Rang & Dales Pharmacology, 7th Edition

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Adverse effects Hypotension, transient sedation, dry mouth, diarrhoea, hypersensitivity reactions. Furthermore, the resulting dopamine has unwanted effects. Carbidopa inhibits DOPA decarboxylase increasing the availabilty of levodopa to the CNS and reducing the its dopamine-mediated side effects. See CNS card Clinical use An adjunct in treatment of Parkinsonism. Note that? Clinical use Inflammatory conditions e. Adverse effects Gastrointestinal disturbances including gastric bleeding; headache, dizziness less commonly, allergic reactions occasionally; renal toxicity rarely.

Used to close patent ductus arteriosus. Similar drugs Diclofenac: moderate potency, half-life 1—2h. Inhibits platelet aggregation see card Half-life only 30min — rapid hydrolysis to salicylate but effects last longer because the COX has been inactivated and new enzyme must be produced. Clinical use Main use: as antithrombotic in myocardial infarction see card set 7.

Other NSAIDs are preferred for anti-inflammatory action and analgesia in musculo-skeletal conditions. Adverse effects Gastrointestinal disturbances, especially gastric bleeding. Special points Should not be used in children. Can cause increased effect of warfarin resulting in bleeding. Has little anti-inflammatory action. Clinical use Mild to moderate pain, especially headache.

Adverse effects Few and uncommon with therapeutic doses. Toxic doses cause firstly nausea and vomiting and then 24h later potentially fatal liver toxicity. No antiplatelet action. Celecoxib is 10—20 x more active on COX-2 than COX-1 — the constitutive enzyme that generates physiologically important prostaglandins. Clinical use Rheumatoid arthritis, osteoarthritis, ankylosing spondylitis. No cardioprotective effect because no antiplatelet action.

Some renal toxicity because COX-2 occurs constitutively in the kidney. See card Methotrexate MTX is cytotoxic in the larger doses used to treat cancer. Half-life 6—9h. Clinical use Drug of first choice for rheumatoid arthritis; also used in psoriasis, ankylosing spondylitis, polymyositis and vaculitis. MTX is also an anti-cancer agent. Adverse effects Gastrointestinal disturbances, dose-related liver toxicity.

Bone marrow depression and pneumonitis can occur. According to X-rays, disease progression is reduced. MOA In the colon the salicylic acid moiety is released, is absorbed and has anti-inflammatory action. Half-life 6—16h. Clinical use Rheumatoid arthritis, juvenile arthritis, inflammatory bowel disease. Rarely bone marrow dyscrasias, liver dysfunction. About a third of patients discontinue the drug because of adverse effects.

MOA Gives rise to a metabolite that inhibits dihydrooratate dehydrogenase; this results in inhibition of T-cell proliferation and decreased production of autoantibodies by B cells. Clinical use Rheumatoid arthritis. Particularly effective in combination with methotrexate. Increased BP, weight gain can occur. The long half-life can lead to cumulative toxicity. Half-life 9—12 days. Adverse effects Nausea, vomiting, headache, upper respiratory tract infections with cough. Because of inactivation of macrophages latent TB and other conditions e.

Blood dyscrasias can occur. Antibodies against infliximab may be produced. MOA Inhibits xanthine oxidase and also the biotransformation of purines to xanthine. Clinical use To prevent episodes of gout. Adverse effects Gastrointestinal disturbances. Rashes and blood dyscrasias can occur. Allopurinol interferes with the metabolism of oral anticoagulants and can increase the effect of azathioprine and cyclophosphamide.

Similar drugs Probenicid is similar in that it is also uricosuric but it acts by increasing uric acid excretion through an effect on the proximal tubule in the nephron; only used to prevent gouty attacks. Phagocytes engulf the crystals and release inflammatory mediators. MOA Inhibits migration into gouty joints of neutrophils by binding to tubulin and preventing its polymerisation into microtubules. It also decreases production of the chemokine leukotriene B4.

