Group —> MoA Flashcards
(190 cards)
Antacids
Gastric Acid Neutralisation
Antacid + Alginate
Gastric Acid Neutralisation
H2 Receptor Antagonist
Blockade of gastric H2 histamine receptors
Proton Pump Inhibitor (PPI)
Blockade of Stomach Acid Transporters (H+ Pump)
Pancreatic Enzymes
Restoration of Pancreatic Enzymes
Bulk Laxatives
Polymers that aren’t broken down by normal digestion bulk up stool.
Water retained in the GI lumen, softening and increasing faecal bulk and promote increased motility.
Faecal Softner
Lower surface tension at oil-water interface allows water or fats to enter the stool and soften it.
Osmotic Laxative
Create an osmotic gradient which pulls water into the lumen of the colon leading to distensión of the colon and purgation.
Stimulant Laxatives
Stimulates rectal mucosa (myenteric plexus) resulting in mass movements.
Opioid Anti-Motility Agents
u-opioid receptor agonist in myenteric plexus blocking intestinal muscarinic receptors.
Loop Diuretics
Inhibits Na/K/2Cl transporter in the Loop of Henle which causes less water to be reabsorbed.
Thiazides
Decreases sodium and chloride reabsorption by inhibiting transporters.
Potassium Sparing Diuretics
Mineralocorticoid receptor blockade prevents production of co transporters leading to decreased K secretion and decreased Na reabsorption. (spironolactone, eplerenone)
Blockade of ENaC leads to decreased sodium reabsorption (amiloride)
Osmotic Diuretic
Increased plasma osmolarity causing water to leave cells and enter blood stream.
Carbonic Anhydrase Inhibitor
Inhibiting carbonic anhydrase prevents the reabsoprtion of Bicarbonate and therefore sodium and water,
H2CO3 reaction in PCT.
Reduces aqueous humour volume
ACEi
Inhibits conversion of Angiotensin 1 to angiotensin 2. Therefore blocking vasoconstriction.
ARBs
Blocks angiotensin 2 receptors and so blocks the renin-angiotensin system.
RAAS aim is to increase BP normally.
Neprilysin Inhibitor
Inhibtion of Natriuretic Peptide breakdown means increased concentration and so increased diuresis.
Given with ARBs because they prevent vasoconstriction?
Beta Blockers
Antagonism of beta adrenergic receptors leads to negative inotropy and chronotropy.
Alpha Blockers
Antagonism of Alpha adrenergic receptors leads to Vasodilation and a decrease in TPR.
CCB
Antagonism of calcium channels leads to blockage of vascular smooth muscle contraction (decreased vasoconstriction)
Nitrates
Nitric oxide release leads to smooth muscle relaxation and vasodilation
Sympathomimetics
Adrenergic stimulation leads to increased inotropy
Antiplatelets
Inhibition of Thromboxane synthesis (aspirin)
Inhibition of platelet activation by Adenosine Diphosphate (ADP) (clopidogrel)