DRUG FORMULARY

Amlodipine Apidra Atorvastatin Azithromycin Ceftriaxone Cefuroxime Celecoxib Clonidine Clopidogrel Co-Amoxiclav Doxorubicin Doxycycline Furosemide Humulin Irbesartan Kalimate Kalium durule eucovorin evofloxacin osartan !efenamic acid methotrexate !etronidazole "orgesic forte #meprazole #xynorm $aracetamol $iaglitazone $iptaz %anitidine &imvastatin 'ramadol (nasyn )ancomycin )incristine DRUG Amlodipine MOA
Amlodipine relaxes peripheral and coronary vascular smooth muscle. It produces coronary vasodilation by

INDICATION
Hypertension* angina* myocardial ischemia+ %educe the ris, of coronary

CONTRAINDICATION
Known sensitivity to dihydropyridines.

ADVERSE REACTION
Headache, peripheral oedema, fatigue, somnolence, nausea,

inhibiting the entry of Ca ions into the voltage-sensitive channels of the vascular smooth muscle and myocardium during depolarisation. It also increases myocardial ! delivery in patients with vasospastic angina. Absorption: "ell absorbed from the #I tract $oral%& pea' plasma concentrations after (-)! hr. Distribution: *rotein-binding+ ,-../. Metabolism: Hepatic+ 0xtensive. Excretion: 1ia urine $mainly as metabolites, )2/ as unchanged%& 3.-.2 hr $elimination half-life%. Apidra *harmacotherapeutic #roup+ Insulin and analogues, fastacting. A7C Code+ A)2A82(. *harmacodynamics+ Insulin glulisine is a recombinant human insulin analogue that is e9uipotent to regular human insulin. Insulin glulisine has a more rapid onset of action and a shorter duration of action than regular human insulin. 7he primary activity of insulins and insulin analogues, including insulin glulisine, is regulation of glucose metabolism. Insulins lower blood glucose levels by stimulating peripheral glucose upta'e, especially by s'eletal muscle and fat and by inhibiting hepatic glucose production. Insulin inhibits lipolysis in the adipocyte, inhibits proteolysis and enhances protein synthesis. Atorvastatin Atorvastatin competitively inhibits H>#-CoA reductase, the en4yme that catalyses the conversion of H>#-CoA to mevalonic acid. 7his results in the induction of the @=@ receptors, leading to lowered @=@-cholesterol concentration. Absorption: 5apid from the #I tract $oral%. Distribution: *rotein-binding+ ,A/. Metabolism: 0xtensively hepatic& converted to active inhibitors of H>#-CoA reductase. Excretion: 6aeces $as metabolites%& )B hr $elimination

revascularization* fetal coronary heart disease* non-fatal !I - stro,e+ Oral Hypertension, Prinzmetal's angina, Stable angina Adult: Initially, . mg once daily increased to )2 mg once daily if necessary. Elderly: Initial dose+ !.. mg once daily. Hepatic impairment: Initial dose+ !.. mg once daily. 7reatment of adults, adolescents : childn ;( yr w< =>, where treatment w< insulin is re9uired.

abdominal pain, flushing, dyspepsia, palpitations, di44iness. 5arely pruritus, rash, dyspnoea, asthenia, muscle cramps. Potentially Fatal: Hypotension, bradycardia, conductive system delay and CC6.

Hypoglycemia.

Hypoglycemia, in? site reactions, lipodystrophy, local : systemic

Mixed dyslipidaemia !on"amilial #yperc#olesterolaemia Heterozygous "amilial #yperc#olesterolaemia I

Hypersensitivity, active liver disease or unexplained persistent elevations of serum transaminase, porphyria, pregnancy, lactation.

Increased ACC for norethindrone and ethinyl estradiol. Concomitant multiple doses of atorvastatin and digoxin increased steady-state digoxin levels. Increased ris' of rhabdomyolysis when used concurently with fibrates. Coadmin with antacid suspensions and colestipol decreased atorvastatin levels.

half-life%. A it!rom"#in A4ithromycin bloc's transpeptidation by binding to .2s ribosomal subunit of susceptible organisms and disrupting 5DA-dependent protein synthesis at the chain elongation step. Absorption: 5educed by food $capsule formulation%& pea' plasma concentrations after !-3 hr. Distribution: 0xtensive into the tissues $concentrations higher than those in blood%, "8C $high concentrations%, CE6 $small amounts%. Metabolism: @iver $demethylation%. Excretion: 1ia the bile $as unchanged drug and metabolites%& via the urine $(/ of the dose%. 0limination Ce$tria%one half-life+ about (A hr. Ceftriaxone binds to one or more of the penicillin-binding proteins .$/$s0 1hich inhibits the final transpeptidation step of peptidoglycan synthesis in bacterial cell 1all* thus inhibiting biosynthesis and arresting cell 1all assembly resulting in bacterial cell death+ A&sorption' $ea, plasma concentrations after 2 hr .I!0+ Distri&(tion' Distributed 1idely into body tissues and fluids3 C&F .therapeutic concentrations0+ Crosses the placenta and enters breast mil,3 bile .high concentrations0+ $rotein-binding4 56-768+ E%#retion' )ia the urine .9:-;68 as unchanged03 via the bile to the faeces .remainder as unchanged and microbiologically inactive compounds03 ;-7 hr .elimination half-life0+ Cefuroxime binds to one or more of the penicillin-binding proteins (PBPs) which inhibits the final transpeptidation step of peptidoglycan synthesis in bacterial cell wall, thus inhibiting biosynthesis and arresting cell wall assembly resulting in bacterial cell death. Absorption: Absorbed from the ! tract with pea" plasma concentrations after #-$ hr (oral)% may be enhanced by the presence of food. Distribution: Pleural and syno&ial fluid, sputum, bone and a'ueous fluids% C() (therapeutic concentrations). Crosses the placenta and enters breast mil". Protein-binding* +p to ,-.. Metabolism: /apidly hydrolysed (intestinal mucosa and blood). Excretion: 0ia the urine by glomerular filtration and renal (ncomplicated gonorrhoea* $rophylaxis of secondary meningococcal meningitis* &usceptible infections* $rophylaxis of surgical infections* 'yphoid fever Hypersensitivity to cephalosporins3 hyperbilirubinaemic neonates+ Do not use calcium or calciumcontaining solutions or products 1ith or 1ithin 95 hr of ceftriaxone administration due to ris, of calcium-ceftriaxone precipitate formation &uperinfection3 anaphylaxis3 diarrhoea3 local reactions3 blood dyscrasias3 rash* fever* pruritus3 elevated transaminases and al,aline phosphatase3 leucopenia* neutropenia+ )otentiall" Fatal' $seudomembranous colitis3 nephrotoxicity respiratory tract infections, s'in and soft tissue infections, typhoid hypersensitivity >ild to moderate nausea, vomiting, abdominal pain, dyspepsia, flatulence, diarrhoea, cramping& angioedema, cholestatic ?aundice& di44iness, headache, vertigo, somnolence& transient elevations of liver en4yme values.

