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Pharmacology > Remaining Movement Disorders > Flashcards

Remaining Movement Disorders Flashcards

1
Q

What is the most common of the movement disorders?

A

Essential tremor

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2
Q

What is essential tremor?

A

rapid oscillating movements with constant frequency and variable amplitude
-alternating contractions of antagonist muscles

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3
Q

What is 1st line treatment for essential tremor?

A

Propanolol-B2 Sandinista

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4
Q

Why is propanolol used?

A

non selective beta blockers depress CNS

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5
Q

T/F Non selective beta blockers are better at tx essential tremor than selective beta blockers

A

TRUE

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6
Q

What are contraindication for use of Propanolol?

A

asthma, DM, and heart block

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7
Q

What are ADE of propanlol?

A

Fatigue
Impotence
Lightheaded
Bradycardia

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8
Q

What can be uses to tx ET in asthma patients?

A

atenolol

metropolol

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9
Q

What is MOA of primidone?

A

Off label use anti-convulsant

-enhances GABA A receptors

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10
Q

What is metabolite of primidone?

A

phenobarbital

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11
Q

What are ADE of primidone? (4)

A

sedation
ataxia
dizziness
vertigo

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12
Q

What is MOA of Topiramate? (3)

A
  • enhances GABA
  • blocks v-gated Na channels
  • antagonizes AMPA/kainite glutamate receptors
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13
Q

What is ADE of topiramate? (1)

A

difficulty concentrating

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14
Q

What is MOA of gabapentin?

A

interacts with auxiliary units of Ca+2 channels

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15
Q

What is ADE of gabapentin?

A

gait unsteadiness

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16
Q

When should you consider use of gabapentin?

A

Last resort, when no other meds are working

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17
Q

What is MOA of botulinum?

A

-blocks release of Ca+2 dependent Ach release and affects only presynpatic neuron at NMJ

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18
Q

What is clinical use of Botulinum?

A

-reduce head and voice tremors

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19
Q

What are ADE of botulinum?

A
  • difficulty swallowing and breathing

- dose dependent hand weakness

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20
Q

What is MOA of Benzodiazepines?

A

-enhances GABA activity

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21
Q

Name 2 benzos used to treat ET?

A
  • Clonazepam

- Alpralozam

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22
Q

What is clinical use of benzos?

A

-ET aggravated by anxiety

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23
Q

Why are benzos 2nd line tx?

A

dependence issues

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24
Q

What are ADE of benzos? (1)

A

sedation

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25
Q

What is Huntington’s disease?

A

loss of GABAnergic neurons?

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26
Q

Which drug depletes dopamine by blocking VMAT2 presynpatic transporter?

A

Tetrabenazine/Xenazine/Deutetrabenazine
Austedo
Reserpine

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27
Q

What are ADE of Tetrabenazine? (2)

A
  • Depression

- Hypotension

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28
Q

What are benefits of Deutetrabenazine?

A
  • less risks

- longer plasma half life, lower dosing

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29
Q

What is MOA of haloperidol?

A

-blocks D2 receptors more than serotonin receptors

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30
Q

What is clinical use of haloperidol?

A

-behavior disturbances

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31
Q

What is ADE of haloperidol?

A

extrapyramidal side effects

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32
Q

What is MOA of atypical anti-psychotics?

A

block 5HT/serotonin more than dopamine

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33
Q

Name 4 atypical anti-psychotics?

A

Risperidone
Clozapine
Olanzapine
Aripriprazole

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34
Q

What is clinical use of atypical anti-psychotics?

A

behavior disturbances

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35
Q

What is ADE of clozapine and olanzapine?

A

DM

-high cholesterol

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36
Q

What is ADE of risperidone?

A

high prolactin

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37
Q

Which atypical anti-psychotics tx TS

A

Aripriprazole

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38
Q

What are the hallmark signs of TS?

A

motor and phonic tics

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39
Q

What is pathology of TS?

A

dis inhibition of motor and limbic system

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40
Q

Which drug is used to tx focal/ motor tics in TS?

A

Botulinum toxin

41
Q

How do you treat mild non disabling tics in TS?

A

Habit Reversal Training (tic awareness and competing response)

42
Q

Which drug is used to tx vocal and motor tics in TS?

A

Haloperidol

43
Q

Which drug is used to treat severe motor and vocal tics after failing standards tx?

A

Pimozide/Orap

44
Q

What is MOA of Pimozide?

A

dopamine antagonist

45
Q

What are ADE of Pimozide?

A

decreased ocular accomodation

  • akithisia
  • sedation
46
Q

What is difference between PLMS vs PLMD?

A

-PLMD: fatigue and sleep fragmentation occur wiht PLMS

47
Q

Which meds can cause RLS? (4)

A
  • caffeine
  • anti-emetics metoclopramide
  • bupropion
  • centrally acting histamines
48
Q

What level of Ferritin is associated with RLS?

A

Ferritin below <45-50mcg/L

49
Q

How do you tx a patient with ferritin levels below 75mcg/L?

A

Give 325mcg 3x/day with Vitamin C (100-200mcg)

-check after 4 months of therapy

50
Q

How do you tx intermittent RLS?

A

Levydopa/Carbydopa not requiring daily use

51
Q

When is Levydopa/Carbydopa also useful?

A

after long travel or spectator events with prolonged sitting

52
Q

What levels should be avoided for Levydopa/Carbydopa?

A

stay below 200mg/day

53
Q

What drug is used to tx intermittent RLS in younger patients?

A

Benzodiazepines

54
Q

What is ADE of treating RLS with benzos?

