A detailed case study of alzheimers disease.

1. AKHIL JOSEPH
REG. NO: 13Q0402
21st September - World Alzheimer's Day

2. • Alzheimer’s disease (AD) is the most common form of
dementing illness, and the prevalence of AD increases with
each decade of life.
• Alzheimer’s disease (AD), first characterized by Alois
Alzheimer in 1907, is a gradually progressive dementia
affecting cognition, behavior, and functional status. The
exact pathophysiologic mechanisms underlying AD are not
entirely known, and no cure exists. Although drugs may reduce
AD symptoms for a time, the disease is eventually fatal.

3. • AD profoundly affects the family as well as the patient. The
need or supervision and assistance increases until the late
stages of the disease, when AD patients become totally
dependent on a family member, spouse, or other caregiver for
all of their basic needs.
• AD affects multiple areas of cognition and is characterized by a
gradual onset with a slow, progressive decline.
• The etiology of AD is unknown, and current pharmacotherapy
neither cures nor arrests the pathophysiology.
• Survival following AD onset is estimated to be 3 to 20 years,
with an average of 8 years after the onset of symptoms.

4. • AD is the most common cause of dementia. AD unassociated with
any other pathology accounts for 50% to 60% of cases of latelife
cognitive dysfunction.
• Approximately 4.5 million Americans have AD. By the year 2050,
1 in 5 people will be older than age 65 years, and the number of
AD patients is projected to be 13.2 million. Most cases present in
persons older than age 65 years, but approximately 5% of cases
occur in persons younger than age 65 years. Onset can be as early
as age 40 years, resulting in the arbitrary age classifications of
early onset (ages 40 to 64 years) and late-onset (ages 65 years and
older).
• Increasing age is the greatest risk factor for AD. The prevalence of
AD increases exponentially with age, affecting approximately 7%
of individuals ages 65 to 74 years, 53% of those ages 75 to 84, and
40% of persons ages 85 years and older.

5. • The exact etiology of AD is unknown; however, several genetic and
environmental causes have been explored as potential causes of AD.
• Dominantly inherited forms of AD account for less than 1% of cases.
• Almost all early onset cases of AD can be attributed to alterations on
chromosomes 1, 14, or 21.
• Genetic susceptibility to sporadic, late-onset AD is thought to be
primarily linked to the apolipoprotein E (apo E) genotype.
• Apo E4 is the only genetic factor that is unequivocally associated with
an increased risk of late-onset AD, but it has been estimated to account
for less than half of the genetic contribution to AD risk.

6. • A number of environmental factors are associated with an increased
risk of AD, including age, decreased reserve capacity of the brain
(reduced brain size, low educational level, and reduced mental and
physical activity in late life), head injury, and risk factors for vascular
disease (hypercholesterolemia, hypertension, atherosclerosis, coronary
heart disease, smoking, obesity, and diabetes).

7. • The signature lesions in AD are neuritic plaques and
neurofibrillary tangles (NFTs) located in the cortical areas
and medial temporal lobe structures of the brain.1 Along with
these lesions, degeneration of neurons and synapses, as well as
cortical atrophy, occurs. Plaques and NFTs may also be present
in other diseases, even in normal aging, but there is a much
higher concentration of plaques and NFTs in patients with AD.
• Several mechanisms have been proposed to explain these
changes in the brain, including βAP aggregation and deposition
leading to the formation of plaques; hyperphosphorylation of
tau protein leading to NFT development, inflammatory
processes; dysfunction of the neurovasculature; oxidative
stress; and mitochondrial dysfunction.

9. • In its original form, the amyloid cascade hypothesis proposed
that altered APP processing drove βAP production, βAP gave
rise to plaques, plaques induced neurodegeneration, and this
neuronal loss resulted in the clinical dementia syndrome typical
of AD.
• While subsequent research failed to show APP mutation was a
common cause of AD, the findings of other genetic and
molecular research also lent support to the amyloid cascade
hypothesis. Specifically, mutations in two other genes,
presenilin 1 on chromosome 14 and presenilin 2 on
chromosome 1, were also shown to cause variants of early
onset, autosomal dominant AD. More recent data suggest the
presenilin gene products comprise part of the γ-secretase
complex that is so intimately involved in APP processing.
• Even so, the amyloid cascade hypothesis seems most

13. • Tau protein provides structural support to microtubules, the
cell’s transportation and skeletal support system. When tau
filaments undergo abnormal phosphorylation at a specific site,
they cannot bind effectively to microtubules, and the
microtubules collapse. Without an intact system of
microtubules, the cell cannot function properly and eventually
dies. The density of the NFTs correlates well with the severity
of the dementia, because they are a hallmark of neuronal death.