Cefuroxime

uncomplicated +1!, respiratory tract infection, uncomplicated gonorrhea, meningitis,

2ypersensiti&ity to cephalosporins.

3arge doses can cause cerebral irritation and con&ulsions% nausea, &omiting, diarrhoea, ! disturbances% erythema multiforme, (te&ens4ohnson syndrome, epidermal necrolysis. Potentially Fatal: Anaphylaxis, nephrotoxicity, pseudomembranous colitis.

tubular secretion (as unchanged)% &ia bile (small amounts)% 5min (elimination half-life)% prolonged in neonates and renal impairment.

Celecoxib

Ciprofloxacin

Celecoxib is a nonsteroidal antiinflammatory drug (6(A!7) 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, fe&er, swelling and tenderness. Celecoxib bloc"s the en8yme that ma"es prostaglandins (cyclooxygenase #), resulting in lower concentrations of prostaglandins. As a conse'uence, inflammation and its accompanying pain, fe&er, swelling and tenderness are reduced. Celecoxib differs from other 6(A!7s 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. !nhibits bacterial 76A topoisomerase !!, thereby including 76A strand brea"age and cell death

Celecoxib is used for the relief of pain, fe&er, swelling, and tenderness caused by osteoarthritis, 9u&enile arthritis, rheumatoid arthritis, and an"ylosing spondylitis. Celecoxib does not pre&ent the progression of either type of arthritis. !t reduces only the symptoms and signs of arthritis. Celecoxib is appro&ed for patients with familial )AP who ha&e not had their colons remo&ed. Celebrex also is also used for the relief of acute pain and the pain of menstrual cramps (primary dysmenorrhea). <ffecti&e against gram-negati&e species, including Psedomonas, 6eisseria, 2aemophilus species and <nterobacter as well as against =ycoplasma and 3egionella species.
#ypertension, prop#ylaxis "or migraine,#ypertensi%e crisis

2ypersensiti&ity including those in whom attac"s of angioedema, rhinitis and urticaria ha&e been precipitated by aspirin, 6(A!7s or sulfonamides. (e&ere hepatic impairment% se&ere heart failure% inflammatory bowel disease% peptic ulcer% renal impairment (CrCl :$- ml;min)% pregnancy and lactation. Component sensiti&ity

Abdominal pain, diarrhea, nausea, oedema, di88iness, headache, insomnia, upper respiratory tract infections% rash. Potentially )atal* (erious s"in reactions such as exfoliati&e dermatitis, (te&ens-4ohnson syndrome, and toxic epidermal necrolysis.

! upset% s"in rash%headache% di88iness% tendonitis and tendon rupture in adults

=ry mouth, drowsiness, di44iness, headache, constipation, impotence, vivid dreams, urinary retention& dry, itching, burning sensation in the eye& fluid or electrolyte imbalance, #I upset, paralytic ileus, orthostatic hypotension, wea'ness, sedation, pruritus, myalgia, urticaria, nausea, insomnia, arrhythmias, agitation. 5educed #I motility at times may cause paralytic ileus. Potentially Fatal: 7ransient hypertension or profound hypotension, respiratory depression, convulsion. Clonidine withdrawal syndrome could be life threatening. 8radycardia, coma and disturbances in conduction $in individuals with preexisting diseases of EA<A1 nodes, overdose or on digitalis%.

Clonidine

Clonidine stimulates alpha-! receptors in brain stem which results in reduced sympathetic outflow from the CDE and a decrease in peripheral resistance leading to reduced 8* and pulse rate. It does not alter normal haemodynamic response to exercise at recommended dosages. $nset: !-3 days $transdermal%. Duration: >aintained for A hr after removal of system $transdermal%. Absorption: "ell absorbed from the #I tract $oral%& pea' plasma concentrations after 3-. hr. Absorbed from the s'in $transdermal%. Distribution: !2-B2/ protein bound. Metabolism: Hepatic+ .2/ of the dose. Excretion: 1ia urine within !B hr $as B2-(2/ as unchanged drug%, via faeces $!2/ of the dose%& (-!B hr $elimination half-life%, prolonged to B) hr in renal

Hypersensitivity. =isorders of cardiac pacema'er activity and conduction. *regnancy and lactation.

Clopidogrel

Co-Amoxicla&

impairment. Clopidogrel inhibits adenosine diphosphate $A=*% from binding to its receptor sites on the platelets and subse9uent activation of glycoprotein #* IIb<IIIa complex thus preventing fibrinogen binding, platelet adhesion and aggregation. Absorption: 5apidly but incompletely absorbed from the #I tract $oral%. Distribution: *rotein-binding+ 0xtensive. Metabolism: Hepatic+ 0xtensive& converted to inactive carboxylic acid derivative and thiol derivative $active%. Excretion: 1ia urine and faeces $as metabolites and unchanged drug%. Inhibits enzymes involved in formation of peptidoglycan layer of bacterial cell 1all*no effect on human cell 1alls+ /actericidal* only 1or,s on dividing bacteria+ <ell absorbed enterally*Clavulanic acid inhibits beta-lactamase Half life4 =hour >limination4%apid clearance from plasma due to active secretion into renal tubular fluid - can be bloc,ed by probenecid Also excreted in bile

$rophylaxis of thromboembolic disorders* hepatic impairment* cute coronary syndrome

Hypersensitivity. Active pathological bleeding. admin within - days after >I and ischaemic stro'e, coagulation disorders. @actation.

=yspepsia, abdominal pain, nausea, vomiting, flatulence, constipation, gastritis, gastric and duodenal ulcers. #I upset, diarrhoea, paraesthesia, vertigo, headache, di44iness, pruritus and rashes. Potentially Fatal: 8leeding disorders including #I and intracranial haemorrhage. 8lood dyscrasias. =iarrhea, nausea : vomiting, s'in rash : urticaria, vaginitis. 5arely, pseudomembranous colitis, stomatitis : candidiasis, erythema multiforme : other s'in effects. Hepatic, renal, hematologic or CDE effects.

