Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology 2 > Parkinsons Disease > Flashcards

Parkinsons Disease Flashcards

1
Q

What are the early signs of PD?

A

Tremor, Bradykinesia, Rigidity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the late sign of PD?

A

Postural Instability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Explain the effect of depigmentation in the substantia nigra.

A

The loss of neuromelanin means the neurons aren’t protected from oxidative stress which can lead to neuronal death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is PD?

A

Movement disorder via dysfunction in the basal ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the general pathophysiology of PD?

A

Dopamine depletion from the basal ganglia which disrupts communication to the thalamus and motor cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the name & function of the extrapyramidal system?

A

Name: Basal Ganglia
Function: Coordinate and perform motor commands at a subconscious level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the 5 components of the basal ganglia?

A
  • Substantia Nigra
  • Striatum
  • Globus Pallidus
  • Subthalamic nucleus
  • Thalamus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the result of the degeneration of neurons in the substantia nigra / nigrostriatal pathway?

A

Decreased dopaminergic influence on striatal neurons

-This usually regulates fine motor activity and depends on ACh / DA balance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the 5 classes of PD drugs?

A
  • Dopamine precursors
  • Dopamine receptor agonists
  • Drugs inhibiting dopamine breakdown
  • Drugs that release dopamine
  • Anticholinergics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How much of Levodopa actually reaches the brain?

A

<1-3% reaches CNS to bind to D1 & D2 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the issue with solely using Levodopa? (3)

A
  • Peripheral conversion of L-Dopa to DA via Dopa decarboxylase
  • Peripheral breakdown of L-Dopa via COMT which competes with L-Dopa to bross BBB
  • Side effects (80% of GI side effects)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why is Levodopa usually given with carbidopa? (4)

A
  • Carbiopa won’t cross BBB but will reduce peripheral conversion to dopamine
  • Levodopa levels can be reduced by 75%
  • 10% will now make it to the CNS
  • less side effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the deterioration in response to levodopa?

A

30-50% of patients after 3-5 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are side effects with DA precursors? (3)

A
  • Anorexia, nausea and vomiting (domperidone)
  • Postural hypotension
  • Psychological effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are management issues with DA precursors? (2)

A
  • Dyskinesia

- On-off phenomena

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the effect on Levodopa + DDC inhibitors when given with anticonvulsants?

A

Decreased (increased metabolism)

17
Q

What is the effect on Levodopa + DDC inhibitors when given with antipsychotics?

A

Decreased (blocks dopamine receptors)

18
Q

What is the effect on Levodopa + DDC inhibitors when given with antihypertensives?

A

Increased risk of postural hypotension

19
Q

What is the effect on Levodopa + DDC inhibitors when given with MAO-A inhibitors?

A

Hypertensive crisis

20
Q

What is the effect on Levodopa + DDC inhibitors when given with MAO-B inhibitors?

A

Increased nausea + CNS effects

21
Q

What is the effect on Levodopa + DDC inhibitors when given with Ferrous sulfate?

A

Decreased (less absorption)

22
Q

What are the 2 types of D-receptor agonists and which one is still used?

A

Ergot derived vs non-ergot derived (non is used)

23
Q

What is the main use of ergot-derived D-agnoists?

A

Acts on D1 + D2 and reduces the ‘on-off’ phenomenon of levodopa

24
Q

What is the main use of non-ergot-derived D-agnoists?

A

Acts on D2 + D3 as an effective initial therapy with mild symptoms

25
Q

List 3 ergot derived D-agonists

A
  • Bromocriptine
  • Pergolide
  • Carbergoline
26
Q

List 3 non-ergot derived D-agonists

A
  • Pramipexole
  • Ropinirole
  • Rotigotine
27
Q

What is a side effect unique to non-ergot derived D-agonist

A
  • Peripheral edema
28
Q

What is Tolcapone and its mechanism of action?

A

COMT inhibitor which prevents peripheral metabolism of levodopa (prolongs clinical response)

29
Q

What is Selegiline and its mechanism of action?

A

Irreversible inhibitor of MAO-B (which usually degrades DA)

- Given as an initial therapy

30
Q

What is Amantadine and its mechanism of action?

A
  • N-methyl-D-aspartate antagonist
  • Increases synaptic dopamine levels
  • Given as therapy for PD with tremor-predominant symptoms
31
Q

What is the mechanism and an example of anticholinergics?

A
  • Releases the inhibition on DA nerve terminals e.g. benztropine
32
Q

What type of parkinsons are anticholinergics given to?

A

Tremor-Predominant

33
Q

List 5 side effects of anticholinergics

A
  • Dry mouth
  • Constipation
  • Blurred vision
  • Urinary retention / prostatic hypertrophy
  • Glaucoma

Pharmacology 2 (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions