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Pharmacology Drugs > Parkinson's Disease > Flashcards

Parkinson's Disease Flashcards

1
Q

What is the mechanism of action of L-DOPA?

A

L-DOPA can cross the blood brain barrier where it is converted to dopamine by dopa decarboxylase

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2
Q

Why isn’t dopamine given directly to the patient?

A

Dopamine can’t cross the blood brain barrier to act directly

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3
Q

What is the pharmacokinetics of L-DOPA?

A
  • Oral administration. Absorbed by active transport
  • 90% inactivated in intestinal wall by monoamine oxidase & DOPA decarboxylase
  • 9% is converted to dopamine in peripheral tissues by DOPA decarboxylase
  • Less than 1% enters CNS -
  • Half-life is 2 hours. Short dose interval and fluctuations in blood levels and symptoms as a result of this.
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4
Q

What are the side effects of L-DOPA?

A
  • Dyskinesia + dystonia + “freezing”
  • Psychosis (schizophrenia-like effects.Hallucination/delusion/paranoia)
  • Nausea/vomiting/hypotension
  • On and Off
  • Wearing off
  • Nausea/Anorexia
  • Hypotension
  • Tachycardia
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5
Q

What are some drug interactions demonstrated with L-DOPA?

A
  • Pyridoxine increases peripheral breakdown of L-DOPA
  • Many antipsychotic drugs block dopamine receptors and parkinsonism is a side effect
  • MAOIs risk antihypertensive crisis
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6
Q

What is the mechanism of action of Dopamine receptor agonists?

A

-Dopamine receptor Agonist

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7
Q

What are examples of non-ergot derived dopamine receptor agonist?

A
  • Ropinirole
  • Pramipexole
  • Rotigotine
  • Apomorphine
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8
Q

What are advantages of dopamine receptor agonists?

A
  • Direct acting
  • Less dyskinesias/motor complication
  • Possible neuroprotection
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9
Q

What are physical side effects of dopamine receptor agonists?

A
  • Nausea
  • Postural Hypotension
  • Psychosis
  • Confusion
  • Sedation
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10
Q

What are disadvantages of dopamine receptor agonists?

A
  • Less efficacy than L-DOPA
  • Impulse control disorder
  • More psychiatric
  • Expensive
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11
Q

What are psychological side effects of dopamine receptor agonists? (impulse control disorders)

A
  • Pathological gambling
  • Hypersexuality, compulsive shopping
  • Desire to increase dosage
  • Punding
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12
Q

What are examples of Monoamine oxidase B inhibitors?

A
  • Selegiline

- Rasagaline

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13
Q

What is the mechanism of action monoamine oxidase B inhibitors?

A
  • MAOB metabolises dopamine
  • Predominates in dopamine containing region
  • MAOB inhibitors enhance dopamine by inhibiting MAOB
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14
Q

What are the advantages of Monoamine oxidase B inhibitors?

A
  • Can be used along
  • Prolong the action of L-DOPA
  • Smooths out motor response
  • May be neuroprotective
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15
Q

What are examples of anticholinergics?

A
  • Trihexyphenidydyl
  • Orphenadrine
  • Procyclidine
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16
Q

What is the mechanism of action of anticholinergics in the treatment of Parkinson’s disease?

A
  • Acetyl choline may have antagonistic effects to dopamine

- Minor role in treatment of Parkison’s Disease

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17
Q

What are the advantages of using anticholinergics in treatment of Parkinson’s disease?

A
  • Treat tremor

- Not acting via dopamine systems

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18
Q

What are the disadvantages of using anticholinergics in treatment of Parkinson’s disease?

A

-No effect on bradykinesia

19
Q

What are side effects of anticholinergics?

A
  • Confusion
  • Drowsiness
  • Usual anticholinergic effects
20
Q

What is the mechanism of action of Amantidine?

A

Unclear but possibly

  • Enhanced dopamine release
  • Anticholinergic NMDA inhibition
21
Q

What are the advantages of Amantadine?

A

-Few side effects

22
Q

What are the disadvantages of amantadine?

A
  • Poorly efficacious

- Little effect on tremor

23
Q

How is surgery used to treat Parkinson’s disease?

