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Psychiatry > Anti-psychotic drugs > Flashcards

Anti-psychotic drugs Flashcards

1
Q

What are the positive symptoms of schizophrenia?

A
  1. delusions
  2. hallucinations
  3. thought disturbances
  4. disorganized speech
  5. paranoia
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2
Q

What are the negative symptoms of schizophrenia?

A
  1. blunted affect
  2. apathy and emotional withdraw
  3. poverty of speech and thought
  4. loss of initiative
  5. disorientation
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3
Q

What is the dopamine hypothesis for schizophrenia?

A

disease is caused by the dysfunction of dopaminergic pathways based on the observation that:

  1. anti-psychotics block dopamine receptors and potency correlates for D2
  2. dopamine-releasing drugs like amphetamines produce positive psychotic symptoms
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4
Q

Schizophrenia is caused by diminished activity of the __________ pathway and enhanced activity of the __________ pathway.

A

diminished activity of mesocortical pathway

  • midbrain region [tegementum] to prefrontal cortex
  • cognition and psychomotor regulation
  • reduced activity–> negative symptoms of schizophrenia

enhancement of the mesolimbic pathway

  • tegmentum to nucleus accumbens, the hippocampus, septal region, amygdala
  • increased activity–> positive symptoms of schizophrenia
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5
Q

What is the nigrostriatal dopaminergic pathway?

A

Substantia nigra–> striatum for muscle control and coordination
Degeneration of this pathway are responsible for the EPS side effects of antipsychotic drugs

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6
Q

What is the dopaminergic tuberoinfundibular pathway?

A

dopamine from the hypothalamus goes to the pituitary to inhibit the release of prolactin, so with anti-psychotic drugs, there will be less inhibition –> galactorrhea, amenorrhea

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7
Q

What is the NMDA hypofunction hypothesis for schizophrenia?

A

Antagonism of NMDA-type glutamate receptors decreases cortical dopamine release and increases mesolimbic release.

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8
Q

What are the 3 main classes of “classic” antipsychotics?
How do they ALL function?
What pathways of the brain have positive effects?
Which areas are responsible for the side effects?

A
  1. phenothiazines
  2. thioxanthenes
  3. butyrophenones

They all function by blocking D2 receptors [but can also bind D1 receptors]

Positive effects: mesocortical, mesolimbic [only alleviates the positive symptoms]
Negative effects: tuberoinfundibular, nigrostriatal

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9
Q

What are the 3 structures of phenothiazines?
What is the main drug of each structure?
Are they low or high potency?
Which structure is LEAST likely to have EPS?
Which is the most likely to cause EPS?

A
  1. aliphatic - chlorpromazine, low potency drug
  2. piperidine -least likely to have EPS
  3. piperazine - fluphenazine, high potency, most likely to cause extrapyramidal symptoms
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10
Q

What is the structure of chlorpromazine?

A

Aliphatic phenothiazine

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11
Q

What is the pharmacokinetics of all phenothiazines?

A

They are all lipophilic so once in the bloodstream they redistribute [large Vd] and get concentrated in the tissues of lung, spleen, liver, and adrenals.

T1/2 = 24 to 48 hrs
Metabolized in the liver to inactive metabolites

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12
Q

What are the 8 major side effects of phenothiazines?

A
  1. EPS
  2. behavioral effects - feeling of indifference [ataraxia]
  3. Muscarinic blockade –> dry mouth, mydriasis, constipation, urine retention, memory, glaucoma exacerbation
  4. Sedation [related to H1 effects]
  5. a1-blockade –> hypotension, reflex tachycardia, long QT
  6. depression of thermoregulation
  7. reduced seizure threshold
  8. “other” - weight gain, agranulocytosis, gynecomastia, lactation, amenorrhea
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13
Q

Why is there an inverse relationship between EPS and muscarinic receptor blockade?

A

Dopamine normally inhibits Ach from nigrostriatal neurons.

With antipsychotics, the dopamine receptors are blocked and Ach is released, but antimuscarinic effects reveres this.

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14
Q

Chlorpromazine has weak or strong effects in the following areas?

