DRUG FORMULARYAmlodipineApidraAtorvastatinAzithromycinCeftriaxoneCefuroximeCelecoxibClonidineClopidogrelCo-AmoxiclavDoxorubicinDoxycyclineFurosemideHumulinIrbesartanKalimateKalium duruleLeucovorinLevofloxacinLosartanMefenamic acidmethotrexateMetronidazoleNorgesic forteOmeprazoleOxynormParacetamolPiaglitazonePiptazRanitidineSimvastatinTramadolUnasynVancomycinVincristine

DRUG MOA INDICATION CONTRAINDICATION ADVERSE REACTIONAmlodipine Amlodipine relaxes peripheral and coronary vascular

smooth muscle. It produces coronary vasodilation by inhibiting the entry of Ca ions into the voltage-sensitive channels of the vascular smooth muscle and myocardium during depolarisation. It also increases myocardial O2 delivery in patients with vasospastic angina.Absorption: Well absorbed from the GI tract (oral); peak plasma concentrations after 6-12 hr.Distribution: Protein-binding: 97.5%.Metabolism: Hepatic: Extensive.Excretion: Via urine (mainly as metabolites, 10% as unchanged); 35-50 hr (elimination half-life).

Hypertension, angina, myocardial ischemia. Reduce the risk of coronary revascularization, fetal coronary heart disease, non-fatal MI & stroke.

OralHypertension, Prinzmetal's angina, Stable anginaAdult: Initially, 5 mg once daily increased to 10 mg once daily if necessary.Elderly: Initial dose: 2.5 mg once daily.Hepatic impairment: Initial dose: 2.5 mg once daily.

Known sensitivity to

dihydropyridines.

Headache, peripheral oedema, fatigue, somnolence, nausea, abdominal pain, flushing, dyspepsia, palpitations, dizziness. Rarely pruritus, rash, dyspnoea, asthenia, muscle cramps.Potentially Fatal: Hypotension, bradycardia, conductive system delay and CCF.

ApidraPharmacotherapeutic Group: Insulin and analogues, fast-

acting. ATC Code: A10AB06.

Pharmacodynamics: Insulin glulisine is a recombinant

human insulin analogue that is equipotent to regular

human insulin. Insulin glulisine has a more rapid onset of

action and a shorter duration of action than regular human

insulin.

The primary activity of insulins and insulin analogues,

including insulin glulisine, is regulation of glucose

metabolism. Insulins lower blood glucose levels by

stimulating peripheral glucose uptake, especially by

skeletal muscle and fat and by inhibiting hepatic glucose

production. Insulin inhibits lipolysis in the adipocyte,

inhibits proteolysis and enhances protein synthesis.

Treatment of adults, adolescents & childn ≥6 yr w/ DM, where treatment w/ insulin is required.

Hypoglycemia.Hypoglycemia, inj site reactions, lipodystrophy, local & systemic 

AtorvastatinAtorvastatin competitively inhibits HMG-CoA reductase,

the enzyme that catalyses the conversion of HMG-CoA to

mevalonic acid. This results in the induction of the LDL

receptors, leading to lowered LDL-cholesterol

concentration.

Absorption: Rapid from the GI tract (oral).

Distribution: Protein-binding: 98%.

Metabolism: Extensively hepatic; converted to active

Mixed dyslipidaemia; Nonfamilial hypercholesterolaemia; Heterozygous familial hypercholesterolaemia I

Hypersensitivity, active liver

disease or unexplained

persistent elevations of serum

transaminase, porphyria,

pregnancy, lactation.

Increased AUC for norethindrone and ethinyl estradiol. Concomitant multiple doses of atorvastatin and digoxin increased steady-state digoxin levels. Increased risk of rhabdomyolysis when used concurently with fibrates. Co-admin with antacid suspensions and colestipol decreased atorvastatin levels.

inhibitors of HMG-CoA reductase.

Excretion: Faeces (as metabolites); 14 hr (elimination

half-life).Azithromycin

Azithromycin blocks transpeptidation by binding to 50s

ribosomal subunit of susceptible organisms and disrupting

RNA-dependent protein synthesis at the chain elongation

step.

Absorption: Reduced by food (capsule formulation); peak

plasma concentrations after 2-3 hr.

Distribution: Extensive into the tissues (concentrations

higher than those in blood), WBC (high concentrations),

CSF (small amounts).

Metabolism: Liver (demethylation).

Excretion: Via the bile (as unchanged drug and

metabolites); via the urine (6% of the dose). Elimination

half-life: about 68 hr.

respiratory tract infections, skin and soft tissue infections, typhoid hypersensitivity

Mild to moderate nausea, vomiting, abdominal pain, dyspepsia, flatulence, diarrhoea, cramping; angioedema, cholestatic jaundice; dizziness, headache, vertigo, somnolence; transient elevations of liver enzyme values.

Ceftriaxone Ceftriaxone binds to one or more of the penicillin-binding proteins (PBPs) which inhibits the final transpeptidation step of peptidoglycan synthesis in bacterial cell wall, thus inhibiting biosynthesis and arresting cell wall assembly resulting in bacterial cell death.Absorption: Peak plasma concentrations after 2 hr (IM).Distribution: Distributed widely into body tissues and fluids; CSF (therapeutic concentrations). Crosses the placenta and enters breast milk; bile (high concentrations). Protein-binding: 85-95%.Excretion: Via the urine (40-65% as unchanged); via the bile to the faeces (remainder as unchanged and microbiologically inactive compounds); 6-9 hr (elimination half-life).

Uncomplicated gonorrhoea, Prophylaxis of secondary meningococcal meningitis, Susceptible infections, Prophylaxis of surgical infections, Typhoid fever

Hypersensitivity to cephalosporins; hyperbilirubinaemic neonates. Do not use calcium or calcium-containing solutions or products with or within 48 hr of ceftriaxone administration due to risk of calcium-ceftriaxone precipitate formation

Superinfection; anaphylaxis; diarrhoea; local reactions; blood dyscrasias; rash, fever, pruritus; elevated transaminases and alkaline phosphatase; leucopenia, neutropenia.Potentially Fatal: Pseudomembranous colitis; nephrotoxicity

Cefuroxime Cefuroxime binds to one or more of the penicillin-binding proteins (PBPs) which inhibits the final transpeptidation step of peptidoglycan synthesis in bacterial cell wall, thus inhibiting biosynthesis and arresting cell wall assembly resulting in bacterial cell death.Absorption: Absorbed from the GI tract with peak plasma concentrations after 2-3 hr (oral); may be enhanced by the presence of food.Distribution: Pleural and synovial fluid, sputum, bone and aqueous fluids; CSF (therapeutic concentrations). Crosses the placenta and enters breast milk. Protein-binding: Up to 50%.

uncomplicated UTI, respiratory tract infection, uncomplicated gonorrhea, meningitis,

Hypersensitivity to cephalosporins.

