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Clinical Pharmacology II > Dementia, Parkinson's, and Movement Disorders > Flashcards

Dementia, Parkinson's, and Movement Disorders Flashcards

1
Q

What is Alzheimer’s Disease?

A

A progressive neurodegenerative disease characterized by a loss of function and death of nerve cells in several areas of the brain

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2
Q

What type of neurons are predominantly lost in Alzheimer’s Disease?

A

Cholinergic neurons

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3
Q

What types of drugs are Alzheimers patients particularly sensitive?

A

Anti-cholinergics

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4
Q

What do drugs for Alzheimers Disease aim to do?

A

Increase ACh activity/concentration either direclty (by using an agonist) or indirectly (by using an AChI)

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5
Q

How does the cholingergic neuron loss cause an exacerbation of Alzheimer’s Disease?

A

The neuron loss causes excess glutamate which is an excitatory Neurotransmitter

The excess glutamate causes noisy brain signaling and increases neuronal cell death in the brain

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6
Q

What drug is used to treat the excess glutamate caused by neuronal cell loss?

A

Memantine

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7
Q

What are the goals of Alzheimer’s Disease therapy?

A

1) Maintain quality of life
2) Maximize function in daily activities
3) Enhance cognition, mood, and behavior
4) Foster a safe environment
5) Promote social engagement, as appropriate

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8
Q

What is the mainstay of Alzheimer’s Disease Therapy?

A

Acetylcholinterase inhibitors (AChI)

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9
Q

What do AChI do to treat Alzheimer’s?

A

They attempt to offset loss of presynaptic cholinergic function to slow decline of memory and enhance ability to perform activities of daily living

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10
Q

The AChI used to treat Alzheimer’s are more specific for what receptors?

A

More selective for ACh muscarinic receptors in the brain

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11
Q

Which AChI is also approved for use in Parkinson’s Dementia?

A

Rivastigmine

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12
Q

What are the AChI ADR’s?

A

mostly muscarinic in nature = SLUDGE BBB

BRADYCARDIA
Dizziness
Lightheadedness
Increased Urinary Frequency
N/D
Concern for dose dependent GI bleed
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13
Q

What is the MOA of Memantine?

A

Less glutamate activity causes less noise and therefore better signal in the brain = improved cognitive test scores and functioning

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14
Q

When is Memantine used in AD treatment?

A

In severe or progressed Alzheimers Disease

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15
Q

What is the ADR of memantine?

A

Headache

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16
Q

What is Parkinson’s Disease?

A

Progressive

Combo of:
Rigidity 
Bradykinesia
Tremor
Hypokinesia
Postural Instability
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17
Q

What is Parkinson’s disease caused by?

A

LOW DOPAMINE

Selective loss of dopaminergic neurons in the nigrostriatal pathway

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18
Q

What drugs cause DA depletion from neurons and cause drug induced Parkinsonism?

A

Drugs of Abuse

Reserpine
Tetrabenazine
Deutetrabenazine

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19
Q

What drugs cause DA receptor blockade and cause drug induced Parkinsonism?

A

Antipsychotics: typical > atypical

Metoclopramide

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20
Q

What are other non-motor symptoms of Parkinson’s?

A 
Affective disorder
Personality changes
Abnormalities of autonomic function
Sensory complaints
Fatigue
Sleep Disorders
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21
Q

What is the hallmark therapy for Parkinson’s?

A

Exogenous Dopamine Supplementation

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22
Q

What are the endogenous barriers to therapy optimization of Parkinson’s?

A 
Blood Brain Barrier
Amino Acid transporter
DOPA decarboxylase
MAO
COMT
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23
Q

What is Levodopa broken down by?

A

In periphery and centrally = COMT

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24
Q

What only breaks down Dopamine in the brain?

A

MAO-B

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25
Q

What is the first line therapy options for Parkinson’s?

A

Dopamine Replacement Therapy (levodopa)
Dopamine Receptor Agonist

+/- enzyme inhibitors to decrease DA breakdown

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26
Q

What are additional lines of therapy for Parkinson’s?

A

Muscarinic Receptor Antagonists
Pimavanserin
Behavioral Therapy
Family/Social dynamic

27
Q

What is the target for Dopamine Receptor Agonists?

A

D2 receptors in basal ganglia

28
Q

Why are Dopamine Receptor Agonists better to use over L-Dopa?

A

1) there are no enzyme conversion concerns
2) They have better BBB penetration; They don’t have to compete with Amino acid transporter like L-dopa
3) They are more selective for DA receptor activation
4) Less response fluctuations and dyskinesias

29
Q

What receptors does Bromocriptine hit?

A

D2/D3/D4

Less selective for these than non-ergot derivatives

30
Q

What other indications is Bromocriptine used in?

A 
Hyperorlactinemia
Pituitary adenoma
Cocaine withdrawal
Alcohol dependence
Mastalgia
31
Q

What are non-ergot DA agonists?

