9363673
Description
Flashcards by Amelia Claire, updated more than 1 year ago
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Created by Amelia Claire
almost 7 years ago
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| Question | Answer |
| Drugs for Anaemia | Iron deficient Anaemia Ferrous fumarate Ferrous sulfate Iron polymaltose Iron sucrose Ferric carboxymaltose B12 and Folic Acid Deficient Anaemia Cyanocobalamin Hydroxocobalamin Folic acid Anaemia linked to Chronic Disease Epoetin Darbepoetin |
| Ferric carboxymaltose | IV least likely to cause an immune reaction to the carbohydrate shell or toxic effects of labile iron from the iron oxyhydroxide core |
| Cyanocobalamin | cyanide moiety synthetic shorter half life oral or IM |
| Hydroxocobalamin | hydroxy group naturally occurring longer half life IM injection |
| Epoetin | Recombinant Human Erythropoietin Epo agonist mimics erythropoietin to stimulate erythropoiesis in the bone marrow, by binding to Epo receptors on progenitor cells. shorter half life |
| darbepoietin alfa | synthetic erythropoietin analogue Epo agonist mimics erythropoietin to stimulate erythropoiesis in the bone marrow, by binding to Epo receptors on progenitor cells. longer half life, less frequent dosing |
| drugs for dyslipidaemia | Statins; Atorvastatin Rosuvastatin Simvastatin Pravastatin Fluvastatin Fibrates: Fenofibrate Gemfibrozil Cholesterol Absorption Inhibitors Ezetimibe Bile Acid Binding Resins: Cholestyramine Colestipol Nitrates: Nicotinic acid (Niacin) PCSK9 inhibitors: Alirocumab Evolocumab Omega-3 fatty acids |
| Statins (DRUGS) | Shorter HALF LIFE Pravastatin Simvastatin Fluvastatin Longer Half life Rosuvastatin Atorvastatin |
| Statins MOA | Competitively inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (a rate-limiting enzyme in cholesterol synthesis). Increase hepatic cholesterol uptake from blood, reduce concentrations of total cholesterol, LDL and triglyceride (modest), and produce a small increase in HDL concentrations. |
| Pravastatin | Class: statin ( HMG-CoA reductase inhibitors) MOA: Competitively inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (a rate-limiting enzyme in cholesterol synthesis). Increase hepatic cholesterol uptake from blood, reduce concentrations of total cholesterol, LDL and triglyceride (modest), and produce a small increase in HDL concentrations. Metabolised: CYP450 |
| Simvastatin | Class: statin ( HMG-CoA reductase inhibitors) MOA: Competitively inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (a rate-limiting enzyme in cholesterol synthesis). Increase hepatic cholesterol uptake from blood, reduce concentrations of total cholesterol, LDL and triglyceride (modest), and produce a small increase in HDL concentrations. Metabolised: CYP3A4 |
| Fluvastatin | Class: statin ( HMG-CoA reductase inhibitors) MOA: Competitively inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (a rate-limiting enzyme in cholesterol synthesis). Increase hepatic cholesterol uptake from blood, reduce concentrations of total cholesterol, LDL and triglyceride (modest), and produce a small increase in HDL concentrations. Metabolised: CYP2C9 |
| Rosuvastatin | Class: statin ( HMG-CoA reductase inhibitors) MOA: Competitively inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (a rate-limiting enzyme in cholesterol synthesis). Increase hepatic cholesterol uptake from blood, reduce concentrations of total cholesterol, LDL and triglyceride (modest), and produce a small increase in HDL concentrations. Metabolised: CYP2C9 |
| Atorvastatin | Class: statin ( HMG-CoA reductase inhibitors) MOA: Competitively inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (a rate-limiting enzyme in cholesterol synthesis). Increase hepatic cholesterol uptake from blood, reduce concentrations of total cholesterol, LDL and triglyceride (modest), and produce a small increase in HDL concentrations. Metabolised: CYP3A4 |
| Adverse Effects of Statins | Pravastatin & Rosuvastatin less lipophilic = less myopathy Common AE’s: mild gastrointestinal symptoms, headache, changes to liver function tests, muscle-related adverse effects Monitor liver function tests Muscle-related side effects (myopathies) Myalgia - muscle pain Myositis – muscle inflammation Rhabdomyolysis – can be life threatening Destruction of striated muscle cells Myoglobin, K+, creatinine kinase (+more) released High myoglobin in bloodstream = kidney injury |
| Fibrates (drugs) | Fenofibrate Gemfibrozil |
| Fibrates MOA | Fibrates activate the peroxisome proliferator activated receptors (PPAR) and modulate lipoprotein synthesis and catabolism. PPAR alters expression of lipid metabolism in genes. PPAR alpha activation leads to increased lipoprotein lipase in muscle Increased uptake and oxidation of fatty acid in muscle cells Increased fatty acid and oxidation in liver reduced TGI synthesis and incased Apoprotein 1 and 2 ligands for specific receptors, increasing HDLs |
| Fenofibrate | Class: Fibrate MOA: Activate peroxisome proliferator-activated receptors (PPAR) & modulate lipoprotein synthesis & catabolism--> PPAR alters expression of lipid metabolism genes |
| Gemfibrozil | Class: Fibrate MOA Activate peroxisome proliferator-activated receptors (PPAR) & modulate lipoprotein synthesis & catabolism--> PPAR alters expression of lipid metabolism genes |
| Fibrates: AEs | Metabolite of fenofibrate = fenofibric acid → photoexcitation → intersystem crossing to triplet excited state → damage to cellular components → inflammation |
| Cholesterol Absorption Inhibitor | Ezetimibe |
