CHAPTER 14 Geriatrics
I. Definitions
A. Geriatrics is the branch of medicine concerned with the health care of the elderly. It aims to promote health and to prevent and treat disease and disabilities in older adults.
B. A geriatrician is a medical doctor who is specially trained to prevent and manage the unique and, oftentimes, multiple health concerns of older adults. Geriatricians are able to treat older patients, manage multiple disease symptoms, and develop care plans that address the special health care needs of older adults.
II. Conditions Commonly Seen in Geriatric Patients
A. Parkinson disease
1. Pathophysiology and epidemiology
a. Progressive, neurologic disorder due to degeneration of presynaptic dopaminergic neurons in the substantia nigra equals the loss of postsynaptic dopamine activity in the striatum (dopamine involved in inhibition of cholinergic and glutamatergic loops and increased activity in these systems)
b. Mean age of diagnosis: 55–60 years; incidence approximately 20/100,000; mortality not greatly increased
c. Etiology of idiopathic Parkinson disease unknown: possibly a combination of genetic predisposition and environmental factors. Hereditary accounts for less than 2% of all diagnosed cases. Oxidative stress and free radical damage may contribute to neuronal degeneration.
d. Drug-induced: Caused by antidopaminergic agents (metoclopramide, prochlorperazine, neuroleptics, reserpine, methyldopa, etc.); rarely amiodarone, selective serotonin reuptake inhibitors (SSRIs), valproic acid, diltiazem, verapamil
e. Treatment for drug-induced Parkinson disease: discontinue drug, administer anticholinergic agents (e.g., diphenhydramine or benztropine)
2. Signs and symptoms (Figure 14-1)
b. Minor: difficulty with fine coordinated movements; postural disturbance (later in disease state); flattened facial expression (masked facies); voice may become hypophonic, monotonal; shuffling gait; micrographia; drooling, difficulty swallowing liquids; pain in affected limb; depression or dementia; constipation; orthostatic hypotension; urinary frequency; sweating; dermatitis; sexual dysfunction
3. Treatment
a. The goal is to improve motor symptoms (tremor, bradykinesia, rigidity), inhibit cholinergic action, ease dopaminergic action
b. Guidelines differ regarding initial therapy: dopamine first line versus last. Treatment should not be initiated in most patients until motor symptoms significantly impair quality of life (QOL) and/or daily function.
1) Mild disease: amantadine (Symmetrel), selegeline (selegline monotherapy provides mild-to-modest relief of motor symptoms and delays need for levodopa)
c. All treatments are patient specific: doses must be tailored and changed according to patient’s disease state, progression, and side effects.
d. Drug holidays: no longer widely recommended due to risk of severe immobility, aspiration pneumonia, venous thromboembolism, depression
5. Medications
a. Levodopa/carbodopa (Sinemet, Sinemet CR)
1) Mechanism of action: Levodopa is a dopamine precursor that can cross the blood-brain barrier and replace dopamine in the brain (metabolized by dopa-decarboxylase to dopamine). Carbidopa inhibits peripheral dopa-decarboxylase and allows more dopamine to enter brain, which allows lower levodopa dose, more-rapid dosage titration, and reduced peripheral side effects (nausea/vomiting, arrhythmias, orthostatic hypotension).
2) Usual dose: minimum 75–100 mg/day carbidopa required. Initial dose is one carbidopa 25 mg/levodopa 100 mg tablet PO three times per day. Levodopa absorption is impaired by high-protein meals.
