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Y4 PPT > B44 - Parkinson's, epilepsy > Flashcards

B44 - Parkinson's, epilepsy Flashcards

1
Q

3 targets of pharma mx for parkinsons

A

Increase dopamine levels
Reduce dopamine breakdown
Directly act on dopamine receptors

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2
Q

drug to Increase dopamine levels

A

– Levodopa

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3
Q

drugs which Reduce dopamine breakdown (2 classes + examples)

A

– MAO-B inhibitors (Selegiline/Rosagiline)

– Catechol-O-methyltransferase (COMT) inhibitors (Entacapone/Tolcapone)

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4
Q

2 drugs which Directly act on dopamine receptors

A

–Pramipexole/Ropinirole

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5
Q

3 things that the choice of drug depends on in parkinson’s

A

the impact of improving motor disability (better with levodopa) compared with the risk of motor complications (more common in younger patients) and neuropsychiatric complications (more common in older and cognitively impaired patients; greater with agonists).

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6
Q

Which treatment is initially recommended in younger patients (3)

A

Oral or transdermal dopamine agonist. Pramipexole, ropinirole and rotigotine are effective.

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7
Q

which drug should be considered if dyskinesia is not adequately managed by modifying existing therapy in parkinsons

A

Amantadine

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8
Q

When should Anticholinergics should not be offered to people with Parkinson’s disease

A

people who have developed dyskinesia and/or motor fluctuations.

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9
Q

What is levodopa and why is it given instead of dopamine

A

Levodopa is an amino acid precursor of dopamine.

Dopamine cannot cross the blood brain barrier, whereas levodopa can where it is converted into dopamine

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10
Q

Why is levodopa often prescribed with an additional drug

A

levodopa can also be converted to dopamine by peripheral dopa-decarboxylase (DDC) before it has chance to enter the brain

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11
Q

Which drugs are prescribed with levodopa

A

peripheral dopa decarboxylase (DDC) inhibitors such as carbidopa or benserazide

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12
Q

Other physiological effects of dopamine (5)

A

Central
Cognition – dopamine plays a role in controlling the flow of information in the frontal lobe. Loss of dopamine there can lead to memory problems. Overstimulation can cause psychosis and Schizophrenia
Lactation – Dopamine is a Prolactin inhibitory hormone, acting on D2 receptors, preventing lactation

Peripheral
Nausea – dopamine has an emetic function (causes nausea) – example of an antagonist is Metoclopramide
GI motility – inhibits gastric stimulation (anti-kinetic effect) – example of an antagonist is Domperidone
Cardiac – dopamine is converted to norepinephrine

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13
Q

Co-careldopa & Co-beneldopa CI (4)

A

Breast feeding
Severe psychiatric illness
Caution in severe pulmonary or cardiovascular disease
Severe nausea/GI motility problems

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14
Q

Co-careldopa & Co-beneldopa SE (7)

A

Nausea and vomiting
Abnormal dreams and sleep disturbances
Dizziness and syncope

!!!
Dyskinesia
Rapid fluctuations in clinical state (“on-off” effect - switching from dyskinesia to immobility within minutes)
Postural hypotension
Psychological effects - dementia, depression, schizophrenia-like syndrome, impulse control disorders

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15
Q

Co-careldopa combination of

A

levodopa with carbidopa

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16
Q

Co-benoldopa combination of

A

levodopa with benserazide

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17
Q

Co-careldopa & Co-beneldopa interactions (3)

A

Monoamine oxidase inhibitors (hypertensive crisis)
•General anaesthetics (arrhythmias)
•Anti-hypertensives (hypotension)

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18
Q

Measures for prevention of ‘wearing off’ SE of co-carel/beneldopa (4)

A

Adjust the dose
Smaller, more frequent doses of levodopa.
Prolonged-release levodopa preparations (ideally taken at bedtime)
Dietary adjustments: take levodopa 30 minutes before food

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19
Q

Measures for prevention of ‘on/off’ SE of co-carel/beneldopa (s)

A

Combine levodopa with a dopamine agonist
Fewer doses of levodopa
Liquid forms of levodopa

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20
Q

Levodopa effects on :

  • motor Sx
  • ADL
  • motor complications
  • adverse events
  • off time
  • hallucinations
A
  • more motor Sx improvement
  • more improvement ADL
  • more motor complications
  • fewer adverse events
  • more off time reduction
  • more hallucinations
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21
Q

Dopamine agonist effects on :

  • motor Sx
  • ADL
  • motor complications
  • adverse events
  • off time
  • hallucinations
A
  • less motor Sx improvement
  • less improvement ADL
  • fewer motor complications
  • more adverse events
  • off time reduction
  • less risk hallucinations
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22
Q

MAO-B inhibitors effects on :

  • motor Sx
  • ADL
  • motor complications
  • adverse events
  • off time
  • hallucinations
A
  • less motor Sx improvement
  • less improvement ADL
  • fewer motor complications
  • fewer adverse events
  • off time reduction
  • less risk hallucinations
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23
Q

Options if PD patients have difficulty/are unable to swallow (4)

A

Crush tablets (do not do this with modified release drugs!)
Consider liquid
Patch (Rotigotine)
NG/NJ/PEG tube

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24
Q

Why should you never stop Parkinson’s drug treatment abruptly?

