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ACTH has a permissive action in aldosterone pro- Although aldosterone is the major duction 30mg paxil for sale. It allows cells to respond optimally to their primary stimulus trusted paxil 40mg, angiotensin II cheap paxil 10mg with mastercard. Synthesis of the Adrenal Androgens with a deficiency of the 11-hydroxylase (the Adrenal androgen biosynthesis proceeds from cleavage of the 2-carbon side chain of P450C11 enzyme), may lead to clinical signs 17-hydroxypregnenolone at C17 to form the 19-carbon adrenal androgen dehy- and symptoms of mineralocorticoid excess droepiandrosterone (DHEA) and its sulfate derivative (DHEAS) in the zona reticu- even though aldosterone secretion is sup- losum of the adrenal cortex (see Fig. These compounds, which are weak pressed in these patients. Androstenedione, another weak adrenal androgen, is produced when the 2-car- bon side chain is cleaved from 17 -hydroxyprogesterone by the C17-C20 lyase Androstenedione can be purchased at health food stores under the name activity of P450C17. This androgen is converted to testosterone primarily in extra- Andros. Although the adrenal cortex makes very little estrogen, the weak letic performance through its ability to be con- adrenal androgens may be converted to estrogens in the peripheral tissues, particu- verted to testosterone. Its use has been banned larly in adipose tissue (Fig. Synthesis of Testosterone year, the drug received a lot of publicity, as the supplement had been used by a player who Luteinizing hormone (LH) from the anterior pituitary stimulates the synthesis of broke the major league home run record. In many ways, the pathways leading to androgen synthesis in the testicle are similar to those described for the adrenal cortex. In the human testicle, the predominant pathway leading to testosterone synthesis is through pregnenolone to 17- - hydroxypregnenolone to DHEA (the ∆5 pathway), and then from DHEA to androstenedione, and from androstenedione to testosterone (see Fig. As for all steroids, the rate-limiting step in testosterone production is the conversion of cholesterol to pregnenolone. LH controls the rate of side-chain cleavage from cholesterol at carbon 21 to form pregnenolone, and thus regulates the rate of Congenital adrenal hyperplasia (CAH) is a group of diseases caused by a geneti- cally determined deficiency in a variety of enzymes required for cortisol synthe- sis. The most common deficiency is that of 21- hydroxylase, the activity of Adrenal which is necessary to convert progesterone to 11-deoxycorticosterone and 17- hydroxy O O progesterone to 11-deoxycortisol. Thus, this deficiency reduces both aldosterone and corti- sol production, without affecting androgen production. If the enzyme deficiency is severe, the precursors for aldosterone and cortisol production are shunted to androgen synthesis, producing an overabundance of androgens, which leads to prenatal masculinization in OH O females and postnatal virilization of males. Another enzyme deficiency in this group of dis- Dehydroepi- Androstenedione eases is that of 11- hydroxylase, which results in the accumulation of 11-deoxycorticos- androsterone terone. An excess of this mineralocorticoid leads to hypertension (through binding of 11- deoxycorticosterone to the aldosterone receptor). In this form of CAH, 11-deoxycortisol Adipose Extra-adrenal also accumulates, but its biologic activity is minimal, and no specific clinical signs and tissue tissues symptoms result. The androgen pathway is unaffected, and the increased ACTH levels may Estrogens Testosterone increase the levels of adrenal androgens in the blood. A third possible enzyme deficiency is that of 17- hydroxylase. A defect in 17- hydroxylase leads to aldosterone excess and Fig. These weak hypertension; however, because adrenal androgen synthesis requires this enzyme, no viril- androgens are converted to testosterone or ization occurs in these patients. In its target cells, the double bond in ring A of testosterone ing androgen is testosterone. Approx- is reduced through the action of 5- reductase, forming the active hormone dihy- imately 50% of the testosterone in the drotestosterone (DHT). Synthesis of Estrogens and Progesterone remaining half is derived from ovarian and adrenal androstenedione, which, after secretion Ovarian production of estrogens, progestins (compounds related to progesterone), into the blood, is converted to testosterone in and androgens requires the activity of the cytochrome P450 family of oxidative adipose tissue, muscle, liver, and skin. The adre- enzymes used for the synthesis of other steroid hormones.