$rophylaxis against infections associated 1? ma@or surgical procedures+ 'reatment of resp tract* A('* s,in - soft tissue* #-A* bone* intra-abdominal - post-op infections

Hypersensitivity to penicillins. *enicillinassociated cholestatic ?aundice or hepatic dysfunction.

Do%or(&i#in

Doxorubicin is a cytotoxic anthracycline antibiotic+ 'he cytotoxic action results from its binding to D"A and inhibition of nucleic acid synthesis+ Doxorubicin has been sho1n to produce regression in a variety of disseminated malignancies+ Absorption4 %apidly cleared from the blood after I) admin+ Distribution4 Distributed into tissues including lungs* liver* heart* spleen and ,idneys .I)03 crosses the placenta3 enters breast mil,+ !etabolism4 Hepatic3 rapidly converted to doxorubicinol+ >xcretion4 /ile .as unchanged drug03 =2 min* B+B hr* B: hr .mean elimination half-lives0+

'reatment of acute leu,emias* lymphomas a variety of solid tumors+

!ar,ed myelosuppression induced by previous chemotherapy or radiotherapy* preexisting heart disease* previous treatment 1? complete cumulative doses of doxorubicin or other anthracyclines+ $regnancy lactation+

!yelosuppression - cardiotoxicity3 alopecia* hyperpigmentation of nailbeds dermal creases primarily in childn3 s,in reaction3 acute nausea vomiting3 mucositis3 ulceration - necrosis of the colon esp the cecum3 vascular phlebosclerosis3 facial flushing .rapid in@ use03 erythematous strea,ing3 anaphylaxis3 crosssensitivity to lincomycin

Do%"#"#line

Doxycycline binds to B:& and 6:& ribosomal subunits thus causing alterations on the cytoplasmic membrane of susceptible organisms+ A&sorption' %eadily and almost completely absorbed from the AI tract .oral03 pea, plasma concentrations after 2 hr+ Absorption not significantly affected by food+ Distri&(tion' ipid-soluble3 into body tissues and fluids+ $rotein-binding4 5:-768+ Meta&olism' Inactivated in the liver+ E%#retion' )ia urine .9:8* may be increased if urine is al,aline03 =2-29 hr .elimination half-life0+ inhibits reabsorption of Da and chloride mainly in the medullary portion of the ascending @oop of Henle. 0xcretion of potassium and ammonia is also increased while uric acid excretion is reduced. It increases plasmarenin levels and secondary hyperaldosteronism may result. 6urosemide reduces 8* in hypertensives as well as in normotensives. It also reduces pulmonary oedema before diuresis has set in. Absorption: 6airly rapidly absorbed from the #I tract $oral%. Distribution: Crosses the placenta and enters breast mil'. *rotein-binding+ ,,/. Excretion: 1ia urine $as unchanged%& ! hr $elimination half-life%, may be prolonged in neonates and renal and hepatic impairment. P#armacology: 7he 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 in?ection, blood supply, temperature and physical activity.

&usceptible infections* (ncomplicated gonorrhoea* &yphilis* %elapsing fever and louse-borne typhus* $rophylaxis of scrub typhus* Acne* &usceptible infections

Children C5 yr3 pregnancy* lactation3 porphyria3 hypersensitivity to tetracyclines3 severe hepatic dysfunction3 prolonged exposure to sunlight or tanning eDuipment+

$ermanent staining of teeth3 rash* superinfection3 nausea* AI upsets* glossitis3 dysphagia3 photosensitivity* hypersensitivity3 haemolytic anaemia* thrombocytopenia* neutropenia and eosinophilia+ )otentiall" Fatal' Anaphylaxis+

F(rosemide

hypertension* edema* heart failure* oliguria in acute or chrnic renal failure

Eevere sodium and water depletion, hypersensitivity to sulphonamides and furosemide, hypo'alaemia, hyponatraemia, precomatose states associated with liver cirrhosis, anuria or renal failure. AddisonFs disease.

6luid and electrolyte imbalance. 5ashes, photosensitivity, nausea, diarrhoea, blurred vision, di44iness, headache, hypotension. 8one marrow depression $rare%, hepatic dysfunction. Hyperglycaemia, glycosuria, ototoxicity. Potentially Fatal: 5arely, sudden death and cardiac arrest. Hypo'alaemia and magnesium depletion can cause cardiac arrhythmias. @ipodystrophy, insulin resistance. @ocal : generalised allergic reactions.

*(m(lin

7reatment of diabetes mellitus for the control of hyperglycemia.

Hypoglycemia.

Ir&esartan

Ibesartan is an angiotensin II type I receptor antagonist and therefore bloc's the vasoconstricting and aldosteronesecreting effects of angiotensin II. Absorption: 5apidly absorbed from the #I7 $oral%& pea' plasma concentrations are achieved after )..-! hrs. Distribution: *rotein-binding around ,(/ Metabolism: Eome hepatic metabolism via cytochrome *B.2 isoen4yme CG*!C, to inactive metabolites.

H&! Diabetic nep#ropat#y in &ype ' DM

Hypersensitivity& pregnancy and lactation.

=iarrhoea, di44iness, fatigue, headache, hyper'alaemia. =yspepsia, oedema, myalgia, insomnia, nasal congestion, )st dose orthostatic hypotension, rash, pharyngitis, urticaria, angioedema, anxiety<nervousness, tachycardia.

Excretion: 1ia bile and urine $as unchanged drug and metabolites%& via urine $!2/ of I1 dose, H!/ as unchanged%. ))-). hrs $elimination half-life%.

>alimate

P#armacology: Kalimate contains --,/ calcium, ) g of which is exchanged for .3--) mg $).3(-).A! m09<g% of potassium in vitro $KCl solution%. 8y administering ).-32 g<day of Kalimate to renal failure patients $adults%, the serum potassium level is reduced by about ) m09<@ $humans%. Cnli'e 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%. Eince Kalimate is a calcium-type resin, it is used even for the patients who restricted ingestion of sodium. >oreover, it can be used without fear of appearance and aggravation of edema, hypertension or cardiac insufficiency induced by sodium $human%. >echanism 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 conse9uence, potassium in the intestinal tract is excreted outside the body. P#armaco(inetics: 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 H. micrometer in si4e has been absorbed through the mucous membrane and deposited on the reticuloendothelial system tissue. Kalimate is controlled in order that such fine

$revention - treatment of hyper,alemia resulting from acute or chronic renal failure+

*atients w< intestinal obstruction : stenosis, constipation.

