q

Why is Risperidone considered like a borderline typical antipsychotic? What drug is an active metabolite of it?

A

Becomes more like typical above 6mg daily -> EPS side effects

  • > also raises prolactin even at low doses
  • > Paliperidone is an active metabolite with fewer side effects
29
Q

What atypical is not associated with EPS? What other diseases is it good for treating other than schizophrenia because of this?

A

Quetiapine (seroquel)

  • > Good for parkinson’s disease dimentia and Lewy Body Dementia
  • > diseases normally highly susceptible to anti-D2 effects of antipsychotics
30
Q

What atypical is associated with DRESS (drug reaction with eosinophilia and systemic syndromes)?

A

Ziprasidone (think of pretty lady with a zipper wearing a DRESS)

31
Q

What drug is most effective in treatment-resistant schizophrenia and its mechanism of action? How is it similar to lithium?

A

Clozapine

5HT2&raquo_space; D2 blockade

Similar to lithium by decreasing suicidality (perhaps due to frequent monitoring needed)

32
Q

Why is frequent monitoring needed for clozapine and what is it?

A

Agranulocytosis is common -> need weekly CBC for 6 months

33
Q

What are the major side effects of concern for clozapine other than agranulocytosis?

A

Myocarditis - heart with a sandglass in it in sketchy
Seizures - shaking clock
Anticholinergic effects - tea party painting behind clozapine closet

34
Q

What depot medications are available for noncompliant patients?

A

Typical - Haloperidol, fluphenazine

Atypical - Risperidone, Paliperidone, Olanzapine, Aripiprazole

35
Q

What is the black box warning for the elderly on antipsychotic drugs?

A

Increased risk of cardiovascular morbidity and mortality for both typical / atypical
-> often used for agitation / aggression in nursing homes, but not an absolute contraindication

36
Q

Why is olanzapine better according to the CATIE RCT?

A

Increased time to discontinuation -> when they couldn’t handle the side effects anymore. Modest efficacy increase

37
Q

What mid-potency typical is as effect as atypical agents for treatment of schizophrenia?

A

Perphenazine
-> did not increased AIMS scores either, although patients with significant EPS history were excluded from group receiving treatment

38
Q

What must be ruled out when treating insomnia? What is the best treatment?

A

Psychiatric illness or medication reaction (i.e. steroids) which is stopping sleep. Also, poor sleep hygiene.

Fixing these is the best treatment -> medications are not first line

39
Q

What are benzos good for in treating insomnia, and what are their main side effects?

A

Good for short term use, decrease sleep latency prolonging total sleep

Main side effects include daytime sedation and rebound insomnia (need to taper)

40
Q

What drug is the benzo of choice for insomnia?

A

Temazepam

-> if you get another benzo, ensure it ends in lam or pam and you’ll be ok

41
Q

What are the non-benzo receptor agonists and their mechanism of action in insomnia?

A

3 Z’s
Zolpidem
Zaleplon
EsZopiclone

Mechanism - binds to GABA-A receptor at allosterically coupled site as benzos

Lack all benzo properties except sedative-hypnotic effect

42
Q

Do non-benzos have abuse potential?

A

Much less, but technically yes -> be aware in patients with history of substance abuse or dependence

43
Q

What type of insomnia is ramelteon good for?

A

Primary insomnia, but not middle insomnia -> little effect on sleep maintenance

44
Q

What drug is used for blind patients unable to obtain a normal circadian rhythm?

A

Tasimelteon (melatonin agonist, same as ramelteon)

-> patients with a non-24 hour sleep-wake disorder

45
Q

What drug is good for both sleep onset and middle insomnia? Does it have abuse potential? Side effect?

A

Suvorexant, no abuse potential
Orexin antagonist

Side effect is next day drowsiness

46
Q

What is the mechanism of action of trazodone in insomnia and possible side effects?

A

Blocks H1 receptors (in addition to antidepressant effects at high doses) at low doses -> causes sleep

Side effects are day-time sedation and anti-a1 effects: Orthostatic hypotension, priapism

47
Q

What tricyclic is used for treatment of insomnia and why?

A

Doxepin - strongly anti-H1 effects at low doses

48
Q

What other antihistamines can be used OTC for insomnia? Problem?

A

Diphenhydramine
Doxylamine

Probable daytime sedation due to long halflife

Psychiatry (23 decks)

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