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In a prospective buy prograf 1mg on line, population-based study of the incidence of shaken baby syndrome prograf 5mg amex, Barlow found a rate of 24 buy prograf with amex. Thirteen to 30% of shaken infants succumb to fatal injuries (American Academy of Ophthalmology, 2002; American 10 11 Academy of Pediatrics, 2001; Dias et al. Half of the remaining infants experience blindness and various global neurological impairments, including seizures, spasticity, paralysis, and developmental delays (A. Shaken baby syndrome is an ominous form of child abuse with devastatingly high rates of morbidity and mortality. Any physician suspecting an infant has been abused is legally obligated to report the case to state or province-specific child welfare agencies. Efforts to educate health care providers about the characteristic features of shaken baby syndrome will serve to increase the detection and reporting of new cases, and hopefully increase the conviction rate of identified perpetrators. Caffey first described the combination of subdural hemorrhages, retinal hemorrhages and long bone fractures in infants without external signs of injury; he named the phenomenon ‘whiplash shaken baby syndrome’ (Caffey, 1972). In his landmark article in 1972, he called for the implementation of a nation-wide prevention campaign. Unfortunately, clinical 11 12 and research efforts remained focused on intervention rather than prevention for several reasons. First, the perceived importance of educating the public about shaken baby syndrome differed among professionals. Some felt it was common knowledge that shaking an infant was dangerous, while others routinely gave advice to shake apneic infants. Second, it was believed that the impulsive act of infant shaking was not amenable to primary prevention through public education. Third, the risk factors associated with shaken baby syndrome were unclear, eliminating the possibility of targeted secondary prevention initiatives (Barron, 2003). Prevention-based research finally began in the United States in the mid 1980’s and has been steadily gaining momentum world-wide. After a 1989 survey by Showers demonstrated that 25 to 50% of adults and adolescents were unaware of the dangers of violent infant shaking, prevention efforts in the form of media campaigns, public education initiatives, male-targeted parenting classes, baby-sitting training courses, and hospital-based programs began to appear. Unfortunately, the impact these programs had on the incidence of shaken baby syndrome remained unknown because the programs were sporadic, fragmented, and unevaluated. In the long term, the total cost of comprehensive medical 12 13 care for a single shaken infant can exceed $1 million (Showers, 1998). These figures do not even begin to capture the hidden costs of shaken baby syndrome, when one considers each victim’s loss of societal productivity and occupational revenue, the cost of prosecuting and incarcerating perpetrators, the cost of foster care and child welfare agency involvement, and the on-going mental, physical, and educational therapy that each victim requires (Dias & Barthauer, 2001, August). Financial costs aside, shaken baby syndrome has devastating effects on the personal lives and emotional health of victims and affected families. Clearly, the hidden costs of treating victims of shaken baby syndrome far exceed the costs of implementing a prevention program. Health professionals, administrators, law enforcement officers, politicians, and affected families have taken a proactive stance in disseminating information about shaken baby syndrome. The conferences provide a unique opportunity for professionals from fields including medicine, 13 14 nursing, law, policing, social work, and psychology to share new research findings, discuss prevention strategies, and educate each other about shaken baby syndrome. On a local level, many shaken baby syndrome prevention initiatives are in operation across North America. The program has been implemented in multiple prisons in the United States, Canada, and Australia; however, its quantifiable effectiveness in reducing the incidence of shaken baby syndrome has never been examined (Dutson, Dulfano, & Nink, 2003). In Wisconsin, the Shaken Baby Association began educating Milwaukee police officers about shaken baby syndrome in 2001. That same year, 18 Milwaukee radio stations simultaneously broadcast a public service announcement urging parents to “Never, ever shake a baby”. Following the announcement, a three month period ensued without a single reported case of shaken baby syndrome. The programs target parents, babysitters, and health professionals in a variety of educational formats, including videos, posters, information cards, pamphlets, and refrigerator magnets (Calgary Injury Prevention Coalition, 2003). Regional public health departments and the Saskatchewan Institute on Prevention of Handicaps have been instrumental in developing and disseminating educational materials to the Canadian public. Although some programs are over 14 15 six years old, however, none have been evaluated with regard to their effect on the incidence rate of shaken baby syndrome. These were complemented by a series of television commercials in 2000, urging parents to “Stop before you cross that line" when coping with a crying infant. Without evidence of effectiveness, the impetus for governments to mandate, fund, and implement prevention programs across large jurisdictions has been minimal. He had extensive experience treating infants with shaken baby syndrome and had conducted a retrospective study in serial radiography for shaken baby syndrome patients. When his own son was born in 1997, Dias experienced firsthand the frustrations that parents are faced with in caring for an inconsolable infant (Lewandowski, 1999, October 14). He realized the ease with which exasperated parents or babysitters could 15 16 impulsively direct their frustrations onto a crying child. Dias resolved to share his expertise in inflicted infant head injuries with new parents to provide them with the necessary knowledge and coping skills to prevent a bout of frustration from resulting in a case of shaken baby syndrome. Dias’ original study provided six years of reliable incidence data for shaken baby syndrome cases in Western New York. The Children’s Hospital of Buffalo, the sole tertiary referral centre for pediatric neurosurgical cases in the region, provided an ideal location for launching his envisioned program. It was to be a comprehensive, hospital-based, universal prevention program that educated parents at the time of the infant’s birth about the dangers of violent infant shaking. Outcome measures were defined as the regional incidence rate of shaken baby syndrome, the number of parents reached by the program, and parental pre and post-program knowledge about shaken baby syndrome. This format was intended to improve upon the multitude of fragmented, unevaluated programs previously in operation. It was also unique in being the first to determine whether improved public knowledge could translate into a reduction in the incidence rate of shaken baby syndrome. Dias’ original study revealed that a total of 33 infants were diagnosed with shaken baby syndrome at the Children’s Hospital of Buffalo between 1992 and 1998, with an average incidence rate of 7. This data, along with Dias’ experience in treating infants with shaken baby syndrome, shaped the following hypotheses that guided the ultimate program design: 16 17 1. Shaken baby syndrome differs from other forms of child abuse in that it seems to result from impulsive acts of adult rage due to infant crying that may be modifiable with timely parental education. Education efforts must be targeted at parents, and particularly, at males, since 71% of perpetrators are parents and paramours, and males comprise the majority. Due to increased public awareness about shaken baby syndrome from public education campaigns and highly publicized infant fatalities, many parents are already aware that violently shaking an infant is dangerous. Therefore, the aim of the education campaign should be to remind parents about shaken baby syndrome at the appropriate time – during a mother’s post-natal stay in the hospital – after which both parents will soon be immersed in the challenges of infant care. Parents are optimal advocates for infant safety and care and may be most effective at disseminating information about shaken baby syndrome to caregivers that will be in contact with their child. Dias conceived that a shaken baby syndrome education campaign could act as a “vaccine” to “inoculate” parents with information and protect infants from acquiring shaking injuries during the first years of life, when they are most susceptible. Given that the average age at which infants incur inflicted head injuries ranges from five to nine months, the goal that parents retain the program information for at least the first year of each child’s life seemed both effective and attainable (Dias & Barthauer, 2001). In addition, a regional Perinatal Outreach Program providing tertiary infant care in conjunction with Western New York hospitals was already in full operation.
Zinc supplements have been shown to increase the growth and weight gain of stunted or underweight children purchase on line prograf. Moreover prograf 1 mg without a prescription, studies have shown that children who receive zinc supplements have lower death rates 5 mg prograf otc. Approximately one third of the world’s population live in areas at high risk of zinc deﬁciency. The most vulnerable population groups are infants, young children, and pregnant and lactating women because of their additional requirements for this essential nutrient. Therefore, interventions to enhance the zinc intake of children in low-income countries are a useful strategy to reducing child mortality rates. Therefore, improving the zinc intake of women before and during pregnancy may help to reduce maternal mortality and beneﬁt infant growth and survival. For young children, complementary feeding practices should be implemented with zinc-rich foods, such as animal source foods, and zinc-fortiﬁed complementary