8397190
Description
Flashcards by Amelia Claire, updated more than 1 year ago
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Created by Amelia Claire
about 7 years ago
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| Question | Answer |
| Ferrous fumarate | equivalent 33% elemental iron (303 mg dose = 100mg elemental iron) oral tablet mechanism = iron for iron deficiency anaemia ADRs iron binds with other drugs to form a complex -absorption of both iron and drug reduced |
| Ferrous sulfate | equivalent 32% elemental iron (310mg dose = 100mg elemental iron) oral tablet mechanism = iron for iron deficiency anaemia ADRs iron binds with other drugs to form a complex -absorption of both iron and drug reduced |
| Iron polymaltose | equivalent 27% elemental iron (370mg dose = 100mg elemental iron) oral tablet mechanism = iron for iron deficiency anaemia ADRs iron binds with other drugs to form a complex -absorption of both iron and drug reduced also available as a IV dose |
| Iron sucrose | IV form of iron more likely to have a toxic effect from labile iron but low likelihood of immune response to the carbohydrate shell |
| Ferric carboxymaltose | IV form of iron, least likely to have the toxic effects and least likely to have the immune response to the carbohydrate shell. |
| Cyanocobalamin | vitamin B12 is required for the methylation of DNA. Cyanocobalamin has a cyanide moiety, is synthetic, has a 'shorter' half life than hydroxocobalamin, available orally or as IM injection, and is converted into methylcobalamin following absorption, used to treat anaemia due to B12 deficiency (pernicious anaemia) |
| Hydroxocobalamin | vitamin B12 is required for the methylation of DNA. Cyanocobalamin has a hydroxy group, is naturally occurring, has a 'longer' half life than cyanocobalamin, available orally or as IM injection, and is converted into methylcobalamin following absorption, used to treat anaemia due to B12 deficiency (pernicious anaemia) |
| Folic acid | Folic acid is required for synthesis of DNA. given orally demethylated in reaction reliant on B12 |
| Epoetin | recombinant human erythropoietin (rhEpo) Epoietin Alpha and Epoietin Beta half life 6-9 hrs |
| Darbepoetin | Synthetic erythropoietin analogue Darbepoetin alfa Two additional carbohydrate chains Longer half-life of 25 h, less frequent dosing |
| Atorvastatin | Statin = HMG-CoA reductase inhibitors Inhibit HMG-CoA reductase in the mevalonate pathway 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. Indications: Hypercholesterolaemia Hypertensive patients with additional risk factors for heart disease longer half life CYP3A4 |
| Rosuvastatin | Statins = HMG-CoA reductase inhibitors Inhibit HMG-CoA reductase in the mevalonate pathway 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. Indications Hypercholesterolaemia High risk of cardiovascular disease longer half life CYP2C9 |
| Simvastatin | Statins = HMG-CoA reductase inhibitors Inhibit HMG-CoA reductase in the mevalonate pathway shorter half life CYP3A4 |
| Pravastatin | Statins = HMG-CoA reductase inhibitors Inhibit HMG-CoA reductase in the mevalonate pathway 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. Indications Hypercholesterolaemia Post MI Unstable angina shorter half life CYP450 |
| Fluvastatin | Statins = HMG-CoA reductase inhibitors Inhibit HMG-CoA reductase in the mevalonate pathway 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. Indications Hypercholesterolaemia Coronary disease after successful PCI shorter half life CYP2C9 |
| Fenofibrate | Class: Fibrate Mode of action: Activate peroxisome proliferator-activated nuclear receptors and modulate lipoprotein synthesis and catabolism. They reduce plasma triglyceride, moderately increase HDL and have a variable effect on LDL concentrations. Indications: Severe hypertriglyceridaemia Dyslipidaemia associated with DMII Hypercholesterolaemia (second line) Reduction in progression of pre-existing diabetic retinopathy associated with type 2 diabetes (with appropriate BP, glycaemic and lipid control) Precautions Photosensitivity from ketoprofen—contraindicated. Pancreatitis, unless due to hypertriglyceridaemia—contraindicated. Treatment with ezetimibe—may further increase risk of gall bladder disease. Treatment with a thiazolidinedione—may further increase risk of paradoxical decrease in HDL concentration. Severe diabetic retinopathy in type 2 diabetes—no data on effect of fenofibrate, as these people were excluded from the clinical trials. |
| Gemfibrozil | Class: Fibrate Mode of action: Activate peroxisome proliferator-activated nuclear receptors and modulate lipoprotein synthesis and catabolism. They reduce plasma triglyceride, moderately increase HDL and have a variable effect on LDL concentrations. Indications: Severe hypertriglyceridaemia with risk of pancreatitis Mixed hyperlipidaemia and dyslipidaemia associated with diabetes (second line) Hypercholesterolaemia (second line) |
| Ezetimibe | Cholesterol absorption inhibitor Inhibits intestinal and biliary cholesterol absorption Mode of action 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. Indications Hypercholesterolaemia Homozygous sitosterolaemia (phytosterolaemia) |
| Cholestyramine | Class:Bile acid binding resins 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. Indications Hypercholesterolaemia Itch associated with partial biliary tract obstruction Diarrhoea following ileal resection or disease |
| Colestipol | Class:Bile acid binding resins 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. Indications Hypercholesterolaemia |
