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In certain skeletal muscles and in most cells during hypoxic crises buy 400 mg etodolac with mastercard, high mutans are major contributors to this rates of glycolysis are associated with rapid degradation of internal glycogen stores process because almost all of their energy is to supply the required glucose-6-P order etodolac 300mg without prescription. Applebod’s dentist explained that bacteria in his dental plaque could con- Anaerobic glycolysis results in acid production in the form of H discount etodolac 400 mg amex. Glycolysis forms pyruvic acid buy etodolac 400 mg on-line, which is reduced to lactic acid order etodolac 200mg overnight delivery. At an intracellular pH of vert all the sugar in his candy into acid in 7. The acid is buffered by bicarbonate and other buffers in saliva, but pKa for lactic acid is 3. Lactate and the H are both transported out of the saliva production decreases in the evening. If the amount of lactate generated exceeds the buffer- atite in his tooth enamel during the night. Major Tissue Sites of Lactate Production in a Resting Man. TISSUES DEPENDENT ON ANAEROBIC GLYCOLYSIS An average 70-kg man consumes about 300 g of carbohydrate per day. Many tissues, including red and white blood cells, the kidney medulla, the tissues Daily Lactate Production (g/day) of the eye, and skeletal muscles, rely on anaerobic glycolysis for at least a portion Total lactate production 115 of their ATP requirements (Table 22. Tissues (or cells) that are heavily depend- Red blood cells 29 Skin 20 ent on anaerobic glycolysis usually have a low ATP demand, high levels of gly- Brain 17 colytic enzymes, and few capillaries, such that oxygen must diffuse over a greater Skeletal muscle 16 distance to reach target cells. The lack of mitochondria, or the increased rate of gly- Renal medulla 15 Intestinal muscosa 8 colysis, is often related to some aspect of cell function. For example, the mature red Other tissues 10 blood cell has no mitochondria because oxidative metabolism might interfere with its function in transporting oxygen bound to hemoglobin. Some of the lactic acid generated by anaerobic glycolysis in skin is secreted in sweat, where it acts as an In the complete oxidation of pyru- antibacterial agent. Many large tumors use anaerobic glycolysis for ATP produc- vate to carbon dioxide, four steps tion, and lack capillaries in their core. The relative proportion of the two pathways depends on the mito- tarate dehydrogenase, and malate dehydro- genase). One step generates FAD(2H) chondrial oxidative capacity of the tissue and its oxygen supply and may vary (succinate dehydrogenase), and one substrate between cell types within the same tissue because of cell distance from the capil- level phosphorylation (succinate thiokinase). When a cell’s energy demand exceeds the capacity of the rate of the electron Thus, because each NADH generates 2. The FAD(2H) generates an Because under these conditions pyruvate dehydrogenase, the TCA cycle, and the additional 1. FATE OF LACTATE tially dependent on anaerobic gly- colysis. Lactate released from cells undergoing anaerobic glycolysis is taken up by other tis- sues (primarily the liver, heart, and skeletal muscle) and oxidized back to pyruvate. Vitreous Ciliary In the liver, the pyruvate is used to synthesize glucose (gluconeogenesis), which is body body returned to the blood. The cycling of lactate and glucose between peripheral tissues Iris Retina and liver is called the Cori cycle (Fig. Lens In many other tissues, lactate is oxidized to pyruvate, which is then oxidized to CO2 Pupil in the TCA cycle. Although the equilibrium of the lactate dehydrogenase reaction Cornea Fovea favors lactate production, flux occurs in the opposite direction if NADH is being rap- Aqueous centralis idly oxidized in the electron transport chain (or being used for gluconeogenesis): humor Choroid Ciliary Lactate NAD S Pyruvate NADH H muscle Sclera The heart, with its huge mitochondrial content and oxidative capacity, is able to The eye contains cells that transmit or focus use lactate released from other tissues as a fuel. During an exercise such as bicycle light, and these cells cannot, therefore, be riding, lactate released into the blood from skeletal muscles in the leg might be used filled with opaque structures such as mito- by resting skeletal muscles in the arm. In the brain, glial cells and astrocytes pro- chondria, or densely packed capillary beds. The corneal epithelium generates most of its duce lactate, which is used by neurons or released into the blood. ATP aerobically from its few mitochondria but still metabolizes some glucose anaerobi- II. The lens of the eye is composed of Glycolysis, in addition to providing ATP, generates precursors for biosynthetic path- fibers that must remain birefringent to trans- ways (Fig. Intermediates of the pathway can be converted to ribose 5- mit and focus light, so mitochondria are phosphate, the sugar incorporated into nucleotides such as ATP.

