Mode Of Action Flashcards
Insulin
Stimulates glucose uptake from circulation into tissues, glycogen, lipid and protein synthesis. Inhibits gluconeogenesis and ketogenesis
Sulphonylureas (Gliclazide)
Stimulates pancreatic insulin secretion by blocking ATP-dependant K+ channels causing depolarisation and opening of voltage gated Ca2+ channels
Biguanides (Metformin)
Increases response to insulin - suppresses hepatic glucose production, increases uptake and utilisation and suppresses intestinal absorbtion
Thyroxine
Replace endogenous hormones
Anti-Thyroid (Carbimazole)
Pro-drug metabolised to thiamazole to inhibit organification of iodine and coupling of iodothyronine which suppresses synthesis of thyroid hormone
Bisphosphonates (Alendronate)
Reduce bone turnover by inhibiting osteoclasts
Mineralocorticoid (Fludrocortisone)
Activates mineralocorticoid receptor to increase ion and H2O transport to raise extracellular volume and BP - lowering K+ levels
NAIDs (Diclofenac)
Inhibit synthesis of prostaglandins from arachidonic acid by inhibiting COX enzyme
Opiates (Codeine)
Metabolised in the liver to produce morphine which agonises Opioid U-receptors
Morphine
Activates Opioid U-receptors in CNS to reduce neuronal excitability.
Blunts response to hypoxia and hypercapnia in the medulla.
Reduce cardiac work and O2 demand
Paracetamol
Not Understood - weak COX 1 inhibitor
Xanthine-Oxidase-Inhibitor (Allopurinol)
Inhibits X-O to reduce metabolism of Xanthine to uric acid
Alpha-Blockers (Doxazocin)
Selective for a-adrenoreceptors found in smooth muscle cells to cause vasodilation and fall in BP
5-alpha-reductase Inhibitors (Finasteride)
Reduce the size of the prostate by inhibiting intracellular 5a-reductase enzyme that converts testosterone into dihydrotestosterone which stimulates pancreatic growth
Penicillins (Amoxicillin)
Inhibit the enzymes responsible for cross linking peptidoglycan in bacterial cell wall
Cephalosporins (Cephradine)
Inhibit the enzymes responsible for cross linking peptidoglycan in bacterial cell wall
Trimethorpim
Inhibit bacterial folate production
Nitrofurantoin
Metabolised by nitrofuran reductase to active component that damages bacterial DNA
`Tetracyclines (Doxyclycline)
Bind to 30s ribosome to inhibit protein synthesis and tRNA unable to bind to mRNA
Aminoglycosides (Gentamicin)
Irreversibly bind to 30s ribosome to inhibit bacterial synthesis
Macrolides (Erythromycin)
Bind 50s ribosome to block translocation
Quinolones (Ciprofloxacin)
Inhibit bacterial DNA synthesis
Anaerobic - Metronidazole
Passive diffusion into cell, then reduced to produce nitroso free radical which bind to DNA and reduces synthesis. (Aerobic bacteria unable to reduce metronidazole)
Glycopeptides (Vancomycin)
Inhibits growth and cross linking of peptidoglycan chains
Antacids (Gaviscon)
Buffer the stomach
H2-antagonists (Ranitidine)
Antagonise histamine receptors in parietal cells which secrete H+ into stomach
PPI (Omeprazole)
Irreversibly inhibit H+/ATP-ase in parietal cells
Anti-diarrhoea (Loperamide)
Opioid that doesn’t penetrate CNS - agonist of opioid u-receptors in GI tract to increase non-propulsive and decrease propulsive movements - slower transport of bowel contents
Laxative (Senna)
Increase water and electrolyte secretion, increasing colonic content and stimulating peristalsis
Aminosalicylate - (Mesalazine)
Releases 5-aminosalicylic acid which has anti-inflammatory effects
Anti-emetics (Metoclopramide)
Blocks dopamine receptors to reduce smooth muscle and LOS relaxation along with inhibiting the ‘vomiting centre’ in the medulla
Loop Diuretics (Furosemide)
Inhibit the Na+/K+/2Cl- transporter on the descending loop of Henle to reduce absorption and therefore water absorption.