Large doses can cause cerebral irritation and convulsions; nausea, vomiting, diarrhoea, GI disturbances; erythema multiforme, Stevens-Johnson syndrome, epidermal necrolysis.Potentially Fatal: Anaphylaxis, nephrotoxicity, pseudomembranous colitis.

Metabolism: Rapidly hydrolysed (intestinal mucosa and blood).Excretion: Via the urine by glomerular filtration and renal tubular secretion (as unchanged); via bile (small amounts); 70 min (elimination half-life); prolonged in neonates and renal impairment.

Celecoxib Celecoxib is a nonsteroidal antiinflammatory drug (NSAID) that is used to treat arthritis, pain, menstrual cramps, and colonic polyps. Prostaglandins are chemicals that are important contributors to the inflammation of arthritis that causes pain, fever, swelling and tenderness. Celecoxib blocks the enzyme that makes prostaglandins (cyclooxygenase 2), resulting in lower concentrations of prostaglandins. As a consequence, inflammation and its accompanying pain, fever, swelling and tenderness are reduced. Celecoxib differs from other NSAIDs in that it causes less inflammation and ulceration of the stomach and intestine (at least with short-term use) and does not interfere with the clotting of blood.

Celecoxib is used for the relief of pain, fever, swelling, and tenderness caused by osteoarthritis, juvenile arthritis, rheumatoid arthritis, and ankylosing spondylitis. Celecoxib does not prevent the progression of either type of arthritis. It reduces only the symptoms and signs of arthritis. Celecoxib is approved for patients with familial FAP who have not had their colons removed. Celebrex also is also used for the relief of acute pain and the pain of menstrual cramps (primary dysmenorrhea).

Hypersensitivity including those in whom attacks of angioedema, rhinitis and urticaria have been precipitated by aspirin, NSAIDs or sulfonamides. Severe hepatic impairment; severe heart failure; inflammatory bowel disease; peptic ulcer; renal impairment (CrCl <30 ml/min); pregnancy and lactation.

Abdominal pain, diarrhea, nausea, oedema, dizziness, headache, insomnia, upper respiratory tract infections; rash.Potentially Fatal: Serious skin reactions such as exfoliative dermatitis, Stevens-Johnson syndrome, and toxic epidermal necrolysis.

Ciprofloxacin Inhibits bacterial DNA topoisomerase II, thereby including DNA strand breakage and cell death

Effective against gram-negative species, including Psedomonas, Neisseria, Haemophilus species and Enterobacter as well as against Mycoplasma and Legionella species.

Component sensitivity GI upset; skin rash;headache; dizziness; tendonitis and tendon rupture in adults

ClonidineClonidine stimulates alpha-2 receptors in brain stem which

results in reduced sympathetic outflow from the CNS and a

decrease in peripheral resistance leading to reduced BP

and pulse rate. It does not alter normal haemodynamic

response to exercise at recommended dosages.

Onset: 2-3 days (transdermal).

Duration: Maintained for 8 hr after removal of system

(transdermal).

Absorption: Well absorbed from the GI tract (oral); peak

plasma concentrations after 3-5 hr. Absorbed from the skin

(transdermal).

Distribution: 20-40% protein bound.

Metabolism: Hepatic: 50% of the dose.

Excretion: Via urine within 24 hr (as 40-60% as

unchanged drug), via faeces (20% of the dose); 6-24 hr

hypertension, prophylaxis for migraine,hypertensive crisis Hypersensitivity. Disorders of

cardiac pacemaker activity and

conduction. Pregnancy and

lactation.

Dry mouth, drowsiness, dizziness, headache, constipation, impotence, vivid dreams, urinary retention; dry, itching, burning sensation in the eye; fluid or electrolyte imbalance, GI upset, paralytic ileus, orthostatic hypotension, weakness, sedation, pruritus, myalgia, urticaria, nausea, insomnia, arrhythmias, agitation. Reduced GI motility at times may cause paralytic ileus.Potentially Fatal: Transient hypertension or profound hypotension, respiratory depression, convulsion. Clonidine withdrawal syndrome could be life threatening. Bradycardia, coma and disturbances in conduction (in individuals with preexisting diseases of SA/AV nodes, overdose or on digitalis).

(elimination half-life), prolonged to 41 hr in renal

impairment.Clopidogrel Clopidogrel inhibits adenosine diphosphate (ADP) from

binding to its receptor sites on the platelets and subsequent activation of glycoprotein GP IIb/IIIa complex thus preventing fibrinogen binding, platelet adhesion and aggregation.Absorption: Rapidly but incompletely absorbed from the GI tract (oral).Distribution: Protein-binding: Extensive.Metabolism: Hepatic: Extensive; converted to inactive carboxylic acid derivative and thiol derivative (active).Excretion: Via urine and faeces (as metabolites and unchanged drug).

Prophylaxis of thromboembolic disorders, hepatic impairment, cute coronary syndrome

Hypersensitivity. Active pathological bleeding. admin within 7 days after MI and ischaemic stroke, coagulation disorders. Lactation.

Dyspepsia, abdominal pain, nausea, vomiting, flatulence, constipation, gastritis, gastric and duodenal ulcers. GI upset, diarrhoea, paraesthesia, vertigo, headache, dizziness, pruritus and rashes.Potentially Fatal: Bleeding disorders including GI and intracranial haemorrhage. Blood dyscrasias.

Co-Amoxiclav Inhibits enzymes involved in formation of peptidoglycan layer of bacterial cell wall,no effect on human cell walls. Bactericidal, only works on dividing bacteria. Well absorbed enterally,Clavulanic acid inhibits beta-lactamaseHalf life: 1hourElimination:Rapid clearance from plasma due to active secretion into renal tubular fluid - can be blocked by probenecidAlso excreted in bile

Prophylaxis against infections associated w/ major surgical procedures. Treatment of resp tract, GUT, skin & soft tissue, O&G, bone, intra-abdominal & post-op infections

Hypersensitivity to

penicillins. Penicillin-

associated cholestatic

jaundice or hepatic

dysfunction.

Diarrhea, nausea & vomiting,

skin rash & urticaria, vaginitis.

Rarely, pseudomembranous

colitis, stomatitis & candidiasis,

erythema multiforme & other

skin effects. Hepatic, renal,

hematologic or CNS effects.

