Alzheimer’s Disease Case Study

Alzheimers Disease Case StudyB. TrimbleCase StudyM. T. an 86-year-old Asian male is brought into the geriatric clinic by his daughter because he is becoming more forgetful. The daughter explains that the patient often does not flat recognize his own grandson. When asked, however, the patient denies memory impairment. The daughter states that her father has been having trouble for almost four years now. She said she did not realize how much her father had changed until she watched a home exposure of her father with his grandson from six years ago. His personality has even seemed to substantiate changed, said the daughter. M.T. is no longer able to take cargon of his house and household chores and is sometimes slow to respond to questions.Past Medical HistoryPeptic Ulcer Disease (PUD) with the last occurrence three years ago.Social HistoryRetired sanitation worker times fifteen years. Lives with his daughter since his wife died five years ago. Previous cigarette smoker quit fiftee n years ago. Denies ethyl alcoholic beverage (ETOH), and intravenous drug abuse.Family HistoryFather died in combat in KoreaMother died at age 92, unknown causeMedications and allergiesNKDAPrevacid 30 mg viva voce one time daily Mylanta 30 ml orally as needed for stomach upsetAspirin EC 81 mg orally once daily Tylenol 325 mg orally as needed for headachePhysical ExaminationGeneral patient is a thin, pleasant man, with on the job(p) memory in no acute distress.Vital signs BP 145/78 , pulse 80 RR 17 , WT 70 kg , Ht 62 BMI 19.8HEENT- Pupils PERLA Ears with cerumen Neck no bruit no JVDCardiovascular Normal sinus rhythm, S1 S2, negative for S3/S4, resp RRRNeuro Aox1 (Oriented to person only), CN XII XII intact, reflex normalAbdomen autocratic bowel sounds, non-tender, non-distendedExternal WNL, no clubbing, cyanosis, or edemaLaboratory TestsAlbumin (3.6-5 g/dL) 3.6g/dL total protein (6.3-8.2g/dL) 6.8g/dLAlk Phos (38-126U/L) 41U/L ALT (7-58 U/L) 21 U/LAST (7-58 U/L) 21 U/L bilirubin (0.2-1.3ug/dL) 0.3ug/dLBUN (8-25mg/dL) 11mg/dL HgB (13.2-15.2 g/dL) 13.5g/dLSCr- (0.5-1.4mg/dL) 0.7mg/dL Hct (40-52%) 39%Na+ (134- 146 meq/dL) 136 mEq/dL Plts (140-450 mm3) 300,000/mm2Cl-(98-107mEq/dL) 103 mEq/dL WBC (4.1-10.9mm3) 8700/mm2Bicarb (22-26 mEq/dL) 24 mEq/dL ESR (Glucose (65-110mg/dL) 101mg/dL B12 (223-1132 pg. /ml) 452pg/mlCa- (8.9-10.4 mEq/dL) 8.5 mEq/dL folate (3.6-20ng/dL) 6.4ng/dLMag (1.6-2.4mEq/dL)1.9 mEq/dLFTI (4-11) 6.3Phos (2.5-4.5 mg/dL) 3.3 mg/dLT3 (75-220ng/dL) 101ng/dLCholesterol- (T4 (4-11mEq/dL) 6.1 mEq/dLTSH (0.35-6.2 microU/uL) 2.0 micro Unit/uLRPR non-reactiveRadiology testCT scan impression mild cortical atrophyDiagnosisDementia (senile dementia) is a syndrome rather than a distinct indisposition entity. It is usually forward and irreversible. It is characterized by a general decline in cognitive abilities that may include losses of memory, abstract reasoning, judgment, and impulse control, as well as changes in perso nality. It is usually subtle in onset and often progresses slowly until symptoms are very obvious and profoundly devastating. The three most common dementias are Alzheimers disease, multi-infarct dementia, and a mixed Alzheimers disease and multi-infarct dementia (Cayton, Graham, Warner, 2004).Alzheimers disease is sometimes called primary degenerative dementia or senile dementia of the Alzheimers type. It accounts for at least 80 percent of all the dementias suffered by the elderly (Whalley, Lawrence, Breitner, 2009). It is a progressive, irreversible, degenerative neurologic disease of unknown origin that begins insidiously. The highest incidence is among persons 65 years and older with increasing incidence after age 70. The life expectancy following the diagnosis varies from six to twenty years (Whalley, Lawrence, Breitner, 2009).The etiology of the disease is unknown, but there are specific neuropathologic and