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Pharmacology III > Alzhiemers > Flashcards

Alzhiemers Flashcards

1
Q

What are the types of dementia?

A 
Mild Cognitive Impairment (MCI)
Alzheimer’s Disease (AD)
Vascular Dementia
Lewy Body Dementia
Parkinson’s Dementia
Frontal Lobe Dementia (Frontotemporal Dementia)
Mixed Dementia
Vascular Dementia and AD
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2
Q

What is a sudden alteration in cognitive function that can last several hours to days?

A

Delirium

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3
Q

What is delirium?

A 
Sudden alterations in cognitive function
Hours to days
Fluctuations in cognition during day
Attention span impaired
Rarely aware of cognitive deficits
Often accompanied by disturbances in sleep-wake cycle and psychomotor disturbances
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4
Q

What are the underlying pathologies associated with delirium?

A

UTI
MI
Pneumonia
Pain

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5
Q

What drugs can induce delirium?

A

Benzodiazepines, anticholinergics, antihistamines, anticonvulsants, beta blockers, sympathomimetics, lithium, diuretics

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6
Q

How is depression differentiated from dementia?

A

Short and long-term memory are selectively impaired
No progression/worsening of cognitive dysfunction
Pt usually aware of deficits (often disturbed by dysfunction)

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7
Q

What is the most common form of dementia?

A

Alzheimer’s Disease

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8
Q

What is alzheimer’s disease?

A

Neurodegenerative disease characterized by non-reversible, progressive cognitive deterioration, together with declining activities of daily living and by neuropsychiatric symptoms or behavioral changes

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9
Q

What are the risk factors for alzheimer’s disease?

A

-Age (most common being over 65)
-Dementia in close family member
-E4 allele of the ApoE gene
-History of psychiatric illness
-Other possible risk factors
Down’s Syndrome, exposure to anesthetic agents, head injury, diabetes

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10
Q

What are the genetics associated with early onset of alzheimers?

A

Almost all early-onset cases are attributable to chromosomal abnormalities
Mutations in 3 genes:
Prensilin 1 on Chromosome 21
Amyloid Precursor Protein (APP) on Chromosome 1
Presenilin 2 on Chromosome 1
Mutations lead to an increase in B-A4 peptide fragments of APP which forms neuritic plaques

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11
Q

What are the genetics associated with late onset alzheimers?

A 
Apolipoprotein E (Apo E) on Chromosome 19
May be more dependant on environmental factors
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12
Q

What family hx is associated with Alzheimer’s Disease?

A

Risk of inheriting AD may be increased four-fold

Apo E4 allele

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13
Q

What is involved with the neuropathology of Alzheimer’s Disease?

A 
Neurofibrillary tangles (NFTs) from abnormally phosphorylated tau protein
Tau essential for axonal transport- stabilizes neuron

Neurons with abnormal tau become unstable and eventually die
NFTs accumulate because not recognized as abnormal
Neuritic plaque lesions with insoluble B-amyloid peptide core
Accumulation leads to neuronal death

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14
Q

What is the pathology Alzheimer’s Disease?

A

Immune System
Glial cells, cytokines (IL-1 and IL-6), and complement cascade
Present near areas of plaque formation

Inflammation (women doesn’t really help)
Occurs secondary to neuronal degeneration

Oxidative damage by free radicals
Tx targets these free radicals

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15
Q

What is the cholinergic system of AD?

A

Multiple neuronal pathways are destroyed by plaques
Leading to shortage of Acetylcholine (this is important for memory and cognition centers)
These cholinergic pathways project to the frontal cortex and hippocampus
Areas strongly associated with memory and cognition

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16
Q

What is involved with the glutamatergic system and AD?

A
  • -Glutamate involved in neuronal pathways essential to learning & memory
  • -B-amyloid aggregation can disrupt transmission of glutamate and lead to excess stimulation of NMDA receptors
  • -Excess stimulation of NMDA receptors can lead to high intracellular Ca++ concentration and excitotoxicity -> neuronal death
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17
Q

What are the cognitive deficits in AD?