This complex activates genes that encode proteins mediating the action of active vitamin D3 purchase paxil 30 mg mastercard. In the intestinal mucosal cell buy cheap paxil 10mg online, for example purchase 30 mg paxil, transcription of genes encoding calcium-transporting proteins is activated. These proteins are capa- ble of carrying Ca2 (and phosphorus) absorbed from the gut lumen across the cell, making it available for eventual passage into the circulation. CHAPTER 34 / CHOLESTEROL ABSORPTION, SYNTHESIS, METABOLISM, AND FATE 649 CH3 CH CLINICAL COMMENTS 3 H 2 CH2 CH2 CH H3C CH Ann Jeina is typical of patients with essentially normal serum triacyl- 3 H3C glycerol levels and elevated serum total cholesterol levels that are repeat- edly in the upper 1% of the general population (e. When similar lipid abnormalities are present in other family members in a pattern HO of autosomal dominant inheritance and no secondary causes for these lipid alter- 7–Dehydrocholesterol ations (e. FH is a genetic disorder caused by an abnormality in one or more alleles respon- CH3 CH 3 sible for the formation or the functional integrity of high-affinity LDL receptors on H CH CH CH 2 2 2 the plasma membrane of cells that normally initiate the internalization of circulat- H3C CH 3 ing LDL and other blood lipoproteins. Heterozygotes for FH (1 in 500 of the pop- H C 2 ulation) have roughly one half of the normal complement or functional capacity of such receptors, whereas homozygotes (1 in 1 million of the population) have essen- HO tially no functional LDL receptors. The rare patient with the homozygous form of Cholecalciferol FH has a more extreme elevation of serum total and LDL cholesterol than does the Liver heterozygote and, as a result, has a more profound predisposition to premature coro- nary artery disease. When this occurs in the medial aspect of the upper and lower eyelids, it is referred to as xanthelasma. Similar deposits known as xanthomas CH3 CH 25 3 may occur in the iris of the eye (arcus lipidalis) as well as the tendons of the hands H 2 CH2 CH2 C OH (“knucklepads”) and Achilles tendons. H3C CH 3 Although therapy aimed at inserting competent LDL receptor genes into the cells of patients with homozygous FH is undergoing clinical trials, the current approach in the heterozygote is to attempt to increase the rate of synthesis of LDL receptors in cells pharmacologically. CH 2 Ann Jeina was treated with cholestyramine, a resin that binds some of the bile 1 salts in the intestine, causing these resin-bound salts to be carried into the feces HO OH rather than recycled to the liver. The liver must now synthesize more bile salts, 1,25–Dihydroxycholecalciferol which lowers the intrahepatic free cholesterol pool. As a result, hepatic LDL recep- (1,25–(OH)2D3) tor synthesis is induced, and more circulating LDL is taken up by the liver. The subsequent decline in the intracellu- skin, ultraviolet (UV) light produces cholecal- lar free cholesterol pool also stimulates the synthesis of additional LDL receptors. A combination of strict dietary and dual pharmacologic therapy, aimed at decreasing the cholesterol levels of the body, is usually quite effective in cor- Vera Leizd’s hirsutism was most likely the result of a problem in her Ann Jeina was treated with a statin (pravastatin) and cholestyramine, a bile acid adrenal cortex that caused excessive sequestrant. With the introduction of the cholesterol absorption blocker ezetimibe, the production of DHEA. Ezetimibe reduces the percentage of absorption of free cholesterol present in the lumen of the gut and hence the amount of cholesterol available to the enterocyte to package into chylomi- crons. This, in turn, reduces the amount of cholesterol returning to the liver in chylomicron rem- nants. The net result is a reduction in the cholesterol pool in hepatocytes. The latter induces the synthesis of an increased number of LDL receptors by the liver cells. As a consequence, the capacity of the liver to increase hepatic uptake of LDL from the circulation leads to a decrease in serum LDL levels. Low-density lipoprotein cholesterol is the primary target of cholesterol- lowering therapy because both epidemiologic and experimental evidence strongly suggest a benefit of lowering serum LDL cholesterol in the pre- vention of atherosclerotic cardiovascular disease. Similar evidence for raising sub- normal levels of serum HDL cholesterol is less conclusive but adequate to support such efforts, particularly in high-risk patients, such as Ivan Applebod, who have multiple cardiovascular risk factors. The first-line therapy in this attempt is non- pharmacologic and includes such measures as increasing aerobic exercise, weight loss in overweight patients, avoidance of excessive alcohol intake, reducing the intake of refined sugars, and cessation of smoking.

