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Flashcards in Antipsychotics Deck (24)
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1
Q

What is the age of onset of SZP (schizophrenia) in males? females?

A

males: 15-24 years
females: 25-34

2
Q

What are positive sx of SZP?

A

hallucinations, delusions, disorganized speech —considered excess cognition

3
Q

What are negative sx of SZP?

A

avolition (lack of motivation), alogia (slowed speech), anhedonia(lack of pleasure), blunted effect
—- considered deficits in behaviour

4
Q

What are the cognitive sx of SZP?

A
  • decline in attention, language, memory, executive function
5
Q

What are affective sx of SZP?

A
  • blunted, inappropriate expression

- often leads to social stigma

6
Q

What is the dopamine hypothesis?

A
  • that there is too much mesolimbic DA pathway activity, leading to the presence of positive sx
  • negative sx occur from low dopaminergic activity in the mesocortical pathway
7
Q

What is the pathway of positive sx for dopamine?

A

ventral tegmental area -> D2 travels down the mesolimbis system-> goes to the nucleus accumbens-> centre for motivation, reward, addiction and reinforcing behaviour

8
Q

What is the pathway for negative symptoms for dopamine?

A

ventral tegmental area-> D1 goes down the mesocortical system -> goes to the prefrontal cortex-> centre for cognition, communication, social function and stress response

9
Q

What do most antipsychotics strongly block?

A

D2 dopamine receptors

10
Q

Drugs that increase what can induce psychosis?

A

dopamine

11
Q

What is the action of typical antipsychotics?

A

MOA thought to be antagonism of D2 receptors in the mesolimbic pathway
- causes effective relief of positive symptoms

12
Q

What are the typical antipsychotics?

A
  • chlorpromazine, fluphenazine, haloperidol, thiothixene
13
Q

What are the adverse effects of typical antipsychotics related to?

A
  • receptor non-selectivity

- blockade of non-mesolimbic D2 dopaminergic pathways

14
Q

Examples of receptor non-selectivity

A
  • chlorpromazine: alpha 1 adrenergic, 5HT2, D2, D1, muscarinic, etc
  • haloperidol: D2, D2, alpa 1, 5HT2, muscarinic, etc
    • result of this is mild to severe.. toxic confusional state, dry mouth, urinary retention (antimuscarinic)
  • orthostatic hypertension, dizziness, tachycardia (a1- adrenergic blockade)
  • weight gain and sedation: histamine blockade
15
Q

What is the nigrostriatal pathway?

A
  • blockade of D2 from the substantia nigra to the stria terminals
  • this causes a blockade of the coordination of voluntary movement
  • can cause parkinson, akathisia, acute dystonic reactions, and tardive dyskinesia
16
Q

What is the tuberoinfundibular pathway?

A
  • blockage of D2 from the hypothalamus to the pituitary gland- increases prolactin production
  • in women: this can cause lactation, amenorrhea, infertility
  • in men: this can cause lactation, impotence,decreased libido
17
Q

What are some other common side effects of antipsychotics?

A
  • pseudo depression related to drowsiness
  • corneal and lens deposits
  • retinal deposits
  • cardiac arrythmias in overdose
  • neuroleptic malignant syndrome (severe muscle rigidity, impaired sweating, fever, autonomic instability, severe agitation)
18
Q

What are the advantages of using atypical antipsychotics?

A
  • blocks D2 in the nucleus accumbent, but also..
  • has a reduced D2 affinity: nigrostiatial= decrease in EPS
  • blocks 5HT receptors- decreases negative symptoms
19
Q

What does increasing the serotonin affinity do?

A
  • decreases negative sx by increasing mesocortical dopamine
20
Q

Examples of antipsychotics

A
  • risperidone (D2=5HT receptor potency)
  • olanzapine (5HT>D2 , also D1)
  • quetiapine (D2= 5HT)
  • zisprasidone (5HT»D2)
  • clozapine (D4= 5HT)
  • ariprazole (D2 partial agonist, 5HT agonist)
21
Q

What are the adverse effects of atypical antipsychotics?

A
  • same as typical antipsychotics, with lower risk, especially go EPS
  • seizures
  • weight gain, hyperlipidemia, hyperglycaemia associated with 5HT blockage - clozapine and olanzapine
  • agranulocytosis
  • higher death rates in patients with dementia
22
Q

What are the main drug interactions?

A
  • excess sedation: anxiolytics, alcohol. antidepressants, antihistamines
  • additive antimuscarinic effects
  • metoclopramide: D2 antagonist, EPS
  • SSRI antidepressants: dopamine suppression in NGS, and EPS
23
Q

How do typical antipsychotics work?

A
  • they block D2 in the mesolimbic (decreases + symptoms), nigrostriatal (EPS) and tuberoinfundibulnar (hyperprolactin) pathways
24
Q

How do atypical antipsychotics work?

A
  • lower affinity block of D2= decreases + symptoms, decreases EPS and prolactin
  • blocks 5HT receptors= decreases - symptoms
  • EPS replaced by weight gain, hyperglycaemia as dominant adverse effect