Doxorubicin Doxorubicin is a cytotoxic anthracycline antibiotic. The cytotoxic action results from its binding to DNA and inhibition of nucleic acid synthesis. Doxorubicin has been shown to produce regression in a variety of disseminated malignancies.Absorption: Rapidly cleared from the blood after IV admin.Distribution: Distributed into tissues including lungs, liver, heart, spleen and kidneys (IV); crosses the placenta; enters breast milk.Metabolism: Hepatic; rapidly converted to doxorubicinol.Excretion: Bile (as unchanged drug); 12 min, 3.3 hr, 30 hr (mean elimination half-lives).

Treatment of acute leukemias, lymphomas & a variety of solid tumors.

Marked myelosuppression induced by previous chemotherapy or radiotherapy, preexisting heart disease, previous treatment w/ complete cumulative doses of doxorubicin or other anthracyclines. Pregnancy & lactation.

Myelosuppression & cardiotoxicity; alopecia, hyperpigmentation of nailbeds & dermal creases primarily in childn; skin reaction; acute nausea & vomiting; mucositis; ulceration & necrosis of the colon esp the cecum; vascular phlebosclerosis; facial flushing (rapid inj use); erythematous streaking; anaphylaxis; cross-sensitivity to lincomycin

Doxycycline Doxycycline binds to 30S and 50S ribosomal subunits thus causing alterations on the cytoplasmic membrane of susceptible organisms.Absorption: Readily and almost completely absorbed from the GI tract (oral); peak plasma concentrations after 2 hr. Absorption not significantly affected by food.Distribution: Lipid-soluble; into body tissues and fluids. Protein-binding: 80-95%.Metabolism: Inactivated in the liver.Excretion: Via urine (40%, may be increased if urine is alkaline); 12-24 hr (elimination half-life).

Susceptible infections, Uncomplicated gonorrhoea, Syphilis, Relapsing fever and louse-borne typhus, Prophylaxis of scrub typhus, Acne, Susceptible infections

Children <8 yr; pregnancy, lactation; porphyria; hypersensitivity to tetracyclines; severe hepatic dysfunction; prolonged exposure to sunlight or tanning equipment.

Permanent staining of teeth; rash, superinfection; nausea, GI upsets, glossitis; dysphagia; photosensitivity, hypersensitivity; haemolytic anaemia, thrombocytopenia, neutropenia and eosinophilia.Potentially Fatal: Anaphylaxis.

Furosemide  inhibits reabsorption of Na and chloride mainly in the medullary portion of the ascending Loop of Henle. Excretion of potassium and ammonia is also increased while uric acid excretion is reduced. It increases plasma-renin levels and secondary hyperaldosteronism may result. Furosemide reduces BP in hypertensives as well as in normotensives. It also reduces pulmonary oedema before diuresis has set in.Absorption: Fairly rapidly absorbed from the GI tract (oral).Distribution: Crosses the placenta and enters breast milk. Protein-binding: 99%.Excretion: Via urine (as unchanged); 2 hr (elimination half-life), may be prolonged in neonates and renal and hepatic impairment.

hypertension, edema, heart failure, oliguria in acute or chrnic renal failure Severe sodium and water

depletion, hypersensitivity to

sulphonamides and

furosemide, hypokalaemia,

hyponatraemia, precomatose

states associated with liver

cirrhosis, anuria or renal

failure. Addison's disease.

Fluid and electrolyte imbalance. Rashes, photosensitivity, nausea, diarrhoea, blurred vision, dizziness, headache, hypotension. Bone marrow depression (rare), hepatic dysfunction. Hyperglycaemia, glycosuria, ototoxicity.Potentially Fatal: Rarely, sudden death and cardiac arrest. Hypokalaemia and magnesium depletion can cause cardiac arrhythmias.

Humulin Pharmacology: The time course of action of any insulin

may vary considerably in different individuals or at different

times in the same individual. As with all insulin

preparations, the duration of action of Humulin is

dependent on dose, site of injection, blood supply,

temperature and physical activity.

Treatment of diabetes mellitus for the control of hyperglycemia. Hypoglycemia.

Lipodystrophy, insulin resistance. Local & generalised allergic reactions.

IrbesartanIbesartan is an angiotensin II type I receptor antagonist

and therefore blocks the vasoconstricting and aldosterone-

secreting effects of angiotensin II.

Absorption: Rapidly absorbed from the GIT (oral); peak

plasma concentrations are achieved after 1.5-2 hrs.

Distribution: Protein-binding around 96%

Metabolism: Some hepatic metabolism via cytochrome

P450 isoenzyme CYP2C9 to inactive metabolites.

HTN; Diabetic nephropathy in Type 2 DM Hypersensitivity; pregnancy

and lactation.

Diarrhoea, dizziness, fatigue, headache, hyperkalaemia. Dyspepsia, oedema, myalgia, insomnia, nasal congestion, 1st dose orthostatic hypotension, rash, pharyngitis, urticaria, angioedema, anxiety/nervousness, tachycardia.

Excretion: Via bile and urine (as unchanged drug and

metabolites); via urine (20% of IV dose, <2% as

unchanged). 11-15 hrs (elimination half-life).Kalimate Pharmacology: Kalimate contains 7-9% calcium, 1 g of

which is exchanged for 53-71 mg (1.36-1.82 mEq/g) of potassium in vitro (KCl solution).

By administering 15-30 g/day of Kalimate to renal failure patients (adults), the serum potassium level is reduced by about 1 mEq/L (humans).

Unlike sodium type resin, Kalimate does not cause the increase in serum sodium and phosphate levels and the decrease in serum calcium level when it is used for renal failure (human).

Since Kalimate is a calcium-type resin, it is used even for the patients who restricted ingestion of sodium. Moreover, it can be used without fear of appearance and aggravation of edema, hypertension or cardiac insufficiency induced by sodium (human).

Mechanism of Action: After administration of Kalimate via oral or rectal route, calcium ion of Kalimate is exchanged for potassium ion in the intestinal tract, particularly around the colon, and Kalimate is excreted as unchanged polystyrene sulfonate resin into the feces without digestion and absorption. In consequence, potassium in the intestinal tract is excreted outside the body.

Pharmacokinetics: It is thought that Kalimate is not absorbed (rabbit). However, it has been reported from the result of the experiment with calf that a fine particle <5 micrometer in size has been absorbed through the mucous membrane and deposited on the reticuloendothelial system tissue. Kalimate is controlled in order that such fine

Prevention & treatment of hyperkalemia resulting from acute or chronic renal failure. Patients w/ intestinal

obstruction & stenosis,

constipation.

Constipation, anorexia & nausea.

Hypopotassemia.

particles are <0.1% in rate.

Kalium Durule Hypokalemia. Prophylaxis during treatment w/ diuretics.

Renal insufficiency, hyperkalemia, untreated Addison's disease, constriction of the esophagus &/or obstructive changes in the alimentary tract.

K salts & K-sparing diuretics, eg spironolactone. Amiloride, triamterene, tacrolimus, ACE inhibitors.

