Anti-psychotics and Lithium Flashcards
Presence of delusions, hallucinations, and grossly disorganized thinking in a clear sensorium (i.e grandiosity and paranoia)
Psychosis
States that stimulation of 5-HT receptors cause hallucinogenic effects
Serotonin hypothesis of schizophrenia
States that there is increased dopamine in schizophrenic patients
Dopamine Hypothesis of Schizophrenia
States that hypofunction of NMDA receptors on GABAergic interneurons leads to diminished inhibitory influences on neuronal function, inducing disinhibition of downstream glutamatergic activity and hyperstimulation of cortical neurons through non-NMDA receptors
Glutamate hypothesis of schizophrenia
T/F Antipsychotics are specific for schizophrenia
False
Antipsychotics are NOT specific for schizophrenia
They are also effective in conditions where psychosis is present, such as schizoaffective disorder, mood disorder, dementia, personality disorder.
Three main psychopathological dimensions of Schizophrenia and examples of each
Positive Sx: psychosis (delusion, hallucination)
Negative Sx: social withdrawal, anhedonia, apathy
Cognitive Sx: attention, memory, executive function
Enumerate the four main dopamine pathways important in schizophrenia and their role
– The mesolimbic pathway (positive symptoms)
– The mesocortical pathway (negative symptoms and cognitive symptoms)
– The nigrostriatal pathway (extrapyramidal symptoms and tardive dyskinesia)
– The tuberoinfundibular pathway (hyperprolactinemia)
Dopamine pathway relevant to positive symptoms of schizophrenia
mesolimbic pathway
T/F: All antipsychotic drugs have the ability to reduce dopaminergic neurotransmission.
True. All antipsychotics are dopamine antagonists and therefore address positive Sx of schizophrenia
Negative and cognitive symptoms of schizophrenia are associated with hypofunction of the
mesocortical pathway
This pathway is related to neurological effects caused by D2 antagonists, such as EPS.
nigrostriatal pathway
Dopaminergic projections in the this pathway influence prolactin release.
tuberoinfundibular pathway
T/F First generation AP affects positive and negative symptoms
F; It only affects positive symptoms
T/F Second generation AP affects positive, negative and cognitive symptoms
T
SE of First generation AP
EPS
First generation AP is aka
Typical
Conventional
Neuroleptic
Second generation AP is aka
Atypical
Serotonin-dopamine antagonists
SE Second generation AP
Less EPS; but more metabolic SE (hyperglycemia, weight gain, dyslipidemia)
MOA of First Gen AP
D2 antagonist
But they can also block H1, M1, and alpha-1 receptors
MOA of Second Gen AP
D2 antagonist
5-HT2A antagonist
5-HT1A agonits
Some are 5-HT1A agonists (ziprasidone, quetiapine, clozapine): causes release in dopamine thereby reducing glutamate release
Acute SE of first gen anti-psychotics
Akathisia
Dystonia
Parkinsonism
Inability to sit still
akathisia
Management of akathisia
beta blockers (propranolol)
sustained contraction of tongue, face, back
acute dystonia
Management of dystonia
antiparkinsonian medication
Clinical features of parkinsonism
Masklike facies, resting tremor, bradykinesia, cogwheel rigidity, shuffling gait, psychomotor retardation
Management of anti-psychotic induced parkinsonsism
Anticholinergic agents
benztropine, biperiden, trihexyphenidyl