By: Edward T. F. Wei PhD
Reports suggest that several oral antimicrobial agents (azithromycin sathuragiri herbals order 30 caps npxl mastercard, ciprofoxacin herbalshopcompanynet discount 30caps npxl overnight delivery, trimethoprim-sulfamethoxazole herbals on demand coupon code cheap npxl 30caps without prescription, and rifampin) and parenteral gentamicin are effective herbs pictures cheap npxl master card, but the role of antimicrobial ther apy is not clear phoenix herbals 50x npxl 30caps with mastercard. The optimal duration of therapy is not known but may be several weeks for systemic disease. Azithromycin or doxycycline are effective for treatment of these conditions; therapy should be administered for several months to prevent relapse in immunocompromised people. Immunocompromised people should avoid contact with cats that scratch or bite and should avoid cats younger than 1 year of age or stray cats. Testing of cats for Bartonella infection is not recommended, nor is removal of the cat from the household. An ulcer begins as an erythematous papule that becomes pustular and erodes over sev eral days, forming a sharply demarcated, somewhat superfcial lesion with a serpiginous border. The base of the ulcer is friable and can be covered with a gray or yellow, purulent exudate. Unlike a syphilitic chancre, which is painless and indurated, the chancroid ulcer often is painful and nonindurated and can be associated with a painful, unilateral inguinal suppurative adenitis (bubo). In most males, chancroid manifests as a genital ulcer with or without inguinal tender ness; edema of the prepuce is common. In females, most lesions are at the vaginal introi tus and symptoms include dysuria, dyspareunia, vaginal discharge, pain on defecation, or anal bleeding. Chancroid is rare in the United States, and when it does occur, it usually is associated with sporadic outbreaks. Because sexual con tact is the only known route of transmission, the diagnosis of chancroid in infants and young children is strong evidence of sexual abuse. Confrmation is made by isolation of Haemophilus ducreyi from a genital ulcer or lymph node aspirate, although sensitivity is less than 80%. Because special culture media and conditions are required for isolation, laboratory personnel should be informed of the suspicion of chancroid. Fluorescent monoclonal antibody stains and polymerase chain reaction assays can provide a specifc diagnosis but are not available in most clinical laboratories. H ducreyi strains with intermediate resistance to ciprofoxacin or erythro mycin have been reported worldwide. Clinical improvement occurs 3 to 7 days after initiation of therapy, and healing is complete in approximately 2 weeks. Adenitis often is slow to resolve and can require needle aspiration or surgical incision. Patients should be reexamined 3 to 7 days after initiating therapy to verify healing. If healing has not occurred, the diagnosis can be incorrect or the patient may have an additional sexually transmitted infection, so further testing is required. Close clinical follow-up is recommended; retreatment with the original regimen usually is effective in patients who experience a relapse. All people having sexual contact with patients with chancroid within 10 days before onset of the patient’s symptoms need to be examined and treated, even if they are asymptomatic. Regular condom use may decrease transmission, and male circumcision is thought to be partially protective. Immunization status for hepatitis B and human papillomavirus should be reviewed and updated if necessary. C pneumoniae can present as severe community-acquired pneumonia in immunocompromised hosts and has been associated with acute respiratory tract exacer bation in patients with cystic fbrosis and in acute chest syndrome in children with sickle cell disease. Physical examination may reveal nonexudative pharyngitis, pulmonary rales, and bronchospasm. Chest radiography may reveal an infltrate(s) of a variety of patterns ranging from pleural effusion and bilateral infltrates to a single patchy subsegmental infltrate. C pneumoniae is distinct anti genically, genetically, and morphologically from Chlamydia species and is grouped in the genus Chlamydophila. The disease occurs worldwide, but in tropical and less developed areas, disease occurs earlier in life than in industrialized countries in temperate climates. In the United States, approximately 50% of adults have C pneumoniae-specifc serum anti body by 20 years of age, indicating prior infection by the organism. Serologic testing has been the primary laboratory means of diagnosis of C pneumoniae infection. Of the serologic tests, the microimmunofuores cent antibody test is the most sensitive and specifc serologic test for acute infection and currently is the only endorsed approach. A fourfold increase in immunoglobulin (Ig) G titer between acute and convalescent sera or an IgM titer of 16 or greater is evidence of acute infection; use of acute and convalescent titers is preferable over an IgM titer. Use of a single IgG titer in diagnosis of acute infection is not recommended, because during primary infection, IgG antibody may not appear until 6 to 8 weeks after onset of illness and increases within 1 to 2 weeks with reinfection. In primary infection, IgM antibody appears approximately 2 to 3 weeks after onset of illness, but caution is advised when interpreting a single IgM antibody titer for diagnosis, because a single result can be either falsely positive because of cross-reactivity with other Chlamydia species or falsely nega tive in cases of reinfection, when IgM may not appear. C pneumoniae can be isolated from swab specimens obtained from the nasophar ynx or oropharynx or from sputum, bronchoalveolar lavage, or tissue biopsy specimens. Specimens should be placed into appropriate transport media and held at 4°C (39°F) until inoculated into cell culture; specimens that cannot be processed within 24 hours should be frozen and held at –70°C. Culturing C pneumoniae is diffcult and often fails to detect presence of the organism. A positive culture is confrmed by propagation of the isolate or a positive polymerase chain reaction assay result. Nasopharyngeal