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Pharmacology > Drugs In Neurological Disorder > Flashcards

Drugs In Neurological Disorder Flashcards

1
Q

What are the clinical features of Parkinson’s disease

A 
Motor:
Bradykinesia
Rigidity
Tremor
Postural instability 
Non-motor: 
Mood changes
Cognitive dysfunction
Urinary incontinence
R.E.M. Sleep behavioural disorder
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2
Q

What is the pathophysiology of PD

A

Lewy bodies
Progressive degeneration of dopaminergic neurones in subtantia nigra pars compacta
Reduced dopamine levels

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3
Q

What is the metabolism pathway of dopamine

A

L-tyrosine to L-dopa
L-dopa to dopamine by DOPA decarboxylase
Dopamine to metabolites by COMT+MAO
Or synthesise Noradrenalin then Adrenalin

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4
Q

What are the medications used in PD

A 
Levodopa
Dopamine receptor agonist
MAOBI
COMTI
Anticholinergics
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5
Q

What is management pathway of PD

A 
GP suspects PD
Referral to specialist for diagnosis
Wait for significant disability
1. Levodopa / Dopamine receptor agonist
2. Consider CR Levodopa, agonist, Entacarpone / CR Levodopa, Entacarpone
3. Consider Surgery, Amorphine
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6
Q

What is the mechanism of action of Levadopa

A

Levadopa is prodrug because Dopamine cannot Cross BBB
Levadopa crosses BBB
Taken up by dopaminergic neurones in brain
Metabolised to dopamine intracellularly by DOPA decarboxylase

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7
Q

What must Levadopa be prescribed with

A

DOPA decarboxylase inhibitor
Inhibit Dopa decarboxylase in periphery
Prevent breakdown of Levadopa in periphery
Thus increased uptake of levodopa in CNS
Allows: less side effects, reduced dosing

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8
Q

What are PK properties of Levodopa

A

Oral admin only
Taken up by Active transport - compete with AA
90% inactivated in GIT - COMT, MAO
9% converted in periphery - DOPA decarboxylase
<1% taken up into CNS - active transport at BBB competing w AA
T1/2 2hours - short dose interval

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9
Q

Give examples of Levadopa

A

Co-careldopa: Sinemet

Co-beneldopa: Madopar

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10
Q

What are side effects of Levadopa

A

N+V (vomiting centre is dopaminergic)
Psychosis
Hypotension
Tachycardia

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11
Q

What happens with long term use of Levodopa

A 
Loss of efficacy - only efficacious in presence of dopaminergic neurones
Gives rise to motor complications:
On/off oscillations
Dyskinesia
Dystonia
Freezing 
End-of-dose deterioration in function
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12
Q

What are DDIs of Levodopa

A 
Vitamin B6 (Pyridoxine): increase peripheral breakdown of Levodopa 
Anti-psychotic Drugs: blocks dopamine receptors 
MAOIs: hypertensive crisis
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13
Q

What are the pros and cons of Levodopa

A

Pros: most efficacious for motor symptoms, low SE profile

Cons: pro drug requiring metabolism, loss of efficacy long term

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14
Q

What are types of formulations of Levodopa

A

All tablet formulations:
Standard dosage
Controlled release
Dispersible Madopar

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15
Q

Give examples of Dopamine Receptor Agonists

A

Non-ergot derived: Ropinirole, Pramipexole
Patch: Rotigotine
SC: Amorphine - for severe motor fluctuations

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16
Q

What are indications of Dopamine receptor agonists

A

De-novo therapy
Add-on therapy
Severe motor fluctuations - Amorphin

17
Q

What are pros and cons of Dopamine Receptor Agonists

A

Pros: no metabolism required, less motor complications w disease progression

Cons: less efficacious, serious SEs (impulse control disorder, more psychosis)

18
Q

What are side effects of Dopamine receptor agonists

A 
Hypotension
Sedation
Psychosis 
Paranoia 
Impulse control disorder: pathological gambling, hyper sexuality - check Hx of obsessive behaviour
19
Q

What is mechanism of action of MAOBIs

A

Inhibit MAO Type B present in dopaminergic neurones
Inhibit breakdown of Dopamine
Enhance Dopamine levels

20
Q

Give examples of MAOBI

A

Selegiline

Rasagaline

21
Q

What are pros and cons of MAOBI

A

Pros: can be used alone, prolongs Levodopa action, allow reduced Levodopa dosage, smooth out motor fluctuations

Cons: low efficacy

22
Q

What is mechanism of action of COMTI

A

COMTI cannot Cross BBB
Inhibit COMT in periphery
Inhibit breakdown of Levadopa in periphery into 3MO
Reduced 3MO competing for active transport at BBB
Increased CNS uptake of Levodpa

23
Q

Give examples of COMTIs

A

Entacarpone

24
Q

What are indications of COMTI

A

Add on therapy only:
Must be prescribed with levodopa + Dopa decarboxylase inhibitor
Allows reduced Levodopa dosing
Prolongs motor response to Levodopa

25
Q

What are types of anticholinergics

A

Trihexyphenidydyl

Procyclidine

26
Q

What are indications of anticholinergics

A

Tremor

27
Q

What are pros and cons of anticholinergics

A

Pros: effective tremor treatment, avoids dopaminergic pathways

Cons: no effect on bradykinesia,cholinergic side effects

28
Q

What are cholinergic side effects

A 
SSLUDGE
Salivation
Sweating 
Lacrimation
Urinary retention 
Diarrhoea 
GI upset + hypermotility 
Emesis
Miosis
29
Q

What are indications for surgery in PD

A

Dopamine responsive
Significant SEs with Levodopa
No psychiatric illness

30
Q

What are types of surgical intervention for PD

A

Deep brain stimulation - Subthalamic nucleus

Lesion:
Thalamus (tremor)
Globus Pallidus interna (dyskinesia)

31
Q

What is Myasthenia Gravis

A

Autoimmune condition of autoantibody-mediated destruction of nAChRs in post synaptic membrane of neuromuscular junction

32
Q

What are the symptoms of Myasthenia Gravis

A 
Fatiguable weakness of skeletal, smooth muscle: 
Ptosis 
Dysphagia, dysarthria, dysphonia
Facial weakness
Dyspnoea (Respiratory muscles)
33
Q

What are complications of Myasthenia Gravis

A

Myasthenia crisis:
respiratory failure
Undertreatment

Cholinergic crisis:
flaccid paralysis + respiratory failure
Overtreatment -muscles stop responding to ACh

34
Q

What medications are used for Myasthenia Gravis

A

Acetylcholinesterase inhibitors

35
Q

Give examples of AChesterase inhibitors

A

Pyridostigmine

Neostimine

36
Q

What is mechanism of action of AChesterase inhibitors

A

Inhibit breakdown of ACh in synaptic cleft
Increase ACh concentration
ACh more likely to bind to remaining nAChR

37
Q

What are PK properties of AChesterase inhibitors

A

Pyridostigmine:
Oral
Duration 3-6hrs
Dose interval crucial

Neostigmine:
Oral or IV
Faster onset
Given in ITU

Pharmacology (19 decks)

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