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Associate Professor, University of California, San Diego School of Medicine

Electrolyte abnormalities occur through a loss of electrolytes in the urine and transmembrane alterations resulting from acidosis menstruation 4 days early purchase premarin 0.625 mg fast delivery. As hydrogen ions accumulate as a result of ketoacidosis women's health clinic rock island buy 0.625 mg premarin amex, intracellular potassium is exchanged for hydrogen ions menstruation or pregnancy spotting buy genuine premarin line. Serum concentrations of potassium increase initially with acidosis then decrease as serum potassium is cleared by the kidney menopause musical cheap 0.625mg premarin visa. Depending on the duration of ketoacidosis, serum potassium concentrations at diagnosis may be increased, normal, or decreased, but intracellular potassium concentrations are depleted. A decreased serum potassium concentration is an ominous sign of total body potassium depletion. Phosphate depletion also can occur as a result of the increased renal phosphate excretion required for elimination of excess hydrogen ions. Sodium depletion is also common ketoacidosis, resulting from renal losses of sodium caused by osmotic diuresis and from gastrointestinal losses from vomiting. If a recent weight measurement is available, the precise extent of dehydration can be calculated. The remaining fluid deficit after the initial bolus should be added to maintenance fluid requirements, and the total should be replaced slowly over 36 to 48 hours. Ongoing losses resulting from osmotic diuresis usually do not need to be replaced unless urine output is large or signs of poor perfusion are present. Osmotic diuresis is usually minimal when the serum glucose concentration decreases to less than 300 mg/ dL. Serum glucose concentrations should decrease at a rate no faster than 100 mg/dL/hour. Insulin therapy decreases the production of free fatty acids and protein catabolism and enhances glucose usage in target tissues. Hence minute-to-minute urine ketone concentrations are not a required index of the adequacy of therapy. Regardless of the serum potassium concentration at presentation, total body potassium depletion is likely. Serum potassium concentrations can decrease rapidly as insulin and then glucose therapy improves acidosis, and potassium is exchanged for intracellular hydrogen ions. Potassium replacement should be given as 50% potassium chloride and 50% potassium phosphate at a concentration of 20 to 40 mEq/L. This combination provides phosphate for replacement of deficits but avoids excess phosphate administration, which may precipitate hypocalcemia. This regimen of multiple daily injections provides the most flexibility but requires the patient to administer many injections per day and to count carbohydrates in food. Insulin pumps provide fast-acting insulin in small basal amounts continuously every hour and will provide bolus insulin when instructed. Insulin pumps may be used by all age groups who are highly motivated to achieve tight control. Serum glucose concentrations should be assessed before each meal, at bedtime, and periodically at 2 to 3 am to provide information for adjustment of the regimen. Patients and their families should begin learning the principles of diabetes care as soon as possible. Demonstration of the ability to administer insulin injections and test glucose concentrations using a glucose meter is necessary before discharge, as is knowledge of hypoglycemia management. Nutrition services must be part of the care delivered to the families from diagnosis. Serum glucose measurement should be repeated every hour during therapy; electrolyte concentrations should be repeated every 2 to 3 hours. Calcium, phosphate, and magnesium concentrations should be measured every 4 to 6 hours during therapy. Any complaints of headache or deterioration of mental status should prompt rapid evaluation for possible cerebral edema. Indicative symptoms include a decreased sensorium, sudden severe headache, vomiting, change in vital signs (bradycardia, hypertension, apnea), a dilated pupil, ophthalmoplegia, or seizure. The pathogenesis of cerebral edema likely involves osmolar shift resulting in fluid accumulation in the intracellular compartment and cell swelling.

