Uroxatral
By Q. Miguel. University of Illinois at Urbana-Champaign.
OTHER TREATMENTS Surgery If there is a clear established focus then maybe the best treatment is to remove it cheap 10 mg uroxatral with amex. This is, of course, both difficult and expensive but its use is expanding with about 500 operations per year in the UK. It is only considered in cases of partial (not general) epilepsy when conventional drug therapy has failed and a clear focus can be established. The advent of sophisticated assessments, such as MIR, long-term EEG telemetry, in- depth electrode recording and PETstudies of blood flow and diazepan binding has now made this possible. Most commonly part of the anterior temperal lobe is removed, 70% of patients become seizure-free and neurological (mainly visual) and psychiatric problems are surprisingly few (5±10%). Gliosis This is not really a treatment but there is a view that glial cells can protect against seizures since the enzyme systems they possess (e. Na±KATPase and carbonic anhydrase) facilitate the regulation of ion movements and reduce the spread of seizures. Certainly ageing, a fatty diet, and phenytoin itself increase glial cell count while decreasing seizure susceptibility. In fact inhibition of carbonic anhydrase and the pro- duction of bicarbonate was one of the first treatments for epilepsy and a recent discovery that under certain circumstances intracellular bicarbonate can depolarise neurons has created a fresh interest in it. In Epileptogenic and Excitotoxic Mechanisms (Eds Avanzini, G, Fariello, R, Heinemann, U and Mutani, R), John Libbey, London pp. Avanzini, G, de Curtis, M, Marescaux, C, Panzica, F, Spriefico, R and Vergnes, M (1992) Role of the thalamic reticular nucleus in the generation of rhythmic thalamo-cortical activities subserving spike and waves. Calabresi, P, Centonze, D, Marfia, GA, Pisani, A and Bernardi, G (1999) An in vitro electro- physiological study on the effects of phenytoin, lamotrigine and gabapentia on striatal neurons. Dodd, PR and Bradford, HF (1976) Release of amino acids from the mature cobalt induced epileptogenic focus.
Glutamic acid can be used in the amination of other -keto acids to form the corresponding Retinol/RBP amino acids generic 10mg uroxatral with amex. It can also be converted to glutamine by cou- complex Chylomicron remnant pling with ammonia, a reaction catalyzed by glutamine containing retinyl ester synthetase. After urea, glutamine is the second most im- Chylo- portant metabolite of ammonia in the liver. It plays an im- micron Lipoprotein lipase portant role in the storage and transport of ammonia in the blood. Through the action of various transaminases, gluta- The metabolism of vitamin A (retinol) by mine can be used to aminate various keto acids to their cor- FIGURE 28. It also acts as an important oxida- tive substrate, and in the small intestine it is the primary substrate for providing energy. Retinol (an alcohol) is transported in chylomicrons mainly as an ester of long-chain fatty acids (see Chapter 27). When chylomicrons enter the circula- THE LIVER AS A STORAGE ORGAN tion, the triglyceride is rapidly acted on by lipoprotein li- pase; the triglyceride content of the particles is signifi- Another important role of the liver is the storage and me- cantly reduced, while the retinyl ester content remains tabolism of fat-soluble vitamins and iron. Receptors in the liver mediate the rapid uptake ble vitamins, particularly vitamin B12, are also stored in the of chylomicron remnants, which are degraded, and the liver. These stored vitamins are released into the circulation retinyl ester is stored. When the vitamin A level in blood falls, the liver mobi- lizes the vitamin A store by hydrolyzing the retinyl ester The Liver Has a Central Role in (see Fig. The retinol formed is bound with retinol- Regulating Coagulation binding protein (RBP), which is synthesized by the liver before it is secreted into the blood. The amount of RBP se- Liver cells are important both in the production and the creted into the blood is dependent on vitamin A status. Most of the known clot- tamin A deficiency significantly inhibits the release of RBP, ting factors and inhibitors are secreted by hepatocytes, whereas vitamin A loading stimulates its release. In addition, several coagulation Hypervitaminosis A develops when massive quantities and anticoagulation proteins require a vitamin K–depend- of vitamin A are consumed. Since liver is the storage organ ent modification following synthesis, specifically factors II, for vitamin A, hepatotoxicity is often associated with hy- VII, IX, and X and proteins C and S, to make them effective.