Adverse effects Diarrhoea and sometimes nausea and vomiting. Special points It can increase the bone marrow depression caused by other drugs. MOA It complexes with cyclophilin to inhibit calcineurin which normally activates the transcription of interleukin-2 IL Metabolised in the liver by the P 3A enzyme system. Can be useful in autoimmune diseases. Often used in combination with glucocorticoids or methotrexate. Adverse effects Nephrotoxicity. Special points Multiple interactions with other drugs.

Similar drug Tacrolimus: indirectly inhibits calcineurin; more potent than ciclosporin with similar adverse effects — myelosuppression etc. MOA Interferes with purine synthesis and has cytotoxic action on dividing cells. Metabolised to mercaptopurine mcp which is the cytotoxic moiety acting by interfering with purine nucleotide metabolism. Mcp is inactivated by xanthine oxidase.

Also used in chronic inflammatory and autoimmune diseases e. Adverse effects Myelotoxicity dose-related. GIT disturbances, hypersensitivity reactions skin rashes, arthralgia etc. Special points Blood should be monitored for myelosuppression. MOA Inhibits de novo purine synthesis specifically in T and B lymphocytes other cells can generate purines by another pathway.

Metabolised to mycophenolic acid which is the active moiety which interferes with purine nucleotide metabolism. Clinical use Used to prevent rejection of organ transplants usually in combination with ciclosporin and glucocorticoids. Also used in autoimmune diseases e. Special points Treatment requires specialist supervision.

Clinical use Used to prevent rejection of organ transplants particulary renal because, unlike ciclosporin, it has no renal toxicity usually in combination with ciclosporin or glucocorticoids. Adverse effects Myelosuppression important , hyperlipidaemia, venous thromboembolism, diarrhoea, rash, osteonecrosis. Special points Drug concentrations in the blood need to be monitored. Other actions : reduction in chronic inflammation, autoimmune and hypersensitivity reactions; various metabolic effects; negative feedback action on ant.

The main effects occur only after 2—8 h because protein synthesis of mediators and enzymes is required see card Clinical use To prevent rejection of organ transplants and to treat rejection episodes. Also used for inflammatory, see hypersensitivity and autoimmune conditions see card MOA Competitive inhibitor of histamine at H1-receptors on smooth muscle. Clinical use Hypersensitivity reactions — hay fever, urticaria, some drug allergies, insect bites, pruritus.

Adverse effects Effects due to action on peripheral muscarinic receptors dry mouth; sometimes blurred vision, constipation, urine retention. Allergen IL-2 1. MOA Competitive inhibitor of histamine at H1-receptors on smooth muscle etc. Clinical use Hypersensitivity reactions — hay fever, urticaria; premedication; sedation; emergency treatment of anaphylaxis; motion sickness. Adverse effects Anticholinergic action on peripheral muscarinic receptors dry mouth; sometimes blurred vision, constipation, urine retention ; headache, drowsiness.

Special points Injection can be painful. Antihistamines Promethazine as specified on cards 4. Antidysrhythmic drugs can affect different phases of the action potential. Also produces some slowing of action potential repolarisation a class III action. Half is excreted unchanged by kidney; half is metabolised in liver. Clinical use Supraventricular and, more usually, ventricular dysrhythmia. Adverse effects Atropine-like effects: blurred vision, dry mouth, constipation, urinary retention.

Negative inotropic action. Procainamide has less antimuscarinic action than either disopyramide or quinidine. The class III actions of these drugs may lead to torsade de pointes.

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Very high first-pass metabolism precludes oral admin. Short T0. Subject to cytochrome P metabolism. Mexiletine and tocainide are orally active. Clinical use Treatment and prevention of ventricular fibrillation especially following infarction. Also digoxin- induced dysrhythmias.

Adverse effects Unwanted CNS effects include drowsiness, tremors and convulsions. Reduces the rate of phase 0 depolarisation causing an increase in the effective refractory period and slowed AV conduction. Associates with and dissociates from sodium channels more slowly than either Ia or Ib agents. Mostly excreted unchanged in urine. Propafenone is metabolised more rapidly by the liver and has a shorter T0.

Clinical use Prevention of paroxysmal atrial fibrillation. Severe ventricular dysrhythmia, unresponsive to other agents. Adverse effects Increases likelihood of dysrhythmia. May increase mortality due to ventricular fibrillation post infarction. Needs careful use. Avoid in patients with structural heart disease.

