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PARKINSONS, SEIZURES, STROKES, MIGRAINES Flashcards

1
Q

What are the 3 pharmacological targets for treating parkinsons?

A

Increase dopamine levels
Reduce dopamine breakdown - MAO-B inhibitors or COMT inhibitors
Directly act on dopamine receptors

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2
Q

An example of a drug that directly increases dopamine levels in the pharmacological management of Parkinson’s disease?

A

Levodopa

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3
Q

Examples of drugs that reduces dopamine breakdown in the pharmacological management of Parkinson’s disease?

A

MAO-B inhibitors - selegiline and rosagiline
COMT inhibitors - entacapone and tolcapone

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4
Q

An example of a drug that directly acts on dopamine receptors in the pharmacological management of Parkinson’s disease?

A

Pramipexone
Ropinirole
Rotigotine

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5
Q

Give examples of MAO-B inhibitors?

A

Selegiline
Rasagiline

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6
Q

Give examples of COMT inhibitors?

A

Entacapone
Tolcapone

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7
Q

What drugs are typically offered for Tx of parkinsons disease when its the early stages and the motor symptoms are not impacting on QOL?

A

Dopamine agonists or MAO-B inhibitors - this can delay the need for levodopa

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8
Q

How are COMT inhibitors used in the Tx of parkinsons disease?

A

They are often given as adjuvant therapy alongside levodopa as they prevent it from breaking down, potentiating the effects

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9
Q

What is levodopa?
Why can’t we just give dopamine directly to treat parkinsons disease?

A

An amino acid precursor of dopamine
As dopamine cannot cross the blood brain barrier but levodopa can and then levodopa is converted to dopamine within the brain

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10
Q

What is carbidopa and benserazide? Why do we give it alongside levodopa?

A

They are dopadecarboxylase inhibitors

Dopadecarboxylase can convert levodopa peripherally into dopamine
So we give a dopa decarboxylase inhibitor alongside levodopa to prevent it being converted to dopamine before it reaches the brain.
This means more of the drug can act within the central NS but also we dont get excessive dopamine peripherally

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11
Q

Central physiological effects of dopamine?

A

Psychosis and mania
Impaired cognition e.g. memory, attention, executive function
Restlessness and agitation
Suppress lactation

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12
Q

Peripheral effects of too much dopamine?

A

Nausea and GI effects
Anti-kinetic effects on the GI system
Vasoconstriction

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13
Q

Peripheral efefcts of too much dopamine?

A

GI e.g. nausea
Anti-kinetic effects on GIT
Vasoconstriction

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14
Q

Which groups of pt should never be prescribed medications containing levodopa?

A

Severe psychiatric illness
Severe pulmonary or cardiovascular disease
Severe nausea or GI motility problems
Breast feeding

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15
Q

Common and important side effects of co-careldopa and co-beneldopa?

A

N&v
Abnormal dreams and sleep disturbances
Dizziness and syncope

Dyskinesia
Rapid fluctuations in clinical state
Postural hypotension
Psychological effects
Impulse control disorders - pathological gambling, binge eating and hypersexuality

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16
Q

Interactions of co-careldopa and co-beneldopa?

A

Monoamine oxidase inhibitors
General anaesthetic
Anti-hypertensives

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17
Q

What must you communicate to the patient when they start co-careldopa or co-beneldopa?

A

The side effects
Not to stop abruptly as can cause maligannt neuroleptic syndrome
They can cause postural hypotension so esp in elderly warn them of this
Warn them of sleepiness if they drive or work

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18
Q

What is co-careldopa?

A

A mixture of carbidopa and levodopa

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19
Q

What is co-beneldopa?

A

A combination of benserazide and levodopa

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20
Q

What should you do if the pt on levodopa treatment is experiencing the wearing off phenomenon?

A

Adjust the dose to smaller, more frequent doses
Use prolonged-release levodopa preperations and take at bedtime
Advise about taking levodopa 30 mins before food to enhance the absorption

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21
Q

What does it mean to Call levodopa a time critical drug?

A

It must be taken at the same time exactly each day to avoid the wearing off phenomenon
This is why in A&E if you get a pt you cannot trust the electronic records you MUST ask the pt how they take their levodopa at home and continue this routine exactly

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22
Q

What are the “on-off” fluctuations seen in levodopa treatment?

A

When the drug is working and symptoms are well controlled and then suddenly/gradually the drug isnt working and motor symptoms appear e..g during the wearing off phase
Can also mean when patients switch from severe dyskinesia to immobility in a few minutes

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23
Q

How can we help a pt struggling with on-off fluctuations when on levodopa treatment?