3) Side effects (levodopa): nausea/vomiting, insomnia or sedation, confusion, hallucinations, dyskinesias, muscle cramping (dystonias), wearing off phenomenon (end-of-dose failure), hypersexuality
4) Levodopa/carbidopa (Sinemet): Approximately 5 years after initiation, many patients experience motor complications (wearing off phenomenon, dyskinesia). Recent guidelines recommend initiating a dopamine agonist early in therapy, which delays need for levodopa and complications of therapy. As disease progresses, dopamine will be needed.
b. Amantadine (Symmetrel): mildly effective against tremor and rigidity
1) Mechanism of action: unclear, may be an NMDA (N-methyl d-aspartate) antagonist; blocks uptake and enhances the release of dopamine
3) Side effects: dry mouth, peripheral edema, livedo reticularis, sedation, confusion, hallucinations; may cause insomnia if taken in late evening (stimulating effect in some patients), may be useful for young patients with fatigue
c. Selegiline (Eldepryl): mild to moderate symptom relief as monotherapy in early disease; also used for adjunctive therapy late in disease to prevent wearing-off phenomenon. Some studies show increased morbidity when used with levodopa. Multiple other studies do not show increased morbidity; however, may want to avoid if patients have history of dementia, frequent falls, or postural hypotension
1) Mechanism of action: selective, irreversible MAO-B inhibitor. Selectivity is lost if the dose is >20 mg/day; metabolized to amphetamine/methamphetamine
2) Side effects: insomnia, sedation, confusion, agitation, hallucinations, vivid dreams; may enhance levodopa-induced dyskinesias
4) Usual dose: 5 mg PO twice daily with breakfast and lunch, may cause insomnia if taken in late evening; consider lowering levodopa dosage by 20% when starting selegiline
d. Dopamine receptor agonists: bromocriptine (Parlodel), pergolide (Permax), pramipexole (Mirapex), ropinirole (Requip)
1) Dopamine agonists may be used as monotherapy early in the disease; adjunctive therapy in late disease to manage motor complications
2) Usual dose: start doses low and titrate slowly. It may take months to achieve therapeutic dosage; taper up and taper down. Reduce the dose in patients with renal disease.
a) Bromocriptine: 1.25 mg PO twice daily, increasing the total daily dose by 2.5 mg every 14–28 days until the desired therapeutic response occurs
c) Pramipexole: initially, 0.125 mg PO three times per day. Gradually increase by 0.125–0.25 mg/dose (0.375–0.75 mg/day) every 5–7 days to a maximum dosage of 1.5 mg PO three times per day (4.5 mg/day).
e. Cateochol-O-methyltransferase (COMT) inhibitors: tolcapone (Tasmar), entacapone (Comtan)
3) COMT inhibitors work with levodopa and prolong its action. Because they affect levodopa metabolism, they are only effective in patients receiving levodopa therapy.
4) Entacapone is a reversible peripheral COMT inhibitor. It is the preferred COMT inhibitor because it does not require liver function test (LFT) monitoring. Tolcapone is a peripheral and central COMT inhibitor. It achieves greater COMT inhibition than entacapone. However, its use is restricted due to occurrence of fatal hepatotoxicity; discontinue tolcapone use after 3 weeks if patient fails to show expected benefit from the drug. Patients must give consent, and LFTs should be performed every 2 weeks for the first 12 months, then every 4 weeks for the next 6 months, and then every 8 weeks for the duration of therapy.
5) Usual dose
a) Tolcapone: initially 100 mg PO three times per day. The maximum recommend dose is 600 mg/day PO given in three divided doses.
6) Side effects: exacerbation of levodopa side effects, such as nausea, urine discoloration (dark yellow to orange-brown), diarrhea (after several weeks). Be alert to signs of liver problems, such as worsening abdominal pain, yellowing of the skin or whites of the eyes (especially with tolcapone). Retroperitoneal fibrosis and other lung problems are rare.
d. Drug side effects
1) Nausea/vomiting: Patients should take levodopa and dopamine agonists with nonprotein snack. If antiemetics are needed, do not use dopamine receptor blockers (see section on drug-induced Parkinson disease).
2) Hallucinations/psychosis: taper off suspected agents until determination of which agent caused the effect; if taper causes significant worsening of Parkinson disease, atypical antipsychotics should be considered (avoid phenothiazine and other traditional antipsychotics).