Propranolol Actions Antidysrhythmic. Also antihypertensive, antianginal. Propranolol has additional class I action. Clinical use Reduction of mortality after infarct where dysrhythmias have a sympathetic input. Paroxysmal atrial fibrillation.

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Adverse effects Bronchoconstriction in asthmatic patients. Cardiac slowing with possible heart block. Propranolol has CNS effects: depression, sedation and sleep disturbances. This increases the refractory period. Sotalol also has class II actions. Sotalol and ibutilide have half-lives of 5—10h.

Clinical use One of the most effective antidysrhythmics. Atrial fibrillation and flutter, ventricular ectopic beats and tachyarrhythmias. Ibutilide i. Adverse effects Torsades de pointes. Less likely with amiodarone than other class III drugs. Amiodarone may cause pulmonary fibrosis, liver damage, photosensitive skin rashes and thyroid malfunction.

Also antianginal and antihypertensive. Shows use-dependence so is more active in tachyarrythmias. Decreases automaticity and slows AV conduction. Clinical use Supraventricular tachycardias. Control of ventricular rate in atrial fibrillation. Adverse effects Side effects due to smooth muscle relaxation: hypotension and dizziness, ankle oedema, constipation. Unwanted cardiac actions include heart block and bradycardia. MOA Activates G-protein-coupled adenosine receptors.

Important actions are its negative chronotropic action on the SA node and slowed AV conduction. Short duration of action. Clinical use Termination of paroxysmal supraventricular tachycardia. Adverse effects Side effects e. Reduces increased cardiac excitability due to hypomagnesaemia, which is common after heart operations. The cellular mechanism of action is not established but is likely to involve effects on membrane ion permeability or transport.

Clinical use Prevention of supraventricular tachycardia and ventricular arrhythmias after bypass surgery. Ventricular dysrhythmias due to digoxin toxicity. Management of torsades de pointes. Adverse effects Muscle weakness. Various pathological factors can disturb the homeostasis and cause hypertension. MOA Inhibits angiotensin-converting enzyme thus reducing synthesis of vasoconstrictor angiotensin II. This decreases aldosterone secretion, resulting in increased salt and water excretion, indirectly decreasing plasma volume and cardiac load see card 6. Lisinopril: half-life 12h.

Enalapril is a prodrug converted to an active moiety by liver enzymes. Clinical use Hypertension; heart failure; ventricular dysfunction following myocardial infarction; diabetic nephropathy. Adverse effects Hypotension; dry cough, angioedema. Renal failure can occur. Special points Hyperkalaemia can occur if given with potassium-sparing diuretics.

The dry cough and angiooedema are due to the drugs producing bradykinin by stimulating the kallikrein-kinin system. Half-life 1—2h; half-life of metabolite 3—4h. Clinical use Hypertension; congestive heart failure; nephropathy. Adverse effects Hypotension, dizziness. Hyperkalaemia can occur. Verapamil acts mainly on the heart, slowing the rate; see card 5. Half-life of amlodipine 35h, of nifedipine 2h. CNS Affects Peripheral sympathetic system releases noradrenaline, which Plasma volume, which affects Stimulates the heart, Constricts blood vessels Vasodilators: increasing: increasing: Calcium channel Cardiac output Peripheral resistance blockers e.

Clinical use Very severe hypertension — particularly in pregnancy. Important drugs in bold. Affects Peripheral sympathetic system? Card decrease sympathetic outflow 2. Card together these control thiazides furosemide MOA Inhibits voltage-gated calcium channels and reduces the contractile process; see Fig.

Clinical use To prevent angina nifedipine, diltiazem. For hypertension; see card 6. For dysrhythmias: verapamil see card 5. Verapamil: constipation an effect on GIT smooth muscle and sometimes heart failure. Can be given by transdermal patch — effects last 24h. Can be given i. Isosorbide mononitrate: given orally; half-life 4h; slow-release preparation available. Nitrates are also used in chronic heart failure; see card 8. The figure below outlines the pathophysiology of angina and myocardial infarction Atherosclerotic plaque Plaque rupture, thrombosis Decreased myocardial perfusion Block of coronary artery Angina Potential Ventricular Myocardial dysrhythmias dysfunction infarction Nifedipine, Glyceryl trinitrate, Diltiazem isosorbide mononitrate PAIN!

