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CPT > Lecture 23 - Neuropharmacology > Flashcards

Lecture 23 - Neuropharmacology Flashcards

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1
Q

What is idiopathic Parkinson’s disease?

A

Neurodegenerative disorder where we lose dopaminergic neurones in the substantia Nigra so the basal ganglia (putamen) receive less dopamine

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2
Q

What structures can form in Idiotpathic Parkinson’s disease?

A

Lewy bodies

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3
Q

What occurs in the basal ganglia due to lack of dopamine in IPD?

A

Loss of dopaminergic neurones in substantia nigra pars compacts means neostriatum isn’t inhibited as much

More ACh is made which impairs mobility

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4
Q

What are the 4 main clinical features of Parkinsonism?

A

Rest tremor
Lead pipe rigidity
Bradykinesia
Postural instability

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5
Q

What is the rest tremor that is seen in Parkinson’s?

A

Its a low frequency pilll rolling tremor which disappears when you ask a patient to do a movement

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6
Q

What is lead pipe rigidity that is seen with Parkinsonism?

A

Where you try and move the patients limb and there’s resisitance all the way

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7
Q

What is bradykinesia?

A

Slow in intiating movements
Shuffling steps
Lack. Of arm swinging

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8
Q

How do you diagnose Idiopathic Parkinson’s disease?

A

Clinical features of Parkinson’s (BRADYKINESIA is main one)

Must also respond to treatment of Levodopa

Structure neuro imaging is normal and other causes of parkinsonism has been ruled out

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9
Q

What are some non motor manifestations of Parkinson’s?

A

Mood changes
Hallucinations
Cognitive change
REM sleep disorder

Restless leg
Fatigue
Pain
Urinary symptoms
Sweating
Low blood pressure

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10
Q

What is the prognosis in Parkinson’s disease after 15years?

A

Most people get:
-dyskinesia (involuntary movements)
-falls
-cognitive decline (some hallucinations)
-somnolence (drowsiness and sleepiness)
-Swallowing difficulty
-hypophonia (quiet)

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11
Q

Describe the process of dopamine release at a synaptic cleft:

A

Depolarisation of dopaminergic neurone leads to Ca2+ influx
Ca2+ binds to vesicles contacting dopamine
Vesicles bind to presynaptic membrane and release contents (dopamine) into synaptic cleft via exocytosis

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12
Q

What is the gold standard drug for treating idiopathic Parkinson’s disease?

A

Levodopa

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13
Q

Why dont we just use dopamine to treat Parkinson’s?

A

Dopamine cant cross BBB whereas levodopa does
Also dopamine would cause peripheral adverse effects

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14
Q

Why does levodopa have a very limited effect in late stage Parkinson’s?

A

Levodopa works by the functioning dopaminergic neurones converting levodopa to dopamine
So in late stage Parkinson’s there are very few functioning dopaminergic neurones so little L-dopa is converted to dopamine

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15
Q

How is levodopa administered?

A

Oral administration

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16
Q

How is levodopa absorbed?

A

Active transport

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17
Q

What enzymes inactivate levodopa in the gut wall?

A

Monoamine oxidase
Dopa decarboxylase

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18
Q

Why does levodopa need regular dosing?

A

Short half life (2hrs)
This leads to fluctuations in blood levels and symptoms

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19
Q

What is levodopa always prescribed with?
Why?

A

Peripheral dopa decarboxylase inhibitor

To prevent the conversion of levodopa into dopamine in the peripheries

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20
Q

What is the drug given with levodopa which is a peripheral dopamine decarboxylase inhibitor?

A

Carbidopa

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21
Q

What is the formulation called which contains levodopa and carbidopa?

A

Sinemet

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22
Q

Why is the sinemet formulation better than just levodopa?

A

Reduces dose required and reduced side effects since more levodopa reaches brain

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23
Q

What are the advantages of levodopa?

A

Highly efficious
Low side effects:
Nausea/anorexia (vomiting)
Hypotension
Psychosis (schizophrenia, hallucinations)
Tachycardia

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24
Q

What drug do you not give as an antiemetic caused by giving levodopa and why?

A

Metoclopramide

Can cause extrapyradimal effects causing Parkinsonian symptoms

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25
Q

What drug can be used as an anti-emetic caused by levodopa?

A

Domperidone

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26
Q

What are the disadvantages of levodopa?

A

Its a precursor so needs conversion

Long term:
-loss of efficacy
-involuntary choreform movements
-motor complications:
May get rigid
Wearing off
Dyskinesias
Dystopia (limb held in abnormal position)
Freezing (will suddenly stop and become rigid)

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27
Q

What vitamin increases the peripheral breakdown of levodopa?

A

Vitamin B6 (pyridoxine)

28
Q

What is the interaction of monoamine oxidase inhibitors with levodopa?

A

Can cause hypertensive crisis

29
Q

What is the interaction of monoamine oxidase inhibitors with levodopa?

A

Can cause hypertensive crisis

30
Q

What is the interaction of monoamine oxidase inhibitors with levodopa?

A

Can cause hypertensive crisis

31
Q

What drugs can block dopamine receptors and cause Parkinsonism as a side effect?

A

Antipsychotic drugs

32
Q

What is the point of giving levodopa with a Catechol-O-methyl Transferase (COMT) inhibitor?

A

Decreases breakdown of levodopa so prolongs the motor repsonse to levodopa

33
Q

What are some COMT inhibitors given with levodopa?
Can they cross the BBB?