A

Combine levodopa with a dopamine agonist
Give fewer doses of levodopa
Use liquid forms of levodopa

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24
Q

What should you do as an F1 if you think the pt does not require their parkinsons meds?

A

NEVER ABRUPTLY DISCONTINUE PARKINSONS MEDICATIONS WITHOUT A SPECIALIST ADVICE

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25
Options for levodopa if pt are unable to swallow?
Crush tablet (not if modified release!!) Consider liquid Patch NG/NJ/PEG tube
26
What is the transdermal drug that can be given for parkinsons called? Whats its MOA?
Rotigotine - a dopamine agonist
27
Why should you not stop parkinsons drugs abruptly?
Neuroleptic malignant syndrome - a rare but life threatening condition!!
28
Pathophysiology of neuroleptic malignant syndrome?
Blockage of D2 receptors in the hypothalamus results in elevated temperature set point and impairment of heat-dissipating mechanisms Blockages of D2 receptors in the nigrostriatal pathway results in muscle rigidity
29
Symptoms of neuroleptic maligannt syndrome?
Pyrexia Muscle rigidity Autonomic lability e.g. hypertension, tachycardia, tachonoea Agitated delirium with confusion
30
Management of neuroleptic maligannt syndrome?
Stop offending drug if that’s the cause IV fluids Dantrolene may be used in selective cases (a muscle relaxant) Bromocroptine may also be used
31
When considering an AED, what factors influence the choice of treatment?
The type of seizure Age Tolerance, compliance, SE Gender - for pregnancy Lifestyle - occupation and driving Coexisting medical condition or medications
32
First line Tx for tonic-clinic seizures?
Sodium valproate first line in males and females unable to conceive Lamotrigine or levetiracetam second line or for fertile females
33
First line Tx for absence seizures?
Ethosuximide
34
First line Tx for myoclonic seizures?
Sodium valproate in males and infertile females Levetiracetam in fertile females
35
First line Tx for atonic or tonic seizures?
Sodium valproate for males and infertile females Lamotrigine for fertile females
36
First line Tx for dravet syndrome?
Sodium valproate males and females due to severity
37
First line Tx for lennox-gustaut syndrome?
Sodium valproate for males and females due to severity
38
Why does drug history influence the choice of AEDs?
Must be aware of other inhibitors or promotes of CYP450 enzyme
39
Sodium valproate MOA/
Inhbits GABA transminase which inhibits GABA breakdown and enhances the inhibitory effect
40
Contraindications for sodium valproate?
Acute porphyria’s Mitrochondrial disorders (higher rates of acute liver failure and liver-related deaths) Personal or FHx of severe hepatic dysfunction Urea cycle disorders Pregnancy
41
Side efefcts of sodium valproate?
GI disturbances Weight gain Transient hair loss with re growth of curly hair Neurological features Blood dyscrasias
42
Interactions with sodium valproate?
CYP450 inhibitor Other AEDs Risk of hepatotoxicity with - statins, alcohol, antibiotics, anti-fungal, chemotherapy
43
Drug monitoring for sodium valproate?
Monitor LFTs before therapy and during first 6 months Measure FBC before starting and before any surgery to assess bleeding risk Only measure drug concentration levels if you suspect non-adherence, toxicity or there is status epilepticus or organ failure
44
What are the teratogenic effects of sodium valproate?
Neural tube defects Significant risk of neurodevelopmental delay
45
What AED is best for pregnancy?
Lamotrigine
46
Moa of lamotrigine?
Sodium channel blocker stabilising presynaptic neuronal membranes and modulating presynaptic release of excitatory neurotransmitters
47
Cautions for lamotrigine?
Can exacerbate myoclonic seizures, dravet syndrome and Lennox-gastat sundrome and parkinsons disease
48
Side efefcts of lamotrigine?
Rashes Steven Johnson syndrome Hypersensitivity syndrome GI disturbance CNS effects Bone marrow supression
49
Interactions with lamotrigine?
Increases CNS effects - Alcohol, anti-psychotics, local anaesthetics, opioids, anti-histamines, benzodiazepines COCP and desogestrel Other AEDs
50
Immediate management of a confirmed non-haemorrhagic stroke?
Aspiring 300mg orally or rectally (immediately if TIA, after 24 hours if thrombolysed) Thrombolysis with alteplase within 4.5 hours of onset of stroke symptoms Thrombectomy can be done in some cases
51
MOA of alteplase?
A recombinant tissue plasminogen activator - converts plasminogen to plasmin
52
Contraindications to thrombolysis?
