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By Q. Gambal. LeTourneau University. 2018.

Hip 593 one child in whom a second acetabular reconstruction was required discount claritin 10mg mastercard; this was successful in maintaining the hip reduced and keeping the child walking until she became a young adult claritin 10mg free shipping. We anticipate discount 10 mg claritin amex, although we have no experi- ence claritin 10 mg low cost, that these individuals should maintain stable hip joints once they reach full adulthood order claritin 10mg mastercard. Inferior Hip Dislocation Direct inferior dislocations of the hip are very rare. We have only treated one such deformity and have had the opportunity to examine another patient (Case 10. Both these individuals had tremendous difficulty with seating because their legs were fixed in a severe, abducted hip and knee-flexed posi- tion making seating almost impossible. A hip radiograph showed inferior hip sub- had a tracheal diversion. A redirectional varus femoral because of difficulty sitting and a complaint from the osteotomy did not greatly change the hip position but al- mother that he sometimes got his knee stuck in his axilla lowed easier sitting and lying in a more normal position when lying. On physical examination he had fixed hip (Figure C10. Our single treatment experience with this type of inferior dislocation is a varus repositioning os- teotomy that allowed this individual to sit much better. The hip did not be- come painful, although this child had severe neurologic involvement that required a tracheostomy. Six years after the varus osteotomy, this child died of aspiration through his tracheal diversion. Hyperabducted and Extended Hip Deformities A small group of children develop severe, bilateral abducted hips. Some of the children have extension contractures and have more or less flexion. This deformity creates great difficulty with seating88 and is a very socially un- appealing posture for adolescents and young adults (Case 10. Etiology There are children in whom the etiology of this hyperextended and abducted position is iatrogenic, related to too much adductor and iliopsoas lengthening with obturator neurectomies. Another large group of children develop this deformity unilaterally and it be- comes a windblown hip posture. The natural history of this hyperabduction deformity is not well docu- mented; however, in our experience, it generally does not get progressively worse as children get older. The problem occurs as children get older and bigger, making it more difficult to accommodate the deformity. With some attention to seating modifications, many of these children develop good pat- terns of sitting and can often spend long periods of time lying in a side lying position. This deformity is a very cosmetically objectionable posture, espe- cially for adolescent and young adult females, to be lying in the hyperab- ducted hip-flexed position every time they are not sitting in their wheelchairs. Some of the children and many caretakers are bothered by this posture. Although it seems that this posture is a precursor to the type II anterior hip dislocation, no good documentation exists to suggest that it leads directly to anterior hip dislocation or inferior hip dislocation. This evolution of defor- mity may occur, but is so rare that it is not recognized as part of the precur- sor posture. A much more common bony deformity that occurs from this position as children grow, and especially as they go into adolescence, is the development of protrusio acetabuli from too much direct medial pressure. This is exactly opposite of what is seen when the widened teardrop with an- terior or posterosuperior dislocations are present. This acetabular protrusio may lead to degenerative arthritis in some young adults. Protrusio acetabuli may also leave children who are osteoporotic at risk for getting an acetabular fracture (Case 10. Treatment Treatment of the hyperabducted hip deformity can be divided into those with mild deformity and those with more severe deformity. Mild deformities are defined as hips having a passive adduction so they can be brought to neutral 10. Her mother, however, was not bothered by the and spastic quadriplegia, was seen for routine follow-up appearance. Physical examination showed the hips with and was noted to have severe hip abduction contractures. Radiographs of the hips showed that she mother did not feel she had any pain.