Muscle Glycogen glycogen is used to generate ATP during muscle contraction buy generic etodolac 400 mg. Liver glycogen is used Glucose Glycogenolysis to maintain blood glucose during fasting and during exercise or periods of enhanced need order etodolac 400 mg fast delivery. UDP-Glucose is also used for the formation of other sugars etodolac 200 mg lowest price, and galactose and Glucose–1–P glucose are interconverted while attached to UDP cheap etodolac 200mg with visa. UDP-Galactose is used for lac- tose synthesis in the mammary gland buy cheap etodolac 200mg. In the liver, UDP-glucose is oxidized to UDP- Glucose–6–P glucuronate, which is used to convert bilirubin and other toxic compounds to glu- Gluconeogenesis curonides for excretion (see Fig. Nucleotide sugars are also used for the synthesis of proteoglycans, glycopro- Glycerol–3–P teins, and glycolipids (see Fig. Proteoglycans are major carbohydrate compo- nents of the extracellular matrix, cartilage, and extracellular fluids (such as the syn- ovial fluid of joints), and they are discussed in more detail in Chapter 49. Most Glycerol extracellular proteins are glycoproteins, i. For both cell membrane glycoproteins and glycolipids, the carbohy- PEP drate portion extends into the extracellular space. Alanine All cells are continuously supplied with glucose under normal circumstances; the body maintains a relatively narrow range of glucose concentration in the blood Pyruvate Lactate (approximately 80-100 mg/dL) in spite of the changes in dietary supply and tissue demand as we sleep and exercise. Low blood glucose levels (hypoglycemia) are prevented by a release of glucose from the OAA large glycogen stores in the liver (glycogenolysis); by synthesis of glucose from lac- TCA tate, glycerol, and amino acids in liver (gluconeogenesis) (Fig. Production of blood glucose from glycemia) are prevented both by the conversion of glucose to glycogen and by its glycogen (by glycogenolysis) and from ala- conversion to triacylglycerols in liver and adipose tissue. Thus, the pathways for nine, lactate, and glycerol (by gluconeogene- glucose utilization as a fuel cannot be considered as totally separate from pathways sis). PEP phosphoenolpyruvate; OAA involving amino acid and fatty acid metabolism (Fig. Overview of the major pathways of glucose metabolism. Pathways for production of blood glucose are shown by dashed lines. FA fatty acids; TG triacylglycerols; OAA oxaloacetate; PEP phosphoenolpyruvate; UDP-G UDP-glucose; DHAP dihydroxyacetone phosphate. Intertissue balance in the utilization and storage of glucose during fasting and feeding is accomplished principally by the actions of the hormones of metabolic homeostasis—insulin and glucagon (Fig. However, cortisol, epinephrine, nor- epinephrine, and other hormones are also involved in intertissue adjustments of supply and demand in response to changes of physiologic state. Glucagon release Blood glucose Insulin release Glycogenolysis Glycogen synthesis Gluconeogenesis Fatty acid synthesis Lipolysis Triglyceride synthesis Liver glycolysis Liver glycolysis Fig 10. Pathways regulated by the release of glucagon (in response to a lowering of blood glucose levels) and insulin (released in response to an elevation of blood glucose levels). Tissue-specific differences occur in the response to these hormones, as detailed in the subse- quent chapters of this section. Insulin and glucagon are Brain the two major hormones that regulate fuel mobilization and storage. Their func- tion is to ensure that cells have a constant source of glucose, fatty acids, and [ATP] amino acids for ATP generation and for cellular maintenance (Fig. Because most tissues are partially or totally dependent on glucose for ATP generation and for production of precursors of other pathways, insulin and glucagon maintain blood glucose levels near 80 to 100 mg/dL (90 mg/dL is the Glucose same as 5 mM), despite the fact that carbohydrate intake varies considerably over the course of a day. The maintenance of constant blood glucose levels (glucose homeostasis) requires these two hormones to regulate carbohydrate, lipid, and Liver amino acid metabolism in accordance with the needs and capacities of individual Ketone bodies tissues. Basically, the dietary intake of all fuels in excess of immediate need is stored, and the appropriate fuel is mobilized when a demand occurs. For example, when dietary glucose is not available in sufficient quantities that all tissues can use it, fatty acids are mobilized and made available to skeletal muscle for use as a fuel (see Chapters 2 and 23), and the liver can convert fatty acids to ketone bod- Fatty [ATP] ies for use by the brain. Fatty acids spare glucose for use by the brain and other acids glucose-dependent tissues (such as the red blood cell). Skeletal The concentrations of insulin and glucagon in the blood regulate fuel storage Adipocyte muscle and mobilization (Fig.

