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The oogonia are transformed to oocytes as they enter the first meiotic division and arrest in prophase antibiotic resistance jobs discount 500 mg cipro with visa. This process 20 begins at 11–12 weeks antibiotics for uti didn't work generic cipro 250mg with mastercard, perhaps in response to a factor or factors produced by the rete ovarii virus from mice discount cipro 750mg amex. Progression of meiosis to the diplotene stage is accomplished throughout the rest of pregnancy and completed by birth bacteria pilorica order 250 mg cipro with visa. Arrest of meiosis at the end of the first stage is probably maintained by inhibiting substances produced by granulosa cells. A single ovum is formed from the two meiotic divisions of the oocyte, one just before ovulation and the second (forming the haploid ovum) at the time of sperm penetration. The excess genetic material is extruded as one polar body at each meiotic division. Gonadotropins and various growth factors (but not sex steroids) can induce resumption of meiosis in vitro, but only in oocytes enclosed by cumulus-granulosa cells. A family of sterols is present in follicular fluid, 21 presumably secreted by the cumulus cells, that activates oocyte meiosis. Loss of germ cells takes place throughout all of these events: during mitosis of germ cells, during the various stages of meiosis, and finally, after follicle formation. The massive loss of oocytes during the second half of pregnancy is the consequence of several mechanisms. Besides follicular growth and atresia, substantial numbers of oocytes regress during meiosis, and those oogonia that fail to be enveloped by granulosa cells undergo degeneration. In addition, germ cells (in the cortical area) migrate to the surface of the gonad and become incorporated into the surface 23, 24 epithelium or are eliminated into the peritoneal cavity. In contrast, once all oocytes are encased in follicles (shortly after birth), the loss of oocytes will be only through the process of follicular growth and atresia. Individuals with Turner syndrome (45,X) experience normal migration and mitosis of germ cells, but the oogonia do not undergo meiosis, and rapid loss of oocytes leaves the gonad without follicles by birth, and it appears as a fibrous streak. The Stage of Follicle Formation At 18–20 weeks, the highly cellular cortex is gradually perforated by vascular channels originating in the deeper medullary areas, and this marks the beginning of 25 follicle formation. As the finger like vascular projections enter the cortex, it takes on the appearance of secondary sex cords. As blood vessels invade and penetrate, they divide the previously solid cortical cell mass into smaller and smaller segments. Drawn in with the blood vessels are perivascular cells that are either mesenchymal or epithelial in origin. The resulting unit is the primordial follicle — an oocyte arrested in prophase of meiosis, enveloped by a single layer of spindle-shaped pregranulosa cells, surrounded by a basement membrane. Residual mesenchyme not utilized in primordial follicle formation is noted in the interstices between follicles, forming the primitive ovarian stroma. The granulosa cells differentiate from coelomic epithelial or mesenchymal precursors (their specific origin is still disputed). This process of primordial follicular development continues until all oocytes in the diplotene stage can be found in follicles, some time shortly after birth. As soon as the oocyte is surrounded by the rosette of pregranulosa cells, the entire follicle can undergo variable degrees of maturation before arresting and becoming atretic. The formation of a primary follicle is marked by a change of the pregranulosa layer to a cuboidal layer of granulosa cells. Further differentiation into a preantral follicle is expressed as more complete granulosa proliferation. Call–Exner body formation (coalescence to form an antrum) and occasionally a minor thecal layer system that differentiates from surrounding mesenchymal cells can be seen. Preantral follicles can be found in the 6th month of gestation, and antral follicles (the Graafian follicle, characterized by a fluid filled space) are present by the end of pregnancy, but not in large numbers. It is only during the