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Pharmacology > Nervous System > Flashcards

Nervous System Flashcards

1
Q

What is meant by a seizure?

A

A seizure is a sudden irregular discharge of electrical activity in the brain.
It involves: sensory disturbance, convulsions (uncontrolled shaking movements) and unconsciousness.

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2
Q

What is epilepsy?

A

A neurological disorder which is marked by recurrent episodes of sensory disturbance/ LOC/ convulsions with abnormal electrical activity in brain.

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3
Q

What is the difference between partial and generalised seizures?

A

Partial= only one bit of the brain affected.

Generalised= many parts of the brain affected.

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4
Q

What are the different types of generalised seizures?

A 
Absence 
Myoclonus 
Tonic clinic 
Tonic 
Atomic
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5
Q

Explain what is meant by the following seizures….

Absence 
Myoclonic 
Tonic clinic 
Tonic 
Atonic
A

Absence= daydreaming
Tonic clinic: muscles tense and then convulse
Myoclonic: brief shock like muscle jerks
Status epileptics: medical emergency
Myocolonic: brief shock like muscle jerks
Atonic: without tone ‘drop attack’
Tons: increased tone (stiffen, then relax).

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6
Q

The causes of epilepsy can be primary (idiopathic)- no apparent cause and may be inherited.
Or
Secondary (symptomatic)
What can some of the causes of epilepsy be?

A 
VITAMIN C 
V= vascular= stroke/TIA 
I= infection= abscess/ meningitis 
T= trauma= jntracerebral haemorrhage 
A= auto immune= systemic lupus erythromatous 
M= metabolic= hypoxia, electrolyte imbalance, hypoglycaemia, thyroid dysfunction 
I= Iatrogenic= drugs/alcohol withdrawal 
N= neoplastic= intracerebral mass
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7
Q

What are some anti epileptic drugs you could use?

A

Carbamazepine, lamotrigine, phenytoin.

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8
Q

How does carbamazepine, lamotrigine and phenytoin work?

A

They are all anti epileptics which are sodium channel blockers, they cause Na channels to be in a constant inactive state so you don’t get action potentials.

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9
Q

What are the side effects of phenytoin?

A

Dizziness
Fatigue
Ataxia
Diplopia
- if used in pregnancy then they can lead to common congenital malformations like: cleft lip palate, congenital heart disease.
You can’t use phenytoin for long as it can become toxic and cause nausea, CNS dysfunction (confusion, nystagmus, ataxia.

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10
Q

What is the first line drug for people with generalised/tonic- clinic seizures?

A

Sodium valproate
Indirect increase in GABA synthesis
Ca2+ channel blocker- prevents depolarisation
As well as being Na+ channel blocker.

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11
Q

Give some side effects of sodium valproate?

A

Dizziness, fatigue, ataxia, diplopia, weight gain.

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12
Q

Why would you have to be careful if taking sodium valproate when taking liver enzyme inhibitors?

A

Liver enzyme inhibitors cause the sodium valproate levels to increases and therefore you have to reduce the dose.

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13
Q

How to levetiracetam work?

A

Binds to synaptic vesicles to inhibit the pre synaptic calcium channel activity, therefore you get inhibition of neurotransmitter release from the pre synaptic neurone.

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14
Q

What are the interactions of carbamazepine, phenytoin and sodium valproate?

A

So carbamazepine and phenytoin, are both liver enzyme inducers so their levels can reduce too rapidly, whereas with sodium valproate, this is a liver enzyme inhibitor so levels can get too high.

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15
Q

What would you advise someone taking the COCP and carbamazepine/phenytoin?

A

As phenytoin and carbamazepine are liver enzyme inducers then they can cause the oestrogen levels of COCP to fall too low, person should have a higher COCP dose and also use other protective measures.

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16
Q

What would you give to someone suffering from epilepsy who is pregnant?

A

Carbamazepine is generally perceived as safe in pregnancy, although can still carry a risk!!!
Sodium valproate should not be used, it is thought to cause decreased serum folate and leads to neural tube defects, craniofacial and skeletal abnormalities, developmental disorders after birth (mental and physical).

17
Q

Why do you have to be careful when prescribing phenytoin?

A

It has a very narrow therapeutic window, if there is a small increase it can go above the therapeutic range and become toxic.
Should have therapeutic drug monitoring
When it reaches toxic levels, it causes nausea, CNS dysfunction (confusion, nystagmus, ataxia), decreased consciousness and coma.

18
Q

What is the treatment of partial seizures (both simple and complex)?

A

Lamb Top Gave Funny Carbs

Lamb= lamotrigine 
Top= topiramate 
G: gabapentin 
F: phenytoin 
C: carbamazepine
19
Q

What is status epileptics and what would you give for it?

A

Epileptic seizures occurring continuously without recovery of consciousness in between
It is neither funny: phenytoin
Or good: benzodiazepines

20
Q

How does benzodiazepine work?

A

It is a GABA potentially, it is an inhibitory neurotransmitter and potentiators enhance the effect of GABA.

