Chapter 15 Flashcards

1
Q

Adjunctive Drugs

A

Drugs that are added as a second drug for combined therapy with a primary drug and may have additive or independent properties

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2
Q

Akinesia

A

Classically defined as “Without movement”. Absence or poverty of movement that results in a mask like facial expression and impaired postural reflexes.

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3
Q

Bradykinesia

A

Slowness of movement; a classic symptom of Parkinson’s disease.

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4
Q

Chorea

A

A condition characterized by involuntary, purposeless, rapid motions such as flexing and extending the fingers, raising and lower the shoulders, or grimacing.

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5
Q

Dyskinesia

A

Abnormal involuntary movements; inability to control movements.

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6
Q

Dystonia

A

Impaired or distorted voluntary movement involving the head, neck, or feet.

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7
Q

Exogenous

A

A term describing any substance produced outside of the body that may be taken into the body (a medication, food, or environmental toxin).

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8
Q

On-off phenomenon

A

A common experience of patients taking medication for Parkinson’s disease in which they experience periods of greater symptomatic control alternating with period of lessor symptomatic control.

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9
Q

Parkinson’s Disease

A

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

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10
Q

Postural instability

A

A decrease or change in motor and muscle movements, often seen in Parkinson’s disease, that leads to unsteadiness and hesitation in movement and gait when the individual starts to stops walking; it can also cause leaning to the left or right when sitting.

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11
Q

Presynaptic

A

Drug that exert their antiparkinson effects before nerve synapse

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12
Q

Rigidity

A

Resistance of the muscles to passive movement leading to the cogwheel rigidity seen in Parkinson’s disease.

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13
Q

TRAP (Tremor, Rigidity, Akinesia, Postural instability)

A

An acronym for symptoms of Parkinson’s disease.

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14
Q

Parkinson’s disease

A

A chronic, progressive neurodegenerative disorder affecting the dopamine producing neurons in the brain.

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15
Q

What is the association of Parkinson’s disease and the sustantia nigra?

A

Parkinson’s disease involves a dopamine deficit in the area of the cerebral cortex called the substantial nigra and it is contained within the basal ganglia.

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16
Q

The Thalamus does not serve as a relay station for the brain; instead, it does muscle coordination?

A

False, The thalamus does serve as a relay station for the brain impulses.

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17
Q

What does the cerebellum regulate?

A

Muscle coordination

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18
Q

Dopamine

A

is an inhibitory neurotransmitter

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19
Q

Acetylcholine

A

is an excitatory neurotransmitter

20
Q

How does Parkinson’s disease result?

A

It results from an imbalance in dopamine and acetylcholine in the basal ganglia. This imbalance is caused by failure of the nerve terminals in the substantial nigra to produce dopamine. Destruction of the substantial nigra by Parkinson’s disease leads to dopamine depletion. this often results in excessive unopposed acetylcholine activity.

21
Q

How is Parkinson’s disease diagnosed?

A

It is usually made on the basis of the classic symptoms and physical findings. The classic symptoms include Bradykinesia, postural instability, and tremors (TRAP, meaning tremor, Rigidity, Akinesia, and postural instability, with akinesia really manifesting as bradykinesia.

22
Q

What does monoamine oxidase do?

A

Causes the breakdown of catecholamines in the body

23
Q

What do catecholamine include?

A

Dopamine, norepinephrine, and epinephrine.

24
Q

What is the primary role of MAO enzymes?

A

It is the breakdown of catecholamines- such as dopamine, norepinephrine, and epinephrine – as well as serotonin.

25
Q

What happens when an MAO-B inhibitor is given?

A

It causes an increase in the levels of dopaminergic stimulation in the CNS.

26
Q

Are Rasagiline (Azilect) and Selegiline (eldepryl) MAO-B inhibitors?

A

Yes, they are indicated for Parkinson’s

27
Q

What is the one drug that is known to function as a dopamine modulator?

A

Amantadine (Symmetrel)

28
Q

What is the Mechanism of action of Amantadine?

A

Amantadine works by causes the release of dopamine and other catecholamines from their storage sites in the presynaptic fibers of nerve cells within the basal ganglia that have not yet been destroyed by the disease process.

29
Q

What happens when Amantadine blocks the reuptake of dopamine?

A

Amantadine blocks the reuptake of dopamine into nerve fibers. This results in higher levels of dopamine in the synapse between nerves and improve dopamine neurotransmission between neurons.

30
Q

Is Amantadine considered to be indirect acting?

A

Yes, because it does not directly stimulate dopaminergic receptors.

31
Q

When is Amantadine provided?

A

It is given in the early stages of Parkinson’s disease, when there are still some intact neurons in the basal ganglia.

32
Q

Is Amantadine used to treat carbidopaa-levodopa?

A

It is often used to treat dyskinesia associated with carbidopa-levodopa. It is also indicated for the treatment of influenza virus infection

33
Q

What are indirect-acting dopaminergic drugs?

A

MAO-A, MAO-B, and COMT

34
Q

How does COMT (catechol ortho methyltransferase) work?

A

COMT is the enzyme that catalyzes the breakdown of the body’s catecholamines.

35
Q

Is Entacopone (Comtan) a COMT inhibitor?

A

Yes, it is indicated for the adjunctive treatment of Parkinson’s and taken with levodopa.

36
Q

Are direct acting dopamine receptors agonist used to treat Parkinson’s?

A

yes, they are often first line agents used upon diagnosis.

37
Q

What are the two subclasses of direct acting dopamine receptors?

A

Nondopamine dopamine receptor agonist (NDDRA) and dopamine replacement drugs.

38
Q

How do the Nondopamine dopamine receptor agonist (NDDRA) work?

A

All of the NDDRAs work by direct stimulation of presynaptic and/or postsynaptic dopamine receptors in the brain. They may be used in early or late stages of the disease

39
Q

What are the subdivisions of NDDRA?

A

They are

  1. ergot derivatives bromocriptine (parlodel)
  2. the non ergot drugs pramipexole (mirapex),
  3. ropinirole (requip),
  4. and rotigotine (Neupro)
40
Q

How does Bromocriptine work?

A

Bromocriptine is an ergot alkaloid similar to ergotamine. Bromocriptine works by activating presynaptic dopamine receptors to stimulate the production of more dopamine.

41
Q

Ergot and non ergot NDDRA are not used to treat Parkinson’s?

A

False, ergot and noergot NDDRA are used to treat Parkinson’s.

42
Q

How has NDDRA’s such as bromocriptine, pramipexole, ropinirole, and rotigotine been used in Parkinson’s?

A

They have been used as adjuncts to levodopa for the management of motor fluctuations; however, they are now often used as first line therapy. They differ from levodopa in that they do not replace dopamine itself but act by stimulating dopaminergic receptors in the brain.

43
Q

What does Bromocriptine do?

A

It stimulates on the D2 receptors and antagonizes the D1 receptors.

44
Q

Can Bromocriptine be given with Carbidopa-levodopa?

A

Yes, so that lower dosages of the levodopa are needed. This results in prolonging the on periods and minimizing the off periods of the disease.

45
Q

Is Pramipexole a non-ergot NDDRA?

A

Yes

46
Q

Pramipexole, ropinirole, and rotigotine can be used in what stage of Parkinson’s?

A

They can be used in early and late stage Parkinson’s and appear to delay the need for levodopa therapy.