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Pharmacotherapy IA: Nervous System > Pharmacotherapeutics of Geriatric Dementias > Flashcards

Pharmacotherapeutics of Geriatric Dementias Flashcards

1
Q

True or False: Alzheimer’s dementia (AD) is the most common cause of dementia.

A

True

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2
Q

What is the second most common type of dementia?

A

Vascular dementia

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3
Q

True or False: the prevalence of vascular dementia increases linearly with age.

A

True

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4
Q

What are the four major anatomical changes that occur in Alzheimer’s Dementia?

A
  • Neurofibrillary tangles
  • Amyloid plaques
  • cortical atrophy
  • Degeneration of cholinergic and other neurons
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5
Q

Describe Acetylcholine imbalance in Alzheimer’s disease

A

Normal Pt: balanced Ach and Dopamine

Alzheimer’s Pt: loss of choline-acetyl transferase (synthesizes Ach) and loss of cholinergic neurons

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6
Q

What are the risk factors of Alzheimer’s Dementia?

A

-age: young (15-19) or old (>40), small head/brain, head trauma, family history, low level of education, vascular disease risk factors (smoking), mild cognitive impairment

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7
Q

What is Mild Cognitive Impairment (MCI)?

A

Categorizes people with cognitive issue insufficient to warrant dementia diagnosis.
-can possibly develop into AD

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8
Q

What does MMSE stand for? What are the categories for it?

A
  • Mini Mental State Exam

- mild, moderate, severe

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9
Q

Mild MMSE

A
  • score 21-26
  • difficulty remembering events
  • Can still complete ADLs and even IADLs
  • may get lost while driving
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10
Q

Moderate MMSE

A
  • score 10-20
  • Requires assistance with ADLs
  • severe impairment of event recall
  • functional fluctuation, may be suspicious
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11
Q

Severe MMSE

A
  • score 0-9
  • lost ability to speak, walk and feed self
  • incontinence of urine and feces
  • needs 24/7 care
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12
Q

True or False: Genetic link of AD accounts for a majority of cases

A

False, it accounts for a minority of cases

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13
Q

Which proteins are involved in the AD genetic link?

A
  • Beta-amyloid
  • Apolipoprotein E (Apo E2, 3, 4)
  • Tau
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14
Q

How does Beta-amyloid function in AD?

A

overproduction linked to alterations in chromosomes 1, 21, or 14
-associated with early onset and senile plaques

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15
Q

How does Apolipoprotein E function in AD?

A

Mutations associated with chromosome 19

-associated with neurofibrillary tangles and late onset AD

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16
Q

How does Tau function in AD?

A
  • soluble protein that supports microtubule function
  • mutations in chromosome 17 associated with PD (not with AD)
  • hyperphosphorylated tau associated with neurofibrillary tangles
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17
Q

AD presents as _____ deficits that occur ______ over time

A
  • cognitive deficits

- progressively over time

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18
Q

What are the major symptoms of AD?

A

cognition: memory loss, apraxia (diff. motor movements), agnosia(can’t identify objects or people), disorientation, impaired executive function
Neuropsychiatric: depression, psychotic symptoms, behavioral disturbances
Functional: impaired ADLS and IADLs

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19
Q

What is used for AD diagnosis?

A
  • DSM-5 criteria
  • extensive neuropsychiatric testing to indicate progressive cognitive decline
  • neuroimaging and serological testing to rule out other causes of cognitive decline
20
Q

What are the pharmacological options for AD?

A
  • Cholinesterase inhibitors (Donepezil, Rivastigmine, Galantamine)
  • NMDA antagonist (Memantine)
  • Biogen’s Aducanumab (new therapy)
21
Q

MOA, dosage forms, and administration of Donepezil (Aricept)

A
  • inhibits AChE
  • oral tablets, ODT
  • Administer at bedtime without regard to meals
  • used for mild, moderate, and severe AD
22
Q

MOA, dosage forms, and administration of Rivastigmine (Exelon)

A
  • inhibits both AChE and BChE (butyrylcholinestrase)
  • available in capsule or patch
  • Used for mild, moderate and severe AD
  • In severe cases, use patch; dosing of patch is the same as in mild to moderate case
  • administer with meals; place patch on upper or lower back
  • starting dose not clinically effective
  • conversion: if oral dose is less than 6 mg, use 4.6 mg patch; if greater than or to 6 mg, use 9.5 mg patch the next day
  • Cautious titration for CrCl less than 50 ml/min
23
Q

MOA, dosage forms, and administration of Galantamine (Razadyne)

A
  • AChE inhibitor; also stimulates nicotininc acetylcholine receptors (nAChRs); may increase glutamate and serotonin
  • used for mild to moderate AD
  • IR tablets, ER capsules, oral solution
  • starting dose not clinically effective
  • can be used off-label for severe AD
  • renal adjustment for CrCl 9-59 ml/min; don’t use if less than 9 ml/min
  • IR or solution with breakfast and dinner; ER with breakfast
24
Q

MOA, dosage forms, and administration if Memantine (Namenda)

A
  • NMDA antagonist/modulator (not complete antagonist; type of glutamate receptor)
  • Used for moderate to severe AD
  • tablet, ER capsule, oral solution, combination package
  • admin without regard to meals; ER swallowed whole or contents sprinkled in applesauce
25
Q

What is the current state of approval of Biogen’s Aducanumab (Aduhelm)?