Leucovorin Leucovorin is frequently used in conjunction with Methotrexate and 5-FU. Leucovorin is not a Chemotherapeutic drug itself, however it is an adjunct to these chemotherapy drugs. Leucovorin is a compound similar to Folic acid, which is a vital Vitamin.

Antidote for folic acid antagonists Begin leucovorin rescue w/in 24 hr of antifolate administration. 10 mg/m2 followed by another dose 6 hrly for 72 hr. If at 24 hr increase in serum creatinine is >50%: 100 mg/m2 3 hrly until serum methotrexate ≥5 x 10-8 M. Counteract hematologic toxicity 5-15 mg/day. Amp Antidote for folic acid antagonists 6-12 mg IM every 6 hrly for 4 doses. Rescue after high-dose methotrexate therapy 15 mg 3 hrly IM or IV, starting 3 hr after the beginning of methotrexate infusion, for 9 doses & then 6 hrly for 3 doses. Advanced colorectal cancer 200 mg/m2 by slow IV inj over a min of 3 min followed by 5-FU (370 mg/m2) or 20 mg/m2 IV followed by 5-FU (425 mg/m2). Treatment is repeated daily for 5 days, this 5-day course may be repeated at 28-day intervals.

Neonates & infants. Vit B12 deficiency anemia.

Allergic sensitization.

Levofloxacin Levofloxacin exerts antibacterial action by inhibiting bacterial topoisomerase IV and DNA gyrase, the enzymes required for DNA replication, transcription repair and recombination. It has in vitro activity against a wide range of gram-negative and gram-positive microorganisms.Absorption: Rapid and complete absorption from the GIT (oral); peak plasma concentrations within 1-2 hr.Distribution: Widely distributed in bronchial mucosa, lungs; CSF (relatively poor). Protein-binding: 30-40%.Metabolism: Limited.Excretion: Mainly via urine (largely as unchanged drug); 6-8 hr (elimination half-life).

sinusitis, chronic bronchitis,CAP, pneumonia, UTI, pyelonephritis, prostatitis

Hypersensitivity to levofloxacin or

other quinolones. Child <18 yr

Oral/IV: Nausea, diarrhoea, constipation, headache, insomnia, inj site reactions (IV). Ophthalmic: Transient decrease in vision, ocular burning, ocular pain or discomfort, foreign body sensation, headache, fever, pharyngitis, photophobia.Potentially Fatal: Anaphylaxis.

Losartan Losartan is an angiotensin II receptor antagonist. The drug and its active metabolite selectively block the vasoconstrictor and aldosterone-secreting effects of angiotensin II by selectively antagonising its binding to AT1receptors.Absorption: Readily absorbed from GI tract with peak plasma concentrations of losartan after around 1 hr and its

Hypertension, type II DM Pregnancy, lactation; children with CrCl <30 ml/min/1.73m2

Headache, dizziness, back pain, myalgia, respiratory tract disorders, asthenia/fatigue, first dose hypotension, rash, angioedema, neutropenia, GI disturbances, transient elevation of liver enzymes, impaired renal

active metabolite after 3-4 hr.Distribution: 98% plasma protein bound.Metabolism: Hepatic metabolism principally by isoenzymes CYP3A4 and 2C9.Excretion: Excreted in faeces and urine as metabolites and unchanged drug. Terminal elimination half life of 2 hr (losartan) and 6-9 hr (active metabolite).

function, taste disturbances and hyperkalaemia.

Mefenamic Acid Pain and inflammation Inflammatory bowel disease; peptic ulcer; neonates; pregnancy (3rd trimester), lactation. Coronary artery bypass graft surgery, severe renal impairment, severe heart failure.

Abdominal pain, dyspepsia, constipation, diarrhoea, nausea, GI ulcers; oedema; bronchospasm; headache, drowsiness, insomnia, visual disturbances; CHF, hypertension, tachycardia, syncope; urticaria, rash; thrombocytopenia, aplastic anaemia, agranulocytosis; tinnitus; elevated liver enzymes; abnormal renal function.

Potentially Fatal: Autoimmune haemolytic anaemia; convulsions (overdosage).

Methotrexate Methotrexate is a folic acid antagonist that inhibits DNA synthesis. It irreversibly binds to dihydrofolate reductase, inhibiting the formation of reduced folates, and thymidylate synthetase, resulting in inhibition of purine and thymidylic acid synthesis.Absorption: Rapidly absorbed from the GI tract at low doses, higher doses are less well absorbed. Rapidly and completely absorbed after IM doses. Peak plasma concentrations after 1-2 hr (oral), 30-60 min (IM).Distribution: Tissues and extracellular fluids; crosses the blood-brain barrier and placenta; enters breast milk. Small amounts in saliva and breastmilk. 50% bound to plasma proteins. Bound as polyglutamate conjugates, bound drug may remain in the body for several mth, particularly in the liver .Metabolism: Partly by intestinal flora. Does not undergo significant metabolism at low dose therapy; 7-hydroxy

Burkitt's lymphoma, Acute lymphoblastic leukaemia, Choriocarcinom,Mycosis fungoides, Rheumatoid arthritis, Psoriasis, Crohn's disease, Meningeal leukaemia, Osteosarcoma, Choriocarcinoma, Breast cancer, Advanced lymphosarcoma, Acute lymphoblastic leukaemia

Severe renal or hepatic impairment, pre-existing profound bone marrow suppression in patients with psoriasis or rheumatoid arthritis, alcoholic liver disease, AIDS, pre-existing blood dyscrasias, pregnancy (in patients with psoriasis or rheumatoid arthritis), breast-feeding.

Ulceration of the mouth and GI disturbances (e.g. stomatitis and diarrhoea), bone marrow depression, hepatotoxicity, renal failure, skin reactions, alopecia, ocular irritation, arachnoiditis in intrathecal use, megaloblastic anaemia, osteoporosis, precipitation of diabetes, arthralgias, necrosis of soft tissue and bone, anaphylaxis, impaired fertility.Potentially Fatal: Pulmonary reactions (e.g. interstitial lung disease); neurotoxicity (e.g. leukoencephalopathy, paresis, demyelination) with intrathecal use; foetal deaths

metabolite is detected at high-doses.Excretion: Primarily via urine; small amounts in bile, faeces. Some evidence of enterohepatic recirculation. Interindividual variation exists, patients with delayed clearance are at an increased risk of toxicity.

