AD

Alzheimer’s disease
Rachelle Crabb

Submitted to Ashley Spurgeon, BSN, in partial fulfillment of Clinical 1
Indian Hills Community College
4/10/15

Alzheimer’s disease
Pathology
Alzheimer’s disease is a deteriorating disease which affects the neurological connections and pathways in the brain. The two main abnormalities are senile plaques, and neurofibrillary tangles. Senile plaques are composed of Beta-Amyloid protein while neurofibrillary tangles are made up of Tau protein. Senile plaques are formed by an increased and unregulated amount of Beta-Amyloid proteins. These proteins build up into little fragments of plaque. Neurons send messages to each other through from the soma, through the axon, and then out through the synapses. Tau protein is what holds the axon skeleton together, therefore it is the boundaries of the microtubules forming the axon. In Alzheimer’s disease, the protein breaks away from the microtubule skeleton, causing the microtubules to break apart from each other. When this happens, messages can’t be sent through the neuron. The Tau protein fragments combine to form neurofibrillary tangles. These tangles prevent any signals or messages to be released from the neuron, and therefore eventually kills the neuron. The accumulation of neurofibrillary tangles originates in the hippocampus. This is the part of our brain responsible for memories, thus contributing the definition of Alzheimer’s disease popular to the public. The following areas are then affected in this order; language, recognition, and the failure to make gestures. Senile plaques are first found in the cortex, and then travel through the hippocampus, and then throughout the rest of our brain. There is no parallel found between the progression of the senile plaques and the symptoms observed for this disease. (Center, n.d.) (Caring for Clients with Cognitive Disorders, 2009)

Causes To this day, a definite cause of Alzheimer’s is unknown, but there are several factors thought to have a hand in the development of the disease. Genetics is thought to contribute the onset and likelihood of the disease. Chromosomes 1, 14, 19, and 21 are linked to the growth of the two proteins involved in Alzheimer’s disease. Chromosome 19’s gene is the most prevalent in the beginning stages of Alzheimer’s. People that have the ApoE4 gene might have a greater chance of cultivating late-stage Alzheimer’s. Heart disease, stroke, high blood pressure, diabetes, and obesity could also potentiate the development of Alzheimer’s as well. (Caring for Clients with Cognitive Disorders, 2009) (Center, n.d.)

Textbook Signs and Symptoms
Patient Signs and Symptoms
1. Memory loss
Can’t remember how she met her first husband. Can’t remember if her last husband passed away or not.
Resident will say the same thing 5 minutes after the first time she said it, and doesn’t remember telling it to you the first time.
2. Difficulty performing familiar tasks
N/A: Resident is currently very independent with ADLs
3. Problems with language
N/A: Speaks clear and coherently
4. Disorientation to time and place
N/A: Knew what day of the week it was when asked, and knew it was spring
5. Reduced judgment
Recorded on chart: Resident would walk out in the streets aimlessly
6. Problems with complex mental tasks
N/A: No observed difficulty with complex mental tasks
7. Misplacing items or valuables
N/A: doesn’t have many things in her room to misplace
8. Changes in mood or behavior
N/A: No