A
  • FDA advisory committee unanimously rejected drug
  • accelerated approval granted based on endpoint (reduced amyloid beta plaque) and not clinical efficacy
  • post approval trials must demonstrate clinical benefit
26
Q

Biogen’s Aducanumab MOA, dosage form(s), admin, ADRs, and pricing

A
  • Used for MCI or mild dementia
  • IV admin
  • diluted in 0.9% sodium chloride and infused over 1 hour every 4 weeks for a year
  • $56,000 per year
  • ADRs: brain edema, headache, cerebral hemorrhage
27
Q

What is the truth regarding managing expectations for AD treatment?

A
  • medications are not curative
  • changes in MMSE are variable
  • possible slight improvement in MMSE (1 or 2 Points)
  • over time MMSE scores will decline despite treatment
28
Q

When should AD therapy be discontinued?

A
  • no clear recommendations on when to d/c
  • patients that can’t speak, ambulate, or provide self-care have little reason to continue medication; risks exceed benefits
29
Q

Which agents used for neuropsychiatric symptoms in dementia should be avoided in elderly?

A
  • Select SSRIs (paroxetine and fluoxetine): paroxetine is highly anticholinergic; fluoxetine has long half-life–>excess CNS stimulation, sleep disturbance, agitation, falls
  • Psychosis-Antipsychotics (clozapine and olanzapine)–>CVD and death
30
Q

What is the extent and time frame of improvement of pharmacological intervention in AD?

A
  • 4-6 weeks for observable benefit

- benefits may last 1-2 years

31
Q

When should a patient switch to another AChE-I in AD?

A
  • if there’s no improvement after 12-24 weeks of treatment

- No need to try a third

32
Q

True or False: Memantine may be used in combo with an AChE-I in moderate to severe AD for added benefit.

A

True

33
Q

What should be done if AChE-I therapy is interrupted for more than a few days in AD?

A

Re-titration from starting dose is recommended

34
Q

True or False: AM dosing is an option with donepezil for alleviation of insomnia and vivid dreams/nightmares in AD

A

True

35
Q

True or False: start low and go slow… but go!

A

True

36
Q

What is Vascular Dementia (VaD)?

A

cognitive disorder caused by vascular disease

  • most common cause is occlusion of cerebral blood vessels by thrombus or embolus leading to ischemic brain injury
  • hemorrhagic brain lesions responsible for some VaD cases
37
Q

Risk factors for VaD

A

advanced age, diabetes mellitus, small vessel cerebrovascular disease, hypertension, heart disease, hyperlipidemia, cigarette smoke, alcohol use, more common in males

38
Q

What is the clinical presentation of VaD?

A
  • stepwise cognitive decline (stability followed by rapid decline due to cerebrovascular insults)
  • personality and mood changes, depression, psychomotor retardation
  • gait disturbance, unsteadiness, unprovoked falls
  • urinary incontinence and frequency
39
Q

Can AChE-Is be used in VaD treatment?

A

deficits in cholinergic transmission and nicotinic binding abnormalities have been observed
-some data indicates improvement in cognition and daily function

40
Q

What are secondary prevention methods for VaD?

A

-Bp regulation, cholesterol control, diabetes control (A1C<7-8%), antiplatelet therapy, smoking cessation, decrease alcohol intake, lifestyle modification

41
Q

Describe Parkinson’s disease related dementia pathology

A
  • Lewy bodies: abnormal proteinaceous inclusions throughout brain
  • Neurofibrillary tau tangles may be present
  • brain atrophy
42
Q

What are the two subtypes of Parkinson’s disease related dementias?

A
  • Lewy Body Dementia (DLB): cognitive symptoms develop less than 1 year after PD diagnosis
  • Parkinson’s Disease Dementia (PDD): cognitive symptoms develop >1 year after PD diagnosis
43
Q

True or False having MCI at PD diagnosis increases risk of conversion to dementia

A

True: risk of conversion increases 6 fold

44
Q

What are the risk factors of Parkinson’s disease related dementias?

A

MCI, advanced age, gait dysfunction, presence of hallucinations

45
Q

What pharmacological treatments can be used for PDD and DLB?

A
  • cholinesterase inhibitors for cognition and memory
  • donepezil and rivastigmine
  • rivastigmine has higher efficacy but more adverse events
  • donepezil used more off label while rivastigmine is FDA approved for PDD
46
Q

Why should anticholinergic agents be avoided in PDD?

A

anticholinergics are indicated in early PD but worsen PDD

Pharmacotherapy IA: Nervous System (2 decks)

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