Constipation, anorexia : nausea. Hypopotassemia.

particles are H2.)/ in rate.

>alium 7urule

Hypo'alemia. *rophylaxis during treatment w< diuretics.

Le(#ovorin

eucovorin is freDuently used in con@unction 1ith !ethotrexate and 6-F(+ eucovorin is not a Chemotherapeutic drug itself* ho1ever it is an ad@unct to these chemotherapy drugs+ eucovorin is a compound similar to Foli# a#id* 1hich is a vital )itamin+

Levo$lo%a#in

3osartan

@evofloxacin exerts antibacterial action by inhibiting bacterial topoisomerase I1 and =DA gyrase, the en4ymes re9uired for =DA replication, transcription repair and recombination. It has in vitro activity against a wide range of gram-negative and gram-positive microorganisms. Absorption: 5apid and complete absorption from the #I7 $oral%& pea' plasma concentrations within )-! hr. Distribution: "idely distributed in bronchial mucosa, lungs& CE6 $relatively poor%. *rotein-binding+ 32-B2/. Metabolism: @imited. Excretion: >ainly via urine $largely as unchanged drug%& (-A hr $elimination half-life%. @osartan is an angiotensin II receptor antagonist. 7he drug and its active metabolite selectively bloc' the vasoconstrictor and aldosterone-secreting effects of angiotensin II by selectively antagonising its binding to A7)receptors. Absorption: 5eadily absorbed from #I tract with pea'

Antidote $or $oli# a#id anta+onists /egin leucovorin rescue 1?in 29 hr of antifolate administration+ =: mg?m2 follo1ed by another dose ; hrly for E2 hr+ If at 29 hr increase in serum creatinine is F6:84 =:: mg?m 2 B hrly until serum methotrexate G6 x =: 5 !+ Co(ntera#t !ematolo+i# to%i#it" 6-=6 mg?day+ Amp Antidote $or $oli# a#id anta+onists ;-=2 mg I! every ; hrly for 9 doses+ Res#(e a$ter !i+!,dose met!otre%ate t!erap" =6 mg B hrly I! or I)* starting B hr after the beginning of methotrexate infusion* for 7 doses - then ; hrly for B doses+ Advan#ed #olore#tal #an#er 2:: mg?m2 by slo1 I) in@ over a min of B min follo1ed by 6-F( .BE: mg?m 20 or 2: mg?m2 I) follo1ed by 6-F( .926 mg?m 20+ 'reatment is repeated daily for 6 days* this 6-day course may be repeated at 25-day intervals+ sinusitis* chronic bronchitis*CA$* pneumonia* ('I* pyelonephritis* prostatitis

5enal insufficiency, hyper'alemia, untreated AddisonFs disease, constriction of the esophagus :<or obstructive changes in the alimentary tract. "eonates - infants+ )it /=2 deficiency anemia+

K salts : K-sparing diuretics, eg spironolactone. Amiloride, triam terene, tacrolimus, AC0 inhibitors.

Allergic sensitization+

Hypersensitivity to levofloxacin or other Duinolones+ Child C=5 yr

ral<I1+ Dausea, diarrhoea, constipation, headache, insomnia, in? site reactions $I1%. phthalmic+ 7ransient decrease in vision, ocular burning, ocular pain or discomfort, foreign body sensation, headache, fever, pharyngitis, photophobia. Potentially Fatal: Anaphylaxis.

Hypertension* type II D!

*regnancy, lactation& children with CrCl H32 ml<min<).-3m!

Headache, di44iness, bac' pain, myalgia, respiratory tract disorders, asthenia<fatigue, first dose hypotension, rash, angioedema, neutropenia, #I disturbances, transient elevation of

plasma concentrations of losartan after around ) hr and its active metabolite after 3-B hr. Distribution: ,A/ plasma protein bound. Metabolism: Hepatic metabolism principally by isoen4ymes CG*3AB and !C,. Excretion: 0xcreted in faeces and urine as metabolites and unchanged drug. 7erminal elimination half life of ! hr $losartan% and (-, hr $active metabolite%.

liver en4ymes, impaired renal function, taste disturbances and hyper'alaemia.

=efenamic Acid

$ain and inflammation

Inflammatory bo1el disease3 peptic ulcer3 neonates3 pregnancy .Brd trimester0* lactation+ Coronary artery bypass graft surgery* severe renal impairment* severe heart failure+

Abdominal pain* dyspepsia* constipation* diarrhoea* nausea* AI ulcers3 oedema3 bronchospasm3 headache* dro1siness* insomnia* visual disturbances3 CHF* hypertension* tachycardia* syncope3 urticaria* rash3 thrombocytopenia* aplastic anaemia* agranulocytosis3 tinnitus3 elevated liver enzymes3 abnormal renal function+ $otentially Fatal4 Autoimmune haemolytic anaemia3 convulsions .overdosage0+

Met!otre%ate

!ethotrexate is a folic acid antagonist that inhibits D"A 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+ A&sorption' %apidly absorbed from the AI tract at lo1 doses* higher doses are less 1ell absorbed+ %apidly and completely absorbed after I! doses+ $ea, plasma concentrations after =-2 hr .oral0* B:-;: min .I!0+ Distri&(tion' 'issues and extracellular fluids3 crosses the blood-brain barrier and placenta3 enters breast mil,+ &mall amounts in saliva and breastmil,+ 6:8 bound to plasma proteins+ /ound as polyglutamate con@ugates* bound drug may remain in the body for several mth* particularly in the liver + Meta&olism' $artly by intestinal flora+ Does not undergo

/ur,ittHs lymphoma* Acute lymphoblastic leu,aemia* Choriocarcinom*!ycosis fungoides* %heumatoid arthritis* $soriasis* CrohnHs disease* !eningeal leu,aemia* #steosarcoma* Choriocarcinoma* /reast cancer* Advanced lymphosarcoma* Acute lymphoblastic leu,aemia

&evere renal or hepatic impairment* pre-existing profound bone marro1 suppression in patients 1ith psoriasis or rheumatoid arthritis* alcoholic liver disease* AID&* pre-existing blood dyscrasias* pregnancy .in patients 1ith psoriasis or rheumatoid arthritis0* breastfeeding+