shedding can occur for months after acute disease, even with treatment. Immunohistochemistry, used to detect C pneumoniae in tissue specimens, requires control antibodies and tissues in addition to skill in recognizing staining artifacts to avoid false-positive results. For suspected C pneumoniae infections, treatment with macrolides (eg, erythromycin, azithromycin, or clarithromycin) is recommended. Tetracycline or doxycycline may be used but should not be given routinely to children younger than 8 years of age (see Tetracyclines, p 801). Newer fuoroquinolones (levofoxacin and moxi foxacin) are alternative drugs for patients who are unable to tolerate macrolide antibiotics but should not be used as frst-line treatment. Duration of therapy typically is 10 to 14 days for eryth romycin, clarithromycin, tetracycline, or doxycycline. However, with all of these antimicrobial agents, the optimal duration of therapy is not clear. Extensive interstitial pneumonia can occur, with radiographic changes characteristically more severe than would be expected from physical examination fnd ings. Endocarditis, myocarditis, pericarditis, thrombophlebitis, nephritis, hepatitis, and encephalitis are rare complications. The term psittacosis com monly is used, although the term ornithosis more accurately describes the potential for nearly all domestic and wild birds to spread this infection, not just psittacine birds (eg, parakeets, parrots, and macaws). In the United States, psittacine birds, pigeons, and turkeys are important sources of human disease. Importation and illegal traffcking of exotic birds is associated with an increased incidence of disease in humans, because ship ping, crowding, and other stress factors may increase shedding of the organism among birds with latent infection. Infection usually is acquired by inhaling aerosolized excrement or secretions from the eyes or beaks of birds. Handling of plumage and mouth-to-beak contact are the modes of exposure described most frequently, although transmission has been reported through exposure to aviaries, bird exhibits, and lawn-mowing. Excretion of C psittaci from birds may be intermittent or continuous for weeks or months. Pet own ers and workers at poultry slaughter plants, poultry farms, and pet shops are at increased risk of infection. This assay has been validated in birds but has yet to be validated for use in humans. Treatment with antimicrobial agents may suppress the antibody response, and in such cases, a third serum sample obtained 4 to 6 weeks after the acute sample may be useful in confrming the diagnosis. Culturing the organism is diffcult and should be attempted only by experienced personnel in laborato ries where strict measures to prevent spread of the organism are used during collection and handling of all specimens because of occupational and laboratory safety concerns. Therapy should be a minimum of 10 days and should continue for 10 to 14 days after fever abates. Erythromycin and azithromycin are alternative agents and are recommended for younger children and pregnant women. All birds suspected to be the source of human infec tion should be seen by a veterinarian for evaluation and management. Birds with C psittaci infection should be isolated and treated with appropriate antimicrobial agents for at least 30 to 45 days. Birds suspected of dying from 1 C psittaci infection should be sealed in an impermeable container and transported on dry ice to a veterinary laboratory for testing. All potentially contaminated caging and housing areas should be disinfected thoroughly before reuse to eliminate any infectious organisms. People cleaning cages or handling possibly infected birds should wear personal protective equipment including gloves, eye wear, a disposable hat, and a respirator with N95 or higher rating. C psittaci is susceptible to many but not all household disinfectants and detergents. Effective disinfectants include 1 National Association of State Public Health Veterinarians. Compendium of Measures to Control Chlamydophila psittaci Infection Among Humans (Psittacosis) and Pet Birds (Avian Chlamydiosis), 2008. People exposed to common sources of infection should be observed for development of fever or respiratory tract symptoms; early diag nostic tests should be performed, and therapy should be initiated if symptoms appear. Neonatal chlamydial conjunctivitis is characterized by ocular congestion, edema, and discharge developing a few days to several weeks after birth and lasting for 1 to 2 weeks and sometimes longer. Pneumonia in young infants usually is an afebrile illness of insidious onset occur ring between 2 and 19 weeks after birth. A repetitive staccato cough, tachypnea, and rales in an afebrile 1-month-old infant are characteristic but not always present. Severe chlamydial pneumonia has occurred in infants and some immunocompromised adults. Genitourinary tract manifestations, such as vaginitis in prepubertal girls; urethri tis, cervicitis, endometritis, salpingitis, and perihepatitis (Fitz-Hugh-Curtis syndrome) in postpubertal females; urethritis and epididymitis in males; and Reiter syndrome (arthritis, urethritis, and bilateral conjunctivitis) also can occur. In postpubertal females, chlamydial infection can progress to pelvic infammatory disease and result in ectopic pregnancy or infertility. However, anorectal infection is associated with anal intercourse and can cause hemorrhagic proctocolitis or stricture among women and men who engage in anal intercourse. The proctocolitis can be moderate to severe and can resemble infammatory bowel disease. Trachoma is a chronic follicular keratoconjunctivitis with neovascularization of the cornea that results from repeated and chronic infection. Blindness secondary to extensive local scarring and infammation occurs in 1% to 15% of people with tra choma. Trachoma usually is caused by serovars A through C, and genital and perinatal infections are caused by B and D through K. A signifcant proportion of patients are asymptomatic, thereby providing an ongoing reservoir for infection.
Penetrating injuries and injuries related to herbs pool order npxl 30caps mastercard instrumentation of the urethra occur much less commonly everyuth herbals skin care products cheapest generic npxl uk. In patients with suspected urethral injuries himalaya herbals buy cheap npxl 30 caps on-line, a urinary catheter should never be inserted until retrograde urethrography is performed to herbs pool 30caps npxl free shipping assess whether the urethra is intact exotic herbals lexington ky purchase genuine npxl line. Retrograde urethography is the gold standard study for the diagnosis of urethral injury. Injuries to the bladder may result from blunt or penetrating trauma, with motor vehicle accidents being the most common mechanism in children. Most bladder injuries (>80%) are associated with pelvic fractures and penetration of the bladder by a bony fragment. Clinical findings associated with bladder laceration may include hematuria, dysuria, and pain in the lower abdomen/pelvis. In cases of complete bladder rupture, patients may develop peritonitis and a palpable fluid wave from leakage of urine into the peritoneal cavity. Although the boy in the vignette presents with hematuria, an anterior urethral injury would be much more likely to result from his mechanism of injury than a bladder laceration. In addition, he has no abdominal pain and no findings suggestive of a pelvic fracture on physical examination. These injuries typically result from the traumatic impact of an erect penis against a hard surface. Patients with penile shaft fractures generally report hearing a cracking sound at the time of injury and present with pain, swelling, and deformity of the penile shaft. Classic signs and symptoms for patients with rhabdomyolysis include weakness, myalgias, red or brown discolored urine, and in some cases, difficulty with urination. Rhabdomyolysis may result from traumatic causes such as crush injuries and compartment syndrome, as well as nontraumatic causes such as excessive exertion, prolonged seizure activity, hypokalemia, metabolic myopathies, illicit and prescription drugs, and infections. Scrotal trauma may occur as a result of straddle injuries, and injuries can range from minor scrotal/testicular contusions to complete testicular rupture (a surgical emergency). Testicular contusion may present with tenderness to palpation over the scrotum, scrotal edema, and ecchymosis. The boy in the vignette has no tenderness on palpation of his testicles and has blood at the urethral meatus that would not be explained by a testicular contusion. Other clinical indicators may include voiding difficulty, scrotal hematoma or perineal ecchymoses, and displacement of the prostate on rectal examination in males. He is currently intubated and sedated because of respiratory failure from pneumonia. Prior to this event, given the progressive nature of his illness, his parents and primary care physician discussed end-of-life care with him. The patient indicated his desire for withdrawal of life-sustaining treatment if he were to develop respiratory failure again. In this setting, therapies should be given with the purpose of alleviating symptoms. The most appropriate medication to treat the symptom of breathing difficulty is intravenous morphine, 0. Palliative care is the practice of integrating medical, spiritual, and psychosocial aspects of care when making medical decisions based on quality of life for a patient in a family-centered manner. Palliative care should begin for all children with progressive medical conditions early enough in the course of disease so that rational decisions can be made with as little stress as possible. As the practice of palliative care expands, primary care physicians will likely play a more integral role. An important aspect of palliative care is defining the goals of end-of-life care for a terminally ill child. Because of repeated respiratory infections from his progressive neuromuscular condition, the child in the vignette prepared an advance directive indicating his desire for withdrawal of life-sustaining therapies in the case of a subsequent episode of respiratory failure. The principle of autonomy, or respect for persons, provides that an appropriately mature 16-year-old child should ideally determine important decisions such as end of-life care. Although the decision-making power legally lies with his parents, every effort should be made to incorporate the child’s wishes into such decisions. Presumably, for the child in the vignette, open discussions occurred and decisions were appropriately made in a relatively low-stress setting. A “do-not-resuscitate” order may be defined in the outpatient setting, and family members can direct caregivers accordingly. It is not uncommon for families to initially choose mechanical ventilation for a child like the boy in the vignette, in case the cause of acute respiratory failure is quickly reversible. However, a chronically ill or weak child often does not then wean from mechanical support easily. Terminal extubation, which involves removal of an endotracheal tube from a ventilator-dependent patient, is a reasonable option in such cases. For the boy in the vignette, because terminal extubation has been chosen and the condition is not likely reversible, noninvasive positive pressure ventilation would not be appropriate. In terminal extubation, the patient and family should be informed that it is uncertain how long it will take for the child to die. Opioids and/or benzodiazepines should be readily available, at doses appropriate for the intent to treat symptoms of distress, as opposed to intentionally causing or hastening death. Although these medications may in fact hasten death, the “doctrine of double effect” provides that if a medication has 2 effects, 1 positive (treating symptoms) and the other negative (hastening death), the intent of the positive effect can be honored. Although it is practiced in some countries, euthanasia is not widely accepted in the medical community. For the boy in the vignette, administration of 5 mg/kg of intravenous morphine would be an intentional overdose and would represent euthanasia. Administration of vecuronium without adequate sedation is inhumane in any setting, and in this setting would also constitute euthanasia. On physical examination, she has erythema, edema, and exudates of both tonsillar pillars, tender bilateral anterior cervical lymphadenopathy, and a scarlatiniform rash. In contrast, growth of Streptococcus pyogenes is easily detected on routine culture media. Detection of A haemolyticum can be enhanced if rabbit or human blood agar is used. Therefore, the differential growth of S pyogenes compared to A haemolyticum using routine culture media is the best way to distinguish these 2 causes of pharyngitis. It is not possible to distinguish pharyngitis caused by S pyogenes from that caused by A haemolyticum on clinical grounds. Fever, pharyngeal exudates, lymphadenopathy, and a scarlatiniform rash can be seen in both infections. A haemolyticum, like S pyogenes, can cause invasive infections, although invasive A haemolyticum infections are quite rare and tend to occur in immunocompromised patients. While A haemolyticum infections occur primarily in adolescents and young adults, individuals in this age group also can develop streptococcal pharyngitis, therefore, age alone cannot distinguish these infections. While the treatment of choice for streptococcal pharyngitis is penicillin, erythromycin is the drug of choice for treating A haemolyticum pharyngitis. His evaluation includes normal blood urea nitrogen, creatinine, electrolytes, thyroid function tests, urinalysis, and head computed tomography. His vitals show a temperature of 37˚C, heart rate of 120 beats/min, respiratory rate of 18 breaths/min, and a blood pressure of 154/96 mm Hg. You discuss the diagnostic evaluation for this patient’s signs and symptoms with your residents. They arise from the chromaffin cells of the adrenal medulla (pheochromocytoma) or the sympathetic ganglia (paraganglioma or extra-adrenal pheochromocytoma). Pheochromocytomas are often diagnosed in patients with classical paroxysmal symptoms of headache, sweating, flushing, diarrhea, and palpitations, a positive history of familial disease, or as an incidental adrenal mass in patients getting abdominal imaging for other reasons. Pheochromocytomas are also reported in association with multiple endocrine neoplasia type 2, von Hippel-Lindau syndrome, neurofibromatosis type 1, and paraganglioma syndromes. Patients with clinical features and family history of these syndromes are periodically screened for pheochromocytomas and are usually asymptomatic at the time of diagnosis. The patient in the vignette has hypertension, tachycardia, and sweating, which is suggestive of pheochromocytoma. His prior histories of recurrent emergency room visits are indicative of the paroxysmal nature of the symptoms. Subsequent laboratory evaluation in this patient should focus on identifying excess catecholamine secretion (plasma-fractionated metanephrines) as the underlying cause of the patient’s symptoms. The diagnostic approach to pheochromocytoma includes biochemical testing for excess catecholamine secretion and subsequent demonstration of tumor by imaging. In patients with pheochromocytomas, the excess catecholamines are converted to metanephrines and normetanephrine metabolites within the tumor by the chromaffin cells. Therefore, excess catecholamine can be measured as increased total or fractionated catecholamines (dopamine, norepinephrine, and epinephrine) or total and fractionated metanephrines (metanephrine and normetanephrine). Measurement of fractionated metanephrines in urine or plasma is considered the most sensitive biochemical test for evaluating patients suspected of having pheochromocytoma. Most laboratories measure fractionated catecholamines and metanephrines by high performance liquid chromatography or tandem mass spectroscopy to overcome the problems with false-positive or false-negative results from fluorometric analysis. Plasma fractionated metanephrines have a high sensitivity (> 95%) and low specificity (85% 89%) for diagnosing pheochromocytoma. In patients with high pretest probability of pheochromocytoma in the presence of clinical symptoms or strong family history, plasma fractionated metanephrines is the initial diagnostic test. A 24-hour urine collection for fractionated catecholamines and metanephrines is reported to have the highest sensitivity (98%) and specificity (98%) for diagnosing pheochromocytoma. Urinary fractionated catecholamines and metanephrines should be the first test in patients with low pretest probability for pheochromocytoma (incidental adrenal mass without imaging characteristics consistent with pheochromocytoma). In younger children in whom obtaining a complete 24-hour urine collection is difficult, plasma fractionated metanephrines is the preferred initial test. Total urinary metanephrines and vanillylmandelic acid on a spot sample have poor diagnostic sensitivity and specificity, compared with fractionated plasma metanephrines, and are not indicated as the next step for this patient. In symptomatic patients, abdominal and pelvic ultrasonography can be the initial imaging. Iodinated contrast media can precipitate hypertensive crisis, and it is advisable to avoid using iodinated contrast without α-adrenergic blockade in patients with suspected pheochromocytoma. Laboratory results obtained at admission and at 12, 24 and 48 hours after admission are shown in Item Q187. As hepatic injury progresses, the patient will experience hypoglycemia, cerebral edema, encephalopathy, and renal failure. Patients with liver failure will have hypoglycemia caused by failure of synthesis and release. Ammonia levels are elevated associated with increased glutamine and poor clearance. Fibrinogen levels are more often low, associated with disseminated intravascular coagulation. Transaminases are elevated in this child because of the acetaminophen toxicity and associated hepatitis. Elevated transaminases are associated with inflammation and are not a good predictor of liver failure. The parents also want to discuss recurrence risk of the achondroplasia for future pregnancies.
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Copyright © 16 the Breast Clinical Gynecologic Endocrinology and Infertility 16The Breast Growth and Development Abnormal Shapes and Sizes Pregnancy and Lactation Prolactin Secretion Prolactin Inhibiting Factor Prolactin Releasing Factor the Prolactin Receptor Amniotic Fluid Prolactin Lactation Breastfeeding by Adopting Mothers Cessation of Lactation Contraceptive Effect of Lactation Inappropriate Lactation — Galactorrheic Syndromes Differential Diagnosis of Galactorrhea the Clinical Problem of Galactorrhea Treatment of Galactorrhea the Management of Mastalgia Cancer of the Breast Scope of the Problem Risk Factors Specific Endocrine Factors Receptors and Clinical Prognosis Tamoxifen and Breast Cancer Needle Aspiration Screening Mammography Screening for Breast Cancer Chapter References the form, function, and pathology of the human female breast are major concerns of medicine and society. As mammals, we define our biologic class by the function of the breast in nourishing our young. As obstetricians, we seek to enhance or diminish function, and as gynecologists, the appearance of inappropriate lactation (galactorrhea) may signify serious disease. In this chapter, the factors involved in normal growth and development of the breast will be reviewed, including the physiology of normal lactation. A description of the numerous factors leading to inappropriate lactation will follow, and, finally, the endocrine aspects of breast cancer will be considered. Growth and Development the basic component of the breast lobule is the hollow alveolus or milk gland lined by a single layer of milk-secreting epithelial cells, derived from an ingrowth of epidermis into the underlying mesenchyme at 10–12 weeks of gestation. Each alveolus is encased in a crisscrossing mantle of contractile myoepithelial strands. The lumen of the alveolus connects to a collecting intralobular duct by means of a thin nonmuscular duct. Contractile muscle cells line the intralobular ducts that eventually reach the exterior via 15–20 collecting ducts in a radial arrangement, corresponding to the 15–20 distinct mammary lobules in the breast, each of which contains many alveoli. Growth of this milk-producing system is dependent on numerous hormonal factors that occur in two sequences, first at puberty and then in pregnancy. Although there is considerable overlapping of hormonal influences, the differences in quantities of the stimuli in each circumstance and the availability of entirely unique inciting factors (human placental lactogen and prolactin) during pregnancy permit this chronologic distinction. The strength of the hormonal stimulus to breast tissue during pregnancy is responsible for the fact that nearly half of male and female newborns have breast secretions. In most girls, the first response to the increasing levels of estrogen is an increase in size and pigmentation of the areola and the formation of a mass of breast tissue just underneath the areola. The development of estrogen receptors in the breast does not occur in the absence of prolactin. The primary effect of estrogen in subprimate mammals is to stimulate growth of the ductal portion of the gland system. Progesterone in these animals 2 influences growth of the alveolar components of the lobule. However, neither hormone alone, or in combination, is capable of yielding optimal breast growth and 3 development. Full differentiation of the gland requires insulin, cortisol, thyroxine, prolactin, and growth hormone. Of course, the ubiquitous growth factors are also involved, but the molecular mechanisms remain to be determined. Nevertheless, experimental evidence in mice indicates that progesterone is the key hormone 2 required for mammary growth and differentiation; estrogen is necessary because the synthesis of progesterone receptors requires the critical presence of estrogen. The pubertal response is a manifestation of closely synchronized central (hypothalamus-pituitary) and peripheral (ovary-breast) events. This suggests a paracrine interaction between gonadotrophs and lactotrophs, linked by estrogen, ultimately with an impact on the breast. Changes occur routinely in response to the estrogen-progesterone sequence of a normal menstrual cycle. During the normal menstrual cycle, estrogen receptors in mammary gland epithelium decrease in number during the luteal phase, whereas progesterone receptors 8 remain at a high level throughout the cycle. Studies using tissue from reduction mammoplasties or from breast tissue near a benign or malignant lesion have 6, 9, 10 demonstrated a peak in mitotic activity during the luteal phase. Using fine needle biopsy tissue, an immunocytochemical marker of proliferation was higher in the 8 luteal phase than in the proliferative phase. However, important studies indicate that 11, 12and 13 with increasing duration of exposure, progesterone imposes a limitation on breast cell proliferation. Therefore, breast and endometrium epithelial cells may be more similar than initially proposed. Final differentiation of the alveolar epithelial cell into a mature milk cell is accomplished by the gestational increase in estrogen and progesterone, combined with the presence of prolactin, but only after prior exposure to cortisol and insulin. The complete reaction depends on the availability of minimal quantities of thyroid hormone. Thus, the endocrinologically intact individual in whom estrogen, progesterone, thyroxine, cortisol, insulin, prolactin, and growth hormone are available can have appropriate breast growth and function. During the first trimester of pregnancy, growth and proliferation are maximal, changing to differentiation and secretory activity as pregnancy progresses. As the years go by, the breasts contain progressively more fat, but after menopause, this process accelerates so that soon into the postmenopausal years, the breast glandular tissue is mostly replaced by fat. Abnormal Shapes and Sizes Early differentiation of the mammary gland anlage is under fetal hormonal control. Abnormalities in adult size or shape may reflect the impact of hormones (especially the presence or absence of testosterone) during this early period of development. This prenatal hormonal influence programs the breast development that will occur in response to the increase in hormones at puberty. With one exception, hormone therapy is totally ineffective in producing a permanent change in breast shape or size. Of course in patients with primary amenorrhea due to deficient ovarian function, estrogen treatment will induce significant and gratifying breast growth. Breast size can be increased in current users of oral contraceptives, but there is no lasting effect 14 associated with past use. Accessory nipples can be found anywhere from the groin to the neck, remnants of the mammary line that extends early in embryonic life (6th week) along the ventral, lateral body wall. Pregnancy and Lactation Prolactin Secretion In most mammalian species, prolactin is a single chain polypeptide of 199 amino acids, 40% similar in structure to growth hormone and placental lactogen. All three hormones are believed to have originated from a common ancestral protein about 400 million years ago. Prolactin is encoded by a single gene on the short arm of chromosome 6, producing a molecule that in its major form is maintained in 3 loops by disulfide bonds. Simultaneous measurements of prolactin by both bioassay and immunoassay reveal discrepancies. Chemical studies have revealed structural modifications that include glycosylation, phosphorylation, and variations in binding and charge. This heterogeneity is the result of many influences at many levels: transcription, 15, 16 translation, post translational modification, and peripheral metabolism. Enzymatic cleavage of the prolactin molecule yields fragments that may be capable of biologic activity. Prolactin that has been glycosylated continues to exert activity; differences in the carbohydrate moieties can produce differences 17 in biologic activity and immunoreactivity. However, the non-glycosylated form of prolactin is the predominant form of prolactin secreted into the circulation. Big prolactin can result from the failure to remove introns; it has little biologic activity and does not cross react with antibodies to the major form of prolactin. The so-called big big variants of prolactin are due to separate molecules of prolactin binding to each other, either noncovalently or by interchain disulfide bonding. Some of the apparently larger forms of prolactin are prolactin molecules complexed to binding proteins. Nevertheless, the routine radioimmunoassay of prolactin is generally clinically reliable, especially at extremely high levels associated with prolactin-secreting pituitary tumors. The anterior pituitary cells that produce prolactin, growth hormone, and thyroid-stimulating hormone (lactotrophs, somatotrophs, and thyrotrophs) require the presence of Pit-1, a transcription factor, for development. Pit-1 also binds to the prolactin gene in multiple sites in both the promoter region and in an adjacent region, designated as a distal enhancer; Pit-1 binding is a requirement for prolactin promoter activity and gene transcription. Many hormones, neurotransmitters, and growth factors influence the prolactin gene, involved in a level of function beyond that allowed by Pit-1. Fundamental modulation of prolactin secretion is exerted by estrogen, 18, 19 producing both differentiation of lactotrophs and direct stimulation of prolactin production. An estrogen response element is adjacent to one of the Pit-1 binding sites in the distal enhancer region, and estrogen stimulation of the prolactin gene involves interaction with this Pit-1 binding site. Estrogen also influences prolactin 20 production by suppressing dopamine secretion. Surfactant synthesis in the fetal lung is influenced by prolactin, and decidual prolactin modulates 21, 22 prostaglandin-mediated uterine muscle contractility. Prolactin also contributes to the prevention of the immunologic rejection of the conceptus by suppressing the maternal immune response. The mechanisms and purpose for mammary production of prolactin remain to be determined, but prolactin in milk is believed to be derived from local synthesis. Transmission of this prolactin to the newborn may be important for immune functions. Dopamine is secreted by the basal hypothalamus into the portal system and conducted to the anterior pituitary. Dopamine binds specifically to lactotroph cells and suppresses the secretion of prolactin into the general circulation; in its absence, prolactin is secreted. Dopamine binds to a G protein-coupled receptor (Chapter 2) that exists in a long form and a short form, but only the D2 (long form) is present on lactotrophs. However, except in hypothyroidism, normal physiologic changes as well as abnormal prolactin secretion are easily explained and understood in terms of variations in the prolactin inhibiting factor, dopamine. A large collection of peptides has been reported to stimulate the release of prolactin in vitro. But it is unknown whether these peptides participate in the normal physiologic regulation of prolactin secretion. The Prolactin Receptor the prolactin receptor is encoded by a gene on chromosome 5p13–14 that is near the gene for the growth hormone receptor. The prolactin receptor belongs to a 25 receptor family that includes many cytokines and some growth factors, supporting a dual role for prolactin as a classic hormone and as a cytokine. Prolactin receptors exist in more than one form, all containing an extracellular region, a single transmembrane region, and a relatively long cytoplasmic domain. There 26 is evidence for more than one receptor, depending upon the site of action. The amino acid identity between prolactin and growth 27 hormone receptors is approximately 30%, with certain regions having up to 70% homology. A protein also exists that functions as a receptor/transporter, translocating prolactin from the blood into the cerebrospinal fluid, the amniotic fluid, and milk. Amniotic Fluid Prolactin Amniotic fluid concentrations of prolactin parallel maternal serum concentrations until the 10th week of pregnancy, rise markedly until the 20th week, and then decrease. Indeed, the source of amniotic fluid prolactin is neither the maternal pituitary nor the fetal pituitary. The failure of dopamine agonist treatment to suppress amniotic fluid prolactin levels, and studies with in vitro culture systems, indicate a primary decidual source with transfer via amnion receptors to the amniotic fluid, requiring the intactness of amnion, chorion, and adherent decidua. This decidual synthesis of 28 prolactin is initiated by progesterone, but once decidualization is established, prolactin secretion continues in the absence of both progesterone and estradiol. Various decidual factors regulate prolactin synthesis and release, including relaxin, insulin, and insulin-like growth factor-I (discussed in Chapter 4).
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Rate of amoxicillin, face and neck, and diarrhea with infection in im-ported trimethoprin Shigellosis* Bacteria blood, mucous and inflammatory monkeys can be high sulfamethoxazole cells Leptospira Animal, human urine Direct contact with urine of Phase 1: headache, muscle ache, 7-12 Days Leptospirosis Doxycycline and interrogans infected dogs, mice or rats. Animals Tick-borne, blood Fever, headache and muscle pain 5-15 days Epidemic relapsing Tetracyclines, recurrentis (louse transfusions that lasts 4-10 days and subsides. Skin lesions, swollen disease for humans, doxycycline, (formerly humans are accidental bacteria and when lymph glands, abscesses septicemia but when left sulfisoxazole, or Melioidosis* Bacteria Pseudomonas hosts contaminated soil comes in or pneumonia untreated, has 95% cotrimoxazole. Animal bite, contact with Headache, fever, malaise, 3-8 weeks Untreated, the fatality Antirabies vaccine genus Lyssavirus All mammals: wild infected saliva or tissue nervousness, dilation of pupils, rate is 100%; Post before clinical onset animals (raccoons, salivation, excessive perspiration, exposure treatment is of symptoms; post rodents, foxes, etc. Can Ranges; 14-25 fever, Denque fever, (except yellow fever Flaviviridae, rodents, etc. Variations several can live in the in (Iodoquinol, humans Cyst is resistant to drying depending on parasites. Can be months to testines for years metronidazole) and frequent urge with high or low even years without causing antibiotics to treat any Parasite volume of stool, with or without some symptoms. Primates, infected meats; ingestion accompanied with fever, sore throat, following human race. Severe intestines 2 and migrates to the alternative infection can cause severe tissue wks; average lungs. Then it travels Strongyloidiasis Nematode damage, systemic damage of various 4-21 days up to the mouth and is tissues in the body and potential swallowed into the death intestinal tract Trichinella spiralis Generally pigs or cattle Eating undercooked flesh Nausea, vomiting, diarrhea, fever, Abdominal Over 100 species of Thiabendazole of animals infected with the neurological disorders, possible symptoms: 1 animals may be a host (Mintezol), larvae cardiac involvement 2 days. Describe the composition of the thin and Chapter Objectives thick flaments, and label the parts of the sarcomere. Compare and contrast skeletal, smooth, and potential in a neuron and ending with the cardiac muscle. Using a drawing, identify and describe the Muscle Energy 243 special features of a skeletal muscle cell, 8. Explain the benefts and disadvantages of different energy sources (creatine Skeletal Muscle Contraction 233 phosphate, glycolysis, and mitochondrial respiration); compare anaerobic and 4. Compare the structure and function of fast Smooth Muscle 252 glycolytic fbers and slow oxidative fbers. Describe the structural and functional differences between skeletal and smooth muscle. List the steps involved in smooth muscle contraction, including the different types of 11. List different causes of muscle fatigue, referring to stimuli that can induce contraction. Explain how a stronger contraction results from antagonist for different body movements at modifying fber length and/or recruiting additional each joint. Provide examples of isometric, concentric isotonic, and eccentric isotonic contractions. For each body region (head and neck, upper limb, torso, and lower limb), label the major skeletal 14. Discuss the effects of resistance training and muscles on a diagram and indicate their insertion endurance exercise on muscles. With the aid of an interpreter she explained that Hammid was becoming increasingly upset by his inability to keep up with the other boys on his soccer team because of the painful muscle cramps that occurred in his legs with strenuous exercise. He had also been complaining that everyday activities requiring signifcant muscle effort, such as climbing stairs, caused him pain. She explained further, “He’s had these pains all of his life, but not so bad as now. The doctor in Herat told me he probably had liver disease because his urine is red or brown sometimes. Physical Examination and Other Data: Hammid was of normal height and weight for his age, and his vital signs were unremarkable. Mild proximal muscle weakness was present in all extremities and he had diffculty walking on his heels or toes more than 8 or 10 steps because cramps developed in his legs. Laboratory evaluation revealed abnormally high levels of creatine kinase (a muscle enzyme) in the blood. A presumptive diagnosis of McArdle syndrome (type V glycogen storage disease, due to a genetic defciency of muscle glycogen phosphorylase, another muscle enzyme) was made and an appointment with a specialist in muscular diseases was arranged. Study of blood lactic acid in a forearm vein was abnormal: the normal increase of lactic acid did not occur during the test. A muscle biopsy was performed; it showed increased amounts of glycogen in the muscle fbers and a severe decrease in muscle content of glycogen phosphorylase. Specialists at the clinic explained to Hammid’s parents that his genetic defect was inherited and that no treatment was currently available. The parents were also reassured that although Hammid would have diffculty with strenuous exercise all of his life, he would be unlikely to suffer other problems. Just as the word bone can refer either to an organ or to a tissue, so can the word muscle; that is, the biceps muscle (a muscle in the arm) is an organ primarily composed of muscle tissue. We derive the word muscle from the Latin mus (for “mouse”), a reference to the rippling motion of muscles, which was thought to resemble the movement of mice beneath the skin. In turn, mus was derived from earlier Greek, where mys (meaning both “mouse” and “muscle”) gives us the prefxes myo and mys-, which refer to muscle. Words referring to muscle tissue may also have the prefx sarco-, which is derived from Greek sarx (for “fesh”). Every movement of our body requires Overview of Muscle skeletal muscle action, from large movements like walking, to smaller movements like breathing or fol Muscle comprises about 40% to 50% of body weight. This ability makes ately obvious, an uninterrupted sequence of tiny, muscle cells responsible for our movements, both visible silent contractions of postural skeletal muscle and invisible: walking, talking, bowel movements, urina keeps us erect when we are standing or sitting and tion, breathing, heartbeats, the dilation and constriction keeps our heads from slumping on our shoulders. And when we A related activity is the stabilization of joints: In are still—sitting or standing—muscle cells keep us erect. The core function of muscle is to convert chemical ● Adjust the volume of hollow structures. Muscle acts to: to unconscious autonomic commands, muscles in the 228 Chapter 7 Muscles 229 walls of hollow structures relax to increase volume Because nearly half of body mass is skeletal muscle, and contract to decrease it. For example: most body heat comes from skeletal muscle contrac ● Muscle in the bladder wall relaxes to allow the tions. And just as waste heat from an automobile bladder to expand to accommodate more urine or engine is used to warm the car’s interior on a frosty contracts to expel it. For vessels and allow more blood fow or contracts to example, when we shiver with cold, the shivers are reduce blood fow. Based on his symptoms, which of the muscle traction power male ejaculation and female orgasm. When it does so, about three-fourths of There are three types of muscle:skeletal, cardiac, and smooth the nutrient energy consumed escapes as heat. Yes No No 230 Human Form, Human Function: Essentials of Anatomy & Physiology is their ability to contract. Their most important differ What’s more, skeletal muscle is voluntary muscle; ences relate to four qualities: that is, we can contract and relax it at will. Skeletal mus cles can also function outside of our conscious control; ● Location for example, the diaphragm contracts and relaxes to ● Microscopic appearance keep us breathing while we sleep, and our neck and ● Whether or not they are subject to conscious control back muscles maintain our seated posture while our ● the type of contraction they generate attention is devoted to our work. Skeletal muscle fbers contract quickly and forcefully Skeletal Muscle Moves the Skeleton and then relax to become ready to contract again. They do not maintain contraction for an extended period of As the name suggests, most skeletal muscle is attached time, and they fatigue after repeated contraction. Microscopically, skeletal muscle is striated muscle; Cardiac Muscle Propels Blood that is, it has cross-stripes (striations) on microscopic through the Body examination, an appearance that is intimately related to its function. Mature muscle cells are especially long and As its name suggests, cardiac muscle tissue is found thin—up to a foot long—and are typically called muscle only in the heart, and accounts for most of its mass (see fbers. We perceive cardiac muscle contractions as our muscle fber is a single mature skeletal muscle cell. Cardiac muscle cells are much shorter than skeletal muscle fbers, but they are branched and inter connected. The end of one branch is connected inti mately to another, producing long cardiac muscle fbers. The result is that cardiac muscle is a network that in many ways behaves like a single huge muscle cell. Of course, cardiac muscle is involuntary muscle: we cannot control its contractions by force of will. That said, some things we deliberately do—such as engaging in meditation—can slow our heartbeat, whereas other things—such as vigorous exercise—can increase it. Like skeletal muscle fbers, cardiac muscle cells con tract quickly and then relax. We will return to cardiac mus Skeletal muscle cle in Chapter 11 in our discussion of the heart. Smooth Muscle Powers Cardiac muscle the Actions of Viscera Smooth muscle tissue is found in thick layers in the walls of hollow organs such as blood vessels, the urinary Smooth muscles bladder, the uterus, and the intestines (Fig. The (stomach, intestines) intestines and other abdominal organs are frequently described as the viscera; therefore, smooth muscle is also called visceral muscle. Cardiac muscle (shown in ume of hollow structures and helps move substances— dark red) keeps blood moving, smooth muscle (orange) from food to blood—throughout the body. Which type of muscle Smooth muscle is named for its microscopic appear makes up the stomach wall? As dis cle is discussed in Chapter 11, and that of smooth cussed further on in this chapter, its lack of striations is muscle is discussed later in this chapter. Smooth muscle is involuntary: we do not command Myoblasts Fuse to Form the wall of our stomach to relax to accommodate a large Muscle Fibers meal. It just happens as the stomach responds automat ically to the mechanical stimulation of food bulk, which During embryonic development, stem cells produce is but one of many stimuli that govern smooth muscle immature muscle cells called myoblasts (blast “pre function. Several myoblasts fuse together to produce can maintain the contraction over a long period. Gener each skeletal muscle fber, so each muscle fber contains ally, smooth muscle fbers do not fatigue. Some muscle stem cells persist into adulthood, hidden between the muscle cell membrane Case Note and the surrounding connective tissue. Which type of muscle is affected by Hammid’s location at the muscle fber’s periphery. However, satellite cell activity is not suffcient to repair major skeletal muscle injuries. A fnal important characteristic of all three types of muscle tissue is its extensibility—its ability to stretch without tear ing. The muscle that normally brings the called satellite cells; they produce myoblasts, which jaws together must relax and lengthen in order to permit fuse to form skeletal muscle fbers. If this muscle were not extensible, your simple action would cause the muscle to tear.