Micronutrient Malnutrition – Detection, Measurement and Intervention: a Training Package for Field Staff

Total Page：16

File Type：pdf, Size：1020Kb

Micronutrient Malnutrition – Detection, Measurement and Intervention: A Training Package for Field Staff Compiled by the Institute of Child Health Photo-cards for Printing For UNHCR Version 1 2003 ICH/UNHCR MNDD Slide Iron Deficiency Anaemia Pale mucous membranes in the eye and the tongue are signs of anaemia. You may see these signs in males and females of all ages. ICH/UNHCR MNDD Slide Vitamin A Deficiency – Xeropthalmia Bitots spots (X1B) are foamy white areas on the white of the eye. Be careful not to confuse them with other types of eye problems. These signs will most often be seen in children. Corneal Xerosis(X2) Keratomalacia (X3) ICH/UNHCR MNDD Slide 20 Iodine Deficiency – Goiter examination Goitre can be examined by looking or by feeling the neck (palpating). If the goiter is not large it may only be seen if the head is tilted gently backwards. The visible goitres seen in the 2 pictures on the top left are Grade 2. Iodine deficiency can also cause developmental problems in children such cretinism ICH/UNHCR MNDD Slide Thiamine Deficiency Riboflavin Deficiency -Beriberi - Ariboflavinosis Lesions of the mouth are seen in Oedema is seen in the wet form of riboflavin deficiency. They are called beriberi. However, it is also caused angular stomatitis if the fissures are at by general malnutrition and can be the corners of the mouth and cheilosis if seen in children and adults. they are elsewhere on the lips. ICH/UNHCR MNDD Slide Niacin Deficiency - Pellagra Casal’s collar Butterfly sign A rash (dermatitis) which is on both sides of the body, and on skin normally exposed to sunlight is a sign of pellagra. Check the face, neck, hands, arms and legs. ICH/UNHCR MNDD Slide Vitamin C Deficiency - Scurvy Bleeding around the bases of the hair on the legs (Perifollicular hemorrhage) and the gums in between the teeth are signs of scurvy. There may be areas of bruising as seen in second picture. There may also be swelling of the bone joints. ICH/UNHCR MNDD Slide Vitamin D deficiency - Rickets Harrison’s Groove or Pigeon Chest Spinal deformity Beading of the rib cage (rachitic rosary) Bow legs ICH/UNHCR MNDD Slide.

