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Exam prep tutorials (Pharmacology) > Drugs used in Epilepsy + Diabetes Mellitus > Flashcards

Drugs used in Epilepsy + Diabetes Mellitus Flashcards

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1
Q

Why do seizures occur?

A

Secondary to repetitive neuronal discharges in the CNS

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2
Q

What drugs are used to control seizures?

A
  • anticonvulsants
  • benzodiazepines
  • anaesthetics agents
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3
Q

What are the mechanisms of action of the anticonvulsants?

A
  • action on CNS Na+ channels
  • potentiating the neurotransmitter GABA
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4
Q

What is the mechanism of action for anticonvulsants acting on the CNS Na+ channels?

A
  1. Inhibiting inactive fast Na+ channels eg phenytoin
    • these drugs have affinity for sodium channels that are opening and closing rapidly (which occurs with increased CNS neuronal activity during a seizure)
    • this means they’re selective for abnormal neuronal discharges involved in the seizure without interfering significantly with normal neuronal transmission
  2. Stabilizing presynaptic Na+ channels by inhibiting the release of excitatory neurotransmitters eg lamotrigine
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5
Q

What are the mechanisms for potentiating GABA?

A
  • Facilitating GABA
    • opening the Cl- channels allows Cl- into the cell, causing cell hyperpolarization and the cell becomes less excitable (eg benzodiazepines and barbiturates)
  • GABA agonists
    • eg baclofen and acamprosate (used for their other effects)
  • Inhibiting GABA transaminase
    • ​GABA transaminase is the enzyme which normally catalyses the breakdown of GABA eg sodium valproate and vigabatrin
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6
Q

What is the chemical structure of phenytoin?

A
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7
Q

What can phenytoin be used in?

A
  • generalized seizures (grand mal)
  • partial seizures (petit mal)
  • status epilepticus (persistent seizures > 30mins without regaining consciousness between)
  • trigeminal neuralgia
  • Class Ib anti-arrhythmic agent (Rx of digoxin toxicity related arrhythmias
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8
Q

What is the MOA of phenytoin?

A
  • binds to inactive or refractory fast Na+ channels after opening
  • therefore most effective against channels opening and closing at a high frequency, like those in seizures
    • PO/IV only
    • narrow therapeutic index - monitor plasma levels
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9
Q

What are the SEs of phenytoin?

A
  • hirsutism
  • gum hyperplasia
  • acne
  • coarse facies
  • peripheral neuropathy
  • megaloblastic anaemia
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10
Q

What toxic effects can phenytoin cause?

A
  • ataxia
  • nystagmus
  • paraesthesia
  • slurred speech
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11
Q

What are the key points about phenytoin?

A
  • teratogenic
  • enzyme inducer (CYP450)
  • 90% protein bound
  • liver metabolism to inactive metabolites
  • renal excretion
  • undergoes saturation kinetics just above therapeutic index
  • zero order kinetics replace 1st order kinetics at high drug concentrations due to enzyme saturation
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12
Q

What is the chemical structure of sodium valproate?

A
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13
Q

What is sodium valproate?

A

Epilim - the sodium salt of valproic acid.

Available IV or slow release capsules/sachets.

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14
Q

What can sodium valproate be used for?

A
  • partial seizures
  • myoclonic seizures
  • grand mal epilepsy
  • petit mal epilepsy (particularly effective)
  • chronic pain (trigeminal neuralgia)
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15
Q

What is the MOA of sodium valproate?

A

Stabilises inactive Na+ channels and increases GABA concentration by inhibiting GABA transaminase (the enzyme that breaks down GABA).

(similar to phenytoin)

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16
Q

What are the SEs of sodium valproate?

A
  • nausea
  • thrombocytopenia
  • hair loss (transient)
  • gastric irritation
  • neural tube defects
  • liver dysfunction
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17
Q

What % protein bound is sodium valproate?

A

90% protein bound

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18
Q

Where is sodium valproate metabolised and excreted?

A

Liver metabolism.

Renal excretion,

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19
Q

What other anticonvulsants can be used as monotherapy or as an adjunct to phenytoin or sodium valproate?

A

Gabapentin

  • increases GABA synthesis in the brain
  • now used in chronic pain almost exclusively
  • modulates voltage gated Ca2+ channels
  • inhibits excitatory glutamate
  • increases 5-HT (serotonin) levels in CNS

Lamotrigine

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20
Q

Why is lamotrigine used?

