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NR 546 FINAL EXAM STUDY GUIDE 2023-2024 WITH 100% VERIFIED SOLUTIONS, Exams of Nursing

NR 546 FINAL EXAM STUDY GUIDE 2023-2024 WITH 100% VERIFIED SOLUTIONS NR 546 FINAL EXAM STUDY GUIDE 2023-2024 WITH 100% VERIFIED SOLUTIONS NR 546 FINAL EXAM STUDY GUIDE 2023-2024 WITH 100% VERIFIED SOLUTIONS

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2023/2024

Available from 08/30/2024

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Download NR 546 FINAL EXAM STUDY GUIDE 2023-2024 WITH 100% VERIFIED SOLUTIONS and more Exams Nursing in PDF only on Docsity! NR 546 FINAL EXAM STUDY GUIDE 2023-2024 WITH 100% VERIFIED SOLUTIONS MDD-- Monoamine hypothesis of depression, prescribing considerations- the theory is that depression is caused by a deficiency in monoamine neurotransmission. And mania is the opposite - due to an excess of monoamine neurotransmission. This hasn't really been proven yet, so then the focus shifted to the monoamine receptor hypothesis - that the abnormality of receptors for monoamine NTs cause depression. In that case, the lack of NT causes upregulation of receptors. Also not proven yet. Right now the focus is on regulation of gene expression, growth factors, environmental factors, and epigenetic changes. Prescribing considerations - do not give antidepressants as monotherapy for bipolar - always combine with mood stabilizer. Must rule out mania or hypomania so don't confuse MDD with BPD and induce mania. Monitor infant irritability when prescribe SNRI for breastfeeding. Also keep in mind: client preference, prior treatment response, anticipated adverse effects, comorbidities, half life and interactions (if they will forget to take med, choose something longer acting), cost. Start patient on drug for 4-8 weeks, on lowest recommended dose. If doesn't work, first increase dose, then switch to diff drug in same class and give adequate trial of high enough dose, then switch to a drug in a different class, then add a second med. For older people - citalopram and escitalopram should be ½ dose, avoid paroxetine if have history of falls, avoid TCAs prescribed with out CNS depressants. SSRIs what screens should be completed prior to prescribing a SSRI? - for SNRIs need to check BP before and during treatment. Which age group is most at risk when prescribed a SSRI? Why? Kids and adults under 25 - increased risk of suicide Which SSRI has the least CYP interactions - escitalopram (Lexapro). Good for forgetful people - fluoxetine (has 2-3 day half life). Also sertraline (27-36 hour ½ life). Longest acting fluoxetine has the longest half life 1-2 weeks. When adding or switching antidepressants use caution for 5 weeks after stopping fluoxetine More likely to cause discontinuation syndrome. - paroxetine Safe in nursing and pregnancy and breastfeeding sertraline Contraindicated in pregnancy paroxetine (risk of atrial septal defect). Which medications are used as adjuncts? Buproprion, Lowest risk of sexual side effects buproprion, mirtazapine What is serotonin syndrome When use two serotonergic drugs together. Symptoms: mental status changes (agitation, hallucinations, delirium, coma), autonomic instability (tachycardia, dizziness, diaphoresis, hyperthermia), neuromuscular symptoms (tremor, rigidity, myoclonus, hyperreflexia, incoordination), seizures, and/or gastrointestinal symptoms (nausea, vomiting, diarrhea). Treatment - stop med, supportive care, benzos. MAOIs black box warning Suicidal ideation in children, adolescents and young adults MAOI half life 2-4 hours SSRIs black box warning suicidal tendencies MAOIs (monoamine oxidase inhibitors) Antidepresents durgs that inhibit the enzyme that deatctiviates dopamine, norepiniphrine, and serotonin. MAOIs appear to be most effective for treating non-endogenous and atypical depressions. Side-effects include anticholnergic effects, insomnia, agitation, confusion, and wieght gain. when taken in conjuction with other drugs or foods containing tyramine, they can cause a hypertensive crisis. • Lithium levels can be increased by nonsteroidal anti- inflammatory drugs (NSAIDs) and angiotensin-converting enzyme (ACE) inhibitors and decreased by caffeine and mania. Role of L-Methylfolate in depression treatment is necessary for the synthesis of monoamines. We generally get l-methylfolate from dietary folic acid, but about 50% of people are deficient. There are small studies that say that supplementing l-methylfolate or regular OTC folate may help as adjunctive treatment of depression. Recommended to try the