A

Entacapone
Opicapone

Can’t cross BBB

34
Q

What is the effect of giving COMT inhibitors by themselves?

Why?

A

No therapeutic effect since doesn’t cross the blood brain barrier so is never given alone

35
Q

What are some dopamine receptor agonists?

A

Ropinirole (tablet)
Pramipexole (tablet)

Rotigotine (patch)

Apomorphine (subcutaneous)

36
Q

When is apomorphine given?
How is it given?
What type of drug is this?

A

For patients with severe motor fluctuations

Subcutaneously

Dopamine receptor agonists

37
Q

What are the advantages of dopamine receptor agonists?

A

Direct acting on receptors
Less dyskinesias and motor complications
Possible neuroprotection

38
Q

What are the disadvantages of dopamine receptor agonists?

A

Less efficacy than levodopa
Impulse control disorders
More psychiatric s/e like hallucinations
Expensive

39
Q

What are some impulse count troll disorders that are caused by dopamine receptor agonists?

A

Can lose ability to control impulsiveness

-pathological gambling
-hypersexuality
-compulsive shopping
-desire to increase dose
-punding

40
Q

What is punding?

A

Compulsive sorting of things

41
Q

What are the side effects of dopamine receptor agonists?

A

Sedation
Hallucinations
Confusion
Nausea
Hypotension

42
Q

What drug do you give to a patient having severe motor fluctuations with Parkinson’s?

How do you administer it?

A

Apomorphine

Subcutaneously (dopamine receptor agonist)

43
Q

What is the function of monoamine oxidase B?
What effect do monoamine oxidase B inhbitors have?

A

Metabolises dopamine

So inhibitors MAOB so dopamine is enchanced/stays around longer

44
Q

What are some examples of monoamine oxidase B inhbitors?

A

Rasagaline
Safinamide

45
Q

What are some examples of anticholinergics to help treat Parkinson’s disease?

A

Trihexyphenidydyl
Orphenadrine
Procyclidine

46
Q

What are the advantages of anticholinergics?

A

Treat tremor
Not acting via dopamine systems

47
Q

What are disadvantages of anticholinergics?

A

Doesnt help the bradykinesia

Confusion
Drowsiness

48
Q

When is Amantadine rarely used for Parkinson’s?

A

When levodopa is inducing dyskinesia (choreiform movements)

49
Q

What are the side effects of amantadine?

A

Hallucinations
Confusion

50
Q

When are Parkinson’s patients eligible for surgery?

A

Need good response to levodopa
No psychiatric illness
Significant side. Effects with levodopa so that’s not an eligible treatment

51
Q

What are some consequences of not reveinving enough l-dopa?

A

L dopa withdrawal
Severe akinnetic mutism
Life threatening neuroleptic malignant syndrome (confusion, rigidity, fever, autonomic dysregulation)

52
Q

What are some consequences of withdrawal from dopamine agonists?

A

Dopamine agonist withdrawal syndrome (DAWS)
Neurophsyciatric symptoms (agitation, antic, anxiety, depression) autonomic symptoms

53
Q

What is the pathophysiology of myasthenia Gravis?

A

Auto immune antibodies attatching to post synaptic ACh receptors blocking signals reaching muscle

54
Q

What are some symptoms of myasthenia Gravis?

A

Flucatuating
Fatiguable
Weakness of skeletal muscle

Extraocularmusucels
Bulbar involvement (Dysphagia, dysphonia)
Limb weakness
Resp. Muscle involvement

55
Q

What is meant by fatiguable in myasthenia gravis?

A

Muscles that are being used get weaker as you use it for seconds to minutes

They will be back to full strength after rest for a couple mins

56
Q

What are some drugs that can worsen myasthenia gravis?

A

Aminoglycosides
B blockers
Chloroquine
Magnesium
ACE inhibitors
Syuccinylcholine

57
Q

What are some complications of myasthenia gravis?

A

Acute exacerbation (myasthenic crisis)

Overtreatment (cholinergic crisis)

58
Q

What is the most commonly used drug to treat myasthenia?

A

Pyridostigmine

59
Q

What is the mechanism of action of pyridostigmine?

A

Acetylcholinesterase inhibitors

60
Q

What drugs except pyridostigmine can be used for myasthenia gravis?

A

Corticosteroids decrease immune response
Steroid sparing drugs like azathioprine

61
Q

What effects does pyridostigmine have?

A

Enhances neuromuscular transmission
Skeletal and smooth muscle
Excess does can cause depolarising block (paralysis) cholinergic crisis
Muscarinic side effects (gut churning, diarrhoea, bradycardia)

62
Q

When is neostigmine given?
How is it given?
Why is it only given here?

A

In the ITU
Oral and IV
Acts much quicker than neostigmine but causes SIGNIFICANT anti Muscarinic side effects

63
Q

Why is the dosing interval for pyridostigmine crucial?

A

If not given on time can get Dysphagia, dysarthria and respiratory depression

64
Q

What are the muscarinic side effects of pyridostigmine?

A

Miosis

SLUDGE

Salivation
Sweating
Lacrimation
Urinary incontinence
Diarrhoea
GI upset and hypermotility
Emesis

65
Q

When do you dose patients withi pyridostigmine in relation to their meals and why?

A

40 to 60mins before meals to optimise swallowing
Since it has peak actioon after 60 mins

CPT (30 decks)

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