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Complication rates of shoulder stabilisation surgery are highly dependent on the surgical technique utilised gasex 100 caps cheap. Reported complications of open shoulder stabilisation include infection gasex 100 caps, bleeding cheap gasex 100 caps with visa, injury to nerves (particularly the axillary and musculocutaneous nerves), loss of shoulder motion (the goal of many older open procedures, such as the Putti-Platt and Magnuson-Stack), recurrent instability (subluxation and/or dislocation) (reports range from three percent to 50%),64 hardware complications, arthritis (often due to loss of shoulder motion), subscapularis detachment/disruption, pain and weakness. The reported complications of arthroscopic stabilisation include infection, bleeding, injury to nerves (including the axillary, 51 12 64 81 83 45 18 9 74 16 14 16 27 79 8 5 23 30 40 2 14 11 20 21 25 24 Treatment of tennis elbow et al stabilisers to lateral opening include the cruciate ligaments and the posterolateral capsule. The PCL is the primary restraint to posterior translation of the tibia in all degrees of flexion where it provides 94% of the restraining force to posterior displacement. Sectioning of the PCL alone produced an increase in straight posterior translation with no change in the rotation or varus and valgus rotation. Therefore the posterior drawer test would be most sensitive at 90 degrees with no change in varus or external rotation. Gollehou 38 studied the contribution of the LCL, posterolateral complex, and PCL in cadaver ligament cutting studies. They confirmed that the LCL is the primary restraint to varus rotation in all degrees of knee flexion with maximum displacement at 30 degrees. Additional sectioning of the deep ligament complex produced an increase in varus rotation (maximum at 30 degrees) as well as an increase in the external rotation (maximum at 30 degrees). If the LCL, posterolateral complex and PCL are sectioned, further increases in both varus rotation and external rotation are observed at 60–90 degrees. Thus, isolated injuries to the posterolateral structures will be most evident at 30 degrees. When seen in combination with PCL injuries, displacement will be the maximum 60–90 degrees. In a refinement of earlier studies when the popliteus was sectioned proximally Veltri 39 identified the popliteal attachment to the tibia and the popliteofibular ligaments as individually important structures contributing to the posterolateral stability of the knee. Sectioning of the LCL, cruciate ligament, popliteofibular, and popliteal attachment to the tibia results in an increase in posterior translation, external rotation, and varus rotation best demonstrated at 30 degrees of flexion. These findings not only further our understanding of the function of the ligaments and capsular structures but have implications for planning reconstructive procedures. The physical examination of the knee must be considered in the context of the patient’s age, history and, if possible, the mechanism of injury. Studies examining the accuracy of clinical examination after injury have found that the correct diagnosis is made pre-operatively from 56% to 83% of the time. The diagnosis of extensor mechanism disorders is based largely on history and a composite picture of multiple soft physical findings. Background 405 Optimal treatment of the acute ACL injury Conservative versus No RCT. One moderate sized A3 operative management unequally randomised study and (activity level) one systematic review showing increased activity level following repair plus augmentation Conservative versus operative No RCT. Two cohort studies showing B management (subsequent low meniscectomy rate following meniscal tear) conservative management Timing of surgery No RCT. Three studies showing B increased stiffness after immediate reconstruction Repair or reconstruction One moderate sized RCT and other A3 non-randomised cohorts showing that primary repair is inferior to repair with reconstruction or augmentation Patellar tendon or hamstring No RCT. Six comparative studies B tendon including non-matched surgical techniques and including combined injuries. One sequential study matched for surgical technique. Generally similar results for each graft * A1: evidence from large RCTs or systematic review (including meta-analysis) A2: evidence from at least one high quality cohort A3: evidence from at least one moderate sized RCT or systematic review A4: evidence from at least one RCT B: evidence from at least one high quality study of non-randomised cohorts C: expert opinion et al et al et al et al Meta-analysis Materials and methods Outcome measure 446 Summary: Advantages of ankle tape and braces Injury prevention 456 5 37 13 24 10 23 2 22 18 11 9 44 3 32 19 17 26 5 9 9 11 30 4 23 57 14 8 19 (p < 0·05). They concluded that the prevention programme, which included prophylactic ankle taping of players with ankle problems, significantly reduces soccer injuries. The main difficulty when interpreting the study in the present context – ankle injury prevention – is that it is difficult to determine which of the seven programme components contributed most to the result. Tropp (1985) compared two different methods – ankle orthoses and ankle disk training – for the prevention of ankle sprains in a prospective study where players were randomised to treatment groups by team. The results were analysed separately for players with and without a history of previous ankle sprains. Among players with previous ankle problems 19 of 75 players (25%) in the control group sustained a sprain during the study period, the corresponding figure for the orthosis group and ankle disk groups were 1 of 45 (2%, p < 0·01) and 3 of 65 (5%, p < 0·01), respectively.