OTC folate first. Role of L-Methylfolate in depression tx Suboptimal folate levels in depressed patients (adjunct to antidepressant) • L-Methylfolate is a bioavailable form of folate • L-methylfolate, or 6-(S)-5-methyl-tetrahydrofolate, is derived from folate and is the form that enters the brain and works directly as a methyl donor and monoamine synthesis modulator Why is L-Methylfolate recommended as an adjunct in depression? Treatment with l-methylfolate seems to be safe, has few if any side effects, and is generally less expensive than augmenting with a second branded antidepressant or atypical antipsychotic Pregnancy • Paroxetine is contraindicated in pregnancy due to the risk of congenital defects, including atrial septal defects. • blue lips Pregnancy • Buprenorphine is an acceptable treatment during pregnancy; however, there is an increased risk of a neonatal withdrawal syndrome in newborns. • Suboxone (buprenorphine/naloxone) cannot be used in pregnancy. • Naloxone increases the risk of neonatal abstinence syndrome. Pregnant clients must be switched to buprenorphine (Subutex) monotherapy. • Methadone is approved in pregnancy for heroin-addicted women. Dosing requires adjustment. • Short-term newborn withdrawal effects may be seen and may require neonatal intensive care unit (NICU) admission for treatment. Breast Feeding • Naltrexone and buprenorphine are not recommended for breastfeeding mothers. • Methadone can be prescribed with special consideration given to feeding intervals (breastfeed prior to or 2-6 hours after dose). Older Adult • Buprenorphine use in the elderly may lead to confusion and drowsiness. • Methadone has a high potential for drug interactions, associated with QT prolongation. • It is difficult to titrate in the elderly and has a risk for accumulation due to the long half-life. Alcohol withdrawal Mild • Anxiety • Irritability • Headache • Insomnia • Tremors • Nausea/vomiting Moderate • Increased blood pressure (BP) • Increased heart rate (HR) • Confusion • Mild hyperthermia • Rapid breathing Severe • Hallucinations • Seizures • Disorientation • Impaired attention • Delirium tremens • Death The use of benzodiazepines on a symptom-triggered regimen is the preferred approach. Symptom-triggered therapy is derived from objectively measured symptoms on the CIWA-Ar standardized instrument as seen below. Administer CIWA-Ar • every 4-8 hours until score is lower than 8-10 for 24 hours Symptom-Triggered Regimen • Administer benzodiazepine when CIWA-Ar score is 8 or above. • PO lorazepam (Ativan), diazepam (Valium), or chlordiazepoxide (Librium) for symptom-triggered therapy • Reassess CIWA-Ar every hour. Benzodiazepines are the first-line treatment for clients having psychomotor agitation associated with alcohol withdrawal. This client has an increased risk of an alcohol- related withdrawal seizure, especially since he had one in the past. carbamazepine, levetiracetam, and phenytoin are not routinely used for alcohol withdrawal due to the lack of evidence demonstrating increased efficacy. Additionally, these drugs may potentially mask hemodynamic signs of withdrawal. Narcan is the common initial treatment for alcohol use disorder. Can be initiated while the client is still drinking. Can also be utilized in those with opioid use disorder, as the drug can treat both conditions. However, the client should be opioid-free for at least 7- 10 days to avoid withdrawal. Acamprosate is used in the treatment of alcohol use disorders but does not have a similar effect to opiates. Disulfiram is utilized for resistant treatment, but this medication should not be administered to clients until they have abstained from alcohol for at least 12 hours, as a disulfiram reaction can occur for up to 14 days after alcohol has been consumed. Diazepam is not indicated at this time, given this client has already gone through acute withdrawal. Pregnancy • Teratogenic effects of alcohol on the developing fetus are well known; however, there is limited data on the safety of withdrawal medications in pregnancy. • Naltrexone is commonly used to treat alcohol use disorder in pregnant women, but its effects on the fetus remain largely unknown. • Acamprosate is not recommended in pregnancy but may be necessary if the mother cannot stop drinking alcohol. • Disulfiram's safety in pregnancy is not established. Older Adult • Frequent monitoring is necessary when prescribing benzodiazepines for alcohol withdrawal in older adults. Acamprosate should be used with caution in older adults. ????Sleep- know the indications for the