Deficiency of 21-hydroxylase is the most common form (95%) and serves as a paradigm for these disorders womens health kalispell purchase premarin in india. The gene for 21-hydroxylase lies on the short arm of chromosome 6; the genotype may be determined in a proband pregnancy jeans order on line premarin, permitting prenatal diagnosis in a subsequent pregnancy women's health clinic lawrence ks order premarin with mastercard. The primary clinical manifestation is the virilization of the external genitalia of the affected female fetus; the development of the uterus womens health reno nv buy premarin 0.625mg with mastercard, ovaries, and fallopian tubes remains unaffected by the androgens. The degree of virilization varies, ranging from mild clitoromegaly to complete fusion of labioscrotal folds, with severe clitoromegaly simulating a phallus (see Chapter 177). A male infant with this defect appears normal at birth, although penile enlargement may be apparent thereafter. The deficiency in aldosterone, found in about 75% of patients, causes salt wasting with shock and dehydration until the diagnosis is established and appropriate treatment is given. The treatment of 21-hydroxylase deficiency requires hydrocortisone and fludrocortisone in the case of the salt-losing form. Overtreatment will cause growth stunting and weight gain (cushingoid features), whereas undertreatment will cause excessive height gain, skeletal advance, and early appearance puberty, ultimately jeopardizing adult height potential. Affected subjects have milder manifestations without ambiguous genitalia, but they may have acne, hirsutism, and in girls irregular menstrual cycles or amenorrhea. The goals of treatment are to achieve normal linear growth and bone age advancement. Long-term therapy consists of providing glucocorticoids at a dose of approximately 10 to 15 mg/m2/24 hours in three divided doses of oral hydrocortisone or its equivalent. Mineralocorticoid therapy for salt losers consists of fludrocortisone at a dose of 0. In addition, the assessment of linear growth and skeletal age, by bone age determination, is required as a reflection of appropriate therapy. To avoid adrenal insufficiency, threefold higher doses of glucocorticoids are given during stressful states such as febrile illnesses and surgery. Intramuscular hydrocortisone is used in severe emergencies or with illnesses involving emesis. Mineralocorticoid therapy is monitored with serum sodium, potassium, and plasma renin activity levels. Chapter 178 androgen production can reduce or eliminate the ambiguity of the external genitalia in affected female fetuses, if begun at approximately 7 weeks of gestation; this remains controversial. Table 178-2 summarizes the clinical and biochemical features of adrenal insufficiency in infancy. The most frequent cause is exogenous administration in the context of numerous conditions requiring long-term pharmacologic doses of glucocorticoids. Diagnostic tests include 24-hour urinary cortisol excretion, low-dose dexamethasone suppression test, highdose dexamethasone suppression test (helps distinguish Cushing syndrome from Cushing disease), and late evening salivary cortisol sampling. Parenteral glucocorticoid therapy is necessary during and immediately after surgical treatment to avoid acute adrenal insufficiency. It is a form of primary adrenal insufficiency with absence of glucocorticoid and mineralocorticoid. Clinical manifestations are hyperpigmentation, salt craving, postural hypotension, fasting hypoglycemia, anorexia, weakness, and episodes of shock during severe illness. Other rare causes of adrenal insufficiency include adrenal leukodystrophy and conditions that affect the hypothalamus-pituitary whether acquired, such as in craniopharyngioma, or iatrogenic, such as in irradiation for treatment of malignancy. Replacement treatment with 10 to 15 mg/m2/24 hours of hydrocortisone is indicated, with supplementation during stress at three times the maintenance dosage or the use of intramuscular hydrocortisone. Mineralocorticoid replacement with fludrocortisone is monitored by plasma renin activity and serum sodium and potassium determinations. The process and interpretation of the neurologic examination varies with age; the newborn is unique with many transient and primitive reflex patterns, whereas the examination of adolescents and adults is similar.

Rapport usually can be established quickly if the parents sense that the clinician respects them and is genuinely interested in listening to their concerns pregnancy nutrition app discount premarin 0.625 mg with amex. The clinician develops rapport with the child by engaging the child in developmentally appropriate conversation or play breast cancer apparel cheap premarin amex, perhaps providing toys while interviewing the parents pregnancy 25 weeks belly purchase premarin 0.625 mg with mastercard, and being sensitive to the fears the child may have womens health running order premarin with american express. Similar to their parents, children feel more comfortable if they are greeted by name 20 Section 2 u Growth and Development and involved in pleasant interactions before they are asked sensitive questions or threatened with examinations. With adolescents emphasis should be placed on building a physician-patient relationship that is distinct from the relationship with the parents. The parents should not be excluded; however the adolescent should have the opportunity to express concerns to and ask questions of the physician in confidence. Two intertwined issues must be taken into consideration-consent and confidentiality. Although laws vary from state to state, in general, adolescents who are able to give informed consent. Physicians should become familiar with the governing law in the state where they practice (see Providing confidentiality is crucial, allowing for optimal care (especially for obtaining a history of risk behaviors). When assessing development and behavior, confidentiality can be achieved by meeting with the adolescent alone for at least part of each visit. However parents must be informed when the clinician has significant and immediate concerns about the health and safety of the child. Often the clinician can convince the adolescent to inform the parents directly about a problem or can reach an agreement with the adolescent about how the parents will be informed by the physician (see Chapter 67). Bright Futures standardizes each of the health maintenance visits and provides resources for working with the children and families of different ages (see Elements of each visit include evaluation and management of parental concerns; inquiry about any interval illness since the last physical, growth, development, and nutrition; anticipatory guidance (including safety information and counseling); physical examination; screening tests; and immunizations (Table 9-1). Histories about developmental and behavioral problems are often vague and confusing; to reconcile apparent contradictions, the interviewer frequently must request clarification, more detail, or mere repetition. By summarizing an understanding of the information at frequent intervals and by recapitulating at the close of the visit, the interviewer and patient and family can ensure that they understand each other. The observations of teachers, relatives, and other regular caregivers may be crucial in sorting out this possibility. The parent also may have a distorted image of the child, rooted in parental psychopathology. A sensitive, supportive, and noncritical approach to the parent is crucial to appropriate intervention. More information about referral and intervention for behavioral and developmental issues is covered in Chapter 10. Health maintenance and immunizations now are covered without co-pays for insured patients as part of the Patient Protection and Affordable Care Act. Children born to families with dyslipidemias or early heart disease should also be screened for lipid disorders. When an infant or child begins care after the newborn period, the pediatrician should perform any missing screening tests and immunizations. Parental concerns about vision should be sought until the child is 3 years of age and about hearing until the child is 4 years of age. For toddlers and older children who cannot cooperate with formal audiologic testing with headphones, behavioral audiology may be used. Sounds of a specific frequency or intensity are provided in a standard environment within a soundproof room, and responses are assessed by a trained audiologist. Vision may be assessed by referral to a pediatric ophthalmologist and by visual evoked responses. Newborn Screening Metabolic Screening Every state in the United States mandates newborn metabolic screening. Each state determines its own priorities and procedures, but the following diseases are usually included in metabolic screening: phenylketonuria, galactosemia, congenital hypothyroidism, maple sugar urine disease, and organic aciduria (see Section 10). Many states now screen for cystic fibrosis, testing for immunoreactive trypsinogen. Hemoglobin Electrophoresis Children with hemoglobinopathies are at higher risk for infection and complications from anemia, which early detection may prevent or ameliorate.