Study These Flashcards
A

For seizures - deemed safer in pregnancy (less teratogenic)

21
Q

What is this?

22
Q

What is this?

23
Q

Why should sodium valproate not be given to children?

Study These Flashcards
A

It should not be used in children <2yrs because it’s been associated with liver dysfunction and rare (but reversible) condition of paroxysmal tonic upgaze of childhood.

Also avoid in pregnancy.

24
Q

How does sodium valproate affect brain concentrations of GABA?

Study These Flashcards
A

It increases them

25
What vitamin deficiency can phenytoin cause?
Vitamin D
26
What is the half life of phenytoin?
24hrs
27
What is gabapentin?
A GABA analogue
28
Why should a FBC be checked with valproate therapy?
Because it can cause thrombocytopenia
29
Why do you need a high initial loading dose of phenytoin?
Because it has a volume of distribution of 0.7 L/kg so needs an initial loading dose.
30
What kind of pharmacokinetics does phenytoin undergo?
1st order kinetics until (at high concentrations) the enzyme system is at full capacity and it converts to saturation kinetics or zero order kinetics
31
What categories of diabetes are there?
1. Absolute insulin deficiency 2. Insulin deficiency or resistance 3. Drug induced 4. Gestational diabetes
32
How long must you be fasted for a fasting blood glucose?
\> 8hrs
33
What is a glucose tolerance test?
2h post 75g glucose load
34
What does a diagnosis of diabetes require?
* random BG \>11 mmol/L * fasting BG \> 7mmol/L * glucose tolerance test \>11 mmol/L
35
What would a non-diabetic's fasting blood glucose and glucose tolerance test results be?
Fasting BG = \< 5.6 mmol/L Glucose tolerance test = \< 7.8 mmol/L
36
What would a person with impaired blood glucose's tests show?
Fasting blood glucose 5.6 - 6.9 mmol/L Glucose tolerance test 7.8 - 11 mmol/L
37
What is insulin?
* anabolic polypeptide hormone * produced by beta cells of Islets of Langerhans * 51 amino acids in 2 chains (A + B) including 2 disulphide bridges between A + B * released by the pancreas in response to increased plasma glucose levels * encourages conversion of glucose to glycogen which is stored in the liver
38
How do you make insulin from proinsulin?
Remove C peptide
39
What things does insulin increase?
* glucose uptake into muscle and fat * glucose synthesis * fat synthesis * protein synthesis * K+ uptake by cells
40
What things does insulin decrease?
* fat breakdown * ketone body synthesis * glycogen breakdown * gluconeogenesis * protein breakdown
41
What are sulphonylureas?
Oral hypoglycaemic used in Type 2 diabetes. Exerts a hypoglycaemic effect which is antagonised by thiazides. Displace bound insulin from pancreatic islet 13 cells. eg gliclazide, glibenclamide (2nd gen) Half life 8-12hrs
42
What is the MOA of sulphonylureas?
* increases insulin release from beta cells * decreases peripheral insulin resistance (long term) * decreases glucagon secretion * decreases hepatic insulinase activity
43
What are the key points about sulphonylureas?
* 80% PO bioavailability * tend to cause hypoglycaemia * bound to albumin * liver metabolism * renal excretion * inhibited by thiazides, corticosteroids, phenothiazines (increases blood glucose)
44
What are biguanides?
* oral hypoglycaemics (eg metformin) * 2 guanidine rings * does not increase the amount of insulin released so tends not to cause hypoglycaemia
45
What is the MOA of biguanides?
* decreases gluconeogenesis * increases peripheral insulin utilisation * delays glucose uptake from gut
46
What are the key points of biguanides?
* tends not to cause hypoglycaemia when administered alone * 60% PO bioavailability * unbound * excreted unchanged in urine (therefore increased duration of action in renal failure * can cause lactic acidosis
47
What are the 2 other types of hypoglycaemic drugs (other than sulphonylureas and biguanides)?
Acarbose * delays intestinal glucose absorption * reduces post-prandial hyperglycaemia Thiazolidinediones (eg rosiglitazone) * regulate genes involved in glucose and lipid metabolism, improving insulin sensitivity
48

Exam prep tutorials (Pharmacology) (8 decks)

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