A
  • -Early symptom is loss of memory (amnesia), which usually manifests as minor forgetfulness that becomes steadily more pronounced with the progression of the illness, with relative preservation of older memories.
  • -As disorder progresses, cognitive impairment extends to domains of language (aphasia), skilled movements (apraxia), recognition (agnosia), and functions related to frontal and temporal lobes (decision-making and planning)
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18
Q

What is the average duration of AD?

A

7-10 years

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19
Q

What stage of AD is no congnitive impairment?

A

Stage 1

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20
Q

What stage of AD is very mild cognitive decline?

A

Stage 2

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21
Q

What stage of AD is mild cognitive decline?

A

Stage 3

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22
Q

What stage of AD is moderate cognitive decline?

A

Stage 4

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23
Q

What stage of AD is moderately severe cognitive decline?

A

Stage 5

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24
Q

What stage of AD is severe cognitive decline?

A

Stage 6

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25
What stage of AD is very severe cognitive decline?
Stage 7
26
What do the initial stages of AD involve?
Initial stages include cognitive deficits and neuropsychiatric symptoms
27
What do the final stages of AD involve?
Final stages of disease often result in placement in long-term care Lose ability to eat, walk, or communicate
28
What are the events that generally result in death of AD patients in the final stages of the dz?
Choking Aspiration Infection
29
How is AD diagnosed?
Made on basis of history, clinical observation, memory tests and intellectual functioning over weeks or months; blood tests and neuroimaging (PET and SPECT scans) to R/O alternative diagnoses No medical tests available to diagnose conclusively pre-mortem
30
What score on the MMSE is considered mild to moderate AD?
10-26 on MMSE
31
What score on the MMSE is considered to be moderate to severe AD?
3-14 on MMSE
32
What are the proposed txs suggested to delay AD progression?
Vitamin E | Selegiline
33
Vitamin E
Recommended that every AD patient go on vit E that is the initial tx Recent meta-analyses suggest that high-dose Vit E (>400 IU/day) may increase all-cause mortality Recommendation: If used, dose
34
Selegiline
Improvements similar to vitamin E in 1 study | Recommendation: Not recommended as adjunctive tx
35
What are the proposed treatments to prevent AD?
Estrogen | NSAIDS
36
Estrogen
The Women’s Health Initiative Memory Study 4500 women aged 65+ Assess incidence of dementia and MCI taking placebo or estrogen + progesterone Study didn’t support a role for estrogen in treating sx of AD Ongoing clinical trials are being conducted for possible preventative treatment role Recommendation: Use only in pts who have another medical reason for HRT
37
NSAIDS
Epidemiologic studies indicate lower incidence of AD or higher MMSE scores Evidence of delaying disease onset and progression, slowed rate of cognitive impairment 2 years of exposure necessary for protective effect Mixed results regarding efficacy once AD has begun Safety profile limits use Recommendation: Do not use as treatment at this time
38
When should lipid lowering agents be used in patients with AD?
If they have a lipid problem not just to tx alzheimers
39
What should be used to tx mild AD?
Donepezil, galantamine, rivastigmine, tacrine* or memantine | + Vitamin E
40
What should be used to tx moderate to severe AD?
Donepezil, galantamine, rivastigmine or tacrine* alone OR donepezil in combination with memantine + Vitamin E * tacrine no longer used due to hepatotoxicity
41
What can be used to evaluate medication response in AD?
MMSE | ADAS-COG
42
What is shown on MMSE to evaluate med response in AD?
Average expected decline in AD is 2-4 points per year in an untreated patient Halting progression or improvement over a 6-12 month time period during clinical trials would be considered response
43
What is shown on ADAS-Cog to evaluate med response in AD?
Average expected decline is 4pts at 6 months and 7pts at 1 year Halting progression or improvement at 6 months or longer considered response
44