Thiazide Diurects (Bendroflumathiazide)
Inhibit Na+/Cl- co-transporter in distal convoluted tubule to prevent reabsorption of Na and associated water - this is compensated for in the long term but does cause vasodilation
Potassium Sparing Diuretics (Spironolactone)
Competes with aldosterone which increases Na+ and H2O excretion and K+ retention
Beta-Blockers (Atenolol)
Block B1-adrenergic receptors on the heart to reduce force of contraction and speed of conduction
Calcium Antagonist (Diltiazem)
Block Ca2+ entry into cardiac cells, causing relaxation and vasodilation in arterial smooth muscle - reduces arterial pressure and myocardial contractility. Also slows contraction across the AV node
ACE Inhibitors (Ramipril)
Blocks conversion of AT1 to AT2 which blocks the action of the vasoconstrictor and reduces aldosterone secretion
AT1 Blockers (Losartan)
Block the action of AT2 on the AT1 receptors which reduces peripheral vascular resistance - work particularly on the efferent glomerular arteriole
Nitrates (Isorbide Mononitrate)
Converted to Nitric Oxide which increases guanosine monophosphate synthesis and reduces intracellular Ca2+ in vascular smooth muscle cells - causing relaxation
Cardiac Glycosides (Digoxin)
Increases Vagal tone to reduce contraction at the AV node and inhibits Na+/K+ ATP-ase pumps causing accumulation of Na+ in cells which causes accumualtion of Ca2+ which increases contractile strength
Anti-dysrhythmics (Amiodarone)
Blocks Na+/Ca2+/K+ channels along with antagonism of alpha and beta adrenergic receptors which reduces spontaneous depolarisation, slows conduction velocity and increases resistance to AV node depolarisation.
Aspirin
Irreversibly inhibits COX to reduce production of the pro-aggregatory factor Thromboxane from Arachidonic acid - reducing platelet aggregation
Clopidogrel
Irreversibly binds to Adenosine Diphosphate receptors on the surface of platelets to reduce aggregation (Process is synergistic with aspirin)
Thrombolytics (Tissue Plasminogen Activator)
Cleaves Zymogen Plasminogen at the Arg561-Val562 bond to convert it to plasmin which breaks down clots
Heparins (Enoxaparin)
Enoxaparin - Inhibits the action of Thrombin and Factor Xa to prevent formation of blood clots
Fondaparinux - Only FXa
Novel Anticoagulants (Rivaroxaban)
Direct Factor Xa inhibitor
Oral Anticoagulants (Warfarin)
Inhibits hepatic production of vitamin K dependant coagulation factors by inhibiting the enzyme vitamin K epoxide reductase to prevent Vit K from being reduced to its active form
Statins (Simvastatin)
Inhibit 3-hydroxy-3methyl-glutaryl co-enzyme A reductase which is used in making cholesterol. Also decrease hepatic production and increase clearance from the blood of LDL.
Beta-2-agonists (Salbutamol)
B2 receptors are in smooth muscle of bronchi, GI tract, Uterus and blood vessels - stimulation causes smooth muscle relaxation.
Also stimulates Na+/K+ ATP-ase pumps causing a shift of K+ into cells (Treat Hyperkalaemia)
Anticholinergics (Tiotropium)
Bind to muscarinic receptor to inhibit acetylcholine to reduce smooth muscle tone and secretions
Corticosteroids (Prednisolone)
Bind to cytosolic glucocorticoid receptors which then translocate to the nucleus and bind to glucocorticoid-response elements which regulate gene expression - Up-regulate anti-inflammatory genes and down-regulate pro-inflammatory genes
Mucolytics (Carbocysteine)
Reduce goblet cell hyperplasia and prevent conversion of serous cells to mucus cells
Theophylline
Xanthine derivative that relaxes smooth muslce to cause bronchodilation
Oxygen
Accelerates reabsorbtion of gas in Pneumothorax by reducing the fraction of N2 in the aveoli, increasing its diffusion out of the body
L-dopa (Modapor/Sinemet)
L-dopa can cross the BBB to increase conc and act as a dopamine receptor agonist and provide stimulation
Anticonvulsants (Phenytoin)
Reduces neuronal excitability and electrical conductance among brain cells by appearing to bind Na+ channels in their inactive state
Carbamazepine
Inhibits neuronal Na+ channels, stabilising their resting potentials and also blocks synaptic transmission in the trigeminal nucleus
Sodium Valproate
Appears to be a weak inhibitor of Na+ channels and also increases brain contents of y-aminobutyric acid (GABA) which is an inhibitory neurotransmitter
Lamotrigine
Na+ channel blocker that inhibits sustained firing of neurons and inhibits release of glutamate
Levitaracetam
Interacts with the synaptic vesicle protein 2A
Tricyclics (Amitryptilline)
Inhibits neuronal reuptake of serotonin and noradrenaline from the synaptic cleft, increasing their availability for neurotransmission by blocking muscarinic, histamine, a-adrenergic and dopamine receptors
SSRI’s (Citalopram)
Inhibit neuronal reuptake of serotonin but not noradrenaline
Benzodiazepines (Diazepam)
Target the y-aminobutyric acid type A receptors (GABA(a)) which is a chloride channel that opens in response to binding by GABA - the main inhibitory neurotransmitter - reducing neuronal excitability
Acetylcholinesterase Inhibitors (Donepezil)
Inhibits the enzyme responsible for the breakdown of acetylcholine which causes an increase in availability in the synapses of the brain allowing for greater conduction and brain activity.
