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Neurology > Pharm 33 - Movement disorders > Flashcards

Pharm 33 - Movement disorders Flashcards

1
Q

Goal of AD treatment is to…

A

improve symptoms and reduce/slow cognitive decline

No available drugs can currently stop or reverse cognitive decline

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2
Q

Drugs approved for AD

A

three cholinesterase inhibitors: donepezil, galantamine, rivastigmine

memantine: blocks neuronal receptors for N-methyl-D-aspartate

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3
Q

clinical uses of cholinesterase inhibitors

A
  • myasthenia gravis
  • reversal of neuromuscular blockade (neostigmine)
  • antidote (physostigmine) for poisoning due to muscarininc antagonists (atropine toxicity)
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4
Q

Common/general ADE of cholinesterase inhibitors

A
  • Gastrointestinal:
    Nausea, vomiting, dyspepsia, diarrhea.
  • Dizziness and headache.
  • Bronchoconstriction
  • Bradycardia, fainting or falls.
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5
Q

Severe acute toxicity of cholinesterase inhibitors

SLUDGE and killer B’s

A 
Salivation
Lacrimation
Urination
Diaphoresis/diarrhea
Gastrointestinal cramping
Emesis

Bradycardia
Bronchorrhea
Bronchospasm

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6
Q

Donepezil use

A

mild, moderate, severe AD

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7
Q

MOA of donepezil

A

reversible inhibition of cholinesterase

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8
Q

ADE of donepezil

A

N/D
Bradycardia
Fainting, falls, fall-related fractures

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9
Q

mild, moderate, severe AD drug

A

donepezil

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10
Q

mild to moderate AD

A

galantamine

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11
Q

MOA of galantamine

A

reversible cholinesterates inhibitor

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12
Q

ADE of galantamine

A 
N/D/V
Weight loss
Anorexia
Bradycardia
Bronchoconstriction 
Fainting, falls, fall-related fractures
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13
Q

galantamine use

A

mild to moderate AD

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14
Q

mild, moderate, or severe Alzehimer dementia and parkinson-related dementia

A

rivastigmine

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15
Q

clinical utilitzation for AD: put these drugs in order of utilization

rivastigmine
donepezil
galantamine

A

donepezil&raquo_space; rivastigmine > galantamine

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16
Q

MOA Rivastigmine

A

Irreversible inhibition of cholinesterase.

 more likely to cause toxicity; 10 hour duration in CSF

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17
Q

ADE of Rivastigmine

A

MORE GI effects than the others:
Nausea, vomiting, diarrhea, abdominal pain, anorexia; may cause undesired weight loss.
Worsening of peptic ulcer disease

Also: bradycardia, urinary obstruction, lung disease, fainting, falls, and fall-related fractures

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18
Q

Memantine MOA

A

An N-methyl-d-aspartate (NMDA) receptor antagonist; reduces the persistent over-activated state in AD

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19
Q

Memantine use

A

for moderate to severe AD

Better tolerated than cholinesterase inhibitors.
Somewhat irrelevant….
almost always used in combination of cholinesterase inhibitors

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20
Q

Memantine ADE

A

Dizziness, headache, confusion

Constipation

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21
Q

use of antipsychotic drugs in AD population will result in…

A
  • A 9-fold risk of stroke in the first four weeks of antipsychotic drug use
  • Almost a doubling in the risk of mortality
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22
Q

Other approaches to behavioral disturbances that occurs with “sun-downing” AD patients

A
  • lifestyle approaches: activities, reminiscence therapy, social interaction
  • antidepressants to reduce agitation/treat apathy
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23
Q

Primary parkinsonism drug MOA’s

A
  1. increase dopamine concentration and availability in the brain
  2. directly stimulate dopamine receptors
  3. inhibit cholinergic neurotransmission
  4. adenosine antagonists
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24
Q

Why can you not just give dopamine to treat PD?

