Goals and Objectives - Geriatrics
From the lecture:
# of 65+ millions by state: 1. California, 2. Florida, 3. NY, 4. PA
% of 65+ millions by state: 1. Florida, 2. WV, 3. PA
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Elderly are 13% of the population
36% of hospital stays
49% of all days of hospital care
50% of all physician hours
Average 75 year old
Has at least 3 chronic conditions
Uses 4.5% of all prescription drugs
1 in 4 has at least one disabling condition
Chronic disease results in 70% of all hospital stays and 60% of all Medicare costs
17% of all hospital admissions are caused by inappropriate drug prescribing
1 out of 5 elderly receive inappropriate prescriptions (in notes under slide)
by age 80 3 of 4 elderly have at least 1 disability (in notes under slide)
Ger 2: Nutrition
1.
Understand physiologic and biologic changes in the digestive system
● Neurodegeneration of enteric nervous system → dysphagia, GI reflux and constipation
● Gastric motility is impaired (small intestine unaffected)
● Reduced gastric acid secretions: due to chronic gastritis, proton pump inhibitors,
vagotomy and gastric resections
○ Reduction of gastric acid predisposes to bacterial overgrowth (71% of pt), which
is linked to reduced body weight and reduced intake of micronutrients
● Structural changes of pancreas: secretagogue-stimulated lipase, chymotrypsin and
bicarbonate concentration decline
● Liver declines in size
● BMI and body weight increase until 50-60 then declines
● Cachexia is involuntary loss of fat free mass (muscles, tissue, organ, skin, and bone);
wasting is involuntary loss of weight
● Sarcopenia is the major age related physiological change (loss of skeletal muscle
mass) - decreased exercise level, increased cytokines, and neuron loss in the spinal
cord
● aging is associated with a impairment of receptive relaxation of the gastric fundus→
rapid antral filling → early satiety
● higher levels of leptin are found in older people (singal for adequate body fat). Reduced
glucose tolerance can exacerbate this
● Small intestine: decline in number of villi and crypts, loss of villi and enterocyte height
○ no clear association w/ intestine morphology and nutrient uptake w/ aging
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unintentional weight loss is one of the best predictors of worse clinical outcome,
significant morbidity and mortality assoc..
2.
Understand specific signs and symptoms of nutrient deficiencies
“a wasted, thin individual w/ dry scaly skin and poor wound healing”
● Hair is thin
● Nails are spooned and depigmented
● Complaints of bone and joint pain
● Edema
3.
Understand causes of weight loss
● Mechanism: cause
● Wasting: “involuntary loss of weight”, commonly due to poor dietary food intake
● Cachexia: “involuntary loss of fat-free mass (muscle, organ, tissue, skin, bone) or body
cell mass”, Cytokines (IL-1,-6, TNFa) cause increased resting energy expenditure,
increased gluconeogenesis, shift of albumin production to acute phase proteins causing
a negative nitrogen balance
● Sarcopenia: “decline in muscle mass”, reduced physical activity, hormonal (sex horm),
glucocorticoids, and catecholamines → increase pro-inflammatory cytokines), neural
(neuron loss → m atrophy), cytokines (increase acute phase reactants which break
down muscle)
● Other causes (pathological and non-pathological) causes of wt loss mentioned in
article
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Medical: CHF, COPD, malabsorption syndrome, H. pylori infection, endocrine
diabetes, stroke, Parkinson’s, pneumonia, UTIs, malignancy, rheumatoid arthritis,
alcoholism, poor dentition, drugs
Psychological: dementia/Alzheimer’s disease, depression, anxiety, alcoholism,
bereavement
Social: poverty, isolation, inability to shop, prepare, or cook meals
Ger 3: Alzheimer's disease
1.
Understand the risk factors and prognosis for Alzheimer's disease
● Risk factors: age,
● Death w/in 3-9yrs after dx
2.
