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The traditional duration of 6 weeks has been altered in some protocols to 3 weeks intravenous and 3 weeks oral based on clinical response antibiotics for acne minocycline order keftab 125 mg with mastercard. These subperiosteal abscesses typically follow breakthrough of the thin cortical bone in the metaphyseal region antibiotic cefdinir purchase 125 mg keftab. As these subperiosteal collections strip the periosteum from the underlying cortex 3m antimicrobial mask order keftab with american express, the cortex is devascularized and segments become avascular antibiotic resistance due to overuse of antibiotics cheap 750mg keftab with visa. In severe cases of acute hematogenous osteomyelitis antibiotic 500 mg cheap 500 mg keftab amex, it is not uncommon to see sequestration of the entire bony diaphysis bacteria klebsiella pneumoniae purchase on line keftab. Septic Arthritis Infection of a child’s joint typically results from one of three pathologic mechanisms: 1. Hematogenous spread: just as in osteomyelitis, organisms can localize in the joint, finding the highly vascular synovium a favorable location for replication. Joint capsule Articular cartilage Epiphysis Epiphyseal line Cancellous bone of metaphysis Periosteum Cortical bone Haversian canals Medullary cavity Figure 5-12. Breakthrough from a metaphyseal osteomyelitis: this occurs in specific joints where a portion of the metaphysis is intraarticular. Anatomically, the synovial reflection extends below the physis and includes a portion of metaphyseal cortical bone. The transverse Volk- mann’s canals provide a conduit for pus in the metaphysis to access the joint. Penetrating trauma: this results in joint sepsis when organisms are directly injected into the joint. Clinical Feature Joint swelling and redness are the typical physical findings that one would expect. In con- tradistinction to acute hematogenous osteomyelitis, children affected with septic arthritis tend to be more toxic, exhibiting high fevers, listlessness, and poor feeding. Diagnosis A workup similar to that for osteomyelitis should be carried out and, at the risk of appearing repetitious, one cannot seriously consider this diag- Figure 5-13. Children’s Orthopedics 187 nosis in the differential without having made an attempt to retrieve organ- isms from the joint. It is important to be sure that the joint is, indeed, being aspirated, and this frequently requires fluoroscopic control, especially if the joint in question is the hip. The pediatric hip is often difficult to enter under the best of circumstances, and radiographic control using an arthro- gram is recommended. Microbiogically, the most common organism retrieved in the child is Staphylococcus aureus. As is the case with osteomyelitis, neonates should be suspected of having unusual organisms including gram negatives. In the adolescent patient, one must never forget the most common cause of septic arthritis: Neisseria gonorrhoeae. Treatment Septic arthritis, in contrast to acute hematogenous osteomyelitis, is a surgi- cal emergency. The articular cartilage is extremely vulnerable and easily damaged by enzymes, those produced by the microorganisms as well as those produced by the white cells. Occasionally, in the older child, arthroscopy is an appropriate tech- nique for cleaning out a more-accessible joint such as the knee. In addition, repetitive aspiration in the child is yet another example of “man’s inhumanity to man. The prognosis for septic arthritis in a child depends on early diagnosis, aggressive drainage, and appropriate antibiotic management. Delay in diagnosis or delay in adequate surgical drainage can have disastrous long-term effects on the joint, typically producing irreversible changes. Complications of Bone and Joint Infections Long-term sequelae can result from bacterial damage to these relatively vulnerable tissues. In addition to the bone and articular carti- lage, the child has a physis, which is likewise exposed to the insult. Septic Joint Destruction Loss of articular cartilage and arthrofibrosis ultimately result in joint con- tracture, deformity, and occasionally bony ankylosis (fusion). Salvage of the irreparably damaged articulations is difficult at best and frequently impossible. Erroneous diagnosis of fibrocystic disease and thrombo- phlebitis resulted in a 2-month delay in diagnosis. Skeletal growth of lower limbs is being followed, and the plan is to perform distal femoral epiphyseodesis on the right at the appropriate age. Children’s Orthopedics 189 Physeal Damage Injury to the plate can have long-term effects, especially when it occurs in a very young child with significant growth remaining. Complete arrest and subsequent limb-length inequality or partial arrest and the resultant angular deformity are the two standard patterns of postinjury deformity. In point of fact, the dense bone is disorganized, its lamellar pattern is disrupted, and therefore it is mechanically less sound. Pathologic fracture can occur even in the immobilized limb, although the risk is less. Chronic Infection Despite aggressive treatment, some infections are not completely eradi- cated, and a “stalemate” is established between the host and the organism. Occasionally, at times of psychologic or environmental stress, the infection will reactivate and produce additional damage (see Chapter 3). Children have systemic symptoms—fever, rash, hepatosplenomegaly—and develop a polyarticular arthritis. This is the most destructive form of the disease and leaves multiple destroyed joints in its wake. Polyar- ticular disease, as the name implies, takes its toll on the joints, but is not associated with systemic findings. Typically, it is a monarticular arthritis, with the knee, elbow, and ankle being the joints most commonly involved. Frequently, children suffering from the pauciarticular form of the disease present with an isolated chronically swollen joint. Diagnostic blood studies are usually negative (rheumatoid factor is positive in only 10% of cases). X-rays usually only show juxtaarticular osteopenia, and frequently a synovial biopsy may be needed. The histology of the synovium is similar to that of the adult disease; namely, hyperplasia and villous hypertrophy of the synovium. Treatment should be directed toward control of the synovitis with medi- cations, physical therapy to maintain joint motion, psychologic support for those chronically impaired children, and ultimately