A
  • does not readily cross the BBB
  • poorly tolerated
  • very short 1/2 life as metabolized by COMT, MOA-B, convereted to NE by dopamine hydroxylase
  • causes peripheral, dose-limiting pharmacologic effects
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25
Q

Best way to replace dopamine in the brain

A

give a dopamine precursor, to be converted to dopamine in the brain

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26
Q

L-DOPA MOA

A

L-DOPA is converted to dopamine by DOPA decarboxylase.

  • Peripherally–> gastrointestinal or vascular “side effects.”
  • Within the CNS–> therapeutic effects and CNS “side effects.”

DA can then be synthesized and released as a neurotransmitter

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27
Q

purpose of carbidopa (decarboxylase) when combo’d with levodopa

A

prevents L-DOPA conversion to dopamine in the peripheral to prevent the ADE in the GI tract (NAUSEA)

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28
Q

what is the daily dose of carbidopa to sufficiently inhibit DOPA decarboxylase

A

Carbidopa doses of 70-100 mg/day

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29
Q

how do you minimize wearing off of the levo-carbidopa (3 ways)

A
  1. shorten the dose interval (more frequent dosing)
  2. give drug that prolong’s plasma 1/2 life
  3. adding a direct-acting dopamine agonist
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30
Q

an acute loss of effects of levo/carbiodpa can occur. to combat this, give a rescue therapy drug…

A

apomorphine

31
Q

what part of the diet inhibits L-DOPA oral absoroption

A

dietary protein

32
Q

what dietary component increases DOPA-decarboxylase acitivity

A

Vitamin B-6: pyridoxine

33
Q

disadvantages of Carbi/levo

A
  • multiple doses per day
  • orthostatic hypotension
  • nausea
  • high rates of ADE
34
Q

ADE of carbi/levo

A 
hallucinations
nausea
vomiting
hypotension
dizziness
35
Q

unusal ADE of carbi/levo

A
  • can activate malignant melanoma
  • discoloration of urine/stool (harmless)
  • problems with impulse control
  • drug induced dyskinesia
36
Q

dopamine receptor agonist classes

A

ergot derivatives

non-ergot (only group indicated for monotherapy)

37
Q

advantages of direct dopamine receptor agonism

A
  • active agents do not require metabolic conversion
  • longer t1/2 than levodopa (minimizes wearing off)
  • can be used as monotherapy or in combo with L-DOPA
  • no dietary protein complications
  • lower incidence of response failure (if not responsive to L-DOPA)
38
Q

disadvantages of direct dopamine receptor agonism

A
  • must start at low dose and increase SLOWLY

- same ADE of L-DOPA, plus: increased rates of somnolence, sleep attacks, psychosis, compulsive behavioral activities

39
Q

bromocriptine

A

ergot derivative for dopamine receptor agonism

  • ADE: high incidence with N/HA/dizziness most common
  • very long time to titrate dosing up (at 2-4 week intervals –> can take months)
40
Q

pramipexole

A

oral non-ergot DA receptor agonists

  • may be used early in therapy as monotherapy
  • como’d with Carbi/levo in advanced disease
  • renally eliminated
41
Q

ropinorole

A

oral non-ergot DA receptor agonists

  • may be used early in therapy as monotherapy
  • como’d with Carbi/levo in advanced disease
  • hepatic eliminated
42
Q

apomorphine

A

A derivative of morphine but devoid of typical opioid effects (for example, NO analgesia, euphoria, respiratory depression)

Used clinically as a “rescue” therapy for acute akinesia

43
Q

apomorphine special property

A

very strong emetic - severe N/V is common and need to be administered with antiemetics

44
Q

apormorphine ADE

A

hypotension

daytime sleep attacks

45
Q

Most common ADE of dopamine agonists (ergot and non-ergot)

A

CV: postural hypotension, peripheral edema, dysrhythmias

GI: N/V, anorexia, constipation, dyspepsia

Dyskinesia ESP in combo with L-DOPA

severe mental disturbances: confusion, hallucinations, impulse control disorders, spontaneous sleep

