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Pharmacology > Alzheimer's and Parkinson's Medication > Flashcards

Alzheimer's and Parkinson's Medication Flashcards

1
Q

Pathophysiology of Parkinson’s Dz

A

Progressive depletion of dopaminergic neurons in the substantia nigra of the basal ganglia

Functional increase in ACh occurs (causing the characteristic resting tremor)

Lewy bodies (protein aggregates) found post-portem in remaining DA cells in the SN

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2
Q

Percentage of dopamine lost by the time a patient presents w/ symptoms

A

70-80%

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3
Q

4 core clinical features of Parkinson’s

A
  1. Bradykinesia
  2. Resting Tremor
  3. Rigidity
  4. Postural Instability
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4
Q

What is needed to make the dx of Parkinson’s?

A

Bradykineasia and at least one of the following:

  • -Resting tremor
  • -Rigidity
  • -Postural Instability

Bradykinesia + 1 = possible PK
Bradykinesia + 2= probably PK
Bradykinesia +2/3 +response to meds = PD

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5
Q

5 predictors of Parkinson’s disease progression (these make a worse prognosis)

A
  1. Older age at onset
  2. Rigidity as presenting symptom
  3. Male
  4. Presence of comorbidities
  5. Decreased response to dopamine
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6
Q

What are the two MAO-B inhibitors used to treat PD? Which is used 1st line?

A

Selegiline and Rasagiline

–>Rasagiline is 1st line

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7
Q

Is levodopa 1st line in a patient w/ PD?

A

You can begin levodopa tx 1st line in a PD pt who is older, has cognitive impairment, or has mod-severe functional impairment. Otherwise hold off on using this and use rasagiline 1st line

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8
Q

Why is Rasagiline used above Selegiline?

A

Rasagiline is neuroprotective so it has fewer adverse effects (Selegiline can cause insomnia, jitteriness, dyskinesias, orthostasis, and serotonin syndrome)

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9
Q

MOA of Amantadine (Symmetrel)

A

Unclear - Augmentation of dopamine release from presynaptic terminals and inhibition of dopamine reuptake. Might also inhibit NMDA (glutamate inhibition)

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10
Q

Place in therapy for Amantadine

A

Initiated early stages w/ mild symptoms of PD and it improves bradykinesia, rigidity, and tremors

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11
Q

Side effects of Amantadine:

A 
Orthostatic hypotension
confusion
nightmares
hallucinations
nervousness
irritability
livedo reticularis
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12
Q

When would you give a Parkinson’s pt an anticholinergic agent?

A

If a patient presents early w/ resting tremor and has minimal bradykinesia or rigidity. Can be monotherapy or adjunct

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13
Q

In what types of patient’s with PD would you want to avoid anticholinergic agents?

A

Pt’s w/ cognitive deficits
BPH
Urinary issues
Glaucoma

**AKA - the elderly!

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14
Q

MOA of dopamine agonists

A

Direct stimulation of striatal dopamine receptors. Have longer half lives than LD so they produce more constant stimulation of dopamine receptors

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15
Q

Dopamine agonsts can delay the need for levodopa by _____ years in ____% of pts

A

4-5 years in 80% of patients

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16
Q

Important note about dosing of dopamine agonists.

A

START LOW AND GO SLOW

Effects will take 4-8 weeks to take effect

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17
Q

A patient who is currently taking LD wants to add a dopamine agonist. What needs to be done to either LD or DA?

A

LD needs to be decreased by 20-30%

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18
Q

Name the 4 dopamine agonists - non-ergot derivatives

A
  1. Pramipexole (Mirapex)
  2. Ropinirole (Requip)
  3. Rotigotine (Neupro)
  4. Apomorphine (Apokyn)
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19
Q

What is apomorphine (amokyn) used for?

A

“Rescue therapy” for “delayed on”/”no on”/ or “freezing episodes”

PRN tx of hypomobility in pts w/ advanced PD

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20
Q

If you want to start a pt on apomorphine what must you also do/prescribe?

A

Start trimethobenzamide 3 days prior to administering apomorphine and then continue trimethobenzamide for the 1st two months of treatment

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21
Q

Do not use apomorphine with _______ because the combination could result in severe hypotension

A

serotonin agonists (ondansetron)

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22
Q

What is the formulation of apomorphine?