(lceration of the mouth and AI disturbances .e+g+ stomatitis and diarrhoea0* bone marro1 depression* hepatotoxicity* renal failure* s,in reactions* alopecia* ocular irritation* arachnoiditis in intrathecal use* megaloblastic anaemia* osteoporosis* precipitation of diabetes* arthralgias* necrosis of soft tissue and bone* anaphylaxis* impaired fertility+ )otentiall" Fatal' $ulmonary reactions .e+g+ interstitial lung disease03 neurotoxicity .e+g+ leu,oencephalopathy* paresis*

Metronidazole

6orgesic forte

significant metabolism at lo1 dose therapy3 E-hydroxy metabolite is detected at high-doses+ E%#retion' $rimarily via urine3 small amounts in bile* faeces+ &ome evidence of enterohepatic recirculation+ Interindividual variation exists* patients 1ith delayed clearance are at an increased ris, of toxicity+ =etronida8ole is con&erted to reduction products that interact with 76A to cause destruction of helical 76A structure and strand leading to a protein synthesis inhibition and cell death in susceptible organisms. !t is effecti&e against a wide range of organisms including <. histolytica, 1. &aginalis, iardia, anaerobes e.g. Bacterioides sp, )usobacterium sp, Clostridiumsp, Peptococc us sp and Peptostreptococcus sp, and moderately acti&e against ardnerella sp and Campylobacter sp. Absorption: /eadily absorbed from the ! tract (oral), poorly absorbed from the &agina (intra&aginal)% pea" plasma concentrations after ?-# hr (oral), ,-?# hr (rectal), @ hr (intra&aginal). =ay be delayed by the presence of food. Distribution: Protein-binding* :#-.. Aidely distributed in body tissues and fluids e.g. bile, bone, breast mil", cerebral abscesses, C(), li&er and li&er abscesses, sali&a, semenal fluid, &aginal secretions (concentrations similar to those in plasma)% crosses the placenta and rapidly enters fetal circulation. Metabolism: 2epatic &ia side-chain oxidation and glucuronide formation. Excretion: =ainly &ia urine (as metabolites)% &ia faeces (small amounts). <limination half-life* @ hr% longer in neonates and se&ere hepatic impairment. Analgesic<s'eletal muscle relaxant.

demyelination0 1ith use3 foetal deaths

intrathecal

Amoebiasis, Balantidiasis, Balantidiasis, 1richomoniasis, iardiasis, Bacterial &aginosis, Acute necrotising ulcerati&e gingi&itis, Acute dental infections, Anaerobic bacterial infections, Prophylaxis of postoperati&e anaerobic bacterial infections, <radication of 2. pylori associated with peptic ulcer disease,3eg ulcers and pressure sores, Antibiotic-associated colitis, Anaerobic bacterial infections, Prophylaxis of postoperati&e anaerobic bacterial infections, Anaerobic infections, Prophylaxis of postoperati&e anaerobic bacterial infections, 1opical;Cutaneous )ungating tumours, /osacea

2istory of hypersensiti&ity to metronida8ole or other nitroimida8ole deri&ati&es. Pregnancy (?st trimester) and lactation.

! disturbances e.g. nausea, unpleasant metallic taste, &omiting, diarrhoea or constipation. )urred tongue, glossitis, and stomatitis due to o&ergrowth of Candida. /arely, antibiotic-associated colitis. Aea"ness, di88iness, ataxia, headache, drowsiness, insomnia, changes in mood or mental state. 6umbness or tingling in the extremities, epileptiform sei8ures (high doses or prolonged treatment). 1ransient leucopenia and thrombocytopenia. 2ypersensiti&ity reactions. +rethral discomfort and dar"ening of urine. /aised li&er en8yme &alues, cholestatic hepatitis, 9aundice. 1hrombophlebitis (!0). Potentially Fatal: Anaphylaxis.

Omepra ole

mepra4ole suppresses gastric acid secretion by specific inhibition of the en4yme system hydrogen<potassium adenosine triphosphatase $HI<KIA7*ase% present on the secretory surface of the gastric parietal cell. $nset: Antisecretory+ approx ) hr& pea' effect+2..-3.. hr. Duration: -! hr. Absorption: 5apid but variable $oral%& dose-dependent.

5elief of painful s'eletal muscle spasm associated with chronic low bac' pain, sprains and strains, prolapsed intervertebral disc, muscle in?ury, nonarticular rheumatism $fibrositis, myositis and myalgia%, FwhiplashF in?uries, acute torticollis, tension headache, dysmenorrhea and other acute or chronic painful muscular conditions. peptic ulcer, #05=,Jollinger-0llison syndrome, acid related dyspepsia, esophagitis,

*atients with glaucoma, prostatic hypertrophy or obstruction at the baldder nec' or myasthenia gravis.

Dausea, dry mouth, blurring of vision, di44iness and restlessness. 5arely, rash or drowsiness may occur. 7hese symptoms disappear rapidly with a reduction in dosage or cessation of medication.

=iarrhoea, nausea, fatigue, constipation, vomiting, flatulence, acid regurgitation, taste perversion, arthralgia, myalgia, urticaria, dry mouth, di44iness, headache, paraesthesia, abdominal pain, s'in rashes, wea'ness, bac' pain, upper respiratory infection, cough. Potentially Fatal: Anaphylaxis.

8ioavailability+

ral+ approx 32-B2/.

Distribution: *rotein-binding+ ,./. Metabolism: 0xtensively hepatic& converted to hydroxyomepra4ole and omepra4ole sulfone. Excretion: 1ia urine $--/% and bile. 0limination half-life+ 2..-3 hr.

Bxynorm

P#armacology: *harmacodynamics+ Capsule+ Central Dervous Eystem+ xycodone is a pure agonist opioid ther whose principal therapeutic action is analgesia.