A

Risk of neuroleptic malignant syndrome

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25
Q

Neuroleptic Malignant Syndrome pathophys

A

Pathophysiology: Depletion of dopamine in the hypothalamus/nigrostriatal pathway

26
Q

Neuroleptic Malignant Syndrome S/Sx

A

rigidity, fever, altered GCS

27
Q

Neuroleptic Malignant Syndrome Mx

A

mainly supportive, some evidence for use dantrole, bromocriptine or Lorazepam

28
Q

When can anti-epileptic drug treatment be commenced

A

AED treatment may be commenced after one seizure if neurological deficit, EEG shows epileptic activity, risk of further seizure deemed unacceptable by the patient or structural abnormality on brain imaging.

29
Q

First line AED focal seizures

A

Lamotrigine or carbamazepine

30
Q

First line AED generalised seizures

A

Sodium valproate

31
Q

Sodium valproate MOA

A

inhibits GABA transaminase (inhibits breakdown of GABA so increases inhibitory effect, reducing excessive neuronal firing)

32
Q

Sodium valproate CI (3)

A

History/family history hepatic dysfunction
Metabolic disorders
Pregnancy

33
Q

Sodium valproate SE (5)

A

GI disturbances(N+V, anorexia, abdominal pain, bowel disturbance to pancreatitis and hepatotoxicity)
Weight gain
Transient hair loss with regrowth of curly hair
Neurological features (ataxia, tremor, confusion, encephalopathy, coma)
Blood dyscrasias (anaemia and thrombocytopenia)

34
Q

Sodium valproate interactions (3)

A

Cytochrome P450 inhibitor
Other anti-epileptic drugs
Risk of hepatoxicity –Statins, alcohol, antibiotics, anti-fungals, chemotherapy agents

35
Q

Sodium valproate monitoring

A

Monitor LFTs before and during first 6 months
Measure FBC before surgery to assess bleeding risk

Routine drug concentration levels are not indicated
Only performed if:
Suspect non-adherence or toxicity
Clinical conditions such as status epilepticus or organ failure

36
Q

Sodium valproate caution in women

A

Valproate is highly teratogenic, leading to neurodevelopmental disorders (30-40% risk) and congenital malformations (10% risk).
Must not be used in women of childbearing potential unless the conditions of pregnancy prevention program (PPP) are met and only if other treatments are ineffective or not tolerate. PPP is the use of highly effective contraception (<1% failure rate). Women must be fully informed of the risk and the need to avoid exposure to valproate medicines in pregnancy.

37
Q

What would be the most appropriate first line drug for a woman in reproductive years?

A

Lamotrigine

38
Q

Lamotrigine MOA

A

Use-dependent inhibition of sodium channels. Selectively targets neurons that synthesise glutamate and aspartate. Stabilises presynaptic neuronal membrane, suppressing release of excitatory amino acid glutamate which plays a key role in the generation of seizures.

39
Q

Lamotrigine cautions (2)

A

Can exacerbate myoclonic seizures and Parkinson’s disease

Renal failure and hepatic failure (reduced dose)

40
Q

Lamotrigine SE (5)

A

Hypersensitivity syndrome (fever, rash, lymphadenopathy and hepatic dysfunction)
Rashes(Stevens-Johnson syndrome and toxic epidermal necrolysis can develop)
GI disturbances
CNS effects(drowsiness, headache, fatigue, dizziness, double vision, ataxia and tremor)
Bone marrow suppression

41
Q

Lamotrigine interactions (3)

A

Increased CNS effects: Alcohol, anti-psychotics, local anaesthetics, opioids, anti-histamines, benzodiazepines

Female hormones: Combined oral contraceptive (moderately reduced lamotrigine exposure, possibly reduced contraceptive efficacy), Desogestrel (increased lamotrigine exposure)

Other anti-epileptic drugs

42
Q

Advice for woman trying for pregnancy with epilepsy

A

folic acid 5mg

43
Q

Driving requirements epilepsy

A

You must tell theDVLA.
You must stop driving straight away.
If you’ve had a seizure while awake and lost consciousness:
Your licence will be taken away
Epilepsy – can re-apply if seizure free for 12 months
Single seizure – can re-apply if seizure free for 6 months

44
Q

When is Thrombolysis with alteplase recommended in stroke.