| Ezetimibe | lass: Cholesterol Absorption Inhibitor / other drugs for dyslipidaemia Mode of action reduces binding of AP2 clathrin to NPC1L1 to ↓ cholesterol absorption Reduces absorption of dietary and biliary cholesterol by inhibiting its transport across the intestinal wall. This leads to an increased demand for cholesterol, an increase in LDL uptake and its removal from the plasma. Doesn’t interfere with absorption of triglycerides, fat-soluble vitamins or fat-soluble drugs Metabolised: in liver, excreted in bile to GI lumen where it can work again → enterohepatic circuit increases half-life |
| Bile Binding Acid Resins (Drugs) | Cholestyramine Colestipol |
| Bile Acid Binding Resins (MOA) | Cholesterol is converted to bile acids in the liver Bile acids are secreted into the GI tract, can be reabsorbed Bile acid binding resins sequester bile in GI tract = ↑ excretion in faeces More LDL cholesterol moves from blood stream to liver to form bile acids Mode of action Bind bile acids in intestinal lumen, preventing reabsorption, and increasing bile acid excretion in the faeces. Increased demand for cholesterol for bile acid synthesis results in an increase in LDL uptake and removal from plasma. |
| Cholestyramine and Colestipol | Cholesterol is converted to bile acids in the liver Bile acids are secreted into the GI tract, can be reabsorbed Bile acid binding resins sequester bile in GI tract = ↑ excretion in faeces More LDL cholesterol moves from blood stream to liver to form bile acids Mode of action Bind bile acids in intestinal lumen, preventing reabsorption, and increasing bile acid excretion in the faeces. Increased demand for cholesterol for bile acid synthesis results in an increase in LDL uptake and removal from plasma. |
| Bile acid binding resins - precautions | May increase triglycerides, cause steatorrhoea & reduce absorption of fat-soluble vitamins Less bile acids available for digestion May need to sup ADEK Ineffective if complete biliary obstruction No bile reaching the resins in the GI lumen May worsen constipation, diverticular disease, haemorrhoids Adding bulk to the stool May bind to & alter absorption of other rx Warfarin, digoxin, thyroxine – need to separate doses |
| Nicotinic Acid / Niacin *Nitrates* | Class: ~ Other drugs for dyslipidaemia Mode of action Mechanism of action is unclear Thought to decrease VLDL, ILD, LDL by: * Suppressing fatty acid release from adipose tissue * Reducing TG synthesis, via inhibition of DGAT2 enzyme * Increasing apoprotein B catabolism Thought to increase HDL by: * Increasing hepatic uptake of & production of apoprotein A * Reducing cholesteryl ester transfer protein * Reducing HDL uptake by inhibiting beta chain ATP synthase |
| Adverse effects of Nicotinic acid | Nicotinic acid induced flushing Nicotinic acid binds to receptor on epidermal Langerh cells → prostaglandin release → vasodilation Prevented by pre-administration of aspirin Hyperglycaemia Niacin receptor GPR109A found on islet cells → islet cell dysfunction Hyperuricaemia, may precipitate gout Increases urate resorption in kidney decreases urate excretion Nicotinate functions as counter-ion for main uric acid transporter URAT1 Myopathy (rare) |
| Proprotein convertase subtilisin-kexin type 9 (PCSK9) inhibitors (DRUGS) | alirocumab evolocumab |
| Proprotein convertase subtilisin-kexin type 9 (PCSK9) inhibitors MOA | Mode of action Human monoclonal antibody that binds to proprotein convertase subtilisin/kexin type 9 (PCSK9). It inhibits PCSK9 degradation of LDL receptors which increases the number of LDL receptors thereby increasing hepatic LDL uptake and reducing serum LDL. |
| alirocumab | Class: Proprotein convertase subtilisin-kexin type 9 (PCSK9) inhibitors MOA: Human monoclonal antibody that binds to proprotein convertase subtilisin/kexin type 9 (PCSK9). It inhibits PCSK9 degradation of LDL receptors which increases the number of LDL receptors thereby increasing hepatic LDL uptake and reducing serum LDL. SUBCUT every 2-4 weeks |
| evolocumab | Class: Proprotein convertase subtilisin-kexin type 9 (PCSK9) inhibitors MOA: Human monoclonal antibody that binds to proprotein convertase subtilisin/kexin type 9 (PCSK9). It inhibits PCSK9 degradation of LDL receptors which increases the number of LDL receptors thereby increasing hepatic LDL uptake and reducing serum LDL. SUBCUT 2-4 weeks |
| Omega-3 fatty acids - Fish oil derivatives MOA + AE | MOA Inhibit release of TGs from the liver Reduces VLDL and therefore LDL Stimulate lipoprotein lipase to increase clearance of TGs from plasma May have anticoagulant and anti-inflammatory effects Adverse effects: gastrointestinal upset, fishy aftertaste |
| drugs for thrombosis | Aspirin ADP, P2Y12 antagonists Clopidogrel Prasugrel Ticagrelor PDE Inhibitor Dipyridamole Glycoprotein IIb/IIIa antagonists Abciximab Tirofiban Warfarin Indirect Thrombin Inhibitors Unfractionated heparin Enoxaparin Fondaparinux Direct Thrombin Inhibitors Dabigatran Factor Xa inhibitors Apixaban Rivaroxaban Tissue plasminogen activator (t-PA) analogues Alteplase Tenecteplase haemostatic agent / Antifibrinolytic Vitamin K Tranexamic acid Protamine Idarucizumab |
| Aspirin - anti platelet (Cyclo-oxygenase (COX) inhibitors) | Mode of action Inhibits platelet aggregation by irreversibly inhibiting cyclo-oxygenase, reducing the synthesis of thromboxane A2 (an inducer of platelet aggregation) for the life of the platelet. Non-selective COX I & II inhibitors can cause adverse effects via reduced production of off-target prostaglandins |
| Adenosine diphosphate (ADP, P2Y12) antagonists (drugs) | Antiplatelets Clopidogrel Prasugrel Ticagrelor |
