neuropharmacology

Question 1

3 main MOAs of anti-epileptic drugs (+ examples)

Answer 1

1. Na+ Ch block -> inhibit APs -> stabilise Na+ Chs => reduce frequency of discharge (e.g. lamotrigine, phenytoin, carbamezepine);
2. enhance GABA transmission (e.g. benzodiazepam - ↑GABA, sodium valporate -↓ GABA-T => ↓ GABA reuptake);
3. reduce glutamate release (e.g. lamotrigine)

Question 2

examples of side effects of Lamotrigine (5)

Answer 2

1. skin reactions;
2. blood disorders;
3. headaches;
4. drowsiness/dizziness;
5. osteoporosis
   (5. interacts w valporate)

Question 3

why should sodium valporate not be given to women

Answer 3

it is tetragenic

Question 4

what should be done if the first line agent doesn’t work (epilepsy)

Answer 4

titrate up 2nd agent while gradually withdrawing the first -> shouldn’t leave them with no treatment at all

Question 5

when can epilepsy treatment begin to be stopped

Answer 5

if 2 years seizure free

Question 6

concerns for pregnant epileptic pts (foetal development)

Answer 6

drugs are all tatragenic -> neural tube defects, cranial facial defects

Question 7

what should be done for pregnant epileptic pts (pharma wise -2)

Answer 7

1. aim for a single drug at the lowest possible dose to prevent seizures that could result in hypoxia;
2. folic acid supplements

Question 8

why can a MAX of 2 doses only be given in status epilepticus

Answer 8

can cause respiratory depression

Question 9

4 parts to parkinson’s mgx (pharma)

Answer 9

1. give DA precursor (L-DOPA)
2. give DA agonoist (bromocriptine, cabergoline etc.)
3. reduce endogenous DA breakdown anzymes (i.e. MOA-Bi e.g. selegilin)
4. release DA from stores + inhibit reuptake (e.g. amantadine)

Question 10

why is levodopa usually given alongside other drugs (2)

Answer 10

reduces its side effects (reduce binding in the periphery); reduces the amount needed to be effective (stops binding at unintended sites)

Question 11

side effects of levodopa

Answer 11

chorea, atonia, nausea, postural hypotension

Question 11

carbidopa and benserazide MOA

Answer 11

dopamine decarboxylase inhibitors -> stops levodopa being metabolised in the periphery => side effects are reduced and lower levodopa dose needed as more reaches the target organ;
can’t cross BBB so has o effect on the CNS

Question 12

selegiline/rasagiline MOA

Answer 12

inhibits the MAO-B pathway => increase in DA travelling to intended site

Question 13

tolcapone MOA

Answer 13

inhibtis COMT pathway => increase in DA travelling to intended site

Question 14

why is L-DOPA used in PD rather than DA itself (3)

Answer 14

1. DA has poor oral absorption;
2. DA cant cross BBB;

Question 15

where is MAO-B found and what does it do

Answer 15

found in the striatum, breaks down DA

Question 16

what does 5-HT control via the CNS (4)

Answer 16

1. mood
2. pain input
3. appetite
4. commiting

Question 17

what does 5-HT control via the PNS (2)

Answer 17

1. pain fibers
2. vascular tone

Question 18

what class of drug should be avoided in migraines

Answer 18

opiods

Question 19

triptans MOA

Answer 19

selective 5-HT receptor agonists with high affinity for 5-HT1B and 5-HT1D receptors -> leads to vasoconstriction of the cranial arteries, which painfully dilate during a migraine attack

Question 20

why must triptans be prescribed with caution in pts w CVD

Answer 20

they can cause vasoconstriction