Running Head: PATHOPHYSIOLOGY OF ALZHEIMER’S DISEASE 1

Pathophysiology of Alzheimer’s Disease:

Case Study 2

Jennifer Pawson

University of New Hampshire

PATHOPHYSIOLOGY OF ALZHEIMER’S DISEASE 2

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

PATHOPHYSIOLOGY OF ALZHEIMER’S DISEASE 3

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.

PATHOPHYSIOLOGY OF ALZHEIMER’S DISEASE 4

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

PATHOPHYSIOLOGY OF ALZHEIMER’S DISEASE 5

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 incontinence and polypharmacy

Active as of nine years ago

PATHOPHYSIOLOGY OF ALZHEIMER’S DISEASE 6

Risk for injury to self and others related to

agitation, confusion, and polypharmacy

Active as of nine years ago

Potential liver damage or disease as evidenced by

elevated bilirubin levels

Active as of current visit

Risk for anemia related to possible increased red

blood cell destruction as evidenced by elevated

bilirubin levels

Active as of current visit, prior history

of iron deficiency 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 HTN

Active as of 20 years ago

Risk for impaired skin integrity related to bladder

incontinence

Active as of current visit

Risk for social interaction impairment related to

inability to remember bridge games, increased

agitation at others, and urinary incontinence

Active as of current visit

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

Risk for self-care deficit related to confusion,

difficulty remembering cooking and home care

(forgot to turn off the stove), neighbors and

family helping her home, and reported “poor

judgment”

Active as of nine years ago

PATHOPHYSIOLOGY OF ALZHEIMER’S DISEASE 7

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

Dark purple indicates clinical manifestations found in this client:

PATHOPHYSIOLOGY OF ALZHEIMER’S DISEASE 8

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/Ebsteins-Anomaly_UCM_307025_Article.jsp/HEARTORG/Conditions/

Arrhythmia/ArrhythmiaToolsResources/Conduction-

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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,

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Risperidone for psychosis of Alzheimer's disease and mixed dementia: Results of a

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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

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