medications on your medication table. Which medications are appropriate for sleep onset and which are more appropriate for waking during the night???????? •Suvorexant (Belsomra) •Lemborexant (Dayvigo) -Sedating Antidepressants •trazodone (Desyrel) •amitriptyline (Elavil) •mirtazapine (Remeron) -Z-drugs (Sedative/hypnotic drugs) First-line agents for insomnia include: •zolpidem (Ambien) •zaleplon (Sonata) •eszopiclone (Lunesta) •PEARLS: potential for abuse/dependence, Drugs may increase suicidal ideations, Abrupt discontinuation can result in rebound insomnia and withdrawal symptoms -Benzodiazepines (BZOs) •not considered a first-line treatment due to the potential for misuse •when first-line agents fail, benzodiazepines may be used with caution for insomnia orexin (hypocretin) neurotransmitter that increases wakefulness and arousal Sleep meds Lifespan Considerations: Pregnancy -Consider the risk-ben A common cause of insomnia is restless legs syndrome (RLS) restless legs syndrome (RLS) typically occurs in the evening or at night -causes uncomfortable uncontrollable urge to move the legs. -may be idiopathic or associated with other conditions such as pregnancy, end-stage renal disease, fibromyalgia, iron deficiency, arthritis, or peripheral neuropathy -Tx: •Dopamine agonists : pramipexole (Mirapex), ropinirole (Requip) •Iron •Gabapentin/ pregabalin for severe or painful RLS Rationale: Ropinirole is a first-line agent for RLS. Iron is not appropriate in a client unless serum ferritin indicates deficiency. Gabapentin is appropriate for RLS but is a second-line medication. Diazepam is not appropriate for this client. Week 8 Genetics The etiology of AD is not fully understood. The development of AD involves a combination of genetic and environmental factors. Genes appear to play a strong role, with late-onset AD showing heritability of 58–79% and early- onset AD showing over 90% (Sims et al., 2020). Neurons in the brains of clients who develop AD may also have genetic coding abnormalities associated with amyloid precursor protein, while mutations of at least three different chromosomes, 21, 14, and 1, are associated with early-onset AD (Stahl, 2021). Neuroanatomy Two hallmarks of AD are amyloid plaques and neurofibrillary tangles. Toxic amyloid plaques are believed to form in the brain of clients with AD due to the abnormal processing of amyloid precursor protein. AD may involve the formation of too many Aβ amyloid-forming peptides or not enough removal of them (Stahl, 2021). Amyloid plaques and neurofibrillary tangles impair the function of neurons, causing them to lose connections with other brain cells and die. Cell death leads to the atrophy of brain tissue, which affects the areas responsible for memory and higher-level thinking, such as the hippocampus and cerebral cortex. Atrophy also leads to enlarged ventricles. Explore the brain changes in AD in 3DLinks to an external site. . Neural Networks In addition to the development of amyloid plaques and neurofibrillary tangles, multiple cellular changes are associated with AD, including damage to synapses, mitochondrial abnormalities, and inflammatory processes. These changes are associated with neurotransmitter failure and neuronal death. Neural Signaling Acetylcholine (ACh) is a neurotransmitter necessary for processing memory and learning. AD leads to decreased acetylcholinesterase activity and a permanent loss of cholinergic neurons. Decreased cholinergic function is linked to memory dysfunction, particularly short-term memory (Stahl, 2021). Neuronal damage may also occur due to abnormal activation of N- methyl-d-aspartate (NMDA) receptors by glutamate (Liu et al., 2019). Progression of AD Early (1-3 years) • short term memory deficits • disoriented to date • diminished recall of recent events • mild language and decision-making deficits • mild problem copying figures (clock drawing) • social withdrawal • mood change • personality changes • problems with managing finances. anxiety, irritability, and sleep disruption Middle (2-8 years) • disoriented to date and place • may get lost in familiar places • impaired learning new skills • agitation, aggression, restlessness, or anxiety • difficulty with activities of daily living (ADLs) such as cooking and grooming Late (6-12 years) • disoriented to person, time, or place • non-verbal • long term memory diminished • unable to groom or dress • progress to need for total care at end stage • When donepezil (Aricept) is added to CYP2D6 or CYP3A4, there is a possibility of peripheral side effects, and inducers of