NURS 660 [STUDY GUIDE] LATEST UPDATE 2024 QUESTIONS AND EXPLAINED ANSWERS

NURS 660 [STUDY GUIDE] LATEST UPDATE 2024 QUESTIONS AND EXPLAINED ANSWERS 1. Identify the emerging neurobiological hypothesis of schizophrenia. o The hypothesis: (focus on the most detail with the Dopamine Theory) ...

NURS 660 [STUDY GUIDE] LATEST UPDATE 2024 QUESTIONS AND EXPLAINED ANSWERS 1. Identify the emerging neurobiological hypothesis of schizophrenia. o The hypothesis: (focus on the most detail with the Dopamine Theory) ❖ The only pharmacological treatment that we have are dopamine (D2 receptors) and serotonin (5HT2A) ❖ Dopamine Theory ▪ Hyperactive dopamine at D2 receptors in the mesolimbic pathway In the mesolimbic pathway is responsible for the positive symptoms; the hypoactivity is responsible for the negative ▪ Mesolimbic pathway it’s overactive dopamine receptors or overactive dopamine on the dopamine receptors in mesolimbic pathways but it is also hypoactive dopamine at the D2 receptors in the mesocortical pathway ▪ Most detailed knowledge about this theory because that has been our foundational understanding of schizophrenia up until the very recent past so the other two, we don’t have as much detail about. But the other two just give us a much fuller understanding as far as why the Dopamine Theory happened in the first place. ❖ Glutamate Theory ▪ Hypoactive dopamine at N-Methyl-D-Asperate (NMDA) receptor ▪ NMDA receptors are hypofunctioning and because of that, it leads to hyperactive dopamine in the mesolimbic pathway and hypoactive dopamine in the mesocortical pathway. ▪ The NMDA receptor is on the GABA interneurons ▪ Emerging one ❖ Serotonin Theory ▪ Hyperactive dopamine at the 5HT2A receptors in the mesocortical pathway 5HT2A receptors are overly active In the mesocortical pathway is responsible for the negative symptoms ▪ 5HT2A receptors are hyperfunctioning, which leads to over functioning or overactive dopamine on those receptors in them as a mesolimbic pathway and hypoactive dopamine receptors in that mesocortical pathway o Positive symptoms ❖ Delusions, Hallucinations o Negative symptoms ❖ Apathy, Anhedonia, Cognitive Blunting, Neuroleptic dysphoria 2. Identify the different dopamine pathways and what role each pathway plays in relation to schizophrenia/psychosis and treatment. o Dopamine Pathways – 2 pathways are related to pathophysiology (nigrostriatal & tuberoinfundibular) and 2 pathways are responsible for signs & symptoms of schizophrenia (mesolimbic & mesocortical) ❖ Mesolimbic ❖ Mesocortical ❖ Nigrostriatal ❖ Tuberoinfundibular o 2 are responsible for the symptoms, the signs & symptoms of schizophrenia (positive/negative signs) ❖ Mesolimbic & Mesocortical ▪ How are the positive/negative manifesting in the mesolimbic area and mesocortical area? What dopamine is doing, and what’s the difference? Mesolimbic Pathway ➢ Hyperactive ➢ Looney pathway, where too much dopamine is happening ➢ The way the medications will work is by blocking the dopamine, can’t get so excessive ➢ You can think of L as lunacy/looney because that is where the positive symptoms are. The positive symptoms are if you saw that individual in the street, you would think they are positively insane because they might be hearing voices, talking to themselves, or responding to internal stimuli. ➢ Negative symptoms are harder to catch because the person is more withdrawn, not social, they tend to not have a lot of emotional expressions ❖ Mesocortical Pathway ▪ Hypoactive ▪ What is dopamine doing in that pathway as far as negative symptoms? Too little Blocking dopamine will make a bad situation worse like anhedonia o These drugs we have currently, do a really good job in reducing the positive symptoms but because these drugs do not have selectivity for just the one pathway that is involved in the positive symptoms, they tend to make the bad situation being too little dopamine