A

SubQ - so pt may require someone else to inject it d/t hypomobility
NO ORAL DOSING!!

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23
Q

Why is carbidopa given with levodopa?

A

Levodopa is metabolized to dopamine by L-amino acid decarboxylase so that it cannot cross the BBB. Levodopa alone also causes significant N/V and the doses we require to get it into the substantia nigra.

Because of this problem, we give carbidopa which is a peripheral decarboxylase inhibitor used to increase LD’s bioavailability.

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24
Q

____ less LD dose required to achieve same effect when it is dosed with carbidopa.

A

80% less

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25
Q

Immediate release CD/LD should be dosed @ ________.

Extended release CD/LD should be dosed @ ________.

A

IR: Take 30 min before a meal or 60 min after

CR: Should be taken with food

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26
Q

A PD pt comes to you explaining that her symptoms are returning just prior to her next dose of CD/LD. To fix this “wearing off effect” you….

A

Decrease dosing interval of LD (inc. it’s frequency)

Could also add MAO-B inhibitor, COMT inhibitor, or DA

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27
Q

How to manage a pt’s PD meds when they are experiencing “peak-dose dyskinesia” or excessive movement secondary to excessive striatal dopamine stimulation.

A

Smaller and more frequent doses of CD/LD

Could add amantadine

28
Q

How do you correct “delayed on” and “no on” problems with a PD pts meds?

A

Since this may be d/t delayed gastric emptying or decreased absorption in the duodenum…

…Give CD/LD on empty stomach before meals using ODT formulation (avoid controlled release)
…Could add apomorphine

29
Q

What is “freezing” or “start hesitation” in relation to PD?

A

Sudden, episodic inhibition of lower-extremity motor function. Often exacerbated by anxiety or when perceived obstacles are encountered

30
Q

How can we fix “freezing?”

A

Inc. CD/LD dose
Add DA or MAO-B inhibitor
Utilize physical therapy and assistive walking devices or sensory cues

31
Q

What is “off period dystonia” and how can we treat this in PD?

A

Sustained muscle contraction that is common in distal lower extremity. These often occur in early morning hours just prior to the first dose of L-dopa.

To tx:

  • -Add CR CD/LD
  • -Add ropinirole CR at bedtime
  • -Initiate Baclofen
  • -Initiate Botulinum toxin
32
Q

A pt is experiencing myoclonic jerks during sleep. They are already on CD/LD. What to do?

A

Decrease nighttime LD dose

Initiate clonazepam

33
Q

MOA of COMT Inhibitors

A

Prevent peripheral conversion of LD to 3-O-Methyldopa

–>Allows more LD across the BBB

34
Q

Can we use COMT-Inhibitors as monotherapy for Parkinson’s?

A

NO! It only works w/ CD/LD

35
Q

2 COMT Inhibitors we use:

A

Entacapone (comtan, stalevo)

Tolcapone (Tasmar)

36
Q

Which COMT-Inhibitor should you monitor LFT’s in d/t its potential serious liver dysfunction

A

Tolcapone

37
Q

What two Parkinson drugs need to be tapered when taking a patient off? (give reasons as to why too)

A
  1. Anticholinergics - could cause withdrawl rxns

2. Amantadine - to avoid rebound Parkinsonism

38
Q

Parkinson drugs that needs to be adjusted if a patient has renal dysfunction

A

Pramipexole (Mirapex)

39
Q

PD drugs that need to have LFTs monitored d/t liver issues

A
  1. Tolcapone

2. Ropinirole

40
Q

Typical progression of Alzheimer symptoms

A

Cognitive impairment –> Behavioral impairment –> Functional impairment

41
Q

Stages of Alzheimer’s and MMSE scores associated

A

Mild Cognitive Impairment - Memory loss only, no evidence of AD

Mild AD: MMSE 26-18 - forgetful, short-term memory loss, hobbies lost, impaired ADLs

Mod AD: MMSE 17-10 - further progression…transition into care, behavioral/psychological symptoms of dementia start

Severe AD: MMSE 9-0 - agitation, altered sleep patterns, assistance required for everything, dementia, speech involved

42
Q

3 cholinesterase inhibitors used to tx AD

A

Donepezil
Galantamine
Rivastigmine

43
Q

NMDA antagonist used to tx AD

A

Memantine (Namenda)

44
Q

What are Cholinesterase inhibitors indicated for?

