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Hepatic Lipidosis Most common form of severe liver disease in cats. Most often seen in obese cats suddenly subjected to dietary deprivation. May also be associated with diabetes mellitus, drug injury and toxicity. Thedisease seems to result from the sudden mobilisation of the bodies fat stores which quickly overwhelms the liver's ability to process the raw fat into useful nutrients. The fat accumulates in the liver rapidly and causes acute liver failure. The end result is a swollen, greasy liver which is fragile and yellow to see. The cats present with complete lack of appetite and many signs of acute liver failure. Treatment is based on the provision of a highly nutritious diet to provide the energy required to run the body, stop the ongoing mobilisation of the fat stores, and drive the liver to decrease the fatty accumulation in the liver. Treatment is difficult and a long process.

Up to 25% of patients with TB of the lymph nodes (TB lymphadenitis) will get worse on treatment before they get better and this usually happens in the first few months of treatment. [ citation needed ] A few weeks after starting treatment, lymph nodes often start to enlarge, and previously solid lymph nodes may soften and develop into tuberculous cervical lymphadenitis . This should not be interpreted as failure of therapy and is a common reason for patients (and their physicians) to panic unnecessarily. With patience, two to three months into treatment the lymph nodes start to shrink again and re-aspiration or re-biopsy of the lymph nodes is unnecessary: if repeat microbiological studies are ordered, they will show the continued presence of viable bacteria with the same sensitivity pattern, which further adds to the confusion: physicians inexperienced in the treatment of TB will then often add second-line drugs in the belief that the treatment is not working. In these situations, all that is required is re-assurance. Steroids may be useful in resolving the swelling, especially if it is painful, but they are unnecessary. Additional antibiotics are unnecessary and the treatment regimen does not need to be lengthened. [ citation needed ]

    Intestinal Neuronal Dysplasia (IND) is a colonic motility disorder first described in 1971 by Meier-Ruge associated to characteristic histochemical changes of the bowel wall (hyperplasia of submucous & myenteric plexus with giant ganglia formation,  isolated ganglion cells in lamina propia and muscularis mucosa, elevation of acetylcholinesterase in parasympathetic fiber of lamina propia and circular muscle, and myenteric plexus sympathetic hypoplastic innervation), also known as hyperganglionosis associated to elevated acetylcholinesterase parasympathetic staining. The condition can occur in an isolated form (either localized to colon or disseminated throughout the bowel), or associated to other diseases such as Hirschsprung's (HD), neurofibromatosis, MEN type IIB, and anorectal malformations. It is estimated that 20-75% of HD cases have IND changes proximal to the aganglionic segment. Clinically two different types of isolated IND have been described: Type A shows symptoms of abdominal distension, enterocolitis, bloody stools, intestinal spasticity in imaging studies (Ba Enema) since birth, is less common and associated with hypoplasia of sympathetic nerves. Type B is more frequent, symptoms are indistinguishable from that of HD, with chronic constipation, megacolon, and repeated episodes of bowel obstruction. Management depends on clinical situation; conservative for minor symptoms until neuronal maturation occurs around the 4th year of life, colostomy and resectional therapy for life threatening situations.
 

Steroid drugs ppt

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