arthroplasties or fusions for those joints most severely involved. Hemophilia Children with bleeding dyscrasias frequently have repeated hemarthroses. Initially, the blood in the joint simply distends the capsular structures and causes a mild synovitis. With repeated bleeds, the synovium becomes hyperplastic and ultimately pannus formation is seen. At this point, the joint changes appear very similar to those seen in rheumatoid disease, such as osteopenia, enzymatic cartilage degradation, bony erosions, and lysis. Lyme Disease In the endemic regions of the Northeast and Middle Atlantic states, the child who presents with a swollen knee needs to be considered as a poten- Figure 5-15. Note the destructive changes with fibrous ankylosis on the right and bony ankylosis on the left. This infectious arthritis is caused by a specific spirochete, Borrelia burgdorferi. These ticks are significantly smaller than the common wood tick, and they are barely visible with the naked eye. Unfortunately, a history of a bite is rare and usually the diagnosis is reached by a high index of suspicion in a susceptible host. The combination of endemic region, erythematous annular skin lesions, and monarticular arthritis should lead the physician to order a Lyme titer. Occasionally, despite adequate treatment, the arthritis can progress to chronic joint destruction, mandating further care. Metabolic Disease Perhaps the classic metabolic disease to affect the pediatric skeleton is rickets. The etiologies of rickets are multiple (Table 5-1), but the important pathophysiologic step is a relative paucity of vitamin D. It will be remem- bered that vitamin D is essential for normal progression of physeal bone 192 J. Complication of Dilantin therapy development, and without it provisional calcification will not occur in the deepest layer of the growth plate. Note the uncalcified osteoid tissue, failure of deposi- tion of calcium along the mature cartilage cell columns, and disorderly invasion of cartilage by blood vessels (×25). The clinically apparent changes of knobby joints, beading of the costochondral joints, and genu varum are all pheno- typic reflections of the underlying histologic disruption of bone formation. Depending on the etiology of the rickets, the histologic pattern varies slightly, but the overall skeletal changes remain relatively constant. Vascular and Hematologic Disease Vascular diseases of the pediatric skeleton are typified by osteochondroses such as Perthes’ disease of the hip and Osgood-Schlatter’s disease of the knee. These are considered regionally, leaving the hematologic diseases to be discussed here. Lauerman Sickle Cell Disease the red cell deformation that occurs in sickle cell patients caused by the abnormal hemoglobin is responsible for the skeletal changes. The abnor- mally shaped cells cause stasis and sludging in small arterioles and capil- laries. The bony infarcts seen in sickle cell disease can occur anywhere in the bone but are more typical in the metaphysis. These children are also predisposed to osteomyelitis, probably because of the already sludged vessels in the metaphysis, making bacterial trapping even easier. Even though Staphylococcus is the most common organism retrieved, this patient population is also susceptible to infection with Sal- monella. This organism gains access to the circulatory system through small infarcts in the intestinal wall and then enters the bone hematoge- nously. The incidence of Salmonella osteomyelitis is approaching that of Staphylococcus in this population. The treatment for the infarcts is appropriate hematologic care, such as hydration and analgesics. Antibiotic selection for osteomyelitis should take into consideration the incidence of Salmonella. Leukemia Leukemia is the most common malignancy of childhood, and the skeleton is not spared its ravages. The bones by X-ray show nondescript lytic changes, most characteristically seen in the metaphyseal region and referred to as Figure 5-19. Although usually the diagnosis has been made well before skeletal com- plications develop, occasionally a child will present for the evaluation of “growing pains” only to have a workup reveal this disease. Any variation from the usual pattern should suggest a basic workup to include X-rays and a white count with differential. Congenital and Neurodevelopmental this group is the largest and most nondescript “wastebasket” of pathologic states, many of which have severe impact on the pediatric skeleton. Included here are congenital birth defects of no known etiology, such as proximal 196 J. Lauerman femoral focal deficiency, as well as genetic diseases transmitted in classic Mendelian fashion . In addition, the neuromuscular diseases frequently have an immense impact on the skeleton, as aberrant and eccentric muscular forces are created. Unfortunately, it is difficult to find many common themes that make an appreciation of the skeletal impact easier to understand. Osteogenesis Imperfecta this disease is transmitted in a classic autosomal dominant pattern with only rare exception. The basic defect is one of abnormal collagen synthesis caused by impotent osteoblasts. Certainly, the osteoblasts are normal in number but are incapable of normal synthetic activity. The collagenous product of their incompetence is poorly formed and poorly cross linked, making it weak. The subsequent bone that is made is similarly architectur- ally thin and mechanically weak. The severity of the disease is as expected, a function of the dose of abnormal genetic material. Some of the severe homozygotes are stillborn as a result of intracranial bleeds occurring in the perinatal period. As with most genetic diseases, penetrance varies such that some children have multiple fractures and severe shortening and others, less involved, have only the occasional fracture. These fractures respond to appropriate treatment, and healing is only slightly prolonged. Occasionally, it is necessary to correct long bone deformities, which is best accomplished operatively by performing multiple osteotomies in a single bone. Scoliosis can also complicate this disease, and its management can be very challenging, especially if surgical management is required to correct the deformity. It is very difficult to use spinal instrumentation in the face of this osteopenic, softened bone. Down Syndrome First described in England by Langdon Down in the 1800s, this syndrome has been shown to result from a trisomy of the number 21 chromosome.

