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Pharmacology Test #6 > Parkinson's Disease and Movement Disorders > Flashcards

Parkinson's Disease and Movement Disorders Flashcards

1
Q

Prognosis of Parkinson’s post-diagnosis

A

10-20 years post-diagnosis

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2
Q

What does Parkinsonism mean?

A

the person has PD-like symptoms, but can be induced by other means, such as antipsychotics

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3
Q

When does Parkinson’s disease usually present?

A

in the 60s-70s, but 5-10% present before age 40

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4
Q

Where is the neurological deficit with Parkinson’s disease?

A

deficit in the extrapyramidal system

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5
Q

Parkinson’s disease

A

chronic, progressive, irreversible disease, leading to tremor and muscular rigidity

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6
Q

Parkinson’s disease symptoms

A

resting tremor; akinesia; muscular rigidity; compromised cognitive functions; comorbid depression (25% of pts)

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7
Q

Describe the rigidity of Parkinson’s disease

A

flexors and extensors both contracted, so pts often quite fatigued

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8
Q

Pathophysiology of PD

A

cell death in the substantia nigra; decreased DAergic innervation in the basal ganglia

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9
Q

Structures in the basal ganglia (striatum)

A

caudate nucleus; putamen; globus pallidus; terminal projection fields from the SNc

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10
Q

What does the striatum do?

A

striatum allows a movement to occur, so damage to normal excitation/inhibition circuitry will disturb normal execution of movements

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11
Q

What kind of circuits are the direct and indirect pathways?

A

inhibitory circuits

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12
Q

Reduced direct pathway activity causes

A

greater inhibition of GPe; GPe is inhibitory, so this results in less inhibition of STN

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13
Q

What does increased activity of STN contribute to

A

overactivity of GPi/SNr

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14
Q

Increased activity of GPi/SNr causes

A

causes increased inhibition of the thalamus

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15
Q

What happens when thalamus activity is decreased/?

A

results in reduced motor commands from cortex, resulting in the motor symptoms of PD

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16
Q

What does the thalamus normally do?

A

thalamus is excitatory and normally provides activation of the cortex to allow execution of motor commands from the basal ganglia

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17
Q

Etiology of PD

A
  1. Age/sex
  2. Environmental factors (pesticide exposure)
  3. Redox hypothesis
  4. Genetic factors (familial, parkin, LRRK2, alpha-synuclein)
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18
Q

Redox hypothesis

A

DA toxic, oxidized, creates ROS and oxidative stress to DA neurons - which may be particularly vulnerable to this stress

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19
Q

What is the correlation between smoking and Parkinson’s Disease?

A

inverse correlation between smoking and PD, which has been theorized to result from nicotine in cigarettes; independent of smoking’s harmful health effects and dose-dependent

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20
Q

Rate-limiting enzyme in DA production

A

Tyrosine hydroxylase

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21
Q

What does the L-dopa approach rely on

A

relies on the remaining, live DA neurons to produce increased amounts of DA

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22
Q

Non-eroglines

A
  1. Pramipexole (Mirapex)
  2. Ropinirole (Requip)
  3. Rotigotine (NeuroPro)
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23
Q

Used to mimic the action of DA in the indirect pathway

A

DA D2 and D3 agonists

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24
Q

Carbidopa is an inhibitor of

A

peripheral L-dopa metabolism, which helps to direct a greater percentage of the L-dopa to the CNS and allows the dose of L-dopa to be reduced

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25
Q

What does reducing the dose of L-dopa help with?

A

helps to reduce the onset of dyskinesias and reduces other side effects like GI problems

26
Q

What enzyme does Carbidopa inhibit?

A

L-aromatic amino acid decarboxylase

27
Q

What is Sinemet?

A

Levo-dopa + Carbidopa

28
Q

Positive aspects of Sinemet

A

better survival; bradykinesia and rigidity improved; mood improvement

29
Q

Problems with Sinemet

A

decreased prolactin; increased GH; arrhythmias; postural hypotension; nausea initially

30
Q

Gold standard for Parkinson’s treatment

A

L-dopa/Carbidopa (Sinemet)

31
Q

How long until L-dopa begins to decrease in efficacy?

