3937497
| Question | Answer |
| Hydrochlorothiazide a) Use b) Mechanism of action c) Administration/duration of action d) Side effects e) Contraindications | a) Thiazide diuretic used in the treatment of hypertension b) Acts on distal convoluted tubule of kidney by inhibiting Na+Cl- co-transporter, which inhibits Na+ reabsorption to increase levels of Na+ and Cl- in urine → increased levels of water which leads to loss of water from body → decreased blood volume → decreased venous return → decreased blood pressure c) Oral administration with diuretic effect within an hour, duration of action of 10 hours, often used in combination with K+ sparing diuretic, ACE inhibitor or AT1-receptor antagonist d) hypokalemia, hyperuricemia e) shouldn’t be given to patient’s prone to gout |
| Amiloride a) Use b) Mechanism of action c) Side effects | a) K+ sparing diuretic used in the treatment of hypertension b) Inhibits sodium channel in collecting duct of kidney to decrease Na+, K+ pumping and the amount to K+ available for secretion. Only has a small diuretic effect, mainly used to prevent K+ loss with thiazide diuretics c) Side effects: hyperkalemia (high potassium) |
| Enalapril a) Use b) Mechanism of action c) Side effects c) Contraindications | a) ACE inhibitor used in the treatment of hypertension b) Decreases levels of angiotensin II and aldosterone and decreases breakdown of bradykinin to lower blood pressure by inhibiting ACE. Metabolised in the gut to enalaprilat c) dry cough, angioderma (both due to high levels of bradykinin) d) pregnancy, eliminated by kidneys so dose needs to be reduced with renal impairment |
| Candesartan a) Use b) Mechanism of Action c) Contraindications | a) AT1-receptor antagonist used in the treatment of hypertension b) Inhibits effects mediated by AT1 receptors to decrease vasoconstriction, hypertrophy, aldosterone secretion and effects of aldosterone c) pregnancy |
| Amlodopine a) Use b) Mechanism of action c) Side effects | a) Calcium channel blocker used in the treatment of hypertension and atypical angina b) Contraction of vascular smooth muscle requires calcium entry into cells through calcium channels, therefore calcium channel blockers are effective against all vasoconstrictors. Has a greater effect on blood vessels than the heart. c) excessive vasodilation – headache, flushing, dizziness |
| Prazosin a) Use b) Mechanism of action | a) α1-Adrenoceptor Antagonist used in the treatment of hypertension b) Activation of sympathetic nervous system → noradrenaline is released → stimulates α1-adrenoceptors on blood vessels → vasoconstriction. Prazosin binds to α1-adrenoceptor to reduce the binding of noradrenaline, effectively causing vasodilation. Only used to cause small decreases in blood pressure |
| Atenolol a) Use b) Mechanism of action c) Contraindications | a) β-Adrenoceptor Antagonist (β-blocker) used in the treatment of hypertension b) Noradrenaline stimulates β1-adrenoceptors on the heart to increase heart rate and force and on the kidney to increase renin production. β-blockers decrease heart rate and force, vasoconstriction and salt & water retention c) Asthma, excreted in urine therefore reduced dosage may be needed in renal failure |
| Nitroglycerin a) Use b) Mechanism of action c) Administration | a) Nitrovasodilator used in angina attacks b) Ends an angina attack by causing venodilation which leads to pooling of blood in the veins → reduces venous return → reduces work done by heart and oxygen demand c) Extensive first pass liver metabolism so used sublingually in spray or tablet. Onset of action is within a minute. Can also be used in a patch or ointment for prevention of attacks |
| Isosorbide Mononitrate a) Use b) Mechanism of action c) Administration | a) Nitrovasodilator used in angina attacks b) Ends an angina attack by causing venodilation which leads to pooling of blood in the veins → reduces venous return → reduces work done by heart and oxygen demand c) Resistant to first pass liver metabolism, active after oral administration and has a longer half-life than nitroglycerin, therefore used after nitroglycerin has ended the attack, to prevent a further attack |