biochemical changes. These include neurofibrillary tangles and sen ile or neuritic plaques. This neuronal damage occurs primarily in the cerebral cortex and results in decreased brain size. These changes are found to a lesser extent in normal brain tissue of older adults. Cells principally affected by this disease are the ones that use the neurotransmitter acetylcholine. Biochemically, the enzyme active in producing acetylcholine is decreased. Acetylcholine is specifically involved in memory processing (Whalley, Lawrence, Breitner, 2009).Clinical manifestationSymptoms of Alzheimers disease are highly variable. Early in the disease, forgetfulness and subtle memory loss occur, but the victim has adequate cognitive function to hide the loss. Social skills and behavior patterns uphold intact problems are difficult to detect on casual observation (Cayton, Graham, Warner, 2004). With further progression of the disease there is an inability to conceal the deficits. Forgetfulness is manifested in some daily actions. The victim may lose his way in a fam iliar environment. He may repeat the same stories because he forgets that he told them. reasoning and reality orientation by caregivers increase the patients anxiety without increasing function, because this is also forgotten (Cayton, Graham, Warner, 2004).Conversations become difficult because the victim forgets what he was about(predicate) to say or may not be able to remember words. Ability to formulate concepts and think abstractly disappears (Cayton, Graham, Warner, 2004). The person can interpret a proverb only in concrete terms. The victim is often unable to appreciate the consequences of his actions and will therefore exhibit impulsive behavior. He will have difficulty with everyday activities such as working simple appliances and handling money (Cayton, Graham, Warner, 2004).Personality changes are usually negative. The patient may become depressed, suspicious, paranoid, hostile, and even combative (Whalley, Lawrence, Breitner, 2009). Progression of the disease intens ifies the symptoms. Speaking skills deteriorate to nonsense syllables agitation and physical practise increase. A voracious appetite often develops because of the high activity level. The patient may wander at night for hours. Eventually he will need help in all areas of personal care including toileting and consume dysphagia occurs and incontinence develops. The terminal stage may last for months (Cayton, Graham, Warner, 2004).TreatmentTreatment for dementia of the Alzheimers type will be Aricept 5 mg once daily at bedtime. After four weeks symptoms will be reviewed, and titration to ten mg once daily may be initiated, depending upon results. Maximum dosage of 23 mg daily if needed after three months of 10-mg treatments (Katzung, Mastes, Trevor, 2012). Follow up in office in four weeks.Discontinued use of Prevacid, as the medicine is implicated in low blood platelet, WBC, HgB and Hct, calcium, and B12 levels (Brunton, Chabner, Knollman, 2011).Follow-up blood work in four wee ks, should include CBC with differential, CMP, liver panel, weight, and blood pressure. Patient is borderline hypertensive and increase in fluid volume may correct this issue. Patient should be encouraged to change diet to a high-protein diet with adequate hydration. If platelet count and WBC count continue to be below normal a hematology consult will be discussed. Referral to Alzheimers support class will be given to the daughter.ReferencesBrunton, L., Chabner, B., Knollman, B. (2011). Goodman Gilmans The pharmacological basis of therapeutics (12 ed.). McGraw-Hill.Cayton, H., Graham, N., Warner, J. (2004). Dementia Alzheimers and other dementias At your fingertips guide (2 ed.). London Class.Katzung, B., Mastes, S., Trevor, A. (2012). Basic clinical pharmacology (12 ed.). McGraw-Hill.Whalley, L., Lawrence, J., Breitner, J. (2009). Dementia (2 ed.). wellness Press.