last third of gestation 19 that theca cells can be found surrounding follicles. Even in fetal life the cycle of follicle formation, variable ripening, and atresia occurs. Although these steps are precisely those typical of adult reproductive life, full maturity, as expressed in ovulation, does not occur. Estrogen production does not occur until late in pregnancy when follicular development takes place, and even then steroidogenesis is not significant. Unlike the male, gonadal steroid production is not required for development of a normal phenotype. The development of the müllerian duct into the fallopian tubes, the uterus, and the upper third of the vagina is totally independent of the ovary. The ovary at birth and in the first year of life can contain cystic follicles of varying size, undoubtedly stimulated by the reactive gonadotropin surge accompanying the 26 withdrawal of the neonatal hypothalamus and pituitary from the negative feedback of fetoplacental steroids. The median eminence is apparent by week 9 of gestation, and the th hypothalamic-pituitary portal circulation is functional by the 12 week. Levels are higher in female fetuses than in males until the last 6 weeks of gestation. The ovary develops receptors for gonadotropins only in the second half of pregnancy. Thus, the loss of oocytes during fetal life cannot be solely explained by the decline in gonadotropins. The follicular growth and development observed in the second half of 27 28 pregnancy, however, is gonadotropin dependent. Hypophysectomy of a fetal monkey is followed by an increase in oocyte loss by atresia. The Neonatal Ovary 29 the total cortical content of germ cells falls to 1–2 million by birth as a result of prenatal oocyte depletion. This huge depletion of germ cell mass (close to 4–5 million) has occurred over as short a time as 20 weeks. Because of the fixed initial endowment of germ cells, the newborn female enters life, still far from reproductive potential, having lost 80% of her oocytes. The ovary is approximately 1 cm in diameter and weighs about 250–350 mg at birth, although sizable cystic follicles can enlarge the total dimensions. Compartmentalization of the gonad into cortex and a small residual medulla has been achieved. The lower male levels are probably due to testicular testosterone and inhibin production. This early activity is accompanied by inhibin levels comparable to the low range observed during the follicular phase of the menstrual cycle. Follicular response to the antral stage is relatively common in the first 6 months of life in response to these elevated 32 gonadotropin levels. The most common cause of abdominal masses in fetuses and newborns is ovarian cysts, a consequence of gonadotropin stimulation. After the postnatal rise, gonadotropin levels reach a nadir during early childhood (by about 6 months of age in males and 1–2 years in females) and then rise slightly between 4 and 10 years. The process of atresia with an increasing contribution of follicular remnants to the stromal compartment yields progressive ovarian enlargement 36 during childhood, about a ten-fold increase in weight. Of course, the lack of gonadotropin support prevents full follicular development and function. The Adult Ovary 7, 38 At the onset of puberty, the germ cell mass has been reduced to 300,000 to 500,000 units. During the next 35–40 years of reproductive life, 400 to 500 will be 39 selected to ovulate, and the primary follicles will eventually be depleted to a point at menopause when only a few hundred remain. In the last 10–15 years before 40, 41 menopause, there is an acceleration of follicular loss. The loss of oocytes (and follicles) through atresia is a response to changes in many factors. Certainly gonadotropin stimulation and withdrawal are important, but ovarian steroids and autocrine and paracrine factors are also involved. The consequence of these unfavorable changes, atresia, is a process called apoptosis, 51 programmed cell death. Indeed, the process is a consequence of an orderly expression of key gene products that either promote or repress the apoptotic events. This neuronal network innervates the ovarian vasculature, interstitial tissue, and developing follicles. However, nerve fibers (not in an organized network) are present in nonprimate ovaries.