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She found her son on the floor hav- increase the utilization of blood glucose and ing severe jerking movements of all muscles (a grand mal seizure) buy cheap gasex 100 caps on-line. The blood In the emergency room order gasex 100 caps otc, the doctors learned that despite the objections of his glucose is normally supplied by the stimula- family and friends safe gasex 100 caps, Jim regularly used androgens and other anabolic steroids in an tion of liver glycogenolysis and gluconeoge- effort to bulk up his muscle mass. On initial physical examination, he was comatose with occasional involuntary jerking movements of his extremities. He had bitten his tongue and had lost bowel and bladder control at the height of the seizure. The laboratory reported a serum glucose level of 18 mg/dL (extremely low). The intravenous infusion of 5% glucose (5 g of glucose per 100 mL of solution), which had been started earlier, was increased to 10%. In addition, 50 g glucose was given over 30 seconds through the intravenous tubing. STRUCTURE OF GLYCOGEN Muscle Glycogen, the storage form of glucose, is a branched glucose polysaccharide com- Glycogen posed of chains of glucosyl units linked by -1,4 bonds with -1,6 branches every 8 to 10 residues (see Fig. In a molecule of this highly branched structure, Glucose–1–P only one glucosyl residue has an anomeric carbon that is not linked to another glu- cose residue. This anomeric carbon at the beginning of the chain is attached to the protein glycogenin. The other ends of the chains are called nonreducing ends (see Glucose–6–P Chapter 5). The branched structure permits rapid degradation and rapid synthesis Glycolysis of glycogen because enzymes can work on several chains simultaneously from the multiple nonreducing ends. ATP Lactate Glycogen is present in tissues as polymers of very high molecular weight 7 8 CO2 (10 –10 ) collected together in glycogen particles. The enzymes involved in glyco- gen synthesis and degradation, and some of the regulatory enzymes, are bound to the surface of the glycogen particles. FUNCTION OF GLYCOGEN IN SKELETAL MUSCLE AND LIVER Glycogen Glycogen is found in most cell types, where it serves as a reservoir of glucosyl Liver units for ATP generation from glycolysis. Glucose–1–P Glycogen is degraded mainly to glucose 1-phosphate, which is converted to glu- cose 6-phosphate. In skeletal muscle and other cell types, the glucose 6-phosphate Glucose–6–P enters the glycolytic pathway (Fig. Glycogen is an extremely important fuel glucose 6glucose 6––phosphatasephosphatase source for skeletal muscle when ATP demands are high and when glucose 6-phos- Gluconeo- Glucose phate is used rapidly in anaerobic glycolysis. In many other cell types, the small genesis glycogen reservoir serves a similar purpose; it is an emergency fuel source that Blood Glucose supplies glucose for the generation of ATP in the absence of oxygen or during restricted blood flow. In general, glycogenolysis and glycolysis are activated Fig. Glycogenolysis in skeletal muscle together in these cells. Glycogen stores serve different func- Glycogen serves a very different purpose in liver than in skeletal muscle and other tions in muscle cells and liver. Liver glycogen is the first and immediate source of glucose and most other cell types, glycogen stores for the maintenance of blood glucose levels. In the liver, the glucose 6-phosphate that serve as a fuel source for the generation of is generated from glycogen degradation is hydrolyzed to glucose by glucose 6-phos- ATP. In the liver, glycogen stores serve as a phatase, an enzyme present only in the liver and kidneys. Futile cycling refers coneogenesis, the synthesis of glucose from amino acids and other gluconeogenic pre- to a situation in which a substrate is con- cursors (discussed in detail in Chapter 31), also forms glucose 6-phosphate, so that glu- verted to a product through one pathway, cose 6-phosphatase serves as a “gateway” to the blood for both pathways (see Fig. Because the biosynthetic pathway is energy-requir- III. SYNTHESIS AND DEGRADATION OF GLYCOGEN ing, futile cycling results in a waste of high- energy phosphate bonds.

