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Pharmacology > Neurological Disorders > Flashcards

Neurological Disorders Flashcards

1
Q

What are the clinical features of Parkinsonism?

A

Tremor
Rigidity
Bradykinesia
Postural instability

  • due to low dopamine and disturbance of other neurotransmitters.
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2
Q

Name some of the non motor manifestations of Parkinson’s?

A
  • mood change
  • pain
  • cognitive change
  • urinary symptoms
  • sleep disorder
  • sweating
  • swallowing issues
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3
Q

What might be required for the diagnosis of IPD?

A

Clinical features, response to treatment, functional neuro imaging and structural neuro imaging being normal.

Exclude other causes of Parkinsonism:
Drug induced 
Vascular 
Progressive supranuclear palsy 
Multiple systems atrophy 
Corticobasal degeneration
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4
Q

What is the pathology of IPD?

A

Neurodegeneration
Lewy bodies - synucleinopathy
Loss of pigment - >50% loss =symptoms, increased turnover and upregulate receptors
Reduced dopamine

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5
Q

What is the amino acid involved in the dopamine synthesis?

A

Tyrosine

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6
Q

What enzyme converts L-DOPA to Dopamine?

A

DOPA decarboxylase

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7
Q

Which two enzymes degenerate dopamine?

A

Monoamine oxidase

Catecholamine-o-methyl transferase

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8
Q

Why is levodopa prescribed instead of dopamine?

A

L-Dopa crosses the blood brain barrier via active transport, whereas dopamine cannot cross.
It can then be taken up by dopaminergic cells in the substantia nigra before being converted to dopamine.

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9
Q

What are the potential problems with levodopa?

A

Absorbed by active transport, in competition with amino acid.
90% inactivated in intestinal wall by MAO and DOPA decarboxylase.
9% converted to dopamine in peripheral tissues and so less than 1% enters CNS.
Short half life 2 hrs, short dose interval and fluctuations in levels and symptoms.

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10
Q

why L-DOPA not advised to be taken with large protein meals?

A

Both are absorbed by active transport and therefore there is competition between L-DOPA and amino acid uptake.

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11
Q

L-DOPA is given in formulations because?

A

Given with a peripheral DOPA decarboxylase inhibitor, therefore up to 10% L-DOPA crosses the BBB.

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12
Q

What tablet formulations can L-DOPA come in?

A 
Standard dosage 
Controlled release preparations 
Dispersible madopar (not soblube)
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13
Q

What are some of the side effects of L-DOPA?

A

Nausea/anorexia
Hypotension
Psychosis
Tachycardia

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14
Q

What are some of the issues with L-DOPA?

A

Requires enzyme conversion and dopaminergic neurones
Involuntary movements
Motor complications

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15
Q

What are the potential interaction problems with L-DOPA?

A

Pyridoxine (vit B6) increases peripheral breakdown of L-DOPA.
MAOIs risk hypertensive crisis
Many antipsychotic drugs block dopamine receptors and cause Parkinsonism.

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16
Q

What drugs may be given to patients with IPD?

A 
Levodopa
Dopamine receptor agonists 
MAOI type B inhibitors 
COMT inhibitors 
Anticholinergics 
Amantidine
17
Q

Why might dopamine receptor agonists be prescribed and what are the advantages?

A

De novo therapy or add on.

Direct acting, less dyskinesia/ motor complications, possible neuroprotection.

18
Q

What are the disadvantages of dopamine receptor agonists?

A
  • less efficacy than L-DOPA
  • expensive
  • more psychiatric side effects
  • impulse control disorders
19
Q

What is impulse control disorders (or dopamine dysregulation syndrome)?

A
  • pathological gambling
  • hypersexuality
  • compulsive shopping
  • desire to increase dosage
  • punding
20
Q

What are some dopamine receptor agonist side effects?

A 
Sedation
Hallucinations 
Confusion
Nausea 
Hypotension
21
Q

What are MAOB inhibitors and why might they be used?

A

Enhance dopamine, by preventing the breakdown by monoamine oxidase.
Includes selegiline and rasagaline.

Can be used alone, prolong action of L-DOPA. Smooth out motor response and may be neuroprotective.

22
Q

How do COMT inhibitors work and why must they be given as a combination?

A

They reduce peripheral breakdown of L-DOPA to 3,o-methyldopa which competes with L-DOPA for active transport across BBB.
Therefore have a sparing effect and prolongs motor response to L-DOPA.

Alone they have no therapeutic effect.

23
Q

What three drugs form stalevo?

A

COMT inhibitor
L-DOPA
Peripheral dopa decarboxylase inhibitor

24
Q

Why might anticholinergics be prescribed to IPD patients?

A

ACh may have an antagonistic effect to dopamine.
Therefore treat tremor and not acting via dopamine system.

Includes trihexyphenidydyl, orphenadrine and procyclidine

25
Q

What are the disadvantages with using anticholinergics for IPD?

A

No effect on bradykinesia

Side effects; confusion, drowsiness and usual anticholinergic side effects

26
Q

Why would amantadine be prescribed as a last line treatment for IPD ?

A

Poorly effective, with little effect on tremor.

Few side effects and mechanism of action is unclear - enhance dopamine release or anticholinergic NMDA inhibition.

27
Q

What is the pathophysiology of myasthenia gravis?

A

Antibody mediated blockage of Ach by IgG.
Causes fluctuating, fatiguable weakness of skeletal muscle.

  • extraoccular
  • bulbar
  • limb weakness
  • respiratory
28
Q

Which drugs may exacerbate myasthenia gravis?

A 
Aminoglycosides 
B-blockers 
ACEi 
CCBs 
Chloroquine
29
Q

What might be the two acute presentations seen with mysasthenia gravis?

A

Acute exacerbation - myasthenic crisis

Over treatment - cholinergic crisis

30
Q

How do AChE inhibitors help manage myasthenia gravis?

A

Enhance neuromuscular transmission, skeletal and smooth muscle.
Excess dose can cause depolarising block -cholinergic crisis.

Either pyridostigmine (oral) or neostigmine (oral or IV). 
Neostigmine is quicker onset of action, with a duration of 4 hours but significant cholinergic side effects.
31
Q

What are the properties of pyridostigmine?

A

Prevents ACh breakdown in NMJ, therefore ACh more likely to engage with remaining receptors. Onset 30 mins, peak 60-120, duration 3-6 hrs. Dose interval and timing crucial.

32
Q

What features might be seen in a cholinergic crisis?

A

MIOSIS

Salivation
Sweating 
Lacrimation
Urinary incontinence 
Diarrhoea
GI upset and hypermotility 
Emesis

Pharmacology (22 decks)

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