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Lum- sionally virus living or nonliving cheap 500 mg cipro mastercard, pain that radiates to the when the stress reaction is unilater- bar radiculopathy and bowel or blad- buttock or posterior thigh virus 07092012 cheap cipro 250 mg fast delivery. Although al and has not yet resulted in cortical der symptoms are rare but may acute injury may precipitate the on- disruption antibiotics for sinus infection and sore throat buy discount cipro 500 mg line. In addition to document- and well-defined lucent defects may Harris and Weinstein20 studied ing a detailed history of the patient’s develop antimicrobial drugs antibiotics generic cipro 1000mg fast delivery. The re- ed nonsurgically were asymptomat- disturbance of bowel or bladder sulting lumbar stenosis may cause ic, 55% had occasional back pain, function rarely occur with spondy- L5 nerve radiculopathy as well as and 45% had neurologic symptoms; lolysis or low-grade spondylolisthe- bowel and bladder dysfunction from none of the patients was inconti- sis, but they may be reported by pa- compression of sacral nerve roots. A history of night plastic spondylolisthesis are more tive lives with only minor adjust- pain is not typical; when present, it like to develop neurologic injury and ments in lifestyle. No patients with unilat- all children and adolescents present- ported a markedly higher frequency eral defects progressed to slippage ing with back pain. Gait should be of progression in the dysplastic type over the course of the study. Marked slowing of slip tients with advanced degrees of Isthmic spondylolysis and progression was observed with each spondylolisthesis (Figure 1). No correlation was found served for scoliosis, but more defin- and adolescents, has an incidence of between slip progression and low itive evaluation of scoliosis is de- 4. A flattened lumbar individuals with isthmic spondylol- Outcomes Study 36-Item Short lordosis is commonly observed in Volume 14, Number 7, July 2006 419 Spondylolysis and Spondylolisthesis: I. Diagnosis, Natural History, and Nonsurgical Management Figure 1 the standard posteroanterior radio- graphic view allows evaluation of coexisting scoliosis that may be sec- ondary to paraspinal spasm, wheth- er idiopathic or olisthetic (ie, the re- sult of asymmetric forward vertebral translation at the level of the spondylolisthesis). The standing lat- eral view is useful for identifying spondylolytic defects and document- ing the degree of spondylolisthesis. Supine oblique and spot lateral ra- diographic views of the lumbosacral junction improve the likelihood of diagnosing stress reactions and spondylolytic defects (Figure 2). The Meyerding classification quantifies the amount of forward translation based on the standing lateral radiograph22 (Figure 3, A). Measurement of the slip angle quan- tifies the degree of lumbosacral ky- phosis that has occurred in associa- tion with this anterior translation. The slip angle is the angle subtend- ed by the intersection of a line drawn along the superior endplate of L5 and the perpendicular of a line drawn along the posterior cortex of the sacrum (Figure 3, B). C, Standing proved to be unreliable because of lateral radiograph of the lumbosacral spine of the same patient, illustrating high- the rounding of the superior sacrum grade dysplastic spondylolisthesis with severe lumbosacral kyphosis (arrows). A rectal examination is indicated greater risk of slip progression, insta- the sacrum appears vertically ori- in patients with bowel or bladder bility, and development of postoper- ented, and a visible or palpable step- dysfunction to assess anal sphincter ative pseudarthrosis. The irritation and popliteal angle mea- the most effective method for de- spinous processes and lumbodorsal surements to assess hamstring tecting spondylolysis when plain ra- fascia, paraspinal muscles, and sa- spasm and contracture complete the diographs are normal and the patient croiliac joints are palpated for ten- examination. Figure 3 A, the Meyerding classification is used to quantify the degree of spondylolisthesis. A=width of the superior endplate of S1, a = distance between the posterior edge of the inferior endplate of L5 and the posterior edge of the superior endplate of S1. A value >50° correlates with a significantly increased risk of progression of spondylolisthesis. A 15-year-old diver presented with upper lumbar back pain of several months’ 26 duration. A, Anteroposterior radiograph of the lumbar spine showing sclerosis of spondylolysis. A high rate of false-positive results superior to those of activity sclerosis at the pars, lamina, or pedi- studies and a low positive predictive restriction alone. Nerve root com- involvement of the pars, adjacent documents progressive bony healing. These muscles sur- spondylolisthesis at 6- to 9-month Surgery is indicated when patients rounding the lumbar spine have the intervals through skeletal maturity. Symptomatic relief can Spondylolytic Defect ability compared with the control be expected in <10% of cases. Con- (Isthmic Spondylolysis) group, who underwent more general sequently, surgical management is the goals of treatment of the physiotherapy treatment. Also rou- recommended for children and ado- young patient with a symptomatic tinely prescribed was stretching of lescents with symptomatic high- spondylolytic defect are