After the postnatal rise antibiotics for uti diarrhea keftab 125mg with visa, 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 antibiotic medications buy discount keftab on-line. If the onset of puberty is triggered by the first hormone to increase in the circulation antibiotic resistance in bacteria order keftab 750 mg with mastercard, then a role for adrenal steroids must be considered antibiotic 4 uti order 500mg keftab fast delivery. However antibiotics for uti with least side effects order keftab 375 mg amex, there is no evidence to suggest that the adrenal steroids are necessary for the proper timing of puberty antibiotic quick guide discount 375 mg keftab with mastercard, and adrenarche appears to be independent, not controlled by the same mechanism 144 that turns on the gonads. Neither is there a definite relationship demonstrated between melatonin secretion and puberty. Because the studies have focused on the amount of melatonin secreted rather than the rhythm of secretion, this question remains open. The clinical onset of puberty is preceded by an increase in 145, 146, 147, 148 and 149 pulse frequency, amplitude, and regularity, especially during the night. This pattern can be detected in individuals who develop increasing and decreasing degrees of hypothalamic suppression (such as in individuals with worsening and improving anorexia nervosa). The rise of gonadotropins at puberty appears to be independent of the gonads in that the same response can be observed in patients with gonadal dysgenesis (who 150 lack functional steroid-producing gonadal tissue). Adolescent girls with Turner syndrome (45,X) also demonstrate augmented gonadotropin secretion during sleep. Thus, maturation at puberty must involve changes in the hypothalamus that are independent of ovarian steroids. The maturational change in the hypothalamus is followed by an orderly and predictable sequence of events. Increased gonadotropins are responsible for follicular growth and development in the ovary and increased sex steroid levels. The trend toward lowering of the menarcheal age and the period of acceleration of growth has halted. In a 10-year prospective study of middle class contemporary 151 American girls, the mean age of menarche was 12. The age of onset of puberty is variable and influenced by genetic factors, socioeconomic conditions, and general health. The earlier menarche today compared to the past is undoubtedly due to improved nutrition and better health. It has 152 been suggested that initiation of growth and menarche occur at a particular body weight (48 kg) and percent of body fat (17%). Although this hypothesis of a critical weight is a helpful concept, the extreme variability in onset of menarche indicates that there is no particular age or size at which an individual girl should be expected to experience menarche. In the female, the typical sequence of events is growth initiation, thelarche, pubarche, and finally menarche. For example, growth of pubic hair and breast development are not always correlated. Puberty is due to the reactivation of the hypothalamic-pituitary axis, once fully active during fetal life but suppressed during childhood. If the systems are potentially responsive, what holds function in check until puberty? The hypothalamic-pituitary-gonadal system is operative prior to puberty but is extremely sensitive to steroids and therefore suppressed. The changes at puberty are due to a gradually increasing gonadotropin secretion that takes place because of a decrease in the sensitivity of the hypothalamic centers to the negative-inhibitory action of gonadal steroids. In addition, there is a qualitative change as a greater increase occurs in the bioactive forms of the gonadotropins. Negative feedback of steroids, however, cannot be the sole explanation for the low gonadotropin levels in children. Agonadal children show the same decline in 153 gonadotropins from age 2 to 6 as do normal children. A very sensitive negative feedback of gonadal steroids (6–15 times more sensitive before puberty). The initial maturational change in the hypothalamus would then be a decrease in this inhibitory influence. This explains the well-known finding of anovulation in the first months (as long as 18 months) of menstruation. There are frequent exceptions, however, and ovulation can occur even at the time of menarche. The overall result of this change in the hypothalamus is the development of secondary sex characteristics, attainment of adult set point levels, and the ability to reproduce. Neoplastic and vascular disorders that alter hypothalamic sensitivity can reverse the prepubertal threshold restraint and lead to precocious puberty. Pellegrini I, Barlier A, Gunz G, Figarella-Branger D, Enjalbert A, Grisoli F, Jaquet P, Pit-1 gene expression in the human pituitary and pituitary adenomas, J Clin Endocrinol Metab 79:189, 1994. Melmed S, the structure and function of pituitary dopamine receptors, Endocrinologist 7:385, 1997. Hardelin J-P, Levilliers J, Young J, Pholsena M, Legouis R, Kirk J, Boulooux P, Petit C, Schaison G, Xp22. Matteo S, the effect of job stress and job interdependency on menstrual cycle length, regularity and synchrony, Psychoneuroendocrinology 12:467, 1987. Knobil E, the neuroendocrine control of the menstrual cycle, Recent Prog Horm Res 36:53, 1980. Ray D, Melmed S, Pituitary cytokine and growth factor expression and action, Endocr Rev 18:206, 1997. Roberts V, Meunier H, Vaughan J, Rivier J, Rivier C, Vale W, Sawchenko P, Production and regulation of inhibin subunits in pituitary gonadotropes, Endocrinology 124:552, 1989. Kitaoka M, Kojima I, Ogata E, Activin-A: a modulator of multiple types of anterior pituitary cells, Biochem Biophys Res Commun 157:48, 1988. Billestrup N, Gonzalez-Manchon C, Potter E, Vale W, Inhibition of somatotroph growth and growth hormone biosynthesis by activin in vitro, Mol Endocrinol 4:356, 1990. Kogawa K, Nakamura T, Sugiono K, Takio K, Titani K, Sugino H, Activin-binding protein is present in pituitary, Endocrinology 128:1434, 1991. Wildt L, Leyendecker G, Sir-Petermann T, Waibel-Treber S, Treatment with naltrexone in hypothalamic ovarian failure: induction of ovulation and pregnancy, Hum Reprod 8:350, 1993. Potential implications for the sexual dimorphism of the stress response and immune/inflammatory reaction, J Clin Invest 92:1896, 1993. Fishman J, Norton B, Brain catecholestrogens: formation and possible functions, Adv Biosci 15:123, 1975. Mohr E, Meyerhof W, Richter D, the hypothalamic hormone oxytocin: From gene expression to signal transduction, Rev Physiol Biochem Pharmacol 121:31, 1992. Menon M, Peegel H, Katta V, Estradiol potentiation of gonadotropin-releasing hormone responsiveness in the anterior pituitary is mediated by an increase in gonadotropin-releasing hormone receptors, Am J Obstet Gynecol 151:534, 1985. Araki S, Chikazawa K, Motoyama M, Ljima K, Abe N, Tamada T, Reduction in pituitary desensitization and prolongation of gonadotropin release by estrogen during continuous administration of gonadotropin-releasing hormone in women: its antagonism by progesterone, J Clin Endocrinol Metab 60:590, 1985. Silman R, Melatonin and the human gonadotrophin-releasing hormone pulse generator, J Endocrinol 128:7, 1991. Kauppila A, Kivela A, Pakarinen A, Vakkuri O, Inverse seasonal relationship between melatonin and ovarian activity in humans in a region with a strong seasonal contrast in luminosity, J Clin Endocrinol Metab 65:823, 1987. Dunkel L, Alfthan H, Stenman U-H, Selstam G, Rosberg S, Albertsson-Wikland