Posted: February 25th, 2021
Respond to at least two of your colleagues by comparing the differential diagnostic features of the disorder you were assigned to the diagnostic features of the disorder your colleagues were assigned.
Support your responses with evidence-based literature with at least two references in each colleague’s response with proper citation in APA Format.
Colleagues Respond # 1
Criteria for Alzheimer’s Disease
Alzheimer’s disease is a slowly progressing disorder where the individual may be asymptomatic for many years in preclinical phase, followed by a period called mild cognitive impairment without functional deficit, and finally leading to dementia or neurocognitive syndrome with cognitive deficits, functional decline with neuropsychiatric symptoms (Gabbard 2014).
According to American psychiatric association (2013), neurocognitive disorders can be either major or mild neurocognitive disorder. To diagnose Alzheimer’s disease, the DSM-5 has given criteria as follows.
Major neurocognitive disorder due to Alzheimer’s disease are diagnosed either as probable and possible Alzheimer’s disease (American psychiatric association 2013). Probable Alzheimer’s disease is diagnosed if either of the following are present otherwise, possible Alzheimer’s disease is diagnosed.
1.Evidence of a causative Alzheimer’s disease genetic mutation from family history or genetic testing
2. All three of the following such as a) Clear evidence of decline in memory and learning and at least one other cognitive domain based on detailed history or serial neuropsychological testing, b) Steadily progressive, gradual decline in cognition, without extended plateaus, c) No evidence of mixed etiology such as absence of other neurodegenerative or cerebrovascular disease, or another neurological, mental, or systemic disease or condition likely contributing to cognitive decline
Mild neuro cognitive disorder due to Alzheimer’s disease can be either Probable or possible Alzheimer’s disease (American Psychiatric association 2013).
Probable Alzheimer’s disease is diagnosed if there is evidence of a causative Alzheimer’s disease genetic mutation from either genetic testing or family history. Possible Alzheimer’s disease is diagnosed if there is no evidence of a causative Alzheimer’s disease genetic mutation from either genetic testing or family history, and all three of the following are present such as a) clear evidence of decline in memory and learning, b) steadily progressive, gradual decline in cognition, without extended plateaus, no evidence of mixed etiology such as absence of other condition likely contributing to cognitive decline. c) The disturbance is not better explained by cerebrovascular disease, another neurodegenerative disease, the effects of a substance, or another mental, neurological, or systemic disorder.
It is important to minimize or eliminate medications that impair cognition such as anticholinergics, opioid analgesics and benzodiazepines before starting pharmacological treatment for Alzheimer’s disease (AD) (Gabbard 2014). The general treatment for AD are anticholinesterase inhibitors (AChEI) and Memantine (Gabbard 2014). Acetylcholinesterase inhibitors reversibly inhibit the activity of acetylcholinesterase, the enzyme responsible for synaptic metabolism of acetylcholine; their administration thereby increases levels of synaptic acetylcholine (Gabbard 2014). The usual AChEI are Donepezil, Galantamine, and Rivastigmine. Donepezil is an oral dissolving tablet and once daily dosing (Gabbard 2014). It is used in mild, moderate and severe AD and it may take up to 6 weeks to have baseline memory improvement (Stahl 2014). The initial dose is 5 mg /day and can reach a target dose of 10 mg /day (Gabbard 2014). Galantamine is a AChEI and allosteric nicotinic receptor modulator and is used in mild to moderate AD (Stahl 2014). The initial dose is 4 mg /Bid for immediate release and 8 mg/day for the extended release with a target dose of 8-12 mg Bid for immediate release and 16-24 mg/day for extended release (Gabbard 2014). It may take up to 6 weeks for improvement in any baseline memory (Stahl 2014). It has reported side effects of bradycardia. Rivastigmine is a AChEI and butyryl cholinesterase (BuChEI) with an initial dose of 1.5 mg Bid (Oral) or 4.6 mg/day transdermal to reach a target dose of 3-6 mg bid oral or 9.6 mg /day transdermal (Gabbard 2014). It is used in mild to moderate AD and may take up to 6 weeks for improvement in mild to moderate memory (Stahl 2014). The transdermal administration decreases GI side effects (Gabbard 2014).
Another medication used to treat AD is Memantine which is a NMDA receptor antagonist. It interferes with postulated persistent activation of NMDA receptors by excessive glutamate release in AD (Stahl 2014). The dosage is 5mg /day (initial) and 10 mg Bid (Gabbard 2014). Memory improvement is not expected with the treatment and takes many months in for stabilization of degenerative course (Stahl 2014). Decreased creatinine clearance is a side effect and dose adjustment is required if it occurs (Gabbard 2014).