15. • Multiple neuronal pathways are destroyed in AD. Damage occurs in
any nerve cell population located in or traveling through plaque
laden areas. Widespread cell destruction results in a variety of
neurotransmitter deficits, with cholinergic abnormalities being the
most prominent. Loss of cholinergic activity correlates with AD
severity. In late AD, the number of cholinergic neurons is reduced,
and there is loss of nicotinic receptors in the hippocampus and
cortex. Presynaptic nicotinic receptors control the release of
acetylcholine, as well as other neurotransmitters important for
memory and mood, including glutamate, serotonin, and
norepinephrine.
• This approach is flawed for two reasons. First, cholinergic cell loss
appears to be a secondary consequence of Alzheimer’s pathology, not
the disease-producing event; second, cholinergic neurons are only
one of many neuronal pathways destroyed in AD.

17. • GENERAL : The patient may have vague memory complaints initially,
or the patient’s significant other may report that the patient is
“forgetful.” Cognitive decline is gradual over the course of illness.
Behavioral disturbances may be present in moderate stages. Loss of
daily function is common in advanced stages.
• Symptoms
• Cognitive
• ■ Memory loss (poor recall and losing items)
• ■ Aphasia (circumlocution and anomia)
• ■ Apraxia
• ■ Agnosia
• ■ Disorientation (impaired perception of time and unable to
• recognize familiar people)
• ■ Impaired executive function.

18. • Noncognitive
• ■ Depression, psychotic symptoms (hallucinations and delusions)
• ■ Behavioral disturbances (physical and verbal aggression,
• motor hyperactivity, uncooperativeness, wandering, repetitive
• mannerisms and activities, and combativeness)
• Functional
• ■ Inability to care for self (dressing, bathing, toileting, and
• eating)
• Laboratory Tests
• ■ Rule out vitamin B12 and folate deficiency
• ■ Rule out hypothyroidism with thyroid function tests
• ■ Blood cell counts, serum electrolytes, liver function tests
• Other Diagnostic Tests
• ■ CT or MRI scans may aid diagnosis

19. • A family member often first brings memory complaints to the attention of
a primary care clinician.
• At present the only way to definitively diagnose AD is through direct
examination of brain tissue at autopsy or biopsy.
• Several criteria have been developed for the detection and diagnosis of
dementia, including the following;
• Mini Mental Status Examination (MMSE,)
• Diagnostic and Statistical Manual of Mental Disorders, 4th ed. Text
Revision (DSM-IV-TR) criteria.
• The Agency for Healthcare Research and Quality (AHRQ) Guidelines.
• TheAmerican Academy of Neurology Guidelines.
• The National Institute of Neurological Disorders and Stroke (NINDS)
criteria.
• The National Institute of Neurological Communicative Disorders and
• Stroke (NINCDS).
• The Alzheimer’s Disease and Related Disorders Association (ADRDA)
Criteria.

20. Mild
(MMSE score
26–18)
Patient has difficulty remembering recent events. Ability
to
manage finances, prepare food, and carry out other
household activities declines. May get lost while driving.
Begins to withdraw from difficult tasks and to give up
hobbies. May deny memory problems.
Moderate
(MMSE score
17–10)
Patient requires assistance with activities of daily living.
Frequently disoriented with regard to time (date, year,
season). Recall for recent events is severely impaired.
May
forget some details of past life and names of family and
friends. Functioning may fluctuate from day to day.
Patient generally denies problems. May become
suspicious
or tearful. Loses ability to drive safely. Agitation,
paranoia, and delusions are common.
Severe
(MMSE score 9–0)
Patient loses ability to speak, walk, and feed self.
Incontinent
of urine and feces. Requires care 24 hours a day, 7 days
a week.

21. • NAME: XYZ
• SEX: Male
• DEPT : PSYCHIATRY
• DOA: 19-12-2016
• AGE: 80
• I.P NO : 43123
• DOD: 21-12-2016

22. • C/O loss of memory.
HISTORY OF PRESENT ILLNESS:
80 year old man, retired teacher since 20 years was
apparently alright till 15 days back then wife noticed loss of
memory, Gradually onset in nature. Pt unable to remember
things such as daily choices, financial duties, and not able to
remember whether he had food or not.

23. • K/C/O Hypertension and on Rx TAB. AMLONG 5 MG O.D,
since 9 days.
• Not a K/C/O DM, ASTHMA, EPILEPSY.
• No H/O Hallucinations / Delusions.

24. • FAMILY HISTORY
• Diet : veg
• Appetite : good
• B/B : normal
• SOCIAL HISTORY
• Habits : NIL
• WIFE’s Comments : Noticed since 15 days, Not able to count
money.
• ALLERGIES
• No known allergies

25. • PT is well built, nourished, concsious and well oriented to time,
place and person.
_ _ _ _ _ _
P I C K L E
• BP: 140/ 80 mmHg
• PR: 74 bpm

26. • CVS : S1, S2 heared, no murmur.
• RS : NVBS +
• CNS : conscious and oriented
• P/A : Soft, non-tender, no organomegaly.
INVESTIGATION
• MRI BRAIN

27. • ALZHEIMERS ? SENILE DEMENTIA ?

28. IMPRESSION ;
• Non-specific white matter isheamic changes (Leukoaraiosis).
• Diffuse cerebral atrophy.
• Time-of-Flight (TOF) MRA : Hypoplasia of right A1 segment and
right cerebral artery.
• Spondylotic changes in whole spine : c3-4, c4-5, c5-6 level.
Osteophyte disc complexes causing anterior thecal sac indentation,
no nerve root / cord compression.
• Bilateral facetal arthropathy, with intra dural osteophytes causing the
thecal space narrowing at D10,D-11 level.
• Diffuse disc bulge with thecal sac indentation all lumbar levels.

29. • Cerebral atrophy is a common feature of many of the diseases that
affect the brain.Atrophy of any tissue means a decrement in the size
of the cell. In brain tissue, atrophy describes a loss of neurons and the
connections between them.
Time of flight angiography
(TOF) is an MRI technique to
visualize flow within vessels,
without the need to
administer contrast.

31. Spondylosis refers to
degenerative changes in
the spine such as bone spurs and
degenerating intervertebral
discs. Spondylosis changes in
the spine are frequently referred to
as osteoarthritis.
diffuse disc bulge causing
ventral thecal sac
Hypoplasia of right A1 segment
and right cerebral artery.

32. • The facet joints connect the vertebral bodies to one another,
They help keep the normal alignment of the spinal vertebrae
and limit motion. The pain and discomfort that is caused by
degeneration and arthritis of this part of the spine is called
facet arthropathy.

33. BRAND NAME GENERIC NAME DOSE ROUTE FREQUENCY DAY 1 DAY 2 DAY 3
CAP.
CLOPITORVA
CLOPIDOGREL
ATORVASTATIN
75mg
10mg
P/O 0-0-1 √ √ √
TAB. AMLONG AMLODIPINE 5mg P/O 0-1-0 √ √ √
TAB.
DONAMEM
DONEPEZIL
MEMANTINE
5mg
5mg
P/O 0-0-1 √
TAB. NUHENZ
MECOBALAMIN,
BENFOTIAMMINE,
FOLIC ACID,
MYO-INOSITOL,
PYRIDOXINE HCL,
CHROMIUM
POLYNICOTINATE.
1.5mg
200mg
1.5mg
100mg
3mg
200mcg
P/O 0-1-0 √ √ √

34. 10-12-2016
• K/C/O HYPERTENSION, newly detected.
• BP : 170/90mmHg
• H/O dementia ( for recent events )
• MMSE score : 18/30
ADVICE
• Brain MRI
• Review patient wife for detailed info.
• TAB. NUHENZ 0-1-0
TAB. AMLONG 5mg 0-1-0
• Revisit on 15-12-2016 with BRAIN MRI report.

35. • MRI REPORT :
IMPRESSION ;
• Non-specific white matter isheamic changes.
• Diffuse cerebral atrophy.
• Time-of-Flight (TOF) MRA : Hypoplasia of right A1 segment and
right cerebral artery.
• Spondylotic changes in whole spine : c3-4, c4-5, c5-6 level.
Osteophyte disc complexes causing anterior thecal sac indentation,
no nerve root / cord compression.
• Bilateral facetal arthropathy, with intra dural osteophytes causing the
thecal space narrowing at D10,D-11 level.
• Diffuse disc bulge with thecal sac indentation all lumbar levels.

