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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
Neuroleptic Malignant Syndrome pathophys
Pathophysiology: Depletion of dopamine in the hypothalamus/nigrostriatal pathway
26
Neuroleptic Malignant Syndrome S/Sx
rigidity, fever, altered GCS
27
Neuroleptic Malignant Syndrome Mx
mainly supportive, some evidence for use dantrole, bromocriptine or Lorazepam
28
When can anti-epileptic drug treatment be commenced
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
First line AED focal seizures
Lamotrigine or carbamazepine
30
First line AED generalised seizures
Sodium valproate
31
Sodium valproate MOA
inhibits GABA transaminase (inhibits breakdown of GABA so increases inhibitory effect, reducing excessive neuronal firing)
32
Sodium valproate CI (3)
History/family history hepatic dysfunction Metabolic disorders Pregnancy
33
Sodium valproate SE (5)
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
Sodium valproate interactions (3)
Cytochrome P450 inhibitor  Other anti-epileptic drugs Risk of hepatoxicity –Statins, alcohol, antibiotics, anti-fungals, chemotherapy agents
35
Sodium valproate monitoring
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
Sodium valproate caution in women
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
What would be the most appropriate first line drug for a woman in reproductive years?
Lamotrigine
38
Lamotrigine MOA
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
Lamotrigine cautions (2)
Can exacerbate myoclonic seizures and Parkinson’s disease | Renal failure and hepatic failure (reduced dose)
40
Lamotrigine SE (5)
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
Lamotrigine interactions (3)
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
Advice for woman trying for pregnancy with epilepsy
folic acid 5mg
43
Driving requirements epilepsy
You must tell the DVLA. 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
When is Thrombolysis with alteplase recommended in stroke.
–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
Alteplase MOA
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
Absolute contraindications for alteplase ischaemic stroke (9)
- 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
Relative contraindications for alteplase ischaemic stroke (8)
- 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
Alteplase SE (5)
``` 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
Following successful treatment with Alteplase, what further treatment should be prescribed in the first few days following thrombolysis?
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
Clopidogrel MOA
Target: ADP Receptor Action: Irreversible Inhibitor Effect: Inhibits binding of adenosine diphosphate (ADP) to its platelet receptor Overall effect: Inhibits platelet aggregation
51
Clopidogrel contraindications (4)
Active bleeding Discontinue 7 days before elective surgery Avoid in pregnancy Caution in hepatic/renal impairment
52
Clopidogrel SE (4)
Bleeding GI disturbances (Abdominal pain, diarrhoea, dyspepsia, constipation, nausea, vomiting, peptic ulcers) Rashes Headache, dizziness, paraesthesia 
53
Clopidogrel interactions (5)
Increased bleeding risk: Anticoagulants and anti-platelets NSAIDs SSRIs Reduced antiplatelet effect fluoxetine PPIs Erythromycin
54
Stroke secondary prevention (8)
``` 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
Provided they are eligible for any resultant intervention investigate ischaemic storke patients for: (3)
Ipsilateral carotid artery stenosis Atrial fibrillation Structural cardiac disease
56
BP target following ischaemic stroke
systolic blood pressure below 130 mmHg
57
Statin MOA
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
Atorvastatin cautions (5)
``` Elderly patients High alcohol intake or liver disease Hypothyroidism Patients at risk of muscle toxicity Haemorrhagic stroke ```
59
Atorvastatin interactions (3)
``` Macrolide antibiotics (increased statin exposure) Penicillin antibiotics (increased risk hepatotoxicity) Colchicine (increased risk of rhabdomyolysis) ```
60
Atorvastating SE (8)
``` GI disturbance CNS effects – dizziness, headache, blurred vision Colchicine (increased risk of rhabdomyolysis) Hepatic effects Muscle effects Skin reactions Hyperglycaemia Weight change Epistaxis ```
61
Stroke driving requirements
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

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