A

5-6 years

32
Q

Eventually develops with long-term administration of L-dopa

A

motor dyskinesias

33
Q

Chorea

A

semi-directed, non-repetitive dancelike movements

34
Q

Dystonia

A

sustained msucle contractions cuase twisting and repetitive movements or abnormal postures

35
Q

Athetosis

A

slow, involuntary, convoluted, writhing movements of the fingers, hands, toes, and feet and in some cases, arms, legs, neck and tongue

36
Q

Why is L-dopa delayed until it is absolutely necessary

A

dyskinesias

37
Q

What should you try first in a parkinson’s patient

A

try non-erogoline DA agonists; Requip is anecdotally slightly better than Mirapex

38
Q

Amantadine

A

DA releasing agent, not much better than l-dopa

39
Q

MAO-B inhibitors are specific for

A

DA (MAO-A more on 5HT and NE)

40
Q

COMT inhibitors prevent

A

methylation in the liver, allows L-dopa doses to last longer (though they don’t allow you to reduce the dose)

41
Q

Inheritance of Huntington’s disease

A

autosomal dominant (complete penetrance); CAG repeats in huntington gene

42
Q

What determines the disease course of Huntington’s?

A

the number of CAG-repeats in the huntington gene

43
Q

Symptoms of Huntington’s

A

choreiform movements, cognitive impairment, behavioral changes

44
Q

What do abnormal huntington proteins do?

A

aggregate and form inclusions

45
Q

What part of the brain is preferentially affected in Huntington’s disease?

A

spiny neurons of the striatum

46
Q

Prognosis of huntington’s after diagnosis

A

20 years after diagnosis; death occurs from pneumonia, suicide, heart disease, aspiration of food, falls

47
Q

Mechanism of HD pathology

A

selective destruction of medium spiny neurons of the neostriatum, particularly those that project from the striatum to the Gpe (earlier than those that proejct to Gpi)

48
Q

How are PD and HD different?

A

HD is the opposite of PD: inhibition of GPi, STN, and dis-inhibition of thalamus and cortex

49
Q

Treatment of HD

A
  1. Antidepressants (w/o anti-Ach effects)
  2. Carbemazepine for depression
  3. low-dose antipsychotics
  4. Tetrabenazine
  5. Benzodiazepines
50
Q

What is tetrabenazine?

A

reversible type of reserpine (which is irreversible), used to deplete monamines such as DA

51
Q

What kind of Huntington’s patients get benzos?

A

for severely agitated, anxious, stressed patients

52
Q

Spasticity

A

muscle stiffness or tightness

53
Q

What does spasticity result from

A

results from imbalance in excitation/inhibition to alpha motor neuron

54
Q

Damage to upper motor neurons causes

A

reduced activity of inhibitory interneurons, overactivity of motor neurons and hyperreflexia

55
Q

Tizanidine

A

alpha2 agonist; acts via presynaptic mechanism to reduce activity of motor neuron

56
Q

Baclofen

A

GABAb agonist that can act directly on the motor neuron and presynaptically on excitatory corticospinal glutamate fiber

57
Q

Dantrolene

A

block Ca2+ release in muscle; interferes with excitation contraction coupling in muscle fiber by blocking release of CA2+ from sarcoplasmic reticulum via inhibition of ryanodine receptors

58
Q

Clinical use of Tizanidine

A

stroke, MS, ALS

59
Q

Clinical use of Baclofen

A

ALS

60
Q

Problems with Baclofen

A

serious, life-threatening side effects possible

61
Q

Cyclobenzaprine

A

mechanism of action unclear, may involve norepinephrine or serotonin in spinal cord, ultimately leads to decreased firing of motor neurons

Pharmacology Test #6 (12 decks)

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