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Preface

Thank God we pray for the presence of God Almighty because it is with mercy, grace, and love
and guidance that we can complete this Alzheimer's Disease paper in Nursing to the extent of
our knowledge and abilities.
We sincerely hope that this paper can be useful in order to add insight and our knowledge about
the implementation of the Pancasila precepts in nursing. We are also fully aware that in this
task there are shortcomings and far from what we expected. For this reason, we hope that there
will be criticism, suggestions and suggestions for improvement in the future, since there is
nothing perfect without constructive means.
Hopefully this simple paper can be understood for anyone who reads it. If this compiled report
can be useful for both ourselves and those who read it. We apologize before, if there are errors
in words that are not pleasing and we request constructive criticism and suggestions for future
improvements.
CHAPTER I
PRELIMINARY

A. Background
Alzheimer's disease is a progressive degenerative brain disease, in which brain cells are
damaged and die resulting in mental disorders such as dementia (disruption of memory
functions), language, language, thinking and behaving. Most dementia is caused by
Alzheimer's disease (60%). Dementia is a manageable disease, and dementia is not a normal
part of the aging process, increasing the number of cases in the younger age group (around 40-
50 years).
Alzheimer's disease was first discovered in 1907 by a psychiatrist and neuropathologist named
Alois Alzheimer. He observed a 51-year-old woman who had intellectual and memory
problems and did not know her place of residence, while the woman did not experience
impaired coordination and reflexes. In the autopsy it appears that the part of the brain
experiences diffuse and symmetrical atrophy, and microscopically appears the cortical part of
the brain to experience neuritis plaque and neurofibrillary degeneration.
Things that are considered to protect someone from Alzheimer's are APO E2 & 3 genes, higher
education (high brain activity), Estrogen use, and the use of anti-inflammatory drugs. Although
the cause is unknown, but this dementia (senility) mental disorder can be managed well through
various efforts.

B. Formulation of the problem


a. What is the definition of Alzheimer's?
b. What is the etiology of Alzheimer's?
c. What are the clinical manifestations of Alzheimer's?
d. What is the pathophysiology of Alzheimer's?
e. What is the medical management of Alzheimer's?

C. Aim
a. To find out the definition of Alzheimer's
b. To find out how the etiology of Alzheimer's
c. To find out how the clinical manifestations of Alzheimer's
d. To find out how the pathophysiology of Alzheimer's
e. To find out how medical management of Alzheimer's
CHAPTER II
DISCUSSION

A. Definition
Alzheimer's is a chronic, progressive and degenerative disorder of the brain and is known to
affect memory, cognitive and the ability to treat oneself. (Brunner &, Suddart, 2002).
Alzheimer's is a degenerative disease characterized by a decrease in memory, intellectual, and
personality. Cannot be cured, treatment is intended to stop the progression of the disease and
increase the independence of the patient. (Dr. Sofi Kumala Dewi, et al, 2008)
Alzheimer's is a disease that destroys and causes paralysis, which mainly affects people aged
65 years and over (pathophysiology: the clinical concept of disease processes, also a disease
with degenerative disorders that affect brain cells and cause impaired intellectual function, this
disease occurs in men and women and according to documents occur to certain people at the
age of 40 years. (Medical Surgery: vol. 1 p. 1003)
So that Alzheimer's is a chronic, degenerative disease characterized by memory loss,
intellectual, personality which can lead to reduced self-care ability. This disease attacks people
aged 65 years and above.

