摘要:

Aluminium is now recognised as an important toxin causing considerable morbidity and mortality, particularly in patients with chronic renal failure. Diseases that have been associated with aluminium include dialysis dementia, renal osteodystrophy and Alzheimer's disease. Aluminium also has an effect on red blood cells, parathyroid glands and chromosomes.Accumulation of aluminium in the body tends to occur when the gastrointestinal barrier is circumvented. This has been identified as a problem during dialysis or intravenous fluid administration. Renal functional impairment results in decreased aluminium excretion and promotes accumulation of the element in the body.Many sources have been shown to be contaminated with aluminium. These include the water used for dialysis; medicines containing aluminium, such as aluminium-containing phosphate binding gels; total parenteral nutrition solutions; processed human serum albumin; intravenous fluids in infants; and other environmental and industrial sources.The management of aluminium toxicity involves the identification of these contaminated sources and subsequent removal of the element. This includes regular monitoring of water used in dialysis. The use of aluminium-containing phosphate binding gels in patients with compromised renal function should be reviewed and alternatives sought. The development of effective aluminium-free phosphate binders is desirable. Once a patient has aluminium toxicity, desferrioxamine (deferoxamine) has been shown to be an effective agent in its chelation and removal.

ISSN:0112-5966    

出版商:ADIS    

年代:1989

数据来源: ADIS

摘要:

Snake envenomation is a major cause of death and disability in the developing countries, particularly India and Southeast Asia. Species variation in venom components, yield, and lethality leads to quite different clinical presentations and mortality. Venomous snakes are divided into 5 families. Bites of the Viperidae. Crotalidae and Colubridae usually cause primarily local effects and bleeding; the Elapidae most commonly cause neurological symptoms, particularly paralysis; while the Hydrophidae cause paralysis and myolysis.Venoms are complex mixtures of enzymes, peptides and metalloproteins. 26 enzymes have been identified, and 10 of those are found in most venoms. Components have been identified that act as procoagulants, anticoagulants, hyaluronidases, RNases, DNases, postsynaptic toxins and presynaptic toxins. Other peptides induce capillary leak syndrome, haemolysis and shock.The clinical results of envenomation vary widely, and there may be no envenomation with a bite. Syndromes reported include oedema, haemolysis, shock, bleeding, pituitary failure, renal failure, myonecrosis, and combinations of the above.First aid measures that have been proposed include tourniquets, constricting bands, tight crepe bandages, incision and suction, cryotherapy, and high voltage electric shock. None of these has been shown to be effective except usage of a crepe bandage for Australian elapid bite. Tourniquets or cryotherapy, if used for extended periods may lead to gangrene. The most important first aid measure is rapid transport to comprehensive medical care.There is some controversy about medical treatment in the United States, but less in other countries. Supportive measures routinely required include intravenous fluids, tetanus prophylaxis and antibiotics. Anticholinergics may be useful in elapid bite. Intubation and ventilation may be necessary. Unproven surgical approaches include excision of envenomated tissues and fasciotomy. The former is disfiguring, the latter should be reserved for those patients with demonstrated increased intracompartmental pressure.More than 100 antivenins are produced by about 36 laboratories worldwide. The products are effective, but carry a high risk of serum sickness and a lesser risk of anaphylaxis. A more effective and less reactive product is under development.

ISSN:0112-5966    

出版商:ADIS    

年代:1989

数据来源: ADIS

摘要:

Although many cases of &bgr;-adrenoceptor antagonist (&bgr;-blocker) poisoning are uneventful, a proportion develop serious and sometimes fatal cardiovascular system depression with severe hypotension. As &bgr;-adrenergic tone is not essential for cardiovascular function in health, there is no physiological reason why total &bgr;-adrenoceptor blockade should have serious consequences in the resting individual. The toxic actions of &bgr;-blockers appear to be related to properties such as membrane depressant activity and possibly due to actions on &bgr;-adrenoceptors distinct from those in the cardiovascular system. Most reports of serious adverse effects following overdosage concern &bgr;-blockers with significant membrane depressant activity, and in particular propranolol and oxprenolol, with which progressive heart block and bradycardia are features. Sotalol toxicity, with its unique electrophysiological action, is a special case. Animal experiments confirm that &bgr;-blockers with membrane depressant activity are more toxic than the newer more selective ones, such as atenolol and nadolol. However, experimental models also reveal that artificial ventilation markedly reduces the toxicity of all &bgr;-blockers tested, suggesting a respiratory depressant action with very high doses. Treatment of serious overdosage in man should include maintenance of adequate ventilation. High dose intravenous glucagon is recommended, because its inotropic action depends on direct stimulation of adenylate cyclase. &bgr;-Agonists such as isoprenaline (isoproterenol) or prenalterol may be effective, but the nature of agonist-competitive antagonist interactions may necessitate the use of unrealistically large doses to overcome very high tissue &bgr;-blocker concentrations.