alleviation tight lumbodorsal fascia and ham- grade spondylolisthesis. For most symptomatic children Spondylolisthesis and adolescents, a period of restrict- In two studies of children and ad- Indications for Surgical ed activity and physiotherapy will olescents with symptomatic low- Management relieve symptoms and allow a safe grade spondylolisthesis, two thirds return to activities. The need for in one study32 and all patients in the Surgical treatment is indicated for the brace treatment is infrequent and is second study34 responded to nonsur- child with persistent pain resulting reserved for patients who do not re- gical measures, including activity re- from a nonhealing stress fracture of spond to rest and physical therapy. When pain, spinal mobil- low-grade spondylolisthesis despite a corset, which limits the extremes of ity, and hamstring spasm are im- minimum of 6 months of nonsurgi- spinal motion, is effective in reduc- proved, the patient may return to cal treatment. Clinical level, and it has a benign clinical defect may be an incidental radio- observation of diminished pain, im- course in the majority of patients. Surgery is also in- proved spinal mobility, and de- their report on the natural history of dicated in young patients with creased hamstring spasm confirm symptomatic low-grade spondylolis- progressive dysplastic spondylolisthe- the efficacy of treatment. Activities thesis, Frennered et al35 found that sis, those presenting with neurologic may be resumed once symptoms only 2 of 47 patients demonstrated deficit, and symptomatic children have resolved after an appropriate progression of slip. Careful clinical and diagnostic group were taught specific strength- rologic deficit, and need for surgical evaluation is important to properly ening exercises to target the deep ab- intervention. The procedure is used for several specific purposes: to relieve pain; to provide stability; to overcome postural deformity resulting from neurologic deficit; and to halt advancing disease. The technique provides access to the spine along the long axis of the spine, as opposed to anterior, posterior or lateral approaches. The surgeon enters the back through a very small incision next to the tailbone and the abnormal disc is taken out. Then a bone graft is placed where the abnormal disc was and is supplemented with a large metal screw. Sometimes, additional, smaller screws are placed through another small incision higher on the back for extra stability. During a direct lateral or extreme lateral approach, a narrow passageway is created through the underlying tissues and the psoas muscle using tubular dilators, without cutting the muscle; which is the major difference between the open approach and lateral approach. The procedure is generally indicated for interbody fusion at the lower levels of the spine . These scores are equal to or more severe than the majority of participants, meaning those participants within two standard deviations ( + /-) of the mean for such scores. Dynamic Stabilization: Also known as soft stabilization or flexible stabilization has been proposed as an adjunct or alternative to spinal fusion for the treatment of severe refractory pain due to degenerative spondylolisthesis, or continued severe refractory back pain following prior fusion, sometimes referred to as failed back surgery syndrome. Dynamic stabilization uses flexible materials rather than rigid devices to stabilize the affected spinal segment(s). These flexible materials may be anchored to the vertebrae by synthetic cords or by pedicle screws. Unlike the rigid fixation of spinal fusion, dynamic stabilization is intended to preserve the mobility of the spinal segment. Facet Arthroplasty: the implantation of a spinal prosthesis to restore posterior element structure and function, as an adjunct to neural decompression Facet Fusion: A minimally invasive back procedure that uses specially designed bone dowels made from allograft material (donated cortical bone) that are inserted into the facet joints. The procedure is designed to stop facet joints from moving and is intended to eliminate or reduce back pain caused by facet joint dysfunction (Gellhorn, 2013). Facet Syndrome: A condition in which arthritic change and inflammation occur and the nerves to the facet joints convey severe and diffuse pain. In this procedure, a specialized cannula and surgical tools are used under fluoroscopic guidance for bone and tissue sculpting near the spinal canal. The damaged portion of the disc is removed to release pressure on the spinal cord and nerves. Allograft Surgical Treatment for Spine Pain Page 3 of 29 UnitedHealthcare Commercial Medical Policy Effective 04/01/2020 Proprietary Information of UnitedHealthcare. A metal implant is inserted to stabilize the spine and secure the spinous ® processes until the fusion takes place . Coflex is a U-shaped device with 2 pair of serrated wings extending from the upper and lower long arms of the U. The U portion is inserted horizontally between 2 adjacent spinous processes (bones) in the back of the spine, and the wings are crimped over bone to hold the implant in place. After implantation the device is opened or expanded to distract (open) the neural foramen and decompress the nerves. Spacers are implanted midline between adjacent lamina and spinous processes to provide dynamic stabilization following decompressive surgery.