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With adequate lev- then oxidizes these fatty acids and produces els of ATP obtained from fatty acid (or ketone body) oxidation gasex 100caps otc, the rate of ketone bodies gasex 100 caps free shipping. The activity of the regulatory enzymes in glycolysis and the TCA cycle (pyruvate dehydrogenase and PFK-1) are decreased by the changes in concentration of their allosteric regulators (ADP purchase 100 caps gasex free shipping, an activator of PDH, 6. Levels of ketone bodies in the blood at various times during fasting. Glucose lev- els remain relatively constant, as do levels of fatty acids. Ketone body levels, however, increase markedly, rising to levels at which they can be used by the brain and other nervous tissue. CHAPTER 23 / OXIDATION OF FATTY ACIDS AND KETONE BODIES 435 decreases in concentration; NADH, and acetyl CoA, inhibitors of PDH, are The level of total ketone bodies in increased in concentration under these conditions; and ATP and citrate, Lofata Burne’s blood greatly inhibitors of PFK-1, are increased in concentration). As a consequence, glucose- exceeds normal fasting levels and the mild ketosis produced during exercise. Glucose-6-P inhibits hexokinase, thereby decreasing the rate of a person on a normal mealtime schedule, entry of glucose into glycolysis, and its uptake from the blood. In skeletal mus- total blood ketone bodies rarely exceed 0. During prolonged fasting, they may centration (see Chapter 36). Preferential utilization of fatty acids does not, how- rise to 4 to 5 mM. Levels above 7 mM are ever, restrict the ability of glycolysis to respond to an increase in AMP or ADP considered evidence of ketoacidosis, levels, such as might occur during exercise or oxygen limitation. Tissues That Use Ketone Bodies tem in the blood and compensatory respira- tion (Kussmaul’s respiration) (see Chapter 4). Skeletal muscles, the heart, the liver, and many other tissues use fatty acids as their major fuel during fasting and other conditions that increase fatty acids in the blood. However, a number of other tissues (or cell types), such as the brain, use ketone bodies to a greater extent. For example, cells of the intestinal muscosa, which trans- port fatty acids from the intestine to the blood, use ketone bodies and amino acids during starvation, rather than fatty acids. Adipocytes, which store fatty acids in tri- acylglycerols, do not use fatty acids as a fuel during fasting but can use ketone bod- ies. Ketone bodies cross the placenta, and can be used by the fetus. Almost all tis- Why can’t red blood cells use sues and cell types, with the exception of liver and red blood cells, are able to use ketone bodies for energy? Regulation of Ketone Body Synthesis A number of events, in addition to the increased supply of fatty acids from adipose triacylglycerols, promote hepatic ketone body synthesis during fasting. The decreased insulin/glucagon ratio results in inhibition of acetyl CoA carboxylase and decreased malonyl CoA levels, which activates CPTI, thereby allowing fatty acyl CoA to enter the pathway of -oxidation. When oxidation of fatty acyl CoA to acetyl CoA generates enough NADH and FAD(2H) to supply the ATP needs of the liver, acetyl CoA is diverted from the TCA cycle into ketogenesis and oxaloacetate in the TCA cycle is diverted toward malate and into glucose synthesis (gluconeogenesis). This pattern is regulated by the NADH/NAD ratio, which is relatively high during -oxidation. As the length of time of fasting continues, increased transcription of the gene for mitochondrial HMG-CoA synthase facili- tates high rates of ketone body production. Although the liver has been described as “altruistic” because it provides ketone bodies for other tissues, it is simply getting rid of fuel that it does not need. CLINICAL COMMENTS As Otto Shape runs, he increases the rate at which his muscles oxidize all fuels. The increased rate of ATP utilization stimulates the electron trans- port chain, which oxidizes NADH and FAD(2H) much faster, thereby increasing the rate at which fatty acids are oxidized. During exercise, he also uses muscle glycogen stores, which contribute glucose to glycolysis. In some of the fibers, the glucose is used anaerobically, thereby producing lactate. Some of the lac- tate will be used by his heart, and some will be taken up by the liver to be converted to glucose.