K, Developmental changes in 24-hour profiles of luteinizing hormone and follicle-stimulating hormone from prepuberty to midstages of puberty in boys, J Clin Endocrinol Metab 74:890, 1992. Copyright © 6 Regulation of the Menstrual Cycle Clinical Gynecologic Endocrinology and Infertility 6Regulation of the Menstrual Cycle the Follicular Phase the Primordial Follicle the Preantral Follicle the Antral Follicle the Preovulatory Follicle Ovulation Luteal Phase the Luteal-Follicular Transition the Normal Menstrual Cycle Chapter References Many superstitious beliefs have surrounded menstruation throughout recorded history. Indeed, attitudes and ideas about this aspect of female physiology have changed slowly. Hopefully, the scientific progress of the last few decades, which has revealed the dynamic relationships between the pituitary and gonadal hormones and the cyclic nature of the normal reproductive process, will yield a new understanding. The hormone changes, correlated with the morphologic and autocrine/paracrine events in the ovary, make the coordination of this system one of the most remarkable events in biology. The diagnosis and management of abnormal menstrual function must be based on an understanding of the physiologic mechanisms involved in the regulation of the normal cycle. To understand the normal menstrual cycle, it is helpful to divide the cycle into 3 phases: the follicular phase, ovulation, and the luteal phase. We will examine each of these phases, concentrating on the changes in ovarian and pituitary hormones, what governs the pattern of hormone changes, and the effects of these hormones on the ovary, pituitary, and hypothalamus in regulating the menstrual cycle. The Follicular Phase During the follicular phase an orderly sequence of events takes place that ensures the proper number of follicles is ready for ovulation. In the human ovary the end result of this follicular development is (usually) one surviving mature follicle. This process, which occurs over the space of 10–14 days, features a series of sequential actions of hormones and autocrine/paracrine peptides on the follicle, leading the follicle destined to ovulate through a period of initial growth from a primordial follicle through the stages of the preantral, antral, and preovulatory follicle. The Primordial Follicle the primordial germ cells originate in the endoderm of the yolk sac, allantois, and hindgut of the embryo, and by 5–6 weeks of gestation, they have migrated to the genital ridge. A rapid mitotic multiplication of germ cells begins at 6–8 weeks of pregnancy, and by 16–20 weeks, the maximum number of oocytes is reached: a total 1 of 6–7 million in both ovaries. The primordial follicle is nongrowing and consists of an oocyte, arrested in the diplotene stage of meiotic prophase, surrounded by a single layer of spindle-shaped granulosa cells. Until their numbers are exhausted, follicles begin to grow and undergo atresia under all physiologic circumstances. Growth and atresia are not interrupted by pregnancy, ovulation, or periods of anovulation. This dynamic process continues at all ages, including infancy and around the menopause. From the maximum number at 16–20 weeks of pregnancy, the number of oocytes will irretrievably decrease. The rate of decrease is proportional to the total number present; thus, the most rapid decrease occurs before birth, resulting in a decline from 6–7 million to 2 million at birth and to 300,000 at puberty. The mechanism for determining which follicles and how many will start growing during any one cycle is unknown. The number of follicles that starts growing each 2, 3 cycle appears to be dependent upon the size of the residual pool of inactive primordial follicles. It is possible that the follicle which is singled out to play the leading role in a particular cycle is the beneficiary of a timely match of follicle “readiness” (perhaps prepared by autocrine/paracrine actions in its microenvironment) and appropriate tropic hormone stimulation. The first follicle able to respond to stimulation may achieve an early lead that it never relinquishes. Nevertheless, each cohort of follicles that begins growth is engaged in a serious competition that ends with only one follicle succeeding. Rescue From Atresia (Apoptosis) 4 the follicle destined to ovulate is recruited in the first few days of the cycle. The early growth of follicles occurs over the timespan of several menstrual cycles, but the 5, 6 ovulatory follicle is one of a cohort recruited at the time of the luteal-follicular transition. The total duration of time to achieve preovulatory status is approximately 85 7 days. The majority of this time (until a late stage) involves responses that are independent of hormonal regulation. The first visible signs of follicular development are an increase in the size of the oocyte and the granulosa cells becoming cuboidal rather than squamous in shape. At this same time, small gap junctions develop between the granulosa cells and the oocyte. Gap junctions are channels that when open permit the exchange of nutrients, ions, and regulatory molecules. Thus, the gap junctions serve as the pathway for nutritional, metabolite, and signal interchange between the granulosa cells and the oocyte. The process of follicular growth is influenced by factors derived from the oocyte. With multiplication of the cuboidal granulosa cells (to approximately 15 cells), the primordial follicle becomes a primary follicle. The granulosa layer is separated from the stromal cells by a basement membrane called the basal lamina. The surrounding stromal cells differentiate into concentric layers designated the theca interna 6 (closest to the basal lamina) and the theca externa (the outer portion). The theca layers appear when granulosa proliferation produces 3–6 layers of granulosa cells. The belief that the initiation of follicular growth is independent of gonadotropin stimulation is supported by the persistence of this initial growth in 11, 12 gonadotropin-deficient mutant mice and in anencephalic fetuses. In the vast majority of instances this growth is limited and rapidly followed by atresia. The general pattern of limited growth and quick atresia is interrupted at the beginning of the menstrual cycle when a group of follicles (after approximately 60 days of 14 development) responds to a hormonal change and is propelled to grow. The following discussion of events, which mark the growth and development of the ovarian follicle from the preantral stage to ovulation, is based on a formulation that assigns a key role to estradiol functioning as a classic hormone to transmit messages to the brain and as a local regulator within the follicle. We will first describe the traditional conventional view regarding ovarian follicular growth and development derived from 10–15 years of scientific pursuit; and then we will consider the differences in primates. Local autocrine/paracrine peptides probably have replaced steroid hormones as the principal regulators within primate ovarian follicles. The Preantral Follicle Once growth is accelerated, the follicle progresses to the preantral stage as the oocyte enlarges and is surrounded by a membrane, the zona pellucida. The granulosa cells undergo a multilayer proliferation as the thecal layer continues to organize from the surrounding stroma. This growth is dependent upon gonadotropins and is correlated with increasing production of estrogen. Molecular studies indicate that all of the granulosa cells in mature follicles are derived from as 18 few as 3 precursor cells.

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Koivunen R virus 3 game generic keftab 250mg online, Laatikainen T antibiotic every 6 hours purchase keftab 250mg visa, Tomas C treatment for sinus infection home remedies cheap keftab online, Huhtaniemi I antibiotic gastroenteritis purchase keftab overnight delivery, Tapanainen J antibiotics gas order cheap keftab on line, vated receptor gamma gene polymorphism and dietary fat intake in Martikainen H antibiotic 9 fk unsri purchase on line keftab. J Clin morphology with regular ovulatory cycles: insights into the pathophys- Endocrinol Metab 2006;91:2–6. Joseph-Horne R, Mason H, Batty S, White D, Hillier S, Urquhart M, over 1000 consecutive patients. Cor- tic ovaries without hyperandrogenaemia exhibit similar disturbances in onary heart disease risk factors in women with polycystic ovary syn- insulin and lipid profiles as thosewith polycystic ovary syndrome. The impact of ethnic- have hyperandrogenic pituitary–ovarian responses to gonadotropin- ity on the presentation of polycystic ovarian syndrome. Variation within the type 2 diabetes susceptibility gene calpain- the prevalence of polycystic ovaries in women with a history of gesta- 10 and polycystic ovary syndrome. An and associated metabolic abnormalities in Indian subcontinent Asian evaluation of the inter-observer and intra-observervariabilityofthe ultra- women. Prediction models for insulin resistance in the polycystic ovary syn- Exon 6 and 2 peroxisome proliferator-activated receptor-gamma poly- drome. Fertil Steril 2005;83: lationship of the metabolic syndrome and obesity to polycystic ovary 1717–23. The prevalence of polycystic ovaries tic ovary syndrome in North Rhine-Westphalia. Polycystic ovary syndrome: the spectrum of the disorder in 1741 have polycystic ovary syndrome? 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Insulin iation in hyperandrogenic women influences the findings of abnormal resistance in the sisters of women with polycystic ovary syndrome: as- metabolic and cardiovascular risk parameters. J Clin Endocrinol Metab sociation with hyperandrogenemia rather than menstrual irregularity. Endocrine disorders associated with inappropriately high aroma- Surv 2004;59:141–54. The indepen- Prevalence of 21-hydroxylase-deficient nonclassic adrenal hyperplasia dent effects of hyperandrogenaemia, hyperinsulinaemia, and obesity and insulin resistance among hirsute women from Puerto Rico. Ad- hyperandrogenic symptoms: implications for the management of poly- verse lipid and coronary heart disease risk profiles in young women cystic ovary syndrome. Clin Endocrinol (Oxf) tein lipid concentrations and cardiovascular risk in women with poly- 2003;59:282–8. Maternal thyroid deficiency during pregnancy and sub- with insulin resistance in women with polycystic ovaries. Am J lence ofthyroid disordersin a middle-aged female population,with spe- Med Genet 1998;76:337–42. Screening for 21-hydroxylase-deficient nonclassic adrenal Thyroid disorders in the general population of Hisayama Japan, with hyperplasia among hyperandrogenic women: a prospective study. Natural history of thyroid abnormalities: prevalence, incidence, and re- N Engl J Med 1990;323:849–54. Bjoro T, Holmen J, Kruger O, Midthjell K, Hunstad K, Schreiner T, 1993;168:889–95. Acquired adrenal hyperplasia: with special reference oxidase antibodies in a large, unselected population. Late-onset adrenal steroid 3 beta-hydroxysteroid dehydrogenase defi- Prolactin has a direct effect on adrenal androgen secretion. Studies of 3 beta-hydroxysteroid dehydrogenase genes metabolic clearance rate of dehydroepiandrosterone sulfate in normal in infants and children manifesting premature pubarche and increased and hyperprolactinemic subjects. J Clin Endocrinol Metab 1986;62: adrenocorticotropin-stimulated delta 5-steroid levels. Clinical review 56: Nonclassic ad- Identification of virilizing adrenal tumors in hirsute women. The Cushing syndromes: changing views of diagnosis and plasia: the great pretender. Androgen-related effects on peripheral glucose metabolism tory value of signs and symptoms aiding early diagnosis. Cushing’s syndrome [erratum appears in N Engl J Med 1995 Mol Genet Metab 2000;71:527–34. Influence of different genotypes on 17- ing’s syndrome in obese women with and without polycystic ovary syn- hydroxyprogesterone levels in patients with nonclassical congenital drome. J Clin Endo- notype-genotype correlation in 56 women with nonclassical congenital crinol Metab 2003;88:2634–43. Menstrual abnormalities in women thosis nigricans syndrome: a common endocrinopathy with distinct with Cushing’s disease are correlated with hypercortisolemia rather pathophysiologic features. Midnight salivary cortisol for the initial diagnosis of Cush- plasma androstenedione to 5 alpha-androstanediol glucuronide in ing’s syndrome of various causes. A clinicopathologic analysis of 17 cases and review of the investigation of hirsutism in a Turkish population: idiopathic hyperan- literature. Ferriman Gallwey association of ovarian tumors with polycystic ovaries with review of the self-scoring I: performance assessment in women with polycystic ovary literature. Consensus on infertility treatment related to renal adenoma with studies on the steroid content of the adrenal venous polycystic ovary syndrome. Diagnosing the diagnosis: why we must standardize the defin- Gynecol 1979;53:36–43. Am J Obstet Gynecol 1988;158: utility, limitations, and pitfalls in measuring testosterone: an Endocrine 1313–22. Alteration in Mizaj al-Rahim, congenital abnormality or biochemical changes in cervical secretion and presence of anti-sperm antibody in the cervix leads to cervical hostility. Therefore the aim of this study was to appraise the usefulness of Unani treatment in infertility due to cervical mucus factor. Materials and Methods: this study was conducted in infertile patients due to cervical mucus factor (n=12) at Govt Nizamia Tibbi hospital, Hyderabad. The inclusion criteria includes infertile married woman aged 18-35 year with normal ovulatory cycles, patent fallopian tubes and normal sperms count of husband. On the basis of Unani Usool-i-Ila’j, Munzij (11 days) and Mushil (3 alternate days) with Tabrid were given in first month of the enrollment. From second month orally Sufuf of Buroode Dandane Feel (2g) and Resha Bargad (2g) with 4g sugar and Majoon Supari Pak 5 g was given twice daily from day 1 to day 10 with vaginal humool (powder of Joazbuwa, Kuzmazij, Phitkari Biryani, and Poste Anar each 2g with Roghan Chameeli 10 g) from day 6 to day 10 was given. Results: In the present study, minimum age was 18 years and maximum age was 31 years. Eight patients had primary infertility and four patients had secondary infertility. Conclusions: this study shows that aforementioned Unani treatment is useful in Uqr. During the pre-ovulatory phase of the cycle and under the influence of oestrogen, cervical Infertility is a chronic illness that causes medical as well mucus (when viewed under a microscope) forms parallel as social and financial problem. It is ―the state of channels that allow sperm to traverse the cervix and then inability to conceive after a period of unprotected and [1] to swim up to the fallopian tubes: the biological valve— regular intercourse for one year. The incidence of this disease [2] phase and under the influence of progesterone, cervical is 10%–15%. The causes of infertility are male, mucus is thick (with a ―cobblestone‖ appearance under peritoneal, ovarian, tubal, uterine, cervical, and the microscope) and blocks the passage of sperm into the unexplained. Cervical mucus is a necessary component uterus: the biological valve of cervical mucus is of human fertility and plays at least two critically [3] ―closed‖. According to Unani concepts, alteration in important physiologic roles in fertility. First, cervical four humours of body and alteration in uterine mucus is essential to sperm survival and transport. The temperament or hard texture of uterine inner layer or duration of the fertile window is six days in couples of whole uterus undergo in hard texture due to absorption of normal fertility: the five days that the sperm can survive phlegmatic fluid in the uterus or abnormal bile and black in fertile-type mucus plus the day of ovulation. Without bile, irregular menstrual cycles, cervical infections, fertile mucus sperm would last only hours in the vagina congenital abnormalities, anovulatory cycles, peritoneal with little chance of meeting and fertilizing the egg infections, and sexually transmitted diseases are common (ovum). Further, eminent ancient ―biological valve,‖ admitting sperm to the uterus at physicians mentioned that infertility due to cervical certain times of the cycle while inhibiting their entrance mucus hostility is caused by temperament changes due to . Alteration in the temperament congestion of cervix and white discharge seen by per of uterus such as su’al mizaj har yabis (hot & dry) causes speculum and tenderness felt by bimanual examination. At every follow up during six known as spinnbarkeit), salinity (evaluated according to months of study period, pregnancy test was done to the number of channels formed by the crystallization of confirm the pregnancy if patient had missed periods. The the mucus when dried on a glass slide also known as study was conducted for a period of 14 days of each ―ferning‖), and the number and motility of surviving cycle upto 3 cycles. In Unani medicine, the Supari Pak 5 g was given twice daily from day 1 to day response in cervical factor infertility has been mentioned 10 with vaginal humool (powder of Joazbuwa, Kuzmazij, in the classical texts. Further, these medicine are safe and Phitkari Biryani, and Poste Anar each 2g with Roghan having no side effects as compared to modern medicine. Therefore the aim of this pilot study was to appraise the usefulness of Unani treatment in infertility due to Joshanda Munzij included Gule banafsha, Maveez cervical mucus factor. Mushil included habbe Study Design: this pilot study was conducted in ayarij 7 tabs orally in the early morning. The tabrid infertile patients due to cervical mucus factor (n=12) at consists of Khameera Gaozaban Sada (5g) with Warqe Govt Nizamia Tibbia hospital, Hyderabad during the Nuqra (1 tola) orally given twice daily on alternate days year 2015-2016 after taking written informed consent. Participants: the inclusion criteria includes infertile Outcome: the outcome was conception. Procedure: Patients were assessed through complete history, physical examination and investigations.

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This axial image of an isthmic spondylolisthesis with severe central canal spondylolisthesis reveals an elongated stenosis and facetal effusion bacteria bacillus cheap keftab 375mg on-line. This T2W image of a football lineman shows facetal effusion (hyperintense on T2) at L4-5 antibiotics for dogs at tractor supply keftab 500 mg lowest price, L5- S1 with a synovial cyst extending posteriorly and caudally from the L5-S1 facet (yellow arrow) infection 3 weeks after wisdom tooth extraction purchase keftab 500mg. These findings correlate with his symptoms and history of pain and traumatic lumbar extensions while playing football antimicrobial wound cream order discount keftab online. Facet effusion can be an indicator of reduced segmental stability in degenerative spondylolisthesis antibiotic resistance exam questions order keftab discount. While it is not fully understood if this finding predisposes the vertebra to lysis or if it occurs as a result of lysis and listhesis antimicrobial underpants purchase 125 mg keftab with amex, experts are leaning toward the thought that this trapezoid deformation occurs over time after the spondylolysis and listhesis occur. This phenomenon is not pathognomonic for an isthmic spondylolisthesis, but is a point of reference that may alert the clinician to a spondylolisthesis. Bony edema and sclerosis of the cortical bone Sclerotic thickening of the vertebral endplate Henry Gray (1821–1865). Bony edema, disc degeneration, and sclerotic changes to the vertebral endplates secondary to spondylolisthesis are clearly visible in figures 8:26 and 27. Bony edema of the pars interarticularis (yellow arrows) is visible on this T2 weighted axial image indicating a probable isthmic spondylolisthesis. The blue line in figure 8:31 shows the level of the slice that was used to create figure 8:29. Incidentally the sagittal images display a perineural cyst affecting the S2 nerve root. By analyzing the sagittal views (figure 8:33) we can see that the L4-5 and L5-S1 facets are approximated by the anterolisthesis of L5 on S1. By following the red line we can clearly see how the facets of L4-5 and L5-S1 could appear on the same axial slice. This finding underscores the importance of comparing sagittal views with axial views to gain a complete perspective of the lumbar Figure 8:32. Another common finding in isthmic spondylolisthesis is the “rolling up” or “peeling” of the disc below the listhesis and less commonly “rolling down” of the disc above the spondylolisthesis. In sagittal imagery of a spondylolisthesis, a line drawn along the posterior body of the lower segment typically shows the disc to be in line with the inferior segment. On axial imagery of a spondylolisthesis, it is not uncommon for the appearance of a pseudo-bulge or pseudo-disc herniation to be seen. The phenomenon of a pseudo-bulge or pseudo-disc herniation occurs when the axial image slice (blue line in the schematic) contains the rolled up portion of the disc along with vertebra listing forward. By integrating axial and sagittal views, the clinician can more fully understand what occurs to the disc in a patient with spondylolisthesis. This series shows not only the L5-S1 disc rolling up, but the L4-L5 disc rolling down following an L5 anterolisthesis. These images of an isthmic spondylolisthesis reveal enlargement of the central canal, anterolisthesis, a trapezoid shaped L5, and a “roll-up” of the adjoining intervertebral discs. This axial T2W image of isthmic spondylolisthesis show a the same patient shows another synovial cyst arising from the inferior synovial cyst arising from the right L5- portion of the right L5-S1 facet. These sagittal T2 weighted images show three synovial cysts arising from the facets adjoining an L5 on S1 spondylolisthesis. The excessive fluid production (effusion) can result in a ballooning of the facet joint’s capsule creating synovial cysts. When synovial cysts project posteriorly, they usually do not require intervention. However, if the synovial cyst projects into the central canal, intervention may be indicated. These images are all of the same patient whose L4-L5-S1 facets produced multiple synovial cysts projecting posteriorly. Given the degeneration of the disc, anterolisthesis, facetal hypertrophy, and ligamentous buckling and thickening, this phenomenon could be particularly contributory to creating central canal and foraminal stenosis. In this case the facets of L4-5 eroded and degenerated to such an extent that they could no longer function to restrain the anterior listhesis of L4 on L5. These two sagittal images display the characteristics that are common in degenerative spondylolisthesis. The image on the right shows anterolisthesis, disc degeneration, disc rolling at the level of listhesis, and stenosis. Note that the posterior vertebral elements of L4 have maintained a normal relationship with the vertebral body; they have not come apart as is seen in most cases of listhesis secondary to spondylolysis. Post-surgical spondylolisthesis of L5 and re-herniation of the L4-L5 disc on a T2W axial image. Post-surgical spondylolisthesis of L5 and re-herniation of the L4-L5 disc on a T2W sagittal image. Lying supine will allow a mobile segment to settle into a lower state of displacement. T2 weighted sagittal showing significant disc rolling of the L4-5 and L5-S1 discs. This case presents an isthmic spondylolisthesis in a patient with transitional anomalies of the lumbosacral anatomy. Of particular interest is the amount of disc roll-up of the L5-S1 disc and disc roll-down of the L4-L5 disc. These T2 weighted sagittal images show the significant disc rolling above and below the L5 vertebra. Clinical imaging: with skeletal, chest and abdomen pattern differentials (third edition). For that reason it has more value in radiology reports than in clinical diagnosis. It is characterized by hypertrophic osteophytic changes, desiccation of the discs, loss of disc height, ligamentous instability, facetal hypertrophy, facetal imbrication, and bony remodeling. Disc bulges, hypertrophic facets, and thickening of the ligamentum flavum all contribute to stenosis of the central canal, lateral recess, and the foramina. Degeneration of intervertebral discs can cause slackening of the spinal ligaments which can lead to degenerative spondylolisthesis. The body responds to slackened ligaments by producing osteophytes as seen particularly at the level of L4 and L5. Clinical imaging: with skeletal, chest and abdomen pattern differentials(third edition). The central canal is the protective conduit that protects the spinal cord and (from L1-L2 caudally) the cauda equina. Stenosis usually occurs at the levels of the intervertebral disc where the disc bulges. Facet hypertrophy and ligament thickening can combine to narrow the central canal. Pedicles can be congenitally