B. Alzheimer disease and dementia
1. Pathophysiology/epidemiology
a. Genetic factors: known to play a role in some cases of Alzheimer disease (AD). Some families with a history of early-onset AD have a mutation on the amyloid beta precursor protein (APP) gene. Another gene, the apolipoprotein (Apo) E gene, also has been implicated in the disease. Apo E is a protein found with beta amyloid (a protein found in the brains of patients with AD) in neuritic (inflamed nerve) plaques. Together, these genetic mutations account for less than 10% of all patients with AD.
b. Plaques and tangles: The causes of AD are poorly understood, but its effect on brain tissue has been demonstrated clearly. AD damages and kills brain cells. Neurons generate electrical and chemical signals that are relayed from neuron to neuron to help an individual think, remember, and feel (physically and emotionally). Brain chemicals called neurotransmitters help these signals flow seamlessly between neurons. Initially in people with AD, neurons in certain locations of the brain begin to die. When they die, lower levels of neurotransmitters are produced, creating signaling problems in the brain. One neurotransmitter, acetylcholine, has been found to be deficient in the brains of those with AD. Medication treatment is based around increasing the amount of acetylcholine in the brain.
1) Plaques and tangles in brain tissue are considered hallmarks of AD. Plaques are made up of beta-amyloid, a normally harmless protein. Although the ultimate cause of neuron death in AD is not known, mounting evidence suggests that a form of beta-amyloid protein may be the cause. The plaque is responsible for memory deterioration in individuals with AD.
c. Inflammation: Researchers have observed inflammation in the brains of some people with AD. As beta-amyloid plaques develop in the spaces between neurons, immune cells are getting rid of dead cells and other waste products in the brain. Although research has found that the inflammation occurs before plaques have fully formed, it is not known how this development relates to the disease process. There is also debate about whether inflammation has a damaging effect on neurons or whether it is beneficial in clearing away plaques.
d. Age is the most important risk factor for AD. The number of people with the disease doubles every 5 years beyond age 65 years.
e. It is estimated that about five million Americans have AD, and about 360,000 people are newly diagnosed every year. AD affects about 10% of people ages 65 years and older, and the number doubles roughly every 10 years after age 65 years. Half of the population ages 85 years and older may have AD.
f. Signs and symptoms
1) Mild symptoms: mental deterioration, such as memory impairment and confusion, difficulty learning and remembering new information, difficulty with daily tasks, and depression (sadness, decreased interest in usual activities, loss of energy)
2) Moderate symptoms: forgetting old facts, continually repeating stories, and/or asking the same questions over and over, deficiencies in intellect and reasoning, a lack of concern for appearance, hygiene, and sleep
3) Severe symptoms: groaning, screaming, mumbling, or speaking gibberish, failing to recognize the faces of family members or caregivers, great difficulty with all essential activities of daily life
g. Medications
1) Cholinesterase inhibitors: donepezil (Aricept), rivastigmine (Exelon), galantamine (Razadyne), and tacrine (Cognex)
a) Mechanism of action: inhibits the degradation of acetylcholine by inhibiting the enzyme acetylcholinesterase
b) Usual doses
(1) Donepezil (Aricept): initial 5 mg/day at bedtime; may increase to 10 mg/day at bedtime after 4–6 weeks
(2) Rivastigmine (Exelon): initial 1.5 mg twice daily; may increase by 3 mg/day (1.5 mg/dose) every 2 weeks based on tolerability (maximum recommended dose 6 mg twice daily)
c) Side effects: gastrointestinal effects (diarrhea, nausea, vomiting, anorexia) are most common and may require dose reductions for some agents (e.g., galantamine). Increased salivation, increased respiratory secretions, bradycardia, headache, fatigue, and vertigo are other side effects. Hepatotoxicity has been attributed to the use of tacrine and has limited the drug’s clinical use.
