(Chapter 15 Antiparkinsonian drugs)

Question 1

Anticholingeric drugs

Answer 1

Drugs that block of impede the activity of the neurotransmitter acetylcholine (ACh) at the cholingeric receptors in the brain

Question 2

Catechol ortho-methyltransferase (COMT) inhibitors

Answer 2

A class of direct acting dopaminergic drugs that work by inhibiting the enzyme COMT, which catalyzes the breakdown of dopamine

Question 3

Dopaminergic drugs

Answer 3

• Drugs used to replace the deficiency of dopamine at dopamine receptors in the nerve endings, especially in the brain when treating Parkinson’s disease (can be direct or indirect acting or replacement drugs)
• The goal of this therapy is to increase levels of dopamine in the brain and reduce the most detrimental complications of PD

Question 4

On-off phenomenon

Answer 4

A phenomenon seen in patients taking levodopa long term, in which patients have periods of good control (on time) and those when they have bad control or breakthrough Parkinson’s disease (off time)

Question 5

Parkinson’s disease (PD)

Answer 5

A slowly progressive, degenerative neurological disorder characterized by resting tremor, pill rolling of the fingers, mask like facies, shuffling gait, forward flexion of the trunk, loss of postural reflexes, and muscle rigidity and weakness

• Affects the dopamine producing neurons in the brain. Caused by an imbalance of neurotransmitters (not enough dopamine and too much ACh)
• Symptoms include Bradykinesia, Rigidity, Tremor and Postural instability

Question 6

Wearing off phenomenon

Answer 6

A gradual worsening of parkinsonian symptoms as a patients medications begin to loose their effectiveness, despite maximal doses with a variety of medications

Question 7

Levodopa therapy

Answer 7

• levodopa is a precursor of dopamine
• The blood–brain barrier does not allow exogenously supplied dopamine to enter, but it does allow levodopa to enter
• levodopa is taken up by the dopaminergic terminal, converted into dopamine, and then released as needed. As a result, the neurotransmitter imbalance is controlled in patients with early PD who still have functioning nerve terminals
• As PD progresses, it becomes more and more difficult to control with levodopa
• Ultimately, levodopa no longer controls the PD, and patient is seriously debilitated. This generally occurs between 5 and 10 years after the start of levodopa therapy

Question 8

Carbidopa

Answer 8

Carbidopa is given with levodopa

Carbidopa, which does not cross the blood–brain barrier, prevents levodopa breakdown in the periphery

Question 9

Drug therapy for PD

Answer 9

• (MAOIs) (monoamine oxidase B) inhibitor: selegiline

- COMT (catechol ortho-methyltransferase) inhibitor: entacapone

Question 10

Selegiline (MAOIs)

Answer 10

• MAOIs break down catecholamines in the central nervous system (CNS), primarily the brain
• selegiline is a newer, potent, irreversible MAOI that selectively inhibits MAO-B
• selegiline causes an increase in the levels of dopaminergic stimulation in the CNS
• Used in combination with levodopa or levodopa–carbidopa. Used as an adjunctive when a patient’s response to levodopa is fluctuating
• Allows the dose of levodopa to be decreased; delays the development of unresponsiveness to levodopa therapy
• Adverse effects include Nausea, lightheadedness, dizziness, abdominal pain, insomnia, confusion, dry mouth

Question 11

Dopaminergic therapy (replacement)

Answer 11

Can be Replacement, Direct acting/replacement, and Indirect acting
- Dopaminergic drugs are used to increase dopamine levels in the brain and to reduce the severity of PD symptoms