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However buy claritin 10mg visa, the quantities of arginine generated by the urea cycle are – HC + CH COO adequate only for the adult and are insufficient to support growth buy 10mg claritin with visa. Therefore generic claritin 10mg amex, during N periods of growth buy claritin 10mg low price, arginine becomes an essential amino acid order claritin 10mg mastercard. It is important to realize H ∆1-Pyrroline 5-carboxylate that if arginine is used for protein synthesis, the levels of ornithine will drop, thereby slowing the urea cycle. This will stimulate the formation of ornithine from glutamate. Arginine is cleaved by arginase to form urea and ornithine. If ornithine is pres- NADPH FAD•2H + H+ ent in amounts in excess of those required for the urea cycle, it is transaminated to glutamate semialdehyde, which is reduced to glutamate. The conversion of an alde- NADP+ FAD hyde to a primary amine is a unique form of a transamination reaction and requires pyridoxal phosphate (PLP). HISTIDINE N H2 Although histidine cannot be synthesized in humans, five of its carbons form gluta- Proline mate when it is degraded. In a series of steps, histidine is converted to formiminog- lutamate (FIGLU). The subsequent reactions transfer one carbon of FIGLU to the Fig. Reactions 1, 3, and 4 occur in mitochon- FH4 pool (see Chapter 40) and release NH4 and glutamate (Fig. Amino Acids Related to Oxaloacetate sis and degradation involve different enzymes. The cyclization reaction (formation of a Schiff (Aspartate and Asparagine) base) is nonenzymatic, i. Aspartate is produced by transamination of oxaloacetate. This reaction is readily reversible, so aspartate can be reconverted to oxaloacetate (Fig. Asparagine is formed from aspartate by a reaction in which glutamine provides the nitrogen for formation of the amide group. Thus, this reaction differs from the synthesis of glutamine from glutamate, in which NH4 provides the nitrogen. How- + ever, the reaction catalyzed by asparaginase, which hydrolyzes asparagine to NH4 Certain types of tumor cells, partic- and aspartate, is analogous to the reaction catalyzed by glutaminase. Amino Acids That Form Fumarate fore, asparaginase has been used as an anti- tumor agent. ASPARTATE asparagine to aspartate in the blood, Although the major route for aspartate degradation involves its conversion to decreasing the amount of asparagine avail- oxaloacetate, carbons from aspartate can form fumarate in the urea cycle (see Chap- able for tumor cell growth. This reaction generates cytosolic fumarate, which must be converted to malate (using cytoplasmic fumarase) for transport into the mitochondria for oxida- tive or anaplerotic purposes. 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.

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Similar evidence for raising sub- normal levels of serum HDL cholesterol is less conclusive but adequate to support such efforts buy generic claritin 10mg on-line, particularly in high-risk patients cheap 10mg claritin amex, such as Ivan Applebod buy claritin 10mg fast delivery, who have multiple cardiovascular risk factors discount 10 mg claritin fast delivery. The first-line therapy in this attempt is non- pharmacologic and includes such measures as increasing aerobic exercise cheap claritin 10 mg with mastercard, weight loss in overweight patients, avoidance of excessive alcohol intake, reducing the intake of refined sugars, and cessation of smoking. If these efforts fail, drug therapy to raise serum HDL cholesterol levels must be considered. Applebod has failed in his attempts to diet and exercise. He could be given an HMG CoA reductase inhibitor such as pravastatin and, perhaps, a bile salt–binding resin such as cholestyramine. Other lipid-lowering drugs such as the fibric acid derivatives and ezetimibe, which also decrease triacylglycerol levels and potentially increase HDL levels, should be considered (Table 34. Vera Leizd was born with a normal female genotype and phenotype, had normal female sexual development, spontaneous onset of puberty, and reg- ular, although somewhat scanty, menses until the age of 20. At that point, she developed secondary amenorrhea (cessation of menses) and evidence of male hormone excess with early virilization (masculinization). The differential diagnosis included an ovarian versus an adrenocortical source of the excess androgenic steroids. Mechanism(s) of Action and Efficacy of Lipid-Lowering Agents Percentage change in serum