| Verapamil a) Use b) Mechanism of action c) Alternate use/mechanism of action d) Administration | a) Calcium channel blocker used in the prevention of angina b) Inhibits the influx of calcium which leads to a decreased heart rate and force thus work and oxygen demand of the heart c) Also a class IV anti-arrhythmia drug. Blocks cardiac calcium channels over vascular calcium channels, inhibiting inward calcium current associated with pacemaking. Also slows conduction through the AV node. Used in arrhythmias with increased excitation of SA or AV nodes d) Active after oral admin but undergoes extensive first pass metabolism. Also used via IV in an emergency |
| Furosemide (frusemide) a) Use b) Mechanism of action c) Administration | a) Diuretic used for the treatment of heart failure b) Inhibits the Na+K+2Cl- cotransporter which leads to retention of ions and water to increase the amount of water loss from the kidney c) Active after oral admin to give diuretic effect in 30 minutes. In an emergency, used intravenously to have an effect in 2-10 minutes |
| Furosemide (frusemide) a) Side effects | Hyponatremia (low levels of sodium), too much fluid loss leading to hypotension, excessive K+ loss from kidney → hypokalaemia → can promote cardiac arrhythmias, hyperuricemia (should be avoided in patients with a hx of gout), hearing loss, hypomagnesemia → can promote cardiac arrhythmias. |
| Metoprolol a) Use b) Mechanism of action | a) β1-adrenoceptor antagonist used in heart failure b) In heart failure the number of β-adrenoceptors is altered and β-adrenoceptor antagonists have been shown to increase cardiac output |
| Digoxin a) Use b) Mechanism of action c) Side effects d) Antidote | a) Derived from natural plant source (the foxglove) and used for heart failure b) Inhibits Na+K+ATP-ase that drives sodium and potassium exchange across membranes which leads to an increase in intracellular Na+ → increased levels of intracellular Ca2+ → increased force of myocardial contraction → reverses decreased cardiac output in heart failure 60% of the toxic dose is required to produce therapeutic effect c) Widespread effects: Can cause cardiac arrhythmias, Can cause gastro-intestinal toxicity d) In life threatening digoxin toxicity, anti-digoxin immunotherapy is used intravenously |
| Lignocaine a) Use b) Mechanism of action | a) Class I anti-arrhythmic drug. Used in serious ventricular arrhythmias to decrease excitability of the conduction system. Also used as a local anaesthetic. b) Blocks sodium channels involved in the rapid depolarisation in the Purkinje system. No effect on sinus rhythm as this is controlled by calcium channels |
| L-Sotalol a) Use | a) Class II anti-arrhythmic drug Non-selective β-adrenoceptor antagonist used in treatment of tachyarrhythmias where an overactive sympathetic nervous system is implicated. 2 isomers – the L-isomer (L-sotalol) is the non-selective β-adrenoceptor antagonist |
| Esmolol a) Use | a) Class II anti-arrhythmic drug. Ultra short acting β-adrenoceptor antagonist used intravenously to treat atrial flutter and fibrillation associated with operations |
| D-Sotalol a) Use b) Mechanism of action | a) Class III anti-arrhythmic drug. Used in a variety of supraventricular and ventricular arrhythmias b) Blocks delayed outward rectifying K+ channel to prolong the action potential in the Purkinje system |
| Amiodarone a) Use b) Mechanism of action c) Unwanted action d) Administration e) Side effects | a) Anti-arrhythmic drug that has activity in all classes b) Potent K+ channel blocker, Na+ channel blocker and Ca2+ channel blocker. Also blocks α and β adrenoceptors c) it is an analog of thyroid hormone thus many adverse effects mimic those of hypothyroidism d) Used orally in recurrent ventricular tachycardia/fibrillation and to convert atrial fibrillation to normal sinus rhythm, Used intravenously for the termination of ventricular or supraventricular arrhythmias in an emergency e) Pulmonary toxicity, hypothyroidism |