2) Memantine (Namenda)
a) Mechanism of action: NMDA antagonist, blocks glutamate activity and prevents excessive influx of calcium and, thereby, neuronal death
b) Usual dose: Initial 5 mg/day; increase dose by 5 mg/day to a target dose of 20 mg/day; wait at least 1 week between dosage changes; doses >5 mg/day should be given in two divided doses.
4) Adjunct therapies
a) Depression that occurs during the early stages is commonly treated with antidepressant medications, such as selective serotonin reuptake inhibitors (SSRI) including fluoxetine (Prozac) and sertraline (Zoloft), and the tricyclic antidepressants (TCA), including amitriptyline (Elavil). Side effects include drowsiness, fatigue, and sedation. TCA may increase mental confusion.
b) Agitation may be treated with an antipsychotic medication, such as haloperidol (Haldol), risperidone (Risperdal), olanzapine (Zyprexa), and quetiapine (Seroquel). NOTE: Antipsychotics are not FDA approved to treat behavioral symptoms of AD and may increase the risk for death in elderly patients with dementia. Side effects include sedation, confusion, and tardive dyskinesia (an irreversible movement disorder characterized by lip smacking, facial grimacing, and unsteady walking).
C. Glaucoma
1. Pathophysiology and epidemiology
a. Glaucoma is the name given to a group of conditions caused by increased intraocular (inside the eye) pressure (IOP), resulting either from a malformation or malfunction of the eye’s drainage system. Left untreated, an elevated IOP may cause irreversible damage to the optic nerve and retinal fibers, resulting in a progressive, permanent loss of vision. However, early detection and treatment can slow or even halt the progression of the disease.
b. It is estimated that more than three million Americans have glaucoma but only half of those know they have it. Most individuals with glaucoma are not aware of problems with their vision. This is because the central vision (for reading and recognizing people) is only affected when glaucoma has advanced to a late stage. Even when central vision is still good, glaucoma may affect the vision needed for driving and other daily functions, including seeing stair steps or reading.
c. Approximately 120,000 are blind from glaucoma, accounting for 9%–12% of all cases of blindness in the United States. About 2% of the population 40–50 years old and 8% older than 70 years of age have elevated IOP.
d. Glaucoma is the second leading cause of blindness in the world, according to the World Health Organization (WHO). Glaucoma is the leading cause of blindness among African Americans.
2. Most common forms of glaucoma
a. Open-angle glaucoma (chronic): Open angle (also called chronic open angle or primary open angle) is the most common type of glaucoma and usually causes no symptoms at first. Even though the anterior structures of the eye appear normal, aqueous fluid builds within the anterior chamber, causing the IOP to become elevated. Left untreated, this may result in permanent damage of the optic nerve and retina.
b. Angle-closure glaucoma (acute): Acute angle closure glaucoma, or closed-angle glaucoma, occurs because of an abnormality of the trabecular mesh work and the canal of Schlemm in the eye that keeps aqueous humor fluid from draining. In most of these cases, the space between the iris and cornea is narrower than normal, putting pressure on the canal of Schlemm and leaving a smaller channel for the aqueous humor to drain. If the flow of aqueous becomes completely blocked, the IOP rises sharply, causing a sudden angle closure attack. Only about 10% of the population with glaucoma has acute angle closure glaucoma.
c. Secondary glaucoma: Secondary glaucoma can develop as complications of other medical conditions, such as inflammation, trauma, previous surgery, diabetes, or a tumor. These types of glaucoma are sometimes associated with eye surgery or advanced cataracts, eye injuries, certain eye tumors, uveitis (eye inflammation), and certain medications (including topical steroid creams, cocaine, chlorpromazine or Thorazine, and phenelzine or Nardil).
5. Medications
a. Prostaglandin analogs
2) Adverse effects: may change the pigment of the iris (may be permanent); may change direction of eyelashes (may be permanent) and increase growth of eyelashes
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