21
Q

What is Parkinson’s?

A

A neurodegenerative disorder, degeneration of dopaminergic neurones (dopamine plays a role in movement).
Parkinson’s symptoms include: tremor, rigidity and bradykinesia.

22
Q

The 3 cardinal signs of Parkinson’s= tremor, bradykinesia, rigidity, but what are the non motor manifestations?

A 
Mood changes 
Pain 
Cognitive change 
Urinary symptoms 
Sleep disorder 
Sweating
23
Q

What is L-DOPA, how does it work, what are it’s side effects?

A

L- DOPA is a central nervous system agent. It is able to cross the blood brain barrier unlike dopamine, which ant.
Normally side effects are low, but you can get:
Nausea/anorexia
Hypotension
Psychosis (scizophrenia like effects, hallucinations, delusion, paranoia) tachycardia

24
Q

Why will L-DOPA not always work?

A

L-DOPA has to be taken up by dopaminergic cells in the Substantia nigra, in order to be converted to dopamine, if there are fewer remaining cells then there is going to be a less reliable effect of levodopa and you will get motor fluctuations.
It doesn’t stop the degeneration of dopaminergic neurones, so doesn’t cure p, just helps with symptoms.

25
Q

What are some formulations of L-DOPA?

A

Co-careldopa and co-beneldopa
These are combinations of L-DOPA and a peripheral DOPA decarboxylase inhibitor, this allows less L-DOPA to be used.
You get reduced side effects and increased L-DOPA reaching the brain.

26
Q

What is it that causes metabolism of L-DOPA, what can be given to reduce this?

A

Peripheral dopa decarboxylase causes metabolism of L-DOPA in the peripheries, to stop this you can give a peripheral dopa decarboxylase inhibitor.

27
Q

How do dopamine receptor agonists work in Parkinson’s, what is there mechanism of action and what are the side effects?

A

They bind to dopamine receptors, they are direct acting and by using them you get less dyskinesia and motor complications.
The side effects= sedation, hallucinations, confusion, nausea, hypotension and impulse control disorders.

28
Q

Give examples of dopamine receptor agonists…

A

Ropinirole, rotifotine, apomorphine

29
Q

What is the difference in route of administration for rotigotine and apomorphine?

A

Rotigotine is patch, whereas apomorphine is given subcut.

30
Q

What are rasagiline and selegiline, how do they work?

A

They are monoamine oxidase B inhibitors, normally monoamine oxidase B metabolises dopamine and predominates in dopamine containing regions in the brain, therefore by inhibiting it you get enhancement of dopamine.
They can be used alone or can be used along side of L-DOPA to prolong the action of L-DOPA.

31
Q

What is Entacopone, how does it work?

A

It is COMT inhibitor
Catechol-o-methyl transferase, it reduces the peripheral breakdown of L-DOPA
It doesn’t have a therapeutic effect along, you do have to use it with L-DOPA as it has an L-DOPA sparing effect, it prolongs the motor response to L-DOPA.

32
Q

Do anticholinergics play a big role in the treatment of PD?

A

No they play a minor role in the treatment, they may have antagonistic effects to dopamine and don’t act via. Dopamine systems, they don’t have an effect on bradykinesia but they do treat the tremor.
Side effects: confusion, drowsiness, tachycardia, vasoconstriction

33
Q

What is myasthenia gravies?

A

A chronic, auto-immune neuromuscular disease which causes weakness in the skeletal muscles, it is fluctuating and fatiguable.

34
Q

Give some drugs which you may need to think about prescribing to a patient who has myasthenia gravis?

A

Drugs which affect the neuromuscular transmission (they exacerbate myasthenia gravis)
Beta blockers, ACE inhibitors, magnesium, aminoglycosides

35
Q

Give some of the signs of myasthenia gravis….

A

Extort ocular muscles
Dysphagia, dysphonia, dysarthria
Limb weakness
Respiratory muscle involvement

36
Q

Explain the pathophysiology of myasthenia gravis…

A

IgG antibodies block Ach binding sites, Ach rarely binds and Ach esterase begins to break it down, normally Ach would have no difficulty binding and would be broken down after binding has already occurred

37
Q

What are the terms for acute exacerbation of myasthenia gravis and overtreatment?

A

Acute exacerbation= myasthenic crisis

Over treatment= cholinergic crisis

38
Q

What are the drugs used for treatment of myasthenia gravis, also give the side effects of these drugs…

A

Acetylcholinesterase inhibitors- they prevent the breakdown of Ach by cholinesterases
They enhance neuromuscular transmission
Skeletal and smooth muscle
Excess dose can cause depolarising block- cholinergic crisis

Pyridostigmine- oral

Neostigmine- oral and IV prep (ITU), quicker action, duration is up to 4 hours

Muscarinic side effects: 
S salivation
L lacrimation
U urinary incontinence 
D diarrhoea 
G GI upset and hypermobility
E Emesis 
(+sweating/miosis)

Pharmacology (15 decks)

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