Revision Drug Names, Functions and Facts Flashcards
Codeine:
Function: Opioid agonist painkiller.
Facts:
- Relatively low affinity for opioid receptors until metabolised by the CytP450 system.
- Metabolised into active form, morphine.
Mechanism of action:
- Mu opioid receptor agonist, see morphine.
Clopidogrel:
Function: Anti-platelet medication used for heart attack and stroke victims.
Facts:
- Inactive until metabolised by the CytP450 system in liver.
Mechanism of action:
- Irreversibly inhibits the P2Y12 component of ADP receptors.
- Two ADP receptors on platelets, P2Y1 and P2Y12, P2Y12 activation causes downstream effects resulting in proliferation. One effect is inhibition of adenylyl cyclase, decreasing cAMP levels (GPCR).
Morphine:
Function: Pain medication.
Facts:
- Comes from poppy seeds originally
- UGT system enzymes glucuronidate morphine into inactive form, and makes it polar, and thus hydrophilic allowing elimination via kidneys.
Mechanism of action:
- Mostly targets mu-opioid receptors.
- G protein-coupled receptor, ligand binding causes structural changes in receptor and G-protein, GDP swapped for GTP, alpha G portion dissociates from beta- and gamma- portions.
- alpha-G inhibits adenylyl cyclase, resulting in lower cAMP, thus PKA.
- Lower PKA results in the inhibition of Ca2+ voltage channels at presynaptic neuron, and opening of K+ channels, less action potential.
- Less excitatory neurotransmitters released (substance P and glutamate), less pain.
Statins:
Function: Lowers LDL-C (low-density lipoprotein cholesterol) concentration in serum.
Mechanism of action:
- Inhibits HMG-CoA reductase, stopping cholesterol synthesis in the liver.
- As a result, liver cells upregulate LDL-C receptors, taking more from the blood, so less cholesterol and triglycerides.
Grapefruit juice:
Mechanism of action:
- ‘Furanocoumarins’ present in juice inhibit CYP3A4 enzymes in small intestine, these can metabolise statins.
- Patients on statins required to refrain from drinking grapefruit juice, or limit consumption.
Ritonavir:
Function: CYP3A4 inhibitor.
Facts:
- Original purpose was antiretroviral against HIV.
Mechanism of action:
- See function.
Ibrutinib:
Function: Chemotherapy drug, useful against leukaemias and lymphomas.
Facts:
- Bruton’s tyrosine kinase facilitates proliferation of WBCs
- B-cell lymphomas commonly upregulate BTK.
Mechanism of action:
- Inhibits Bruton’s tyrosine kinase.
- Reduces cell proliferation.
Warfarin:
Function: Anti-coagulant.
Facts:
- Can be displaced from plasma proteins by fluoxetine
- CYP2D6 enzyme also competitively inhibited by fluoxetine, affects metabolism
- Mainly metabolised by CYP2C9
Mechanism of action:
- Inhibits vitamin K epoxide reductase, vital in vitamin K synthesis. Vitamin K vital in blood clotting, used as cofactor for clotting factors (II (prothrombin)
Fluoxetine:
Function: Anti-depressant
Facts:
- Inhibits CYP2D6 in liver, can interact with other drugs via this. Such as warfarin, though this is moreso from the plasma protein displacement effect.
Mechanism of action:
- Blocks serotonin reuptake channel proteins in presynaptic membrane.
Aspirin:
Function: Painkiller/Anti Inflammatory
Facts:
- Prodrug
- Activated by esterases in the GI tract and liver (~80% in liver)
to form salicylic acid from acetylsalicylic acid.
- Inhibition of target is completely irreversible.
- Metabolised by UGT mainly, and CYP2C9.
Mechanism of action:
- Inhibits COX-1 and 2 enzymes.
- COX-1 and 2 responsible for arachidonic acid cascade to produce prostaglandins, which can be responsible for pain and fever, but also gastric protection in the case of COX-1.
Celecoxib:
Function: Painkiller/ Anti Inflammatory
Mechanism of Action:
- Selectively inhibits COX-2, responsible more specifically for the prostaglandins responsible for fever and pain in arachidonic acid cascade. Avoids gastric side effects such as ulcers seen in continuous aspirin use.
L-DOPA + Carbidopa:
Function: Dopamine treatment for Parkinson’s.
Mechanism of Action:
- L-DOPA is a precursor to dopamine and is converted by DOPA decarboxylase.
- Don’t want excess dopamine metabolism outside of the brain, so Carbidopa (designed to not cross BBB) inhibits DOPA decarboxylase.
Ethanol:
Function: シ
Facts:
- Zero-order kinetic drug.
- 10mg/hour metabolised by alcohol dehydrogenase to acetaldehyde, a toxic compound that is responsible for hangovers.
Mechanism of Action:
- Acts as an agonist for GABA receptors, and weakly for glycine receptors. Inhibitory on brain.
- Inhibitor of NMDA receptors in higher concentrations, responsible for brain plasticity and memory making, drinking too much can cause blackout.
Disulfiram (Antabuse):
Function: Management of alcohol abuse.
