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PENYAKIT DEGENERATIF
Why do we age?
What particular
breakdowns lead to aging?
CELLULAR AGING
Penuaan seluler
mekanisme
Genetik
Lingkungan
Nutrisi
Faktor yg mempengaruhi
penuaan biologik
Non-modifiable Aspects of
Aging
Cardiac reserve
Dental decay
Glucose tolerance
Intelligence tests
Memory
Osteoporosis
Physical endurance
Physical strength
Pulmonary reserve
Reaction time
Serum cholesterol
Social ability
Skin aging
Elevated blood pressure
Exercise, nonsmoking
Prophylaxis, diet
Weight control, exercise, diet
Training, practice
Training, practice
Weight-bearing exercise, diet
Exercise, weight control
Exercise
Exercise, nonsmoking
Training, practice
Diet, weight control, exercise
Practice
Sun avoidance
Salt limitation, weight control,
exercise
Age-related development of
hypertension possibly related to
increased sympathetic system
activity
Impaired glucose intolerance
Diminished thyroid function
Decline in gonadal function
Changes in Physical
Appearance with Age
Age-Dependent Diseases
Cataracts
Hearing Impairment
Osteoporosis
Osteoarthritis
Vulvovaginalatrophy
Nodular prostatic hyperplasia
(BPH)
Age-Related Diseases
Atherosclerosis
Temporal arteritis
Myelodysplasticsyndro
me
Hypertension
Type II diabetes
Vulnerability to
infections
Alzheimers disease
Parkinsons disease
Some cancers, e.g.,
prostate, breast, colon
Calcificaortic stenosis
Multiple myeloma
Glaucoma
Metabolic syndrome
Changes in Hormone
Regulation and Reproduction
Simpulan
Universal
Alamiah, tidak terelakkan, irreversible,
progresif seiring waktu
Bervariasi antar individu
Laju bervariasi antar organ, jaringan
Dipengaruhi fx nonbiologis
proses penyakit
Rentan sakit
perubahan terkait penuaan faktor
risiko
Osteoporosis
Dementia
Metabolic syndrome
Degenerative disease
affecting
cortex
Alzheimers Disease
Alzheimer disease
Alzheimer disease,
morphology
neurofibrilar tangles :
hyperphosphorylated protein tau
- axonal microtubules protein
not spesific to Azlheimer
Causes of Alzheimers
Disease
amiloid : congo
red
Morphology Alzheimer
Other Dementias
Degenerasi Ganglia
basalis dan batang otak
Parkinson disease
Huntington disease
multiple system atrofi
Parkinsons Disease-associated
with dementia in 15-40% of cases
Pseudodementia-the clinical
picture of depression in the elderly
Symptoms may be apathy,
psychomotor retardation, impaired
concentration, confusion
Drugs, alcohol, toxins and physical
illnesses may also cause reversible
dementia
Parkinson disease
Morfologi Parkinson
disease
Parkinson disease
substansia nigra, Lewy
bodies
Huntington disease,
otosom dominan
Morphology Huntington
disease
Huntington disease
Huntington disease
clinical features
decades 4/5
early : dementia
affective
severe dementia
suicide
infection death
morphology
atrofi serebelum, pons
neuronal loss, cytoplasmic and
nuclear inclusion
Gejala :
Parkinsonism dan disfungsi otonom
(hipotensi ortostatik)
Spinocerebellar
degeneration
Ataxia spinocerebellar tdd :
- ataxia Friedreich
ataxia teleangiectasia
Otosom resesive
DEGENERATIVE MOTOR
NEURON
Lower motor neuron
lower motor neuron cranial
upper motor neuron
Gejala : denervasi otot : otot lemah,
atrofi, fasikulasi
Tanda klinis : paresis, spastis,
hiperefleksi
Amyotrophic Lateral
Sclerosis
atrofi otot
Sering wanita, dekade ke 5
5-10% otosom dominan
cornu anterior korda spinalis :
menipis
girus precentral atrofi
mikroskopik : neuron cornu
anterior berkurang
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