| Adenosine diphosphate (ADP, P2Y12) antagonists MOA | Mode of action: (clopidogrel, prasugrel) The active metabolite of the thienopyridines irreversibly binds to the platelet P2Y12 receptor and inhibits platelet aggregation for the life of the platelet. MOA: Ticagrelor binds reversibly to the P2Y12 receptor. |
| Clopidogrel | Class: Adenosine diphosphate (ADP, P2Y12) antagonists The active metabolite of the thienopyridines irreversibly binds to the platelet P2Y12 receptor and inhibits platelet aggregation for the life of the platelet. Prodrug - 2 CYP450 Dependent Steps Daily Dosing |
| Prasugrel | Class: Adenosine diphosphate (ADP, P2Y12) antagonists MOA: Delivered as Prodrug: 1x plasma esterase + 1 CYP450 dependent step to become active metabolite. The active metabolite of the thienopyridines irreversibly binds to the platelet P2Y12 receptor and inhibits platelet aggregation for the life of the platelet. |
| Ticagrelor | Class: Adenosine diphosphate (ADP, P2Y12) antagonists MOA: Ticagrelor binds reversibly to the P2Y12 receptor. Non-competitively inhibits ADP dependent platelet activation & aggregation |
| Phosphodiesterase (PDE) inhibitors drug and MOA | Dipyridamole Mode of action Inhibiting reuptake of adenosine Inhibiting PDE to increase cAMP within platelets -> decreases Ca2+ Platelet aggregation and activation inhibited Inhibits platelet function by inhibiting phosphodiesterase, which increases platelet cAMP. |
| Dipyridamole | Class: Phosphodiesterase (PDE) inhibitors Mode of action Inhibiting reuptake of adenosine Inhibiting PDE to increase cAMP within platelets -> decreases Ca2+ Platelet aggregation and activation inhibited from AMH Inhibits platelet function by inhibiting phosphodiesterase, which increases platelet cAMP. |
| Glycoprotein IIb/IIIa antagonists drugs and MOA | Abciximab Tirofiban Mode of action Prevent binding of fibrinogen to platelet, by occupying glycoprotein IIb/IIIa receptor, thereby blocking platelet aggregation. |
| Abciximab | Class: Glycoprotein IIb/IIIa antagonists Mode of action Prevent binding of fibrinogen to platelet, by occupying glycoprotein IIb/IIIa receptor, thereby blocking platelet aggregation. Abciximab is a chimeric monoclonal antibody. |
| Tirofiban | Class: Glycoprotein IIb/IIIa antagonists Mode of action Prevent binding of fibrinogen to platelet, by occupying glycoprotein IIb/IIIa receptor, thereby blocking platelet aggregation. Tirofiban is a non-peptide antagonist |
| Warfarin | Class: Vitamin K Antagonist Mode of action Vitamin K antagonist; inhibits synthesis of vitamin K-dependent clotting factors (II, VII, IX, X) and the antithrombotic factors protein C and protein S. Racemic mix: S-warfarin 2-5x more anticoagulant Narrow therapeutic index Susceptible to drug-drug & drug-food interactions |
| indirect thrombin inhibitors drugs and MOA | heparin enoxaparin fondaparinux Induce conformational change to increase in antithrombin III to its efficacy inhibiting Xa (and thrombin for heparin) |
| heparin | Class: indirect thrombin inhibitors MOA: inhibits factor Xa and thrombin by Inducing conformational change to increase in antithrombin III to its efficacy inhibiting Xa and thrombin |
| enoxaparin | Class: indirect thrombin inhibitors MOA: inhibits factor Xa and thrombin by Inducing conformational change to increase in antithrombin III to its efficacy inhibiting Xa |
| fondaparinux | Class: Factor Xa inhibitor // indirect thrombin inhibitors MOA: inhibits factor Xa and thrombin by Inducing conformational change to increase in antithrombin III to its efficacy inhibiting Xa Selectively inhibit factor Xa, blocking thrombin production, conversion of fibrinogen to fibrin, and thrombus development. |
| Direct thrombin inhibitors Drugs and MOA | dabigatran MOA: Reversibly inhibit both free and fibrin-bound thrombin, preventing conversion of fibrinogen to fibrin, preventing thrombus formation. Thrombin-induced platelet aggregation is also inhibited. Reversible, competitive inhibitor of thrombin → prevents conversion of fibrinogen to fibrin: |
| dabigatran | Class: Direct Thrombin Inhibitor MOA: Reversibly inhibit both free and fibrin-bound thrombin, preventing conversion of fibrinogen to fibrin, preventing thrombus formation. Thrombin-induced platelet aggregation is also inhibited. Reversible, competitive inhibitor of thrombin → prevents conversion of fibrinogen to fibrin |
| Factor Xa inhibitors drugs and MOA | apixaban rivaroxaban MOA: Selectively inhibit factor Xa, blocking thrombin production, conversion of fibrinogen to fibrin, and thrombus development. Both metabolized CYP3A4 & both substrates of P-gp -> risk of drug interactions |
| apixaban | Class: Factor Xa Inhibitors MOA: Selectively inhibit factor Xa, blocking thrombin production, conversion of fibrinogen to fibrin, and thrombus development. metabolized: CYP3A4 & both substrates of P-gp -> risk of drug interactions |
| rivaroxaban | Class: Factor Xa Inhibitors MOA: Selectively inhibit factor Xa, blocking thrombin production, conversion of fibrinogen to fibrin, and thrombus development. metabolized: CYP3A4 & both substrates of P-gp -> risk of drug interactions |
| Tissue plasminogen activator (t-PA) analogues drugs and MOA | Alteplase Tenecteplase Fibrinolytic/thrombolytic agents. Convert plasminogen to plasmin, which catalyses the breakdown of fibrin. Analogues of human tPA developed More specific to clot-bound plasminogen, no immune response |
| Alteplase | Class: Fibrinolytic/thrombolytic agents // Tissue plasminogen activator (t-PA) analogues MOA: Convert plasminogen to plasmin, which catalyses the breakdown of fibrin. Exact copy of human t-PA Short half-life, need IV infusion |