| Nicotinic acid (Niacin) | Mode of action Mechanism unclear. Probably suppresses fatty acid release from peripheral tissue, especially adipose tissue. In doses >1 g daily, nicotinic acid reduces LDL and triglycerides, increases HDL and uniquely lowers potentially atherogenic lipoprotein(a). Indications Hypercholesterolaemia, mixed hyperlipidaemia or severe hypertriglyceridaemia Pellagra |
| Alirocumab | NOAC Indications Use with a statin (unless statin-intolerant) and other lipid-lowering drugs if appropriate for: heterozygous familial hypercholesterolaemia after inadequate response or intolerance to statins primary hypercholesterolaemia and ischaemic cardiovascular disease (CVD) after inadequate response or intolerance to statins Comments reduces LDL by 39–62% but, unlike statins, reduction in cardiovascular events and death has not been demonstrated long-term safety and efficacy is unknown; longest trial was 18 months not marketed in Australia |
| Evolocumab | class: proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor 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. Indications Use with a statin (unless statin-intolerant) and other lipid-lowering drugs if appropriate for: homozygous familial hypercholesterolaemia heterozygous familial hypercholesterolaemia after inadequate response or intolerance to statins primary hypercholesterolaemia and pre-existing ischaemic cardiovascular disease (CVD) after inadequate response or intolerance to statins |
| Omega-3 fatty acids | Fish oil is rich in polyunsaturated fatty acids: Eicosapentaenoic acid (EPA) & docosahexaenoic acid (DHA) Sourced from oily fish (e.g. salmon, herring, mackerel) 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 |
| Aspirin | Class: COX inhibitor 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. Indications ACS History of symptomatic atherosclerosis |
| Dipyridamole | class: Phosphodiesterase (PDE) inhibitors Mode of action Inhibits platelet function by inhibiting phosphodiesterase, which increases platelet cAMP. Indications Prevention of recurrent ischaemic stroke and TIA, including fixed-dose combination with aspirin |
| Clopidogrel | Class: ADP P2Y12 antagonists prodrug: 2 CYP450 dependent steps Mode of action: The active metabolite of the thienopyridines irreversibly binds to the platelet P2Y12 receptor and inhibits platelet aggregation for the life of the platelet. |
| Prasugrel | Class: ADP P2Y12 antagonists Prodrug: plasma esterase + 1 CYP450 dependent step Mode of action: 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: ADP P2Y12 antagonists Ticagrelor binds reversibly to the P2Y12 receptor. |
| Abciximab | Class: Glycoprotein IIb/IIIa antagonists Prevent binding of fibrinogen to platelet, by occupying glycoprotein IIb/IIIa receptor, thereby blocking platelet aggregation. Abciximab is a chimeric monoclonal antibody Indications Percutaneous transluminal coronary angioplasty (PTCA) and intracoronary stenting Unstable angina refractory to conventional treatment where PCI is planned |
| 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 Indications Unstable angina and non-STEMI in high-risk patients |
| 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. |
| Unfractionated heparin | Class: indirect thrombin inhibitors Method of Action: Induce conformational change to increase in antithrombin III to its efficacy inhibiting Xa and thrombin IV or subcut |
| Enoxaparin | Class: indirect thrombin inhibitors Method of Action: Induce conformational change to increase in antithrombin III to its efficacy inhibiting Xa Indications: Treatment of venous thrombosis Prevention of extracorporeal thrombosis during haemodialysis Treatment of acute STEMI, non-STEMI and unstable angina |
| Fondaparinux | Class: ? Factor Xa Inhibitor on AMH website indirect thrombin inhibitor on lecture slides Mode of action Mode of action from Factor Xa inhibitors Selectively inhibit factor Xa, blocking thrombin production, conversion of fibrinogen to fibrin, and thrombus development. |
| Dabigatran | Class: direct thrombin inhibitor Method of Action: Reversibly inhibit both free and fibrin-bound thrombin, preventing conversion of fibrinogen to fibrin, preventing thrombus formation. Thrombin-induced platelet aggregation is also inhibited. |
| Apixaban | Class: Factor Xa Inhibitor Mode of action Selectively inhibit factor Xa, blocking thrombin production, conversion of fibrinogen to fibrin, and thrombus development. *** metabolized by CYP3A4 & both substrates of P-gp -> risk of of drug interactions |
| Rivaroxaban | Class: Factor Xa Inhibitor Mode of action Selectively inhibit factor Xa, blocking thrombin production, conversion of fibrinogen to fibrin, and thrombus development. *** metabolized by CYP3A4 & both substrates of P-gp -> risk of of drug interactions |
| Alteplase | Class: Tissue plasminogen activator (t-PA) analogues (?thrombolytic on AMH) Mode of action Convert plasminogen to plasmin, which catalyses the breakdown of fibrin. known as recombinant t-PA (rt-PA) Exact copy of human t-PA Short half-life, need IV infusion Indications Acute STEMI Massive pulmonary embolism |
| Tenecteplase | Class: Tissue plasminogen activator (t-PA) analogues (?thrombolytic on AMH) Mode of action 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) Indications Acute STEMI |
| Vitamin K | 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 |
| Tranexamic acid | Class; anti-Fibrinolytic Mode of action Inhibits breakdown of clots by blocking binding of plasminogen and plasmin to fibrin. |
| Idarucizumab | 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 |
| Protamine | class: drug specific reversal agent (heparin & enoxaparin reversal) Mode of action Combines with heparin to form a stable inactive complex, reversing its anticoagulant effect. Indications Heparin, dalteparin or enoxaparin overdose in patients with, or at high risk of, severe haemorrhage. |
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