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Pathophysiology of Alzheimer’s Disease:

Case Study 2

Jennifer Pawson

University of New Hampshire

The following case study information is based on the client outlined on p. 88 in Bruyere’s 100 Case Studies in Pathophysiology (2009).

1. Identify this patient’s two major risk factors for Alzheimer disease.

This client has two of the primary risk factors for developing late onset Alzheimer’s disease (AD): a positive family history for the disease and advanced age. Clients who have first-degree relatives with Alzheimer’s disease have a 10-30% increased risk of developing the disease themselves (Shadlen & Larsen, 2010). This client had two first degree relatives, her mother and her sister, with diagnosed Alzheimer’s disease, and therefore the client is at an increased risk. The client’s age of 83 also puts her at risk for having this disease. The incidence rate of AD in clients, ages 80-85, is 3.3% while the general population ages 65-69 only has a rate of 0.6% (Shadlen & Larsen, 2010). Aside from genetic risk factors, studies have shown conflicting evidence that hypertension, diabetes, and other pathological processes are indicative of increased risk for AD (Shadlen & Larsen, 2010). Therefore the highest indicators of risk for this client remain her age and family history of the disease.

2. Review the blood tests in table 38.2 and discuss if they are normal or abnormal.

The blood tests in table 38.2 are normal with the exception of the following results: HDL, TSH, triglycerides, direct bilirubin, total bilirubin (Taylor et al., 2008; Porth, 2007; American Heart Association, 2010). The HDL cholesterol result was below optimal levels, while the triglyceride result was borderline high (Porth, 2007; American Heart Association, 2010). Also, given this client’s family history, it is recommended that her LDL levels should be below 100 (Porth, 2007). Additionally, this client has a higher than expected serum TSH levels, which can be indicative of thyroid dysfunction (Porth, 2007). The only remaining abnormal results were a high direct bilirubin and high normal total bilirubin levels (Taylor et al., 2008).

3. Identify any lab blood test results in Table 38.2 that might explain the patient’s deteriorating neurologic function

High serum levels of bilirubin could be contributing to this client’s neurological deterioration. In studies with rodents, bilirubin toxicity has been linked to cognitive dysfunction and memory changes (Chang, Lee, Huang, & Hsu, 2009; Huang et al., 2004). Additionally, elevated conjugated (or direct) bilirubin levels may indicate illnesses with system effects, such as cirrhosis and hepatitis (Dugdale, 2009; Porth, 2007). However, this client has no other signs or symptoms of hepatic impairment, including a normal abdominal exam and normal AST and ALT levels (Kaplan, 2010). Therefore, it is more likely that this client’s history of constipation may have impaired the client’s ability to excrete direct bilirubin through bowel elimination (Taylor et al., 2008).

Aside from bilirubin levels, a high TSH level could indicate a thyroid problem (Porth, 2007). Hypothyroidism could cause cognitive impairment; however, aggressive behavior and irritability are more likely to be caused by hyperthyroidism (Porth, 2007). Without an abnormal T4 level though, it is unlikely that this client’s issues are solely dependent on a thyroid issue. An additional cause for neurological dysfunction in adults is electrolyte imbalances, and this client’s electrolyte values are within normal range (Bruyere, 2009; Porth 2007). Given the current evidence, Alzheimer’s disease is the most likely cause for this client’s cognitive decline.

4. Multi-infarct (vascular) dementia has to be ruled out as a possible cause of this patient’s changes in cognitive function as they present in a similar manner:

a. Identify two risk factors that predispose this patient to multi-infarct dementia

Risk factors for this client developing multi-infarct dementia include a history of hypercholesteremia and hypertension, though some research has shown that cardiovascular disease may not be indicative of vascular dementia risk level (Porth, 2007; Wright, 2010). However, current lab test results have shown normal levels of cholesterol, which in turn reduces the clients risk for developing emboli and other heart disease (Porth, 2007).

b. Discuss CT scan findings associated with Alzheimer disease compared to multi-infract dementia

Findings on neuroimaging tests may help in diagnosing AD, particularly when attempting rule out other causes of dementia (Alzheimer’s Foundation of America, 2010a). Findings associated with CT scans in clients with AD include sulci widening and ventricular dilatation (Bruyere, 2009). This contrasts with findings found in other forms of dementia, such as multi-infarct, also known as vascular, dementia. Some clinical manifestations of neurological damage found in vascular dementia include vascular damage and signs of cerebral infarct and ischemia on CT scans (Porth, 2007; Condefer, Haworth, & Wilcock, 2004). However, research has shown that CT scans may be unnecessary for determining the cause of dementia, when a client’s overall history is taken into account (Condefer, Haworth, & Wilcock, 2004).

5. Why might a trial of risperidone be appropriate for this patient?

This client’s family has reported recent aggression and emotional outbursts, which are two psychotic features of late-stage Alzheimer’s disease (Alzheimer’s Foundation of America, 2010b). A review of risperidone trials by Katz et al. (2007) found that risperidone was effective in reducing the aggressive symptoms of psychosis related to AD. An additional study by Brodaty et al. (2005) found that risperidone treatment for clients with AD, who scored less than 23 on the MMSE and had aggressive tendencies, saw improvement in psychotic features and global functioning in as little as 2 weeks. However, it should be noted that risperidone has a significant increased incidence compared to placebo of somnolence and constipation (p-value less than 0.05 and 0.1, respectively) (Brodaty et al., 2005). As this client has developed psychotic features of AD, and her score on the MMSE was 18, risperidone should be discussed with the family as a potential treatment for some of the client’s symptoms.