lipid level (monotherapy) Total HDL Agent Mechanism of Action cholesterol LDL-cholesterol cholesterol Triacylglycerols Statins Inhibits HMG-CoA T15–60% T 20–60% c 5–15% T10–40% reductase activity Bile acid Increase fecal T15–20% T10–25% c 3–5% Variable, depending on pretreatment level of resins excretion of bile salts triacylglycerols (may increase) Niacin Activates LPL; T 22–25% T10–25% c 15–35% T 20–50% reduces hepatic production of VLDL; reduces catabolism of HDL Fibrates Antagonizes PPAR- T12–15% Variable, c 5–15% T 20–50% causing an increase depending on in LPL activity, a pretreatment levels decrease in of other lipids apoprotein C-III production, and an increase in apoprotein A-I production. Ezetimibe Reduces intestinal T10–15% T 15–20% c 1–3% T 5–8% if triacylglycerols are high absorption of free pretreatment cholesterol from the gut lumen Abbreviations: LPL, lipoprotein lipase; LDL, low-density lipoprotein; HDL, high-density lipoprotein; triacylglycerols, triglycerides; PPAR, peroxisome proliferators-acti- vated receptor (the Table is adapted from Circulation 2002; 106:3145–3457). CHAPTER 34 / CHOLESTEROL ABSORPTION, SYNTHESIS, METABOLISM, AND FATE 651 the adrenal cortex or the ovary is the source of excess male hormone involves the measurement of the concentration of dehydroepiandrosterone sulfate (DHEAS) in the patient’s plasma, because the adrenal cortex makes most of the DHEA, and the ovary makes little or none. Vera’s plasma DHEAS level was moderately elevated, identifying her adrenal cortices as the likely source of her virilizing syndrome. If the excess production of androgens is not the result of an adrenal tumor, but the result of a defect in the pathway for cortisol production, the simple treatment is to administer glucocorticoids by mouth. The rationale for such treatment can be better understood by reviewing Fig. If Vera Leizd has a genetically deter- mined partial deficiency in the P450C11 enzyme system needed to convert 11- deoxycortisol to cortisol, her blood cortisol levels would fall. By virtue of the nor- mal positive feedback mechanism, a subnormal level of cortisol in the blood would induce the anterior pituitary to make more ACTH. The latter would not only stim- ulate the cortisol pathway to increase cortisol synthesis to normal but, in the process, would also induce increased production of adrenal androgens such as DHEA and DHEAS. The increased levels of the adrenal androgens (although rel- atively weak androgens) would cause varying degrees of virilization, depending on the severity of the enzyme deficiency. The administration of a glucocorticoid by mouth would suppress the high level of secretion of ACTH from the anterior pitu- itary gland that occurs in response to the reduced levels of cortisol secreted from the adrenal cortex. Treatment with prednisone (a synthetic glucocorticoid), there- fore, will prevent the ACTH-induced overproduction of adrenal androgens. How- ever, when ACTH secretion returns to normal, endogenous cortisol synthesis falls below normal. The administered prednisone brings the net glucocorticoid activity in the blood back to physiologic levels. Vera’s adrenal androgen levels in the blood returned to normal after several weeks of therapy with prednisone (a synthetic glu- cocorticoid). As a result, her menses eventually resumed, and her virilizing fea- tures slowly resolved. Because Vera’s symptoms began in adult life, her genetically determined adrenal hyperplasia is referred to as a “nonclassic” or “atypical” form of the disorder. A more severe enzyme deficiency leads to the “classic” disease, which is associated with excessive fetal adrenal androgen production in utero and, therefore, manifests itself at birth, often with ambiguous external genitalia and virilizing features in the female neonate. BIOCHEMICAL COMMENTS Defects in the LDL receptor gene are responsible for the elevated blood levels of LDL, and thus of cholesterol, in FH. Over 300 mutations have been found in the LDL receptor gene, affecting all stages in the production and functioning of the receptor. The LDL receptor gene, which contains 18 exons and is 45 kilobases (kb) in length, is located on the short arm of chromosome 19. The exons share sequences for the C9 component of complement (a blood protein involved in the immune response), and the N-linked oligosaccharide domain is homologous to the genes for the precursor of EGF and also for three proteases of the blood clotting system, Fac- tors IX and X and protein C (see Chapter 45).