  1. antipsychotic, antiemetic
  2. EPS
  3. muscarinic blockade
  4. H1-blockade
  5. a-blockade
A

It is a low potency phenothiazine so:

  1. weak
  2. weak
  3. strong - constipation, dry mucus membranes
  4. strong - sedation
  5. strong- hypotension, rebound tachycardia
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15
Q

What are the advantages of chlorpromazine?

Disadvantages?

A

Advantages: least EP symptoms of the phenothiazines
Disadvantage: hypotension, sedation, antimuscarinic

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16
Q

Fluphenazine has weak or strong effects in the following areas?

  1. antipsychotic, antiemetic
  2. EPS
  3. muscarinic blockade
  4. H1-blockade
  5. a-blockade
A

It is high potency phenothiazine so:

  1. strong
  2. strong
  3. low
  4. low
  5. low
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17
Q

What are the advantages and disadvantages of fluphenazine?

A

Advantages: depot form, low sedation/hypotension/antimuscarinic

Disadvantages: high EPS

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18
Q

Is haliperidol more similar to chlorpromazine or fluphenazine in terms of antipsychotic effect, EPS, muscarinic blockade, a1 and H1 effects?
What are the pros and cons of haliperidol?

A

It is closer to fluphenazine except haliperidol has:
Cons: most EPS
Pros: least anticholinergics, low incidence of liver disease

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19
Q

What are the 3 main uses of phenothiazines?

A
  1. antipsychotic effects:
    - less agitation, improved thinking
    - less or terminated hallucinations [including drug induced]
    - no tolerance, physical or psychological dependence
  2. manic phase of bipolar disorder [although usually 2nd generation are used]
  3. anti-emetic for digitalis, apomorphine, opioids
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20
Q

What is the structure of thioxanthenes?

A

like phenothiazines but with carbon instead of N in the middle of the three rings.
-side chains can be aliphatic OR piperazine

21
Q

Butyrophenones tend to be potent ______________ with low ___________ activity.

A

D2-antagonists with low anticholinergic activity [making them similar to fluphenazine]

22
Q

What is the most commonly prescribed butyrophenone?

What are it’s 4 major uses?

A

Haloperidol

  1. manic episodes in bipolar
  2. Tourette’s
  3. chorea
  4. psychotic episodes in depressed patients
23
Q

What are the 6 EPS that arise from antipsychotic blockage of dopamine receptors?

A
  1. Parkinsonism
  2. Tardive Dyskinesia
  3. Acute dystonia
  4. acute akathisia [inability to sit]
  5. perioral tremor [rabbit syndrome]
  6. Neuroleptic malignant syndrome
24
Q

Which EPS usually occurs first [1-5 days after start of therapy]?
What is treatment?

A

Acute dystonia - twisting and spasm of the face, tongue, neck

Treat with anticholinergic drugs [relief w/in minutes]

  • benzotropine, antihistamine with antimusc. action
  • IV single injection [second injection if persists for 10 minutes]
25
Q

After acute dystonia, the next EPS to appear with antipsychotic use [5-60 days with 40% in the first month] is what?
What is treatment?

A

Acute akathisia- “unable to sit”
The patient will be restless and unable to sit still. They have emotional unease because they cannot get comfortable. Crossing/uncrossing legs.

Treatment:

  1. reduce dose of antipsychotic
  2. change drug
  3. propanolol
  4. anticholinergic
26
Q

When are parkinsonism symptoms likely to show up in a patient on a classic antipsychotic?
What is treatment?

A

They show up 5-30 days after initiation of medication.
Treat by:
1. reduce dosage
2. anticholinergic drugs
**AVOID L-Dopa as it will aggravate schizophrenia symptoms
3. amantidine

27
Q

What is perioral tremor?
When does it occur after taking a classic antipsychotic?
What is treatment?

A

Tremor of muscle around the mouth [“rabbit syndrome”]
It occurs months-> years after

Treatment
1. anticholinergic

28
Q

What is neuroleptic malignant syndrome?
When is onset after taking classic anti-psychotic?
What is treatment?