A research study by Forstmeier et al. (2015) has concluded that cognitive behavior therapy has shown benefit to both the individual with Alzheimer’s disease having neuropsychiatric symptoms and to the care giver where it helps reduce the use of medication and delayed nursing home placement. insight oriented therapy and less verbal therapies such as music therapy and art therapy can be helpful in alleviating negative emotions and minimizing problematic behaviors (Betty 1994)
Supportive treatment such as education, counseling about diagnosis and prognosis, comfort, and emotional support including instructions on safe and effective caregiving, problem solving, and crisis intervention are important for patients and caregivers (Gabbard 2014). It is also important to consider safety concerns, including driving (and its eventual restriction), living independently, medication administration, and fall risks (Gabbard 2014). They can be helped with a safe predictable place to live with support for activities of daily living, assistance with managing medical comorbidities, and assistance with advanced planning and end-of-life decisions (Gabbard 2014)
Benefits and Risks of Neurocognitive Therapies
The treatments for Alzheimer’s disease are anticholinesterase inhibiters and memantine. These medications are not expected to cure the disease but the beneficial part of the treatment is that it helps delay the progression of neurocognitive and physical decline. There are some side effects for Donepezil (which is a acetylcholinesterase inhibitor ) such as atrioventricular block, decreased appetite, diarrhea, dizziness, headache, hypertension, nausea, syncope, torsades de pointes, vomiting, weight loss are the major side effects (Boice, Dunay, Epperly 2017). Galantamine has additional side effects such as nausea, vomiting and weight loss and Rivastigmine side effects are Abdominal pain, atrial fibrillation, atrioventricular block, decreased appetite, diarrhea, dizziness, headache, myocardial infarction, nausea, vomiting (Boice, Dunay, Epperly 2017). The side effects of Memantine are confusion, constipation, diarrhea, dizziness, vomiting; rarely, cerebrovascular event or acute kidney injury (Boice, Dunay, Epperly 2017
Differential Diagnostic Features of Alzheimer’s Disease
Almost 80% of dementia in older people are related to Alzheimer’s disease, however the diagnosis can be difficult where the patients may exhibit similar pathologies and symptoms (Alzheimer’s association n. d). Based on the major clinical differences between major dementias, a correct diagnosis can be made. The common dementias with similar symptoms are Frontotemporal dementia, Levy body disease, vascular dementia, Creutzfeldt-Jakob Disease and Alzheimer’s disease (Alzheimer’s association n. d). Vascular dementia is related to cerebral vascular disease and are seen in patients with preexisting hypertension or other cardiovascular risk factors (Ruiz, Sadock & Sadock 2014). Frontotemporal dementia is characterized by preponderance of atrophy in the frontotemporal regions (Ruiz et al., 2014). In Levy body disease the patients often have cap grass syndrome in addition to hallucination and parkinsonian features (Ruiz et al., 2014).
Colleagues Respond # 2
Diagnosis of Dementia
Dementia is a general term used for loss of problem-solving, language, memory, and other thinking capabilities, which are severe and have the intensity to affect an individual’s daily life. The most common cause of dementia is Alzheimer’s (Mosk et al., 2017). It can be challenging diagnosing dementia. Individuals with this condition have a cognitive impairment, and they have lost the ability to attend to their daily duties such as driving safely, paying bills, and their medications. During the diagnosis, the doctor must recognize the oaters for the loss of functions and skills and determine what the person can do at that moment. Recently there has been a more accurate diagnosis from the biomarkers of Alzheimer’s disease. The doctors do cognitive and neuropsychological tests to evaluate the patient’s thinking. Several tests involve measuring thinking skills, language skills, judgments, reasoning, orientation, and attention. Neurological evaluation is where the doctor will evaluate attention, visual perception, memory, language, senses, and movements, balance, problem-solving, and reflexes, among other areas. Brain scans include CT or MRI, which checks the evidence of bleeding, tumor or stroke, or hydrocephalus. PET scans checks on the patterns of the brain. Laboratory tests include blood samples to determine the physical problems that can affect the brain functioning, such as deficiency of vitamin B-12 or thyroid gland underactive.
Treatment of Dementia
Psychopharmacologic treatment includes the use of the following: cholinesterase inhibitors, which include galantamine (Razadyne), donepezil (Aricept), and rivastigmine (Exelon) which works by boosting the levels of chemical messenger which are involved in judgment and memory. They are used to treat Alzheimer’s disease in the primary case. Doctors might be prescribed these drugs to other dementias, including Lewy body dementia, Parkinson’s disease dementia, and vascular dementia. There are side effects of these drugs that include diarrhea, vomiting, and nausea. Memantine (Namenda) regulates the activity of glutamate, which is a chemical messenger involved in brain functions such as memory and learning. This can also be prescribed with a cholinesterase inhibitor and had dizziness as one of the most common side effects. Psychotherapy includes occupational therapy, which teaches one coping behaviors and ensures that one is home safer. This prevents accidents and manages behaviors as well as preparing one for the dementia progression. Modifying the environment is another psychotherapy that reduces noise and clutter, making it easier for dementia to function and focus (Carrion et al., 2018). This involves hiding objects that threaten the safety and monitoring system, alerting when a person with dementia wanders. Simplifying tasks will break tasks into smaller portions and hence make one focus on success and not a failure. Routine and structure also help to reduce confusion among people with dementia.
Research has identified several risks involved in the treatment of patients with dementia. Many of the patients have been prescribed some medications which act on the nervous system and the brain, but they are not meant to treat dementia. These kinds of interventions have special risks for older people (Gnjidic et al., 2018). These drugs have been linked with worse cognitive symptoms in older adults. Depressants do not treat dementia, but most doctors prescribe these drugs nearly triple to the older adults. These have negative impacts and mild side effects on the patients.
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