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Flashcards in Antipsychotics Deck (24)

Name the “Typical” aka Older Antipsychotic drugs.


Name some of the “Atypicals”


  • Chlorpromazine, Fluphenazine, Perphenazine, Haloperidol


Atypical: “Heterocyclics”

  • Clozapine, Quetiapine, Risperidone, Zotepine, Olanzapine


What are common adverse effects for the Typical Antipsychotics?

Anticholinergic Effects


Orthostatic Hypotension


EPS and movement disorders

Less Expensive 


What are the common adverse effects for the Atypical Antipsychotics?

Less likely to have EPS

Instead associated with weight gain, hyperglycemia, and diabetes

Nausea, dizziness, HA and hypotension


Clozapine – Agranulocytosis 


What is the main mechanism of action of Antipsychotic Medications? What are the 4 major pathways that they act on? 

Block D2 Receptors!!!!



Mesolimbic – target for positive symptoms

Mesocortical – target for negative symptoms



Which have higher affinity for D2 receptors: Atypicals or Typicals? What is the significance of affinity? How does it relate to potency?

Typicals have high affinity for D2 receptor

Atypicals are less “sticky” and have less affinity so can block both D2 and 5HT receptors – this allows them to act more for negative symptoms


Higher affinity then less you need for effective dose (higher potency) but also cause more EPS


Lower affinity/potency tend to cause more sedation, anti-Ach, orthostatic hypotension


Of the Typicals, which ones most block the M1 cholinergic receptors in addition to D2?

Which ones block Alpha 1 more than others?

Which ones block H1 more than others?

Which one has the highest affinity for blocking D2 and least affinity for other receptor subtypes? 

M1 Bloc k Thioridazine


A1 and H1 – Chlorpromazine


Haloperidol is the best!


What are the effects of blocking D2 in the Tuberoinfundibular Pathway? 

Tuberoinfundibular pathway controls Prolactin secretion (hypothal to arcuate nucleus)


Blocking D2 --> Increase in prolactin secretion

= Hyperprolactinemia!!! With breast secretions, amenorrhea and infertility


What are the effects of blocking D2 in the Mesocortical Pathway? 

Mesocortical Pathway – mediates negative and cognitive symptoms likely through Da deficit


Blockade of D2 here where you already have deficit in Da leads to:

  • Emotional blunting
  • Cognitive problems
  • Essentially, mimicking negative symptoms


What are the effects of blocking D2 in the Nigrostrial Pathway?







Blocking D2 here, from SN to BG, leads to EPS and movement disorders including:

  • Dystonia
  • Tremor
  • Akinisia – decreased movement spontaneity
  • Akathisia – Motor restlessness/constant urge to move

Tardive Dyskinesia – MAY BE PERMANENT


What is Tardive Dyskinesia? What causes this?

Hyperkinetic Movement Disorder characterized by repetitive, involuntary and purposeless movements


Facial and Tongue movements – tics and jercs

Rapid movements of arms, trunk and legs may appear

Involuntary movements of fingers


Mechanism: D2 Blockade leads to Up-Regulation of Receptors!!! Permanent reorganization unless blockade is removed early enough



What is the relationship between Da and Ach in the BG? How can imbalance cause EPS? How can you alleviate EPS? 

Normally, there’s a balance between Da and Ach

Da suppresses activity of Ach neurons and limits release when acting through receptors, when you block Da receptors you get increased Ach release/activity associated with EPS (muscarinic rec in BG)


*Anticholinergic properties of typical antipsychotics help to overcome excess Ach activity and reduce EPS but does NOT alleviate the risk for Tardive Dyskinesia


What’s the general MOA for the heterogenous group of Atypical Antipsychotics?


What are their clinical effects? 

Da Antagonism – lower affinity for D2 receptors and so only occupy and block a few of those


5HT2A receptor Blockade


Clinically – effective for negative symptoms from 5HT blockade and lessen positive symptoms with lower risk of EPS


What role does the Serotonin inhibition play in the different clinical effects of the atypical antipsychotics? 