Understand the pathology of AD
“accumulation of misfolded proteins in the brain results in oxidative and inflammatory damage,
which in turn leads to energy failure and synaptic dysfunction”
● B-amyloid peptide:
○ amyloidgenic mechanism initiated by beta-site amyloid precursor protein-cleaving
enzyme (BACB-1) a B-secretase
○ severity of AD correlates to levels of oligomers in brain (soluble oligomers and
intermediate amyloids are the most neurotoxic), not the total B-amyloid
○ Neprilysin- protease, degrades B-amyloid mono/oligomers
○ Insulin-degrading enzyme: a thiol metalloendopeptidase, degrades B-amyloid
and other small peptides
○ THEREFORE, decreased neprilysin or insulin-degrading enzyme → B-amyloid
accumulation
■ INCREASED amounts of neprilysin or insulin-degrading enzyme →
prevents plaque formation
● Dystrophic neurites:
● Neurofibrillary tangles in medial temporal-lobe structures: filamentous inclusions in
pyramidal neurons. The number of tangles is a marker of severity of AD. The major
component of the tangles is an abnormally hyperphosphorylated (insoluble) and
aggregated form of tau. Elevated amino acids T181, T231 and tau in the CSF predict
incipient AD in patients with mild cognitive impairment.
○ tau mutations do not occur in AD
○ oxidative stress, impaired protein folding by the ER and deficient
proteasome/autophagic mediated clearance are assoc. with aging and drive
amyloid accumulation.
● Loss of neurons and white matter: observed in patients at all stages
● Congophilic (amyloid) angiopathy:
● Inflammation:
● Oxidative damage: B-amyloid is a potent mitochondrial poison, especially affecting
synaptic pool
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B-amyloid inhibits key enzymes in brain and mitochondria, specifically
cytochrome C oxidase → electron transport, ATP-production, oxygen
consumption and mitochondrial mem potential all become impaired
Increased mitochondrial superoxide radical formation and conversion into
hydrogen peroxide cause oxidative stress, release of cytochrome c and
apoptosis
Alcohol dehydrogenase is targeted by B-amyloid
The antihistamine dimebolin hydrochloride is a putative mitochondrial stimulant,
reported to improve cognition and behavior in pts with AD
Dysfunctional mitochondria release oxidizing free radicals
Markers of oxidative damage precede pathological changes
B-amyloid is a potent generator of reactive oxygen species and reactive nitrogen
species
Stimulated microglia are a major source of highly diffusible NO radical
Peroxidation of membrane lipids yields toxic aldehydes
Increased permeability of Ca impaired glucose transport and aggravate energy
imbalance
Zinc, typically thought to be toxin in AD, might at lower concentrations protect
cells by blocking B-amyloid channels or compete with copper for B-amyloid
binding.
3.
Understand the mechanisms of synaptic failure in AD
● AD may be a primarily a disorder of synaptic failure
● In mild AD, there is about a 25% reduction of presynaptic vesicle protein synaptophysin
and with advancing disease there’s a disproportionately large loss of synapses
compared to neurons **and this loss best correlates w/ dementia
● synaptic loss particularly affects the dentate region of the hippocampus
● “long-term potentiation”, an experimental indicator of memory formation at synapses are
impaired in mice with plaque-bearing disease after B-amyloid was applied to brain
● Disruptions of the release of presynaptic neurotransmitters and postsynaptic glutamatereceptor ion currents occur partially as a result of endocytosis of N-methyl-D-aspartate
(NMDA) surface receptors and endocytosis of a-amino-3-hydroxy-5-methyl-4-isoxazole
(the ladder further weakens currents synaptic currents after a high-frequency stimulus
train) **intraneuronal B-amyloid triggers these synaptic deficits even earlier
● Depletion of neurotrophin and neurotransmitters
○ Neurotrophin- promote proliferation, differentiation and survival of neurons and
glia, mediate learning, memory and behavior. Normally high levels in receptors in
cholinergic neurons and are reduced in late-stages of AD
○ Deficiency of cholinergic projections in AD is linked to buildup of B-amyloid and
tau
○ Presynaptic a-7 nicotinic acetylcholine receptors are essential for cognitive
processing. Levels are initially elevated in AD, then decrease. B-amyloid binds
to a-7 receptor, impairing the release of acetylcholine and maintenance of “longterm potentiation”
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Activation of nicotinic acetylcholine receptors or M1 receptors limits tau
phosphorylation
○ Muscarinic receptors are also reduced in AD: normally activate protein kinase C,
favoring amyloid to be processed into a non-amyloid molecule
Summary: B-amyloid triggers endocytosis of crucial surface receptors and impairs the
release of AcH resulting in synaptic failure. The reduction of synaptophysin best
correlates with dementia.
