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A comprehensive set of questions and answers for an exam in psychopharmacology, specifically focusing on the course nurs660. It covers key neurotransmitters involved in schizophrenia, adverse reactions to antipsychotics, serotonin syndrome, and the mechanisms of action of various antipsychotic medications. The document also includes information on extrapyramidal side effects, their types, and management strategies. This resource is valuable for students studying psychopharmacology and preparing for exams.
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Major neurotransmitters involved in schizophrenia - ANS ✓-Dopamine
Conventional Antipsychotics - ANS ✓First-Generation drug for Schizophrenia
SE: Retinal deposits, RPE hyperpigmentation, dry eye, mydriasis, increased IOP (watch in narrow angle), hypotension, weight gain QTc prolongation. Interactions: levodopa, dopamine agonists, CNS depressants, antihypertensives Indications: schizophrenia pts who fail to respond to other antipsychotics. Perphenzaine (Trilafon) - ANS ✓Potent D2 antagonist SE: neuroleptic induced deficit syndrome, akathisia, EPS, parkonsonism, TD, galactorrhea, urinary retention, sexual dysfunction Interactions: Fluoxetine, paroxetine, and bupropion can increase levels. Antihypertensives have synergistic interaction, increasing risk for hypotension. Serious adverse events: NMS, jaundice, seizures, CV death in elderly The "Done" family - ANS ✓Bind more potently to 5HT2A than D2, have less affinity to 5HT1A than the pines, lower 5HT2C potency than pines. Risperidone, Lurasidone, paliperidone Second generation antipsychotics Lurasidone (Latuda) - ANS ✓Treats schizophrenia and depression. SE: must be taken with 350 calories of solid food for max absorption. Low risk of weight gain Paliperidone (Invega) - ANS ✓If patient has a lot of SE from risperidone, will most likely have a lot of SE with this med. Interactions: Can enhance risk of QT prolongation in other medications with SE. Increases effects of antihypertensivies. Serious adverse effects: hyperglycemia/ DKA, NMS, increased risk of death in elderly pts with dementia indications: oral or LAI (monthly and every 3 month doses)
Acute dystonia - ANS ✓Sustained muscle contraction in the face, neck, trunk, or extremities, can affect the larynx. Oculogyric crisis can be a dystonic reaction. Painful. Onset- quickly, within hours. Reversible with treatment of an anticholinergic, benadryl, benzotropine, or congentin. Akathisia - ANS ✓Uncontrollable motor restlessness. Pace, fidget, rock back and forth. Often misdiagnosed as anxiety, difficult to diagnose Onset: typically occurs within days to weeks but within a month. Reversible with beta blockers, benzos, can switch pt's medication. First generation antipsychotics with high potency are highly likely to produce akathisia. pseudo-parkinsonism - ANS ✓Rigidity, pill-rolling tremors, bradykinesia (top 3), masked face, and shuffling gait. Does not progress to Parkinson's, usually reversible. Onset- Months to years (weeks but within a month-Langford) Treat with amantadine and benzos Tardive dyskinesia (TD) - ANS ✓Late-onset (6 months to years) Irreversible neurologic side effect, only 50% reversible characterized by abnormal, involuntary movements such as lip smacking, tongue protrusion, chewing, excessive blinking, grimacing, irregular finger movements, and choreiform movements of the limbs and feet Older adults are at higher risk Treatment- valbenazine, deutetrabenazine, benzos Do not treat with anticholinergics. Can test severity with AIMS test
Upregulation of dopamine 2 receptors - ANS ✓Long term blockade of D receptors in the nigrostritrial dopamine pathway can cause upregulation of those receptors. May lead to TD as well as quick, jerky, limb movements. Upregulation may be the consequence of the neuron's futile attempt to overcome drug induced blockade of its dopamine receptors Downregulation of dopamine 2 receptors - ANS ✓Process wherein the postsynaptic neuron can make itself less sensitive to stimulation. If a neuron is being activated too often, it can reduce the number of receptors available on it's membrane, making itself less sensitive to acitvation. Dopamine D2 - ANS ✓Possible benefits- reduced positive symptoms SE: EPS, akathisia, endocrine effects such as prolactin secretion, menstrual changes, sexual dysfunction Serotonin - ANS ✓5HT2A- benefits: reduced EPS. SE: sexual dysfunction 5HT2C- benefits: unknown. SE: weight gain Histamine H1 - ANS ✓Benefits: sedation Se: sedation, increased appetite, weight gain, hypotension Muscarinic cholinergic - ANS ✓Benefits: reduced EPS SE: autonomic side effects such as blurred vision, dry mouth, constipation, urinary retention, tachycardia, memory dysfunction. Adrengeric receptors - ANS ✓Benefits unknown. possible side effects: a1- orthostatic hypotension, dizziness, reflex tachycardia a2- drug interactions
Greater risk for EPS, NMS, tardive dyskinesia, QTC prolongation. Haldol, fluphenazine. Low potency first generation antipsychotics - ANS ✓1st gen antipsychotics that have a lower affinity for dopamine receptors have a lower potency (need more of a drug to get an effect). More anticholinergic effects. High H1 (weight gain, sedation) and M1 (dry mouth, tachycardia, urinary retention, constipation, visual changes, visual changes, or blurred vision) More antiadrenergic (A1) effects (orthostatic hypotension, cardiac problems, sexual dysfunction (priapism). More antihistamine effects Decreased incidence of EPS. Positive Symptoms of Schizophrenia - ANS ✓Delusions, hallucinations, distortions, agitation, disorganized speech, disorganized behavior Where do positive symptoms originate? - ANS ✓Mesolimbic dopamine pathway Medications to treat positive symptoms - ANS ✓Antipsychotics Negative symptoms of schizophrenia - ANS ✓Flat affect, alogia, affective blunting, asociality, anhedonia, avolition. Where do negative symptoms originate? - ANS ✓Mesocortical dopamine pathway. May also involve mesolimbic regions such as nucleus accumbens Medications to treat negative symptoms - ANS ✓Vraylar, amisulpride
Hypotheses of Schizophrenia - ANS ✓-Mesolimbic pathway is hypothesized to be hyperactive resulting in excess dopamine at the synapse.