Group —> MoA Flashcards
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)
Anticoagulant - Coumarin
Inhibition of Vitamin K epoxide reductase leads to decreased clotting.
Anticoagulant - Direct Thrombin Inhibitor
Inhibition of Thrombin
Anticoagulants - Direct Factor Xa inhibitors
Inhibition of Factor Xa in the coagulation cascade
Anticoagulants - Heparins
Inactivation of thrombin and factor Xa via complexing antithrombin III
Thromoblytics/Fibrinolytics
Activation of plasminogen for proteolytic breakdown of thrombus fibrin
HMG-CoA Reductase inhibitors
Inhibition of mavelonate pathway required for cholesterol synthesis
Class 1 Antiarrythmic
Voltage gated sodium channel blockage
Prolongs QT interval leading to increased QRS duration. Decrease chance of arrythmia
Class 2 Antiarrythmic
Beta adrenergic receptor blockage
reduction in adrenergic effects on rate and inotropy
Class 3 Antiarrythmic
Potassium channel blockage.
Evidence of beta blocker and calcium channel blocker properties
Prolongs QT interval
Class 4 Antiarrythmic
Cardiac calcium channel blockade
Reduction of action potential and cardiac output.
Cardiac Glycosides
Reduces conductivity of AV node.
Decreased HR
Adenosine
Activates adenosine receptors
Causes hyperpolarisation
Slows conduction through AV node.
Antimuscarinic (Anticholinergic)
Blockage of vagal muscarinic ACh receptors
Increases HR
Magnesium
Unclear
Possibly alters Na K Ca ion balance via channels and transporters.
Beta-2-Adrenergic Agonist
Dilation of bronchial smooth muscle
Antimuscarinics
Blocks muscarinic receptors to promote bronchial dilation
Methylxanthines
Bronchodilator by increasing cAMP in smooth muscle
Glucocorticoids
Reduction of inflammation and mucus production
Leukotriene Antagonist
Blockage of leukotriene receptors to reduce inflammation.
Mucolytic
Synthetic DNAse 1 - breakdown of extracellular DNA to reduce sputum viscosity. (dornase alfa)
Cleavage of mucous glycoproteins to reduce viscosity (Carbocisteine)
Dopaminergics
Increased dopamine synthesis and dopaminergic function. (Basal Ganglia)
Dopa-decarboxylase inhibitor
Stops breakdown of Levodopa in the periphery by inhibiting dopa-decarboxylase.
Monoamine Oxidase B Inhibitors (MAOI)
Inhibit the breakdown of dopamine
Catechol-O-methyl transferase inhibitor (COMT)
Blockade of dopamine precursor breakdown by inhibition of COMT.
Anticholinergics
Muscarinic cholinergic receptor antagonist.
Dopamine-depleting drugs
Blocks VMAT (vesicular monoamine transporter) preventing uptake of DA into vesicles.
Selective Serotonin reuptake inhibitors (SSRIs)
Inhibition of serotonin (5HT) reuptake pump in synaptic cleft
Reversible inhibitor of monoamine oxidase type A (RIMA)
Inhibits monoamine oxidase A, preferentially decreases breakdown of serotonin and noradrenaline
Tricylic Antidepressants (TCA)
Inhibition of noradrenaline and serotonin reuptake in synaptic cleft.
H1 antagonist
M1 antagonist
Adrenergic Antagonist.
Atypical Antidepressants Venlafaxine and Reboxetine
Noradrenaline reuptake inhibitor
Atypical Antidepressant Buproprion
Noradrenaline and Dopamine reuptake inhibitor
Atypical Antidepressant Agomelatine
Melatonin agonist
Atypical Antidepressant Mirtazepine
Alpha-2-antagonist
Antipsychotic 1st Generation
Selective D2 dopamine receptor blockade
Antipsychotic 2nd Generation
Selective D2 doapmine receptor blockade
5-HT receptor blockade
Mood Stabiliser
Unclear - possible neuronal calcium channel blockade.
Cholinesterase Inhibitor
Inhibition of Acetylcholinesterase (reversible)
NMDA receptor antagonist
VD blocker of NDMA
Anxiolytics
GABA Positive Allosteric Modulator (PAM) (y-subunit) increase GABA receptor acitivity.
5HT partial Agonist (buspirone)
Non-Benzodiazepine Hypnotic
GABA Positive Allosteric Modulator (PAM) (y-subunit) increase GABA receptor acitivity. (y-subunit)
Anti-Epilepsy Drugs (AEDs)
Sodium channel blockers.
Ethosuximide = Calcium channel blocker
Slows down action potentials to make seizures less likely.
Benzodiazepines
GABA positive allosteric modulator (PAM) (y-subunit) causing increased activity of GABA receptors to enhance GABA effects.
Benzodiazepine Antagonist
Antagonises GABA receptors and signalling.
Barbiturates
GABA Positive Allosteric Modulate (B-subunit) –> enhanced effect of GABA.
Weak Analgesic / Antipyretic
Unclear - Possible COX inhibitor in CNS.
NSAID
Non-selective COX inhibitors, blockade of prostaglandin (healing proteins) synthesis
COX2-selective NSAIDs
COX-2 inhibition, localised prostaglandin (healing proteins) blockade
Weak Opioid Analgesics
Stimulation of analgesic opioid receptors
Strong Opioid Analgesics
Stimulation of analgesic opioid receptors
Partial/mixed agonist opioid analgesics
Modulation of analgesic opioid receptors (u and k)
Opioid Antagonist
Opioid Receptor Antagonist
Opioid Addiction Management
Narcotic opioid replacement, opioid receptor agonist/modulator