COMA UREMICO PDF

History[ edit ] Urea was crystallized and identified between and It was hypothesized that excess urea may lead to specific disorders. Later in , it was confirmed that the body did produce urea and that it was excreted by the kidneys. In , urea was produced in vitro via oxidation of proteins. It was in that Thomas Dutrochet seeded the idea of dialysis with the discovery of separating smaller molecules from larger molecules through a semipermeable membrane. They also suggested that harm may be caused by this.

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History[ edit ] Urea was crystallized and identified between and It was hypothesized that excess urea may lead to specific disorders. Later in , it was confirmed that the body did produce urea and that it was excreted by the kidneys. In , urea was produced in vitro via oxidation of proteins. It was in that Thomas Dutrochet seeded the idea of dialysis with the discovery of separating smaller molecules from larger molecules through a semipermeable membrane.

They also suggested that harm may be caused by this. Later research suggested that major neurological disorders like coma and convulsions did not correlate with physical findings which included generalized edema of the brain. This suggested that uremia was a form of blood poisoning. Frerich described clinical uremic syndrome and suggested that a toxicity was the mechanism of its cause.

It was in that J. Picard developed a sensitive method to reproducibly measure blood urea. This work solidified the fact that renal failure coincided with an increase in blood urea. It was J. Picard with E. The patients may present with ammonia-like taste and smell in mouth, stomatitis, gingivitis, decreased salivary flow, xerostomia and parotitis.

It is an ammonia odour in the mouth caused by the high concentration of urea in the saliva which subsequent breakdown to ammonia. Uremic stomatitis appears as a pseudo membrane or the frank ulcerations with redness and a pultaceous coat in the mouth.

It is believed to be caused by loss of tissue resistance and failure to withstand traumatic influences. It is a white plaque found on the skin or in the mouth, it is caused by residual urea crystals left on the epithelial surface after perspiration and saliva evaporation or as a result of reduced salivary flow. Uraemia can lead to alteration of platelet aggregation. This situation, combined with the use of heparin and other anticoagulants in haemodialysis, causes the patients to become predisposed to ecchymosis , petechiae , and haemorrhages in the oral cavity.

In addition, patients might also experience altered taste sensations, dysgeusia , and be predisposed to bacterial and candidiasis infections.

Candidiasis is more frequent in renal transplant patients because of generalized immunosuppression. The abnormalities of dental development correlate with the age at which metabolic disturbances occur. For example, enamel hypoplasia in the form of white or brown discoloration of primary teeth is commonly seen in young children with early-onset renal disease.

The salivary pH will usually be above the critical pH level for demineralization of the enamel to occur and this helps to prevent the formation of caries. Any alterations in drugs or other aspects of treatment must be previously agreed upon by the nephrologist.

All potential foci of infection should be intercepted; these include periodontal and endodontic lesions, residual roots, partially erupted and malpositioned third molars, peri-implantitis, and mucosal lesions. When periodontitis is suspected, a periodontal chart should be recorded.

Orthodontic appliances can be maintained if they do not interfere with oral hygiene. For hemodialysis patients, it is important to determine the treatment schedule. Dental treatment should be started on the day after hemodialysis due to several reasons: there is no accumulation of uremic toxins in the blood, and circulating heparin is absent. Treatment should not commence on the same day as hemodialysis as patients usually feel unwell and their blood is heparinized, which might cause excessive bleeding.

For patients undergoing peritoneal dialysis, there are no contraindications to dental treatment except in cases of acute peritoneal infections, where elective procedure should be deferred. Any injections or blood pressure measurement should not be performed on an arm with an arteriovenous AV fistula.

If the AV site is located on a leg, the patient should avoid sitting for lengthy periods, as venous drainage may be obstructed. During long dental procedures, the dentist should allow patients with AV sites on their legs to take a brief walk or stand for a while every hour. Hemostatic aids should be instituted in cases of excessive bleeding, which is commonly seen in uremia and renal failure. To manage postoperative bleeding, primary closure techniques and local hemostatic agents should be used routinely.

To reduce bleeding during and after a procedure, tranexamic acid, both as a rinse or administered orally, can be used. It is important to adopt infection control measures to avoid cross-contamination in the dental clinic and prevent risk of exposure to dental personnel. Due to renal failure, the plasma half-lives of drugs normally excreted in urine will be prolonged, leading to increased toxicity.

Many drugs which are normally safely administered cannot be given to patients with reduced renal function. Besides, some drugs can be given, but the dosage must be reduced. However, in patients undergoing dialysis, reduced plasma half-lives of drugs will be observed. The antibiotics of choice are penicillins, clindamycin, and cephalosporins, which can be administered at normal doses even if the therapeutic range will be extended.

Aspirin is characterized by an anti-platelet activity and thus its use should be avoided in uremic patients. Only one is listed.

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Uremia - Cause e Sintomi

Ket Increased tyrosine nitration of the brain in chronic renal insufficiency: Pregnancy-associated hemolytic uremic syndrome revisited in the era of complement gene mutations. Eculizumab for the treatment of two recurrences of atypical hemolytic uremic syndrome in a kidney allograft. Guanidino compound levels in brain regions of non-dialyzed uremic patients. Myocardial infarction is a complication of factor H-associated atypical HUS.

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