A

Used as monotherapy in mild parkinson’s or as an adjunct to Sinemet in advanced disease

D2/D3 receptors only

Often used for Restless leg syndrome also

32
Q

What are the two DOC’s for Non-ergot DA agonists?

A

Pramipexole

Ropinirole

33
Q

What are the Dopamine Receptor Agonists ADRs?

A

GI
Cardiovascular
Dyskinesias
Mental Disturbances

34
Q

Who do you have to be cautious in using Dopamine Receptor Agonists in?

A

Patients with:

Psychotic illness (schizophrenia)
Recent MI
Uncontrolled Hypertension

35
Q

What is Levodopa?

A

Oral Dopamine Replacement

Enters brain by LAT

Rarely used as monotherapy

Peripheral DA ADRs by activating chemotrigger zone

Need for combo with enzyme inhibitor

36
Q

What is carbidopa?

A

DOPA decarboxylase inhibitor

Inhibits peripheral conversion of L-DOPA to DA

Never given as monotherapy

37
Q

When levodopa is given alone, what percentage of the dose actually gets into the brain?

A

1-3%

38
Q

When Sinemet is given, what percentage of the levodopa dose actually gets into the brain?

A

10%

39
Q

What symptom of Parkinson’s is Sinemet most effective at treating?

A

Bradykinesia

40
Q

What may reduce levodopa entry into the brain due to competition for LAT?

A

Protein

41
Q

What are the ADRs of Sinemet?

A 
N/V
Tachycardia
Ventricular Abnormalities
Hypertension
Increased peripheral catecholamine formation
Depression
Anxiety
Dose related dyskinesias
Response fluctuations
42
Q

When are the best results of Sinemet therapy seen and what are the disadvantages?

A

Best results in first 3-4 years of treatment

Must dose adjust over time due to DA related ADRs

Does not stop progression of the disease

43
Q

What are the response fluctuations seen in Sinemet therapy?

A

End of Dose Akinesia

On/Off Phenomenon

44
Q

What is the end of dose akinesia?

A

Related to dosing times

Wearing off reaction towards time when next dose is due

45
Q

What is the on/off phenomenon?

A

Unrelated to dosing

On = marked akinesia
Off = improved mobility, often marked dyskinesia

Less incidence with more continuous DA exposure

46
Q

What can occur due to Carbidopa use?

A

Increased metabolic breakdown of levodopa through COMT and MAO-B pathways

47
Q

What is Catechol-O-Methyltransferase (COMT)?

A

Central DA metabolizer

Peripheral L-DOPA metabolizer

48
Q

What is Monoamine Oxidase (MAO)?

A

Metabolizes catecholamines

MAO-B = DA selective

49
Q

What is Tolcapone?

A

Inhibits central and peripheral COMT

HEPATOTOXICITY

50
Q

What is Entacapone?

A

Inhibits Peripheral COMT only

51
Q

What is Selegiline?

A

MAO-B irreversible inhibitor

Dietary restrictions with tyramine by formulation/dose

Metabolized to amphetamine derivatives

52
Q

What is Rasalgaline?

A

Irreversible MAO-B Inhibitor

53
Q

What is Safinamide?

A

Reversible MAO-B inhbitor

54
Q

What are the drug interactions to be aware of with MAO-B inhibitors?

A

Serotonin Syndrome with SSRIs

55
Q

What do antimuscarinics help with in Parkinson’s treatment?

A

relieves tremor and rigidity

56
Q

What is Apomorphine?

A

Potent DA receptor agonist used as a “RESCUE” from off phenomenon

Injection that works within 10 minutes

ADR: NAUSEA

57
Q

What is Pimavanserin used to treat in Parkinson’s?

A

Treats the hallucinations and delusions associated with the psychosis that can come if too much DA is given to the patient

58
Q

Who must you be cautious in using Pimarvanserin with?

A

Elderly

Qtc prolongation

59
Q

What is Huntington’s Disease?

A

Autosomal dominant inherited disorder

Causes progressive chorea and dementia

60
Q

What is the chorea related to in Huntington’s disease?

A

Imbalance of DA, ACh, and GABA in basal ganglia causing overactivity of DA nigrostatial pathway and GABA neuron degeneration which reduces and imapirs GABA activity

61
Q

What is Reserpine?

A

Inhibits VMAT to reduce reuptake of catecholamines

Binds to and destroys catecholamine stroage vesicles, not allowing them to be stored resulting in sympathetic dysfunction

ADRs: Hypotension, depression, sedation, diarrhea, nasal congestion

62
Q

What is Tetrabenazine?

A

More selective than reserpine for dopamine

Depletes pre-synpatic DA stores; mildly antagonizes D2 receptors

Less ADRs

63
Q

What are the treatment considerations for Restless Leg syndrome?

A 
D2 agonists (non-ergot)
Gabapentin
64
Q

What are the treatment considerations for tremors?

A

Propanalol

Benztropine

Clinical Pharmacology II (25 decks)

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