Myocardial infarction is a medical emergency requiring hospitalisation. Anti-platelet agents Statins see section 10 see card 9. Shock Increased Opioids sympathetic see cards Slows AV conduction. Prolongs AV node refractory period. Increases force of contraction in failing heart. Clinical use Atrial fibrillation. Adverse effects Dysrhythymias, due to block of AV Increased force of Contraction conduction and ectopic pacemaker action; yellow vision; nausea and vomiting. Special points Narrow margin between effective dose and toxic dose. Have a go at giving examples.

Myocardial disease, hypertension, vascular disease can cause: exacerbates exacerbates Increased pre-load Cardiac failure Increased after-load i. Increased increase output peripheral Decreased resistance Increased central renal blood venous pressure flow Reduced tissue Renin perfusion release Vasoconstriction?

Also produces some lowering of plasma triglyceride and some increase in HDL-C. Plasma half-life: 1—3h. Clinical use Hypercholesterolaemia. Used to prevent atherosclerosis in patients with high C serum levels and to prevent cardiac infarction in patients who already have atherosclerosis. Adverse effects Usually mild: muscle pain, GIT distubances, insomnia, rash. Rarer severe effects: severe myositis risk increased if given with fibrates ; angioedema.

Special points Statin action is increased by Estimibe. Clinical use Used for mixed dyslipidemia i. Adverse effects GIT upsets; rash; moderate increased risk of gall stones; myositis — which can be severe. Special points Avoid use of statins with fibrates. Main effect: decrease of plasma LDL concentration. MOA Blocks a sterol carrier protein in the brush border of enterocytes and thus reduces the amount of biliary and dietary C delivered to the liver via chylomicrons. Plasma half-life: 22h. Clinical use Hypercholesterolaemia, usually as adjunct to a statin.

Adverse effects These are few. GIT upsets may occur as may headache, rashes and myalgia. MOA It is a positively charged drug that binds the negatively charged bile acids inhibiting their absorption. This reduces the pool of bile acids in the liver which decreases the hepatic store of C.

The drug also lowers C by decreasing its absorption from the GIT. Clinical use Hypercholesterolaemia, often used with a statin. Adverse effects GIT disturbances: constipation and bloating, sometimes diarrhoea. Special points Prevents absorption of fat-soluble vitamins, statins, gemfibrozil and other drugs e. Decreases plasma triglyceride synthesis and reduces the release of VLDL from the liver which results in decreased plasma triglycerides and LDL levels.

Clinical use As an adjunct to a statin in dyslipidaemia, or when a statin is contraindicated. Adverse effects Vasodilatation with uncomfortable flushing ; GIT disturbances, pruritus, rashes. Less commonly: palpitations, dyspnoea, headache, giddiness, peripheral oedema. High doses can impair liver function as well as glucose tolerance and can precipitate gout. Special points Unwanted effects can limit its clinical use.

Pretreatment with ibuprofen can reduce the flushing. Excretion in urine, increased inhibitor thrombotic, if urine is alkalinised. Also used to of thrombosis treat acute stroke. Toxic doses cause respiratory alkalosis followed by acidosis. Metabolised to an active compound. Because action is irreversible, the effects last several days until platelets are replaced.

Often given with aspirin. Adverse effects Unwanted effects: bleeding; GIT discomfort; rashes. Rarely neutropaenia. It binds and inactivates the receptor preventing the binding of fibrinogen thus inhibiting platelet aggregation. Half life 10—30min. Clinical use Adjunct to heparin and aspirin in high-risk patients undergoing coronary angioplasty an operation to unblock coronary artery. Prevents restenosis and reinfarction. Adverse effects Bleeding; thrombocytopaenia. Special points For specialist use. Used just once because of immunogenicity.