7reatment of moderate to severe pain in patients with cancer and postoperative pain. 6or the treatment of severe pain re9uiring the use of strong opioids

*atients with 'nown hypersensitivity to oxycodone or any of the other ingredients, or in any situation where opioids are contraindicated. 7his 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 H)2 m@<min%, chronic constipation, concurrent administration of monoamine oxidase inhibitors or within ! wee's of discontinuation of their use& pregnancy. )se in lactation: xycodone

Capsule+

xycodone has been in

clinical use for -. years. Eerious adverse reactions which may be associated with xynorm 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 shoc' $see verdosage%. 7he nonserious adverse events seen on initiation of therapy with xynorm are typical opioid side effects. 7hese events are dosedependent and their fre9uency depends upon the dose, the clinical setting, the patientFs level of opioid tolerance and host factors specific to the individual. 7hey should be expected and managed as a part of opioid analgesia. 7he most fre9uent $K./% include+ Constipation, nausea,

members of the class 'nown as opioid agonists include substances eg, morphine, hydromorphone, fentanyl, codeine and hydrocodone. *harmacological effects of opioid agonists include anxiolysis, euphoria, feelings of relaxation, respiratory depression, constipation, miosis and cough supression as well as analgesia. @i'e all pure opioid agonist analgesics with increasing doses, there is increasing analgesia. 7his is unli'e mixed agonist<antagonists or non-opioid analgesics where there is a limit to the analgesic effect with increasing doses. 7he ceiling to analgesic effectiveness is imposed only by side effects, the more serious of which may include somnolence and respiratory depression. "hile the precise mechanism of analgesic action is un'nown, specific CDE opioid receptors for endogenous compounds with opioid-li'e activity have been identified throughout the brain and spinal cord and play a role in the analgesic effects of oxynorm. xycodone 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.

may be secreted in breast mil' and may cause respiratory depression in the newborn. xycodone should therefore not be used in breastfeeding

somnolence, di44iness, vomiting, xycodone depresses the cough reflex by direct effect on the cough center in the medulla. Antitussive effects may occur with doses lower than those usually re9uired for analgesia. xycodone causes miosis even in total dar'ness. *inpoint pupils are a sign of opioid overdose but are not pathognomonic $eg, pontine lesions of hemorrhagic or ischemic origin may produce similar findings%. >ar'ed mydriasis rather than miosis may be seen with hypoxia in the setting of oxynorm overdose $see #astrointestinal 7ract and verdosage%. mothers. pruritus, headache, dry mouth, sweating and asthenia. In many cases, the fre9uency of these events during initiation of therapy may be minimi4ed by careful individuali4ation of starting dosage, slow titration and the avoidance of large swings in the plasma concentrations of the opioid. 6ollowing are the common adverse ther Emooth >uscle+ events associated with immediaterelease oxycodone

xycodone causes a reduction in motility associated with an increase in smooth muscle tone in the antrum of the stomach and duodenum. =igestion in the small intestines is delayed and propulsive contractions are decreased. *ropulsive peristaltic waves in the colon are decreased while tone may be increased to the point of spasm resulting in constipation. ther opioid-induced effects may ddi and transient include a reduction in gastric, biliary and pancreatic secretions, spasm of sphincter of elevations in serum amylase. Cardiovascular Eystem+ xycodone may produce release

of histamine with or without associated peripheral vasodilation. >anifestations of histamine release and<or peripheral vasodilation may include pruritus, flushing, red eyes, sweating and<or orthostatic hypotension. Concentration-0fficacy 5elationships+ Etudies in normal volunteers and patients reveal predictable relationships between oxycodone dosage and plasma 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 individuali4ed titration of dosage to the desired effect. 7he 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. ConcentrationAdverse 0xperience 5elationships+ xynorm is associated with typical opioid-related adverse experiences. 7here is a general relationship between increasing oxycodone plasma concentration and increasing fre9uency of doserelated opioid adverse experiences eg, nausea, vomiting, CDE 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 individuali4ed $see =osage : Administration% because the effective analgesic dose for some patients will be too high to be tolerated by other patients. Ampule+ xycodone is a full opioid agonist with no xycodone is

antagonistic properties. It has an affinity for L, mc and M opioid receptors in the brain and spinal cord. similar to morphine in its action. 7he therapeutic effect is mainly analgesic, anxiolytic, antitussive and sedative. P#armaco(inetics: Capsule+ delivery of oxycodone. xynorm provide immediate

ral bioavailability of (2-A-/. Cpon

repeated dosing in normal volunteers in pharmaco'inetic studies, steady-state levels were achieved within !B-3( hrs. xycodone is extensively metaboli4ed and eliminated primarily in the urine as both con?ugated and uncon?ugated metabolites. 7he apparent elimination tN of oxycodone is 3.! hrs. Absorption+ About (2-A-/ of an oral dose of oxycodone reaches the central compartment in comparison to a parenteral dose. 7his high oral bioavailability is due to low presystemic and<or first-pass metabolism. In normal volunteers, the tN of absorption is 2.B hrs for immediaterelease oral oxycodone.#iven the short tN of elimination of oxycodone, steady-state plasma concentrations of oxycodone are achieved within !B-3( hrs of initiation of dosing with oxycontin. =istribution+ 6ollowing I1 administration, the volume of distribution $1ss% for oxycodone was !.( @<'g. about B./. brain. xycodone binding to plasma protein at 3-OC and a pH of -.B was nce absorbed, oxycodone is distributed to s'eletal muscle, liver, intestinal tract, lungs, spleen and xycodone has been found in breast mil' $see *recautions%. >etabolism+ xycodone hydrochloride is extensively

metaboli4ed to noroxycodone, oxymorphone and their glucuronides. 7he ma?or circulating metabolite is noroxycodone with an ACC ratio of 2.( relative to that of oxycodone. Doroxycodone is reported to be a considerably wea'er analgesic than oxycodone. xymorphone, although possessing analgesic activity, is

present in the plasma only in low concentrations. 7he correlation between oxymorphone concentrations and opioid effects was much less than that seen with oxycodone plasma concentrations. 7he analgesic activity profile of other metabolites is not 'nown. 7he formation of oxymorphone, but not noroxycodone, is mediated by cytochrome *-B.2, !=( and as such, its formation can, in theory, be affected by other drugs $see =rug-=rug Interactions in the following texts%. 0xcretion+ xycodone and its metabolites are excreted

primarily via the 'idney. 7he amounts measured in the urine have been reported as follows+ 6ree oxycodone up to ),/& con?ugated oxycodone up to .2/& free oxymorphone 2/& con?ugated oxymorphone )B/& both free and con?ugated noroxycodone have been found in the urine but not 9uantified. 7he total plasma clearance was 2.A @<min for adults.

