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WGU D027 CCM1 Advanced Patho pharmacological
Foundations Task 1 | Passed on First Attempt |Latest Update
with Complete Solution
MSN Core Word E-Portfolio Template
Student Name: Shanna Oakley
Course Name: D027 Advanced Patho pharmacological Foundations
Required CPE Activities Estimated Time Anticipated
(Deliverables) (hours and Completion
1 | Page
, 2
minutes) Date
1a. CPE schedule table 3 min 11/25/25
1b. Feedback and Synthesis 2 hrs 11/25/25
Improvement Plan
1c. GoReact Video 15 min 11/26/25
1c. Peer Responses 25 min 11/26/25
1c. Reflection Summary 30 min 11/25/25
2a. Feedback and Synthesis 2 hrs 11/26/25
Improvement Plan
2b. GoReact Video 15 min 11/26/25
2b. Peer Responses 25 min 11/26/25
2b. Reflection Summary 30 min 11/26/25
3a. Feedback and Synthesis 2 hrs 11/26/25
Improvement Plan
3b. Feedback and Synthesis 2 hrs 11/26/25
Improvement Treatment Plan
3c. GoReact Video 15 min 11/27/25
3c. Peer Responses 25 min 11/27/25
3c. Reflection Summary 30 min 11/27/25
2 | Page
, 3
Phase 1: Advanced Professional Nurse or Colleague Pathophysiology Synthesis
1b. Feedback and Synthesis Improvement Plan: Alzheimer’s Disease
I. Pathophysiology
As the most common cause of dementia and sixth leading cause of death,
Alzheimer’s disease (AD) is affecting the lives of more than 5 million Americans
(Rosenthal & Burchum, 2018). The exact cause is unknown; therefore, it is believed to
be a result of a combination of factors. Collective pathophysiology includes low levels
of acetylcholine, neuronal degeneration, and neurofibrillary tangles. Known to be a
progressive condition, degeneration begins in the hippocampus initially affecting
memory, but spreads to the cerebral cortex, to eventually include more severe
compromises, like that of speech or even daily self-care. Neuritic plaques continue to
form containing beta-amyloid cores and the neurofibrillary tangles develop as deformed
structures of a protein, called tau, become twisted (Rosenthal & Burchum, 2018). The
presence of all the tangles and plaques disrupts normal neuronal activity leading to the
demise of nerve cells, and ultimately cognitive dysfunction (Alzheimer’s Association,
2025).
II. Clinical Manifestations
Throughout the aging process, normal brain changes cause slight difficulty with
memory recall or slower speeds of processing information. Due to this and the fact
that, typically, AD has an onset of symptoms after the age of 65 years, the disease may
be easily mistaken for age. The progression of symptoms from mild to severe can vary
3 | Page
WGU D027 CCM1 Advanced Patho pharmacological
Foundations Task 1 | Passed on First Attempt |Latest Update
with Complete Solution
MSN Core Word E-Portfolio Template
Student Name: Shanna Oakley
Course Name: D027 Advanced Patho pharmacological Foundations
Required CPE Activities Estimated Time Anticipated
(Deliverables) (hours and Completion
1 | Page
, 2
minutes) Date
1a. CPE schedule table 3 min 11/25/25
1b. Feedback and Synthesis 2 hrs 11/25/25
Improvement Plan
1c. GoReact Video 15 min 11/26/25
1c. Peer Responses 25 min 11/26/25
1c. Reflection Summary 30 min 11/25/25
2a. Feedback and Synthesis 2 hrs 11/26/25
Improvement Plan
2b. GoReact Video 15 min 11/26/25
2b. Peer Responses 25 min 11/26/25
2b. Reflection Summary 30 min 11/26/25
3a. Feedback and Synthesis 2 hrs 11/26/25
Improvement Plan
3b. Feedback and Synthesis 2 hrs 11/26/25
Improvement Treatment Plan
3c. GoReact Video 15 min 11/27/25
3c. Peer Responses 25 min 11/27/25
3c. Reflection Summary 30 min 11/27/25
2 | Page
, 3
Phase 1: Advanced Professional Nurse or Colleague Pathophysiology Synthesis
1b. Feedback and Synthesis Improvement Plan: Alzheimer’s Disease
I. Pathophysiology
As the most common cause of dementia and sixth leading cause of death,
Alzheimer’s disease (AD) is affecting the lives of more than 5 million Americans
(Rosenthal & Burchum, 2018). The exact cause is unknown; therefore, it is believed to
be a result of a combination of factors. Collective pathophysiology includes low levels
of acetylcholine, neuronal degeneration, and neurofibrillary tangles. Known to be a
progressive condition, degeneration begins in the hippocampus initially affecting
memory, but spreads to the cerebral cortex, to eventually include more severe
compromises, like that of speech or even daily self-care. Neuritic plaques continue to
form containing beta-amyloid cores and the neurofibrillary tangles develop as deformed
structures of a protein, called tau, become twisted (Rosenthal & Burchum, 2018). The
presence of all the tangles and plaques disrupts normal neuronal activity leading to the
demise of nerve cells, and ultimately cognitive dysfunction (Alzheimer’s Association,
2025).
II. Clinical Manifestations
Throughout the aging process, normal brain changes cause slight difficulty with
memory recall or slower speeds of processing information. Due to this and the fact
that, typically, AD has an onset of symptoms after the age of 65 years, the disease may
be easily mistaken for age. The progression of symptoms from mild to severe can vary
3 | Page