4.
Understand risk factors for progression to AD
● Age: incidence of dx doubles every 5 yrs after 65yo, exceeding ⅓ of people over 85
● strokes and white matter lesions contribute greatly to cognitive decline
● APOE genetic risk (APOE4 specifically exponentially increases the risk).
○ major determinant of late-onset alz.
○ apolipoprotein J is a newly discovered that deposits AB
● Sortillin-related receptor being reduced
● general anesthesia
Ger 4: Mild Cognitive Impairment
1.
2.
Contrast the clinical features between mild cognitive impairment and dementia
Contrast the clinical features between MCI and normal aging
Mild Cognitive
Impairment
(amnesic)
Normal Aging
Dementia
Signs/Symptoms
more prominent
forgetfulness – forget
important
information or
appointments and
conversations
Misplacing
objects or
difficulty recalling
words
Cognitive deficits
affect daily
functioning = loss of
independence in
community
Tests To Run
Short Test of Mental
Status and Montreal
Cognitive Assessment
3.
Functional Activities
Questionnaire
According to the reading, identify treatments that have potential benefit
● Cognitive rehabilitation programs
○ Using mnemonics, association strategies and computer assisted
training programs has shown some improvement
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Since a risk factor for progressing to dementia include cardiovascular risk
factors, brisk walking of 150 min per week showed that the exercise
group had better cognitive function than the group that did not exercise
high dose vitamin E or donepezil (reduced progression in up to 24
months, at 36 no significant effect; vitamin E did not significantly reduce
the risk of progression)
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4.
Understand the types of MCI
o 2 Subtypes of MCI:
● Amnestic (memory impairment)
○ Clinically significant memory impairment that does not meet criteria for
dementia
○ Pt. is aware of increasing forgetfulness
○ Other cognitive capacities are preserved with only mild inefficiencies
● Non-Amnestic (no memory impairment)
○ Subtle decline in functions not related to memory, or affecting attention,
language or visual-spatial function
○ Less common
○ May be forerunner for dementias other than Alzheimer’s
Ger 5: Depression
1.
Understand diagnostic criteria for depression
● major depression can be made if a patient has five or more of the following symptoms during
the same 2-week interval with at least one of the symptoms being either depressed mood or
loss of interest or pleasure in activities that were previously pleasurable:
○ 1 dx must be depressed mood and loss of interest or pleasure in previously pleasurable
activities
○ 2nd dx can be: Significant weight gain or loss, in/hypersomnia, psychomotor agitation or
retardation, fatigue, feelings of worthlessness or inappropriate guilt, impaired
concentration, recurrent thoughts of death.
● dysthymia - less severe but longer lasting than depression (chronic low mood)
○ dx requires 2 (or more) of the following: poor appetite/overeating, in/hypersomnia,
fatigue, low self esteem, impaired concentration, hopelessness
○ chronicity is an essential element; specifically,for the majority of the time they must
exhibit the above sxs over 2 years and not be asx for more than 2 mos. (during those 2
years)
2.
Understand risk factors for depression
a. Increased chronic conditions = increased depression (both can affect each other)
b. Living environment, nursing homes have higher depression rates
c. Inability to perform ADLs
3.
1.
Understand how depression affects comorbidities
a. depression is not the most prevalent in the elderly but has the highest impact on
their health when it is present. So, an elderly person is more likely to commit
suicide when depressed.
b. depression is an independent risk factor for ACS (SSRIs have been shown to be
beneficial for both depression and ACS)
c. depression is an independent risk factor for mortality
Ger 6: Delirium
Identify risk factors for delirium
Predisposing Factors (chronic):
Precipitating Factors (acute that initiate)
• Advanced age
• Preexisting dementia
• History of stroke
• Parkinson disease
• Multiple comorbid conditions
• Impaired vision
• Impaired hearing
• Functional impairment
• Male sex
• History of alcohol abuse
• New acute medical problem
• Exacerbation of chronic medical
problem
• Surgery/anesthesia
• New psychoactive medication
• Acute stroke
• Pain
• Environmental change
• Urine retention/fecal impaction
• Electrolyte disturbances
• Dehydration
• Sepsis
An Old Alcoholic Male with parkinson,
strokes, and dementia who can’t see, hear or
be functional.
