BACKGROUND
Mr. Akkad is a 76 year old Iranian male who is brought to your office by his eldest son for “strange behavior.” Mr. Akkad was seen by his family physician who ruled out any organic basis for Mr. Akkad’s behavior. All laboratory and diagnostic imaging tests (including CT-scan of the head) were normal.
According to his son, he has been demonstrating some strange thoughts and behaviors for the past two years, but things seem to be getting worse. Per the client’s son, the family noticed that Mr. Akkad’s personality began to change a few years ago. He began to lose interest in religious activities with the family and became more “critical” of everyone. They also noticed that things he used to take seriously had become a source of “amusement” and “ridicule.”
Over the course of the past two years, the family has noticed that Mr. Akkad has been forgetting things. His son also reports that sometimes he has difficult “finding the right words” in a conversation and then will shift to an entirely different line of conversation
SUBJECTIVE
During the clinical interview, Mr. Akkad is pleasant, cooperative and seems to enjoy speaking with you. You notice some confabulation during various aspects of memory testing, so you perform a Mini-Mental State Exam. Mr. Akkad scores 18 out of 30 with primary deficits in orientation, registration, attention & calculation, and recall. The score suggests moderate dementia.
MENTAL STATUS EXAM
Mr. Akkad is 76 year old Iranian male who is cooperative with today’s clinical interview. His eye contact is poor. Speech is clear, coherent, but tangential at times. He makes no unusual motor movements and demonstrates no tic. Self-reported mood is euthymic. Affect however is restricted. He denies visual or auditory hallucinations. No delusional or paranoid thought processes noted. He is alert and oriented to person, partially oriented to place, but is disoriented to time and event [he reports that he thought he was coming to lunch but “wound up here”- referring to your office, at which point he begins to laugh]. Insight and judgment are impaired. Impulse control is also impaired as evidenced by Mr. Akkad’s standing up during the clinical interview and walking towards the door. When you asked where he was going, he stated that he did not know. Mr. Akkad denies suicidal or homicidal ideation.
Diagnosis: Major neurocognitive disorder due to Alzheimer’s disease (presumptive)
Select what you should do:
Begin Exelon (rivastigmine) 1.5 mg orally BID with an increase to 3 mg orally BID in 2 weeks
RESULTS OF DECISION POINT ONE
Decision Point Two
Increase Exelon to 4.5 mg orally BID
RESULTS OF DECISION POINT TWO
Client returns to clinic in four weeks
Client’s son reports that the client is tolerating the medication well, but is still concerned that his father is no better
He states that his father is attending religious services with the family, which the son and the rest of the family is happy about. He reports that his father is still easily amused by things he once found serious
At this point, the client is reporting no side effects and is participating in an important part of family life (religious services). This could speak to the fact that the medication may have improved some symptoms. you needs to counsel the client’s son on the trajectory of presumptive Alzheimer’s disease in that it is irreversible, and while cholinesterase inhibitors can stabilize symptoms, this process can take months. Also, these medications are incapable of reversing the degenerative process. Some improvements in problematic behaviors (such as disinhibition) may be seen, but not in all clients.
At this point, you could maintain the current dose until the next visit in 4 weeks, or you could increase it to 6 mg orally BID and see how the client is doing in 4 more weeks. Augmentation with Namenda is another possibility, but you should maximize the dose of the cholinesterase inhibitor before adding augmenting agents. However, some experts argue that combination therapy should be used from the onset of treatment.
Finally, it is important to note that changes in the MMSE should be evaluated over the course of months, not weeks. The absence of change in the MMSE after 4 weeks of treatment should not be a source of concern.
QUESTIONS TO ANSWER
1) Summarize case study and medication chosen above in full details
a) what is Alzheimer’s disease
2)Based on the decisions you recommended for the patient case study, explain whether you believe the decisions provided were supported by the evidence-based literature. Be specific and provide examples. Be sure to support your response with evidence and references from outside resources.
3What were you hoping to achieve with the decisions you recommended for the patient case study you were assigned? Support your response with evidence and references from outside resources.
4)Explain any difference between what you expected to achieve with each of the decisions and the results of the decisions in the exercise.
a) Describe whether they were different. Be specific and provide examples
In the presented case study, Mr. Akkad is a 76-year-old Iranian male with a history of alcoholism and symptoms suggestive of moderate dementia. He exhibits forgetfulness, confabulation, disorientation, impaired judgment, and restricted affect. The mental status exam indicates cognitive deficits and a Mini-Mental State Exam (MMSE) score of 18 out of 30, consistent with a diagnosis of major neurocognitive disorder due to Alzheimer’s disease (AD). The initial treatment decision was to start Exelon (rivastigmine) at 1.5 mg orally twice daily (BID) with a planned increase to 3 mg orally BID after two weeks. The follow-up visit after four weeks showed no improvement in Mr. Akkad’s symptoms, and his MMSE score remained unchanged.
The decision to initiate treatment with Exelon (rivastigmine), a cholinesterase inhibitor, is supported by evidence-based literature for the treatment of Alzheimer’s disease. Cholinesterase inhibitors have shown to improve cognitive function, activities of daily living, and global functioning in patients with AD (Birks, 2006). However, it is important to note that the response to cholinesterase inhibitors can take months, and not all patients may show significant improvement. The decision to increase the dose to 4.5 mg orally BID after the second visit is also in line with the recommended dosing regimen for Exelon in the treatment of AD (Exelon prescribing information).
The initial goal of initiating Exelon in Mr. Akkad was to improve his cognitive function and behavior, particularly his disinhibited behaviors and disinterest in religious activities. The expected outcome was to stabilize his symptoms and potentially see improvements in certain problematic behaviors associated with AD, such as disinhibition. However, it was important to communicate to Mr. Akkad’s son that the degenerative process of AD is irreversible, and cholinesterase inhibitors aim to manage symptoms rather than cure the disease.
The expected outcome of the decisions made for Mr. Akkad was to see some improvement in his symptoms, especially in relation to disinhibited behaviors and religious participation. However, the actual results after four weeks did not show significant improvement, as indicated by the unchanged MMSE score. It is essential to remember that the response to cholinesterase inhibitors may vary among individuals, and not all patients may experience noticeable improvements in the short term. Thus, it is crucial to assess the effectiveness of treatment over several months and not base outcomes solely on short-term changes.
The case study of Mr. Akkad illustrates the challenges of managing Alzheimer’s disease in a real-world clinical setting. The treatment decisions to initiate Exelon (rivastigmine) were supported by evidence-based literature, but the expected outcomes were not fully achieved in the short term. It is vital to communicate realistic expectations to patients and their families and to monitor treatment response over a more extended period to assess the full impact of medication therapy on cognitive function and behavior in Alzheimer’s disease.
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