| Tenecteplase | Class: Fibrinolytic/thrombolytic agents // Tissue plasminogen activator (t-PA) analogues MOA: Convert plasminogen to plasmin, which catalyses the breakdown of fibrin Higher binding affinity for plasmin vs alteplase Longer half-life, can give IV bolus Not inactivated by plasminogen activator inhibitor (PAI-1) |
| Tissue plasminogen activator (t-PA) analogues adverse effects and risks | Alter haemostasis more profoundly than any other anticoagulants → Greatest risk for bleeding complications Many contraindications to fibrinolysis Concurrent antiplatelet or anticoagulant drugs increase risk of bleeding but combinaGons can be required |
| haemostatic agent / Antifibrinolytic | Tranexamic acid Vitamin K |
| Tranexamic Acid | Class: haemostatic agent / Antifibrinolytic Mode of action Inhibits breakdown of clots by blocking binding of plasminogen and plasmin to fibrin. Inhibits fibrinolysis: Competitive inhibitor of plasminogen activation At high doses = non-competitive inhibitor of plasmin Onset of action 5-15 min Cleared renally – may require dose adjustment |
| Vitamin K | Class: haemostatic agent / Antifibrinolytic/ antidote reversal agent Mode of action Essential cofactor in the synthesis of blood clotting factors II, VII, IX and X, and proteins C and S; reverses effect of vitamin K antagonists. Indications Haemorrhage or threatened haemorrhage due to severe hypoprothrombinaemia, eg from excessive dose of warfarin, hypovitaminosis K Prevention and treatment of haemorrhagic disease of the newborn |
| Drugs for reversing anticoagulation | Idarucizumab Protamine Vitamin K |
| Protamine | class: Drugs for reversing anticoagulation Mode of action Combines with heparin to form a stable inactive complex, reversing its anticoagulant effect. heparin & enoxaparin reversal Indications Heparin, dalteparin or enoxaparin overdose in patients with, or at high risk of, severe haemorrhage |
| Idarucizumab | class: Drugs for reversing anticoagulation Mode of action Humanised monoclonal antibody fragment (Fab) that binds with dabigatran and its metabolites to form a stable inactive complex, reversing their anticoagulant effect. Indications Rapid reversal of anticoagulant effects of dabigatran: in life-threatening or uncontrolled bleeding for emergency surgery or urgent procedures |
| drugs for Ischaemic Heart Disease | BBs Metoprolol Atenolol CCBs Amlodipine Nifedipine Diltiazem Verapamil organic nitrates Glyceryltrinitrate Isosorbide mononitrate Isosorbide dinitrate other drugs for angina Nicorandil Ivabradine Perhexiline |
| Beta Blockers drugs to know for exam and basic MOA | Metoprolol Atenolol Competitive antagonism of beta-adrenoceptors Reduce myocardial oxygen demand Reduced heart rate Reduced contractility |
| Atenolol | class: beta blocker Beta-1 selective ‘cardioselective’ antagonists Competitive antagonism of beta-adrenoceptors Reduce myocardial oxygen demand Reduced heart rate Reduced contractility renal clearance longer half life |
| Metoprolol | class: beta blocker Beta-1 selective ‘cardioselective’ antagonist Competitive antagonism of beta-adrenoceptors Reduce myocardial oxygen demand Reduced heart rate Reduced contractility hepatic Clearance short half life |
| Calcium channel blockers Dihydropyridines (end with ‘pine’ ) | Amlodipine Nifedipine Dihydropyridines act mainly on arteriolar smooth muscle to reduce peripheral vascular resistance and BP. They have minimal effect on myocardial cells. Block inward current of calcium into cells in vascular smooth muscle, myocardium and cardiac conducting system via L‑type calcium channels. Act on coronary arteriolar smooth muscle to reduce vascular resistance and myocardial oxygen requirements, relieving angina symptoms. |
| Calcium Channel Blockers Non-dihydropyridine | Diltiazem (a Benzothiazepine) Verapamil (a Phenylalkylamine) |
| Amlodipine | Class: Calcium Channel Blocker - Dihydropyridines Block inward current of calcium into cells in vascular smooth muscle, myocardium and cardiac conducting system via L‑type calcium channels. Act on coronary arteriolar smooth muscle to reduce vascular resistance and myocardial oxygen requirements, relieving angina symptoms. Dihydropyridines: * act mainly on arteriolar smooth muscle to reduce PERIPHERAL vascular resistance and BP. * They have minimal effect on myocardial cells. |
| nifedipine | Class: Calcium Channel Blocker - Dihydropyridines Block inward current of calcium into cells in vascular smooth muscle, myocardium and cardiac conducting system via L‑type calcium channels. Act on coronary arteriolar smooth muscle to reduce vascular resistance and myocardial oxygen requirements, relieving angina symptoms. Dihydropyridines: * act mainly on arteriolar smooth mscle to reduce PERIPHERAL vascular resistance and BP. * They have minimal effect on myocardial cells. |
| diltiazem ( a Benzothiazepine) | Class: Calcium Channel Blockers / non-dihydropyeridine MOA: Block inward current of calcium into cells in vascular smooth muscle, myocardium and cardiac conducting system via L‑type calcium channels. Act on coronary arteriolar smooth muscle to reduce vascular resistance and myocardial oxygen requirements, relieving angina symptoms. Non-dihydropyridines: diltiazem acts on cardiac and arteriolar smooth muscle to reduce cardiac contractility, heart rate and conduction. |
