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Alanine (the major gluconeogenic amino acid) and other amino acids enter the liver generic viagra extra dosage 130 mg amex, where their nitrogen is converted to urea cheap viagra extra dosage 120 mg with mastercard, which is excreted in the urine, and their carbons to glucose and ketone bodies, which are oxidized by various tissues for energy. CHAPTER 38 / FATE OF AMINO ACID NITROGEN: UREA CYCLE 699 severe malaise, loss of appetite, nausea, vomiting, and arthralgias (joint pains). He A had a low-grade fever and noted a persistent and increasing pain in the area of his Amino acid1 α–Keto acid1 liver. His friend noted a yellow discoloration of the whites of Percy’s eyes and skin. PLP Percy’s urine turned the color of iced tea, and his stool became a light-clay color. Serologic testing for viral hepatitis type B, C, and D were nonreactive, but fecal B – – studies showed “shedding” of hepatitis virus type A. Tests for antibodies to antigens COO COO + of the hepatitis A virus (anti-HAV) in the serum were positive for the immunoglob- H3N C H C O ulin M type. CH CH 2 2 A diagnosis of acute viral hepatitis type A was made, probably contracted from – – COO COO virus-contaminated food Percy had eaten while on his cruise. His physician Aspartate Oxaloacetate explained that there was no specific treatment for type A viral hepatitis but recom- mended symptomatic and supportive care and prevention of transmission to others PLP by the fecal–oral route. Percy took acetaminophen 3 to 4 times a day for fever and – – COO COO arthralgias throughout his illness. Transamination Reactions – – COO COO Transamination is the major process for removing nitrogen from amino acids. In α–Ketoglutarate Glutamate most instances, the nitrogen is transferred as an amino group from the original Fig. The amino group amino acid to -ketoglutarate, forming glutamate, whereas the original amino acid from one amino acid is transferred to another. For example, the amino Pairs of amino acids and their corresponding acid aspartate can be transaminated to form its corresponding -keto acid, oxaloac- -keto acids are involved in these reactions. In the process, the amino group is transferred to -ketoglutarate, which is con- ketoglutarate and glutamate are usually one of verted to its corresponding amino acid, glutamate. The reactions, which are readily All amino acids except lysine and threonine undergo transamination reactions. For most of these reactions, -ketoglutarate and glutamate serve as one of or aminotransferases. A generalized reac- the -keto acid–amino acid pairs. Whereas pyridoxal phosphate is Overall, in a transamination reaction, an amino group from one amino acid used primarily for reactions involv- becomes the amino group of a second amino acid. Because these reactions are read- ing amino acids, it is also required ily reversible, they can be used to remove nitrogen from amino acids or to transfer for the glycogen phosphorylase reaction, in nitrogen to -keto acids to form amino acids. Thus, they are involved both in amino which it acts as a general acid/base catalyst. Removal of Amino Acid Nitrogen as Ammonia Cells in the body and bacteria in the gut release the nitrogen of certain amino acids as ammonia or ammonium ion (NH4 ) (Fig. Because these two forms of nitrogen can be interconverted, the terms are sometimes used interchangeably. Ammonium ion releases a proton to form ammonia by a reaction with a pK of 9. Therefore, at physiologic pH, the equilibrium favors NH4 by a factor of approximately 100/1 (see Chapter 4, the Henderson-Hasselbalch equation).
In such muscles viagra extra dosage 120 mg low price, the glycolytic capacity is high because the enzymes of glycol- ysis are present in large amounts (thus order viagra extra dosage 120 mg, the overall Vmax [maximum velocity] is large). The levels of hexokinase, however, are low, so very little circulating glucose is used. The low levels of hexokinase in fast-twitch glycolytic fibers prevent the muscle from drawing on blood glucose to meet this high demand for ATP, thus avoiding hypoglycemia. Glucose 6-phosphate, formed from glycogenolysis, further inhibits hexokinase. The tissues rely on endogenous fuel stores (glycogen and cre- atine phosphate) to generate ATP, following the pathway of glycogen breakdown to glucose 1-phosphate, the conversion of glucose 1-phosphate to glucose 6-phos- phate, and the metabolism of glucose 6-phosphate to lactate. Thus, anaerobic gly- colysis is the main source of ATP during exercise of these muscle fibers. CHAPTER 47 / METABOLISM OF MUSCLE AT REST AND DURING EXERCISE 873 3. ANAEROBIC GLYCOLYSIS FROM GLYCOGEN Glycogenolysis and glycolysis during exercise are activated together because both PFK-1 (the rate-limiting enzyme of glycolysis) and glycogen phosphorylase b (the inhibited form of glycogen phosphorylase) are allosterically activated by AMP. AMP is an ideal activator because its concentration is normally kept low by the adenylate kinase (also called myokinase in muscle) equilibrium [2 ADP 4 AMP ATP]. Thus, whenever ATP levels decrease slightly, the AMP concentration increases manyfold (Fig. To compensate for the low ATP yield of anaerobic glycolysis, fast-twitch glycolytic fibers have a much higher content of glycolytic enzymes, and the rate of glucose 6-phosphate utilization is more than 12 times as fast as slow-twitch fibers. Muscle