Adverse effects Headache common ; GIT disturbances; hypotension, hypersensitivity reactions. Clinical use Myocardial infarction, deep vein thrombosis, pulmonary embolism, acute ischaemic stroke. Special points It needs to be given within 12 hours of the onset of the condition, preferably within 1 hour. Similar drug Reteplase long half-life. Clinical use To reduce haemorrhage following dental extraction or prostatectomy.

For menorrhagia, epistaxis, hereditary angioedema, thrombolytic overdose. Adverse effects GIT disturbances. Rare: hypersensitivity skin reactions, disturbed colour vision. Elimination Factor X Xa half-life 40—90min; renal excretion. Thrombocytopaenia, hypersensitivity reactions, osteoporosis. Special points Dosage is adjusted according to the activated partial thromboplastin time. Overdose treated with protamine sulfate.

Similar drugs Low molecular weight heparins. Elimination half-life IXa — min; renal excretion. To treat deep vein thrombosis, pulmonary Factor II IIa thrombin embolism, myocardial infarction, unstable prothrombin angina. Less likely than heparin to cause thrombocytopaenia, hypersensitivity reactions, osteoporosis.

Special points No need to monitor the activated partial thromboplastin time. Similar drugs Other low molecular weight heparins: e. K hydroquinone Vit. K reductase Vit. K quinone Vit. To prevent embolisation in atrial fibrillation. Adverse effects Bleeding; treated by giving natural Vit K or fresh plasma or coagulation factor concentrates. Special points Prothrombin time must be monitored. Antiplatelet drugs are used mainly for thromboembolism in Anticoagulants e. Antiplatelet drugs e.

Anticoagulants have little effect on arterial thrombi. Thrombosis The diagram shows the events leading up to platelet aggregation. Platelet adhesion? Synthesis of TXA2? There are, of course, others. In the tetrahydrofolate FH4 form it is a cofactor in the synthesis of purines and pyrimidines being particularly important in thymidylate synthesis. The functionally inactive methyl-FH4 is demethylated in a Vit Bdependent reaction see card Clinical use To treat megaloblastic anaemias caused by folate deficiency.

To prevent the development of folate deficiency in susceptible individuals e.

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To treat toxicity caused by methotrexate a folate antagonist. Adverse effects Rare; occasionally GIT disturbances. Special points Should not be used in undiagnosed megaloblastic anaemias because if the anaemia is due to Vit B deficiency the anemia may improve but the neurological lesions will persist and could get worse. Clinical use To treat pernicious anaemia and other causes of vitamin B12 deficiency. Adverse effects Nausea, dizziness, headache and hypersensitivity reactions; hypokalaemia at start of treatment.

Drug with Cyanocobalamin. Clinical use To treat the anaemia of chronc renal failure and of AIDS; to alleviate anaemia caused by cytotoxic anticancer drugs; to prevent anaemia in premature infants. Adverse effects GIT disturbances; hypertension. It can mobilise haemopoietic stem cells from bone marrow to blood.

Clinical use Neutropenia associated with cytotoxic cancer chemotherapy, bone marrow transplantation or HIV infection.

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Adverse effects GIT disturbances, bone pain, muscle pain, fever, rash, alopecia. Similar drug Lenograstim. Special points For use only by experienced clinicians. Clinical use Iron-deficiency anaemia. Adverse effects Dose-related GIT disturbances — nausea, epigastric pain, abdominal cramps, diarrhoea. Drugs with Ferrous fumarate, ferrous gluconate — given orally.

Iron dextran given by deep i. Special points Iron toxicity both acute due to excessive ingestion of iron salts or chronic e. Folic acid is usually given to pregnant women as a supplement — to prevent the development of neural tube defects e. Chemotaxins e. See also card 2. Short-acting 3—5h ; can be given i. Mainly excreted unchanged. To prevent exercise-induced asthma. For chronic obstructive airways disease.

Unwanted Tremors, tachycardia, sometimes dysrhythmias, nervousness, some peripheral dilatation. Long-acting 8—12h ; Mostly metabolised by P with significant amount lost in faeces.