A

It is a lethal side effect of antipsychotics with:

  • muscle rigidity, dystonia
  • hyperthermia, sweating
  • catatonia
  • coma

Onset is after a single dose or after years OR when anticholinergic therapy is withdrawn

Treatment:

  1. withdrawal from neuroleptic
  2. administer bromocriptine [dopamine agonist]
  3. muscle relaxant [diazepam or dantrolene]
29
Q

When is maximum risk of developing tardive dyskinesia?
What is the incidence rate?
What group of people are most at risk?

A

Maximum risk is YEARS after starting therapy.
30% at 5 years, 70% at 25 years
Elderly are most at risk [half affected in 3 years]

30
Q

How is tardive dyskinesia treated?

A
  1. use lowest effective dose of classic antipsychotic
    OR
  2. substitute clozapine or atypical antipsychotic
31
Q

What is the mechanism by which tardive dyskinesia occurs with antipsychotic use?

A

DA-Ach-GABA imbalance

32
Q

How does withdrawal-emergence dyskinesia differ from tardive dyskinesia?

A

Withdrawal resolves over 1-2 weeks after withdrawing from the neuroleptic

33
Q

What differentiates the new generation anti-psychotics from the classic?

A
  1. less EPS

2. little propensity to increase prolactin

34
Q

What 3 properties allow for the “atypical behavior” of antipsychotics?

A
  1. high affinity for 5HT2 serotonin receptors
  2. high affinity for D4 receptors
  3. specific action on mesolimbic rather than nigrostriatal pathways
35
Q

When is clozapine used?

What are the drawbacks?

A

It is used :

  1. when other medications have failed
  2. in patients with unmanagable EPS

It is the most effective antipsychotic due to broad spectrum [mult DA, 5HT, a1, H1, muscarinic receptors]
But is limited due to:
1. agranulocytosis - requires weekly blood counts, costly
2. lower seizure threshold

36
Q

One of the side effects of clozapine is lowering the seizure threshold. What anticonvulsant CANNOT be given with clozapine? Why?

A

Carbamazepine - bone marrow toxicity

37
Q

What receptors does resperidone have high affinity for?

What are adverse effects?

A

It acts on 5HT2a&raquo_space; D2

Adverse effects: insomnia, drowsy, agitation, headache, runny nose, constipation, weight gain

38
Q

What drug is olanzapine most similar to?

What differentiates them?

A

Olanzapine is most like clozapine because it binds 5HT2a» D1,2 and has affinity for D4 receptors.

It does NOT have agranulocytosis

39
Q

Of the atypical antipsychotics, which has the least antipsychotic potential?

A

Clozapine

40
Q

Of the atypical antipsychotics, which has the least EPS?

A

Clozapine < olanzapine < resperidone

41
Q

Which atypical antipsychotic has NO antimuscarinic effect?

A

risperidone

42
Q

What are the major advantages of clozapine?

Disadvantages?

A

Advantages: lowest EPS, effective in refractory patients

Disadvantages: agranulocytosis, low seizure threshold, salivation, MOST WEIGHT GAIN

43
Q

What are the advantages and disadvantages of risperidone?

A

Advantages: minimal EPS at <6mg/day, low weight gain
Disadvantages: cardiac arrthmia, increased prolactin

44
Q

What are the advantages and disadvantages of olanzapine?

A

Advantages: low EP, effective in refractory

Disadvantages : weight gain

45
Q

What receptor does aripiprazole work on?

What is the major advantage?

A

It is a partial D2 agonist, therefore there is very little risk of EPS

46
Q

Which atypical antipsychotic is a partial D2 agonist?

A

Aripiprazole

47
Q

On what receptors does ziprasidone work?
What does it treat?
What are the side effects?

A

Antagonism of D2, 5HT2a, 5HT1d, 5HT2c
Agonist of 5HT1a

It is effective at treating negative symptoms of schizophrenia because it is a moderate 5HT, NE reuptake blocker

Low weight gain or sexual disfunction
Side effect: prolonged QT

48
Q

For which 2 atypical antipsychotics does the side effect of weight gain appear the greatest?

A

clozapine, olanzapine

Psychiatry (18 decks)

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