B. Etiology
The exact cause is unknown. Some alternative causes that have been hypothesized are metal
intoxication, impaired immunity function, viral infection, air / industrial pollution, trauma,
neurotransmitters, cell-selfilament formation deficits, herititary precipitations. The basic
pathological disorder of Alzheimer's disease consists of neuronal degeneration, the death of
specific areas of brain tissue which results in impaired cognitive function with progressive
memory loss.
A deficiency of growth factors or amino acids can play a role in the selective death of neurons.
The possibility of these cells degenerating caused by an increase in intracellular calcium,
failure of energy metabolism, the formation of free radicals or the presence of non-specific
abnormal protein production. Alzheimer's disease is a genetic disease, but several studies have
proven that the role of genetic factors, but several studies have proven that the role of non-
genetic factors (environment) is also involved, where environmental factors only trigger
genetic factors.
• Genetic factors
Some researchers revealed 50% of the prevalence of this Alzheimer's case was revealed
through the dominant autosomal gene. Individuals of the first line descent in families with
Alzheimer's sufferers have a risk of suffering from dementia 6 times greater than the normal
control group
• Factors of infection
There is a hypothesis that the cause of viral infection in families with Alzheimer's sufferers
who were carried out immuno-blot analysis was found to be reactive antibodies.
• Environmental factor
Ekmann (1988), said that environmental factors can also play a role in the pathogenesis of
Alzheimer's disease. Environmental factors include, aluminum, silicon, mercury, zinc.
• Immunological factors
Behan and Felman (1970) reported that 60% of patients suffering from Alzheimer's had serum
protein abnormalities such as decreased albumin and increased alpha protein, anti trypsin
alphamarcoglobuli and haptoglobuli.
Heyman (1984), reported a significant and increasing association of Alzheimer's patients with
thyroid sufferers. Hashimoto's thyroid is a chronic inflammatory disease that is often found in
young women because of the role of the immunity factor
• Factors of trauma
Several studies have shown an association between Alzheimer's disease and head trauma. This
is associated with boxers suffering from pugilistic dementia, where in the autopsy there are
many neurofibrillary tangles.
• Neurotransmitter factors
Changes in neurotransmitters in the brain tissue of people with Alzheimer's have a very
important role such as, Acetylcholine, Noradrenaline, Dopamine, Serotonin, and MAO
(Monoamine Oxidase) (Dr. Iskandar Japardi, 2002).

C. Pathophysiology
There are some typical biochemical and neuropathological changes found in Alzheimer's
disease, including: tangled neuron fibers (the tangled period of neurons that don't work) and
art or neuritis plaques (beta-amyloid protein deposits, parts of a large protein, amyloid
premenessor protein ( APP) Damage to these neurons occurs primarily in the cerebral cortex
and results in damage to brain size.
Mascopically, brain changes in Alzheimer's involve severe damage to cortical and
hippocampal neurons, as well as amyloid accumulation in intracranial blood vessels.
Microscopically, there are morphological (structural) and biochemical changes in neurons.
Morphological changes consist of 2 characteristic lesions which eventually develop into soma
degeneration and or axons and or dendrites. One sign of lesions in AD is the neurofibrillary
tangles, which are intracellular structures that contain tangled fibers and most consist of "know"
proteins. In the SSP, tau protein is mostly a structural forming inhibitor that is bound and
stabilizes microtubules and is an important component of the cytokleton neuron cells. In AD
neurons there is abnormal phosphorylation of tau proteins, chemically causing changes in tau
so that they cannot be bound to microtubules together. The abnormal Tau is twisted into a
double helical filament, each of which is wounded. With the collapse of the internal transport
system, intercellular relationships are the first to not function and ultimately followed by cell
death. The formation of tangled neurons and the development of damaged neurons causes
Alzheimer's.
Another typical lesion is senile plaque, consisting mainly of beta amyloid (A-beta) which forms
in tissue fluid around neurons rather than in neuronal cells. A-beta is a fragment of amyloid
precursor protein (APP) which normally adheres to a neuronal membrane that plays a role in
neuronal growth and defense. APP is divided into fragments by proteases, one of which is A-
beta, a sticky fragment that develops into a soluble clot. These clots eventually mix with glia
cells which eventually form fibrils - frozen plaque fibrils, solid, mature, insoluble, and believed
to be toxic to intact neurons. Another possibility is that A-beta produces free radicals, which
disrupts intracellular relationships and decreases blood vessel response, resulting in more
susceptible neurons to stressors. In addition to lesions, biochemical changes in the SSP also
influence AD. Neurochemically abnormalities in the brain
D. Pathway

Predisposing factors : slow virus, immune process, poisoning and genetics.

decreased metabolism and blood flow in the superior parietal cortex

Degeneration of cholinergic neurons

Diffuse neurofibillar tangling Loss of cholinergic nerve fibers in the


cerebral cortex

Senile plaque occurs Decreased cell cholinergic neurons that


project into the hippocampus and amygdala

Neurotransmitter disorder

Acetylcholine in the brain

Dementia

The change in the Lose the ability to solve the The doings of the strange
ability to take care of problem of an eye on the chaotic tend to wandering
myself state of complex and have encouragement
thinking abstract emotion violence
labil forgetful and apathetic

self-care deficit High risk of trauma

Changes in the process of


barriers to social
interaction, barriers to
Changes in nutrition and
verbal communication,
less than the body's
needs
ineffective coping
E. Clinical manifestations
Clinical manifestations / symptoms that appear in patients with Alzheimer's include:
1. Loss of memory / memory
2. Difficulty doing regular routine activities
3. Language difficulties.
4. Difficulty sleeping
5. Disorientation of time and place
6. Decreased ability to decide something
7. Unstable emotion
8. Apathy
9. Muscle tone / muscle stiffness
10. Inability to detect danger

