Parkinson's Disease and Movement Disorders Flashcards Preview

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

Flashcards in Parkinson's Disease and Movement Disorders Deck (61)
Loading flashcards...
1

Prognosis of Parkinson's post-diagnosis

10-20 years post-diagnosis

2

What does Parkinsonism mean?

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

3

When does Parkinson's disease usually present?

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

4

Where is the neurological deficit with Parkinson's disease?

deficit in the extrapyramidal system

5

Parkinson's disease

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

6

Parkinson's disease symptoms

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

7

Describe the rigidity of Parkinson's disease

flexors and extensors both contracted, so pts often quite fatigued

8

Pathophysiology of PD

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

9

Structures in the basal ganglia (striatum)

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

10

What does the striatum do?

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

11

What kind of circuits are the direct and indirect pathways?

inhibitory circuits

12

Reduced direct pathway activity causes

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

13

What does increased activity of STN contribute to

overactivity of GPi/SNr

14

Increased activity of GPi/SNr causes

causes increased inhibition of the thalamus

15

What happens when thalamus activity is decreased/?

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

16

What does the thalamus normally do?

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

17

Etiology of PD

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

18

Redox hypothesis

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

19

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

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

20

Rate-limiting enzyme in DA production

Tyrosine hydroxylase

21

What does the L-dopa approach rely on

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

22

Non-eroglines

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

23

Used to mimic the action of DA in the indirect pathway

DA D2 and D3 agonists

24

Carbidopa is an inhibitor of

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

25

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

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

26

What enzyme does Carbidopa inhibit?

L-aromatic amino acid decarboxylase

27

What is Sinemet?

Levo-dopa + Carbidopa

28

Positive aspects of Sinemet

better survival; bradykinesia and rigidity improved; mood improvement

29

Problems with Sinemet

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

30

Gold standard for Parkinson's treatment

L-dopa/Carbidopa (Sinemet)