Running Head: PATHOPHYSIOLOGY OF ALZHEIMER’S DISEASE
Pathophysiology of Alzheimer’s Disease:
Case Study 2
Jennifer Pawson
University of New Hampshire
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PATHOPHYSIOLOGY OF ALZHEIMER’S DISEASE
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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 firstdegree 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
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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.
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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
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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
Active as of nine years ago
than 65, urinary incontinence and polypharmacy
PATHOPHYSIOLOGY OF ALZHEIMER’S DISEASE
Risk for injury to self and others related to
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Active as of nine years ago
agitation, confusion, and polypharmacy
Potential liver damage or disease as evidenced by
Active as of current visit
elevated bilirubin levels
Risk for anemia related to possible increased red
Active as of current visit, prior history
blood cell destruction as evidenced by elevated
of iron deficiency anemia four years ago
bilirubin levels
HTN as evidenced by current reading
Active as of 20 years ago
Risk for heart disease and vascular issues related
Active as of 20 years ago
to pathophysiology of HTN
Risk for impaired skin integrity related to bladder
Active as of current visit
incontinence
Risk for social interaction impairment related to
Active as of current visit
inability to remember 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,
Active as of nine years ago
difficulty remembering cooking and home care
(forgot to turn off the stove), neighbors and
family helping her home, and reported “poor
judgment”
PATHOPHYSIOLOGY OF ALZHEIMER’S DISEASE
Flow Chart – Additional reference used (Alzheimer’s Association, 2010).
Dark purple indicates clinical manifestations found in this client:
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References
Alzheimer’s Foundation of America. (2010). About Alzheimer’s Disease: Definition. Retrieved
from http://www.alzfdn.org/AboutAlzheimers/definition.html
Alzheimer’s Foundation of America. (2010). About Alzheimer’s Disease: Symptoms. Retrieved
from http://www.alzfdn.org/AboutAlzheimers/symptoms.html
Alzheimer’s Association. (2010). Stages. Retrieved from
http://www.alz.org/alzheimers_disease_stages_of_alzheimers.asp#stage5
American Heart Association. (2010). What your cholesterol levels mean. Retrieved from
http://www.heart.org/HEARTORG/Conditions/CongenitalHeartDefects/AboutCongenital
HeartDefects/EbsteinsAnomaly_UCM_307025_Article.jsp/HEARTORG/Conditions/Arrhythmia/ArrhythmiaT
oolsResources/ConductionDisorders_UCM_302046_Article.jsp/HEARTORG/Conditions/Cholesterol/AboutCholest
erol/What-Your-Cholesterol-Levels-Mean_UCM_305562_Article.jsp
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.
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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
http://www.nlm.nih.gov/medlineplus/ency/article/003479.htm
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
http://www.uptodate.com.libproxy.unh.edu/online/content/topic.do?topicKey=hep_dis/14
026&selectedTitle=3~150&source=search_result#H1
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.
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Shadlen,M. & Larsen, E. B. (2010). Risk factors for dementia. Retrieved from
http://www.uptodate.com/online/content/topic.do?topicKey=nuroegen/5651&selectedTitl
e=1~150&source=search_result#H1
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
http://www.uptodate.com.libproxy.unh.edu/online/content/topic.do?topicKey=nuroegen/
7230&selectedTitle=9~150&source=search_result#H1