foods. Summary of Study Session 7 In Study Session 7 you have learned that: 1 If the vitamin A status in the body is very low, the immune system becomes weak and illness is more common and more severe, increasing under-ﬁve death rates. In adults, anaemia reduces work capacity and mental performance as well as tolerance to infections. Iron deﬁciency anaemia can also cause increased maternal mortality due to bleeding problems. In addition, zinc reduces the frequency and severity of diarrhoea, pneumonia, and possibly malaria. Write your answers in your Study Diary and discuss them with your Tutor at the next Study Support Meeting. You can check your answers with the Notes on the Self-Assessment Questions at the end of this Module. In this session you will be introduced to the issue of the overall shortage of food at the household level (household food insecurity). You will learn about its causes, consequences and prevention as well as nutrition emergency interventions. Coping strategies that may be adopted by households in response to constrained food supplies will be described, using local examples. Learning Outcomes for Study Session 8 When you have studied this session, you should be able to: 8. Utilisation (the capacity to transform food into the desired nutritional outcome). If these conditions are not fulﬁlled then the household is said to be in the state of food insecurity. Chronic food insecurity is commonly described as the result of 97 overwhelming poverty indicated by a lack of assets (means of living). Acute food insecurity is usually considered to be more of a short-term phenomenon related either to manmade or unusual natural shocks, such as drought. While the chronically food insecure population may experience food deﬁcits relative to need in any given year, irrespective of the impact of shocks, the acutely food insecure require short term assistance to help them cope with unusual circumstances that impact temporarily on their lives and livelihoods. Both chronic and acute problems of food insecurity are widespread and severe in Ethiopia. Rural Urban Others Chronic Resource poor Low income Refugees households households employed in informal sector Displaced people Landless or land-scarce households Those outside the labour market Poor pastoralists Elderly, disabled and sick Female-headed households Some female-headed households Elderly, disabled and sick Street children Poor non-agricultural households Newly established settlers Acute Resource poor Urban poor vulnerable Groups affected by households vulnerable to economic shocks, temporary civil unrest to shocks, especially especially those drought causing food price rises Farmers and others in drought prone areas Pastoralists Others vulnerable to economic shocks (eg. People living in low income households, with informal employment are also very vulnerable. In Ethiopia natural and man- made disasters are the commonest causes of household food insecurity. Drought and conﬂict are the main factors that increase problems of food production, distribution and access. High rates of population growth and poverty also play a part, within an already difﬁcult environment of fragile ecosystems where it might be difﬁcult to produce sufﬁcient food. The fact that almost 80% of the population in Ethiopia depends almost exclusively on agriculture for its consumption and income needs means that measures to address the problems of poverty and food insecurity must mainly be found within the agricultural sector. Other natural disasters such as pest infestations destroy area-speciﬁc production levels and the threat of locust swarms is often present. Currently there is an ineffective weather and pest early warning system in the country. Depending only on rainwater for farming when there is variable rainfall in some of the arid areas is not reliable for producing sufﬁcient food supply. Initiatives in Ethiopia, such as using irrigation systems, water harvest technology and drip irrigation, are encouraging steps that need to be strengthened further. Causes of food insecurity Mechanism (how it leads to food insecurity) Rapid population growth A high rate of population growth calls for more food production and the need for ploughing more land. Population may exceed the carrying capacity of the fragile environment in some areas At the household level the food produced from the same plot of land that the household has may not be sufﬁcient. The chances of drought occurring in parts of Ethiopia have increased the probability of food insecurity, especially in the arid and pastoralist areas (northern and eastern parts of Ethiopia) Traditional rain-dependent farming systems Lack of agricultural intensiﬁcation and low agricultural productivity means that many of those in rural areas remain subsistence producers. Therefore, the large quantity of food at low prices which is essential for economic growth in urban areas is not available Stop reading for a while and think of the causes of food insecurity in your area. Indirect indicators can also give clues to the presence of household food insecurity. These include measuring the percentage