Daniel J. Wallace, MD

• Clinical Professor of Medicine, Cedars-Sinai Medical
• Center, David Geffen School of Medicine at University
• of California Los Angeles, Los Angeles, CA, USA

They also have difficulty in spelling because of underlying problem with word decoding gastritis symptoms itching discount gasex 100 caps online. The difficulty in reading impairs their ability to cope up with the academic syllabus and is often associated with low self-confidence and feeling of frustra tion gastritis zimt order gasex online now, which increases the risk of developing psychological and emotional problems diet gastritis kronik 100caps gasex otc. Diagnosis of dyslexia is clinical gastritis disease definition buy gasex 100caps otc, based on presence of unexpected difficulties in reading at the level of phono logic processing of words gastritis diet ������ purchase generic gasex line. Standardized tests are used to test speed gastritis dietz cheap gasex 100caps with amex, accuracy and comprehension in reading and spelling ability, in relation to the age and school grade. Affected children are best taught in small groups by teachers trained in the principle of phonics. Usually these programs improve the reading accuracy significantly and fluency to a lesser extent. For older children, the management stresses more on accommodation rather than remediation. There is difficulty in pronouncing the initial consonants caused by spasm of lingual and palatal muscles. Parents of a young child with primary stuttering should be reassured that stuttering between the age of 2-5 yr usually resolves on its own. Making the child conscious of his stutter or pressurizing him to repeat the word without stuttering will further increase the stress and the stutter. Children who continue to have significant stuttering require referral to a speech therapist. In older children with late onset of stuttering, the help of a child psychologist should be sought. Intelligence is variable, although most children fall in the functionally retarded category by conventional psychological testing. Testing for associated neurological disorders such as tuberous sclerosis and fragile X is recommended. Older children and adolescents with relatively higher intelligence but poor social skills and psychiatric symptoms. Factors associated with better prognosis are early diagnosis, intensive behavioral therapy, higher intelligence level and presence of functional speech. Children with better prognostic factors may grow up to be self-sufficient and employed, though socially isolated. On the other hand, those with poor prognosis remain dependent on family or require placement in facilities outside home. Data from developed countries suggest that 1 in 150 children is affected by such disorders. To meet full criteria for diagnosis, a child must demonstrate the following symptoms: (i) qualitative impairment in social interaction as manifested by two of the following: impairment in the use of multiple nonverbal behaviors. In Munchausen by proxy, the abusing caregiver gains attention from the relation ships formed with health care providers, or her own family as a result of the problems created. Apnea, seizures (which may be induced by suffocating the child or injecting insulin), fever, diarrhea and skin conditions are the common symptoms. Confirmation of diagnosis needs careful history and reviewing of past and current hospital records. Once the diagnosis is made, the offending caregiver should be confronted, separated from the child and provided psychotherapy. The overriding feature is the repetitive and persistent pattern of behaviors that violate societal norms and the rights of other people, for a period of at least one year. The diagnosis of conduct disorder is made if three or more of the above behaviors are present, with at least one having taken place in the previous six months. Various child behavior management techniques, such as positive reinforcement to increase desirable behavior, and extinction and time out to decrease problem behavior, are taught to the parents. The children are taught anger coping, peer coping and problem-solving skills, so that they are able to deal better with problematic interpersonal situations. Oppositional Defiant Disorder Oppositional defiant disorder is a repetitive and persistent pattern of opposition, defiant, disobedient and disruptive behaviors towards authority figures persisting for at least 6 months. Although the disorder does not include the more aggressive aspects of conduct disorder, many children go on to be later diagnosed with conduct disorders. The management should focus on alleviating known risk factors or stresses that might be contributing to the development of oppositional behavior. Juvenile Delinquency Children who show oppositional defiant behavior or conduct disorder and come in to conflict with the juvenile justice system because of such behavior are called juvenile delinquents. The term refers to a person under 18 yr who is brought to the attention of the juvenile justice system for committing a criminal act or displaying a variety of other behaviors not allowed under the law, such as, truancy, use of alcohol or illicit drugs. Family and parenting interventions have been shown to reduce the rate of re-incarceration and criminal behaviour by juvenile delinquents. In some cases, placement in foster care is recommended with similar interventions being administered by the foster family. Godbole, Vijayalakshmi Bhatia Adolescence is a stage of transition from childhood to adulthood. During this stage of life, a youth undergoes rapid changes in body structure, mediated by the sex hormones. The appearance of sexual characters is coupled with changes in cognition and psychology. Whereas adolescence refers to this entire process, puberty refers to the physical aspect. The age group 10-19 yr is considered as the period of adolescence, and puberty marks the early half of adolescence. Though it is a continuous process, for convenience sake, adolescence is generally divided in to three phases: early (10-13 yr), mid (14-16 yr) and late (1719 yr) puberty. Mild degree of breast enlargement is normally seen in more than half of boys in early puberty which subsides spontaneously over several months. Physical Growth and Nutritional Requirements During puberty, boys gain about 20-30 cm and girls about 16-28 cm. Peak growth velocity in girls occurs before attainment of menarche (stage 3) in girls whereas boys have their peak growth velocity during later stages of puberty (stages 4-5). The growth spurt affects the distal skeleton first, hence enlargement of limb and extremities is followed by increase in trunk size. Gonadal sex steroids bring about secondary sexual characters (breast develop ment, increase in penile and testicular size and menarche), whereas adrenal androgens cause development of sexual hair, acne and underarm odor. The details of hormonal mechanisms of onset and progression of puberty are dealt with in Chapter 17. Onset and Sequence of Puberty Puberty in girls starts with breast development (thelarche) any time between 8 and 13 yr. This is followed by appearance of pubic hair (pubarche) and subsequently