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Albertazzi P treatment for dogs eating rat poison order cipro 250mg free shipping, Pansini F virus 43215 purchase cipro 750mg without prescription, Bonaccorsi G antibiotic resistance usa discount cipro 250mg with amex, Zanotti L antimicrobial foods purchase 250 mg cipro visa, Forini E, Aloysio D, the effect of dietary soy supplementation on hot flushes, Obstet Gynecol 91:6, 1998. Adlercreutz H, Mazur W, Phyto-oestrogens and western diseases, Ann Med 29:95, 1997. Ingram D, Sanders K, Kolybaba M, Lopez D, Case-control study of phyto-oestrogens and breast cancer, Lancet 350:990, 1997. Gennari C, Agnusdei D, Crepaldi G, Isaia G, Mazzuoli G, Ortolani S, Bufalino L, Passeri M, Effect of ipriflavone–a synthetic derivative of natural isoflavones–on bone mass loss in the early years after menopause, Menopause 5:9, 1998. Jorgensen T, Gallstones in a Danish population: fertility, period, pregnancies, and exogenous female sex hormones, Gut 29:433, 1988. Haarbo J, Marslew U, Gotfredsen A, Christiansen C, Postmenopausal hormone replacement therapy prevents central distribution of body fat after menopause, Metabolism 40:1323, 1991. Ley C, Lees B, Stevenson J, Sex- and menopause-associated changes in body-fat distribution, Am J Clin Nutr 55:950, 1992. Boston Collaborative Drug Surveillance Program, Surgically confirmed gallbladder disease, venous thromboembolism, and breast tumors in relation to postmenopausal estrogen therapy, New Engl J Med 290:15, 1974. Jick H, Derby L, Myers M, Vasilakis C, Newton K, Risk of hospital admission for idiopathic venous thromboembolism among users of postmenopausal oestrogens, Lancet 348:981, 1996. Meilahn E, Kuller L, Matthews K, Kiss J, Hemostatic factors according to menopausal status and use of hormone replacement therapy, Ann Epidemiol 2:445, 1992. Conard J, Gompel A, Pelissier C, Mirabel C, Basdevant A, Fibrinogen and plasminogen modifications during oral estradiol replacement therapy, Fertil Steril 68:449, 1997. A long-term study of “untreated” hyperplasia in 170 patients, Cancer 56:402, 1985. Grady D, Gebretsadik T, Kerlikowske K, Ernster V, Petitti D, Hormone replacement therapy and endometrial cancer risk: a meta-analysis, Obstet Gynecol 85:304, 1995. Persson I, Adami H-O, Bergkvist L, Lindgren A, Pettersson, Hoover R, Schairer C, Risk of endometrial cancer after treatment with oestrogens alone or in conjunction with progestogens: results of a prospective study, Br Med J 298:147, 1989. Schairer C, Adami H-O, Hoover R, Persson I, Cause-specific mortality in women receiving hormone replacement therapy, Epidemiology 8:59, 1997. Adami H-O, Persson I, Hoover R, Schairer C, Bergkvist L, Risk of cancer in women receiving hormone replacement therapy, Int J Cancer 44:833, 1989. Parazzini F, La Vecchia C, Negri E, Franceschi S, Moroni S, Chatenoud L, Bolis G, Case-control study of oestrogen replacement therapy and risk of cervical cancer, Br Med J 315:85, 1997. Ploch E, Hormonal replacement therapy in patients after cervical cancer treatment, Gynecol Oncol 26:169, 1987. Persson I, Yuen J, Bergkvist L, Schairer C, Cancer incidence and mortality in women receiving estrogen and estrogen-progestin replacement therapy–long-term follow-up of a Swedish cohort, Int J Cancer 67:327, 1996. Bergkvist L, Adami H-O, Persson I, Hoover R, Schairer C, the risk of breast cancer after estrogen and estrogen-replacement, New Engl J Med 321:293, 1989. Persson I, Yuen J, Bergkvist L, Adami H-O, Hoover R, Schairer C, Combined oestrogen-progestogen replacement and breast cancer risk, Lancet 340:1044, 1992. Persson I, Thurfjell E, Bergstrom R, Holmberg L, Hormone replacement therapy and the risk of breast cancer. Nested case-control study in a cohort of Swedish women attending mammography screening, Int J Cancer 72:758, 1997. Ewertz M, Influence of non-contraceptive exogenous and endogenous sex hormones on breast cancer risk in Denmark, Int J Cancer 42:832, 1988. Sillero-Arenas M, Delgado-Rodriguez M, Rodigues-Canteras R, Bueno-Cavanillas A, Galvez-Vargas R, Menopausal hormone replacement therapy and breast cancer: a meta-analysis, Obstet Gynecol 79:286, 1992. Collaborative Group on Hormonal Factors in Breast Cancer, Breast cancer and hormone replacement therapy: collaborative reanalysis of data from 51 epidemiological studies of 52,705 women with breast cancer and 108,411 women without breast cancer, Lancet 350:1047, 1997. Hunt K, Vessey M, McPherson K, Coleman M, Long-term