fatigue during exercise generally results from a lowering of the pH of the tissue to approximately 6. Both aerobic and anaerobic metabolism lowers the pH. Both the lowering of pH and lactate production can cause pain. Metabolic fatigue also can occur once muscle glycogen is depleted. Muscle glycogen stores are used up in less than 2 minutes of anaerobic exercise. The muscle used in pushups, a high- strength exercise, is principally fast-twitch glycolytic fibers. No matter how well you have trained, you probably cannot do pushups for as long as 2 minutes. Furthermore, you will feel the pain as the mus- cle pH drops as lactate production continues. The regulation of muscle glycogen metabolism is complex. Recall that glycogen degradation in muscle is not sensitive to glucagon (muscles lack glucagon receptors), so there is little change in muscle glycogen stores during overnight fasting or long-term fasting, if the individual remains at rest. Glycogen synthase is inhibited during exercise but can be activated in resting muscle by the release of insulin after a high-carbohy- drate meal. Unlike the liver form of glycogen phosphorylase, the muscle isozyme con- tains an allosteric site for AMP binding. When AMP binds to muscle glycogen phos- phorylase b, the enzyme is activated even though it is not phosphorylated. Thus, as muscle begins to work and the myosin-ATPase hydrolyzes existing ATP stores to ADP, AMP will begin to accumulate (due to the myokinase reaction), and glycogen degra- dation will be enhanced. The activation of muscle glycogen phosphorylase b is further enhanced by the release of Ca2 from the sarcoplasmic reticulum, which occurs when muscles are stimulated to contract.
He was placed in solid ankle AFOs and discount viagra extra dosage 130mg amex, after 1 year of phys- ical therapy effective 200 mg viagra extra dosage, he was able to walk slowly in the posterior walker, but could not get into the walker by himself. By age 4 years, through continued therapy, he learned to get up into a standing position and increased his walking speed. By age 5 years, he was walking well with the walker, and in therapy, he was working on balance development with the use of quad canes, which were nonfunctional for am- bulation outside the therapy environment. By age 6 years, he was practicing with Lofstrand crutches and by age 8 years, he was starting to practice walking independently. He was finding more stability and walking more with back-kneeing and ankle dorsiflexion even though he did not have equinous contractures (Figure C7. It was clear at this time, however, that he would be a permanent crutch user as age 8 years is a common plateau point, and he had been receiving intensive therapy, which means sig- nificant additional improvement cannot be expected. He had no significant structural limitations that could be Figure C7. Over the next 4 years, he continued to work on his balance, but as he entered puberty, it was clear that he would never be able to walk independent of the crutches except for very short times in home areas. A surgical plan is made and the actual surgery planned to least disturb families’ normal activities. First, a decision has to be made if a tone reduction procedure is indicated or if the treatment is to be all musculoskeletal based. If children are independent ambulators and the physical examination demonstrates increased tone throughout the lower extremities and minimal fixed muscle contractures, the kinematics demonstrate decreased range of motion at the hip, knee, and ankle, and there are no transverse plane deformities, these children are considered excellent candidates for a tone reduction procedure. Children who meet all these criteria are very rarely seen, so there are almost always relative contraindi- cations. At this time, the reported data from rhizotomy in this age group suggests that ambulatory ability is not improved much over physical ther- apy alone. Gait 359 dorsal rhizotomy, with the only report suggesting a better chance of in- dependent ambulation following muscle surgery than dorsal rhizotomy. The use of intrathecal baclofen for this population has not been reported. The large size of the pump and the need for frequent refills has made families hes- itant to have these pumps implanted. We know of no center using the pump for this indication, although theoretically it would be an ideal indication. The pump would allow controlling the spasticity and allow children to be as func- tional as possible. Part of the problem with dorsal rhizotomy is that too much tone is removed and children are left weak. Clearly, the mainstay of surgical treatment of children with diplegia is direct correction of the deformities that are causing the functional impair- ment to gait. The goal should be to correct all the impairments that can be corrected with one surgery. If there is a varus foot deformity with equinus that seems to be causing toe walking, there is a temptation to suggest that this should be corrected. In early and middle childhood diplegia, unless the varus foot deformity is fixed, no surgery should be done on the tibialis anterior or tibialis posterior. Al- most all these children will convert to planovalgus later, and any surgery on the foot at this age will only speed up that process. If children have a plano- valgus deformity that is supple and are tolerating an orthotic, continuation of the orthotic is in order.