short or asymmetrical in length, contributing to stenosis. A transection of a vertebral vertebral body along with the arch of the segment showing the canal’s position within the pedicles and lamina comprise the bony portion vertebra. A T2 weighted sagittal image of a patent central canal traveling the length of Images adapted from Henry Gray (1821–1865). Note the congenitally narrowed canal, ligamentum flavum hypertrophy, and facetal hypertrophy. Note that stenosis typically occurs at the vertebral interspace where a disc bulge, ligamentum flavum hypertrophy, and facet hypertrophy combine to narrow the central canal. Even in patients with central canal stenosis, the canal is usually patent at the middle of the vertebral body. Only the intervertebral region where the combination of disc, facet hypertrophy, and ligamentum flavum hypertrophy or enfolding combine to narrow the central canal. These images expose a lumbar stenosis at L2-L3 arising from a congenitally narrow canal, ligamentum flavum hypertrophy, an L2-L3 disc bulge, and facetal hypertrophy. Lumbar stenosis of the central this T2 weighted axial image clearly canal and lateral recesses secondary to facet demonstrates a patent central canal. The combination of decreased disc height, enfolding and thickening of spinal ligaments, and bony hypertrophy contribute to this slowly progressing condition. The image on the left (figure 10:12) shows a widely patent central canal, lateral recesses (subarticular zone), and intervertebral foramina. The image on the right (figure10:13) reveals a moderately severe stenosis that affects the central canal, lateral recesses, and foramina. The point at which a narrowing of the canal becomes a stenosis is imprecise and is usually left to the interpretation of the radiologist. This T2W axial image shows significant ligamentum flavum hypertrophy and facet hypertrophy from degeneration. This T2W sagittal image shows an L4-5 central canal stenosis that is caused by the convergence of a disc bulge, disc degeneration, degenerative spondylolisthesis of L4 on L5, ligamentum flavum hypertrophy, and facet hypertrophy. Disc bulging at L4-L5 compounds the narrowing effects of the hypertrophic changes of the ligamentum flavum and the zygapophyseal joints. This case compiles ligamentum flavum hypertrophy, a synovial cyst, degenerative spondylolisthesis, disc bulging, facetal hypertrophy, and epidural lipomatosis to narrow the central canal. This T2W sagittal image reveals a stenosis of the central canal caused by an accumulation of various factors. This image reveals a degenerative spondylolisthesis, ligamentum flavum hypertrophy, facet hypertrophy, an L4-L5 disc bulge, and a large synovial cyst at L4-L5. A facet that is inflamed and effused (white arrow) can give rise to a synovial cyst (red arrow). Facetal effusion denoted by the white arrow and spinal epidural lipomatosis denoted by the red arrow. Figure: 10:21 Central canal stenosis from facet hypertrophy, ligamentum flavum hypertrophy (yellow arrows), and a disc bulge. Redundant ligamentum flavum combines with a disc bulge and facetal hypertrophy to create a central canal stenosis visible in this T2 weighted axial image of the L2-L3 interspace. A developmentally narrowed central canal, usually attributed to congenitally short pedicles, predisposes a spine to develop a central canal stenosis as normal age-related degeneration contributes to a narrowing of the canal. These age-related changes include ligamentum flavum enfolding (redundant ligamentum flavum) and hypertrophy, facet hypertrophy, and disc bulges. A developmentally narrowed central canal tends to produce stenosis symptoms earlier and with a more profound clinical presentation than a more patent canal. A congenital canal tends to have a more rapid onset of stenosis with less spinal degeneration. The difference between a congenitally narrowed canal and a stenosis is that a stenosis refers to a focal narrowing of the canal, whereas a congenitally narrowed canal is the generalized narrowing of the canal. Clinically, patients with congenital stenosis will report with multiple levels of stenosis, and they present with symptoms at a younger age. A congenitally narrowed this T2 weighted axial image clearly shows central canal in a 32 year-old female. The image in figure 10:32 shows a widely patent central canal with ample room for the spinal nerves of the cauda equina. In stark contrast is the image in figure 10:33; it has a tight canal that has little room to spare for the contents of the thecal sac. Significance of the small lumbar spinal canal: cauda equina compression syndromes due to spondylosis. Clinical imaging: with skeletal, chest and abdomen pattern differentials(third edition). It can also provide insight into the degree of bony edema and the formation of epidural hematomas. When a spine fractures, fragments of bone may be pushed backwards into the spinal canal or cord. The retropulsion of bony fragments into the canal and possibly even into the cord is a great concern in compression fractures of the spine. The next few pages will present a gallery of images revealing common presentations of vertebral fractures. The loss of height attributed to compression fractures can lead to crowding of internal structures. In this case of multiple fractures, the aorta is forced into a torturous contorted path, the lungs and heart have lost chest space, and the bone fragments have migrated posteriorly into the central spinal canal. This image reveals a number of significant findings: compression fractures, post-surgical changes, spondylolisthesis, endplate disruption, fusion, spondylosis, disc derangements and degeneration, and cord effacement. While most compression fracture are stable and do not endanger the spinal cord, this patient has a significant posterior displacement (retropulsion) of bony fragments at T12. Burst fractures or compression fractures in healthy non-osteoporotic patients are usually the result of significant trauma. This patient experienced significant compressive forces that caused an L3 burst fracture. Axial image of the compression fracture of L2 with bony retropulsion into the central canal and cauda equina. Note the bony edema in L1 and L2 and the hematoma posterior to the spinous processes of L3 and L4 (yellow arrows). Note the significant central canal stenosis resulting from the retropulsion of bone posteriorly. Clinical imaging: with skeletal, chest and abdomen pattern differentials(third edition). Retrospective review of biopsy results following percutaneous fixation of vertebral compression fractures. Most practitioners want to know if there is a need for surgical referral or a referral to an oncologist: (Is there neurological defect? However, recent studies have found that vertebral marrow edema is clinically significant and can be progressive.

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