In most areas of the brain, serotonin inhibits Da release BUTTTTTT in the nigrostriatal pathway, 5HT2A antagonism results in an increase in Da activity and lowers the EPS


Also, bc the Da antagonism is weaker, Da release can compete with the atypicals 


How do the atypicals work in the Mesocortical pathway? What is the significance? 

5HT2A antagonism releases the brake on Da in the Mesocortical pathway


High density of 5HT2A in cerebral cortex leads to more effective block and an increase in Da release which can outcompete the D2 Antagonist part


What is Neuroleptic Malignant Syndrome?

Life-threatening illness associated with antipsychotic therapy occurs within 30 days of new medication or dose increase


Clinical Manifestation: F.E.V.E.R.

  • Fever
  • Encephalopathy – delirium, agitation, coma
  • Vital Signs unstable – Autonomic instability: high BP, tachypnea, Diaphoresis
  • Elevated enzymes – CPK increased
  • Rigidity of Muscles


What is the treatment for Neuroleptic Malignant Syndrome? 

Immediate discontinuation of the antipsychotic and Hydration

Maintain Vitals


Give Bromocritptine and/or Dantrolene


What is Clozapine? How does it work? What are the major side effects? 

First Atypical Antipsychotic with weak D2 Antagonism and 5HT2A-C antagonism

  • Works for pts when all else fails!!

Causes very few EPS, NO TARDIVE DYSKINESIA, NO elevation in Prolactin

Side Effects:

  • Agranulocytosis – can be life threatening
  • M1 Anticholinergic Effects
  • Alpha Adrenergic Effects – low BP and dizziness
  • H1 Anti-Histamine – drowsiness and weight gain
  • 5HT2C Blocker – weight gain


What is Risperidone? What are the Side Effects? 

Atypical Antipsychotic and higher doses lead to more EPS --> Less is better


Effective mood stabilizer and has efficacy for both positive and negative effects


Side Effects:

  • Prolactin Elevation
  • Weight Gain
  • Decreased TD


What is Olanzapine? What are the Side Effects? 

Atypical Antipsychotic and higher doses lead to more EPS à Less is better


Effective mood stabilizer and has efficacy for both positive and negative effects


Side Effects:

  • Slight prolactin elevation
  • Somewhat sedating
  • Decreased TD


What is Quetiapine? What are the Side Effects?




Atypical Antipsychotic where more is better bc very low risk EPS and TD


Side Effects:

  • Some weight gain
  • Sedating
  • Dose titration necessary to decrease dizziness

*Low Dose may be useful in Borderline Disorder


What is Ziprasidone? What is unique about it? 

Newer Antipsychotic where EPS is dose related BUT it has NO WEIGHT GAIN AND LOW RISK DIABETES


Can be used as an antidepressant!!!

Causes Nausea and sleep disturbances 


What is Aripiprazole? How does it work? What is unique about it? 

Aripiprazole = Abilify


D2 Partial Agonist and 5HT2A Antagonist

  • Partial Agonist – binds receptor but does not cause full activity, only attenuated activity


Causes little to no weight gain, little EPS, little sedation and little effect on heart function – YAY!


What is Zotepine? What is unique about it? Side effects? 

Zotepine is an antagonist at Da and 5HT receptors with high affinity for D1 and D2 and affects 5HT2A


Also inhibits reuptake of NE!!! Has high efficacy for negative symptoms


Most common side effects:

  • Weight gain
  • Somnolence
  • Constipation
  • Asthenia
  • Dry mouth
  • Akathisia


Review: What are the Atypical Antipsychotics? Which ones are particularly risky for weight gain/diabetes/worsening lipids? 

Clozapine, Olanzapine, Risperidone, Zotepine and Quetiapine – weight gain, DB, Lipids


Aripiprazole and Ziprasidone – no weight gain or other metabolic risk