Postexercise increases in plasma levels of ketones have been observed in racing sled dogs (Hammel et al womens health practice order premarin. Plasma 3-hydroxybutyrate concentrations increased two- to three-fold 5 to 60 minutes postexercise compared to preexercise levels womens health facts buy 0.625mg premarin visa. Primary ketosis in the high-producing dairy cow: clinical and subclinical disorders pregnancy 4 weeks ultrasound discount 0.625 mg premarin with amex, treatment menstrual irregularities in perimenopause purchase premarin 0.625mg fast delivery, prevention, and outlook. Influence of sodium -hydroxybutyrate on glucose and free fatty acid metabolism in normal dogs. Metabolic changes in liver associated with spontaneous ketosis and starvation in cows. Plasma cholesterol and lipoprotein concentrations in the dog: the effects of age, breed, gender and endocrine disease. Normal canine lipid profiles and effects of experimentally induced pancreatitis and hepatic necrosis on lipids. Lipoprotein cholesterol distribution in experimentally induced canine cholestasis. Production and utilization of metabolites by the alimentary tract as measured in portal and hepatic blood. The metabolism of glucose, acetate, lipids and amino acids in lactating dairy cows. An effect of ketones on the concentrations of glucose and References 109 of free fatty acids in man independent of the release of insulin. Plasma cholesterol esterification and plasma lipoproteins in bile-duct-ligated dogs. Effects of various synthetic glucocorticoids on milk production and blood glucose and ketone body concentrations in normal and ketotic cows. Regulation of carnitine palmitoyltransferase activity by malonyl-CoA in mitochondria from sheep liver, a tissue with a low capacity for fatty acid synthesis. On alimentary acetonuria and ketonuria in dairy cattle induced by feeding grass silage of the butyric acid type. Utilization of long chain fatty acids by rat liver: studies of the role of fatty acid binding protein. Acute pancreatitis with hyperlipemia: evidence for a persistent defect in lipid metabolism. Chemical interference by drugs and other substances with clinical laboratory test procedures. Comparison of mitochondrial acyl coenzyme A synthetase activity and substrate specificity in different tissues. The effects of palmitate on intracellular potentials recorded from Langendorff-perfused guinea-pig hearts in normoxia and hypoxia, and during perfusion at reduced flow rate. False-positive results for ketone with the drug mesna and other free-sulfhydryl compounds. Glucagon, insulin, growth hormone, and some blood metabolites during energy restriction ketonemia of lactating cows. Enzymatic microdetermination of free fatty acids in plasma of animals using paraoxon to prevent lipolysis. Enzymic and chemical-extraction determinations of free fatty acids in serum compared. Hepatic ketogenesis in newborn pigs is limited by low mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase activity. Severe hypertriglyceridaemia in clinically ill horses: diagnosis, treatment and outcome. Clinical application of parenteral nutrition in the treatment of five ponies and one donkey with hyperlipaemia. Alterations in plasma corticosteroids, insulin and selected metabolites in horses used in endurance rides.

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