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Nr 546 Final Exam Study guide, Study Guides, Projects, Research of Nursing

Harvard UniversityNursing

Nr 546 Final Exam Study guideNr 546 Final Exam Study guide

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Nr 546 Final Exam Study guide
Finale
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
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Nr 546 Final Exam Study guide

Finale 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?

  • Paroxetine is contraindicated in pregnancy due to the risk of congenital defects, including atrial septal defects.

Breast Feeding

  • Infant irritability should be monitored when SNRIs are prescribed. Older Adult
  • Older adults may not respond to antidepressants as robustly as younger people if the first episode of depression occurs after age 65.
  • Citalopram and escitalopram should be dosed at 1/2 dose due to the risk of QTc prolongation.
  • 2019 American Geriatric Society (AGS) Beers Criteria include the following recommendations:
  • Avoid paroxetine in clients with a history of falls/fractures.
  • Avoid tricyclic antidepressants prescribed with other central nervous system (CNS) depressants. Children
  • Antidepressants increase the risk of death by suicide in children and adults younger than 25.
  • Mood-stabilizing drugs require baseline and routine laboratory monitoring to help determine medical appropriateness for the initiation of therapy and monitoring of adverse effects.
  • Pre-conception and contraceptive counseling should be provided for women of childbearing age. Risk-benefit ratio should be discussed. If a woman is desiring future pregnancy select medications that are not contraindicated in pregnancy.
  • The Federal Drug Administration (FDA) requires the product labeling for all antidepressants to contain language about the potential risk of inducing a mood switch to mania.
  • Lurasidone (Latuda) should be taken with food, at least 350 calories, for maximum absorption.
  • Lithium carbonate (Lithobid) starting dose is reduced by at least 50% in clients with renal impairment.
  • Lithium levels can be increased by nonsteroidal anti- inflammatory drugs (NSAIDs) and angiotensin-converting enzyme (ACE) inhibitors and decreased by caffeine and mania. Pregnancy
  • Lithium, valproic acid, and carbamazepine are teratogenic and are contraindicated during pregnancy.
  • Lurasidone has been used in pregnancy without teratogenic effects. Breast Feeding
  • Avoid breastfeeding for clients prescribed carbamazepine, lithium, and lamotrigine. Older Adult Use caution. Reduced renal and hepatic function may impact metabolism and elimination. Reduce dose as necessary. 2019 American Geriatric Society (AGS) Beers Criteria include the following recommendations :
  • 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

your medication table. Which medications are

appropriate for sleep onset and which are more

appropriate for waking during the night????????

Week 7 Phasic firing is hypothetically associated with reward, feelings of euphoria, and abuse potential. Immediate-release stimulants rapidly increase DA and NE, especially increasing phasic firing, not tonic firing. Therefore, immediate- release stimulants have a higher risk of abuse. Extended-release formulations of stimulants lead to a gradual and sustained increase in NE and DA, enhancing tonic firing, which is hypothetically linked to the therapeutic effects of stimulants. They are amplifying tonic NE and DA signals, which are thought to be low in ADHD. The extended-release formulations occupy the NE transporter in the prefrontal cortex with slow enough onset and for long enough to enhance tonic NE and DA signaling; however, they do not block DA transporters fast or long enough in the nucleus accumbens to increase phasic signaling, thus reducing abuse potential. The prefrontal cortex lacks high concentrations of dopamine transporters (DAT), so in this brain region, DA gets inactivated by norepinephrine transporters (NET). Therefore, inhibiting NET in the prefrontal cortex increases both DA and NE. As only a few NET exist in the nucleus accumbens, atomoxetine does not induce an increase in DA and NE in the nucleus accumbens, the reward center of the brain, thus atomoxetine does not have abuse potential. In the nucleus accumbens, there are only a few NE neurons and NE transporters. Inhibiting NET in the nucleus accumbens will not lead to an increase in NE or DA. Atomoxetine does not modulate serotonin levels. The striatum and the anterior cingulate cortex are not brain areas involved in reward. Center in the brain that tells you to go to sleep VLPO (Ventrolateral preoptic area) -tells the 7 wakefulness areas of the brain to "shut off" excitatory neurotransmitters that stimulate wakefulness: acetylcholine norepinephri ne histamine serotonin orexin dopamine sleep-promoting neurotransmitters: Gamma aminobutyric acid (GABA) melatonin Sleep Medications -Over-the-Counter Sleep Aids

  • antihistamines such as diphenhydramine (Benadryl)
  • Valerian root -Melatonin Agonist Medications -ramelteon (Rozerem)
  • prescription melatonin -Orexin Receptor Antagonists

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

adverse effects.

  • 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
  • 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.