Dementia/Geriatric Psych Flashcards
Geriatric Epidemiology Info
By 2045 - life expectancy will be 80
2030 – 20% of Americans will be 65 or older
Proportion of Hispanics will double to 10.9%
80% of seniors will have at least one chronic illness, 50% will have at least TWO
TO diagnose dementia
One must have a cognitive deficit that involves BOTH MEMORY LOSS AND ONE/MORE COGNITIVE DISTURBANCE (aphasia, apraxia, agnosia, problems with exec functioning)
Deficits must cause significant impairment in the patient’s life and NOT be attributable to another problem
Treatable causes of Dementia
B12 deficiency Thyroid Abnormalities Syphilis Depression Delirium Medications (benzos, narcotics, anticholinergics, Lithium) Alcohol
Most common cause of dementia
ALZHEIMER’S DISEASE
Alzheimer’s
Most common cause, 4-5 million Americans, approximately 14 million by 2050
Avg course is 8-10 years
Present when they can no longer perform their IADL’s (instrumental ADLs) –> these are not necessary for normal functioning, but necessary for living on one’s own, caring for themselves, etc
Neurobio of AD
NT affected is ACETYLCHOLINE - reduce activity of choline acetyltransferase, which makes ACh and a reduction in the number of cholinergic neurons/receptors in the hippocampus and cortex
AMYLOID PLAQUES, NEUROFIBRILLARY TANGLES
Major risk factor is INCREASED AGE
Others - female gender, African American or Latino ethnicity, hx of head injury, lower educational level, high cholesterol WITH APOE 1-3
Some genetic factors APOE4….APOE-2 may be protective!
SLOW ONSET
PROGRESSIVE cognitive loss, does NOT fluctuaate
COGNITIVE, NO motor involvement
Vascular Dementia
Type of progressive dementia that can occur IMMEDIATELY after a stroke, or up to 3 months later
Multi-infarct dementia – occurs due to numerous micro-infarcts (lacunar strokes) in the brain from reduced blood flow
These patients more likely to experience balance/gait difficulties than those with AD
Risk factors include CAD, MI, hyperlipidemia, HTN, diabetes, male gender, African American race
Diffuse Lewy Body Disease
Often characterized as having components of BOTH AD and PD, as motor impairments tend to appear within a year of the beginning of cognitive decline
RAPID ONSET and patients experience functional decline relatively quickly
Can experience FLUCTUATING changes in cognition and alertness, as well as visual hallucinations
Shuffling gait, blank expression, soft voice, cogwheel rigidity (LESS PROMINENT TREMOR than PD)
Cytoplasmic alpha-synucleuin inclusions (Lew Bodies) DIFFUSELY scattered throughout the brain (Parkinson’s just in Substantia Nigra)
Also see loss of DA from the substantia nigra, loss of ACh from the basal forebrain, and cerebral cortical atrophy
Frontotemporal Dementia
Used to be known as Pick’s Disease
2nd most common form of dementia in middle aged adults (45-65) and typically has an 8 year course
**Patient experience a gradual progression of personality change (blunted emotions, lack of empathy and insight) to drastic behavioral disturbances (poor hygiene, distractibility, diet changes, speech changes)***
M = F, those with family history have a higher risk
Subtypes – disinhibited, apathetic, sterotypic
Intracellular TAU proteins
HIV-associated Dementia
HIV patients have activated macrophages and microglia that release chemical and inflammatory mediators –> leads to neuronal cell damage and death, which can lead to dementia
Dramatically decreased with HAART (highly active antiretroviral) therapy
Risk in OLDER HIV patients
Symptoms – motor slowing, poor concentration/attention, memory loss, slowed processing, lower extremity weakness, poor coordination and balance, loss of bladder/bowels, hand weakness
Need more TIME to accomplish cognitive tasks (don’t necessarily lose the ability)
INACTIVE subtype – deficits are fixed and do not improve OR get worse
GRADUALLY PROGRESSIVE subtype - worsening function over time
After HAART - 44 months life expectancy once symptoms kick in (before HAART - 6 months)
Lab tests to order for Dementia
CBC (rule out infection), basic metabolic panel, thyroid function tests, B12/Folate, VDRL/RPR, maybe anti-HIV Ab
Urinalysis for UTI, as this could make them delirious
MRI of brain perhaps
Treating Dementia
No cure for progressive dementias, focus on improving function and slowing the progression of the disease
Pharmacological Intervention geared toward INCREASING AVAILABLE ACH:
AChE Inhibitors –> Tacrine, Donezepil, Rivastigmine, Galantamine (side effects GI upset, gastric ulcers, peripheral edema, dizziness, bradycardia)
Memantine – NMDA receptor antagonist given WITH AChE inhibitor
Together they successfully delay the progression of dementia symptoms compared with placebo
Treat other conditions that are risk factors as well (hyperlipidemia, HTN)
Antipsychotics?
How do we treat a patient who is exhibitin aggressive behavior that is difficult to manage?
NOT antipsychotics –> no effect compared with placebo, actually INCREASED MORTALITY!!!
What is the ONE THING that may help to prevent AD for us and our patients?
PHYSICAL ACTIVITY for 60 min/day 3x/week
Pseudodementia
Depression with COGNITIVE findings
Has a 5 year time frame – many start out with pseudodementia and may develop clinically significant dementia later on
Patients may give “I don’t know” answers to questions, but after a while, depressed patients with “pseudodementia” will be able to come up with the answer
A patient with dementia would not say “i don’t know” - they’d just give the answer as, July 1 1942.
Cognitive symptoms WILL resolve with treatment (antidepressants)