Metronidazole Metronidazole is converted to reduction products that interact with DNA to cause destruction of helical DNA structure and strand leading to a protein synthesis inhibition and cell death in susceptible organisms. It is effective against a wide range of organisms including E. histolytica, T. vaginalis, Giardia, anaerobes e.g. Bacterioides sp, Fusobacterium sp, Clostridiumsp, Peptococcus sp and Peptostreptococcus sp, and moderately active against Gardnerella sp and Campylobacter sp.Absorption: Readily absorbed from the GI tract (oral), poorly absorbed from the vagina (intravaginal); peak plasma concentrations after 1-2 hr (oral), 5-12 hr (rectal), 8 hr (intravaginal). May be delayed by the presence of food.Distribution: Protein-binding: <20%. Widely distributed in body tissues and fluids e.g. bile, bone, breast milk, cerebral abscesses, CSF, liver and liver abscesses, saliva, semenal fluid, vaginal secretions (concentrations similar to those in plasma); crosses the placenta and rapidly enters fetal circulation.Metabolism: Hepatic via side-chain oxidation and glucuronide formation.Excretion: Mainly via urine (as metabolites); via faeces (small amounts). Elimination half-life: 8 hr; longer in neonates and severe hepatic impairment.

Amoebiasis, Balantidiasis, Balantidiasis, Trichomoniasis, Giardiasis, Bacterial vaginosis, Acute necrotising ulcerative gingivitis, Acute dental infections, Anaerobic bacterial infections, Prophylaxis of postoperative anaerobic bacterial infections, Eradication of H. pylori associated with peptic ulcer disease,Leg ulcers and pressure sores, Antibiotic-associated colitis, Anaerobic bacterial infections, Prophylaxis of postoperative anaerobic bacterial infections, Anaerobic infections, Prophylaxis of postoperative anaerobic bacterial infections, Topical/CutaneousFungating tumours, Rosacea

History of hypersensitivity to

metronidazole or other

nitroimidazole derivatives.

Pregnancy (1st trimester) and

lactation.

GI disturbances e.g. nausea, unpleasant metallic taste, vomiting, diarrhoea or constipation. Furred tongue, glossitis, and stomatitis due to overgrowth of Candida. Rarely, antibiotic-associated colitis. Weakness, dizziness, ataxia, headache, drowsiness, insomnia, changes in mood or mental state. Numbness or tingling in the extremities, epileptiform seizures (high doses or prolonged treatment). Transient leucopenia and thrombocytopenia. Hypersensitivity reactions. Urethral discomfort and darkening of urine. Raised liver enzyme values, cholestatic hepatitis, jaundice. Thrombophlebitis (IV).Potentially Fatal: Anaphylaxis.

Norgesic forte Analgesic/skeletal muscle relaxant. Relief of painful skeletal muscle spasm associated with chronic low back pain, sprains and strains, prolapsed intervertebral disc, muscle injury, non-articular rheumatism (fibrositis, myositis and myalgia), 'whiplash' injuries, acute torticollis, tension headache, dysmenorrhea and other acute or chronic painful muscular conditions.

Patients with glaucoma, prostatic hypertrophy or obstruction at the baldder neck or myasthenia gravis.

Nausea, dry mouth, blurring of vision, dizziness and restlessness. Rarely, rash or drowsiness may occur. These symptoms disappear rapidly with a reduction in dosage or cessation of medication.

OmeprazoleOmeprazole suppresses gastric acid secretion by specific

inhibition of the enzyme system hydrogen/potassium

adenosine triphosphatase (H+/K+ATPase) present on the

secretory surface of the gastric parietal cell.

Onset: Antisecretory: approx 1 hr; peak effect:0.5-3.5 hr.

Duration: 72 hr.

Absorption: Rapid but variable (oral); dose-dependent.

Bioavailability: Oral: approx 30-40%.

peptic ulcer, GERD,Zollinger-Ellison syndrome, acid related dyspepsia, esophagitis,

Diarrhoea, nausea, fatigue, constipation, vomiting, flatulence, acid regurgitation, taste perversion, arthralgia, myalgia, urticaria, dry mouth, dizziness, headache, paraesthesia, abdominal pain, skin rashes, weakness, back pain, upper respiratory infection, cough.Potentially Fatal: Anaphylaxis.

Distribution: Protein-binding: 95%.

Metabolism: Extensively hepatic; converted to

hydroxyomeprazole and omeprazole sulfone.

Excretion: Via urine (77%) and bile. Elimination half-life:

0.5-3 hr.Oxynorm Pharmacology: Pharmacodynamics: Capsule: Central

Nervous System: Oxycodone is a pure agonist opioid

whose principal therapeutic action is analgesia. Other

members of the class known as opioid agonists include

substances eg, morphine, hydromorphone, fentanyl,

codeine and hydrocodone. Pharmacological effects of

opioid agonists include anxiolysis, euphoria, feelings of

relaxation, respiratory depression, constipation, miosis and

cough supression as well as analgesia. Like all pure opioid

agonist analgesics with increasing doses, there is

increasing analgesia. This is unlike mixed

agonist/antagonists or non-opioid analgesics where there

is a limit to the analgesic effect with increasing doses. The

ceiling to analgesic effectiveness is imposed only by side

effects, the more serious of which may include somnolence

and respiratory depression.

While the precise mechanism of analgesic action is

unknown, specific CNS opioid receptors for endogenous

compounds with opioid-like activity have been identified

throughout the brain and spinal cord and play a role in the

analgesic effects of oxynorm.

Oxycodone produces respiratory depression by direct

action on brain stem respiratory centers involving both a

reduction in the responsiveness of the brain stem

respiratory centers to increases in carbon dioxide tension

and to electrical stimulation.

Treatment of moderate to severe pain in patients with cancer and postoperative pain. For the treatment of severe pain requiring the use of strong opioids

Patients with known

hypersensitivity to oxycodone

or any of the other ingredients,

or in any situation where

opioids are contraindicated.

This includes patients with

respiratory depression,

paralytic ileus, acute abdomen,

chronic obstructive airways

disease, cor pulmonale,

chronic bronchial asthma,

hypercarbia, moderate to

severe hepatic impairment,

severe renal impairment (CrCl

<10 mL/min), chronic

constipation, concurrent

administration of monoamine

oxidase inhibitors or within 2

weeks of discontinuation of

their use; pregnancy.

Use in lactation: Oxycodone

may be secreted in breast milk

and may cause respiratory

depression in the newborn.

Oxycodone should therefore

not be used in breastfeeding

mothers.

Capsule: Oxycodone has been in

clinical use for 75 years.

Serious adverse reactions which

may be associated with Oxynorm

therapy in clinical use are those

observed with other opioid

analgesics including respiratory

depression, apnea, respiratory

arrest and (to an even lesser

degree) circulatory depression,

hypotension or shock (see

Overdosage).

The nonserious adverse events

seen on initiation of therapy with

Oxynorm are typical opioid side

effects. These events are dose-

dependent and their frequency

depends upon the dose, the

clinical setting, the patient's level

of opioid tolerance and host

factors specific to the individual.