menstruation (menarche), occurring at an average of 12. However, many experts believe that the normal age of menarche is advancing to as early as 9 yr in many populations. The breast buds may be tender and there may be asymmetry in the breast size during early phases of puberty. In boys, the earliest change is increase in testicular size (testicular volume reaching 4 ml or length 2. Estrogen and androgen enhance calcium accretion by bone but favor early fusion of epiphyses. Increase in body structure is paralleled by increase in blood volume and muscle mass. There is lack of sun-exposure due to our modest tradition of clothing coupled with dark skin pigment. The resulting low bone mineral density is more pronounced in underprivileged girls as they have low protein intake in addition to calcium and vitamin D deficiency. Vitamin A deficiency is also an important issue in economically deprived adolescents. Undernutrition often delays the onset of puberty and sexual maturation, and results in stunting, poor bone mass accrual and reduced work capacity. Anorexia nervosa and bulimia are being increasingly reported among urban Indian youth. Teens are impulsive and have limited ability to perceive future implications of their current behavior. Curiosity about sexual anatomy and comparison with peers is common during this stage. The youth starts to think beyond self and there is beginning of abstract reasoning. The youth becomes career oriented and starts short and longterm planning for his or her goals in life. Knowledge about contraception is improving among adolescents and most of them are aware of at least some method of contraception. Adjustment disorder, anxiety disorders, depression, suicide, delinquent behavior, poor body image and low self-esteem are the psychological problems faced by adolescents. Suicide rates are increasing in adolescents, with higher number of completed suicide in boys and attempted suicides in girls. Adolescents are at higher risk of committing suicide because of their cognitive immaturity and increased impulsivity. Many urban adolescents do not get enough sleep due to various reasons like increasing academic activity, parents working in shifts or watching television late in to the night. Poor sleep habits and inadequate sleep are likely to reflect in school performance and cause daytime drowsiness, aggressive behavior, conduct disorders, anxiety, restless leg syndrome and depression. Various biological (immature and incompletely estrogenized mucosa) and psychosocial factors (lack of preparedness, lack of familiarity with barrier contraceptives) make an adolescent susceptible to these infections. There is increase in nutritional requirements during this period of rapid growth, micronutrients being as important as energy and protein (see Chapter 6). Vaginal discharge is common in adolescent girls and may signify physiological leucorrhea of puberty or endogenous or sexually transmitted infections. Candidal infections become common with starting of menstruation and often have a cyclic nature. Obesity is the other end on the spectrum of malnutrition and is epidemic in the urban settings. Obesity has strong association with asthma, sleep disorders, reflux disease, Blount disease, slipped femoral epiphysis, gallstones, fatty liver and numerous metabolic derange ments like type 2 diabetes, dyslipidemia, hypertension and polycystic ovary disease. There is a close relationship between obesity, hypertension and type 2 diabetes mellitus. Sedentary lifestyle, increased consumption of calorie dense food and decreased outdoor activity contribute to these disorders. It is common to have anovulatory and irregular menstrual cycles during first two years after menarche. The condition has association with other metabolic derangements like obesity, insulin resistance and type 2 diabetes. Road traffic accidents, burns and poisoning are leading causes of trau matic mortality and disability in Indian youth. Motor vehicle and industrial accidents are common in boys whereas burns are commoner in girls. Many adolescents migrate from rural to urban settings for labour or educational opportunities. Traffic king of youth is a serious problem in India and happens for industrial or domestic labour, forced marriages and prostitution. Unmarried adolescents are likely to resort to unsafe methods of abortions, which increase the risk of compli cations like septicemia and also mortality. As compared to adult pregnancy, they are also at a higher risk for pre eclampsia, preterm labor and postpartum hemorrhage. Prolonged and obstructed labor is common in adolescent pregnancies and young girls are two to four times more likely to die during childbirth as compared to adult pregnant females. Environmental and Social Challenges from rapid changes in their body structures, various other factors like peer acceptance, discrimination, academic burden, parental expectations, changing social environ ments cause stress among youth. Switching from verna cular to English medium schools, long hours of school and tuitions are additional stress factors that are unaddressed. While most adolescents have adequate coping skills, some may have serious adjustment problems resulting in various psychological and somatic effects. Young people are often treated as second class citizens, under the control of adults and often not involved in any decision making. Adolescent girls are often asked to limit their outdoor or extracurricular activities and are involved in any decision making. Adolescent girls are often confined to their houses and expected to do the household work. There is ongoing research in to the role of electromagnetic exposure from communication devices in disorders like childhood leukemia, brain tumors and immune dysregulation. With reduction in poverty and increased avail ability of electronic media, adolescents are exposed to information from all across the world. This exposure is often unsupervised because of working parents and increasing use of personal electronic gadgets. Due to inability to separate fact from fantasy, adolescents succumb to the glamorous portrayal of tobacco or alcohol consumption, unrealistic expectations, physical aggres sion, destructive behavior and unprotected sex. In urban areas, spending much of their spare time indoors on social networking sites, teenagers are actually deprived of sunlight and physical activity and are socially isolated. Pressure for conforming to norms drives many of their actions and decisions, including risk taking behavior and initiation of substance abuse. Studies have shown that children belonging to poorer families had higher chances of having depression, antisocial behavior and engaging in drugs or sexual activity at earlier ages.

L-Ascorbic Acid (Vitamin C (Ascorbic Acid)). Gasex.

• Preventing type 2 diabetes.
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• Improving physical performance and strength in the elderly.
• Reducing skin problems in people being treated for cancer with radiation.
• Treating the common cold. But it is not effective for preventing the common cold.
• Treatment and prevention of vitamin C deficiency, including a condition called "scurvy."