A

–Treatment is started as early as possible within 4.5 hours of onset of stroke symptoms, and
–Intracranial haemorrhage has been excluded by appropriate imaging technique

45
Q

Alteplase MOA

A

Alteplase is a copy of tissue plasminogen activator (t-PA), which is a naturally occuring enzyme covering plasminogen to plasmin. Plasmin is the major enzyme responsible for clot breakdown and fibrinolysis.

46
Q

Absolute contraindications for alteplase ischaemic stroke (9)

A
  • Intracranial haemorrhage, neurosurgery/head trauma/stroke in past 3 months, uncontrolled hypertension, previous intracranial haemorrhage, known AV malformation/neoplasm/aneurysm, active internal bleeding, suspected endocarditis, bleeding diathesis, abnormal blood glucose
47
Q

Relative contraindications for alteplase ischaemic stroke (8)

A
  • Minor/rapidly improving symptoms, seizure at stroke onset, severe stroke, major surgery or serious trauma in previous 2 weeks, previous GI/urinary tract haemorrhage in previous 3 weeks, recent lumbar puncture or arterial puncture at non-compressible site, post MI pericarditis, pregnancy
48
Q

Alteplase SE (5)

A 
Haemorrhage
Anaphylactic reactions
Hypotension - thought to be due to enzymatic release of the vasodilator bradykinin. If the infusion is stopped/slowed the blood pressure usually recovers rapidly and treatment can be continued.
Nausea and vomiting
Cerebral oedema -caused by reperfusion.
49
Q

Following successful treatment with Alteplase, what further treatment should be prescribed in the first few days following thrombolysis?

A

Aspirin (300 mg, PO/PR)
Started in all patients with acute ischaemic stroke within 24 hours
Patients treated with thrombolysis should start treatment after 24 hours
Continued for 2 weeks before converting to long-term anti-thrombotic treatment
Standard anti-thrombotic treatment is clopidogrel 75mg daily

50
Q

Clopidogrel MOA

A

Target: ADP Receptor
Action: Irreversible Inhibitor
Effect: Inhibits binding of adenosine diphosphate (ADP) to its platelet receptor
Overall effect: Inhibits platelet aggregation

51
Q

Clopidogrel contraindications (4)

A

Active bleeding
Discontinue 7 days before elective surgery
Avoid in pregnancy
Caution in hepatic/renal impairment

52
Q

Clopidogrel SE (4)

A

Bleeding
GI disturbances (Abdominal pain, diarrhoea, dyspepsia, constipation, nausea, vomiting, peptic ulcers)
Rashes
Headache, dizziness, paraesthesia

53
Q

Clopidogrel interactions (5)

A

Increased bleeding risk:
Anticoagulants and anti-platelets
NSAIDs
SSRIs

Reduced antiplatelet effect
fluoxetine
PPIs
Erythromycin

54
Q

Stroke secondary prevention (8)

A 
Investigations for risk factors
Lipid modification (statins)
Blood pressure
Physical activity
Smoking cessation (if applicable)
Diet optimisation
Reduce alcohol consumption
Control of other co-morbidities (e.g. diabetes)
55
Q

Provided they are eligible for any resultant intervention investigate ischaemic storke patients for:
(3)

A

Ipsilateral carotid artery stenosis
Atrial fibrillation
Structural cardiac disease

56
Q

BP target following ischaemic stroke

A

systolic blood pressure below 130 mmHg

57
Q

Statin MOA

A

HMG-CoA reductase inhibitors competitively inhibit the enzyme that catalyses the rate-limiting step in the synthesis of cholesterol by the liver. The fall in hepatic cholesterol levels produces a compensatory upregulation in the number of LDL receptors on hepatocytes, with increased clearance of circulatory LDL cholesterol.

58
Q

Atorvastatin cautions (5)

A 
Elderly patients
High alcohol intake or liver disease
Hypothyroidism
Patients at risk of muscle toxicity
Haemorrhagic stroke
59
Q

Atorvastatin interactions (3)

A 
Macrolide antibiotics (increased statin exposure)
Penicillin antibiotics (increased risk hepatotoxicity)
Colchicine (increased risk of rhabdomyolysis)
60
Q

Atorvastating SE (8)

A 
GI disturbance
CNS effects – dizziness, headache, blurred vision Colchicine (increased risk of rhabdomyolysis)
Hepatic effects
Muscle effects
Skin reactions
Hyperglycaemia
Weight change
Epistaxis
61
Q

Stroke driving requirements

A

Must not drive for one month
Thereafter driving may resume if there has been a satisfactory clinical recovery
DVLA should be informed if there is residual neurological deficit

Y4 PPT (10 decks)

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