They should be expected and

managed as a part of opioid

analgesia. The most frequent

(>5%) include: Constipation,

nausea, somnolence, dizziness,

Oxycodone depresses the cough reflex by direct effect on

the cough center in the medulla. Antitussive effects may

occur with doses lower than those usually required for

analgesia.

Oxycodone causes miosis even in total darkness. Pinpoint

pupils are a sign of opioid overdose but are not

pathognomonic (eg, pontine lesions of hemorrhagic or

ischemic origin may produce similar findings). Marked

mydriasis rather than miosis may be seen with hypoxia in

the setting of oxynorm overdose (see Overdosage).

Gastrointestinal Tract and Other Smooth Muscle:

Oxycodone causes a reduction in motility associated with

an increase in smooth muscle tone in the antrum of the

stomach and duodenum. Digestion in the small intestines

is delayed and propulsive contractions are decreased.

Propulsive peristaltic waves in the colon are decreased

while tone may be increased to the point of spasm

resulting in constipation. Other opioid-induced effects may

include a reduction in gastric, biliary and pancreatic

secretions, spasm of sphincter of Oddi and transient

elevations in serum amylase.

Cardiovascular System: Oxycodone may produce release

of histamine with or without associated peripheral

vasodilation. Manifestations of histamine release and/or

peripheral vasodilation may include pruritus, flushing, red

eyes, sweating and/or orthostatic hypotension.

Concentration-Efficacy Relationships: Studies in normal

volunteers and patients reveal predictable relationships

between oxycodone dosage and plasma oxycodone

vomiting, pruritus, headache, dry

mouth, sweating and asthenia. In

many cases, the frequency of

these events during initiation of

therapy may be minimized by

careful individualization of starting

dosage, slow titration and the

avoidance of large swings in the

plasma concentrations of the

opioid. Following are the common

adverse events associated with

immediate-release oxycodone

concentrations, as well as between concentration and

certain expected opioid effects, eg, pupillary constriction,

sedation, overall drug effect, analgesia and feelings of

relaxation. As with all opioids, the minimum effective

plasma concentration for analgesia will vary widely among

patents, especially among patients who have been

previously treated with potent agonist opioids. As a result,

patients must be treated with individualized titration of

dosage to the desired effect. The minimum effective

analgesic concentration of oxycodone for any individual

patient may increase over time due to an increase in pain,

the development of a new pain syndrome and/or the

development of analgesic tolerance. Concentration-

Adverse Experience Relationships: Oxynorm is associated

with typical opioid-related adverse experiences. There is a

general relationship between increasing oxycodone

plasma concentration and increasing frequency of dose-

related opioid adverse experiences eg, nausea, vomiting,

CNS effects and respiratory depression. In opioid-tolerant

patients, the situation is altered by the development of

tolerance to opioid-related side effects and the relationship

is not clinically relevant. As with all opioids, the dose must

be individualized (see Dosage & Administration) because

the effective analgesic dose for some patients will be too

high to be tolerated by other patients.

Ampule: Oxycodone is a full opioid agonist with no

antagonistic properties. It has an affinity for κ, mc and δ

opioid receptors in the brain and spinal cord. Oxycodone is

similar to morphine in its action. The therapeutic effect is

mainly analgesic, anxiolytic, antitussive and sedative.

Pharmacokinetics: Capsule: Oxynorm provide immediate

delivery of oxycodone. Oral bioavailability of 60-87%. Upon

repeated dosing in normal volunteers in pharmacokinetic

studies, steady-state levels were achieved within 24-36

hrs. Oxycodone is extensively metabolized and eliminated

primarily in the urine as both conjugated and unconjugated

metabolites. The apparent elimination t½ of oxycodone is

3.2 hrs.

Absorption: About 60-87% of an oral dose of oxycodone

reaches the central compartment in comparison to a

parenteral dose. This high oral bioavailability is due to low

presystemic and/or first-pass metabolism. In normal

volunteers, the t½ of absorption is 0.4 hrs for immediate-

release oral oxycodone.Given the short t½ of elimination of

oxycodone, steady-state plasma concentrations of

oxycodone are achieved within 24-36 hrs of initiation of

dosing with oxycontin.

Distribution: Following IV administration, the volume of

distribution (Vss) for oxycodone was 2.6 L/kg. Oxycodone

binding to plasma protein at 37°C and a pH of 7.4 was

about 45%. Once absorbed, oxycodone is distributed to

skeletal muscle, liver, intestinal tract, lungs, spleen and

brain. Oxycodone has been found in breast milk (see

Precautions).

Metabolism: Oxycodone hydrochloride is extensively

metabolized to noroxycodone, oxymorphone and their

glucuronides. The major circulating metabolite is

noroxycodone with an AUC ratio of 0.6 relative to that of

oxycodone. Noroxycodone is reported to be a considerably

weaker analgesic than oxycodone.

Oxymorphone, although possessing analgesic activity, is

present in the plasma only in low concentrations. The

correlation between oxymorphone concentrations and

opioid effects was much less than that seen with

oxycodone plasma concentrations. The analgesic activity

profile of other metabolites is not known.

The formation of oxymorphone, but not noroxycodone, is

mediated by cytochrome P-450, 2D6 and as such, its

formation can, in theory, be affected by other drugs (see

Drug-Drug Interactions in the following texts).

Excretion: Oxycodone and its metabolites are excreted

primarily via the kidney. The amounts measured in the

urine have been reported as follows: Free oxycodone up to

19%; conjugated oxycodone up to 50%; free oxymorphone

0%; conjugated oxymorphone 14%; both free and

conjugated noroxycodone have been found in the urine but

not quantified. The total plasma clearance was 0.8 L/min

for adults.

Paracetamol The main mechanism of action of paracetamol is considered to be the inhibition of cyclooxygenase (COX), and recent findings suggest that it is highly selective for COX-2. While it has analgesic and antipyretic properties comparable to those of aspirin or other NSAIDs, its peripheral anti-inflammatory activity is usually limited by several factors, one of which is high level of peroxides present in inflammatory lesions. However, in some circumstances, even peripheral anti-

PO/Rectal 0.5-1 g 4-6 hrly when needed.

Max: 4 g/day.

IV >50 kg: 1 g 4-6 hrly (Max: 4 g/day); <50 kg: 15 mg/kg 4-6 hrly (Max: 60 mg/kg/day).

Renal or hepatic impairment; alcohol-dependent patients; G6PD deficiency.