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At the end of puberty gastritis y embarazo buy gasex us, linear growth is nearly complete as a result of the effects of gonadal steroids on skeletal maturation and epiphyseal fusion gastritis diet 0 cd purchase generic gasex on line. The first evidence of puberty in the majority of boys is enlargement of the testes to a volume greater than 4 mL or a length greater than 2 chronic gastritis stomach gasex 100 caps sale. It is not until midpuberty gastritis diet list of foods to avoid buy generic gasex from india, when testosterone levels are rapidly rising gastritis diet cabbage purchase gasex with visa, that boys experience voice change gastritis diet �������� order gasex on line amex, axillary hair, facial hair, and the peak growth spurt. The initial pubertal event is typically the appearance of breast buds, although a small percentage of girls will develop pubic hair first. Initial breast development often occurs asymmetrically and should not be of concern. Breast development is primarily under the control of estrogens secreted by the ovaries, whereas growth of pubic hair and axillary hair results mainly from adrenal androgens. Unlike in boys, the pubertal growth spurt in girls occurs at the onset of puberty. Menarche usually occurs 18 to 24 months after the onset of breast development (mean age: 12. Consequently, age of menarche is not necessarily a good predictor of final adult height. Precocious puberty is defined as pubertal development occurring below the limits of age set for normal onset of puberty. For boys, precocious puberty is development occurring before 9 years in white and Hispanic boys and 8 years in black boys. Girls showing signs of puberty between 6 and 8 years often have a benign, slowly progressing form that requires no intervention. Girls who are short and start puberty between 6 and 8 years may also benefit from evaluation. In children who present with early pubertal signs, precocious puberty must be distinguished from normal variants of puberty, such as benign premature thelarche and benign premature adrenarche. Benign premature adrenarche, which occurs in both sexes, is defined as the early development of pubic hair with or without axillary hair, body odor, and acne. There are no signs of gonadarche in benign premature adrenarche; girls have no breast development, and boys have no testicular enlargement. Several characteristics of benign premature thelarche distinguish it from the breast development that occurs in precocious puberty. First of all, benign premature thelarche is most common in girls who are either less than 2 years old or between 6 and 8 years of age. Girls with benign premature thelarche may have a history of slowly progressing breast development or waxing and waning of breast size. The natural course of benign premature thelarche is for the breast tissue to regress or fail to progress. Because of the benign nature of this condition, treatment is not necessary except for reassurance and follow-up. Follow-up is critical because premature thelarche occasionally is the first sign of what later becomes apparent as central precocious puberty. Measurement of breast tissue diameter during the clinic visit can be helpful for comparison at a later visit. As in premature thelarche, growth rate and bone age are typically not accelerated. The natural course of benign premature adrenarche is a slow progression of the signs of adrenarche with no effect on the timing of true puberty. Because pubic hair development may be the first sign of puberty, follow-up is necessary to evaluate for evidence of gonadarche. Precocious puberty, regardless of the cause, is associated with accelerated linear growth and skeletal maturation secondary to elevated sex steroid levels. However, skeletal maturation may become more advanced than stature, thus leading to premature fusion of the epiphyseal growth plates and a compromised final adult height. In addition to the physical consequences of early puberty, social and psychological aspects may need to be considered. The disparity in overall prevalence of precocity is explained by the large numbers of girls with central idiopathic precocity, a condition that is less common in boys. In both boys and girls, a complete history should be taken, with careful consideration of any exposure to exogenous steroids or estrogen receptor agonists. Height measurements should be plotted on a growth chart to determine growth pattern and growth velocity. One of the early steps in evaluating a child with early pubertal development should be to obtain a radiograph of the left hand and wrist to determine skeletal maturity (bone age). Sex steroid levels should be measured, especially in boys, because testosterone levels higher than the prepubertal range (. For girls, estradiol measurements are less reliable indicators of puberty, because most commercial assays are not sufficiently specific or sensitive to demonstrate an increase during early puberty. Consequently, the sequence of hormonal and physical events in central precocious puberty is identical to the progression of normal puberty. Although the possible causes of peripheral precocious puberty are more numerous (Box 43-1), central precocity accounts for most cases. If random gonadotropins are measured, a third-generation assay is recommended because it has better discrimination between prepubertal and pubertal levels. Projected final adult height often increases because of a slowing of skeletal maturation. After discontinuation of therapy, pubertal progression resumes, and normal rates of fertility are expected. Girls with ovarian cysts, ovarian tumors, or McCune-Albright syndrome generally have signs of estrogen excess such as breast development and possibly vaginal bleeding. In these girls, a pelvic ultrasound scan is diagnostic, and estradiol levels are markedly elevated. In girls, breast development and vaginal bleeding occur with sporadic increases in estradiol from autonomously functioning ovarian cysts. Endocrine cells with this mutation have autonomous hyperfunction and secrete excess amounts of their respective hormones. Girls with McCune-Albright syndrome are generally treated with a medication that inhibits the aromatization of testosterone to estrogen, such as letrozole. Other trials have been performed using tamoxifen, an estrogen receptor antagonist. In boys, treatment consists of either inhibiting androgen production with ketoconazole or using a combination of an aromatase inhibitor that blocks the conversion of androgen to estrogen and an antiandrogen that antagonizes the effects of androgens at the receptor. Familial testotoxicosis is a male-limited autosomal dominant, gonadotropin-independent form of male precocious puberty. Boys with this condition begin to develop true precocity with bilateral