Clinical Pearls of Antipsychotics
Schizophrenia (SZ) is a chronic psychiatric disorder with impairment in reality
perception, which we cannot cure with medications yet. Antipsychotics only provide
symptomatic treatment for this “thought process” disorder. One pathophysiologic
hypothesis is excessive synaptic pruning beginning at/after 2 yo (more neural
connections are needed as newborns to 2 yo at which time synaptic pruning begins
until puberty to “streamline” neural connections) which results in SZ as young adults
usually. The patient’s first psychotic episode can frequently occur when they move
away from home and are at college (different environment, stress, drug abuse-
another reason to say no to drugs!). Suicide rates are high in this population and
suicidal attempts are even higher so we want to closely monitor these patients,
especially since SZ is debilitating. It is a struggle for patients with SZ to function
and/or “fit” in society and in relationships. Because with antipsychotics, we are
targeting the positive (word salad-the words are there but don’t make sense
together-a jumble of words), negative and cognitive symptoms, be sure to know
these-see slides for symptoms.
Antipsychotics have many significant side effects. When thinking of side effects, it
may be helpful to think of the effects of the receptors where these medications can
work, which is related to MOA of the particular drug- note antipsychotics
antagonize/block these receptors.
Receptor Antagonism Effect Clinically
Dopamine (+) symptom reduction, EPS (extrapyramidal symptoms),
hyperprolactinemia (galactorrhea), worsen (-) & cognitive symptoms
Acetylcholine
(muscarinic)
Anticholinergic SE (delirium, confusion, blurred vision, constipation,
urinary retention, tachycardia, dry eyes), EPS reduction
Histamine Drowsiness (forget non-sedating antihistamine which are outliers)
and metabolic AE (weight gain, hyperlipidemia, glucose
intolerance/new onset diabetes, hypertension)
5HT (Serotonin) Cognitive and (-) symptom reduction/improvement, antidepressant
effects (remember our AD), EPS reduction, metabolic AE (weight
gain, hyperlipidemia, glucose intolerance, new onset diabetes,
hypertension)
Norepinephrine
(Alpha)
Orthostatic hypotension, drowsiness, cardiac AE
When you review the MOA and SE charts in the slides, in 1 and 2 generation
stnd
antipsychotics, you can see why they cause these SE based on the receptor where
they are acting. The antipsychotics that work on blocking multiple receptors have
many different AE. If we generalized FGA (first generation antipsychotics or typical
antipsychotics), they generally have more EPS incidence, less metabolic AE, and can
worsen negative and/or cognitive symptoms. Therefore, these are not considered
1stline usually. SGA (second generation or atypical antipsychotics) generally have
less EPS incidence, may improve negative symptoms, but have increased metabolic
AE. Of course, there are always outliers. All antipsychotics have BBW for increased
mortality in elderly patient with dementia related psychosis treated with
antipsychotics. Some antipsychotics have additional BBW (clozapine for one), which
you should know.
Here is a link to SZ assessment and AIM (Abnormal Involuntary Movement Scale) for
tardive dyskinesia from antipsychotics.
https://www.google.com/url?
sa=t&rct=j&q=&esrc=s&source=web&cd=&ved=2ahUKEwib9t3BjYLqAhVlTT
ABHYCRBWUQFjAAegQIBBAC&url=https%3A%2F
%2Fwww.medicalhomeportal.org%2Flink
%2F6544&usg=AOvVaw1dst8JlPICT3u_KFZJOceH
Clozapine has a REMS (Risk Evaluation and Mitigation Strategies) because of its BBW
for agranulocytosis. All prescribers, pharmacists, and patient must enroll in this
program prior to treatment to ensure monitoring requirements for ANC (Absolute
Neutrophil Count) are met. Here is the address for this REMS and for enrollment:
https://www.clozapinerems.com/CpmgClozapineUI/home.u
Dr. Donna Hudson