Mechanism of Action:
- Inhibits aldehyde dehydrogenase, which normally quickly converts acetaldehyde into acetic acid.
- Higher levels of acetaldehyde cause extremely unpleasant, hangover-like effects.
Benzodiazepines:
Function: Anxiolytic/Sedative drug
Facts:
- The target, GABA receptors, are ion channel-linked receptors. Binding of ligand opens these and Cl- ions flow into neuron,
Mechanism of Action:
- Enhances the binding of GABA to its receptor, prevents inhibition by this neurotransmitter.
- Inhibition results in less release of neurotransmitters such as glutamate, norepinephrine, dopamine, serotonin.
Propranolol:
Function: Decrease heart rate and contractility.
Facts:
- The class of drugs are called ‘Beta-blockers’, because the target is beta-adrenergic receptors.
Mechanism of Action:
- Non-selective beta-blocker, targets beta-1 and beta-2 adrenergic receptors.
- These receptors are GPCRs that when stimulated by norepinephrine and epinephrine in the sympathetic nervous response to increase heart rate and contractility.
- Stops binding of these neurotransmitters.
Amlodipine:
Function: Increased systemic vasodilation of arteries, lowering blood pressure. Heart doesn’t work as hard and pain in chest is reduced.
Facts:
- It is a ‘dihydropyridine
Mechanism of Action:
- Calcium channel blocker, blocks L-type voltage-gated calcium channels (in the vasculature mostly).
- These channels predominantly found in smooth muscle of blood vessels and in the heart muscle.
- Blocks influx of calcium into smooth muscle, necessary for contraction.
Digoxin:
Function: Increases contractility of the heart muscle, and steadies the heart rate (vagus nerve effects). Used in heart failure and arrhythmia.
Facts:
- Derived from the Digitalis plant
Mechanism of Action:
- Inhibits sodium-potassium pump, and in cardiac muscle cells, this causes build-up of Na+.
- Sodium-calcium exchange protein relies on export of 1 Ca2+ ion for 3 Na+ ions, when many Na+ in cell, pump is less efficient.
- Increase in Ca2+ causes positive inotropic effect (more actin/myosin interactions).
- Increased Ca2+ in baroreceptors (pressure receptors in heart), leads to stimulation of the vagus nerve, and a steadying of heart rate.
Verapamil:
Function: Negative inotropic effect, and negative chronotropic effect.
Facts:
- Belongs to group ‘non-dihydropyridines’.
Mechanism of action:
- Blocks L-type calcium channels (in the heart mostly)
- Decreases levels of Ca2+ in cardiac muscle cells
- Less interaction of actin and myosin, negative inotropic effect.
- Lower calcium leads to reduced firing of the sinoatrial node, negative chronotropic effect.
- Lower calcium causes negative dromotropic effect on AV node, leading to a steadier heart rate.
Heroin:
Function: Narcotic
Facts:
- Most heroin deacetylated in the liver to 6-monoacetylmorphine, then to morphine.
- ‘Diacetylmorphine’ can cross the blood-brain barrier
- Also deacetylated in the brain to intermediate 6-MAM, which is also more potent than morphine.
Mechanism of Action:
- Same as morphine.
Fosinopril:
Function: Lowers blood pressure and increases blood flow to the heart. Used to treat hypertension.
Facts:
- Angiotensin II is the main effector molecule in renin-angiotensin-aldosterone system, playing a critical role in the blood pressure, fluid and electrolyte balance.
- When blood pressure falls, decrease in NaCl in kidneys, renin cleaves angiotensinogen to become angiotensin I, ACE primarily in lungs converts to angiotensin II.
- Angiotensin II vasoconstrictor, stimulates release of aldosterone (promotes sodium and water retention in kidneys) and also triggers release of antidiuretic hormone.
Mechanism of Action:
- Inhibits ACE in lungs.
- Less angiotensin II
- Blood pressure drop, blood volume drop, and promotes diuresis.
Angiotensin II type 1 receptor blockers:
Function: Lower blood pressure and volume
Facts:
- Avoids inhibiting angiotensin II action on potentially protective effects from type 2 receptors, such as vasodilation and anti-inflammatory effects.
Mechanism of Action:
- Inhibits the GPCR Angiotensin II type 1.
- Angiotensin II cannot exert vasoconstrictive, fluid retention effects.
Nitrates:
(Nitroglycerine)
Function: Relieves chest pain associated with coronary heart disease. Protect heart by decreasing work done by heart and increasing blood flow to heart (coronary arteries).
Mechanism of Action:
- Converted to nitric oxide in the body
- Nitric oxide stimulates guanylate cyclase, increased cGMP.
- Higher cGMP leads to increase in protein kinase G.
- Higher PKG leads to vasodilation of smooth muscle.
Loop diuretics:
Function: Management of fluid overload syndromes (e.g. in heart failure), and edema.
Facts:
- Called so because it affects ‘Loop of Henle’
Mechanism of Action:
- Inhibits the Na/K/2Cl cotransporter in Loop of Henle.
- No ion movement out of Loop of Henle to blood.
- No reabsorption of water into blood at this point.
