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

Drugs used in Epilepsy + Diabetes Mellitus Flashcards

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?

A

For seizures - deemed safer in pregnancy (less teratogenic)

21
Q

What is this?

A

Gabapentin

22
Q

What is this?

A

Lamotrigine

23
Q

Why should sodium valproate not be given to children?

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?

A

It increases them

25
Q

What vitamin deficiency can phenytoin cause?

A

Vitamin D

26
Q

What is the half life of phenytoin?

A

24hrs

27
Q

What is gabapentin?

A

A GABA analogue

28
Q

Why should a FBC be checked with valproate therapy?

A

Because it can cause thrombocytopenia

29
Q

Why do you need a high initial loading dose of phenytoin?

A

Because it has a volume of distribution of 0.7 L/kg so needs an initial loading dose.

30
Q

What kind of pharmacokinetics does phenytoin undergo?

A

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
Q

What categories of diabetes are there?

A
  1. Absolute insulin deficiency
  2. Insulin deficiency or resistance
  3. Drug induced
  4. Gestational diabetes
32
Q

How long must you be fasted for a fasting blood glucose?

A

> 8hrs

33
Q

What is a glucose tolerance test?

A

2h post 75g glucose load

34
Q

What does a diagnosis of diabetes require?

A
  • random BG >11 mmol/L
  • fasting BG > 7mmol/L
  • glucose tolerance test >11 mmol/L
35
Q

What would a non-diabetic’s fasting blood glucose and glucose tolerance test results be?

A

Fasting BG = < 5.6 mmol/L

Glucose tolerance test = < 7.8 mmol/L

36
Q

What would a person with impaired blood glucose’s tests show?

A

Fasting blood glucose 5.6 - 6.9 mmol/L

Glucose tolerance test 7.8 - 11 mmol/L

37
Q

What is insulin?

A
  • 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
Q

How do you make insulin from proinsulin?

A

Remove C peptide

39
Q

What things does insulin increase?

A
  • glucose uptake into muscle and fat
  • glucose synthesis
  • fat synthesis
  • protein synthesis
  • K+ uptake by cells
40
Q

What things does insulin decrease?

A
  • fat breakdown
  • ketone body synthesis
  • glycogen breakdown
  • gluconeogenesis
  • protein breakdown
41
Q

What are sulphonylureas?

A

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
Q

What is the MOA of sulphonylureas?

A
  • increases insulin release from beta cells
  • decreases peripheral insulin resistance (long term)
  • decreases glucagon secretion
  • decreases hepatic insulinase activity
43
Q

What are the key points about sulphonylureas?

A
  • 80% PO bioavailability
  • tend to cause hypoglycaemia
  • bound to albumin
  • liver metabolism
  • renal excretion
  • inhibited by thiazides, corticosteroids, phenothiazines (increases blood glucose)
44
Q

What are biguanides?

A
  • oral hypoglycaemics (eg metformin)
  • 2 guanidine rings
  • does not increase the amount of insulin released so tends not to cause hypoglycaemia
45
Q

What is the MOA of biguanides?

A
  • decreases gluconeogenesis
  • increases peripheral insulin utilisation
  • delays glucose uptake from gut
46
Q

What are the key points of biguanides?

A
  • 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
Q

What are the 2 other types of hypoglycaemic drugs (other than sulphonylureas and biguanides)?

A

Acarbose

  • delays intestinal glucose absorption
  • reduces post-prandial hyperglycaemia

Thiazolidinediones (eg rosiglitazone)

  • regulate genes involved in glucose and lipid metabolism, improving insulin sensitivity
48
Q
A

Exam prep tutorials (Pharmacology) (8 decks)

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