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Chemwatch:4650.13 Page 12 of 18 Issue Date:11/12/2018
<br /> Version No:7.1.1.1 API Pond Ammonia Test Solution#1 Print Date:06/21/2019
<br /> be separated into two general classes which could loosely be regarded as"good prostaglandins"and"bad prostaglandins",
<br /> according to the structure of a particular enzyme involved in their biosynthesis,cyclooxygenase(COX).
<br /> Prostaglandins whose synthesis involves the cyclooxygenase-I enzyme,or COX-1,are responsible for maintenance and
<br /> protection of the gastrointestinal tract,while prostaglandins whose synthesis involves the cyclooxygenase-II enzyme,or
<br /> COX-2,are responsible for inflammation and pain.
<br /> The existing non-steroidal anti-inflammatory drugs(NSAIDs)differ in their relative specificities for COX-2 and COX-1
<br /> There has been much concern about the possibility of increased risk for heart attack and stroke in users of NSAID drugs,
<br /> particularly COX-2 selective NSAIDs.The cardiovascular risks associated with NSAIDs are controversial,with apparently
<br /> contradictory data produced from different clinical trials and in published meta-analyses. Cardiovascular risk of COX-2
<br /> specific inhibitors is not surprising since prostaglandins are involved in regulation of blood pressure by the kidneys.
<br /> COX-inhibitors produce blood dyscrasias(abnormal conditions of the blood),and interfere with platelet function.
<br /> Phototoxic or photoallergic skin reactions may also occur.Anaphylactoid reactions characterised by maculopapular rash,
<br /> urticaria,pruritus,bronchospasm,and syncope have been described.Other effects include oedema,metabolic acidosis,
<br /> hyperkalaemia,azotemia,cystitis and urinary tract infections,visual and hearing disturbances,conjunctivitis,corneal
<br /> deposits,retinal degeneration,ear pain and occasionally,deafness.Idiosyncratic responses include asthma,allergic
<br /> interstitial nephritis,hypersensitivity hepatitis,aplastic anaemia and exfoliative dermatitis.
<br /> Non-steroidal anti-inflammatory drugs with an inhibitory effect on prostaglandin synthesis,when given during the latter
<br /> stages of pregnancy,cause premature closure of the foetal ductus arteriosus(1).When given at term they prolong labour
<br /> and delay parturition.Evidence(1)from animal experimental studies,clinical investigations in humans,and epidemiological
<br /> studies supports the hypothesis that NSAIDs are chemopreventative agents against colon cancer.This is corroborated by
<br /> I knowledge of the underlying path ophysiological mechanisms and the effects of arachidonic metabolites,Le
<br /> prostaglandins,on the carcinogenic process and the influence of cyclooxygenase(COX)inhibitors such as NSAIDs on
<br /> these metabolites.1.Berkel et al;Epidemiol Rev.,Vol 18,No.2,1996
<br /> Because of the known effects of NSAIDs drugs on the foetal cardiovascular system(closure of ductus arteriosus),use
<br /> during pregnancy(particularly late pregnancy)should be avoided.In rat studies with NSAIDs,as with other drugs known to
<br /> inhibit prostaglandin synthesis,an increased incidence of dystocia,delayed parturition,and decreased pup survival
<br /> occurred
<br /> Aspirin and NSAIDs may cause anaphylactic or anaphylactoid reactions.Constitutively-expressed cyclooxygenase
<br /> (COX-1)inhibition is likely to be responsible for the cross-reactions and side effects associated with these drugs,as well
<br /> as the anaphylactoid reactions sometimes seen in aspirin-sensitive respiratory disease.Though anaphylactic and
<br /> anaphylactoid reactions may be clinically indistinguishable,they involve different mechanisms.Anaphylactic reactions
<br /> are due to immediate hypersensitivity involving cross-linking of drug-specific IgE.Regardless of COX selectivity pattern,
<br /> NSAIDs may function as haptens capable of inducing allergic sensitization.Unlike anaphylaxis,anaphylactoid reactions
<br /> are most likely related to inhibition of COX-1 by NSAIDS.Thus,an anaphylactoid reaction caused by a particular COX-1
<br /> inhibiting NSAID will occur with a chemically unrelated NSAID which also inhibits COX-1 enzymes.Selective COX-2
<br /> inhibitors appear to be safe in patients with a history of NSAID-related anaphylactoid reactions but can function as
<br /> haptens,with resulting sensitisation and anaphylaxis upon next exposure.Eva A Berkes Clinical Reviews in Allergy and
<br /> Immunology 24,pp 137-147 2003.
<br /> COX-2 inhibitors reduce inflammation(and pain)while minimising gastrointestinal adverse drug reactions(e.g.stomach
<br /> ulcers)that are common with non-selective NSAIDs. COX-1 is involved in synthesis of prostaglandins and thromboxane,
<br /> but COX-2 is only involved in the synthesis of prostaglandin.Therefore,inhibition of COX-2 inhibits only prostaglandin
<br /> synthesis without affecting thromboxane and thus has no effect on platelet aggregation or blood clotting.
<br /> Chronic abuse of analgesics has been associated with nephropathy.Patients invariably have a history of regular ingestion
<br /> of substantial or excessive doses over a period of years.In mild cases the condition is reversible.The initial renal lesion
<br /> is papillary necrosis proceeding to secondary atrophic changes in the renal cortex body.An abnormally high incidence of
<br /> transitional cell carcinoma of the renal pelvis and bladders has been reported in patients with analgesic nephropathy.
<br /> Mild chronic salicylate intoxication,or"salicylism",may occur after repeated exposures to large doses. Symptoms
<br /> include dizziness,tinnitus,deafness,sweating,nausea and vomiting,headache and mental confusion. Symptoms of
<br /> more severe intoxication include hyperventilation,fever,restlessness,ketosis,and respiratory alkalosis and metabolic
<br /> acidosis. Depression of the central nervous system may lead to coma,cardiovascular collapse and respiratory failure.
<br /> Chronic exposure to the salicylates(o-hydroxybenzoates)may produce metabolic and central system disturbances or
<br /> damage to the kidneys.Persons with pre-existing skin disorders,eye problems or impaired kidney function may be more
<br /> susceptible to the effects of these substances.Certain individuals(atopics),notably asthmatics,exhibit significant hyper-
<br /> sensitivity to salicylic acid derivatives.Reactions include urticaria and other skin eruptions,rhinitis and severe(even
<br /> fatal)bronchospasm and dyspnea.Chronic exposure to the p-hydroxybenzoates(parabens)is associated with
<br /> hypersensitivity reactions following application of these to the skin.Hypersensitivity reactions have also been reported
<br /> following parenteral or oral administration.Cross-sensitivity occurs between the p-hydroxybenzoates Hypersensitivity
<br /> reactions may include by acute bronchospasm,hives(urticaria),deep dermal wheals(angioneurotic oedema),running nose
<br /> (rhinitis)and blurred vision.Anaphylactic shock and skin rash(non-thrombocytopenic purpura)may also occur.Any
<br /> individual may be predisposed to such anti-body mediated reaction if other chemical agents have caused prior
<br /> sensitisation(cross-sensitivity).
<br /> Exposure to the material for prolonged periods may cause physical defects in the developing embryo(teratogenesis).
<br /> API Pond Ammonia Test TOXICITY ' , IRRITATION -
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