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Procedures that will provide stability have the most reliable outcome purchase 200mg etodolac free shipping. For example order 200mg etodolac visa, correction of planovalgus feet with a fusion is a reliable procedure buy etodolac 300mg fast delivery. There is no benefit of trying muscle balancing or joint preservation treatment in the face of athetosis discount etodolac 300mg with visa. Although the post- operative course may be difficult safe 300mg etodolac, the outcome of the surgical treatment of fixed knee flexion contractures is usually good. Often, these patients have very high cognitive function and are very hesitant to undertake the correction, even if severe deforming musculoskeletal problems are clearly limiting their activities. Both a full analysis and an experienced surgeon will usually be able to convince them of the benefit if the problem is clear and straightforward. These patients also need an explanation of the corrections planned, which are limited to bony correction, joint fusion, or muscle lengthening. There is no role for tendon transfer in individuals with significant athetosis. Most of the surgery should be planned in late middle childhood or adolescence, as these individuals seldom have fixed deformities that cause problems earlier. Dystonia The first and most important thing to address in individuals with dystonia is to diagnose the dystonia and make sure it is not misinterpreted as spasticity. Diagnosing dystonia was addressed fully in the motor control chapter. Of- ten, a foot will look like it has severe varus deformity, then on another day, the foot will be in valgus. If surgeons do not have a video record and are not very attentive, a presumption of a spastic equinovarus foot deformity may easily be made. These feet may look like ideal feet for tendon transfers be- cause they are supple; however, tendon transfers tend to cause severe over- reaction in the opposite direction. We had one patient in whom we did a rectus transfer, not recog- nizing that it was dystonia and not spasticity. This individual spent 9 months with a flexed knee every time she tried to walk. With persistent therapy and bracing, and under the threat of reversing the transfer, the muscle suddenly went silent and knee flexion in stance stopped. Botulinum toxin is an ex- tremely effective agent to block the muscle effects of dystonia, with its major side effect being that it only works for three to four injection cycles, then the body becomes immune. If the individual has a foot deformity that is symp- tomatic, the correct treatment is fusion, usually a triple arthrodesis with tran- section of the offending muscles. Very little other surgery except for fusion is of benefit in ambulatory individuals with dystonia. Ambulatory problems related to chorea and ballismus are rare, and we have never had occasion in which surgery was required. Again, if there is foot instability, a fusion would be a reasonable option. Complications of Gait Treatment There are many real and potential complications in the treatment of gait problems in children with CP. Often, there is the presumption that nonop- erative treatment has no complications; however, this is false. The most severe complication of nonoperative treatment is to continue to treat a de- formity that is clearly getting worse but the progression is ignored (Case 7. A typical example is a child who is increasing in crouch with increasing knee flexion contracture, but there is no decision to address the problem. When the knee flexion contracture finally gets to the point that the child can no longer walk, a decision has to be made to put him in a wheelchair or try surgery. This poor judgment will be the direct cause of the child being in a wheelchair for the remainder of his life, or it may be the direct cause of the complications, which are incurred much more commonly in correcting se- vere knee flexion contractures than in correcting milder deformities. Indi- viduals who are good community ambulators at age 7 or 8 years of age do 7. Gait 375 not go into wheelchairs at age 15 years unless there is some complication or supervening medical problem unrelated to CP. Also, the use of inappropri- ate orthotics can lead to severe skin breakdown or permanent scars on the calf from breakdown of the subcutaneous fat layer. Another complication of nonoperative management is to have children in walking aids that are in- appropriate.