| Adenosine a) Use b) Mechanism of action c) Administration | a) Naturally occurring substance that has receptor mediated effects, produced in ischaemia and slows heart rate b) Acts at the A1-receptors in the heart to slow sinus node activity and conduction through the AV node c) Used via IV in an emergency for acute treatment of supraventricular arrhythmias where its rapid onset is a major advantage |
| Low dose aspirin a) Use b) Mechanism of action c) Why not high dose aspirin? | a) Used to prevent myocardial infarction and stroke b) Inhibits COX-1 in platelets, decreasing the amount of intermediates available to be converted to TXA2, leading to decreased platelet aggregation. Has no effect on the COX-1 in the endothelial cells or on the production of PGI2 from the endothelial cells and PGI2-mediated inhibition of platelet aggregation c) High dose aspirin inhibits bot PGI2 and TXA2 formation and has no effect on platelet aggregation, therefore not used to prevent myocardial infarction and stroke |
| Clopidogrel a) Use b) Mechanism of action c) Can it be used in combination with low dose aspirin? | a) Anti-platelet drug b) Antagonist at P2Y receptors and inhibits ADP-induced platelet aggregation. Reduces cardiovascular events in patients with unstable angina c) Clopidogrel and low dose aspirin work by different mechanisms therefore have an additive effect and can be used in combination to prevent vascular events in patients with unstable angina, recent myocardial infarction and in stenting |
| Abciximab a) Use b) Mechanism of action c) Administration d) Side effects | a) Anti-platelet drug. Used in combination with low dose aspirin and heparin when angioplasty or stenting is undertaken for coronary thrombosis. b) Antibody to the GPIIb/IIIa receptor and prevents platelet aggregation. Decreases the incidence of recurrent myocardial infarction and death c) Administered via IV, followed by continuous infusion of a lower dose for 12 hours d) Increased incidence of bleeding |
| Heparin a) Use b) Mechanism of action c) Administration | a) Anticoagulant drug b) Inhibits all clotting factor proteases to inhibit clotting quickly c) Ineffective when administer orally. Used intravenously or subcutaneously |
| Dabigatran a) Use b) Mechanism of action c) Administration | a) Anticoagulant drug. Used after hip and knee replacements to prevent thromboembolism b) Direct thrombin inhibitor, inhibits the conversion of fibrogen to fibrin c) Active after oral administration and has an immediate effect |
| Fondaparinux a) Use b) Mechanism of action c) Administration | a) Anticoagulant drug used to prevent thromboembolism after hip fracture and hip and knee replacements b) Factor Xa inhibitor c) Used subcutaneously and effective quite quickly |
| Streptokinase a) Use b) Mechanism of action c) Side effects d) Administration | a) Drug used to activate fibrinolysis to breakdown clots b) Activates plasma form of plasminogen to produce plasmin to breakdown thrombi. Also breaks down clots where blood vessel repair is occurring c) High incidence of bleeding. Can lead to allergic reaction/anaphylaxis d) Administered via IV. Loading dose and maintenance dose used |
| Alteplase a) Use b) Mechanism of action c) Trade name? d) Side effects | a) Drug used to activate fibrinolysis to breakdown clots B) Activates fibrin form of plasminogen and also forms plasmin for fibrinolysis C) Tissue type plasminogen activator (TPA) d) Claimed to be clot selective but high incidence of bleeding |
| Simvastatin a) Use b) Mechanism of action | a) Statin used to decrease levels of LDL (low density lipoprotein) cholesterol (bad cholesterol) b) Inhibits HMG CoA reductase which leads to decreased cholesterol synthesis and increased synthesis of LDL receptors to decrease plasma LDL cholesterol |