A

Mild to moderate AD

45
Q

What are NMDA antagonists indicated for?

A

Moderate to severe AD

46
Q

MMSE and ADAS improvements w/ cholinesterase inhibitors

A

MMSE: 1-1.5 improvement

AGAS: 2.8-4 improvement

47
Q

Average MMSE and ADAS decline in a patient w/ AD on NO MEDICATIONS.

A

MMSE: 2-4 points/year
ADAS: 7 points/year

48
Q

MOA of Donepezil (Aricept)

A

Reversible CI that has specificity for acetylcholinesterase and NOT butyrylchoinesterase

49
Q

MOA of Galantamine (Razadyne)

A
  1. Inhibits acetylcholinesterase

2. Modulates nicotinic receptors… inc. release and enhancement of cholinergic function

50
Q

MOA of Rivastigmine (Exelon)

A

Reversible CI but has a very slow dissociation w/ ACHe

Substantially inhibits butyrylcholinesterase

51
Q

Dosing for Donepezil

A

5mg, 10mg, 23mg. Start @ 5mg and titrate up to 10mg in 4-6 weeks
–>If pt has mod-severe AD can wait 3 months and again titrate up to 23mg daily.

Package insert recommends dosing at bedtime but most people favor administration w/ lunch to reduce nightmares/vivid dreams

52
Q

Drug interactions of donepezil

A

Anticholinergics
NSAIDs
CYP2D6 or 3A4 inhibitors

53
Q

Which cholinesterase inhibitor has the worst adverse rxn’s? Which has the best?

A

Worst – Rivastigmine

Best – Donepezil

54
Q

Dosing of galantamine:

A

Comes in IR, ER, and oral solutions

Titrate every 4 weeks..start dose @ 8mg/day

55
Q

Renal dose adjustments of galantamine:

A

If CrCl < 70 do not exceed 16mgs daily

If CrCl < 9 DO NOT GIVE GALANTAMINE

56
Q

Dosing of Rivastigmine

A

Comes in capsules, oral solution, transdermal patch

Start dose (capsule) @ 1.5mg BID and titrate up q4weeks to a max dose of 12mg

Take w/ food

57
Q

MOA of Memantine

A

interfers/slows glutamatergic excitotoxic neurotoxicity. It is specific and noncompetitive antagonist (no interactions w/ other enzymes, receptors, transporters

Rapid association/dissociation w/ the receptor

58
Q

Dosing/titration schedule of Memantine

A 
Titrated weekly:
5mg daily
5mg BID
5mg morning, 10mg afternoon
10mg BID
*Also comes in XR formulation that is titrated similiar:
7mg daily
14mg daily
21mg daily
28mg daily
59
Q

Dose reduction of Memantine if renally impaired

A

If CrCl < 30 then Max of 10mg/day

60
Q

Is vitamin E indicated for either Parkinson’s or Alzheimers?

A

NO!

61
Q

Besides the pharmacotherapies discussed in the AD lecture (CI and NMDA antagonists) what other therapies can we add to a patient with AD?

A

Aspirin
Vitamin B (6,9,12)
Ginkgo Biloba

62
Q

A pt diagnosed w/ AD presents with hallucinations and delusions. What is an additional therapy that can be added to address these new symptoms?

A

Antipsychotic drugs

  • -> Haloperidol
  • -> Atypicals
63
Q

A pt diagnosed w/ AD presents with poor appetite, suicidal thoughts, and depression. What is an additional therapy that can be added to address these new symptoms?`

A

Antidepressants

–>SSRI’s are tx of choice (Citalopram, escitalopram, sertraline)

64
Q

A pt diagnosed w/ AD presents with restlessness, anxiety, and insomnia. What can we add to this pts existing meds to address these new presenting symptoms?

A

Benzodiazepines

–>Lorazepam

65
Q

A pt diagnosed w/ AD presents with agitation and aggression. What can we give to this pt to address these new presenting symptoms

A

Anticonvulsants

  • ->Carbamazepine
  • ->Valproic Acid

Pharmacology (17 decks)

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