Clinical use To prevent bronchconstriction with exercise-induced asthma or at night in patients needing prolonged bronchodilator therapy. For chronic obstructive pulmonary disease. Unwanted Tremors, tachycardia, sometimes dysrhythmias, nervousness, some peripheral vasodilatation. Aminophylline can be given i.

Aminophylline i. Unwanted GIT disturbances, tachycardia, anxiety. High plasma levels can cause serious dysrhythymia effects or seizures. Special points Plasma levels should be monitored. Relaxes airway smooth muscle in mild asthma. Metabolised in liver and excreted mainly in bile; half-life 3—5h.

Effective in aspirin-induced asthma. Unwanted Few. No effect on the late phase. MOA Competitively antagonises acetylcholine action on muscarinc receptors. No effect on the immediate phase. See also card MOA Reduces the activation of inflammatory cells and the release of mediators especially cytokines see cards 4. Clinical use Added to bronchodilator therapy if this is inadequate. Unwanted Hoarse voice; oral candidiasis thrush.

MOA It is a monoclonal antibody that inhibits the binding of IgE to mast cells and eosinophils thus reducing mediator release. Unwanted Hypersensitivity reactions. No effect on bronchial spasm. MOA Inhibits mast cell degranulation and the response of sensory C fibres to irritants early phase and eosinophil activation delayed phase possibly by an action on chloride channels in the plasma membranes. Clinical use Prophylaxis of asthma, mainly in older children. To reduce symptoms of allergic rhinitis.

Unwanted Irritation of throat by the powder. Pathobiology of asthma: bronchial hyper-reactivity, bronchial spasm and inflammation of the airways Immediate phase of the asthma attack Cromoglicate Delayed phase of the asthma attack can inhibit bronchial hyper-reactivity and spasm bronchial hyper-reactivity, spasm and airway inflammation Cromoglicate Triggers: Allergen e.

Step 1 Patient is started on Drug A. How would A be given? How would B be given? Step 3 If asthma is not adequately controlled, add Drug C. How would it be given? Step 4 If asthma is still not adequately controlled, add other drug s. Step 5 If asthma is still not adequately controlled, add another drug.

Step 2 If inhalation of the short-acting bronchodilator is needed more than once a day, regular inhaled beclometasone is added. Step 3 If the asthma is not adequately controlled, a long-acting bronchodilator salmeterol taken regularly by inhalation is added rather than increasing the doses of beclometasone.

Step 4 If the asthma is still not adequately controlled, oral theophylline or montelukast is added — or the dose of inhaled beclometasone is increased. Step 5 If the asthma is still not adequately controlled, a regular single daily dose of an oral corticosteroid e.

Half-life 90min. Clinical use Pulmonary oedema, chronic heart failure, ascites due to liver cirrhosis, hypercalcaemia, hyperkalaemia. Adverse effects Hypokalaemic alkalosis; hyperuricaemia can precipitate gout ; hypovolaemia and hypotension in elderly patients; reversible ototoxicity. Some vasodilator action. Clinical use Hypertension. Also mild heart failure; nephrogenic diabetes insipidus; kidney stones.

Adverse effects Potassium loss; metabolic alkalosis; hyperuricaemia can precipitate gout ; increased insulin requirement; erectile dysfunction. MOA Inhibits the sodium channel in the luminal membrane of the collecting tubule, reducing sodium influx. Triamterene has more rapid onset and shorter duration of action than amiloride. Adverse effects Hyperkalaemia; may cause acidosis. MOA It is a competitive antagonist of aldosterone; causes diuresis by preventing the production of the aldosterone mediator that normally causes influx of sodium by activating the sodium channel in the luminal membrane of the collecting tubule.

Eplerenone has no active metabolite and a shorter half-life. Primary and secondary hyperaldosteronism. Adverse effects Hyperkalaemia; hyperchloraemic acidosis. Can cause gynaecomastia less likely with eplerenone. MOA It is an inert compound that passes across into the filtrate at the glomerulus and is not resorbed. Acts in those parts of the nephron that are freely permeable to water.

Clinical use Cerebral oedema; increased intraocular pressure. Adverse effects Temporary expansion of the extracellur fluid compartment and hyponatraemia due to osmotic extraction of intracellular water. Pulmonary oedema may occur. Inhibits action of histamine released from mast cell-like cells in the gastric mucosa. Partially inhibits acid secretion stimulated by gastrin or vagal stimulation.

