Drugs Flashcards
Methylprednisolone
Treats: MS
MOA: Unbound glucocorticoid crosses cell membranes, binds to cytoplasmic receptors, modifying transcription and protein synthesis. This inhibits leukocyte infiltration at the inflammatory site, supressing inflammatory and immune responses.
Dalfampridine
Treats: MS
MOA: Potassium channel blocker. Exposed potassium channels, due to demyelination, leak K+ ions. This repolarises cells and makes it difficult to trigger an action potential. By blocking the voltage gated K+ channels conduction blocks in demyelinated axons are relieved.
Alemtuzumab/Lemtrada
Treats: MS and leukaemia
MOA: Human monoclonal antibody. It targets CD52 proteins on B-cells and T-cells, leading to cell lysis.
Baclofen
Treats: Spasticity associated with MS
MOA: Muscle relaxant stimulating GABA-B receptors, decreasing frequency and intensity of muscle contractions.
Beta Interferon
Treats: Relapsing Remitting (and Secondary Progressive) MS
MOA: Reduces inflammation by binding to interferon receptors IFNAR1 and IFNAR2c, resulting in phosphorylation of the receptors.
Reserpine
MOA: Blocks the vesicular monoamine transporter (VMAT) causing MDD. Neurotransmitter is available to be taken back up into the vesicles by VMAT, therefore resepine decreases levels of 5-HT and NA.
Phenelzine/Tranylcypromine/Moclobomide
Treats: Depression
MOA: These are MAO-A inhibitors, which stop the degradation of 5-HT and NA, increasing their concentration in the synaptic cleft. Patients on MAOIs should be on a tyramine free diet.
Desipramine, amitriptyline, comipramine
Treats: Depression
MOA: TCAs that block SERT and NAT, increasing neurotransmitter synaptic concentration.
Fluoxetine, paroxetine, fluvoxamine, sertraline, citalopram, escitalopram
Treats: Depression
MOA: SSRIs have a high affinity for SERT but not NAT or DAT, and hence primarily increase 5-HT synaptic concentration.
Mirtazipine
Treats: Depression
MOA: Antagonist to adrenergic alpha 2 receptors. Inhibits the negative feedback which reduces NA release, increasing synaptic concentrations of NA, and therefore 5-HT via alpha 1 receptor stimulation.
Propofol
Use: IV anaesthetic for induction and maintenance
MOA: Positive allosteric modulator (PAM) for GABA at GABA-A receptors. Rapid acting with little excitation.
Isoflurane
Use: Induction and maintenance of general anaesthesia. Also induces muscle relaxation and pain reduces pain sensitivity.
MOA: Induces a reduction in junctional conductance by decreasing gap junction opening times and increasing gap junciton closing times. It activates calcium dependent ATPase in the SR by increasing the fluidity of the lipid membrane. Isoflurane also binds to GABA receptors, large conductance Ca2+ activated K+ channels, glutamate receptors and glycine receptors.
Fentanyl
Use: Opioid analgesic that also causes sedation
MOA: Interacts with the mu opioid receptor, which are coupled with a G protein complex. Binding stimulates the excahnge of GTP for GDP on the G protein complex. This decreases intracellular cAMP by inhibiting adenylate cyclase. Subsequently, nociceptive neurotransmitter release (substance P, glutamate, GABA, dopamine, acetlycholine and noradrenaline etc.) is inhibited.
Suxamethonium
Use: Rapid onset/brief duration depolarising muscle relaxant used in general anaesthesia and intubation.
MOA: Persistently depolarises the NMJ by binding to cholinergic receptors. Not broken down rapidly by AChE and so blocks the receptors, leading to muscle desensitisation.
Atracurium
Use: Non-depolarising muscle relaxant used in general anaesthesia and intubation.
MOA: Atracurium is a cholinergic receptors antagonist at the motor end plate. It is a competitive antagonist to ACh, blocking it from binding to its receptors. As such to reverse the neuromuscuar block, AChE inhibitors are given.