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Ann O’Rexia was receiving psychological counseling for anorexia ner- vosa paxil 30mg visa, but with little success (see Chap order paxil 20mg line. She saw her gynecologist because she had not had a menstrual period for 5 months generic paxil 20mg amex. The physician recognized that Ann’s body weight of 85 lb was now less than 65% of her ideal weight. The admission diag- nosis was severe malnutrition secondary to anorexia nervosa. Clinical findings included decreased body core temperature, blood pressure, and pulse (adaptive responses to malnutrition). Her physician ordered measurements of blood glucose and ketone body levels and made a spot check for ketone bodies in the urine as well as ordering tests to assess the functioning of her heart and kidneys. THE FASTING STATE Blood glucose levels peak approximately 1 hour after eating and then decrease as tissues oxidize glucose or convert it to storage forms of fuel. By 2 hours after a meal, the level returns to the fasting range (between 80 and 100 mg/dL). This decrease in blood glucose causes the pancreas to decrease its secretion of insulin, and the serum insulin level decreases. The liver responds to this hormonal signal by starting to degrade its glycogen stores and release glucose into the blood. If we eat another meal within a few hours, we return to the fed state. However, if we continue to fast for a 12-hour period, we enter the basal state (also known as the postabsorptive state). A person is generally considered to be in the basal state after an overnight fast, when no food has been eaten since dinner the previous evening. By this time, the serum insulin level is low and glucagon is rising. Percy Veere had not eaten much on his first day of hospitalization. Blood Glucose and the Role of the Liver on the morning of his second day of hospi- during Fasting talization was 72 mg/dL (normal, overnight fasting 80–100 mg/dL). Thus, in spite of his The liver maintains blood glucose levels during fasting, and its role is thus critical. Most neurons lack enzymes required for oxidation of fatty nearly normal levels through gluconeogene- acids, but can use ketone bodies to a limited extent. Red blood cells lack mitochon- sis using amino acid precursors. If his blood dria, which contain the enzymes of fatty acid and ketone body oxidation, and can glucose had decreased below 50 to 60 mg/dL use only glucose as a fuel. Therefore, it is imperative that blood glucose not during fasting, his brain would have been decrease too rapidly nor fall too low. Although liver glycogen levels may increase to 200 to 300 g coma and eventual death. Although many after a meal, only approximately 80 g remain after an overnight fast. Fortunately, other tissues, such as the red blood cell, are the liver has another mechanism for producing blood glucose, known as gluconeo- also totally or partially dependent on glu- genesis. In gluconeogenesis, lactate, glycerol, and amino acids are used as carbon cose for energy, they are able to function at sources to synthesize glucose. As fasting continues, gluconeogenesis progressively lower concentrations of blood glucose than adds to the glucose produced by glycogenolysis in the liver.

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In individuals with hemiplegia proven 10 mg paxil, the position of the flexed elbow causes a significant cosmetic concern buy 10mg paxil with amex. Usually best 20 mg paxil, by young adulthood, the contracture is fixed and not progressive. Treatment In young childhood and middle childhood the use of extension splinting may be helpful, although there is no good documentation. Injection of the elbow flexors with botulinum toxin has been reported, but none of these reports 400 Cerebral Palsy Management suggest that any significant lasting benefits occurred. As the contracture becomes very severe and causes problems with hygiene, a surgical release of the elbow flexors is indicated. In individuals with severe quadriplegia and severe contractures, the release should include a complete transection of the distal biceps, brachialis, and brachioradialis. This level of release usually allows el- bow extension to be between approximately 60° and 90° of flexion, which is enough to allow for bathing and keeping the elbow clean. In individuals with hemiplegia, the release of the flexion contracture is indicated because of a cosmetic concern of the elbow always being in a flexed position. If individuals are very functional with their arms and the contrac- tures are mainly dynamic, a Z-lengthening of the biceps tendon is indicated. If the arms are less functional or a fixed contracture of 10° to 20° is present, a complete release of the biceps tendon is indicated. For children with more severe positioning, especially if their arms are held to almost 90° during am- bulation, a myofascial lengthening of the brachialis is added. Elbow flexor lengthening during late childhood and adolescence does seem to provide a permanent improvement in elbow extension. In rare occasions, a severe contracture may present in hemiplegia, where there is an indication to gain extension for a specific func- tional gain or cosmetic concern. Treatment with an extension osteotomy of the distal humerus is a safer and simpler approach than trying to do a com- plete capsulotomy. Elbow joint resection with a flexor release has been re- ported as a treatment of severe elbow flexion contractures,19but we have no experience with this procedure. Complications of Treatment Complications of elbow flexor release are rare. The most serious com- plication is injury to the brachial artery or the medial nerve during flexor lengthening. This complication is best avoided by doing the lengthenings through an open incision and under tourniquet control for optimal visuali- zation of the operative field. Loss of elbow flexor power is only of con- cern in a few individuals with very heavy use of the extremity. Lack of ac- tive flexion has never been encountered and complaints of elbow weakness are almost never reported. Most individuals are happy with the degree of improvement. Radial Head Dislocation Radial head dislocation is a relatively common problem in severe quadri- plegia with elbow flexion contracture and pronation contracture. Radial head dislocation reportedly occurs in 2% of all children with CP involving the upper extremity when elbow radiographs are carefully evaluated. Most of these dislocations are posterior, which is also the position into which the radial head would move with elbow flexion. Natural History In middle childhood, the radial head starts to migrate posteriorly and later- ally as the pronation and flexion contracture increase. Upper Extremity 401 the elbow may develop pain as the radial head dislocates and then reduces again. Most children develop a fixed dislocation rather quickly and no more pain is noted. For a few children, this pain is increasing and parents may want to have the problem treated. As the radial head becomes dislocated, both the contracture and the radial head dislocation usually limit elbow extension and forearm supination.

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