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Pharmacology Exam #3 > Parkinsons > Flashcards

Parkinsons Flashcards

1
Q

Etiology of Parkinsons

A

Dopamin deficiency OR Ach excess

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2
Q

Feature of Parkinsons

A
  1. Resting tremor
  2. Rigidity
  3. Bradykinesia
  4. Postural instability
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3
Q

Amyotrophic Lateral Sclerosis (ALS)

A

Sporadic or familial progressive neurodegenerative disease

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4
Q

Essential Tremor

A

Nerve disorder characterized by uncontrollable shaking while moving

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5
Q

Guillan-Barre

A

Immune system attack the nerves with weakness and tingling in the feet and legs–>ascending paralysis

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6
Q

Huntington’s Disease

A

Inherited adult-onset neurologic disease with dementia and bizarre involuntary movements

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7
Q

Myasthenia Gravis

A

Chronic autoimmune neuromuscular disorder with fluctuating weakness

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8
Q

Restless Leg Syndrome (RLS)

A

Urge to move the legs

Associated with iron deficiency

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9
Q

Tourettes Syndrome

A

Repetitive movements or unwanted sounds (tics) that can’t be easily controlled
Inherited (genetic) and environmental factors

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10
Q

Wilsons disease

A

Inherited autosomal recessive disorder of copper accumulation in liver, brain, kidneys, and eyes

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11
Q

List a monoamine Oxidase Inhibitor (MAO-B)

A

Rasagline

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12
Q

Rasagline ADEs

A
  1. Confusion
  2. Insomnia
  3. Hallucinations
  4. Nausea
  5. Orthostatic hypotension
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13
Q

Rasagline Drug interactions with Meperidine

A

Serotonin Syndrome

  • N/V
  • Tremor
  • Agitation/restlessness
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14
Q

What would be the best treatment of choice in a 71-year-old PD patient?

A

Amantadine

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15
Q

Amantadine MOA

A
  1. Enhances Dopamine release

2. Blocks glutamatergic NMDA receptors

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16
Q

Amantadine Benefits

A

Decreases:

  1. Tremor
  2. Rigidity
  3. Bradykinesia
17
Q

Amantadine ADEs

A

Anti-cholinergic effects:

  1. Dry as a bone-Dry mouth, urinary retention
  2. Blind as a bat-Dilated pupils/Mydriasis
  3. Mad as a hatter-Confused/hallucinations
  4. Red as a beet-Flushing
18
Q

List the prototype Dopamine Agonist

A

Pramipexole

19
Q

Pramipexole MOA

A

Stimulate dopamine activity on the nerves in the substantial nigra and striatum

20
Q

Pramipexole ADE’s

A
  1. Postural Hypotension
  2. Impulsive Behavior-Tend to gamble
  3. Psychosis- Confusion, hallucinations, sedation, vivid dreams
21
Q

Levodopa MOA

A

Dopamine Precursor

  • Crosses the blood brain barrier
  • Once crossed, converted to Dopamine
22
Q

Carbidopa MOA

A

Prevents the metabolism of Levodopa in the peripheral blood via dopa decarboxylase
–>higher blood levels and good portion gets into the brain

23
Q

Levodopa/Carbidopa drug interactions

A

COMT and MAO type B inhibitors diminish doses and prolongs action= Excess Dopamine

24
Q

Levodopa/Carbidopa ADEs

A
  1. Drowsiness
  2. Nausea
  3. Dyskinesias-MOTOR COMPLICATIONS
25
Q

List the two COMT inhibitors

A
  1. Entacapone

2. Tolcapone

26
Q

COMT inhibitor effect on L-Dopa

A

1Blocks conversion of L-Dopa into the inactive form of 3-O-Methyldopa (3-OMD) = Greater % that will cross BBB

27
Q

COMT inhibitor effect on Dopamine

A

Prevents conversion of Dopamine to 3-methoxytyramine (3-MT)

28
Q

What are we going to monitor when using COMT inhibitors?

A

LFTs due to liver toxicity

29
Q

What drug is the most useful as monotherapy in patients under 70 years of age with disturbing tremor who do not have significant bradykinesia or gait disturbances?

A

Anticholinergic/Antimuscaranic

30
Q

List the two Anticholinergic/Antimuscaranic used in PD

A
  1. Benztropine

2. Trihexyphenidyl

31
Q

What is Duopa

A

Carbidopa/Levodopa in Gel form that goes directly to your intestine through a tube

32
Q

Benefits of Duopa

A
  1. Treat motor sx’s
  2. Improve absorption
  3. Reduce off-times by delivering directly to small intestines
33
Q

End-of-dose “wearing off” (motor fluctuation) treatment

A
  1. Increase frequency of carbidopa/L-dopa doses
  2. Add COMT or MAO-B inhibitor
  3. Add Dopamine Agonist
34
Q

“Delayed on” or “no on” response treatment

A
  1. Give carbidopa/L-dopa on empty stomach

2. Use carbidopa/L-dopa ODT

35
Q

Start hesitation (“freezing”) treatment

A
  1. Increase frequency of carbidopa/L-dopa doses
  2. Add MAO-B inhibitor
  3. Add Dopamine Agonist
  4. Physical Therapy
  5. Sensory cues
36
Q

Peak-dose dyskinesia treatment

A
  1. Provide smaller does of carbidopa/L-dopa
  2. Reduce dose of adjunctive dopamine agonist
  3. Add Amantadine
37
Q

What do we want to give to your patients who are on Entcapone/Talcapone (COMT inhibitors) to help avoid one of the SE’s?

A

Anti-diarrheal agents due to diarrhea SE

38
Q

What are we going to monitor in Amantadine?

A
  1. Mental status

2. Renal function

Pharmacology Exam #3 (6 decks)

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