MOA Selective, reversible, competitive antagonism of histamine H2 receptors on parietal cells. Clinical use Peptic and duodenal ulcers. Gastro-oesophageal reflux disease. Adverse effects Uncommon. Headache, GIT disturbances. Confusion, disorientation in elderly. Antiandrogenic effects with cimetidine but not other H2 blockers — gynaecomastia in men and galactorrhoea in women. Special points Cimetidine but not the other H2 antagonists is a potent cytochrome P inhibitor. Many interactions due to increased plasma concentration of other drugs e. Cimetidine and ranitidine also inhibit renal tubular secretion of other drugs.

Omeprazole like other PPIs is a prodrug. The acidic conditions in the parietal cell canaliculi convert the drug to the active form. The production of new PP molecules determines the rate of recovery. Needs enteric coating to prevent action of acid before absorption. Clinical use Duodenal and peptic ulcer. Zollinger-Ellison syndrome. As part of the triple therapy for Helicobacter pylori-dependent ulcers. PPIs are more effective than H2 antagonists.

Adverse effects Generally very safe. Occasionally, headache, abdominal pain, diarrhoea, flatulence and nausea. Long-term use can cause hypergastrinaemia which may increase risk of gastric carcinoid tumours. MOA Kills bacteria by binding to their ribosomes to inhibit protein synthesis.

Metabolised by liver with significant first-pass metabolism. Clinical use Many peptic ulcers occur secondary to H. Triple therapy a combination of two antibiotics with a proton pump inhibitor or H2 antagonist is an effective treatment. Amoxicillin may be replaced by metronidazole in patients allergic to penicillins. Adverse effects Gastrointestinal upsets — diarrhoea, nausea. MOA Antibacterial action against H. May also enhance prostaglandin synthesis. Clinical use I Duodenal ulcers in combination with metronidazole and tetracycline.

Ranitidine bismuth citrate is used with antibiotics to eradicate H. Adverse effects Low frequency of side effects: nausea, vomiting, black stools. Stimulates mucosal secretion of mucus, bicarbonate and prostaglandins. MOA Sucralfate is a complex of aluminium hydroxide and sulfated sucrose. This forms a viscous paste which adheres to ulcer bases to provide a protective barrier. Antacids and drugs reducing acid secretion will inhibit its action. Local action, virtually no absorption.

Clinical use Gastric and duodenal ulcer. Adverse effects Constipation. Formation of solid complexes bezoars within stomach. Aluminium toxicity in patients with renal impairment. Special points Sucralfate will reduce the absorption of many drugs and food substances. This can be minimised by taking them 2h before sucralfate. The elevation of pH also usefully reduces the activity of pepsin.

Stimulates prostaglandin synthesis. Clinical use Short-term symptom relief for duodenal ulcers. Needs to be taken 5—7 times daily. Adverse effects Al OH 3 causes constipation. Mg OH 2 has a strong laxative action osmotic purgative. CaCO3 causes hypercalcaemia. Special point Calcium and aluminium salts complex with orally administered tetracyclines to prevent their absorption.

Effects mediated by Gi-mediated inhibition of adenylate cyclase. Additionally stimulates bicarbonate and mucus secretion. Rapidly hydrolysed to free acid which is the active moiety. Adverse effects Diarrhoea, abdominal cramps. Should be avoided in pregnancy because of contractile action on uterus. Use in hay fever see card 4.

MOA Reversible competitive antagonist at H1 receptors. Significant first-pass metabolism. Meclizine longer T0. Clinical use Motion sickness and other emesis of vestibular origin e. Vomiting in early pregnancy. Emesis due to local stimuli in the gut acting via the vagus. Adverse effects Sedative action may not be desirable — contraindicated for driving etc. Confusion in elderly.

Cyclizine and cinnarizine are less sedating. Dry mouth anticholinergic action. Potentially fatal respiratory depression in infants under 2y. Other actions consistent with antagonism of parasympathetic nervous system see card 1. MOA Reversible competitive antagonism of muscarinic receptors. Antiemetic effects due to blockade of receptors in vestibular nucleus and in the vomiting centre.