| Gemfibrozil a) Use b) Mechanism of action | a) Fibric acid derivative used to increase levels of HDL (high density lipoprotein) cholesterol (good cholesterol). Used in patients with high levels of triglycerides and low levels of HDL cholesterol b) Stimulates Peroxisome Proliferation-Activated Receptor (PPAR) α for fatty acid oxidation, reduction of triglycerides, stimulation of lipoprotein lipase to clear triglycerides and increase HDL-cholesterol |
| Ezetimibe a) Use b) mechanism of action c) Administration | a) Drug used to decrease LDL cholesterol. Used as an alternative to statins for patients with high LDL cholesterol b) Inhibits the transporter for cholesterol absorption from the GI tract to reduce cholesterol absorption. Leads to decreased LDL cholesterol but does not effect HDL cholesterol or triglycerides c) Active after oral administration |
| Insulin lispro a) Use b) Administration c) Side effects/drug reactions | a) Rapid acting insulin replacement therapy used to mimic meal levels of insulin b) Administered as an injection with insulin glargine c) Can cause hypoglycaemia. If taken in combination with ethanol (alcohol), excessive reduction in glucose may occur resulting in hypoglycaemia. Combination of aspirin and insulin replacement therapy may also lead to hypoglycaemia. β-adrenoceptor antagonists reduce levels of glucose and when used in combination with insulin replacement therapy, can cause hypoglycaemia. Glucocorticoids increase the ability of adrenaline to generate glucose, thus when used in combination with insulin replacement therapy, may cause hyperglycaemia |
| Insulin Glargine a) Use b) Administration c) Side effects/drug reactions | a)Long acting insulin replacement therapy used to mimic fasting levels of insulin b) Administered as an injection with insulin lispro c) Can cause hypoglycaemia. If taken in combination with ethanol (alcohol), excessive reduction in glucose may occur resulting in hypoglycaemia. Combination of aspirin and insulin replacement therapy may also lead to hypoglycaemia. β-adrenoceptor antagonists reduce levels of glucose and when used in combination with insulin replacement therapy, can cause hypoglycaemia. Glucocorticoids increase the ability of adrenaline to generate glucose, thus when used in combination with insulin replacement therapy, may cause hyperglycaemia |
| Metformin a) Use b) Mechanism of action | a) Oral anti-hyperglyceic used in treatment of type 2 diabetes b) Inhibits gluconeogenesis (conversion of amino acids to glucose in the liver), increases sensitivity to insulin in type 2 diabetes and increased glucose uptake. Reduces hyperglycemia to normoglycemia but not normoglycemia to hypoglycaemia c) GI disturbances (nausea, diarrhoea), lactic acidosis. No weight gain with metformin as opposed to other anti-diabetic drugs |
| Acarbose a) Use b) Mechanism of action c) Administration d) Side effects | a) Anti-diabetic drug b) Inhibits α-glucosidase which then inhibits glucose in the gut c) Active after oral admin and only used in type 2 diabetes. Can be used in combination with metformin. d) produces carbohydrates in the faeces which causes flatulence and diarrhoea |
| Sulfonylureas (glibencalmide) a) Use b) mechanism of action c) Administration d) Side effects | a) Group of oral hypoglycaemic agents (includes glibenclamide) used in type 2 diabetes only (not type 1) b) Inhibits K+ATP channel in the pancreatic beta cells to increase insulin secretion c) Active after oral administration and taken once or twice daily d) hypoglycaemia which is enhanced by alcohol, weight gain. May become less effective over time and patient might have to proceed to insulin replacement therapy |
| Glitazones (pioglitazone) a) Use b) Mechanism of action c) Administration d) Side effects | a) Group of anti-diabetic drugs (type 2 only, not type 1) b) Stimulates the nuclear receptor PPARϒ to modulate the levels of a number of proteins which leads to reduced glucose output from the live, increased glucose uptake into muscle and reduced insulin resistence. These effects all combine to decrease plasma glucose c) Active after oral admin d) weight gain, oedema, anaemia |