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The LPL in the capillaries of muscle cells has a lower Km than adipose LPL cheap 10mg claritin overnight delivery. Thus cheap claritin 10mg otc, muscle cells can obtain fatty acids from blood lipoproteins whenever they are needed for energy buy claritin 10mg otc, even if the concentration of the lipoproteins is low order claritin 10 mg visa. HDL The glycerol released from chylomicron triacylglycerols by LPL may be used for triacylglycerol synthesis in the liver in the fed state claritin 10 mg with mastercard. ApoB-48 The portion of a chylomicron that remains in the blood after LPL action is ApoCII Mature known as a chylomicron remnant. This remnant binds to receptors on hepatocytes chylomicron (the major cells of the liver), which recognize apoprotein E, and is taken up by the ApoE process of endocytosis. Lysosomes fuse with the endocytic vesicles, and the Fig. Newly synthesized chylomi- Heparin is a complex polysaccharide that is a component of proteoglycans (see crons (nascent chylomicrons) mature as they Chapter 49). Isolated heparin is frequently used as an anticoagulant, because it receive apoproteins CII and E from HDL. As LPL is bound to the capillary teins and also in transfer of cholesterol from endothelium through binding to proteoglycans, heparin also can bind to LPL and dis- peripheral tissues to the liver (see Table 1 in lodge it from the capillary wall. This leads to loss of LPL activity and an increase of the introduction to this section). CHAPTER 32 / DIGESTION AND TRANSPORT OF DIETARY LIPIDS 591 Lymph Chylomicrons Capillary Blood walls Chylomicrons Chylomicrons Intestinal epithelial cell Chylo- L micron P TG L FA CO2 + H2 O Lysosomes Liver CII Muscle Endocytic vesicle Chylomicron FA + remnants Glycerol FA Cholesterol FA TG Stores Receptors Amino acids Adipose tissue Glycerol Fig. Chylomicrons are synthesized in intestinal epithelial cells, secreted into the lymph, pass into the blood, and become mature chylomicrons (see Fig. On capillary walls in adipose tissue and muscle, lipoprotein lipase (LPL) activated by ApoCII digests the triacylglycerols (TG) of chylomicrons to fatty acids and glycerol. Fatty acids (FA) are oxidized in muscle or stored in adipose cells as triacylglycerols. The remnants of the chylomicrons are taken up by the liver by receptor-mediated endocytosis. Lysosomal enzymes within the hepatocyte digest the remnants, releasing the products into the cytosol. CLINICAL COMMENTS The upper abdominal ultrasound study showed a large gallstone lodged in Will Sichel’s common duct with dilation of this duct proximal to the stone. Michael was scheduled for endoscopic retrograde cholangiopancreatogra- phy (ERCP). If common duct obstruction is severe enough, bilirubin flows back into the venous blood draining from the liver. As a consequence, serum bilirubin levels, par- ticularly the indirect (unconjugated) fraction, increase. Tissues such as the sclerae of the eye take up this pigment, which causes them to become yellow (jaundiced). Will Sichel’s condition was severe enough to cause jaundice by this mechanism. Alcohol excess may produce proteinaceous plugs in the small pancreatic ducts, causing back pressure injury and autodigestion of the pancreatic acini drained by these obstructed channels. Al Martini had an episode of acute alcohol-induced pancre- atitis superimposed on a more chronic alcohol-related inflammatory process in the pancreas—in other words, a chronic pancreatitis. As a result of decreased secretion of pancreatic lipase through the pancreatic ducts and into the lumen of the small intestine, dietary fat was not absorbed at a normal rate, and steatorrhea (fat-rich 592 SECTION SIX / LIPID METABOLISM stools) occurred. If abstinence from alcohol does not allow adequate recovery of the enzymatic secretory function of the pancreas, Mr. Martini will have to take a commercial preparation of pancreatic enzymes with meals that contain even mini- mal amounts of fat. BIOCHEMICAL COMMENTS The assembly of chylomicrons within the endoplasmic reticulum of the enterocyte requires the activity of microsomal triglyceride transfer protein (MTP). The protein is a dimer of two nonidentical subunits. The smaller subunit (57 kDa) is protein disulfide isomerase (PDI, see Chapter 7, section IX. A), whereas the larger subunit (97 kDa) contains the triglyceride transfer activity. MTP accelerates the transport of triglycerides, cholesterol esters, and phospholipids across membranes of subcellular organelles.

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