Alzheimer's disease is a progressive neurodegenerative disease that causes problems with memory, thinking, and behavior. It is the most common cause of dementia among older adults. The document discusses the definition, epidemiology, etiology, symptoms, stages, pathophysiology, diagnosis, and treatment of Alzheimer's disease. It provides statistics on prevalence and risk factors. Symptoms usually develop slowly and get worse over time, eventually becoming severe enough to interfere with daily life. A diagnosis involves medical history, physical exams, neuropsychological testing, and brain imaging to rule out other potential causes. Current treatment focuses on medications to improve symptoms as well as supportive care and lifestyle interventions, as there is no cure for Alzheimer's disease currently.
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Alzheimer's Disease Presentation
1. PRESENTED BY:
KATTA. AMULYA
( IV Pharm-D )
13AB1T0014
UNDER THE GUIDANCE OF :
DEAN OF ACADEMICS
MR.SATHEESH.S.GOTTIPATI
DEPARTMENT OF PHARMACY PRACTICE
SUBMITTED TO:
CHAIRPERSON OF SEMINAR COMMITTEE
DR. K. RAJYA LAKSHMI
ASSOCIATE PROFESSOR
ALZHEIMERS
3. DEFNITION:-
Alzheimer’s Disease is a chronic, neuro-degenerative disease with
symptoms that are treatable but has no known cure.
It is a progressive disease that destroys memory and other
important mental functions.
It is a type of dementia that causes problems with memory,
thinking and behavior. Symptoms usually develop slowly and get
worse over time.
Figure:-1 [ Alzheimer’s Disease]
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EPIDEMIOLOGY
35 million people worldwide have Alzheimer’s disease.
5.3 million people in the US have Alzheimer’s disease.
Every 70 seconds someone in America develops Alzheimer’s
disease.
Alzheimer’s is the fifth leading cause of death in people 65 and
older.
Death from Alzheimer’s rose 46.1% from 2000 to 2006 .
54% of the U.S. population has been touched in some way by
Alzheimer’s disease.
Approximately 454,000 people will develop Alzheimer’s in 2010.
At current rates, 19 million Americans will have Alzheimer’s by the
year 2050.
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AETIOLOGY
Advancing age, head trauma, metabolic syndrome,
hypercholesterolemia, hypertension, atherosclerosis, coronary
heart disease, smoking, obesity, and diabetes.
genetic factors, Mutations of geans on chromosomes 1, 14, or21.
Reduction in the enzyme choline acetyltransferase in the
cerebral cortex and hippocampus.
AD is the result of β-amyloid (Aβ) accumulation in the brain
Figure:-2[Aetiology]
6. PATHOPHYSIOLOGY
Alzheimer’s disease (AD) is a progressive dementia with loss of
neurons and the presence of two main microscopic
neuropathological hallmarks:- extracellular amyloid plaques and
intracellular neurofibrillary tangles
Mutation in one of three genes: (amyloid precursor protein), (,
presenilin 1) or (, presenilin 2).
Figure:-3[Neurofibrillary tangles, Amyloid plaques]
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10. STAGES OF ALZHEIMER’S
-Stage 1: Normal
Mentally healthy person
-Stage 2: Normal aged forgetfulness
Persons over the age of 65 experience subjective complaints of cognitive and/or
functional difficulties
-Stage 3: Mild cognitive impairment
The capacity to perform executive functions also becomes compromised. Commonly,
for persons who are still working, job performance may decline.
-Stage 4: Mild Alzheimer’s disease
The most common functioning deficit in these patients is a decreased ability to
manage instrumental (complex) activities of daily life.(ability to manage finances and
to prepare meals for guests etc.)
- Stage 5: Moderate Alzheimer’s disease
This is manifest in a decrement in the ability to choose proper clothing to wear for the
weather conditions and/or for the daily circumstances (occasions).
-Stage 6: Moderately severe Alzheimer’s disease
At this stage, the ability to perform basic activities of daily life becomes
compromised.
-Stage 7: Severe Alzheimer’s disease
At this stage, AD patients require continuous assistance with basic activities of daily
life for survival.
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DIAGNOSIS
Medical history
An interview or questionnaire to identify past medical problems.
Physical examination
Includes evaluations of hearing and sight, heart and lungs, as
well as temperature, blood pressure and pulse readings.
Neuropsychological testing
Doctors use a variety of tools to assess memory, problem-
solving, attention, vision-motor coordination and abstract
thinking, such as performing simple calculations in your head.
Brain-imaging scan
MRI and CT scans look at the structure of the brain and are used
to rule out brain tumors or blood clots in the brain as the reason
for symptoms.
Mini-Mental State Examination (MMSE)
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TREATMENT
Pharmacological / drug
therapy.
Non pharmacological
treatment / non drug therapy.
• SUPPORTIVE CARE
Figure:-10
•CHOLINESTERASE INHIBITORS
•N-METHYL-D-ASPARTATE RECEPTOR
PARTIAL ANTAGONIST
•ANTIDEPRESSANTS
• ANTIPSYCHOTICS
• COGNITIVE ENHANCERS ARE USED
LIKE VITAMIN E, ESTROGEN, NSAID’S.
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DRUG BRAND NAME DOSE ADVERSE EFFECTS
TACRINE COGNEX 40–160 mg/day qid
dosing, titration
necessary
Diarrhea,Anorexia
Dyspepsia,Gastritis
Nausea
DONEPEZIL ARICEPT 5–10 mg/day once daily,
begin with 5 mg
N/V,Diarrhea, Fatigue
Anorexia
RIVASTIGMINE EXELON 6–12 mg/day twice
daily, titration necessary
N/V,Anorexia,Dyspepsia
Asthenia
GALANTAMINE RAZADYNE 16–32 mg/day twice
daily, titration necessary
N/V,Anorexia,Dyspepsia
Weight loss
TABLE NO: 1 TREATMENT
CHOLINESTERASE INHIBITORS:
15. N-METHYL-D-ASPARTATE RECEPTOR PARTIAL ANTAGONIST
Antidepressants, Antipsychotics and cognitive enhancers are used like
vitamin E, Estrogen, NSAID’s.
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DRUG BRAND NAME DOSE ADVERSE EFFECTS
MEMANTINE NAMENDA 5 mg once daily and
titrate above
headaches,
dizziness, insomnia,
and
agitation
TABLE NO: 2 TREATMENT
16. CASE STUDY:
A 74 yr old female patient, complaines of fatigue and epigastric
tenderness, distracted from work. She became more agitated and
was unable to sleep. She often started tasks but did not finish
them, she seemingly forgot what she was doing. She was 20
pounds under her ideal body weight and she was pale. Lab tests
revealed iron deficiency anemia, low albumin, and dehydration.
Case Study Questions:
List the signs of confusion seen in this case ?
Which stage of Alzheimer's disease would you assign?
.
What are appropriate diagnoses?
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17. REFERENCES
ERIC. T. HERFINDAL, DICK R. GOURLEY, HART; Epilepsy
; Clinical pharmacy & Therapeutics; 8h
Edition; p.g.no: 1812 -
1820
JOSEPH T. DIPIRO et.al; Epilepsy ; Pharmacotherapy A
Pathophysiologic approach; 6th
edition; p.g.no: 1050 – 1058
www. medicinet. com
www. healthline. com
www. emedicinehealth.com
www. medical newstoday. com
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