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Simul- taneously cheap gasex 100 caps overnight delivery, to regulate the amount of fatty acids released into circulation generic 100 caps gasex fast delivery, triglyceride synthesis occurs along with glyceroneogenesis buy 100 caps gasex with amex. Fed state TG Glucose Glucose Blood + Insulin DHAP Chylomicrons + Glycerol–3–P Remnants L VLDL TG P LPL + L FACoA IDL CII LDL FA FA Glycerol Adipose cell Fig. Conversion of the fatty acid (FA) from the triacylglycerols (TG) of chylomicrons and VLDL to the TG stored in adipose cells. Note that insulin stimulates both the transport of glucose into adipose cells and the secretion of LPL from the cells. Glucose provides the glycerol 3-phosphate for TG synthesis. Insulin also stimulates the synthesis and secretion of lipoprotein lipase (LPL). Their levels of chylomicrons and VLDL (which contain large amounts of lipase (inactive) triacylglycerols) are elevated because they TG Blood are not digested at the normal rate by LPL. LPL can be dissociated from capillary protein kinase A walls by treatment with heparin (a gly- + hormone cosaminoglycan). Measurements can be sensitive cAMP made on blood after heparin treatment to lipase– P (active) + Low insulin/high glucagon determine whether LPL levels are abnormal. ATP FA FA other FA FA lipases FA FA Glycerol Glycerol Adipose cell Fig. In the fasted state, when insulin levels are low and glucagon is elevated, intracellular cAMP increases and activates protein kinase A, which phosphorylates hormone-sensitive lipase (HSL). Phosphorylated HSL is active and initiates the breakdown of adipose TG. Recall, however, that re-esterification of fatty acids does occur, along with glyceroneogenesis, in the fasted state. The fatty acids, which travel in the blood complexed with albumin, enter cells of muscle and other tissues, where they are oxidized to CO2 and water to produce energy. During prolonged fasting, acetyl CoA produced by -oxidation of fatty acids in the liver is converted to ketone bodies, which are released into the blood. The glycerol derived from lipolysis in adipose cells is used by the liver during fast- ing as a source of carbon for gluconeogenesis. METABOLISM OF GLYCEROPHOSPHOLIPIDS AND SPHINGOLIPIDS Fatty acids, obtained from the diet or synthesized from glucose, are the precursors of glycerophospholipids and of sphingolipids (Fig. These lipids are major com- ponents of cellular membranes. Glycerophospholipids are also components of blood lipoproteins, bile, and lung surfactant. They are the source of the polyunsaturated fatty acids, particularly arachidonic acid, that serve as precursors of the eicosanoids (e. Ether glycerophospho- lipids differ from other glycerophospholipids in that the alkyl or alkenyl chain (an alkyl chain with a double bond) is joined to carbon 1 of the glycerol moiety by an ether rather than an ester bond. Examples of ether lipids are the plasmalogens and platelet activat- ing factor. Sphingolipids are particularly important in forming the myelin sheath sur- rounding nerves in the central nervous system, and in signal transduction. In glycerolipids and ether glycerolipids, glycerol serves as the backbone to which fatty acids and other substituents are attached. Sphingosine, derived from ser- ine, provides the backbone for sphingolipids. GLYCEROPHOSPHOLIPIDS The initial steps in the synthesis of glycerophospholipids are similar to those of tri- acylglycerol synthesis. Glycerol 3-phosphate reacts with fatty acyl CoA to form CHAPTER 33 / SYNTHESIS OF FATTY ACIDS, TRIACYLGLYCEROLS, AND THE MAJOR MEMBRANE LIPIDS 609 Glycerolipids Phospholipids Sphingolipids Triacylglycerols Glycerophospholipids Ether glycerolipids Sphingophospholipids Glycolipids Adipose stores Phosphatidylcholine Plasmalogens Sphingomyelin Cerebrosides Blood lipoproteins Phosphatidylethanolamine Platelet activating Sulfatides Phosphatidylserine factor Globosides Phosphatidylinositol Gangliosides bisphosphate (PIP2) Phosphatidylglycerol Cardiolipin Fatty acid Fatty acid Ether Fatty acid Fatty acid Fatty acid Fatty acid Fatty acid P Head P Head P Head Carbohydrate Fatty acid group group group Fig.

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