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SA Clinical Pharmacology & Therapeutics > S12) Neuropharmacology > Flashcards

S12) Neuropharmacology Flashcards

1
Q

Identify four clinical features of Parkinsonism

A
  • Tremor
  • Rigidity
  • Bradykinesia
  • Postural instability
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2
Q

what are some added features of Parkinsonism

A

→ sometimes they can’t stop their movements so keep moving

→ sometimes can’t start their own movements without a push

→ lead pipe rigidity (resistance in movement)

→ cog wheeling → moving joints slowly

→ shuffle gait

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3
Q

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

A
  • Mood changes
  • Pain
  • Cognitive change
  • Urinary symptoms
  • Sleep disorder
  • Sweating
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4
Q

After 15 years, what clinical features will patients with PD have during follow up?

A
  • Dyskinesia (94%)
  • Falls (81%)
  • Cognitive decline (84%)
  • Somnolence (80%)
  • Swallowing difficulties (50%)
  • Severe speech problems (27%)
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5
Q

How does one make a diagnosis of Idiopathic Parkinson’s Disease?

A
  • Clinical features: Bradykinesia
  • Exclude other causes of Parkinsonism
  • Response to treatment: 70-80% levadopa,
  • Normal structural neuro-imaging
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6
Q

what is bradykinesia

A

movements get slower as movement continues

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7
Q

Describe the pathological features of IPD

A
  • Neurodegeneration
  • Lewy bodies synucleinopathy
  • Loss of pigment
  • Reduced dopamine
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8
Q

what percentage of dopaminergic neurones are lost in the basal ganglia before any motor signs are visible

A

50% lost

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9
Q

Describe three ways in which the basal ganglia circuitry is affected in IPD

A
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10
Q

Identify six different drug classes used to treat IPD

A
  • Levodopa (L-DOPA)
  • Dopamine receptor agonists
  • MAOI type B inhibitors
  • COMT inhibitors
  • Anticholinergics
  • Amantidine
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11
Q

catecholamine synthesis

A
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12
Q

dopamine degradation

A
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13
Q

Why is L-DOPA used to treat IPD instead of Dopamine?

A
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14
Q

How is Levodopa administered?

A

Oral administration

→ not soluble but can be dispersed

→ dispersable Madopar

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15
Q

In five steps, describe the absorption of L-DOPA

A

⇒ Absorbed by active transport

⇒ Competes with amino acids

⇒ Taken up by dopaminergic cells in substantia nigra to be converted to dopamine

⇒ 90% inactivated in intestinal wall

→ 9% converted into dopamine in peripheral tissues by dopa decarboxylase

⇒ Forms monoamine oxidase & DOPA decarboxylase

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16
Q

Despite the patient being on medication why will the medication be less useful over time

A

→ over time the patient is still losing dopaminergic neurones

→ There wont be enough neurones to convert the dopamine

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17
Q

Which formulation of L-DOPA is used to increase the amount that gets to the brain?

A

L-DOPA is used in combination with a peripheral DOPA decarboxylase inhibitor – co-careldopa / co-beneldopa

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18
Q

What is the half life of L-DOPA?

A

T1/2 = 2 hours

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19
Q

What are the advantages of L-DOPA?

A
  • Highly efficacious
  • Low side effects e.g. nausea, vomiting, hypotension, tachycardia, psychosis
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20
Q

What are the disadvantages of L-DOPA?

A
  • Loss of efficacy (only effective in presence of dopaminergic neurones)
  • Needs enzyme conversion
  • Involuntary movements
  • Motor complications
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21
Q

what is levodopa always given in conjunction with

A

→ peripheral dopa decarboxylase inhibitor

→ you want the dopamine to work centrally not peripherally otherwise you will get unwanted side effects

→ this means a reduced dose is required and more levodopa reaching brain

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22
Q

what are some examples of peripheral dopa decarboxylase inhibitor

A

→ Co-careldopa (sinemet

→ Co-beneldopa (madopar)

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23
Q

what are some advantages of taking levodopa

A

→ highly efficacious

→ few side effects:

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24
Q

what are some disadvantages of taking levodopa

A
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25
Q

Describe the drug-drug interactions of L-DOPA with the following:

  • Pyridoxine (Vitamin B6)
  • MAOIs
  • Antipsychotic drugs
A
  • Pyridoxine: increases peripheral breakdown of L-DOPA
  • MAOIs: risk hypertensive crisis
  • Antipsychotic drugs: lead to parkinsonism (block dopamine receptors)
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26
Q

Identify some different types of dopamine receptor agonists

A
  • Ergot derived
  • Non Ergot
  • Patch
  • Subcutaneous
27
Q

Provide two examples of non ergot dopamine receptor agonists

A
  • Ropinirole
  • Pramipexole
28
Q

Provide an example of a patch dopamine receptor agonist

A

Rotigotine

29
Q

Provide an example of a subcutaneous dopamine receptor agonist

A

Apomorphine

30
Q

What are the advantages of dopamine receptor agonists?

A
  • Direct acting
  • Less dyskinesia / motor complications
  • Possible neuroprotection
31
Q

What are the disadvantages of dopamine receptor agonists?

A
  • Less efficacy than L-DOPA
  • Impulse control disorders
  • More psychiatric side effects
  • Expensive
32
Q

Provide five examples of impulse control disorders

A
  • Pathological gambling
  • Hypersexuality
  • Compulsive shopping
  • Desire to increase dosage
  • Punding
33
Q

What are the side effects of dopamine receptor agonists?