testicular and phallic enlargement and growth acceleration by 4 years of age. Girls usually develop virilization in utero, resulting in a degree of sexual ambiguity. Boys have normally formed genitalia and therefore are not identified on physical examination at birth. In the more common salt-losing form of the disease, boys present with vomiting, shock, and electrolyte disturbances at 7 to 10 days. Fortunately, with neonatal screening for 21-hydroxylase deficiency, boys are being diagnosed before they develop life-threatening electrolyte abnormalities. Small subsets of affected boys and girls do not waste salt and may present in early or late childhood with signs of adrenarche, such as pubic hair, acne, body odor, acceleration of linear growth, and skeletal maturation. Insufficient glucocorticoid replacement leads to a compromise in final adult height secondary to advanced skeletal maturation, whereas excessive glucocorticoid replacement leads to short stature because of the direct effects of glucocorticoids on bone. Serum markers, growth curves, and bone age radiographs must be carefully monitored. Rarely, severe primary hypothyroidism may cause breast development in girls and increased testicular size in boys. These children generally present with growth deceleration as typically seen in hypothyroidism, rather than growth acceleration as typically seen in precocious puberty. Thyroid hormone replacement results in regression of pubertal changes, and no other therapy is necessary. Breast development generally starts during early puberty and resolves within 2 years. The cause of gynecomastia is not clearly understood, but it may be related to an elevated ratio of estradiol to testosterone. However, if resolution does not occur or if breast enlargement is excessive, surgery may be warranted. Surgery should be avoided until puberty is complete, to avoid recurrence of gynecomastia. Pathologic conditions associated with gynecomastia include Klinefelter syndrome and various other testosterone-deficient states. Some prescription medications, such as atypical antipsychotics, may cause gynecomastia and galactorrhea. Delayed puberty should be evaluated if there are no pubertal signs by 13 years in girls and by 14 years in boys. An abnormality in the pubertal axis may also manifest as a lack of normal pubertal progression, which is defined as more than 4 years between the first signs of puberty and menarche in girls or more than 5 years for completion of genital growth in boys. There is a high incidence of delayed puberty and primary amenorrhea in girls with anorexia nervosa and in girls who are highly competitive athletes. These girls have hypogonadotropic hypogonadism that appears to be directly related to their low body fat. Leptin is a hormone produced by adipocytes that is important in hypothalamicpituitary-gonadal feedback signaling. Leptin deficiency has been associated with both anorexia and obesity, with hypogonadotropic hypogonadism present in both phenotypes. There appears to be a minimum leptin level that is permissive for pubertal development. Children with this growth pattern generally have a fall-off in their linear growth within the first 2 years of life. After this, growth returns to normal, but along a lower growth channel than would be expected for parental heights. Skeletal maturation is also delayed, and the onset of puberty is commensurate with bone age rather than chronologic age. For example, a 14-year-old boy with a bone age of 11 years will start puberty when his bone age is closer to 11. This delay in puberty postpones the pubertal growth spurt and closure of growth plates, so that the child continues to grow after his or her peers have reached their final adult height. A key feature of this growth pattern is normal linear growth after 2 years of age. Functional or permanent hypogonadism should be considered when there are no signs of puberty and bone age has advanced to beyond the normal ages for puberty to start. A eunuchoid body habitus is often evident in children with abnormally delayed puberty; a decreased ratio of upper to lower body and a long arm span characterize this habitus. As a rule, serum gonadotropin levels are measured first to determine whether the child has hypogonadotropic hypogonadism (gonadotropin deficiency) or hypergonadotropic hypogonadism (primary gonadal failure). Normal or suppressed gonadotropins indicate a failure of the pituitary to stimulate gonadal steroid production. Hyperprolactinemia can also manifest as delayed puberty, and only 50% of the time will there be a history of galactorrhea. Other endocrinopathies such as diabetes mellitus, glucocorticoid excess, and hypothyroidism can cause hypogonadotropic hypogonadism when untreated. Permanent gonadotropin deficiency is suspected if these conditions are ruled out and gonadotropin levels are low. Gonadotropin deficiency may be associated with other pituitary deficiencies from conditions such as septo-optic dysplasia, tumors such as craniopharyngioma, trauma, empty sella syndrome, pituitary dysgenesis, Rathke pouch cysts, or cranial irradiation. Various syndromes, such as Kallmann syndrome, Laurence-MoonBardet-Biedl syndrome, and Prader-Willi syndrome are also associated with gonadotropin deficiency, so a karyotype or other genetic testing may be necessary. Drug abuse, particularly with heroin or methadone, has been associated with hypogonadotropic hypogonadism. If gonadotropin deficiency cannot be clearly distinguished from delayed puberty, a short course of sex steroids can be given. Patients with constitutional delay often enter puberty after such an intervention. If spontaneous puberty does not occur after this treatment or after a second course, the diagnosis of gonadotropin deficiency may be made. Kallmann syndrome is one of a class of disorders referred to as idiopathic hypogonadotropic hypogonadism or idiopathic hypothalamic hypogonadism. The classic form is characterized by hypogonadotropic hypogonadism with hyposmia or anosmia. It is caused by aplasia or hypoplasia of the olfactory bulbs and is associated with hypoplasia or aplasia of other structures of the rhinencephalon. Elevated gonadotropin levels indicate a failure of the gonads to produce enough sex steroids to suppress the hypothalamic-pituitary axis. These levels are diagnostic for gonadal failure at two periods of time: before 2 to 3 years of age and after the bone age is at or beyond the normal age for puberty to start. The incidence is 1 in 1000 male births, and eunuchoid body proportions are often present from early childhood. Associated features include gynecomastia, tall stature, small testes, low testosterone, and elevated serum gonadotropins. Many boys with Klinefelter syndrome have spontaneous onset of pubic hair growth, but they fail to progress completely through puberty.

