Pharm part 2 Flashcards
(14 cards)
Noradrenaline reuptake inhibitor
Atomoxetine (used in ADHD)
Agomelatine
M1/M2 agonist and 5HT2C antagonist
5HT2C promotes noradrenaline and dopamine in the prefrontal cortex
LFTs should be monitored whilst taking this drug
Risperidone MOA
D2 & 5HT2A antagonist
Undergoes first pass metabolism to make the active metabolite for 9-OH Risperidone which is the active metabolite
Risperidone is also an alpha 1 blocker → leading to hypotension on the first dose
Half life is 15 hours
Quetiapine MOA
D2 & 5HT2A
Shorter half -life of 6-12 hours thus requiring multiple daily dosing
This can be mitigated through extended release
Clozapine
D2 & 5HT2A
But with the highest dissociation from D2 receptors
Potent anti-cholinergic
Abilify
Partial D2 agonist & 5HT2A
Long half life - 94 hours, due to the metabolite dehydoapripazole
Highly protein bound 99%
Lithium
Mechanism not perfectly understood
But Lithium works on multiple levels
Neuroprotective ( BDNF,BCL-2)
Changes areas in the brain → anterior cingulate , ventral prefrontal cortex , hippocampus and amygdala
Inhibits intracellular proteins: PKC, MARKS, GSK-3 IP Pase IM Pase.
Half-life f 18 hours, but eith chronic use increases to 36 hours.
Not metabolised by liver and is renally excreted
Valproate
At least three possibilities exist for how valproic acid works:
1.inhibiting voltage-sensitive sodium channels (Figure 8-5),
2 boosting the actions of the neurotransmitter GABA - preventing by either preventing re-uptake of GABA or preventing metabolism of GABA
3. regulating downstream signal transduction cascades ( Activates extracellular signal-regulated kinase (ERK) & pathway thus altering synaptic plasticity)
Valproate is well absorbed with bioavailability close to 100%. Its has a half-life of 16 hours and 90% protein bound
Valproate can cause gastric irritation and hyperammonemia.
S/E → hair loss, peripheral oedema, thrombocytopenia, leucopenia & pancreatitis
Asymptomatic rise LFTs may occur
Carbamazepine
Blocks voltage dependant sodium channels thus inhibiting repetitive neuronal firing
It reduces glutamate release and decreases turnover of dopamine and noradrenaline
It has an erratic absorption and bioavailability of 80%. It is 75% bound to plasma proteins.
Carbamazepine induces its own metabolism, and hence the half life pre auto induction is 24 hours, followed by 8 hours after auto induction.
Potent inducer of CYP 450
Lamotrigine MOA
Blocks voltage sodium channels with secondary effect on calcium transport.
This leads to neural stabilisation and decrease in glutamate release
Half - life 28 hours
Carbamazepine decreases lamotrigine levels by 50% whilst valproate increases lamotrigine by 50%
0.1% steven Johnson sydrome
Must be stopped as soon as a rash is seen
MOA Gabapentin
Binds to the α2δ of the voltage dependent calcium channel - inhibits this channel
Pregabalin does the same
Cholinesterase Inhibators Names and MOA
Donepezil , Galantamine, and rivastigmine
likely due to the increase or preservation of ACh in the CNS and preservation of hippocampal function
These medications stop the enzyme acetylcholine esterase. This enzyme purpose is to degrade and lower ACh in the synapse.
Donepezil Half-life 70 hours,
rivastigmine is not metabolised by the liver and has a half-life of 1.5 hours
Memantine
Acts by blocking NMDA glutamate receptors, therefore lowering glutamate activity and neuronal depolarisation.
This may slow the rate of neuronal death
Non hepatic and Half life of 60-80 hours
ADHD medications and MOA
Methylphenidate → inhibits the dopamine transporter DAT. and noradrenaline transporter NET. leading to increase in dopamine and noradrenaline in the synaptic space
Monitor BP, apittite, growth, sleep, and development of TICs
Atomoxetine can also be used - onset of action is usually 4-6 weeks, it is useful when TICs are present and stimulant diversion may be an issue
