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Psychopharmacology of Psychotic Illness - Coggle Diagram
Psychopharmacology of Psychotic Illness
Brain Pathways
Dopamine Brain Pathway
Mesolimbic Dopamine Pathway
Ventral tegmental area to the nucleus accumbens and amygdala
Mesocortical Dopamine Pathway
Ventral tegmental area to the frontal cortex
Nigrostriatal Dopamin Pathway
Substantia nigra to striatum
Tuberoinfundibular Dopamine Pathway
Hypothaalmus, and dopamine release in portal circulation tot he pituitary gland
Psychosis Mesolimbic Pathway
Hyperactive Dopamine Activity
AMygdala, meidal prefrontal cortex, hippocampus
+ve symptoms of schizophrenia
Delusions, hallucinations
Psychosis Mesocortical Pathway
Dopamine depleted Activity
Negative symptoms of schizophrenia
Cognitive dulling, flat affect
First Generation Antipsychotics
Examples
Haloperidol, Loxapine, methotrimeprazine, Chlorpromazine, Zuclopentixole, Flupentixole
Haloperidol
Typical antipsychotic, blcosk dopmaine receptors (Eliminates hallucinations and delusions)
Mechanism Of action
Blocks cholinergic receptors, histamine receptors, adrenergic receptors
Balance betwen dopmaine and acetylcholine is needed for normal movement
As doppamine increases, Ach increases and leads to EPS
Anticholinergics work by blocking Ach, and reducing Ach restores balance from antipsychotic dopamine blockade
Dopamine Blockade
Substantia Nigra
Parkinsonian Sx
Tremor, Rigidity, Akinesia, Bradykinesia, Postuire stooped
Risk Factors
Elderly female, Hx of neurological problems, High dose/potency AP
Onset
Acute/Insidious
Treatment
Anticholinergic Meds, Benztropine, Procyclidin, Trihexyphenidyl
Akathisia
Description
Feeling of motor restless
RIsk Factors
Middle age female, high caffieine intake, iron deificency, high potentncy AP use
Treatmetn
Beta blocker, benzodiazepine
Dystonia
Description
Torsions/Spasm of muscle Groups
Onset
Usually early in course of treatment
Risk Factors
Young men, recent cocaine use, neroleptic, low Ca,PTH
Treatment
Diphenhydramine, Benztopine
Blocks dopamine in this area of brain
Tuberoinfundibular
Characteristics
Increased prolactin
Onset
Incur with PRL 31-50
Risk Facotrs
WIith FGA (risperidone)
Treatment
Decrease dose, cabergoline, SIldenafil, endo consult
Tardive Dyskinesea
Characteristics
Repetitive involuntary choreoathetoid movements, lip smacking, puckering, pruisng, tongue thrusting or protrustion, grimacing, repetitive chewing motions
Onset
Risk increases with >3 mother of antipsychotic use
Risk Factors
Elderly, female, prolonged AP uise
Treatment
Monitor progression, switch to AP with less TD potential (Clozapine, tetrabenazine)
Neuroleptive Malignant Syndorme
Symptoms
FRAME
Fever, Rigidity, Autonomic Instability, Mental Status Changes, Extra Lab Changes
Risk Factors
Rapid Dose increase, psychomotor abnormalities, dehydration
Treatment
Go to ER, supportive treatment, Benzodiazepines
Preventative
AP with anticholinergic effects seem les liely to cause NMS
Second Generation Antipsychotics
Examples
Risperidone, Paliperiodne, Olanzapine, Quetiapine, ZIprasidone, ASenapine, Lurasidone, Aripiprazole, Brexpiprazole, Clozapine
Mechanism of Action
Bind to D2 receptors, Blocks Serotonin 2A receptors, More targeted effect
Monitoring
Baseline and Repeat: Weight, BP, abdominal girth, fasting glucose/lipid, ECG, black box for diabetes
Risperidone
Mechanism of Actioon
5HT2A/D2 Antagonist
Advantage
Strong AP, cheap, less weight gain
Disadvantage
High dose results in too much D2 antagonism, EPS, Hyperprlactinemia, Sedtation
Paliperidone
Mechanism of Action
5HT2A/D2 antagonist
Advantages
Strong AP, quick effect, less weight gain, no restriction for liver
Disadvantage
High dose results in too much D2 antagonism, EPS, hyperprolactemia, ALpha 2 blockade
Olanzapine
Mechanism of Action
5HT2A/D2 antagnosit
Advantage
Strong AP, effective in mania, very sedative
Disadvantage
Antihistaminergic, sometimes too much sedation, weight gain, postural hypotension, constipation
Quetiapine
Mechanism of Action
5HT2A/D2 antagnosit
Advantages
Less permanent binding at substantia nigra, higher affinity for 5HT2A repcetors than D2, 5HT1A partial agonism
Disadvantage
Antihistaminergic, significant weight gain, constipation, hypotension
Ziprasidone
Mechanism
5HT2A/D2 antagonist
Advantage
weight neutral, short acting
Disadvantages
QTc prolognation
Ansenapine
Mehcanism
5HT2A/D2 Antagonist
Advantages
Weight neutral, sedating, less side effects
Disadvantages
Newer, no eating or drinking
Lurasidone
Mechanism
5HT2A/D2 Antagonism
Advantages
Blocks 5HT7a receptoprs which may help mood, sleep, cognition impairment, 5HT1A partial agonism, less anticholinergic and less antihistaminergic
Disadvantages
Must take with food, newer AP, still has hyperlipidemia/hyperglycemia risk
Aripiprazole
MEchanism
5HT2A antagonist and partial D2 agonist/Antagonist
Advantages
Less weight gain, impact on glucose/cholesterole, EPS, sedation, no hepatic/renal impariments
Disadvantages
Akathisia common
Clozapine
Mechanism of action
5Ht2A/D2 antagonism and more
Interacts with many other neurotransmitters (Blcoks D3
Indications
2 Failed AP trials, severe TD or EPS
Advantages
Effective AP, less EPS/TD/motor risks
Disadvantage
Glucose/lipid dysregulatioon, agranulocytosis, myocarditis
Monitoring
Glucose/lipid monitoring, agranulocytosis
Approach
Choose antipsychotic based on desired effect
If no response after 4-6 weeks, switch
If partial response, increase dose or add another agent
Discontinutation
1st episode
If remission for 1-2 years, consider withdrawal over 6-12 months
Multiple episodes
Minimum 5 years stability, and consider withdrawal over 6-24 months