The proportion of undemutrition starts rising after 4-6 months of age because of the introduction of unhygienic foods that cause infections such as diarrhea gastritis diet 50 cheap gasex online mastercard. Late introduction of complementary feeding and inade quate food intake leads to increasing predisposition to undernutrition gastritis unusual symptoms gasex 100 caps low price. Clinical classification of undernutrition as marasmus gastritis unusual symptoms trusted 100 caps gasex, kwashiorkor and marasmic kwashiorkor is helpful (discussed below) gastritis with chest pain purchase gasex with paypal. The standard used in this classification for reference population was the 50th centile of the old Harvard standards gastritis diet 8 day purchase gasex australia. In severe malnutrition it can be passed above the elbow gastritis diet soda order gasex online, in normal children it cannot. Triceps skin fold is the most representative of the total subcutaneous fat up to sixteen years of age. It is usually above 10 mm in normal children whereas in severely malnourished it may fall below 6 mm. This has prompted many attempts to devise methods of interpreting anthropometric data, which do not require knowledge of precise age. Various variables change slowly over certain broad age ranges and thus are regarded as independent of age over these ranges (Table 6. Certain tools have been developed to simplify the measurement for field workers and give a visible indicator of the degree of malnutrition. It increases rapidly in the first year (11-16 cm) and then been found to be relatively stable between the ages 1 and 5 yr at a value of between 16 and 17 cm. Etiology the causes of malnutrition could be viewed as immediate, underlying and basic as depicted in. They include low birthweight, illnesses (particularly infections such as diarrhea and pneumonia) and inade quate dietary intake (Box 6. Underlying determinants the immediate determinants are in turn influenced by three household determinants namely food, health and care. Political and economic structure Sociocultural environment Underlying determinants Resources for health Safe water supply Adequate sanitation Health care availability Environmental safety. Diarrhea causes nutrition loss in stool Pathological Features Malnutrition affects almost all organ systems. It is the sustainable access to safe food of sufficient quality and quantity, paying attention to energy, protein and micronutrients. This in-turn depends on having financial, physical and social access as distinct from mere availability. Care refers to a process taking place between a caregiver and the receiver of care. It translates food availability at the household level and presence of health services in to growth and development of the child. Households may have an abundance of food but still have malnourished children attributed to absence of care. Care includes care for women, breastfeeding and complementary feeding, home health practices, hygiene practices, psychosocial care and food preparation. The factors that determine adequate household food security, care and health are related to resources, their control and a host of political, cultural and social factors that affect their utilization. Basic Determinants Finally, the underlying determinants are influenced by the basic determinants. These include the socioeconomic Moderate to Severe Malnutrition Moderate to severe malnutrition is associated with one of classical syndromes, namely, marasmus, kwashiorkor, or with manifestations of both (Table 6. The loss of buccal pad of fat creates the aged or wrinkled appearance that has been referred to as monkey facies. There is no edema Less than kwashiorkor High in early stage Recover early Slow recovery Less prone More prone Kwashiorkor spreading, in more advanced cases, to the hands and face. Because of edema, children with kwashiorkor may look healthy so that their parents view them as well fed. Acute starvation or acute illness over a borderline nutritional status could precipitate this form of under nutrition. It is characterized by marked wasting of fat and muscle as these tissues are consumed to make energy. The main sign is pitting edema, usually starting in the legs and feet and It General appearance. The skin lesions consist of increased pigmentation, desquamation and dyspigmentation. Pigmentation may be confluent resemblingflaky paint or in individual enamel spots. Changes include dyspigmentation, loss of characteristic curls and sparseness over temple and occipital regions. A flag sign which is the alternate bands of hypopigmented and normally pigmented hair pattern is seen when the growth of child occurs in spurts. Stools may be watery or semisolid, bulky with a low pH and may contain unabsorbed sugars. The findings include cold, pale extremities due to circulatory insufficiency and are associated with prolonged circulation time, brady cardia, diminished cardiac output and hypotension. Maternal and child undemutrition: consequences for adult health and human capital. It is, therefore, vital to intervene in children with mild and moderate malnutrition at the community level before they develop complications. In order to achieve these high energy intakes, frequent feeding (up to seven times a day) is often necessary. Because energy is so important and because carbohydrate energy sources are bulky, oil is usually used to increase the energy in therapeutic diets. It is recognized increasingly that a relatively small increase over normal protein requirements is sufficient for rapid catchup growth, provided energy intake is high. Milk is the most frequent source of the protein used in therapeutic diets, though other sources, including vegetable protein mixtures, have been used successfully. The best measure of the efficacy of treatment of mild and moderate malnutrition is weight gain. At the community level, the four criteria listed previously should be used to diagnose severe acute malnutrition. The child with severe malnutrition has a complex backdrop with dietary, infective, social and economic factors underlying the malnutrition. Socioeconomic history and family circumstances should be explored to understand the underlying and basic causes. While mild to moderate malnutrition can be managed on ambulatory basis, severe malnutrition is preferably managed in hospital. These alterations and coexisting infections put severely malnourished children at particular risk of death from hypoglycemia, hypo thermia, electrolyte imbalance, heart failure and untreated infection. Symptomatic hypoglycemia manifesting as lethargy, unconsciousness, seizures, peripheral circulatory failure or hypothermia is more common in marasmus, where energy stores are depleted or when feeding is infrequent. Blood glucose levels must be estimated every 30 min till the glucose level becomes normal and stabilizes. Most episodes of symptomatic hyp oglycemia can be prevented by frequent, regular feeds and the child should be fed regularly throughout the night. Children with marasmus, concurrent infections, denuded skin and infants are at a greater risk. If the temperature does not register on a normal thermometer, hypothermia should be assumed and treated. The child should be rewarmed providing heat using radiation (overhead warmer) or conduction (skin contact) or convection (heat convector). If clinical condition allows the child to take orally, warm feeds should be given immediately or else the feeds should be administered through a nasogastric tube. Temperature monitoring must be ensured especially at night when the ambient temperature falls. On the other hand a decrease in the heart rate and respiratory rate (if increased initially) and increase in the urine output indicate that rehydration is proceeding. The return of tears, a moist oral mucosa, less sunken eyes and fontanelle and improved skin turgor are also indicators of rehydration. Loss of elasticity of skin may either be due to loss of the subcutaneous fat in marasmus or loss of extracellular fluid in dehydration. In dehydration, the oral mucosa feels dry to the palpating finger gently rolled on the inner side of the cheek. Presence of thirst, hypothermia, weak pulses and oliguria are other signs of dehydration in severely malnourished children. It is important to recognize that low blood volume (hypovolemia) can coexist with edema. Since estimation of dehydration may be difficult in severely malnourished children, it is safe to assume that all patients with watery diarrhea have some dehydration. Refeeding must be initiated with starter F75 within 2-3 hr of starting rehydration. Intravenous therapy should be given only for severe dehydration and shock or if the enteral route cannot be used. The exact amount actually depends on how much the child wants, volume of stool loss and whether child is vomiting. The frequent passage of small unformed stools should not be confused with profuse watery diarrhea as it does not require fluid replacement. Severe dehydration with shock It is important to recognize severe dehydration in malnourished children. Patients should be monitored for features of overhydration and cardiac decompensation. Step 4: Correct Electrolyte Imbalance In severely malnourished children excess body sodium exists even though the plasma sodium may be low. Sodium intake should be restricted to prevent sodium overload and water retention during the initial phase of treatment. All severely malnourished children have deficiencies of potassium and magnesium, which may take two weeks or more to correct. Severely malnourished children may develop severe hypokalemia and clinically manifest with weakness of abdominal, skeletal and even respiratory muscles. Once severe hypokalemia is corrected, all severely malnourished children need supplemental potassium at the progress of rehydration should be monitored every half hourly for first 2 hr and then hourly for the next 410 hr. Pulse rate, respiratory rate, oral mucosa, urine frequency or volume and frequency of stools and vomiting should be monitored. It is essential that adequate safety measures are taken to prevent the spread of hospital acquired infections, since these children are at higher risk of acquiring infections due to their compromised immune status. The most common sites for infection are the skin, the alimentary tract, the respiratory tract (including the ears, nose and throat) and the urinary tract. Therefore, all severely malnourished children should be assumed to have a serious infection on their arrival in hospital. In addition, hypoglycemia and hypothermia are considered markers of severe infection in children. Antimalarial and antituberculous treatment should only be given when the particular conditions are diagnosed. Response to treatment will be indicated by resolution of initial symptoms and signs of infection, if any. In presence of xerophthalmia, the same dose should be repeated on the next day and 2 weeks later. In presence of clinical evidence of xerophthalmia the administration of vitamin A should be considered an emergency as the changes may progress to keratomalacia within hours. Micronutrients should be used as an adjunct to treatment in safe and effective doses. Up to twice the recommended daily allowance of various vitamins and minerals should be used. Although anemia is common, iron should not be given initially due to danger of promoting free radical generation and bacterial proliferation. It should be added only after a week of therapy when the child has a good appetite and starts gaining weight. Prevention of Hospital Acquired Infection the health care personnel should follow standard precautions. If the severely anemic child has signs of cardiac failure, packed cells rather than whole blood should be transfused. In mild to moderate anemia, iron should be given for two months to replete iron stores but this should not be started until after the initial stabilization phase has been completed. The preparation should be easy to prepare and socially acceptable and there should be facilities for adequate storage, cooking and refrigeration. The volume of feeds are increased gradually while decreasing the frequency of administration. The calories are increased only after the child can accept the increased volume of feeds. Step 8: Achieve Catchup Growth Once appetite returns, higher intakes should be encouraged. It is recommended that each successive feed is increased by 10 ml until some is left Table 6. Household measure should be used only as an alternative, as they may not be standardized the above charts give the composition for 100 ml diet. This energy dense, mineral and vitamin enriched ready to use therapeutic food with a similar nutrient profile but greater energy and nutrient density than F-100 has greatly improved cost effectiveness of treating severe malnutrition.

Cardiac transplantation with and without bone marrow transplantation is currently under investigation gastritis zoloft buy gasex online from canada, as is the role of chemotherapy for some patients with cardiac involvement caused by primary amyloidosis gastritis diet cure order gasex 100caps visa. High-dose melphalan and autologous stem-cell transplantation in patients with amyloid light-chain amyloidosis appears to have a significant benefit on survival in patients without cardiac amyloid gastritis symptoms nausea gasex 100 caps on line. Treatment should start as soon as a definitive diagnosis of streptococcal infection has been made; the treatment is either a single dose of benzathine penicillin (1 gastritis symptoms pms gasex 100caps overnight delivery,200 gastritis sore throat discount 100 caps gasex free shipping,000 units for adults and half this dose for children) or a full 10-day course of oral penicillin V (for children gastritis and gerd purchase generic gasex, 250 mg two or three times daily456; empirically double this for adults). Thereafter, in selected patients in whom recurrences are feared, the penicillin injection is repeated monthly, or penicillin V is given as 125 to 250 mg twice daily continuously. The best route is by injection, which is used for 5 years, followed by oral prophylaxis possibly for life. As surgical techniques for valve repair and the performance of prosthetic valves have improved, so have the surgical indications become less stringent. An essential component of this strategy is the local results in regard to mitral valve repair 518 12 - Which Therapy for Which Condition Aortic Stenosis In valvular stenosis, the basic problem is obstructive and requires surgical relief. Improved surgical techniques allow