| Verapamil (a Phenylalkylamine) | Class: Calcium Channel Blockers / non-dihydropyeridine MOA: Block inward current of calcium into cells in vascular smooth muscle, myocardium and cardiac conducting system via L‑type calcium channels. Act on coronary arteriolar smooth muscle to reduce vascular resistance and myocardial oxygen requirements, relieving angina symptoms. Non-dihydropyridines: Verapamil acts on cardiac and arteriolar smooth muscle to reduce cardiac contractility, heart rate and conduction, with verapamil having the greater effect. |
| Calcium Channel Blockers AEs | Depend on type/properties of CCB Headache, flushing, peripheral oedema Constipation, dyspepsia Gingival hyperplasia Overgrowth of gums Rare, most common with nifedipine Reversible when CCB ceased Most CCBs susceptible to CYP3A4 mediated drug interactions |
| organic nitrates - drugs and MOA | Glyceryltrinitrate (GTN or nitroglycerin) Isosorbide mononitrate (ISMN) Isosorbide dinitrate (ISDN) Mode of action Decrease myocardial oxygen demand Dilates veins to decrease preload At high doses dilates arteries to reduce afterload Improve myocardial oxygen supply by Inducing coronary vasodilation Relaxation of coronary vessels decreases spasms (variant angina) |
| Glyceryltrinitrate (GTN or nitroglycerin) | Provide exogenous source of nitric oxide (which mediates vasodilator effects). Predominantly venodilators; reduce venous return and preload to the heart, reducing myocardial oxygen requirement.. DFD = Sublingual spray & tablets, transdermal patch, IV infusion metabolism: 1. Denitration to dinitrates (t1/2 = 40 min) 2. Glucuronidation very very short half life 1- 3 minutes |
| Isosorbide mononitrate (ISMN) | Provide exogenous source of nitric oxide (which mediates vasodilator effects). Predominantly venodilators; reduce venous return and preload to the heart, reducing myocardial oxygen requirement. DFD = Controlled release tablets Metabolism: 1. Denitration to isosorbide 2. Glucuronidation |
| Isosorbide dinitrate (ISDN) | Provide exogenous source of nitric oxide (which mediates vasodilator effects). Predominantly venodilators; reduce venous return and preload to the heart, reducing myocardial oxygen requirement.DFD = sublingual and oral tablets Metabolism: 1. Denitration to mononitrates (t1/2 2-4 h) 2. Glucucronidation |
| Tolerance to nitrates | Tolerance to vasodilator effect develops in 60% of patients if used continuously to prevent angina Need a nitrate free period each day to maintain efficacy GTN patch on 0800, off 2000 or min 8 h off each night Time nitrate free period when symptoms least likely Mechanism of tolerance not fully understood ?? Related to reduced production of nitric oxide (NO) |
| Potassium channel activators drug and MOA | Nicorandil Mode of action Produces venous and arterial dilation due to its nitrate moiety and its effect on potassium channels in vascular smooth muscle; improves myocardial oxygen balance and decreases angina. |
| Nicorandil | lass: Potassium Channel Activator / drugs for angina Opens K+ channels of vascular smooth muscle → K+ moves out of cell → hyperpolarisation → muscle contraction inhibited Also a nitrate donor Decreases myocardial oxygen demand Dilation of arteries to reduce afterload Some dilation of veins to decrease preload |
| Ivbradine | Class; other drugs for angina MOA: simple Blocks sodium channels in the sino-atrial node Increases interval between depolarisation Reduces heart rate Decreases myocardial oxygen demand Mode of action: technical Ivabradine inhibits a current regulating the interval between depolarisations of the sinoatrial (SA) node. It reduces heart rate (by about 10 beats/minute) which in turn lowers cardiac workload and myocardial oxygen demand. |
| Perhexiline | MOA: Inhibits enzyme involved in long-chain fatty acid metabolism in the heart → Glucose metabolism predominates Oxidation of glucose requires less oxygen than oxidation of fatty acids = reduces myocardial oxygen requirements Narrow therapeutic index Requires therapeutic drug monitoring Non-linear pharmacokinetics Adverse effects: neurotoxicity, hepatotoxicity Metabolised by polymorphic CYP2D6 = large interindividual variation in dose required |
| Drugs for Heart Failure | ACE inhibitors Captopril Enalapril Perindopril Ramipril Sartans Candesartan Irbesartan Neprilysin Inhibitor Sacubitril BBs Bisoprolol Carvedilol Metoprolol Diuretics Frusemide (furosemide) Aldosterone Antagonist Spironolactone Digoxin |
| Angiotensin I converting enzyme (ACE) inhibitors drugs and MOA | Captopril - active drug Enalapril - prodrug Perindopril - prodrug Ramipril - prodrug ACE inhibitors block conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. They reduce the effects of angiotensin II-induced vasoconstriction, sodium retention and aldosterone release. They also reduce the effect of angiotensin II on sympathetic nervous activity and growth factors. |
| Captopril | MOA: ACE inhibitors block conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. They reduce the effects of angiotensin II-induced vasoconstriction, sodium retention and aldosterone release. They also reduce the effect of angiotensin II on sympathetic nervous activity and growth factors. Shorter Half Life - Active Drug, chance of rash due to sulphur moiety |
| Enalapril | Class: ACE inhibitor MOA: ACE inhibitors block conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. They reduce the effects of angiotensin II-induced vasoconstriction, sodium retention and aldosterone release. They also reduce the effect of angiotensin II on sympathetic nervous activity and growth factors. Prodrug |