F. Complications
Possible complications in patients with Alzheimer's disease include:
1. Infection
2. Malnutrition
3. Death
G. Diganostic examination
For certainty of the diagnosis, a diagnostic test is needed as follows:
a. Neuropathology
Definitive diagnosis cannot be established without confirmation of neuropathology.
Generally found:
• bilateral atrophy, symmetrical more prominent in the temporoparietal lobe, anterior frontal,
while the occipital cortex, primary motor cortex, somatosensory system remains intact
• the weight of the brain ranges from 1000 gr (850-1250gr).

Neuropathological abnormalities in Alzheimer's disease consist of:


1) Neurofibrillary tangles (NFT)
A neuronal cytoplasm made of abnormal filaments containing neurofilament proteins,
ubiquine, epitoque. NFT density correlates with the severity of dementia.

2) Senile plaque (SP)


It is a complex structure that occurs due to the degeneration of the nerve ending which
contains abnormal filaments, extracellular amyloid fibers, astrocytes, microglia. Amyloid
precursor protein contained in SP is strongly associated with chromosome 21. Senile plaque
is mainly found in the neocortex, amygdala, hippocampus, piriformis cortex, and is slightly
found in the primary motor cortex, somatosensory cortex, visual cortex, and auditory. Senile
plaque is also found in peripheral tissues. Senile plaque density is associated with decreased
cholinergic. Both histopathological features (NFT and senile plaque) are characteristic
features for patients with Alzheimer's disease.

3) Neuronal degeneration
On microscopic examination of changes and death of neurons in Alzheimer's disease is very
selective. Neuronal death in the neocortex is mainly found in the temporal and frontal
pyramidal neurons. Also found in the hippocampus, amigdala, brain stem nuclei including the
locus serulues, raphe nucleus and substanasia nigra. Cell death of cholinergic neurons,
especially in the basal nucleus of meynert, and noradrenergic cells, especially in the locus
seruleus and serotogenic cells in the nucleus of the dorsal raphe, nucleus tegmentum dorsalis.
Nerve growth factors in cholinergic neurons that degenerate in lesions have been found to be
an expectation in the treatment of Alzheimer's disease.
4) Vakuoler change
Is a neuronal cytoplasm that is oval shaped and can shift the nucleus. This number of
vakuoler is significantly associated with the number of NFT and SP, these changes are often
found in the temporomedial cortex, amygdala and insula. Never found in the frontal, parietal,
occipital, hippocampal, cerebellar and brainstem cortex

5) Lewy body
It is a part of the intraneuronal cytoplasm which is mostly found in the enterhinal, cingulate
gyrus, insular cortex, and amygdala. Small amounts of the frontal, temporal, parietal,
occipital cortex. This cortical Lewy body is the same as immunoreactivity that occurs in the
brain stem body in the histopathology of Parkinson's disease. Hansen et al. Stated that Lewy
body is a variant of Alzheimer's disease.

b. Neuropsychological examination

• The function of this neuropsychological examination is to determine the presence or


absence of disturbances in general cognitive function and to know in detail the deficit
patterns that occur.
• This psychological test also aims to assess the functions displayed by different parts of the
brain such as memory disorders, loss of expression, calculations, attention and understanding
of language
Systematic neuropsychological evaluation has important diagnostic functions because:
1) There is a cognitive deficit: early dementia that can be known if there are minor changes
that occur due to normal aging.
2) Comprehensive neuropsychological examination: to distinguish cognitive abnormalities in
global dementia with selective deficits caused by focal dysfunction, metabolic factors, and
psychiatric disorders
3) Identify the picture of neuropsychological abnormalities caused by dementia due to
various causes.

c. CT Scan and MRI


It is a high resolution non-invasive method to see quantification of changes in brain tissue
volume in antemortem Alzheimer's patients.
CT Scan:
• Get rid of possible causes of dementia other than Alzheimer's such as multiinfarction and
cerebral tumors. Overall cortical atrophy and ventricular enlargement are both images of the
dominant marker that is very specific to this disease
• Thinning of cerebral white matter and ventricular enlargement correlates with the severity
of clinical symptoms and the results of mini mental status checks

MRI:
• increased intensity in the cortical and periventricular regions (Capping anterior horn in the
lateral ventricle). This capping is a predilection for early dementia. In addition to cortical
abnormalities, atrophy is also seen in subcortical areas such as hippocampal atrophy,
amygdala, and enlargement of the basal cysterna and sylvii fissure.
• MRI is more sensitive to differentiating dementia from Alzheimer's disease from other
causes, taking into account the size (atrophy) of the hippocampus.