CYP2D6 and CYP3A4 may increase the rate of elimination (Chisholm-Burns, et al., 2019). Rivastigmine (exelon) Mechanism of Action • rivastigmine (Exelon) acts centrally for both acetylcholinesterase and butyrylcholinesterase, thereby potentially increasing its efficacy. Common Side Effects • gastrointestinal symptoms (anorexia, nausea, vomiting, or diarrhea) • weakness • dizziness • tremor Precautions • asthma or chronic obstructive pulmonary disorder (COPD) • sick sinus syndrome • gastrointestinal (GI) Bleeding • weight < 50 kg Prescribing Pearls • rivastigmine (Exelon) is administered orally or topically (transdermal patch). • The transdermal patch is used for dementia associated with Parkinson's disease. • Medications that induce or inhibit CYP450 metabolism will not modify rivastigmine (Exelon) metabolism (Chisholm- Burns, et al., 2019). Galantamine (razadyne) Mechanism of Action galantamine (Razadyne, Razadyne ER) acts by elevating acetylcholine (Ach) in the cerebral cortex, modulating the nicotinic Ach receptors to increase Ach release from existing presynaptic nerve terminals. It also increases glutamate and serotonin levels; however, the benefits of this action are unknown (Chisholm-Burns, et al., 2019). Common Side Effects • gastrointestinal symptoms (nausea, vomiting, diarrhea, anorexia, and weight loss) • headache • dizziness • fatigue Precautions • nonsteroidal anti-inflammatory drug (NSAID) use • GI bleed • asthma or COPD • concurrent use with medications that slow or decrease heart rate Contraindications • severe hepatic impairment • severe renal impairment Prescribing Pearls • There are two major metabolizing enzymes CYP3A4 and CYP2D6 that increase galantamine (Razadyne, Razadyne ER) concentrations or reductions in clearance and anticholinergic side effects when given concurrently with inhibitors of these enzymes (Chisholm- Burns, et al., 2019). *Memantine is the only NMDA approved to manage moderate to severe AD. Based on clinical trials, improvement is modest (Chisholm-Burns, et al., 2019). Click the section below to learn more about NMDA receptor antagonists. Mechanism of Action This drug prevents glutamate, an excitatory neurotransmitter, from binding at the receptor site. NMDA receptors control activity throughout the brain by regulating how much calcium enters the nerve cell. An overproduction of the NMDA receptor and excess glutamate can lead to excessive calcium entering the cell and disrupting information processing. Blocking NMDA receptors protects neurons from the effects of too much glutamate without affecting normal neurotransmission (Chisholm-Burns, et al., 2019). Common Side Effects • gastrointestinal symptoms (constipation, diarrhea, and weight gain) • urinary frequency • confusion • dizziness • headache • cough Precautions • concurrent use with (amantadine, rimantadine, ketamine, or dextromethorphan) • severe hepatic impairment • severe renal impairment • medications or conditions that increase the pH of the urine Prescribing Pearls • This is used as monotherapy or in conjunction with ChEIs; when given with ChEIs, fall precautions are required and driving is forbidden due to delayed reactions. • Minimal inhibition of CYP450 enzymes CYP1A2, CYP2A6, CYP2C9, CYP2D6, CYP2E1, and CYP3A4 occurs, which means there are no pharmacokinetic interactions with medications metabolized by these enzymes (Chisholm-Burns et al., 2019). PrescribingPearls • Memantine is associated with an increased life expectancy when compared to donepezil. • If treatment failure occurs, 50% of individuals respond to a different agent. • Educate clients and families that medications cannot halt or reverse the progression of Alzheimer's disease. • donepezil at a higher dose has a higher incidence of adverse effects without increased cognitive benefit. • rivastigmine (Exelon) is available in oral form or transdermal patch. • The transdermal patch is used for dementia associated with Parkinson's disease. Medications that induce or inhibit CYP450 metabolism will not modify rivastigmine metabolism (Chisholm-Burns et al., 2019). Antipsychotics are not recommended for the treatment of dementia- related to agitation and behavioral symptoms (Stahl, 2021). * Cholinesterase inhibitors are not recommended in pregnancy and lactation. * Researchers are investigating whether consistent and measurable changes in blood levels of specific markers may be reliably associated with Alzheimer's related changes. These markers may include tau, beta-amyloid or other biomarkers the could be measured before and after symptoms appear.