A

morning cognitive impairment

55
Q

Which dopamine agonist are used in persistent leg syndrome?

A
  • Pramiprexole

- Ropinirole

56
Q

What are ADE of ropinirole?

A
  • fatigue
  • nasal stuffiness
  • leg edema
  • impulsive behavior issues
57
Q

Which drugs are alpha 2 delta calcium channels ligands?What type of RLS type do they tx?

A

gabapentin
pregabalin
-persitent RLS

58
Q

If a patient has impulse control issues which medication is preferred dopamine agonist or gabapentin?

A

-gabapentin

59
Q

What is ADE of gabapentin/pregabalin?

A

insomnia

60
Q

How do you tx refractory RLS? Would you refer to neurology?

A
  • Opioids

- Yes

61
Q

What is MOA of opioids?

A

interaction with spinal opiods and dopamine

62
Q

What are ADE of opiods? (2)

A
  • constipation

- tolerance

63
Q

What is ADE of gabapentin? (1)

A

dizziness

64
Q

What is ADE of oral zinc? (2)

A

GI upset, constipation

65
Q

What is ADE of Levydopa/Carbidopa? (Dopamine Agonist)

A

augmentation of symptoms

66
Q

What is Wilson’s disease?

A

impaired metabolism of copper

-copper builds up in liver, brain and cornea

67
Q

Name 2 copper chelating agents?

A
  • D-Pencilliamine

- Trientiene

68
Q

What is MOA of D-penicllinamine?

A

free sulfhydryl group acts as cooper binding moiety

69
Q

How do you tx pyridoxal phosphate insufficiency from use of D-peniclliamine?

A

give pyridoxine 25mg/day

70
Q

What are ADE of D-penicllinamine?

A

early: fever, lymphadenopathy, neutropenia, thrombocytopenia
late: proteinuria

71
Q

What is MOA of trientiene? (3)

A
  • 4 nitrogens bind cooper
  • increases renal excretion
  • obtains copper from less strongly bound sites in proteins and membranes
72
Q

What are ADE with trientene? (3)

A
  • chelates iron, can cause liver toxicity when Cu goes to low
  • dont give iron, can cause nephrotoxicty
  • can cause neuro worsening
73
Q

What should you monitor for pt taking trientene?

A
  • 24 hour copper urine

- nonceruloplasmin bound copper <15mcg/daily

74
Q

Oral zinc is used to tx what disease?

A

Wilson’s disease

75
Q

What is MOA of oral zinc?

A

reduces absorption in small intestine so it gets excreted in feces
zinc acetate>zinc gluconate>zinc sulfate

76
Q

T/F zinc acetate has the best absorption?

A

True

77
Q

What are ADE or oral zinc? (2)

A
  • GI upset

- elevated amylase and lipase but no injury to pancreatitis

78
Q

What is tx for liver failure due to WD?

A

liver transplant

79
Q

What is monitored for pt with WD?

A

CBC, serum ceruloplasmin, copper, urinalysis, LFT’s

-24 hour copper urine yearly

80
Q

What is initial therapy for WD?

A

chelation therapy

81
Q

What is Myasthenia Gravis?

A

weakness in skeletal muscle due to autoimmune attack of ACh receptors at post synaptic cleft

82
Q

Name the two drugs used to treat Myasthenia?

A
  • Neostigmine

- Pyridostigmine

83
Q

What is MOA of Neostigmine and Pyridostigmine?

A

blocks acetylcholinesterase to stop degradation of Ach

84
Q

What is ALS? (3)

A

UMN -affected cortical neurons that provide afferent input to UMN
LMN-disease that affects the ventral horns of spinal cord
-gultamate re-uptake is abnormal (increased glutamate causes excitotoxic injury)

85
Q

T/F Sensory, autonomic, sensory and oculomotor spared in ALS?

A

TRUE

86
Q

What are signs of ALS?

A
  • spasticity
  • respiratory issues
  • dysarthria: slow speech
87
Q

Whats is MOA of Riluzole/Rilutek?

A
  • inhibits glutamate release
  • inactivates v-Na channels
  • blocks intracellualr events that follow NT binding of receptor
88
Q

What are pharmacodynamics of Rilutek?

A
  • oral, high fat meals block absorption

- CYP mediated liver metabolism

89
Q

What are ADE of Riluzole/Rilutek?

A 
Hypotension
Abdominal pain
Neurolagia and arthralgia tremor
Decreased lung function 
Elevated serum transaminases
90
Q

What is MOA of edaravone?

A

free radical scavenger

91
Q

When do you tx with edaravone:

A

ALS pt with less than 2 yrs dx adn FVC >80%

92
Q

What is ADE of edaravone?

A
  • sulfites can cause asthma issues

- injection site contusion

93
Q

What are the 3 drugs that tx spasticity in ALS? (3)

A
  • Baclofen
  • Tinzaidine
  • Clonazepam
94
Q

What is ADE of baclofen?

A

sedation

95
Q

What is MOA of baclofen?

A

GABA receptor agonist

-restores lost inhibition by stimulating post synaptic GABA receptors

96
Q

What is MOA of Tinzanidine?

A

alpha adrenergic A2 agonist

-increases GABA release from inhibitory interneuron in spinal cord

97
Q

What is ADE of Tinzanidine? (3)

A
  • asthenia
  • dizziness
  • drowsiness
98
Q

T/F Diazepam and Clonazepam are used to tx spasticity in ALS

A

True

99
Q

T/F Benzos act by enhancing the inhibitory effect of GABA receptors to tx ALS spasticity

A

True

Pharmacology (47 decks)

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