surveillance of mortality and cancer incidence in women receiving hormone replacement therapy, Br J Obstet Gynaecol 94:620, 1990. Hunt K, Vessey M, McPherson K, Mortality in a cohort of long-term users of hormone replacement therapy: an updated analysis, Br J Obstet Gynaecol 97:1080, 1990. Magnusson C, Holmberg L, Norden T, Lindgren A, Persson I, Prognostic characteristics in breast cancers after hormone replacement therapy, Breast Cancer Res Treat 38:325, 1996. LeLorier J, Grégoire G, Benhaddad A, Lapierre J, Derderian F, Discrepancies between meta-analyses and subsequent large randomized, controlled trials, New Engl J Med 337:536, 1997. Ron E, Lunenfeld B, Menczer J, Blumstein T, Katz L, Oelsner G, Serr D, Cancer incidence in a cohort of infertile women, Am J Epidemiol 125:780, 1987. Gompel A, Malet C, Spritzer P, Lalardrie J-P, Kuttenn F, Mauvais-Jarvis P, Progestin effect on cell proliferation and 17-hydroxysteroid dehydrogenase activity in normal human breast cells in culture, J Clin Endocrinol Metab 63:1174, 1986. Foidart J-M, Colin C, Denoo X, Desreux J, Béliard A, Fournier S, de Ligniéres B, Estradiol and progesterone regulate the proliferation of human breast epithelial cells, Fertil Steril 69:963, 1998. Lambe M, Hsieh C, Trichopoulos D, Ekbom A, Pavia M, Adami H-O, Transient increase in the risk of breast cancer after giving birth, New Engl J Med 331:5, 1994. Sankila R, Heinavaara S, Hakulinen T, Survival of breast cancer patients after subsequent term pregnancy: “healthy mother effect,” Am J Obstet Gynecol 170:818, 1994. Andersson B, Mattsson L, Hahn L, Mårin P, Lapidus L, Holm G, Bengtsson B, Björntorp P, Estrogen replacement therapy decreases hyperandrogenicity and improves glucose homeostasis and plasma lipids in postmenopausal women with noninsulin-dependent diabetes mellitus, J Clin Endocrinol Metab 82:638, 1997. Pschera H, Hjerpe A, Carlström K, Influence of the maturity of the vaginal epithelium upon the absorption of vaginally administered estradiol-17b and progesterone in postmenopausal women, Gynecol Obstet Invest 27:204, 1989. Johnston A, Estrogens — pharmacokinetics and pharmacodynamics with special reference to vaginal administration and the new estradiol formulation — Estring , Acta Obstet Gynecol Scand 75(Suppl 163):16, 1996. Henriksson L, Stjernquist M, Boquist L, Cedergren I, Selinus I, A one-year multicenter study of efficacy and safety of a continuous, low-dose, estradiol-releasing vaginal ring (Estring) in postmenopausal women with symptoms and signs of urogenital aging, Am J Obstet Gynecol 174:85, 1996. Copyright © 19 Obesity Clinical Gynecologic Endocrinology and Infertility 19 Obesity Definition of Obesity Physiology of Adipose Tissue Clinical Obesity Leptin and the Ob Gene (the Lep Gene in Humans) Inherited Aspects of Obesity Endocrine Changes Anatomic Obesity Management of Obesity Chapter References Because approximately one-third of American adults are obese, the unrewarding fight against obesity is all too common, not only with our patients but also with 1 2 ourselves. Unfortunately, for over 100 years the incidence of obesity has been 1, 3, 4 increasing in the United States and Europe, a reflection of an affluent society with an increasingly sedentary life combined with high caloric foods. This change in 5 lifestyle has produced an increasing prevalence of obesity that is similar in adults and children. The lack of success in treating obesity is not due to an unawareness of the implications of obesity; there is a clear-cut, well recognized relationship between mortality 6, 7 and weight. The death rate from diabetes mellitus, for example, is approximately 4 times higher among obese diabetics than among those who control their weight. The death rate from appendicitis is double, presumably from anesthetic and surgical complications. Even the rate of accidents is higher, perhaps because fat people are awkward or because their view of the ground or floor is obstructed. The incidence of hypertension, heart disease, noninsulin-dependent diabetes mellitus, gout, gallbladder disease, colorectal cancer, endometrial cancer, 8 postmenopausal breast cancer, and osteoarthritis is elevated in overweight people. Being overweight in adolescence is even a more powerful predictor of 9 cardiovascular adverse health effects than being overweight as an adult. When the personal and social problems encountered by obese people are also considered, it is no wonder that a clinician without a weight