of children under ﬁve years old who are malnourished and other early warning signs of vulnerability such as low rainfall or the presence of other disasters. One of the most common methods for identifying food-insecure households or regions is to look at the frequency and types of coping strategies. The different types of coping strategies are markers of the severity of conditions, often categorised into four distinct stages of food insecurity. Stage 1: Insurance strategies The ﬁrst stage of household food insecurity is marked by the initial shortage of food, or inability to provide sufﬁcient quantities of food to all members of the household. Households may have prepared for a food quantity shortfall, as in the case of seasonal production, by storing quantities of grain or owning livestock that can be quickly sold, traded, or used for food (in the case of agricultural societies). These are often referred to as insurance (reserve food crisis), and are not intended to be a main source of income or an integral part of income generation, simply crisis insurance. But, before any assets are sold, changes in diet and frequency of meals per day are the ﬁrst adaptations undertaken. Rationing of food consumption is a very common response, and is started and planned generally far in advance of selling any assets. The frequency and severity of coping strategies practiced will vary according to the causes of the food shortage (chronic vs. Stage 2: Crisis strategies I The second stage of food insecurity is marked by the sale of assets, speciﬁcally non-productive assets. At this point, in the food security crisis, food consumption becomes more important than holding onto assets. Jewellery, goats, chickens, other livestock and any other asset that serves as crisis insurance would be sold. Generally, the assets that are preserved are those related to income generation, such as land, farming equipment, oxen and cattle. In addition to non-productive asset sales, the second stage also sees the onset of loans or credit from merchants (as opposed to family), which also has serious implications for the future security of the household and recovery to their original livelihood systems.
While these strategies are not guaranteed to maintain metabolism generic prograf 5 mg line, they do help prevent muscle loss and may increase energy levels buy prograf pills in toronto. Because stress activates cortisol release buy 5mg prograf free shipping, and cortisol slows metabolism, avoiding stress, or at least practicing relaxation techniques, can also help. Lipid metabolism entails the oxidation of fatty acids to either generate energy or synthesize new lipids from smaller constituent molecules. Lipid metabolism is associated with carbohydrate metabolism, as products of glucose (such as acetyl CoA) can be converted into lipids. Lipid metabolism begins in the intestine where ingested triglycerides are broken down into smaller chain fatty acids and subsequently into monoglyceride molecules (see Figure 24. Within the intestinal cells, these triglycerides are packaged along with cholesterol molecules in phospholipid vesicles called chylomicrons (Figure 24. The chylomicrons enable fats and cholesterol to move within the aqueous environment of your lymphatic and circulatory systems. Chylomicrons leave the enterocytes by exocytosis and enter the lymphatic system via lacteals in the villi of the intestine. Once in the circulation, they can either go to the liver or be stored in fat cells (adipocytes) that comprise adipose (fat) tissue found throughout the body. They function to carry these water-insoluble molecules from the intestine, through the lymphatic system, and into the bloodstream, which carries the lipids to adipose tissue for storage. Lipolysis To obtain energy from fat, triglycerides must first be broken down by hydrolysis into their two principal components, fatty acids and glycerol. The resulting fatty acids are oxidized by β- oxidation into acetyl CoA, which is used by the Krebs cycle. Because one triglyceride molecule yields three fatty acid molecules with as much as 16 or more carbons in each one, fat molecules yield more energy than carbohydrates and are an important source of energy for the human body. Triglycerides yield more than twice the energy per unit mass when compared to carbohydrates and proteins. The breakdown of fatty acids, called fatty acid oxidation or beta (β)-oxidation, begins in the cytoplasm, where fatty acids are converted into fatty acyl CoA molecules. This fatty acyl CoA combines with carnitine to create a fatty acyl carnitine molecule, which helps to transport the fatty acid across the mitochondrial membrane. Once inside the mitochondrial matrix, the fatty acyl carnitine molecule is converted back into fatty acyl CoA and then into acetyl CoA (Figure 24. Ketogenesis If excessive acetyl CoA is created from the oxidation of fatty acids and the Krebs cycle is overloaded and cannot handle it, the acetyl CoA is diverted to create ketone bodies. Ketones serve as fuel in times of prolonged starvation or when patients suffer from uncontrolled diabetes and cannot utilize most