| Ramipril | Class: ACE Inhibitor MOA: ACE inhibitors block conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. They reduce the effects of angiotensin II-induced vasoconstriction, sodium retention and aldosterone release. They also reduce the effect of angiotensin II on sympathetic nervous activity and growth factors. Prodrug |
| Perindopril | Class: ACE inhibitors MOA: ACE inhibitors block conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. They reduce the effects of angiotensin II-induced vasoconstriction, sodium retention and aldosterone release. They also reduce the effect of angiotensin II on sympathetic nervous activity and growth factors. Prodrug |
| Angiotensin II receptor blockers (ARBs) or ‘Sartans’ | Irbesartan Candesartan Mode of action Competitively block binding of angiotensin II to type 1 angiotensin (AT1) receptors. They reduce angiotensin II-induced vasoconstriction, sodium reabsorption and aldosterone release. They also reduce the effect of angiotensin II on sympathetic nervous activity and growth factors. |
| Ibersartan | Class: Sartan /ARB Mode of action Competitively block binding of angiotensin II to type 1 angiotensin (AT1) receptors. They reduce angiotensin II-induced vasoconstriction, sodium reabsorption and aldosterone release. They also reduce the effect of angiotensin II on sympathetic nervous activity and growth factors. |
| Candesartan | Class; Sartan / ARB MOA: Mode of action Competitively block binding of angiotensin II to type 1 angiotensin (AT1) receptors. They reduce angiotensin II-induced vasoconstriction, sodium reabsorption and aldosterone release. They also reduce the effect of angiotensin II on sympathetic nervous activity and growth factors. Prodrug |
| Neprilysin inhibitors | sacubitril Mode of action The active metabolite of sacubitril inhibits neprilysin reducing degradation of natriuretic peptides. It also increases angiotensin II concentration which is blocked by valsartan. The combination produces vasodilation, increases glomerular filtration rate, reduces sympathetic tone and aldosterone release, and increases bradykinin levels. |
| Sacubitril | Class: Neprilysin Inhibitor Mode of action The active metabolite of sacubitril inhibits neprilysin reducing degradation of natriuretic peptides. It also increases angiotensin II concentration which is blocked by valsartan. The combination produces vasodilation, increases glomerular filtration rate, reduces sympathetic tone and aldosterone release, and increases bradykinin levels. Heart Failure |
| beta blockers for heart failure | Bisoprolol β1 Carvedilol β1, β2, α1 Metoprolol β1 |
| Bisoprolol | Class: Beta Blocker - β1 selective (hepatic CL + renal CL) Indication: heart failure MOA: Competitively block beta receptors in heart, to slow heart rate. Beta-blockers reduce heart rate, BP and cardiac contractility; also depress sinus node rate and slow conduction through the atrioventricular (AV) node, and prolong atrial refractory periods. The affinity of individual beta-blockers for beta receptors varies |
| metoprolol | Class: Beta Blocker selective β1 - hepatic clearance Indication: heart failure MOA: Competitively block beta receptors in heart, to slow heart rate. Beta-blockers reduce heart rate, BP and cardiac contractility; also depress sinus node rate and slow conduction through the atrioventricular (AV) node, and prolong atrial refractory periods. The affinity of individual beta-blockers for beta receptors varies |
| Carvedilol β1, β2, α1 | Class: Beta Blocker non selective (β1, β2, α1) hepatic CL Indication: heart failure MOA: Competitively block beta receptors in heart, to slow heart rate. Beta-blockers reduce heart rate, BP and cardiac contractility; also depress sinus node rate and slow conduction through the atrioventricular (AV) node, and prolong atrial refractory periods. The affinity of individual beta-blockers for beta receptors varies |
| frusemide (loop diuretic) | Class: Loop Diuretic Indication: heart failure / oedema related to heart failure MOA: Inhibit reabsorption of sodium and chloride in the ascending limb of the loop of Henle. This site accounts for retention of approximately 20% of filtered sodium; therefore, these are potent diuretics. Produce a rapid and intense diuresis and have a short duration of action (4–6 hours). They are effective over a wide dose range with a dose-related response. |
| loop diuretics most potent | loop diuretics most potent, increase water and sodium excretion in kidney, reducing intravascular volume, reducing preload. |
| Aldosterone Antagonist | Spironolactone Indication: heart failure MOA: Inhibit sodium absorption in the distal tubule by antagonising aldosterone, increasing sodium and water excretion and reducing potassium excretion; they are weak diuretics. Aldosterone may contribute to the pathophysiology of heart failure; by reducing aldosterone activity, aldosterone antagonists improve outcome. |
| Digoxin | Class: Antiarrhythmic Indication: heart failure MOA: Slows heart rate and reduces AV nodal conduction by an increase in vagal tone and a reduction in sympathetic activity. Increases the force of myocardial contraction by increasing the release and availability of stored intracellular calcium. inhibits Na+/K+ ATPase transport pump, increases intracellular calcium, increasing ejection fraction and cardiac output. |
| drugs for allergic rhinitis | Cromoglycate Nedocromil Ipratropium Dexchlorpheniramine Promethazine Loratadine Cetirizine Fexofenadine |
| Cromoglycate | class: other drugs for rhinitis intranasal / inhaled / eyedrops allergic rhinitis only mast cell stabiliser - prevents then degranulation and release of histamine from mast cells |