Nausea, allergic reactions, skin rashes, acute renal tubular necrosis.Potentially Fatal: Very rare, blood dyscrasias (e.g. thrombocytopenia, leucopenia, neutropenia, agranulocytosis); liver damage.

inflammatory activity comparable to other NSAIDs can be observed.Because of its selectivity for COX-2 it does not significantly inhibit the production of the pro-clotting thromboxanes.

PiaglitazonePioglitazone is as a potent and highly selective agonist

for the peroxisome proliferator activated receptor-

gamma (PPAR). Activation of these receptors promotes

the production of gene products involved in lipid and

glucose metabolism. It also improves insulin response

to target cells witho increasing the pancreatic secretion

of insulin.

Onset: Delayed.

Absorption: Peak plasma concentrations after 2 hr.

Distribution: Protein-binding: >99%.

Metabolism: Extensively metabolised by hydroxylation

and oxidation.

Excretion: Urine (15-30%); faeces (as metabolites); 3-

7 hr (elimination half-life, parent drug).

Hypersensitivity. Type 1

diabetes mellitus,

symptomatic or history of

heart failure, diabetic

ketoacidosis, childn <18 yr.

Lactation.

Pharyngitis, oedema,

headache, upper resp tract

infection, sinusitis, anaemia; GI

disturbances, wt gain, visual

disturbances, dizziness,

arthralgia, haematuria,

impotence.

PiptazPiperacillin, an extended-spectrum penicillin, exerts its

antimicrobial action in growing and dividing bacteria by

interfering with septum formation and cell wall synthesis of

susceptible bacteria. It binds to penicillin-binding proteins

on the bacterial cell wall and blocks peptidoglycan

synthesis. Peptidoglycan is a heteropolymeric structure

that gives the cell wall its mechanical stability. The final

stage of the peptidoglycan synthesis involves the

Treatment of infections in the lower resp tract eg severe community-aquiredpneumonia & healthcare pneumonia; uncomplicated & complicated skin & skin structure infections; intra-abdominal infections w/ peritonitis eg complicated appendicitis; complicated & uncomplicated UTI; gynecologic infection eg postpartum endometritis or pelvic inflammatory disease; bacterial infection in neutropenic patients; bone & joint infections; bacterialsepsis.

Hypersensitivity to penicillins,

cephalosporins & β-lactam

inhibitors.

Rash, pruritus, fever; diarrhea, nausea, constipation, vomiting, dyspepsia, stool changes, abdominal pain, transient leucopenia, neutropenia, thrombocytopenia; hepatic & renal effects; headache, insomnia, agitation, dizziness, anxiety; HTN, chest pain, edema, moniliasis, rhinitis, dyspnea, hypotension, ileus, syncope, rigors, phlebitis, pain, inflammation, thrombophlebitis.

completion of the cross-linking with the terminal glycine

residue of the pentaglycine bridge linking to the fourth

residue of the pentapeptide. The transpeptidase that

performs this step is inhibited by piperacillin. The bacterial

cell wall weakens leading to swelling and rupture of the

microorganism.

Tazobactam, a penicillin acid sulfone with β-lactamase

inhibitory properties, is similar to sulbactam although it is

regarded as more potent. It irreversibly inactivates many

plasmid-mediated and some chromosome-mediated β-

lactamases. Tazobactam can inhibit staphylococcal β-

lactamases and β-lactamases classified as Richmond-

Sykes types II, III, IV and V. Unlike clavulanic acid, it

generally does not induce production of type I

chromosomally mediated cephalosporins in Pseudomonas

or Enterobacteriaceae.

Pravastatin Pravastatin is structurally similar to the HMG, a substituent of the endogenous substrate of HMG-CoA reductase. Unlike its parent compound, mevastatin, and statins such as lovastatin and simvastatin, pravastatin does not need to be activated in vivo. Its hydrolyzed lactone ring mimics the tetrahedral intermediate produced by the reductase allowing the agent to bind with a much greater affinity than its natural substrate. The bicyclic portion of pravastatin binds to the coenzyme A portion of the active site.

For the treatment of hypercholesterolemia and to reduce the risk of cardiovascular disease.

Hypersensitivity; active liver disease; childn <8 yr. Pregnancy, lactation

GI symptoms, headache, insomnia, chest pain, rash, fatigue, dizziness, myalgia, hypersensitivity, anaphylaxis, angioedema, rhabdomyolysis, renal failure, hepatitis, alopoecia, paraesthesia, impotence, gynaecomastia.

Ranitidine Ranitidine blocks histamine H2-receptors in the stomach and prevents histamine-mediated gastricg7 acid secretion. It does not affect pepsin secretion, pentagastrin-stimulated factor secretion or serum gastrin.Absorption: 50% with peak plasma concentrations after 2-3 hr (oral); rapid with peak plasma concentrations after 15 min (IM).Distribution: Widely distributed. Crosses the placental barrier and enters breast milk. Protein-binding: 20%Metabolism: Hepatic; converted to N-oxide, S-oxide and desmethylranitidine.

Benign gastric and duodenal ulceration, H.pylori infection, Gastro-oesophageal reflux disease, Hypersecretory conditions, Acid aspiration during general anaesthesia, Dyspepsia, Prophylaxis of acid aspiration during general anaesthesia, Hypersecretory conditions, Stress ulceration of upper gastrointestinal tract

Porphyria Headache, dizziness. Rarely hepatitis, thrombocytopaenia, leucopaenia, hypersensitivity, confusion, gynaecomastia, impotence, somnolence, vertigo, hallucinations.Potentially Fatal: Anaphylaxis, hypersensitivity reactions.

Excretion: Urine (as unchanged drug) within 24 hr; faeces; 2-3 hr (elimination half-life).

Simvastatin Simvastatin is a prodrug metabolised in the liver to form the active β-hydroxyacid derivative. This inhibits the conversion of HMG-CoA to mevalonic acid by blocking HMG-CoA reductase, an early and rate-limiting step in cholesterol biosynthesis. It reduces total cholesterol, LDL-cholesterol and triglycerides and increases HDL-cholesterol levels.Onset: 3 days.Absorption: Absorbed from the GI tract (oral).Distribution: Protein-binding: 95%.Metabolism: Extensively hepatic; undergoes metabolism by CYP3A4.Excretion: Mainly excreted in the faeces as metabolites. Urine (10-15% inactive form); 1.9 hr (elimination half-life, active metabolite).

hyperlipidemia, renal impairment, cardiovascular risk reduction

Acute liver disease or unexplained persistent elevations of serum transaminases. Pregnancy, lactation. Porphyria. Patients of Chinese descent should not take 80 mg dose w/ lipid-modifying dose of niacin-containing products (≥1 g/day).