of the circulating glucose. In both cases, fat stores are liberated to generate energy through the Krebs cycle and will generate ketone bodies when too much acetyl CoA accumulates. Ketone Body Oxidation Organs that have classically been thought to be dependent solely on glucose, such as the brain, can actually use ketones as an alternative energy source. The carbon dioxide produced can acidify the blood, leading to diabetic ketoacidosis, a dangerous condition in diabetics. The carbon within the acetoacetyl CoA that is not bonded to the CoA then detaches, splitting the molecule in two. These two acetyl CoA molecules are then processed through the Krebs cycle to generate energy (Figure 24. Lipogenesis When glucose levels are plentiful, the excess acetyl CoA generated by glycolysis can be converted into fatty acids, triglycerides, cholesterol, steroids, and bile salts. This process, called lipogenesis, creates lipids (fat) from the acetyl CoA and takes place in the cytoplasm of adipocytes (fat cells) and hepatocytes (liver cells). When you eat more glucose or carbohydrates than your body needs, your system uses acetyl CoA to turn the excess into fat. Although there are several metabolic sources of acetyl CoA, it is most commonly derived from glycolysis. Lipogenesis begins with acetyl CoA and advances by the subsequent addition of two carbon atoms from another acetyl CoA; this process is repeated until fatty acids are the appropriate length. However, the creation of triglycerides and lipids is an efficient way of storing the energy available in carbohydrates. Although lipogenesis occurs in the cytoplasm, the necessary acetyl CoA is created in the mitochondria and cannot be transported across the mitochondrial membrane. Oxaloacetate forms via the action of pyruvate carboxylase, whereas the action of pyruvate dehydrogenase creates acetyl CoA. Oxaloacetate and acetyl CoA combine to form citrate, which can cross the mitochondrial membrane and enter the cytoplasm. There is protein in bones (collagen), muscles, and tendons; the hemoglobin that transports oxygen; and enzymes that catalyze all biochemical reactions. Amid all these necessary functions, proteins also hold the potential to This OpenStax book is available for free at http://cnx. Proteins are not stored for later use, so excess proteins must be converted into glucose or triglycerides, and used to supply energy or build energy reserves. Although the body can synthesize proteins from amino acids, food is an important source of those amino acids, especially because humans cannot synthesize all of the 20 amino acids used to build proteins. The pancreas releases most of the digestive enzymes, including the proteases trypsin, chymotrypsin, and elastase, which aid protein digestion. In order to avoid breaking down the proteins that make up the pancreas and small intestine, pancreatic enzymes are released as inactive proenzymes that are only activated in the small intestine. Once released into the small intestine, an enzyme found in the wall of the small intestine, called enterokinase, binds to trypsinogen and converts it into its active form, trypsin. Trypsin and chymotrypsin break down large proteins into smaller peptides, a process called proteolysis. These smaller peptides are catabolized into their constituent amino acids, which are transported across the apical surface of the intestinal mucosa in a process that is mediated by sodium-amino acid transporters. The sodium can be reused in the transporter, whereas the amino acids are transferred into the bloodstream to be transported to the liver and cells throughout the body for protein synthesis. If amino acids exist in excess, the body has no capacity or 1176 Chapter 24 | Metabolism and Nutrition mechanism for their storage; thus, they are converted into glucose or ketones, or they are decomposed. Urea Cycle The urea cycle is a set of biochemical reactions that produces urea from ammonium ions in order to prevent a toxic level of ammonium in the body. In these reactions, an amine group, or ammonium ion, from the amino acid is exchanged with a keto group on another molecule. This transamination event creates a molecule that is necessary for the Krebs cycle and an ammonium ion that enters into the urea cycle to be eliminated. Because the processing of amino acids results in the creation of metabolic intermediates, including pyruvate, acetyl CoA, acetoacyl CoA, oxaloacetate, and α-ketoglutarate, amino acids can serve as a source of energy production through the Krebs cycle (Figure 24. Treatments can include diet modification, vitamin supplementation, and gene therapy; however, damage to the central nervous system usually cannot be reversed. Because of this, levels of phenylalanine rise to toxic levels in the body, which results in damage to the central nervous system and brain. Symptoms include delayed neurological development, hyperactivity, mental retardation, seizures, skin rash, tremors, and uncontrolled movements of the arms and legs. Babies exposed to excess phenylalanine in utero may present with heart defects, physical and/or mental retardation, and microcephaly.