| Ipratropium | anticholinergic Class: Other Drugs for Rhinitis Dries nasal secretions and may reduce rhinorrhoea. |
| Nedocromil | cromone mast cell stabilisation Act by inhibiting release of inflammatory mediators from mast cells. |
| sedating antihistaines | Dexchlorpheniramine Promethazine inverse agonist MOA: Reduce the effects of histamine by binding to the H1 receptor and stabilising it in an inactive form. Promethazine also has anticholinergic activity and alpha-blocking activity |
| Dexchlorpheniramine Promethazine | sedating antihistamines inverse agonist MOA: Reduce the effects of histamine by binding to the H1 receptor and stabilising it in an inactive form. Promethazine also has anticholinergic activity and alpha-blocking activity |
| less-sedating antihistamines | Loratadine Cetirizine Fexofenadine Class: less sedating antihistamine inverse agonist Reduce the effects of histamine by binding to the H1 receptor and stabilising it in an inactive form. |
| Loratadine Cetirizine Fexofenadine | Class: less sedating antihistamine inverse agonist Reduce the effects of histamine by binding to the H1 receptor and stabilising it in an inactive form. |
| Drugs for Glaucoma | Latanoprost Bimatoprost Timolol Betaxolol Apraclonidine Brimonidine Acetazolamide Brinzolamide Dorzolamide |
| prostaglandin analogues (eye) | Latanoprost bimatoprost indication: glaucoma MOA: Reduce intraocular pressure by increasing uveoscleral outflow of aqueous humour. |
| beta blockers for glaucoma | Timolol (non selective) Betaxolol (β1 selective) MOA: Reduce aqueous humour formation, probably by blockade of beta receptors on the ciliary epithelium. |
| Timolol (non selective) | Class - beta blockers for glaucoma MOA: Reduce aqueous humour formation, probably by blockade of beta receptors on the ciliary epithelium. |
| Betaxolol (β1 selective) | Class - beta blockers for glaucoma MOA: Reduce aqueous humour formation, probably by blockade of beta receptors on the ciliary epithelium. |
| α2 agonists for glaucoma | apraclonidine and brimonidine MOA: Reduce intraocular pressure by suppressing formation and increasing uveoscleral outflow of aqueous humour. |
| apraclonidine | sympathomimetic / vasoconstriction Indication: Glaucoma MOA: Reduce intraocular pressure by suppressing formation and increasing uveoscleral outflow of aqueous humour. |
| brimonidine | class: α2 agonist sympathomimetic / vasoconstriction Indication: Glaucoma MOA: Reduce intraocular pressure by suppressing formation and increasing uveoscleral outflow of aqueous humour. |
| Systemic carbonic anhydrase inhibitor drug and MOA | Acetazolamide Inhibits carbonic anhydrase and therefore bicarbonate synthesis; in the eye this reduces aqueous humour secretion and thereby intraocular pressure; in the brain this leads to the accumulation of carbon dioxide, reducing the spread of seizure activity. |
| carbonic anhydrase inhibitors | Brinzolamide Dorzolamide MOA: Inhibit carbonic anhydrase II (predominant subtype found in the eye), which reduces aqueous humour formation. |
| Brinzolamide | Class: Carbonic anhydrase inhibitors Indication: Glaucoma MOA: Inhibit carbonic anhydrase II (predominant subtype found in the eye), which reduces aqueous humour formation. |
| Dorzolamide | Class: Carbonic anhydrase inhibitors Indication: Glaucoma MOA: Inhibit carbonic anhydrase II (predominant subtype found in the eye), which reduces aqueous humour formation. |
| Other eye drugs: | Atropine Cyclopentolate Tropicamide Phenylephrine Naphazoline Tetrahydrozoline Carmellose Hypromellose |
| anticholinergics (eyes) drugs and MOA | atropine, cyclopentolate, tropicamide MOA: Reversibly block acetylcholine receptors on iris sphincter and ciliary muscle. |
| Atropine (eye) | Class: anticholinergic Indications from Anticholinergics Mydriasis (dilation of pupil): examination of peripheral lens and retina; prevention or breakdown of posterior synechiae from iritis; prevention of pupil constriction in iritis Cycloplegia (relaxation of ciliary body): diagnostic refraction; pain relief in uveitis; chemical occlusion for treatment of suppression amblyopia; ciliary block glaucoma (rare) MOA: Reversibly block acetylcholine receptors on iris sphincter and ciliary muscle. |
| Cyclopentolate | anticholinergic Reversibly block acetylcholine receptors on iris sphincter and ciliary muscle. |
| Tropicamide | anticholinergic Reversibly block acetylcholine receptors on iris sphincter and ciliary muscle. |
| vasoconstrictors (eyes) drugs and MOA | phenylephrine, naphazoline, tetrahydrozoline MOA: Alpha-adrenoreceptor agonists constrict conjunctival blood vessels, reducing ocular redness and discomfort. |
| phenylephrine, | MOA: Alpha-adrenoreceptor agonists constrict conjunctival blood vessels, reducing ocular redness and discomfort. |
| naphazoline, | MOA: Alpha-adrenoreceptor agonists constrict conjunctival blood vessels, reducing ocular redness and discomfort. |
| tetrahydrozoline | MOA: Alpha-adrenoreceptor agonists constrict conjunctival blood vessels, reducing ocular redness and discomfort. |
| Carmellose & Hypromellose | ocular lubricants |
| Urigenitory Drugs | Propantheline Imipramine Oxybutynin Tolterodine Solifenacin Mirabegron Oestrogen/estrogen Finasteride Tamsulosin Prazosin Tadalafil |
| Imipramine | Class: Tricyclic antidepressants Indiction: *for urinary issues* Nocturnal enuresis MOA: TCAs inhibit reuptake of noradrenaline and serotonin into presynaptic terminals. Although unrelated to the therapeutic effects of the TCAs, they also block cholinergic, histaminergic, alpha1-adrenergic and serotonergic receptors. beta3 mimetic properties to RELAX detrusor muscle |
