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Maddie’s Neuro > Neurological Phamacology > Flashcards

Neurological Phamacology Flashcards

1
Q

Describe the three classic motor symtoms of Parkinson’s Disease. (6)

A

Tremour - low frequency, pill rolling
Rigidity - cog wheeling and lead pipe
Bradykinesia - only responds to dopaminergic drugs.

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2
Q

Describe non-motor symtoms of Parkinson’s disease. (6)

A

Mood changes, pain, cognitive change, urinary change, sleep disorders, sweating.

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3
Q

Describe the diagnostic criteria for Parkinson’s Disease. (3)

A

No structural abnormalities on imaging.
Must be a response to dopaminergic drugs.
No other cause of Parkinsonism - drugs, vascular, degeneration.

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4
Q

Describe the special scan used to diagnose Parkinson’s disease and the findings in PD. (2)

A

A DAT scan labels the ability to reuptake dopamine in the brain.
In PD it will be asymmetrical.

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5
Q

Describe the pathophysiology of PD. (3)

A

Neurodegeneration of dopaminergic neurones in the substantia nigra leading to Lewy Body deposition. A 50% loss of neurones leads to symptomatic PD.

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6
Q

Describe the pathway of conversion between intermediates of the production and degradation of dopamine. (11)

A

Tyrosine > L-DOPA >(DOPAdecarboxylase)> Dopamine > Noradrenaline > adrenaline

Dopamine >(monoamine oxidase)> Intermediate >(Catechol-O-methyl transferase)> Homovanillic acid.

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7
Q

Describe the mechanism of action of LDOPA. (2)

A

Taken up by dopaminergic cells in the substantia nigra and converted to dopamine there.

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8
Q

Explain why LDOPA can’t be taken with certain meals. (2)

A

Absorbed through the intestinal wall by active transport in competition with amino acids. Can’t be taken with a high protein meal.

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9
Q

What is the T1/2 of LDOPA? (1)

A

2 hours.

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10
Q

Explain why LDOPA is often given in conjunction with an enzymatic inhibitor. Name this inhibitor. (5)

A

DOPA decarboxylase inhibitor
Only 1% of LDOPA reaches the CNS: 90% inactivated in the intestinal wall, and 9% is converted in the peripheral tissues and then can’t cross the BBB.
Given with this inhibitor to prevent peripheral conversion to increase the amount that reaches the brain.

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11
Q

Explain why LDOPA can get less efficacious as a treatment over time. (2)

A

It needs functional dopaminergic neurones in the substantia nigra, but as the disease progresses, these are lost.

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12
Q

Describe 2 advantages of LDOPA as a treatment for PD. (3)

A

Initially highly efficacious

Low occurance of side effects - nausea, hypotension, paychosis, tachycardia.

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13
Q

Describe 3 disadvantages of LDOPA as a treatment for PD. (3)

A

Given as a precursor which needs enzymatic conversion.
Long term loss of efficacy.
Motor complications like freezing or dystonia.

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14
Q

Describe 2 DDIs of LDOPA. (2)

A

Vitamin B6 suppliments prompts peripheral conversion of LDOPA.
Antipsychotics block dopamine receptors (why they have Parkinsonism as a side effect).

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15
Q

Describe the three classes of dopamine receptor agonist. Give an example of each, and give their indications. (13)

A

Non-Ergot - Ropinirole, Pramipexole - add on therapy.
Patch - Rotigotine - if can’t take LDOPA orally.
Subcutaneous - Apomorphine - severe motor complications only.

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16
Q

Describe 3 advantages of using dopamine receptor agonists to treat PD. (3)

A

Direct acting
Loss dyskinesias / motor complications
Possible neuroprotection.

17
Q

Describe 5 disadvantages of using dopamine receptor agonists to treat PD. (5)

A

Less efficatious that LDOPA
Can lead to impulse control disorders (compulsive gambling, sexuality, shopping)
Psychiatric side effects esp hallucinations
Expensive
Other side effects (hypotension, nausea, sedation, confusion).

18
Q

Describe the mechanism of action on MOAB inhibitors. (2)

Give two examples. (2)

A

Monosmine oxidase B normally metabolises peripheral dopamine, so inhibiting it will increase dopamine.
Selegiline, Rasagaline

19
Q

Describe one indication of MOAB inhibitors
Give two advantages.
(3)

A

Will prolong the life of LDOPA.

Smooth out motor responses, and may be neuroprotective.

20
Q

Describe the use of anticholinergics to treat Parkinson’s Disease. Describe main side effects of this class of drug. (5)

A

May have antagonistic effects to dopamine (so anticholinergics would have reduced these effects) to reduce tremour but will not help bradykinesia or rigidity as these are specifically dopaminergic.
They can cause side effects like dry mouth, confusion, drowsiness.

21
Q

Describe the use of Amantadine for Parkinson’s Disease. (2)

Give one other use for it. (2)

A

Thought to enhance dopamine release, but mechanism of action uncertain. Has a slight effect on tremour.
Also an antiviral against influenza A.

22
Q

Describe the two main types of surgery undergone in severe cases of Parkinson’s Disease. (5)

A

Lesions - thalamus for tremor, globus pallidus international for dyskinesia.
Deep Brain Stimulation - subthalamic nuclei.

23
Q

Describe the criteria to be met for surgery to be undertaken in severe Parkinson’s Disease. (3)

A

Low dopamine repsonsiveness
Significant side effects with LDOPA
No present psychiatric illness.

24
Q

Define the characteristic features of myasthenia gravis. (3)

A

Fluctuating, fatiguable, weakness in skeletal muscle.

25
Q

Describe the common presentations of Myasthenia Gravis. (7)

A 
Extraoccular muscle failure (Diplopia / ptosis)
Bulbar involvement (dysphagia, dysarthria, dysphonia).
26
Q

Describe the commonest cause of death in patients with Myasthenia Gravis. (1)

A

Respiratory muscle failure.

27
Q

Describe the drugs that can affect neuromuscular transmission can exacerbate myasthenia Gravis. (9)

A 
Aminoglycosides
Beta blockers
Calcium channel blockers
Quinidine
Procainamide
ACEi 
Chloroquine 
Succinylcholine
Magnesium
28
Q

Describe two complications of treatment of myasthenia Gravis. (4)

A

Acute exacerbation due to inadequate treatment - myasthenic crisis
Overtreatment with acetylcholineesterase inhibitors - cholinergic crisis

29
Q

Describe 5 treatments of myasthenia Gravis. (10)

A

Acetylcholineesterase inhibitors - treat acute symptoms
Corticosteriods - decrease immune response
Azathioprine - T cell inhibitors to act as steroid sparing Immunosuppressants.
IV immunoglobulin - acute emergency
Plasmapheresis - removes nAChR antibodies.

30
Q

Name two acetylcholineesterase inhibitors. (2)
Describe the pharmacodynamic properties of one of these drugs. (3)
Describe the side effects of this class of drugs. (1)

A

Pyridostigmine and Neostigmine.
The duration of pyridostigmine is e-6 hours, onset is 30 minutes. Needs to be taken at least 30 minutes before eating so they can actually eat.
Can cause SLUDGE syndrome.

Maddie’s Neuro (17 decks)

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