on that cortical pathway even worse. Thus far there is not a specific agent that treats the negative symptoms. The newer meds have a tendency not to make the problem worse but do not fix the problem either. o The other 2, what is involved in collateral damage of the treatment that we administer for schizophrenia ❖ Nigrostriatal Pathway ❖ Tuberoinfundibular Pathway ❖ What happens to the nigrostriatal pathway and the tuberoinfundibular pathway when we are treating schizophrenia? Under normal circumstances individuals with schizophrenia there is nothing wrong with schizophrenia. When we throw our treatments at them, is when we cause problems. What kinds of problems happen we have when we block dopamine in those pathways? ▪ Nigrostriatal Has to do with extrapyramidal systems like motor function, Parkinsonian type activity like rigidity and tremors Too little dopamine causes movement disorders like Parkinson’s disease, akathisia, and dystonia Too much dopamine causes hyperkinetic movementdisorders like chorea, dyskinesias, and tics Chronic blockade of D2 receptors can lead to tardivedyskinesia ▪ Tuberoinfundibular When dopamine is blocked, prolactin levels rise Increased prolactin level (hyperprolactinemia) ➢ Gynecomastia – breast enlargement of breast development ➢ Amenorrhea – loss of menstrual periods ➢ Galactorrhea – breast secretions o Tip to help remember: ❖ Nigrostriatal – think “stride” because this area impacts movement. When we don’t move, we get stiff and sluggish. Decreased dopamine in this area causes Parkinsonism. ❖ Mesolimbic – think four limbs like a plus sign. Too much dopamine in this area causes positive symptoms. ❖ Mesocortical – think about the core of who you are (emotions). Decreased dopamine in this area causes depression (and negative symptoms) ❖ Tuberoinfundibular – think about infants depending on lactation. Blocked dopamine causes too much prolactin. 3. Know the major neurotransmitters and their roles related to schizophrenia. o Dopamine D2 ❖ Possible benefits – reduced positive symptoms ❖ Possible side effects – EPS including Parkinsonism, akathisia, tardive dyskinesia, endocrine effects such as prolactin secretion, menstrual changes, sexual dysfunction ❖ Inhibitory – normally blocks motor movement o Dopamine D1 ❖ Excitatory – stimulates movement o Serotonin 5HT2A ❖ Possible benefits – reduced EPS (?) ❖ Possible side effects – sexual dysfunction o Serotonin 5HT2c ❖ Possible benefits - unknown ❖ Possible side effects – weight gain o Histamine H1 ❖ Possible benefits - sedation ❖ Possible side effects – sedation, increased appetite, weight gain, hypotension o Muscarinic cholinergic ❖ Possible benefits – reduced EPS ❖ Possible side effects – autonomic side effects such as blurred vision, dry mouth, constipation, urinary retention, tachycardia, memory dysfunction o Alpha 1 adrenergic ❖ Possible benefits - unknown ❖ Possible side effects – orthostatic hypotension, dizziness, reflex tachycardia o Alpha2 adrenergic ❖ Possible benefits - unknown ❖ Possible side effects – drug interactions 4. Identify potential medical emergencies associated with antipsychotic medications and how to manage these emergencies. o The 2 major medical emergencies that is encountered in psychiatry ❖ Neuroleptic Malignant Syndrome (NMS) ▪ Medical emergency needs to be managed in the hospital. Do not manage in an outpatient setting! Provide supportive care, reduce fever (cooling blankets), correct dehydration (IVF), correct electrolyte imbalances, maintain cardiorespiratory stability Stop antipsychotic agent IV benzodiazepine (like Lorazepam or Diazepam) IV Dantrolene (skeletal muscle relaxant) Bromocriptine (dopamine agonist) Amantadine (dopamine agonist with anticholinergic effects ▪ Understand NMS is NOT the same as like an overdose situation, it not like antipsychotic toxicity! ❖ Serotonin Syndrome ▪ Serotonin toxicity ▪ Supportive care ▪ No antidote