6. Develop a problem list for this client.

Problems for this client include:

|Problem |Status of Problem |

|Low HDL levels |Active as of current visit |

|Elevated serum creatinine |Active as of current visit |

|Risk for falls related to confusion, age greater than 65, urinary |Active as of nine years ago |

|incontinence and polypharmacy | |

|Risk for injury to self and others related to agitation, confusion, and |Active as of nine years ago |

|polypharmacy | |

|Potential liver damage or disease as evidenced by elevated bilirubin |Active as of current visit |

|levels | |

|Risk for anemia related to possible increased red blood cell destruction |Active as of current visit, prior history of iron deficiency |

|as evidenced by elevated bilirubin levels |anemia four years ago |

|HTN as evidenced by current reading |Active as of 20 years ago |

|Risk for heart disease and vascular issues related to pathophysiology of |Active as of 20 years ago |

|HTN | |

|Risk for impaired skin integrity related to bladder incontinence |Active as of current visit |

|Risk for social interaction impairment related to inability to remember |Active as of current visit |

|bridge games, increased agitation at others, and urinary incontinence | |

|Bladder incontinence as evidenced by self-report |Active as of current visit |

|Risk for self-care deficit related to confusion, difficulty remembering |Active as of nine years ago |

|cooking and home care (forgot to turn off the stove), neighbors and family| |

|helping her home, and reported “poor judgment” | |

Flow Chart – Additional reference used (Alzheimer’s Association, 2010).

Dark purple indicates clinical manifestations found in this client:

References

Alzheimer’s Foundation of America. (2010). About Alzheimer’s Disease: Definition. Retrieved from

Alzheimer’s Foundation of America. (2010). About Alzheimer’s Disease: Symptoms. Retrieved from

Alzheimer’s Association. (2010). Stages. Retrieved from

American Heart Association. (2010). What your cholesterol levels mean. Retrieved from

Bowen, J., Kamin, R., Leverenz, J., Fishel, M., McCormick, W., Kukull, W., et al. (2005). Interrater Reliability and Accuracy in Identifying Ischemic Strokes Using Computed Tomography Scans in People with Dementia. Journal of the American Geriatrics Society, 53(10), 1743-1747. doi:10.1111/j.1532-5415.2005.53507.x.

Brodaty, H., Ames, D., Snowdon, J., Woodward, M., Kirwan, J., Clarnette, R., et al. (2005). Risperidone for psychosis of Alzheimer's disease and mixed dementia: Results of a double-blind, placebo-controlled trial. International Journal of Geriatric Psychiatry, 20(12), 1153-1157. doi:10.1002/gps.1409.

Bruyere, H. J. (2009). 100 case studies in pathophysiology. Philadelphia, PA: Wolters Kluwer Health.

Chang, F. Y., Lee, C. C., Huang, C. C., Hsu, K. S. (2009) Unconjugated Bilirubin Exposure Impairs Hippocampal Long-Term Synaptic Plasticity. PLoS ONE 4(6): e5876. doi:10.1371/journal.pone.0005876.

Condefer, K., Haworth, J., & Wilcock, G. (2004). Clinical utility of computed tomography in the assessment of dementia: a memory clinic study. International Journal of Geriatric Psychiatry, 19(5), 414-421. doi:10.1002/gps.1028.

Dugdale, D. (2009). Bilirubin – blood. Retrieved from

Huang, L., Hsieh, C., Chou, M., Chuang, J., Liou, C., Tiao, M., et al. (2004). Obstructive jaundice in rats: cause of spatial memory deficits with recovery after biliary decompression. World Journal Of Surgery,28(3), 283-287. Retrieved from MEDLINE database.

Kaplan, M. (2010). Liver function tests that detect injury to hepatocytes. Retrieved from

Katz, I., de Deyn, P., Mintzer, J., Greenspan, A., Zhu, Y., & Brodaty, H. (2007). The efficacy and safety of risperidone in the treatment of psychosis of Alzheimer's disease and mixed dementia: A meta-analysis of 4 placebo-controlled clinical trials. International Journal of Geriatric Psychiatry, 22(5), 475-484. doi:10.1002/gps.1792.

Porth, C. M. (2007). Essentials of pathophysiology: Concepts of altered health states (2nd ed.). Philadelphia, PA: Lippincott Williams & Wilkins.

Shadlen,M. & Larsen, E. B. (2010). Risk factors for dementia. Retrieved from

Taylor, C., Lillis, C., LeMone, P., & Lynn, P. (2008). Fundamentals of nursing: The art and science of nursing care (6th ed.). Philadelphia, PA: Wolters Kluwer Health.

Wright, C. B. (2010). Etiology, clinical manifestations, and diagnosis of vascular dementia. Retrieved from

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