A
  • Thalamus for tremor
  • Globus Pallidus Interna for dyskinesias
  • Deep brain stimulation of subthalamic nucleus
24
Q

What are the uses of Surgery in Parkinson’s disease?

A

Of value in highly selected cases

  • Dopamine response
  • Significant side effect with L-DOPA
  • No psychiatric illness
25
Q

What are examples of Carbidopa?

A
  • Co-careldopa (Sinemet)

- Co-beneldopa (Madopar

26
Q

What is the mechanism of action of Carbidopa?

A

Peripheral decarboxylase inhibitor to prevent breadown of L-DOPA in peripheries

27
Q

Why is carbidopa used with L-DOPA?

A

Used in combination with L-DOPA:

  • Reduces dosage of L-DOPA required
  • Decreases peripheral side effects
  • Increased L-DOPA reaching the brain
28
Q

What are examples of COMT inhibitors?

A

-Entacapone

29
Q

What is the mechanism of action of COMT inhibitors?

A
  • Prevents breakdown of L-dopa in the peripheries
  • Also reduces peripheral breakdown of L-DOPa to 3-O-methyl dopa which competes with L-DOPA active transport into CNS
  • Therefore, prolongs clinical effects of levodopa (motor response) and reduce wearing off)
30
Q

What are the pharmacokinetics of COMT inhibitors?

A
  • Doesn’t cross blood brain barrier

- No therapeutic effect alone

31
Q

What are some physical manifestations of Parkinson’s disease?

A
  • Tremor
  • Rigiditiy
  • Bradykinesia
  • Postural Instability
32
Q

What are some non-motor manifestations of Parkinson’s disease?

A
  • Mood changes - depression and anxiety
  • Pain
  • Cognitive change
  • Urinary symptoms
  • Sleep disorder
  • Sweating
  • Constipation
33
Q

How does Myasthenia Gravis present?

A
  • Extraocular muscles - commonest presentation
  • Bulbar involvement (dysphagia, dysphonia, dysarthria)
  • Limb weakness (proximal symmetric)
  • Respiratory muscle involvement
34
Q

What are some drugs that exacerbate Myasthenia Gravis?

A
  • Aminoglycoside
  • Beta blocker, CCBs, Quinidine, Procainamide
  • Chloroquine, Penicillamine
  • Succinylcholine
  • Magnesium
  • ACE inhibitors
35
Q

What are some complications associated with Myasthenia Gravis?

A
  • Acute exacerbation (Myasthenia Crisis)
  • Overtreatment (Cholinergic crisis)

Both have the same presentations with over and under-treatment

36
Q

How is myasthenia graves treated?

A

-Acetylcholinesterase Inhibitors

37
Q

What are some examples of acetylcholinesterase inhibitors?

A

Pyridostigmine (oral)

Neostigmine (oral and IV preparations)

38
Q

What are some features of Neostigmine?

A
  • Used in ITU
  • Quicker action, duration up to 4 hours
  • Significant anti-muscarininic side effects
39
Q

Whats the mechanism of action of acetylcholinesterase inhibitors?

A
  • Enhance neuromuscular transmission by preventing breakdown of Each in neuromuscular junction
  • Skeletal and smooth mucle
  • Excess dose cause depolarising block (cholinergic crisis)
  • Muscarinic side effects with low dose
40
Q

What is the mechanism of acton of pyridostigmine?

A
  • Prevents breakdown of ACh in neuromuscular junction

- ACh is more likely to engage with remain receptors

41
Q

What are some features of Pyridostimine therapy?

A
  • Onset is 30 mins
  • Peaks at 50-120 mins
  • Duration of action is 3-6 hours

Give 30-40 mins before food

42
Q

What are the anti muscurinic side effects of pyridostigmine?

A

Miosis and the SLUDGE syndrome

  • Salivation
  • Sweating
  • Lacrimation
  • Urinary incontinence
  • Diarrhoea
  • GI upset and Hyper motility
  • Emesis
43
Q

What are examples of ergot derived dopamine receptor agonist?

A

-Bromocriptine

44
Q

Why are ergot derived dopamine receptor agonists no longer used?

A

-Too many side effects

Pharmacology Drugs (22 decks)

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