36. • Find up;
• BP : 150/100mmHg
• MMSE : 17/30
• ALZHEIMERS DISEASE
ADVICE,
• Admit for detailed evaluation
• TAB. CLOPITORVA (75/100) 0-0-1
• TAB. AMLONG 5mg 0-1-0
• TAB. NUHENZ 0-1-0

37. • BP : 140/80 mmHg
• Psycho education done to wife regarding age realated cognitive
defects.
ADVICE
• TAB. CLOPITORVA (75/100) 0-0-1
• TAB. AMLONG 5mg 0-1-0
• TAB. NUHENZ 0-1-0

38. • Pt is conscious and oriented.
• No fresh complaints.
• BP : 140/80mmHg.
• ADVICE
• TSH,T3,T4
• TAB. CLOPITORVA (75/100) 0-0-1
• TAB. AMLONG 5mg 0-1-0
• TAB. NUHENZ 0-1-0

39. • Pt is conscious and oriented.
• No fresh complaints.
• BP : 140/90mmHg.
• TAB. CLOPITORVA (75/100) 0-0-1
• TAB. AMLONG 5mg 0-1-0
• TAB. NUHENZ 0-1-0
• TAB. DONAMEM (5/5mg) 0-0-1

40. • ALZHEIMER’S DEMENTIA, SENILE DEMENTIA with
DIFFUSE CEREBRAL ATROPHY and OSTEO
ARTHRITIS.

41. BRAND NAME GENERIC NAME DOSE ROUTE FREQUENCY DURATION
CAP.
CLOPITORVA
CLOPIDOGREL
ATORVASTATIN
75mg
10mg
P/O 0-0-1 30 DAYS
TAB. AMLONG AMLODIPINE 5mg P/O 0-1-0 30 DAYS
TAB. DONAMEM
DONEPEZIL
MEMANTINE
5mg
5mg
P/O
0-0-1
Followed by
1-0-1
(5mg/10mg)
7 DAYS
TO
CONTINUE
TAB. NUHENZ
MECOBALAMIN,
BENFOTIAMMINE,
FOLIC ACID,
MYO-INOSITOL,
PYRIDOXINE HCL,
CHROMIUM
POLYNICOTINATE.
1.5mg
200mg
1.5mg
100mg
3mg
200mcg
P/O 0-1-0 30 DAYS

42. • Review in Neurology OPD on Tuesday / Thursday / Saturday
after 15 days, with TFT reports.

43. SUBJECTIVE EVIDENCE :
• C/O loss of memory.
• K/C/O Hypertension and on Rx TAB. AMLONG 5 MG O.D, since 9 days.
OBJECTIVE EVIDENCE :
BP: 150/100mmHg
MRI BRAIN - IMPRESSION ;
• Non-specific white matter isheamic changes.
• Diffuse cerebral atrophy.
• Time-of-Flight (TOF) MRA : Hypoplasia of right A1 segment and right cerebral
artery.
• Spondylotic changes in whole spine : c3-4, c4-5, c5-6 level. Osteophyte disc
complexes causing anterior thecal sac indentation, no nerve root / cord compression.
• Bilateral facetal arthropathy, with intra dural osteophytes causing the thecal space
narrowing at D10,D-11 level.

44. ASSESSMENT : By observing the subjective and objective
evidences the patient was diagnosed as ALZHEIMER’S DISEASE,
SENILE DEMENTIA, DIFFUSE CEREBRALATROPHY WITH
OSTEO ARTHRITIS.

45. PLANNING
THERAPEUTIC GOALS TO BE ACHIEVED;
• The primary goal of treatment in AD is Slowing the progression of
the decline and to symptomatically treat cognitive difficulties and
preserve patient function as long as possible.
• Secondary goals include treating the psychiatric and behavioral
sequelae that occur as a result of the disease (help them to remain as
active, engaged and independent as possible ).
• Providing support for both the person with the disease and their
family caregiver.

46. • GOALS ACHIEVED;
• AD specific treatment has been initiated and to treat the
symptoms.
• Psychoeducation provided to patients wife.

47. • AMLODIPINE BESYLATE CLOPIDOGREL - HYDROGEN
SULFATE – MAJOR - Concurrent use of AMLODIPINE and
CLOPIDOGREL may result in decreased antiplatelet effect and
increased risk of thrombotic events.
• ATORVASTATIN CALCIUM CLOPIDOGREL - HYDROGEN
SULFATE – MODERATE -Concurrent use of CLOPIDOGREL and
CYP3A4 METABOLIZED STATINS may result in decreased
formation of clopidogrel active metabolite resulting in high On-
treatment Platelet reactivity.
• VIT B12 and folate deficiency not ruled out.

48. • ABOUT DISEASE : Alzheimer's disease (AD), also known as
just Alzheimer's, is a chronic neurodegenerative disease that usually
starts slowly and gets worse over time. It is the cause of 60% to 70%
of cases of dementia. The most common early symptom is difficulty
in remembering recent events (short-term memory loss).
• ABOUT MEDICATION :
• TAB. DONAMEM has to be taken at bed time.
• Avoid nonprescription (over-the-counter) medications that increase
bleeding (aspirin, NSAIDs) or decrease effectiveness (omeprazole,
esomeprazole ) on concurrent use with clopidogrel.