Paracetamol

'he main mechanism of action of paracetamol is considered to be the inhibition of cyclooxygenase .C#I0* and recent findings suggest that it is highly selective for C#I-2+ <hile it has analgesic and antipyretic properties comparable to those of aspirin or other "&AIDs* its peripheral antiinflammatory activity is usually limited by several factors* one of 1hich is high level of peroxides present in inflammatory lesions+ Ho1ever* in some circumstances* even peripheral anti-

PO/Rectal :+6-= g 9-; hrly 1hen needed+ !ax4 9 g?day+ IV F6: ,g4 = g 9-; hrly .!ax4 9 g?day03 C6: ,g4 =6 mg?,g 9-; hrly .!ax4 ;: mg?,g?day0+

%enal or hepatic impairment3 alcoholdependent patients3 A;$D deficiency+

"ausea* allergic reactions* s,in rashes* acute renal tubular necrosis+ )otentiall" Fatal' )ery rare* blood dyscrasias .e+g+ thrombocytopenia* leucopenia* neutropenia* agranulocytosis03 liver damage+

inflammatory activity comparable to other "&AIDs can be observed+ /ecause of its selectivity for C#I-2 it does not significantly inhibit the production of the pro-clotting thromboxanes+
Piaglita8one
*ioglita4one is as a potent and highly selective agonist for the peroxisome proliferator activated receptorgamma $**A5%. 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. $nset: =elayed. Absorption: *ea' plasma concentrations after ! hr. Distribution: *rotein-binding+ K,,/. Metabolism: 0xtensively metabolised by hydroxylation and oxidation. Excretion: Crine $).-32/%& faeces $as metabolites%& 3- hr $elimination half-life, parent drug%. Hypersensitivity. 7ype ) diabetes mellitus, symptomatic or history of heart failure, diabetic 'etoacidosis, childn H)A yr. @actation. *haryngitis, oedema, headache, upper resp tract infection, sinusitis, anaemia& #I disturbances, wt gain, visual disturbances, di44iness, arthralgia, haematuria, impotence.

)ipta

*iperacillin, 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 bloc's peptidoglycan synthesis. *eptidoglycan is a heteropolymeric structure that gives the cell wall its mechanical stability. 7he final stage of the peptidoglycan synthesis involves the

7reatment of infections in the lower resp tract eg severe community-a9uiredpneumonia : healthcare pneumonia& uncomplicated : complicated s'in : s'in structure infections& intra-abdominal infections w< peritonitis eg complicated appendicitis& complicated : uncomplicated C7I& gynecologic infection eg postpartum endometritis or pelvic inflammatory disease& bacterial infection in neutropenic patients& bone : ?oint infections& bacterialsepsis.

Hypersensitivity to penicillins, cephalosporins : P-lactam inhibitors.

5ash, pruritus, fever& diarrhea, nausea, constipation, vomiting, dyspepsia, stool changes, abdominal pain, transient leucopenia, neutropenia, thrombocytopenia& hepatic : renal effects& headache, insomnia, agitation, di44iness, anxiety& H7D, chest pain, edema, moniliasis, rhinitis, dyspnea, hypotension, ileus, syncope, rigors, phlebitis, pain, inflammation, thrombophlebitis.

completion of the cross-lin'ing with the terminal glycine residue of the pentaglycine bridge lin'ing to the fourth residue of the pentapeptide. 7he transpeptidase that performs this step is inhibited by piperacillin. 7he bacterial cell wall wea'ens leading to swelling and rupture of the microorganism.

7a4obactam, a penicillin acid sulfone with P-lactamase inhibitory properties, is similar to sulbactam although it is regarded as more potent. It irreversibly inactivates many plasmid-mediated and some chromosome-mediated Plactamases. 7a4obactam can inhibit staphylococcal Plactamases and P-lactamases classified as 5ichmondEy'es types II, III, I1 and 1. Cnli'e clavulanic acid, it generally does not induce production of type I chromosomally mediated cephalosporins in *seudomonas or 0nterobacteriaceae.

*ravastatin

Ranitidine

*ravastatin is structurally similar to the H>#, a substituent of the endogenous substrate of H>#-CoA reductase. Cnli'e its parent compound, mevastatin, and statins such as lovastatin and simvastatin, pravastatin does not need to be activated in vivo. Its hydroly4ed lactone ring mimics the tetrahedral intermediate produced by the reductase allowing the agent to bind with a much greater affinity than its natural substrate. 7he bicyclic portion of pravastatin binds to the coen4yme A portion of the active site. %anitidine bloc,s histamine H2-receptors in the stomach and prevents histamine-mediated gastricgE acid secretion+ It does not affect pepsin secretion* pentagastrin-stimulated factor secretion or serum gastrin+ Absorption4 6:8 1ith pea, plasma concentrations after 2-B hr .oral03 rapid 1ith pea, plasma concentrations after =6 min .I!0+ Distribution4 <idely distributed+ Crosses the placental barrier and enters breast mil,+ $rotein-binding4 2:8 !etabolism4 Hepatic3 converted to "-oxide* &-oxide and desmethylranitidine+

6or the treatment of hypercholesterolemia and to reduce the ris' of cardiovascular disease.

Hypersensitivity& active liver disease& childn HA yr. *regnancy, lactation

#I symptoms, headache, insomnia, chest pain, rash, fatigue, di44iness, myalgia, hypersensitivity, anaphylaxis, angioedema, rhabdomyolysis, renal failure, hepatitis, alopoecia, paraesthesia, impotence, gynaecomastia. Headache* dizziness+ %arely hepatitis* thrombocytopaenia* leucopaenia* hypersensitivity* confusion* gynaecomastia* impotence* somnolence* vertigo* hallucinations+ $otentially Fatal4 Anaphylaxis* hypersensitivity reactions+

/enign gastric and duodenal ulceration* H+pylori infection* Aastro-oesophageal reflux disease* Hypersecretory conditions* Acid aspiration during general anaesthesia* Dyspepsia* $rophylaxis of acid aspiration during general anaesthesia* Hypersecretory conditions* &tress ulceration of upper gastrointestinal tract

$orphyria

(im&astatin

7elmisartan

>xcretion4 (rine .as unchanged drug0 1ithin 29 hr3 faeces3 2-B hr .elimination half-life0+ Eimvastatin is a prodrug metabolised in the liver to form the active P-hydroxyacid derivative. 7his inhibits the conversion of H>#-CoA to mevalonic acid by bloc'ing H>#-CoA reductase, an early and rate-limiting step in cholesterol biosynthesis. It reduces total cholesterol, @=@cholesterol and triglycerides and increases H=@cholesterol levels. $nset: 3 days. Absorption: Absorbed from the #I tract $oral%. Distribution: *rotein-binding+ ,./. Metabolism: 0xtensively hepatic& undergoes metabolism by CG*3AB. Excretion: >ainly excreted in the faeces as metabolites. Crine $)2-)./ inactive form%& )., hr $elimination half-life, active metabolite%. angiotensin II receptor bloc'ers $A58s% such as telmisartan bind to the angiotensin II type ) $A7)% 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.

hyperlipidemia* renal impairment* cardiovascular ris, reduction

Acute liver disease or unexplained persistent elevations of serum transaminases. *regnancy, lactation. *orphyria. *atients of Chinese descent should not ta'e A2 mg dose w< lipidmodifying dose of niacincontaining products $;) g<day%.