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ASPARTATE asparagine to aspartate in the blood generic etodolac 300mg without a prescription, Although the major route for aspartate degradation involves its conversion to decreasing the amount of asparagine avail- oxaloacetate generic etodolac 400 mg line, carbons from aspartate can form fumarate in the urea cycle (see Chap- able for tumor cell growth etodolac 300 mg mastercard. This reaction generates cytosolic fumarate buy 200mg etodolac mastercard, which must be converted to malate (using cytoplasmic fumarase) for transport into the mitochondria for oxida- tive or anaplerotic purposes discount 200 mg etodolac mastercard. An analogous sequence of reactions occurs in the purine nucleotide cycle. Aspartate reacts with inosine monophosphate (IMP) to 722 SECTION SEVEN / NITROGEN METABOLISM + form an intermediate (adenylosuccinate) which is cleaved, forming adenosine NH3 monophosphate (AMP) and fumarate (see Chapter 41). PHENYLALANINE AND TYROSINE Glutamate semialdehyde Phenylalanine is converted to tyrosine by a hydroxylation reaction. Tyrosine, pro- ornithine duced from phenylalanine or obtained from the diet, is oxidized, ultimately form- Transamination aminotransferase ing acetoacetate and fumarate. The oxidative steps required to reach this point are, + surprisingly, not energy-generating. The conversion of fumarate to malate, followed NH3 + – by the action of malic enzyme, allows the carbons to be used for gluconeogenesis. H3N CH2 CH2 CH2 CH COO The conversion of phenylalanine to tyrosine and the production of acetoacetate are Ornithine considered further in section IV of this chapter. Amino Acids That Form Succinyl CoA arginase Urea cycle The essential amino acids methionine, valine, isoleucine, and threonine are + degraded to form propionyl-CoA. The conversion of propionyl CoA to succinyl NH NH3 CoA is common to their degradative pathways. Propionyl CoA is also generated H C CH CH CH COO– from the oxidation of odd-chain fatty acids. The carbons of ornithine are derived from NH+ 3 glutamate semialdehyde, which is derived from – CH2 CH COO glutamate. Reactions of the urea cycle convert ornithine to arginine. Arginase converts argi- N N nine back to ornithine by releasing urea. Histidine – histidase NH+ COO 4 CH2 – C CH CH COO COO– N N Oxaloacetate Urocanate transamination PLP – COO – – OOC CH CH2 CH2 COO CH2 NH H C + 3 CH – COO NH ATP Aspartate Glutamine + N-Formiminoglutamate NH4 (FIGLU) asparagine synthetase asparaginase FH 4 Glutamate H2O Glutamate O AMP + PPi C NH2 N5-Formimino-FH 4 CH2 NH+ H C + 4 3 – N5,N10-Methylene-FH COO 4 Asparagine H2O Fig. Synthesis and degradation of aspar- N10-Formyl-FH 4 tate and asparagine. Note that the amide nitro- gen of asparagine is derived from glutamine. The highlighted portion of histidine forms glutamate. The D-methylmalonyl CoA is racemized to L-methylmalonyl CoA, which is rearranged in a vitamin B12-requiring reaction to produce succinyl CoA, a TCA cycle intermediate (see Fig. METHIONINE Methionine is converted to S-adenosylmethionine (SAM), which donates its methyl group to other compounds to form S-adenosylhomocysteine (SAH). Methionine can be regenerated from homo- cysteine by a reaction requiring both FH4 and vitamin B12 (a topic that is consid- ered in more detail in Chapter 40). Alternatively, by reactions requiring PLP, homo- cysteine can provide the sulfur required for the synthesis of cysteine (see Fig. Carbons of homocysteine are then metabolized to -ketobutyrate, which undergoes oxidative decarboxylation to propionyl-CoA. The propionyl-CoA is then converted to succinyl CoA (see Fig. The conversion of -ketobutyrate to propionyl-CoA is catalyzed by either 2. THREONINE the pyruvate or branched-chain - keto dehydrogenase enzymes. In humans threonine is primarily degraded by a PLP-requiring dehydratase to ammonia and -ketobutyrate, which subsequently undergoes oxidative decarboxy- Homocystinuria is caused by defi- lation to form propionyl CoA, just as in the case for methionine (see Fig. The 5 deficiencies of CH3-FH4 or of methyl-B12 are N CH3 FH4 B12 SAM due either to an inadequate dietary intake of FH4 B12 CH3 folate or B12 or to defective enzymes “CH3” donated Homocysteine involved in joining methyl groups to tetrahy- Serine drofolate (FH4), transferring methyl groups S-Adenosyl homocysteine from FH4 to B12, or passing them from B12 PLP to homocysteine to form methionine (see Cystathionine Chapter 40). Is Homer Sistine’s homocystinuria caused PLP by any of these problems? Cysteine Threonine α-Ketobutyrate NH3 CO2 Propionyl CoA Isoleucine CO2 Biotin Acetyl CoA Valine D-Methylmalonyl CoA L-Methylmalonyl CoA Vitamin B12 Succinyl CoA TCA cycle Glucose Fig. The amino acids methionine, threo- nine, isoleucine, and valine, all of which form succinyl CoA via methylmalonyl CoA, are essential in the diet.

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