49. • LIFE STYLE MODIFICATION :
• Physical exercise, proper nutrition, good general health, and socialization are
important for people with Alzheimer's disease.
• COUNSELLING PATIENTS CARE TAKER
• Consider vision, hearing, or other sensory impairments.
• Find optimal level of autonomy and adjust expectations for patient
performance over time.
• Avoid confrontation. Remain calm, firm, and supportive if the patient
becomes upset.
• Plan daily activities to help provide structure, meaning, and a sense of
accomplishment for the person with Alzheimer's.
• Choose the best times to do activities according to the part of the day when
the person is usually at his/her best.
• Keep activities familiar and satisfying, and keep instructions simple.
• Allow the person with Alzheimer's to complete as many things as possible by
him/herself, even if you have to initiate the activity.
• As a caregiver, it is important to understand and act according to your own
physical and emotional limitations. Be sure to take care of yourself, and
allow yourself periods of rest and relaxation.

51. • I am going to ask you some questions and give you some problems to solve. Please try
to answer as best as you can.
• 1. Time: 10 seconds for each reply: 1 MARK FOR EACH
• a) What year is this? (accept exact answer only).
• b) What season is this? (accept either: last week of the old season or first week of a
new season).
• c) What month is this? (accept either: the first day of a new month or the last day of
the previous month).
• d) What is today’s date? (accept previous or next date).
• e) What day of the week is this? (accept exact answer only).
• 2. Time: 10 seconds for each reply: 1 MARK FOR EACH
• a) What country are we in? (accept exact answer only).
• b) What province are we in? (accept exact answer only).
• c) What city/town are we in? (accept exact answer only).
• d) (In home) What is the street address of this house? (accept street name and house
number or equivalent
• in rural areas).
• (In facility) What is the name of this building? (accept exact name of institution only).
• e) (In home) What room are we in? (accept exact answer only).
• (In facility) What floor of the building are we on? (accept exact answer only).

52. • 3. Time: 20 seconds, 3 MARKS
• Say: I am going to name three objects. When I am finished, I want you to repeat them. Remember
what they
• are because I am going to ask you to name them again in a few minutes. (Say the following
words slowly at
• approximately one-second intervals): Ball / Car / Man.
• For repeated use: Bell, jar, fan; Bill, tar, can; Bull, bar, pan.
• Please repeat the three items for me. (score one point for each correct reply on the first attempt.)
• If the person did not repeat all three, repeat until they are learned or up to a maximum of five
times
• (but only score first attempt).
• 4.Time: 30 seconds 5MARKS
• Spell the word WORLD. (you may help the person to spell the word correctly) Say: Now spell it
backwards
• please. If the subject cannot spell world even with assistance, score 0. Refer to Page 3 for
scoring instructions.
• 5. Time: 10 seconds 3 MARKS
• Say: Now what were the three objects I asked you to remember?
• (score one point for each correct answer regardless of order)
• 6. Time: 10 seconds 1 MARK
• Show wristwatch. Ask: What is this called?
• (score one point for correct response: accept “wristwatch” or “watch”; do not accept “clock” or
“time”, etc.).

53. • 7. Time: 10 seconds 1 MARK
• Show pencil. Ask: What is this called?
• (score one point for correct response; accept ”pencil” only; score 0 for pen)
• 8. Time: 10 seconds 1 MARK
• Say: I would like you to repeat a phrase after me: No ifs, ands or buts
• Score one point for a correct repetition. Must be exact, e.g. no ifs or buts, score 0).
• 9. Time: 10 seconds
• Say: Read the words on this page and then do what it says. Then, hand the person the sheet with CLOSE
YOUR
• EYES on it. If the subject just reads and does not close eyes, you may repeat: Read the words on this page and
• then do what it says, (a maximum of three times. Score one point only if the subject closes eyes. The subject
• does not have to read aloud.
• 10. Time: 30 seconds 1 MARK
• Hand the person a pencil and paper (Page 3). Say: Write any complete sentence on that piece of paper.
• Score one point. The sentence must make sense. Ignore spelling errors.
• 11. Time: 1 minute maximum 1 MARK
• Place design, eraser and pencil in front of the person. Say: Copy this design please. Allow multiple tries. Wait
• until the person is finished and hands it back. Score one point for a correctly copied diagram. The person must
• have drawn a four-sided figure between two five-sided figures.
• 12. Time: 30 seconds 3 MARKS
• Ask the person if he is right or left handed. Take a piece of paper, hold it up in front of the person and
• say: Take this paper in your right/left hand (whichever is non-dominant), fold the paper in half once with both
• hands and put the paper down on the floor. Score one point for each instruction executed correctly.