problem cannot comprehend why fat individuals remain overweight. The frequency with which a practitioner encounters the obese patient whose weight does not decrease despite a sworn adherence to a limited-calorie diet makes one question if there is something physiologically different about this patient. Is the problem due to lack of discipline and cheating on a diet, or does it also involve a pathophysiologic factor? Modern studies of obesity strongly indicate that this is a multifactorial problem, and that lack of willpower and laziness are not the simple answers. Definition of Obesity 10 Obesity is an excess storage of triglycerides in adipose cells. The ideal weight for any adult is believed to correspond to his or her ideal weight from age 20 to 30. The following formulas give ideal weight in pounds: Women:100 + (4 x (height in inches minus 60)) Men: 120 + (4 x (height in inches minus 60)) At a weight close to ideal weight, individuals may be overweight, but not overfat. An estimate of body fat, therefore, is more meaningful than a measurement of height and weight. The most accurate method of determining body fat is to determine the density of the body by underwater measurement (hydrodensitometry). It certainly is not practical to measure density by submerging individuals in water in our offices; therefore, skinfold measurements with calipers have become popular as an index of body fat, or expensive imaging techniques can be utilized.

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Other Soft Tissue Masses Benign soft tissue masses are very common in the hand and wrist antibiotics for sinus infection in pregnancy cheap cipro 500 mg visa. They can arise in any of the tissues making up the hand including nerves antibiotic resistance executive order order 250 mg cipro visa, vessels antibiotic bomb cheap cipro 750 mg on line, fat bacteria that causes strep throat cheap 250mg cipro with mastercard, and fascia. The most common “tumors” of the hand arise from the synovium and include ganglions, mucous cysts, and giant cell tumors of the tendon sheath. A ganglion on the dorsum of the wrist or over the flexor tendon sheath can be aspirated, although rates of recurrence are fairly high. Aspiration of a volar wrist ganglion should be approached cautiously, if at all, because of the proximity of the radial artery. Surgical resection is a more definitive option, with only 5% to 10% recurrence rates when done cor- rectly. Giant cell tumors of the tendon sheath are solid lesions arising from the synovium of the tendon sheath or from the finger joints. Other common benign soft tissue masses include foreign-body granulo- mas, epidermal inclusion cysts, arteriovenous malformations and heman- giomas, neurilemmoma, and glomus tumors. The most common ones are epithelioid sarcomas, synovial cell sarcomas, and malignant fibrous histiocytoma. Note the enchondroma of the metacarpal with callus from a healed pathologic fracture. Tumors of Bone Benign tumors of the hand bones are often diagnosed incidentally on radiographic examination for trauma. Osteochondromas, fibrous dysplasia, and giant cell tumor of bone can also present in the small hand bones and may require surgery for diagnosis or treatment. Partial or total hand amputation may be required along with adjuvant radiation therapy or chemotherapy. Metastatic tumors of the hand seldom occur as isolated metastases but are not uncommon during widespread metastatic disease, especially from lung or breast lesions. Management Protocols As one can see, a broad variety of complex problems can affect the hand and wrist. It is, therefore, important to have in mind a standardized approach to patients with these problems to help arrive at the correct diagnosis and management options. The physician should start with a careful and detailed history of the chief complaint, then with a differential diagnosis in mind should perform a directed but thorough physical examination. We have developed algorithms beyond this to help streamline a patient’s care and avoid missing important diagnoses. Although the algorithms are overall quite complete, one should be wary of unusual presentations or diagnoses that are not included. These rare occurrences may require further evaluation or consultation by a hand specialist. The algorithms divide patients into groups with or without a specific history of injury. If the initial radiographs show a fracture, dislocation, or carpal instability pattern, appropriate