What is the primary goal for the treatment of AD?
Primary goal is to maintain patient functioning for as long as possible and symptomatically treat cognitive symptoms
45
What is the secondary goal for the tx of AD?
Secondary goal is to treat the psychiatric and behavioral sequelae
46
What is used to treat mild to moderate AD?
Cholinesterase inhibitors
47
What is used to treat moderate to severe AD?
Memantine +/- cholinesterase inhibitor | donepezil
48
What are the cholinesterase inhibitors?
``` Tacrine (Cognex) – no longer clinically used (hepatotoxicity) Donepezil (Aricept)- oral Galantamine (Reminyl)- oral Rivastigmine (Exelon)- oral or patch No P450 interactions with metabolite ```
49
What is the goal of cholinesterase inhibitors?
To slow down rate of decline NOT USED TO CURE
50
Cholinesterase inhibitors- MOA
Augment cholinergic transmission at remaining synapses
51
Donepezil (Aricept®)- MOA
Long acting, selective for AChE, reversible inhibitor
52
Donepezil (Aricept®)- indications
Mild, moderate, and severe Alzheimer’s dementia
53
Donepezil (Aricept®)- pharmacokinetics
Metabolized by CYP 2D6 and 3A4 Minimal risk of clinically significant drug-interactions Partial renal elimination
54
What is the drug of choice of the cholinersterase inhibitors for AD?
Donepezil
55
Rivastigmine (Exelon®)- MOA
Selective for AChE (G1) | Pseudo-irreversible, non-competitive
56
Rivastigmine (Exelon®)- indications
Mild to moderate Alzheimer’s dementia | Mild to moderate Parkinson’s dementia
57
Rivastigmine (Exelon®)- pharmacokinetics
Not significantly metabolized by CYP450 (avoids a lot of drug interactions) Low probability of drug-drug interactions Available as 2mg/ml oral solution
58
Galantamine (Razadyne®)- MOA
Reversible, competitive inhibitor of AChE | Also stimulates nicotinic receptor sites (risk additional side effects)
59
Galantamine (Razadyne®)- indications
Mild to moderate Alzheimer’s dementia
60
Galantamine (Razadyne®)- pharmacokinetics
``` Available as a once daily ER tablet 8mg daily with food Available as 2mg/ml oral solution Metabolized by CYP450 2D6 and 3A4 Avoid in patients with renal or liver impairment ```
61
Cholinesterase inhibitors- Side effects
``` N/V Diarrhea Anorexia Dizziness Dyspepsia Agitation ```
62
What should you be cautious with for cholinesterase inhibitors?
Bradycardia Monitor carefully in pts on concomitant medications that decrease heart rate Ulcers Increased gastric acid secretion (may need prophylaxis) COPD or Asthma bronchoconstriction Exaggerate succinylcholine neuromuscular blockade during anesthesia The patient may require different dosing. Anticholinergic medications will negate effects of cholinesterase inhibitors A lot of drugs that they patient cant take cuz it will stop this drug from working.
63
Memantine (Namenda®)- MOA
NMDA receptor antagonist Moderate-affinity noncompetitive receptor antagonist Shows neuroprotective effects, slows rate of memory loss in vascular and Alzheimer’s dementia. No evidence of prevention or slowed neurodegeneration in AD
64
Memantine (Namenda®)- indications
moderate to severe AD (MMSE 3-14)
65
Memantine (Namenda®)- dose reductions
Dose reductions in pts with renal impairment is recommended CrCl 40-60 ml/min 5mg twice daily Up to 80% excreted unchanged in urine Partially eliminated by tubular secretion Alkaline conditions reduce clearance (80% at pH = 8) Carbonic anhydrase inhibitors and sodium bicarbonate
66
Memantine (Namenda®)- drug interactions
Minimal CYP-450 metabolism Use caution with other NMDA-antagonists (amantadine (used for parkinsons), ketamine (anesthetic), dextromethorphan(cough syrup OTC))
67
Memantine (Namenda®)- Side effects
Agitation, insomnia, diarrhea, urinary incontinence, UTI
68
What can be used as combination therapy in AD?
Memantine + Donezepil Vitamin E Often recommended as adjunctive treatment because of antioxidant properties Potential effectiveness and favorable side effect profile Doses of no greater than 400 International Units / day
69
What is the treatment for behavioral and psychological sx of dementia (BPSD)?
-Should begin with nonpharmacologic but may also include antipsychotic and/or antidepressants -No medications are approved to treat Behavioral and Psycological Symptoms of Dementia (BPSD) -Use low doses of antipsychotics in patients with dementia Risperidone, olanzipine

Pharmacology III (19 decks)

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