2.
Understand use of lab work, imaging and other studies in evaluation of delirium
a. the Dx is based entirely on the H&P: evaluation confirms and identifies causes
i.
Key aspects of hx: acute onset more common with delirium as well as
fluctuations in mental status
ii.
Key aspects of PE: evaluation of mental status, most importantly,
inattention and abnormal level of consciousness
b. labs and imaging are for etiology and correctable factors
CBC
infection/severe anemia
Chem-7
hyper/hyponatremia
BUN/Cr
dehydration
UA
UTI is common in frail elders
CXR
Pneumonia/CHF
ECG
MI/Arrhythmia
ABG
COPD (hypercarbia)
Drugs
even with normal levels of some drugs (Meperidine has a high risk factor for
delerium)
Tox Screen
for younger pts usually
CT/MRI
younger pts
Lumbar
Puncture
younger pts
EEG
diffuse slow wave activity
Glucose
hypo/hyper and hyperosmolar state (Type II DM)
LFT/INR*
rare
3.
Understand use of medication for agitated delirium
● non-pharm is the cornerstone of tx
● All drug tx is off label. Must be used cautiously and having someone to console the pt
may be preferable.
● high-potency antipsychotics (haloperidol is best in young AIDS pts) are considered
the treatment of choice for agitation in delirium because of their low anticholinergic
potency and minimal risks for hypotension or respiratory depression
● Table 3 summary:
○ Haloperidol is typical but CI in parkinson/Lewy body disease bc of Sx (EPS).
ALso has QT prolongation.
○ Lorazepam is second line (also used in alcohol withdrawal/neuroleptic malignant
sx)
○ Olanzapine/Quetiapine can be substituted in pts with parkinson/lewy body
disease as they have less EPS.
○ If sedation is an issue with other txs use Risperidone.
● Meperidine - high risk for delirium
● Benzos - high risk for delirium
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1.
2.
Ger 7: AGS Beers Criteria
Understand the intent of Beers Criteria
Understand clinical application of the criteria
Geri 7a: Mallet L, Spinewine A, Huang A. Prescribing in elderly people 2: The challenge
of managing drug interactions in elderly people. The Lancet 2007; 370: 185-191.
1. Describe categories of drug interactions that may occur in elderly patients
2. Identify considerations for prescribing medications for elderly patients
3. Describe elderly patients that may be at a higher risk of drug interactions
1.
2.
3.
Falls
Identify causes and risk factors for falls
Understand evaluation of a fall patient
Understand recommendations for fall prevention
1.
2.
3.
Frailty Syndrome
Discuss the pathophysiology of frailty
Understand the frailty cycle
Understand indicators and measures of frailty
1.
2.
3.
4.
Osteoporosis
Understand indications for measuring bone mineral density
Understand pharmacologic options for treatment of osteoporosis
Understand adverse effects of pharmacologic treatments
Understand risk stratification for falls
1.
2.
3.
Deficits in Communication and Information Transfer
Identify ways to improve communication between hospital and outpatient setting
Identify adverse events that may occur due to poor communication
Understand benefit of efficient communication between providers
1.
2.
3.
4.
Elder Maltreatment
Identify physical findings abuse
Understand mimickers of abuse
Understand types of abuse
Identify those at risk of being abused
Pressure Ulcers
1.
2.
3.
4.
Understand Braden Scale
Understand etiology of pressure ulcers
Understand ulcer staging system
Understand pressure ulcer management
1.
2.
Ger 14: Palliative Care
Understand the role of palliative care
Understand approaches to common symptoms of terminally ill
3.
Understand coordination of care in each stage of serious chronic illnesses