EEG
• Useful for identifying physical generation activities. While in Alzheimer's disease, slow
wave changes occur in the non-specific frontal lobe

PET (Positron Emission Tomography)


In Alzheimer's patients, PET results are found:
• decreased blood flow
• O2 metabolism
• glucose in the cerebral area

SPECT (Single Photon Emission Computed Tomography)


• This disorder correlates with the level of functional damage and cogitive deficits. Both of
these checks (SPECT and PET) are not routinely used.

Blood laboratory
There is no specific laboratory examination in Alzheimer's patients. This laboratory
examination is only to rule out other causes of dementia, such as routine blood tests, B12,
calcium, phosphorus, renal and hepatic function, thyroid, folic acid, syphilis serology,
selective antibody screening. (Yulfran, 2009)

H. Management
Treatment of Alzheimer's disease is still very limited because the causes and pathophysiology
are still unclear. Symptomatic and supportive treatment as if only giving satisfaction to the
patient and family.
Symptomatic treatment:
1) Cholinesterase inhibitors
 Purpose: To prevent a decrease in acetylcholine levels, anti-cholinesterase can be used
which works centrally
 Examples: fisostigmine, THA (tetrahydroaminoacridine), donepezil (Aricept), galantamin
(Razadyne), & rivastigmin
 Provision of this drug is said to improve memory and apraxia during administration
O ESO: worsens intellectual appearance in normal people and sufferers
Alzheimer's, nausea & vomiting, bradycardia, ↑ HCl, and ↓ appetite.

2) Thiamin
In Alzheimer's patients, there is a decrease in thiamin pyrophosphatase dependent enzyme,
which is 2 ketoglutarate (75%) and transketolase (45%), this is due to neuronal damage to the
basal nucleus.
Example: thiamin hydrochloride
Dosage 3 gr / day for 3 months orally
Objective: significant improvement in cognition function compared to placebo during the
same period.

3) Nootropic
Nootropic is a psychotropic drug
- Purpose: improve the function of cognition and the learning process. But giving 4000 mg to
Alzheimer's sufferers does not show significant clinical improvement.

4) Clonidine
Impaired intellectual function in Alzheimer's patients can be caused by cortical noradrenergic
damage.
 Example: clonidine (catapres) which is a noradrenergic alpha 2 receptor agonist
 Dosage: maximum 1.2 mg orally for 4 weeks
 Purpose: unsatisfactory to improve cognitive function

5) Haloperiodol
In Alzheimer's patients, it often happens:
 Psychotic disorders (delusions, hallucinations) and behavior: Giving oral Haloperiodol 1-5
mg / day for 4 weeks will improve these symptoms
 If Alzheimer's sufferers suffer from depression, give tricyclic anti-depressant
(Amitryptiline 25-100 mg / day)

6) Acetyl L-Carnitine (ALC)


An endogenous substrate synthesized in the mitochondria with the help of the ALC
transferase enzyme.
- Purpose: increase the activity of acetyl cholinesterase, choline acetyltransferase. - Dosage:
1-2 gr / day / peroral for 1 year in treatment
- Effects: improve or inhibit the progression of cognitive function damage (Yulfran, 2000)
CHAPTER III
FINAL

A. Conclusion
Alzheimer's is a chronic, degenerative disease characterized by memory loss, intellectual,
personality which can lead to reduced self-care ability. This disease attacks people aged 65
years and above. Patients with Alzheimer's disease experience a lot of loss of hypocarpus
neurons and cortex without being accompanied by loss of brain parenchyma, there is also a
neuro fibrillar tangling. Until now the cause of this disease is not yet known. Factors that
affect there are several, namely
1. genetic factors
2. infection factor
3. environmental factors
4. immunological factors
5. trauma factors
6. neurotransmitter factors

B. Suggestions
Thus this paper we compiled as it should hopefully be useful for us all especially for the
drafting team and all students and health students in general. Our advice, more reading to
increase knowledge
BIBLIOGRAPHY

http://abdurrahman-adhie.blogspot.com/2012/05/alzheimer.html

http://stikes-baramuli123.blogspot.com/2015/06/makalah-penyakit-alzheimer.html

http://sufihjuwita.blogs.uny.ac.id/2015/12/17/111/