| Exenatide a) Use b) Mechanism of action c) Administration d) Side effects | a) Anti-diabetic drug. Only used when there is a lack of control of type 2 diabetes with treatment with metformin and glibenclamide b) Peptide agonist at GLP-1 receptors which mimics effects of GLP-1 to stimulate insulin secretion while inhibiting glucagon secretion c) Used subcutaneously prior to a meal d) hypoglycaemia |
| Sitagliptin a) Use b) Mechanism of action c) Administration d) Side effects | a) Anti-diabetic drug. Used in combination with other anti-diabetic drugs b) Inhibitor of dipeptigyl peptidase-4 which leads to a build up of GLP-1 meaning it mimics the effects of GLP-1 to increase insulin secretion and inhibit glucagon secretion c) Active after oral admin d) Only causes hypoglycaemia when used in combination with a sulfonylurea |
| Mylanta a) use b) constituents c) side effects of constituents d) drug interactions | a) Antacid used to neutralise the acid in the stomach. Used in treatment of dysesia, heartburn, GERD, peptic ulcers, NSAIDs-induced ulcers b) Mixture of aluminium hydroxide and magnesium hydroxide c) aluminium hydroxide: chalky taste, constipation. magnesium hydroxide: chalky taste, diarrhoea, belching d) Antacids increase pH of stomach which affects dissolution, absorption and bioavailability of some drugs. There should be a 2 hour gap between taking antacids and other drugs |
| Gaviscon a) Use b) constituents c) Role of alignate d) Side effects of constituents e) drug interactions | a) Antacid used to neutralise the acid in the stomach. Used in treatment of dysesia, heartburn, GERD, peptic ulcers, NSAIDs-induced ulcers b) Mixture of calcium cabonate, sodium bicarbonate, alignate (viscous gum) c) Helps protective mucus stick to the oesphagus to prevent acid damage d) Calcium carbonate: belching, flatulence, constipation. Sodium bicarbonate: belching, abdominal distention e) Antacids increase pH of stomach which affects dissolution, absorption and bioavailability of some drugs. There should be a 2 hour gap between taking antacids and other drugs |
| Omeprazole a) use b) administration c) drug interactions d) combinations | a) Proton pump inhibitor used to inhibit acid secretion in GERD, peptic ulcers and prevention of NSAIDs-induced ulcers b) Administered orally as enteric coated granules that dissolve only at an alkaline pH. Carried in blood until activated in acid environment of stomach c) Inhibits activity of some cytochrome P450 enzymes and may decrease the clearance of benzodiazeines, phenyoin and warfarin. d) used in combination with pH dependent antibiotics to enhance effectiveness of antibiotic |
| Ranitidine a) use b) effectiveness? | a) Histamine H2 receptor antagonist used for dyspepsia, heartburn and GERD b) Only effective against H2 receptor stimulants of acid secretion not other stimulants e.g. gastrin, acetylcholine |
| Misoprostol a) use b) mechanism of action c) side effects d) contraindications | a) inhibits acid secretion. Used to prevent mucosal injury caused by NSAIDs b) selective agonist at prostaglandin EP receptors, stimulates EP1 receptors to inhibit secretion of acid from the stomach c) diarrhoea d) pregnancy |
| Sucralfate a) Use b) mechanism of action c) drug interactions | a) Inhibits ulcers from digesting mucosal proteins b) produces viscous, sticky gel that sticks to ulcers to inhibit digestion of mucosal proteins c) Should not be taken at the same time a antacids, can prevent the absorption of some drugs so should be taken after other drugs |
| Prokinetics a) use in GERD b) use in Gastroparesis c) use in IBS | a) Prevent heartburn by increasing motility in the oesophagus b) Gastroparesis = impaired emptying of stomach not cause by obstruction. Prokinetics increase stomach motility and emptying c) used in constipation associated with IBS |
| Doperidone | a) |
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