46
Q

Benefits of COMT inhibitors

A

add entacapone or tolcapone to prolong the effects of L-DOPA

CANNOT be given as monotherapy

47
Q

MOA of COMT-I

A

prevents degradation of L-DOPA, and other monoamines

48
Q

COMT-I ADE

A

brownish urine discoloration
diarrhea
liver toxicity

49
Q

COMT-I monitoring

A

LFT’s

50
Q

worse hepatotoxicity of the COMT-I’s

A

tolcapone > entacapone

51
Q

MOA-I place in parkinson’s disease treatment

A

adjunct with carbi-levo, esp. late in disease

can be monotherapy, but usually not selected for this due to greater benefits of carbi-levo

52
Q

drug names of MAO-I

A

selegiline
rasagiline
safinamide

53
Q

ADE of selegiline

A

metabolites are amphetamine and methamphetamine: can cause anxiety and insomnia

54
Q

Most commonly used MAO-I

A

rasagline: dosed once, generic, no amphetamine metabolites, fewer ADE

55
Q

role of antimuscarinic drugs in PD

A

used early in disease with younger patients with only/primary manifestation being tremor

will NOT improve bradykinesia with mediocre benefits for rigidity

56
Q

antimuscarinics worsen what in PD

A

postural instability
dementia
constipation
then typical antimuscarinic side effects: dry mouth, urinary retention, blurred vision, confusion

57
Q

amantadine place in PD treatment

A

response occurs within 2-3 days with a little less efficicay than with L-DOPA or dopamine agonists

responses can diminish in 3-6 months

58
Q

amantadine role for PD common effects

A

helpful for dyskinesias caused by levodopa

causes stimulant-like effects to help with fatigue

59
Q

toxicity of amantadine

A

renal toxicity –> renal adjustment required

60
Q

ADE of amantadine

A

CNS: confusion, anxiety, lightheadness

Peripheral: blurry vision, urinary retention, dry mouth, constipation

61
Q

Restless leg syndrome (RLS) may be due to…

A

may be due to IDA

62
Q

How do you treat RLS?

A

dopaminergic supplementation or dopamine agonists: pramipexole or ropinirole or carbi/levo

63
Q

how do you treat tremor

A
  • r/o intentional tremor, rest tremor, drug causes, underlying CNS disorder
64
Q

tremor pharmacologic treatments

A
  1. non-selective beta blocker (if not contraindicated)
  2. primidone
  3. topiramate
  4. gabapentin
  5. benzos
65
Q

how to treat huntington’s disease

A

want to reduce over-activity:

  • inhibit dopaminergic activity to alleviate chorea:
    1. deplete central monoamines (riserpine)
    2. dopamine receptor blockers (haloperiodl)
    3. increased dopaminergic activity (levodopa supplementation) tends to exacerbate chorea
66
Q

only FDA approved drug for treatment of chorea in HD

A

tetrabenazine

FDA boxed warning: depression and suicidality

67
Q

treatment of tics

A

dopamine antagonism: haloperidol, pimozide, fluphenazine

secondly: clonidine, clonazepam, carbamazepine

68
Q

wilson’s disease treatment

A
  1. chelating agents: deplete many minerals and vitamins in addition to copper
  2. restrict copper
  3. zinc supplement to decrease copper absorption

**only treated in specialty care

69
Q

ALS treatment

A

spasticity: baclofen

first/only disease-modifying drug: riluzole –> prolongs life/time to tracheostomy by ~3months

70
Q

treating acute attacks of MS

A
  1. make sure it’s a real attack and treat with IV high dose steriods 3-5 days (methylprednisolone)
  2. then oral prednisone or dexamethasone
71
Q

dosing of steriods in acute attacks of MS

A

methylprednisolone 500-1000mg per day for 5 days

prednisone (oral) 625-1,250mg per day for 3-7 days

72
Q

Concomitnat drug therapy with high dose steroids for MS treatment of acute attacks

A

benzos for bedtime to combat mood changes and insomnia

Li if manic

low salt diet to combat salt retention/HTN

H2RAs or PPIs for gastric distress

73
Q

common treatments for MS patients in primary care:

A
  • depression
  • neuropathic pain
  • drugs for spasticity/muscle spasms
  • ataxia/tremor
  • constipation
  • bladder dysfunction
  • UTI
  • cognitive impairment

Neurology (12 decks)

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