valve replacement even in patients with heart failure of such severity that the aortic valve gradient is low. Peripheral vasoconstriction can contribute to critically severe heart failure, when careful vasodilator therapy improves the hemodynamic status,418 so that aortic valve replacement becomes feasible. The potential but unproven role of medical therapy by statins and other drugs is based on the hypothesis that aortic stenosis in older adults has risk factors similar to coronary artery disease462 and that hypercholesterolemia is associated with disease progression. In patients with decompensated heart failure caused by systolic dysfunction and severe aortic stenosis, intravenous nitroprusside may play a role as a bridge to valve replacement, but meticulous monitoring is mandatory. In truly asymptomatic aortic stenosis, which is nonetheless hemodynamically significant, the key to management is careful and regular supervision, with intervention as soon as symptoms appear. Exercise testing should help to identify asymptomatic patients likely to develop symptoms in the near future. Surgery can relieve the hypertrophy, improve the coronary perfusion pressure, and often also correct any accompanying coronary artery disease. The combination of aortic stenosis and gastrointestinal bleeding suggests type 2A von Willebrand disease, which improves with 12 - Which Therapy for Which Condition The initial enthusiasm for percutaneous aortic balloon valvuloplasty has been tempered by the longterm results, which are disappointing, but it does offer an alternative for patients in whom surgery is contraindicated and in some patients as a bridge to aortic valve replacement, if for one reason or another immediate surgery is inadvisable. There are also subsets of patients with low gradients and poor ventricular function in whom the symptomatic response to balloon valvuloplasty may provide a guide to the success of surgery in the future. It has been increasingly recognized that bicuspid aortic valve is a manifestation of an inherited aortopathy and that first-degree relatives should be screened with comprehensive transthoracic echocardiography. This may be particularly helpful in patients with symptomatic mitral stenosis during pregnancy. Percutaneous balloon mitral commissurotomy is now well established for relief of symptoms. Excellent longterm results for up to 15 years have been reported, and predictors of event-free survival are the valve echocardiographic score and age. Balloon mitral valvuloplasty gives excellent early and late results in rheumatic mitral stenosis. All patients with symptomatic mitral stenosis should be considered for this procedure. The degree of commissural opening resulting in the larger mitral valve area, the better the patient outcome after balloon valvuloplasty. The surgical alternatives are open mitral commissurotomy or mitral valve replacement. Marfan Syndrome In Marfan syndrome with aortic root dilatation the trend is to be increasingly aggressive with aortic surgery including aortic valve-sparing techniques. Paravalvular leaks, particularly in patients with prosthetic valves, are increasingly being treated by percutaneous transcatheter closure. The ability to perform a mitral valve repair is based on the skill and the experience of the surgeon and on the location and type of mitral valve disease that caused mitral regurgitation. In the United States, for isolated mitral regurgitation the rate of repair is increased steadily, and this has been accompanied by a decline of operative mortality rates. Currently direct annuloplasty by retrograde catheterization of the left ventricle from the aorta is under test with the aim of reducing the regurgitant orifice. Many clinical trials attest that ischemic heart disease is a leading but underrecognized cause of death in chronic obstructive pulmonary disease. Multifocal atrial tachycardia is associated with chronic lung disease and is a difficult arrhythmia to treat, although success with verapamil has been reported. For example, albuterol (salbutamol) has relatively little effect on the heart rate while unloading the left heart by peripheral vasodilation. The three major pathogenetic mechanisms that may influence therapy are an imbalance between vasodilation and vasoconstriction in the pulmonary circulation; vascular smooth muscle and endothelial cell proliferation; and coagulation abnormalities, which may lead to thrombosis in situ. Long-term anticoagulants are frequently used on the assumption that there is thromboembolism or thrombosis in situ. A number of studies, but no randomized trials, suggest a better survival in patients treated with warfarin. Current treatments are based on the concept of a primarily vasoconstrictive pathophysiologic finding and use three classes of vasodilated drugs: prostacyclins, endothelin receptor antagonists, and phosphodiesterase-5 inhibitors. Treprostinol is a prostacyclin analogue that is approved in the United States for both subcutaneous and intravenous use,510 and its use in Europe is limited to a few centers. Alternatives include oral analogues and inhaled iloprost, neither of which have data for long-term benefit. The emerging paradigm shift is addressing the vascular remodeling process with the aim of "reverse remodeling. Trials of simvastatin, which could enhance endothelial function by actions on the bone morphogenic protein receptive pathway, and endogenous and intestinal vasoactive peptides have been negative. Among the new vasodilators, riociguat, an activator of soluble guanylate cyclase, and the direct prostaglandin receptor antagonist selexipag deserve attention. Heart-lung and lung transplantation have been performed for primary pulmonary hypertension for more than 20 years, but this has been hampered by the lack of centers with expertise, shortage of donors, and long waiting times. Waiting times remain long and complications such as organ rejection and infections pose formidable obstacles, with survival times with the first transplant of approximately 5 years in approximately 50% of patients. Infective Endocarditis* Infective endocarditis remains potentially fatal if not aggressively treated by antibiotics, with or without surgery. Optimal therapy requires identification of the causative organism, so that appropriate therapy is initiated even though this may delay the start of therapy for a short period. Definitive antibiotic therapy is based on pathogen identification and susceptibility testing and requires the advice of an expert in infectious diseases. In culture-negative endocarditis, therapy is empirical and requires an evaluation of the epidemiologic findings of infection to attempt to define the optimal therapeutic regimen. Streptococcus viridans and Streptococcus bovis are sensitive to penicillin and are still often the causative organisms in community-acquired endocarditis in nonaddicts. If a highly penicillin-resistant streptococcus is suspected, even if not proven, a combination of ampicillin or ceftriaxone with gentamicin is suggested. For highly resistant streptococci518 or for penicillin allergy, vancomycin is used. In general, the duration of therapy in current responders is 4 weeks for native valve endocarditis and 6 weeks for prosthetic valve endocarditis. Staphylococcus aureus is also a common