A
  • Sedation
  • Hallucinations
  • Confusion
  • Nausea
  • Hypotension
34
Q

Describe the mechanism of action of monoamine oxidase B inhibitors

A
  • Inhibits metabolism of dopamine by MAO
  • Prolongs action of L-DOPA
  • Smooths out motor response
35
Q

Provide two examples of monoamine oxidase B inhibitors

A
  • Selegiline
  • Rasagaline
36
Q

Describe the mechanism of action of Catechol-O-methyl Transferase (COMT) inhibitors

A
  • Reduce peripheral breakdown of L-DOPA to 3-O-methyldopa (3-O-methyldopa competes with L-DOPA for active transport into CNS)
  • Prolongs motor response to L-DOPA

→ they have no therapeutic effect by themselves always have to use levodopa and dopa decarboxylase inhibitor)

37
Q

Provide an example of a COMT inhibitor

A

Entacapone (doesn’t cross BBB)

Opicapone (doesn’t cross BBB)

38
Q

Dopamine receptor agonists

A

→ you can start on these before giving ladopa

Non Ergot: Ropinirole, Pramipexole

Patch: if they have swallowing difficulties (Rotigotine)

Subcutaneous: Apomorphine

39
Q

when do you use dopamine receptor agonist

A

→ de novo therapy

→ apomorphine (for patients with severe motor fluctuations) subcutaneous:

→ bolus

→ continuous infusion

40
Q

advantages for dopamine receptor agonist

A

→ no peripheral effect

41
Q

disadvantages for dopamine receptor agonist

A
42
Q

dopamine receptor agonists side effects

A

→ sedation

→ hallucinations

→ confusion

→ nausea

→ hypotension

43
Q

Describe the use of anticholinergics in the treatment of PD

A
  • Acetyl choline may have antagonistics effects on dopamine
  • Minor role in treatment of PD
44
Q

Provide three examples of anticholinergics

A
  • Trihexyphenidydyl
  • Orphenadrine
  • Procyclidine
45
Q

What are the advantages of anticholinergics?

A
  • Treat tremor
  • Not acting via dopamine systems
46
Q

What are the disadvantages of anticholinergics?

A
  • No effect on bradykinesia
  • Several side effects
47
Q

What are the side effects of anticholinergics

A
  • Confusion
  • Drowsiness
48
Q

The mechanism action of amantadine is uncertain.

Provide some suggestions

A
  • Enhanced dopamine release
  • Anticholinergic NMDA inhibition
49
Q

What are the disadvantages of amantadine?

A
  • Poorly effective
  • Few side effects
  • Little effect on tremor
50
Q

Illustrate the differences in the post synaptic membrane of a normal neuromuscular junction with that of one in myasthenia gravis

A

→ autoimmune, immunoglobulin blocks the Act receptors so Ach can’t get in

51
Q

Describe the presentation of Myasthenia gravis

A
  • Extraocular muscles – commonest presentation (ptosis)
  • Bulbar involvement – dysphagia, dysphonia, dysarthria
  • Limb weakness – proximal symmetric
52
Q

what does movement look like in myasthenia graves

A

→ muscle movements become more slow, eg: eye is open and it slowly closes as there is a depletion in the amount of Ach

→ once the eye is rested then there is more Ach and the eye can be kept open again

cycle repeats

53
Q

Identify some drugs which affect the neuromuscular transmission and thus, exacerbate Myasthenia gravis

A
  • Aminoglycosides
  • Beta-blockers
  • CCBs
  • Quinidine
  • ACE inhibitors
54
Q

What are the complications of Myasthenia gravis?

A
  • Acute exacerbation – Myasthenic crisis (respiratory failure, swallowing problems)
  • Overtreatment – cholinergic crisis (muscle paralysis)
55
Q

What is the therapeutic management of Myasthenia gravis?

A

Acetylcholinesterase inhibitors – enhance neuromuscular transmission at skeletal and smooth muscle

56
Q

Provide two examples of acetylcholinesterase inhibitors

A
  • Pyridostigmine (oral)
  • Neostigmine (oral/IV) → quicker action, duration up to 4 hours
57
Q

pyridostigmine

A

onset 30 mins, peak 60-120 mins, duration 3-6 hours

→ must make sure to give 40 mins before eating so that patients can actually swallow

58
Q

What are the antimuscarinic side effects of acetylcholinesterase inhibitors?

A
  • Miosis
  • SSLUDGE syndrome: salivation, sweating, lacrimation, urinary incontinence, diarrhea, GI upset and hypermotility, emesis
59
Q

what are some impulse control disorders

A

→ pathological gambling

→ hyper sexuality

→ compulsive shopping

→ desire to increase dose

→ pending (constantly rearranging things)

60
Q

Monoamine oxidase B inhibitors use

A

→ can be used alone

→ prolong action of levodopa

→ smooths out motor response

61
Q

how do monoamine oxidase B inhibitors work?

A

→ monoamine oxidase B metabolises dopamine and is mainly found in the dopamine regions in the brain

→ these inhibitors will enhance dopamine in the brain

62
Q

what are some examples of monoamine oxidase B inhibitors

A

→ Selegiline

→ Rasagaline

→ Safinamide

63
Q

when is surgery used

A

→ stereotactically

→ deep brain stimulation: insert electrode into brain

→ controlled trials

SA Clinical Pharmacology & Therapeutics (36 decks)

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