active internal bleeding recent haemorrhage, trauma or surgery (including dental extraction) coagulation and bleeding disorders intracranial neoplasm stroke < 3 months aortic dissection recent head injury severe hypertension
53
Side effects of thrombolysis?
haemorrhage N&V Cerebral oedema hypotension - more common with streptokinase allergic reactions may occur with streptokinase
54
What should you do about the aspirin given after a stroke?
Continue for 2 weeks before converting to a long-term anti-thrombotic treatment
55
What is the standard anti-thrombotic treatment given as secondary prevention after a stroke?
Clopidogrel 75mg
56
How does clopidogrel work?
Antagonist of P2Y12 adenosine diphosphate receptor, inhibiting the activation of platelets
57
How does Ticagrelor work differently to clopidogrel?
Ticagrelor does reversible inhibition due to a different binding site whereas clopidogrel does not
58
Contraindications for clopidogrel?
Active bleeding Discontinue 7 days before elective surgery Pregnancy Caution in hepatic and renal impairment
59
Side effects of clopidogrel?
Bleeding GI disturbances Rashes Headaches Dizziness Paraesthesia
60
Interactions with clopidogrel?
Anticoagulants and anti-platelets - increase bleeding risk NSAIDs - increase bleeding risk SSRIs - may make clopidogrel less effective PPIs - omeprazole and esomeprazole may make clopidogrel less effective (lansoprazole should be ok) Erythromycin
61
Secondary prevention after stroke?
Clopidogrel 75mg Check lipids, BP - start statin and hypertensive Physical activity Smoking cessation Diet and exercise Reduce alcohol consumption Optimise control of other co-morbidities
62
Systolic bp target post-stroke in the acute phase?
<130 (In the acute phase you don’t control bp unless its between 150-220 and presenting within 6 hours OR if its >220mmHg)
63
Post-stroke statin?
High intensity statin such as atorvastatin 20-80mg
64
Cautions for statins?
Elderly High alcohol intake or liver disease Hypothyroidism (must be managed adequately before starting statin) Pt at risk of muscle toxicity e.g. muscle disorders Known genetic polymorphism Haemorrhagic stroke
65
Interactions for statins?
Macrolide antibiotics - increase statin levels Penicillin antibiotics - increased risk of hepatotoxiity Colchicine - increased risk of rhabdomyolysis
66
SE of statins?
GI disturbances - diarrhoea, constipation, flatulance, nausea CNS effects - dizziness, headache, blurred vision Hepatic effects Myopathy Sleep disorders Skin reactions Hyperglycaemia Weight gain Epistaxis/thrombocytopemia
67
Example of antimuscarinic used in parkinsons?
Orphenadrine Procyclidine
68
When might you use antimuscarinic drugs in parkinsons disease?
For disabling tremor or excessive salivation
69
Na+ channel blocking AEDs?
Carbamazepine Phenytoin Lamotrigine
70
GABA receptor agonist AEDs?
Clonazepam Diazepam Lorazepam Phenobarbital
71
MOA of vigabatrin?
GABA transaminase inhibitor - prevents breakdown of GABA
72
Moa of gabapentin and pregabalin?
GABA analogues
73
MOA of topiramate?
Glutamate receptor antagonist
74
MOA of ethosuximide?
Neuronal calcium channel blocker
75
Whats the MOA of Triptans?
Selective 5-HT receptor agonists with a high affinity for 5HT1B and 5HT1D receptors - this causes cranialvasoconstriction
76
Examples of 5HT 1B and 1d agonists?
Sumatriptan Zolmitriptan
77
Drugs used for prophylaxis of migraines?
Beta adrenoreceptor antagonists - propranolol AED and TCAs - topiramate, sodium valproate, gabapentin, amitryptiline
78
Acute migraine Tx?
Monotherapy with aspirin, ibuprofen or a triptan as soon as they know they are developing a migraine (if aura they should take sumatriptan)
79
Prophylaxis Tx for migraines?
Propranolol hydrochloride is first line Other beta blockers can be considered Topiramate can be used if BB is unsuitable Amitryptiline can be considered
80
Contraindications for topiramate?
Pregnancy Hypersensitivity Renal or liver issues Acute porphyria Glaucoma
81
What drug is best for menstrual migraine prophylaxis?
Frovatriptan
82
Contraindications for sumatriptan?
Coronary vasospas, IHD, moderate hypertension, PVD, previous cerebrovascular accident, previous MI/TIA, prinzmetals angina
83
Side effects of Triptans?
Nausea and vomiting Dizzy or drowsy Flushing Angina pectoris, palpitations, MI
84
What drugs do Triptans interact with?
SSRIs MAOIs - risk of serotonin syndrome
85
Why is it beneficial to delay the need for levodopa treatment by starting parkinsons patients on dopamine agonists or MAOIs in the early stages of disease?
As overtime levodopa efficacy can reduce Levodopa comes with motor side effects

PPT (6 decks)

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