Headache, nausea, flatulence, heartburn, abdominal pain, diarrhoea/constipation, dysgeusia; dose-related myopathy (e.g. myalgia, muscle weakness and dark urine); serum transaminases and CPK elevations; hypersensitivity; lens opacities; blurring of vision; dizziness; sexual dysfunction; insomnia; depression and upper respiratory symptoms.Potentially Fatal: Severe rhabdomyolysis with acute renal failure.

Telmisartan  angiotensin II receptor blockers (ARBs) such as telmisartan bind to the angiotensin II type 1 (AT1) receptors with high affinity, causing inhibition of the action of angiotensin II on vascular smooth muscle, ultimately leading to a reduction in arterial blood pressure.

Treatment of essential hypertension.Prevention of cardiovascular morbidity and mortality in patients ≥55 years at high risk in cardiovascular disease

Hypersensitivity to the telmisartan or to any of the excipients of Pritor.Second and 3rd trimesters of pregnancy and lactation.Biliary obstructive disorders and severe hepatic impairment.

Back pain; diarrhea; dizziness; sinus pain or congestion; sore throat; upper respiratory tract infection.

Tramadol Tramadol inhibits reuptake of norepinephrine, serotonin and enhances serotonin release. It alters perception and response to pain by binding to mu-opiate receptors in the CNS.Onset: Oral (conventional tablet): 1 hr.Duration: Oral (conventional tablet): 3-6 hr.Absorption: Readily absorbed from the GI tract (oral).Distribution: Widely distributed. Crosses the placenta and enters breast milk.Metabolism: Extensive hepatic first-pass metabolism; converted to O-desmethyltramadol (active) by N- and O-demethylation via the cytochrome P450 isoenzymes CYP3A4 and CYP2D6 and glucuronidation or sulfation.Excretion: Via urine (as metabolites); 6 hr (elimination half-life).

Moderate to severe pain, postoperative pain Suicidal patients, acute alcoholism; head injuries; raised intracranial pressure; severe renal impairment; lactation.

Sweating, dizziness, nausea, vomiting, dry mouth, fatigue, asthenia, somnolence, confusion, constipation, flushing, headache, vertigo, tachycardia, palpitations, miosis, insomnia, orthostatic hypotension, seizures, CNS stimulation e.g. hallucinations.Potentially Fatal: Respiratory depression.

Unasyn Upper & lower resp tract infections, UTI & pyelonephritis; intra-abdominal infections, bacterial septicemia, soft tissue, bone & joint infections, gonococcal infections. Incidence of post-op wound infections.

History of allergic reaction to any penicillins.

GI disturbances. Phlebitis, skin rashes, itching, blood disorders, anaphylaxis & superinfection.

Vancomycin Vancomycin, a glycopeptide antibiotic, is used in the treatment of severe staphylococcal or other gram positive infections where other drugs cannot be used due to resistance or intolerance. It prevents the transfer and addition of muramylpentapeptide building blocks that make up the peptidoglycan molecule thus inhibiting formation of peptidoglycan polymers of the bacterial cell wall. It is active aginst Staphylococci eg, S. aureus, S. epidermidis, S. pneumoniae, Str. pyrogenes and some strains of Group B streptococci, Clostridium difficile, Actinomyces species, Bacillus anthracis, Corynebacterium species, some lactobacilli and Listeria species. Vancomycin demostrates concentration-independent or time dependent killing.Absorption: Poorly absorbed from the GI tract; may be increased if GI tract is inflamed. 60% of intraperitoneal dose absorbed through the peritoneal cavity in 6 hr.Distribution: Extracellular fluids eg, pleural, ascitic, synovial, pericardial fluids; bile (small amounts), CSF (little diffusion); crosses the placenta and enters breast milk. Protein-binding: 55%.Metabolism: Minimal or no metabolism.Excretion: Via the kidneys by glomerular filtration (80-90% as unchanged); 4-6 hr (elimination half-life), prolonged in renal impairment (7.5 days in anephric).

Staphylococcal enterocollitis, antibiotic-associated colitis, renal impairment, severe staphylococcal or other gram-positive infections, osteomyelitis,septicemia, soft tissue infections, prophylaxis of endocarditis

Hypersensitivity to the drug; history of impaired hearing; IM administration.

Ototoxicity, nephrotoxicity, eosinophilia, "red-man" syndrome (e.g. flushing, hypotension, erythema), urticaria, thrombophloebitis, hypersensitivity reactions.Potentially Fatal: Stevens-Johnson syndrome; toxic epidermal necrolysis, blood dyscrasias such as neutropenia or thrombocytopenia.

Vincristine Vincristine arrests cell division at the metaphase stage by inhibiting microtubule formation in the mitotic spindle.Absorption: Poorly absorbed from the GI tract.Distribution: Does not cross the blood-brain barrier in significant amounts. Protein-binding: Extensive.Metabolism: Metabolised in liver.Excretion: Excreted mainly via bile into feces (as unchanged drug and metabolites, 70-80%), urine; 85 hrs (elimination half-life)

Acute lymphoblastic leukaemia, AIDS-related Kaposi's sarcoma, Hodgkin's disease, Neuroblastoma, Small cell lung cancer, Wilm's tumour, Brain tumours, Non-Hodgkin's lymphoma, Acute myeloid leukaemiaFor children: Usual recommended dosage: 1.5-2 mg/m2 once wkly; for patients ≤10 kg: Initiate at 0.05 mg/kg once wkly. Subsequent doses may be modified based on clinical and haematological responses and tolerance of the patient. May be used in combination with other drugs. Prescribers should consult published protocols for the dosage, method and sequence of admin.

Patients with demyelinating form of Charcot-Marie-Tooth syndrome. Pregnancy and lactation. Intrathecal admin (may be fatal). Patients receiving radiation therapy through ports which include liver.

Dose limiting neurotoxicity (e.g. motor function impairment, gait abnormalities), hyperuricaemia, bronchospasm, azospermia, amenorrhoea, alopoecia, leucopenia, urinary dysfunction, abdominal cramps, vomiting, diarrhoea, severe constipation, paralytic ileus, convulsions, hypertension, orthostatic hypotension, ptosis, hoarseness, optic neuropathies, hallucinations, blindness, neurological deafness, difficulty in walking, syndrome of inappropriate ADH secretion.Potentially Fatal: Myelosuppression.

Love the Lord your God with all your heart and with all your soul and with all your mind and with all your strength. (Mark 12:30)

Do you not know? Have you not heard? The LORD is the everlasting God, the Creator of the ends of the earth. He will not grow tired or weary, and his understanding no one can fathom. He gives strength to the weary and increases the power of the weak. Even youths grow tired and weary, and young men stumble and fall; but those who hope in the LORD will renew their strength. They will soar on wings like eagles; they will run and not grow weary, they will walk and not be faint. (Isaiah 40:28-31)

GOD BLESS GUYS! -KIM TAGS