cause of endocarditis, moving up to first place in intravenous drug users, who are also at increased risk of gram-negative bacilli, fungal, and polymicrobial infections, some of which carry a high mortality. Staphylococcus aureus is usually penicillin resistant; use naxoline or cefazolin if the infecting strain is methicillin susceptible. If the isolator is vancomycin resistant or the patient is intolerant of vancomycin, then there are few options, including daptomycin or linezolid and co-trimoxazole. Coagulase-negative staphylococci are an important cause of prosthetic valve endocarditis, particularly within the first 2 months of valve placement. Many of these strains are methicillin resistant and require vancomycin, in combination with rifampin, for at least 6 weeks of treatment and 2 weeks of gentamicin. Enterococcus species, even when fully susceptible to penicillin, require the addition of a minor glycoside such as gentamicin to achieve an attempted cure. Increasing numbers of enterococci have acquired resistance to vancomycin and penicillin. An increasingly aggressive approach to early cardiac surgery has favorably influenced the outcome of infective endocarditis. Surgery outperformed conventional therapy for the primary endpoint of in-hospital death plus embolic events within 6 weeks of randomization (3% versus 23%, P 5 0. In the face of hemodynamic decompensation, surgery should not be delayed pending completion of antibiotic therapy. Relative indications for early surgical intervention include apparent failure of medical therapy as evidenced by persistent bacteremia or fever, or an increase in the size of vegetation during treatment. The issues regarding anticoagulant and antiplatelet therapy are complex and characterized by a lack of hard data. The decision to initiate or continue anticoagulant therapy in patients with infective endocarditis is often difficult. In the event of a cerebral thromboembolic complication, the risk of anticoagulant-induced hemorrhage must be balanced against the alternate risk of recurrent embolism. In general, aspirin has not been indicated in the early management of infective endocarditis, being without effect on vegetation resolution and valvular dysfunction. Rather, the stress is on sustained prophylactic maintenance of strict oral hygiene. Antibiotic prophylaxis is only indicated for patients with those serious underlying cardiac conditions that are associated with the highest risk of adverse outcomes, such as prosthetic valves, severe congenital heart disease, or cardiac transplantation (Table 12-8). For dental procedures in these individuals, only those procedures that involve manipulation of gingival tissue or perforation of the oral mucosa should be covered by antibiotics. Recommended antibiotics reflect changed organism sensitivities (Tables 12-8 and 12-9). Overall, note that there are no recommendations with Class I and Level of Evidence A. Prophylaxis is recommended for procedures on infected respiratory tract or skin, on skin structures, or on musculocutaneous tissue. The new guidelines also simplify antibiotic prophylaxis for patients 526 12 - Which Therapy for Which Condition Table 12-7 Cardiac Conditions with the Highest Risk of Infectious Endocarditis592 Antibiotic prophylaxis during dental procedures recommended by American Heart Association. Prosthetic cardiac valve or prosthetic material used for cardiac valve repair (class 1C). Mitral valve prolapse without mitral regurgitation or thickened leaflets (class 1C). Dental procedures for which endocarditis prophylaxis is reasonable in these groups of patients: All dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa. Prophylaxis is reasonable because endothelialization of prosthetic material occurs within 6 months after the procedure, per the American Heart Association recommendations (2007). Or other first- or second-generation oral cephalosporin in equivalent adult or pediatric dosage. Cephalosporins should not be used in an individual with a history of anaphylaxis, angioedema, or urticaria with penicillins or ampicillin. No antibiotic coverage is suggested even for high-risk patients, but for those with existing gastrointestinal or genitourinary infections, an antienteroccocal agent is "reasonable" without, however, supporting trial data. Despite common perceptions, most infectious endocarditis is not preceded by medicosurgical or dental interventions, so the real answer lies in primary prevention. Cephalosporins should not be used in patients with anaphylaxis, antiooedema, or urticaria after intake of penicillin and ampicillin. Revascularization, either percutaneous or surgical, is indicated for patients with refractory symptoms causing significant disability or the presence of limb-threatening ischemia. The basis of medical therapy lies in risk-factor modification, exercise training, and aspirin. Class I recommendations include a statement that all smokers or former smokers should be asked about their smoking status at every visit, and smokers should be assisted with counseling and the development of a quit-smoking treatment plan that includes pharmacologic therapy with varenicline, bupropion, or nicotine-replacement therapy. Ongoing major trials of statins, antiplatelet agents, recombinant growth factors, and immune modulators may result in clinically relevant new advances in the medical management of peripheral vascular disease in the future, but trials of gene therapy for therapeutic 528 12 - Which Therapy for Which Condition Cilostazol, a phosphodiesterase-3 inhibitor, was approved in 2000 in the United States for intermittent claudication. It is metabolized by the cytochrome P-450 3A4 system, and hence open to interaction with ketoconazole, erythromycin, and diltiazem, as well as grapefruit juice, which should all be avoided. Pentoxifylline (Trental) decreases blood viscosity and maintains red cell flexibility of the erythrocytes as they are squeezed through the capillary bed. Yet in a randomized trial of pentoxifylline and cilostazol, only cilostazol improved both functional status and the walking impairment questionnaire. Mechanisms of action are unclear, but a recent consensus statement recommended its addition to cilostazol. Levocarnitine and l-propionyl-carnitine favorably improve the metabolic status of skeletal muscle to lengthen the walking distance. Ineffective therapies that should be discouraged include estrogen replacement, chelation therapy, and vitamin E supplementation. Nifedipine is best tested, and one 10-mg capsule may be taken intermittently at the start of an attack. Several reports attest to the efficacy of topical glycerol trinitrate in this condition. Common in Africa and Asia, in Western countries it is underdiagnosed especially in alcoholics and in those on "fad diets" or occasionally in patients receiving parenteral nutrition. Even in Shoshin beriberi with peripheral circulatory shock and severe metabolic acidosis, thiamine remains the mainstay of treatment because the acidosis responds poorly to treatment. Cardiovascular Drugs in Pregnancy Most cardiovascular drugs are not well studied for safety in pregnancy. For pregnancy hypertension, methyldopa is best validated, and the diuretics are not as bad as often thought.

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