Headache, nausea, flatulence, heartburn, abdominal pain, diarrhoea<constipation, dysgeusia& dose-related myopathy $e.g. myalgia, muscle wea'ness and dar' urine%& serum transaminases and C*K elevations& hypersensitivity& lens opacities& blurring of vision& di44iness& sexual dysfunction& insomnia& depression and upper respiratory symptoms. Potentially Fatal: Eevere rhabdomyolysis with acute renal failure. 8ac' pain& diarrhea& di44iness& sinus pain or congestion& sore throat& upper respiratory tract infection.

7reatment of essential hypertension. *revention of cardiovascular morbidity and mortality in patients ;.. years at high ris' in cardiovascular disease

1ramadol

7ramadol inhibits reupta'e of norepinephrine, serotonin and enhances serotonin release. It alters perception and response to pain by binding to mu-opiate receptors in the CDE. $nset: ral $conventional tablet%+ ) hr. Duration: ral $conventional tablet%+ 3-( hr. Absorption: 5eadily absorbed from the #I tract $oral%. Distribution: "idely distributed. Crosses the placenta and enters breast mil'. Metabolism: 0xtensive hepatic first-pass metabolism& converted to -desmethyltramadol $active% by D- and demethylation via the cytochrome *B.2 isoen4ymes CG*3AB and CG*!=( and glucuronidation or sulfation. Excretion: 1ia urine $as metabolites%& ( hr $elimination half-life%.

!oderate to severe pain* postoperative pain

Hypersensitivity to the telmisartan or to any of the excipients of *ritor. Eecond and 3rd trimesters of pregnancy and lactation. 8iliary obstructive disorders and severe hepatic impairment. Euicidal patients, acute alcoholism& head in?uries& raised intracranial pressure& severe renal impairment& lactation.

Eweating, di44iness, nausea, vomiting, dry mouth, fatigue, asthenia, somnolence, confusion, constipation, flushing, headache, vertigo, tachycardia, palpitations, miosis, insomnia, orthostatic hypotension, sei4ures, CDE stimulation e.g. hallucinations. Potentially Fatal: 5espiratory depression.

+nasyn

(pper - lo1er resp tract infections* ('I - pyelonephritis3 intraabdominal infections* bacterial septicemia* soft tissue* bone - @oint infections* gonococcal infections+ Incidence of post-op 1ound

History of allergic reaction to any penicillins+

AI disturbances+ $hlebitis* s,in rashes* itching* blood disorders* anaphylaxis superinfection+

infections+
0ancomycin
1ancomycin, 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 bloc's that ma'e up the peptidoglycan molecule thus inhibiting formation of peptidoglycan polymers of the bacterial cell wall. It is active aginst Etaphylococci eg, E. aureus, E. epidermidis, E. pneumoniae, Etr. pyrogenes and some strains of #roup 8 streptococci, Clostridium difficile, Actinomyces species, 8acillus anthracis, Corynebacterium species, some lactobacilli and @isteria species. 1ancomycin demostrates concentration-independent or time dependent 'illing. Absorption: *oorly absorbed from the #I tract& may be increased if #I tract is inflamed. (2/ of intraperitoneal dose absorbed through the peritoneal cavity in ( hr. Distribution: 0xtracellular fluids eg, pleural, ascitic, synovial, pericardial fluids& bile $small amounts%, CE6 $little diffusion%& crosses the placenta and enters breast mil'. *rotein-binding+ ../. Metabolism: >inimal or no metabolism. Excretion: 1ia the 'idneys by glomerular filtration $A2-,2/ as unchanged%& B-( hr $elimination half-life%, prolonged in renal impairment $-.. days in anephric%. )incristine arrests cell division at the metaphase stage by inhibiting microtubule formation in the mitotic spindle+ Absorption4 $oorly absorbed from the AI tract+ Distribution4 Does not cross the blood-brain barrier in significant amounts+ $rotein-binding4 >xtensive+ !etabolism4 !etabolised in liver+ >xcretion4 >xcreted mainly via bile into feces .as unchanged drug and metabolites* E:-5:80* urine3 56 hrs .elimination half-life0 &taphylococcal enterocollitis* antibioticassociated 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& I> administration.

totoxicity, nephrotoxicity, eosinophilia, Qred-manQ syndrome $e.g. flushing, hypotension, erythema%, urticaria, thrombophloebitis, hypersensitivity reactions. Potentially Fatal: EtevensRohnson syndrome& toxic epidermal necrolysis, blood dyscrasias such as neutropenia or thrombocytopenia.

Vin#ristine

Acute lymphoblastic leu,aemia* AID&-related KaposiHs sarcoma* Hodg,inHs disease* "euroblastoma* &mall cell lung cancer* <ilmHs tumour* /rain tumours* "onHodg,inHs lymphoma* Acute myeloid leu,aemia For children4 (sual recommended dosage4 =+6-2 mg?m2 once 1,ly3 for patients J=: ,g4 Initiate at :+:6 mg?,g once 1,ly+ &ubseDuent doses may be modified based on clinical and haematological responses and tolerance of the patient+ !ay be used in combination 1ith other drugs+ $rescribers should consult published protocols for the dosage* method and seDuence of admin+

$atients 1ith demyelinating form of Charcot-!arie-'ooth syndrome+ $regnancy and lactation+ Intrathecal admin .may be fatal0+ $atients receiving radiation therapy through ports 1hich include liver+

Dose limiting neurotoxicity .e+g+ motor function impairment* gait abnormalities0* 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 1al,ing* syndrome of inappropriate ADH secretion+ $otentially Fatal4 !yelosuppression+

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 ever astin! "od# the $reator o% the ends o% the earth& He wi not !row tired or weary# and his understandin! no one 'an %atho(& He !ives stren!th to the weary and in'reases the )ower o% 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 li e eagles; they will run and not grow weary, they will wal and not be faint. (*saiah +0:2,-31) "OD .L/00 "1203 -4*M T5"0