A transdermal patch applied behind ear is particularly effective, lasting for up to 3 days. Clinical use Particularly effective, when given prophylactically, against motion sickness. No efficacy against chemotherapy-induced emesis mediated via the CTZ. Effective against local gut stimuli. Adverse effects Drowsiness. Actions attributable to muscarinic receptor block dry mouth, tachycardia, blurred vision, urinary retention. Avoid in closed-angle glaucoma. Metabolised by cytochrome P system in liver. Clinical use Main agents for nausea and vomiting due to cytotoxic, anticancer drugs. Often given a short time before starting chemotherapy.

Nausea and vomiting arising postoperatively or after radiation treatment. Limited effectiveness in motion sickness. Adverse effects Well tolerated. Headache, GIT upsets. Antipsychotic see card Some of the side effects are due to antagonism of other receptors e. P metabolism in liver. Clinical use Nausea and vomiting associated with cancer chemotherapy, radiation therapy and general anaesthesia. Prolactin release — galactorrhoea. Antihistamine and antimuscarinic actions e. High doses used for nausea and vomiting of chemotherapy esp.

Generally used in combination with other antiemetics. Cannabinoids Action via CB1 receptors. Used for nausea and vomiting associated with cancer chemotherapy. Dronabinol is the main active ingredient tetrahydrocannabinol of cannabis; nabilone is a synthetic analogue.

May cause dependence.

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Nabilone is active by mouth; T0. Neurokinin E. Adjunct for treatment of receptor chemotherapy-induced and post-operative nausea and vomiting. Orally active. MOA These agents are poorly absorbed and raise the osmotic load within the gut lumen. This causes ingested water to be retained and water also to be withdrawn from the blood stream. The increased fluid volume promotes movement along the gut. Purgation occurs within 2h. Not absorbed.


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Clinical use Bowel cleansing prior to surgery or examination MgSO4. Constipation macrogols and lactulose. The effects of lactulose develop after 2—3 days. Adverse effects Abdominal cramps. Few systemic actions because of low absorption. MOA These agents are poorly absorbed and, being hygroscopic, form a soft faecal mass which distends the gut to promote peristalsis. Clinical use Constipation. Used if increasing dietary fibre is inadequate.

Beneficial in various bowel disorders e. Maintain fluid intake to prevent intestinal obstruction. Adverse effects Flatulence. The enhanced secretion of chloride ion is accompanied by water leading to an increase in intraluminal fluid. Local action in the gut — little systemic absorption. Clinical use Chronic constipation. Irritable bowel syndrome with constipation. Adverse effects Nausea. Also increases fluid volume by promoting net fluid secretion. Senna is activated in the colon by bacteria.

Action of bisacodyl is more rapid rectally 30min than orally 6h. Tolerance to action with atony of the colon if used excessively. MOA Surfactant with emulsifying action. Adverse effects Well-tolerated — possible abdominal cramping. Liquid paraffin may impair the absorption of fat-soluble vitamins. The slower transit time allows for more fluid absorption and more solid stools. Effects can be reversed by naloxone. Loperamide and diphenoxylate, but not codeine, achieve low concentrations in CNS, so have few central effects including analgesia and addiction.

Metabolised by hepatic cytochrome P system. Diphenoxylate is hydrolysed to an active metabolite. Uploaded on. Number of pages. Written in. Book Title. Author s. Graeme Henderson, James M. LvanZonsbeek Member since 4 year ago 16 documents sold. Reviews received:. Send Message. Additional information. Wageningen University. Voeding en Gezondheid. HNE Pharmacological aspects of nutrition Master. More courses of Voeding en Gezondheid - Wageningen University. The best study guides. Avoid resits and achieve higher grades with the best study guides, textbook notes, and class notes written by your fellow students.

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Rang & Dales Pharmacology, 7th Edition Rang & Dales Pharmacology, 7th Edition
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Rang & Dales Pharmacology, 7th Edition Rang & Dales Pharmacology, 7th Edition
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