ISSN:0112-5966    

出版商:ADIS    

年代:1989

数据来源: ADIS

摘要:

Priapism is characterised by a persistent erection that cannot be relieved by sexual intercourse or masturbation. Although priapism subsides spontaneously in a few days, impotence frequently follows. Both vascular and neural mechanisms are implicated in the pathophysiology of priapism, but it is not clear which initiates the process.Idiopathic cases of priapism are the most frequent (near 50%); other medical conditions that can result in priapism are haematological diseases (mainly sickle cell anaemia and leukaemia), traumatism, and neoplastic processes. Drug-induced priapism comprises about 30% of cases. The drugs most frequently implicated are psychotropic drugs (phenothiazines and trazodone), antihypertensives (mainly prazosin) and heparin. Recently, the intracavernosal injection of vasoactive drugs (papaverine and phentolamine) has been described in patients treated for impotence. With the exception of heparin, an &agr;-adrenergic blocking mechanism has been suggested in the priapism-inducing action of these drugs.A significant number of anecdotal case reports link priapism and drugs, and it is possible that certain cases of idiopathic priapism could be reclassified if accurate pharmacological anamnesis were to be performed.Priapism must be considered a urological emergency. Surgical procedures are the most preferred treatment for this condition but, in selected cases, drug treatment seems to be an alternative approach.

ISSN:0112-5966    

出版商:ADIS    

年代:1989

数据来源: ADIS

摘要:

Scores of drugs in common clinical use are capable of inflicting various degrees of damage to the kidney. Similarly, a large number of widely employed chemicals may adversely affect renal tissue as part of their toxic potential. A xenobiotic may damage the kidney by more than one mechanism. For example, NSAIDs may cause decreased renal perfusion, interstitial nephritis, primary glomerulopathy and/or altered potassium homeostasis. A large number of drugs and chemicals inflict their damage on the renal tubular cell secondary to intracellular accumulation to concentrations substantially higher than in the plasma or in other tissues. These include aminoglycosides, mercury and carbon tetrachloride and cephaloridine.Drug-induced interstitial nephritis is characterised by inflammatory lesions of the renal interstitium developed after at least 7 to 10 days of therapy. The immunological nature of this reaction is suggested by the associated fever, maculopapular rash and arthralgia observed in some of the patients. Although eosinophilia, eosinophiluria, and raised blood IgE levels are characteristic, immunoglobulins are not deposited in renal tissue, and the basic mechanism has not been elucidated. Renal biopsy demonstrates oedema and interstitial inflammatory reaction, mainly with lymphocytes, monocytes, eosinophils and plasma cells. Less frequent, vasculitis of small vessels or granulomatous reaction may develop, leading to necrotising glomerulonephritis. The drugs most commonly causing acute interstitial nephritis are methicillin, ampicillin, cephalosporins, rifampicin (rifampin), sulphonamides, phenindione and allopurinol. Other penicillins, NSAIDs, phenytoin, thiazides and frusemide (furosemide) are less frequently associated with this syndrome.Drugs and chemicals may affect renal function by pharmacologically decreasing glomerular filtration rate and/or renal blood flow. These include the NSAIDs, radiological contrast media and cyclosporin.Normal renal function depends upon an intact glomerular apparatus. Many drugs and chemicals are capable of damaging the glomerulus, causing its increased permeability to large molecules such as proteins. Several drugs includingd-penicillamine, thiopronine, captopril, pyrithioxine and methimazole, are believed to exert their damage through their sulfhydryl group which bind with high affinity to glomerular structures.A variety of xenobiotics or their metabolites may be deposited in the renal tubule causing obstruction of urine flow and a secondary damage to tubular epithelium. Sulphonamides, methotrexate and ethylene glycol are good examples.Drugs and chemicals may adversely affect renal handling of water and electrolytes by a variety of mechanisms. While chlorpropamide enhances the secretion and pharmacological action of antidiuretic hormone, lithium may lead to nephrogenic diabetes insipidus.The most important step in approaching drug- or chemical-induced nephrotoxicity is the recognition of the role played by the specific agent.Before institution of therapy with a known nephrotoxin, it is imperative to obtain baseline measurements of renal function (plasma creatinine and urea, creatinine clearance and uronalysis). Drug-induced nephrotoxicity is often augmented by dehydration and pre-existing renal failure; maintaining adequate urine output with mannitol minimises the nephrotoxic risk of radiocontrast media, methotrexate and cisplatin. The clinician should be aware of possible drug interactions which are likely to increase the nephrotoxic risk of a given agent. Similarly, disease states may augment renal toxicity in a specific manner.Following exposure to a known nephrotoxin, it is important to assure that dose schedules of drugs excreted by the kidney are modified to correct for changes in their clearance rate.

ISSN:0112-5966    

出版商:ADIS    

年代:1989

数据来源: ADIS

摘要:

Chlordiazepoxide 40mg daily was used to prevent delerium tremens in a 64-year-old female with alcoholic liver disease. After 20 days, the drug was stopped because of the onset of progressive drowsiness. The kinetics of chloridazepoxide were within the predicted range for patients with liver disease, but the elimination half-lives of desmethylchlor-diazepoxide and demoxepam were greatly prolonged at 346 hours and 150 hours, respectively. It is suggested that metabolite accumulation may have contributed to the coma, which is an unusual reaction to chlordiazepoxide.

ISSN:0112-5966    

出版商:ADIS    

年代:1989

数据来源: ADIS