operative or nonoperative treatment should be initiated. When X-rays are negative, a soft tissue injury may have occurred or an occult fracture may be present. When a specific soft tissue injury is noted, appro- priate treatment should be initiated. If none is found and the patient’s symptoms cannot be explained, either further imaging should be per- formed or splinting or casting for a period of time followed by reevaluation should be considered. Figure 10-8 concerns patients who have had no specific history of trauma or injury. Unless patients have a very classic history and physical examina- tion for a soft tissue process, plain X-rays should be taken. If they are positive for arthritis, tumor, or occult bony injury, appropriate operative or nonoperative management should be undertaken. If they are negative, further evaluation or indicated treatment should be initiated according to the algorithm. Which of the following conditions can be causative factors in carpal tunnel syndrome? Which of the following congenital hand differences is associated with visceral anomalies? Avoid documentation of injury until definitive management in the Operating Room 10-8. Which of the following bacteria must be covered when a human bite wound is involved? Any altera- tion of the function of the lower extremities will result in an alteration in the ability to walk and run. Alteration in the hip as a result of disease will significantly effect the biomechanics of gait and place abnormal stress on the joints above and below the hip. This chapter briefly reviews the anatomy of the hip and its relationship to normal and pathologic gait. The important history and physical exami- nation findings of hip pathology are discussed. Surgical management of end- stage disease of the hip commonly are treated by one of several options, and these are reviewed. In addition, trauma to the pelvis, acetabulum, and proximal femur are summarized and treatment alternatives outlined. Anatomy Development the hip joint is a ball-and-socket joint with the round femoral head articu- lating within the round acetabular socket. The acetabulum is formed from the confluence of three bones: the ischium, the ilium, and the pubis. In skeletally immature patients these three bones are joined in the medial acetabulum by the triradiate cartilage, which is a growth plate for the ace- tabulum. There is also appositional growth from the edges of the acetabu- lum and pelvis, resulting in increased depth of the acetabulum and size of the pelvis. Normal development of the acetabulum requires the femoral head to articulate with the acetabular cartilage. The severity of this condition is determined by the degree of subluxation of the femoral head. If the hip is left subluxed or dislocated, the acetabulum will be shallow and predispose the patient to develop osteoarthritis as an adult. This condition is reviewed in greater detail in the chapter on pediatric orthopedic conditions. Osteology and Musculature the innominate bone consists of the ilium, ischium, and pubis, which are joined in the area of the acetabulum. The ischium joins the ilium superiorly and the pubis inferiorly through the inferior pubic ramus. The ischium also serves as the origin of the hamstring and short external rotator muscles of the hip. The pubis consists of the superior pubic ramus, the inferior pubic ramus, and the pubic symphysis. The superior pubic ramus joins the pubic symphysis with the ilium, and the inferior pubic ramus connects the pubic symphysis with the ischium. The pubis serves as the site of insertion of the musculature of the abdominal wall as well as the site of origin for the adductor muscles of the thigh. The Hip and Femur 417 Fovea on head Piriformis Head Greater trochanter Gluteus Neck minimus Epiphyseal Intertrochanteric lines line Psoas Lesser trochanter Vastus major lateralis Vastus Capsular medialis attachment Figure 11-2. The lateral opening of the acetabulum forms a horseshoe with the open end directed inferiorly. The medial base of the acetabulum contains a depres- sion called the acetabular fovea, which is filled with a fatty tissue called the pulvinar and the ligamentum teres. The ligamentum teres is a ligament that extends from the acetabular fovea and the fovea of the femoral head. The artery of the ligamentum teres is a branch of the obturator artery and supplies approximately 10% to 20% of the bone of the femoral head.

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