| anticholinergics (genitourinary) drugs | Propantheline Oxybutynin Tolterodine Solifenacin Darifenacin |
| Oxybutynin | Class: anticholinergic (genitourinary) Indication: urinary urge incontinence works by blocking muscarinic receptors, inhibiting spontaneous detrusor contractions |
| Tolterodine | Class: anticholinergic (genitourinary) Indication: urinary urge incontinence works by blocking muscarinic receptors, inhibiting spontaneous detrusor contractions |
| Solifenacin | Class: anticholinergic (genitourinary) Indication: urinary urge incontinence works by blocking muscarinic receptors, inhibiting spontaneous detrusor contractions |
| Darifenacin | Class: anticholinergic (genitourinary) Indication: urinary urge incontinence works by blocking muscarinic receptors, inhibiting spontaneous detrusor contractions |
| beta 3 agonist (genitourinary) | Mirabegron indication: Urinary urge incontinence MOA: Beta3-adrenoceptor agonist; relaxes bladder muscle during the storage phase of micturition, increasing bladder capacity. |
| Oestrogen/estrogen | Ratio of plasma oestrogen to testosterone increases with age This may result in stromal (the supporting tissue) overgrowth Greater amount of hormone receptors in the stroma compared with the epithelium This theory explains why BPH is chiefly a stromal disease |
| Selective alpha blockers (genitourinary) | Tamsulosin Prazosin |
| Tamsulosin | Class: selective alpha blocker (genitourinary) Indication: Symptom relief in BPH MOA: Block alpha1 receptors, relaxing smooth muscle in the bladder neck and prostate, and decreasing resistance to urinary flow. Tamsulosin is more selective for the alpha1-receptor subtypes found in the bladder and prostate. |
| Prazosin | Class: selective alpha blocker (genitourinary) Indication: Symptom relief in BPH MOA: Block alpha1 receptors, relaxing smooth muscle in the bladder neck and prostate, and decreasing resistance to urinary flow. Tamsulosin is more selective for the alpha1-receptor subtypes found in the bladder and prostate. Prazosin and terazosin are also arterial and venodilators due to blockade of postsynaptic alpha1 receptors and therefore inhibition of catecholamine-mediated vasoconstriction. Unlike nonselective alpha-blockers (eg phenoxybenzamine), they have little effect on presynaptic alpha2 receptors and are therefore less likely to cause reflex tachycardia. |
| Phosphodiesterase 5 inhibitors | Tadalafil Finasteride MOA: Inhibit 5‑alpha-reductase, which converts testosterone to dihydrotestosterone (a potent cellular androgen that stimulates prostate growth). They reduce prostate size and improve symptoms and urinary flow rate. |
| Finasteride | Class: Phosphodiesterase 5 inhibitors MOA: Inhibit 5‑alpha-reductase, which converts testosterone to dihydrotestosterone (a potent cellular androgen that stimulates prostate growth). They reduce prostate size and improve symptoms and urinary flow rate. |
| Tadalafil | Class: Phosphodiesterase 5 inhibitors MOA: Inhibit 5‑alpha-reductase, which converts testosterone to dihydrotestosterone (a potent cellular androgen that stimulates prostate growth). They reduce prostate size and improve symptoms and urinary flow rate. |
| drugs for skin conditions | steroids etc |
| Hydrocortisone | Mildly potent topical corticosteroid. Alters transcription of inflammatory mediators Reduce inflammation and itching. TCS misuse associated with skin atrophy and corticoid acne (unlikely) |
| phenergan (promethazine) | Dermatitis is not caused by histamine release. Reduces awareness of itchiness resulting in less scratching and skin damage Drowsiness, dry mouth. |
| Betamethasone diproprionate | Very potent topical corticosteroid. Alters transcription of inflammatory mediators Reduce inflammation and itching, and minimises skin thickening TCS misuse associated with skin atrophy and corticoid acne (possible) |
| Methotrexate | dihydrofolate reductase inhibitor, direct keratolytic and reduced T-cell activity Reduce inflammation and keratinisation Severe liver, kidney, lung, WBC and mucosal DNA damage. Cytotoxic!! |
| Calcipotriol (+/- betamethasone) | Vitamin D analogue, controls keratinocyte proliferation / differentiation. Returns cells to normal function. Reducing, inflammation, erythema and itching. Dry / irritated skin and mucosal layers Hypocalcaemia, |
| Benzoyl peroxide | Antibacterial effect by free radical formation and desquamation Reduce bacterial load, unblock comedones and clear spots Skin redness, peeling. |
| Doxycycline | Antibacterial and anti-inflammatory effect. Bind to 30s microbial ribosome subunit Reduce lesion number and appearance, swelling, pain associated with acne. Photosensitivity, incorporation into calcifying tissue in under 8 year olds. |
| Adapalene | Interact with retinoid receptors.Modulate cell proliferation Modulate cell differentiation Reduce sebum secretion, Reduce P. acnes load, Anti-inflammatory Skin redness, peeling in the first 6 -8 weeks. Teratogen? |
| Miconazole | Imidazole antifungal. Fungistatic, inhibits Lanosterol 14-alpha demethylase Reduce itching, broken skin, smell. Safe, minimal risk of drug interactions if used topically |
| Terbinafine | Allylamine antifungal. Fungicidal. Inhibits squalene epoxidase. Reduce itching, broken skin, smell. Safe, minimal risk of drug interactions if used topically. (oral tablets, liver issues) |
| Griseofulvin | Halts fungal mitosis, by altering mitotic spindle formation. Used for resistant fungal infections Potentially cause mutation of DNA. |
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