Copy Link

Recommended publications

A Review of the Biochemistry, Metabolism and Clinical Benefits of Thiamin(E) and Its Derivatives
View metadata, citation and similar papers at core.ac.uk brought to you by CORE Advance Access Publication 1 February 2006 eCAM 2006;3(1)49–59provided by PubMed Central doi:10.1093/ecam/nek009 Review A Review of the Biochemistry, Metabolism and Clinical Benefits of Thiamin(e) and Its Derivatives Derrick Lonsdale Preventive Medicine Group, Derrick Lonsdale, 24700 Center Ridge Road, Westlake, OH 44145, USA Thiamin(e), also known as vitamin B1, is now known to play a fundamental role in energy metabolism. Its discovery followed from the original early research on the ‘anti-beriberi factor’ found in rice polish- ings. After its synthesis in 1936, it led to many years of research to find its action in treating beriberi, a lethal scourge known for thousands of years, particularly in cultures dependent on rice as a staple. This paper refers to the previously described symptomatology of beriberi, emphasizing that it differs from that in pure, experimentally induced thiamine deficiency in human subjects. Emphasis is placed on some of the more unusual manifestations of thiamine deficiency and its potential role in modern nutri- tion. Its biochemistry and pathophysiology are discussed and some of the less common conditions asso- ciated with thiamine deficiency are reviewed. An understanding of the role of thiamine in modern nutrition is crucial in the rapidly advancing knowledge applicable to Complementary Alternative Medi- cine. References are given that provide insight into the use of this vitamin in clinical conditions that are not usually associated with nutritional deficiency. The role of allithiamine and its synthetic derivatives is discussed.
[Show full text]
OCULAR MANIFESTATIONS of VITAMIN a DEFICIENCY*T
Br J Ophthalmol: first published as 10.1136/bjo.51.12.854 on 1 December 1967. Downloaded from Brit. J. Ophthal. (1967) 51, 854 OCULAR MANIFESTATIONS OF VITAMIN A DEFICIENCY*t BY G. VENKATASWAMY Department of Ophthalmology, Madurai Medical College, Madurai, India NUTRITIONAL deficiencies are a frequent cause of serious eye disease in India. Oomen (1961) reported a mortality of nearly 30 per cent. in young children with keratomalacia and an even higher proportion in those with protein malnutrition; about 25 per cent. of the survivors became totally blind, and about 60 per cent. were left with reduced vision in one or both eyes. Deficiency diseases revealed by dietary surveys have included xerophthalmia, Bitot's spots, angular stomatitis, and phrynoderma. Gilroy (1951) observed xerophthalmia in 250 out of 4,191 children from 44 estates in Assam. Sundararajan (1963) found signs of vitamin A deficiency in 35 to 45 per cent. of schoolchildren in Calcutta. Chandra, Venkatachalam, Belavadi, Reddy, and Gopalan (1960) reported that lack of protein and vitamin A was the most frequent cause of nutritional deficiency disorders in India; out of copyright. 14,563 children examined in a 5-year period, 2,245 showed malnutrition, 551 vitamin A deficiency, and 157 keratomalacia. Rao, Swaminathan, Swarup, and Patwardhan (1959) observed two to five cases ofvitamin A deficiency for every case ofkwashiorkor. A world-wide survey ofxerophthalniia carried out in nearly fifty countries (including countries in Asia) by WHO in 1962-1963 revealed that this was often the most important cause of blindness in young children. Scrimshaw (1959), McLaren (1963), and UNICEF (1963) concluded that vitamin A deficiency was one of the http://bjo.bmj.com/ main nutritional problems in tropical and subtropical areas.
[Show full text]
Nutrition 102 – Class 3
Nutrition 102 – Class 3 Angel Woolever, RD, CD 1 Nutrition 102 “Introduction to Human Nutrition” second edition Edited by Michael J. Gibney, Susan A. Lanham-New, Aedin Cassidy, and Hester H. Vorster May be purchased online but is not required for the class. 2 Technical Difficulties Contact: Erin Deichman 574.753.1706 [email protected] 3 Questions You may raise your hand and type your question. All questions will be answered at the end of the webinar to save time. 4 Review from Last Week Vitamins E, K, and C What it is Source Function Requirement Absorption Deficiency Toxicity Non-essential compounds Bioflavonoids: Carnitine, Choline, Inositol, Taurine, and Ubiquinone Phytoceuticals 5 Priorities for Today’s Session B Vitamins What they are Source Function Requirement Absorption Deficiency Toxicity 6 7 What Is Vitamin B1 First B Vitamin to be discovered 8 Vitamin B1 Sources Pork – rich source Potatoes Whole-grain cereals Meat Fish 9 Functions of Vitamin B1 Converts carbohydrates into glucose for energy metabolism Strengthens immune system Improves body’s ability to withstand stressful conditions 10 Thiamine Requirements Groups: RDA (mg/day): Infants 0.4 Children 0.7-1.2 Males 1.5 Females 1 Pregnancy 2 Lactation 2 11 Thiamine Absorption Absorbed in the duodenum and proximal jejunum Alcoholics are especially susceptible to thiamine deficiency Excreted in urine, diuresis, and sweat Little storage of thiamine in the body 12 Barriers to Thiamine Absorption Lost into cooking water Unstable to light Exposure to sunlight Destroyed
[Show full text]
Alcohol Related Dementia and Wernicke-Korsakoff Syndrome
About Dementia - 18 ALCOHOL RELATED DEMENTIA AND WERNICKE-KORSAKOFF SYNDROME This Help Sheet discusses alcohol related dementia and Wernicke-Korsakoff syndrome, their causes, symptoms and treatment. What is alcohol related dementia? Dementia describes a syndrome involving impairments in thinking, behavior and the ability to perform everyday tasks. Excessive consumption of alcohol over many years can sometimes result in brain damage that produces symptoms of dementia. Alcohol related dementia may be diagnosed when alcohol abuse is determined to be the most likely cause of the dementia symptoms. The condition can affect memory, learning, reasoning and other mental functions, as well as personality, mood and social skills. Problems usually develop gradually. If the person continues to drink alcohol at high levels, the symptoms of dementia are likely to get progressively worse. If the person abstains from alcohol completely then deterioration can be halted, and there is often some recovery over time. Excessive alcohol consumption can damage the brain in many different ways, directly and indirectly. Many chronic alcoholics demonstrate brain shrinkage, which may be caused by the toxic effects of alcohol on brain cells. Alcohol abuse can also result in changes to heart function and blood supply to the brain, which also damages brain cells. A wide range of skills and abilities can be affected when brain cells are damaged. Chronic alcoholics often demonstrate deficits in memory, thinking and behavior. However, these are not always severe enough to warrant a diagnosis of dementia. Many doctors prefer the terms ‘alcohol related brain injury’ or ‘alcohol related brain impairment’, rather than alcohol related dementia, because alcohol abuse can cause impairments in many different brain functions.
[Show full text]
Vitamins a and E and Carotenoids
Fat-Soluble Vitamins & Micronutrients: Vitamins A and E and Carotenoids Vitamins A (retinol) and E (tocopherol) and the carotenoids are fat-soluble micronutrients that are found in many foods, including some vegetables, fruits, meats, and animal products. Fish-liver oils, liver, egg yolks, butter, and cream are known for their higher content of vitamin A. Nuts and seeds are particularly rich sources of vitamin E (Thomas 2006). At least 700 carotenoids—fat-soluble red and yellow pigments—are found in nature (Britton 2004). Americans consume 40–50 of these carotenoids, primarily in fruits and vegetables (Khachik 1992), and smaller amounts in poultry products, including egg yolks, and in seafoods (Boylston 2007). Six major carotenoids are found in human serum: alpha-carotene, beta-carotene, beta-cryptoxanthin, lutein, trans-lycopene, and zeaxanthin. Major carotene sources are orange-colored fruits and vegetables such as carrots, pumpkins, and mangos. Lutein and zeaxanthin are also found in dark green leafy vegetables, where any orange coloring is overshadowed by chlorophyll. Trans-Lycopene is obtained primarily from tomato and tomato products. For information on the carotenoid content of U.S. foods, see the 1998 carotenoid database created by the U.S. Department of Agriculture and the Nutrition Coordinating Center at the University of Minnesota (http://www.nal.usda.gov/fnic/foodcomp/Data/car98/car98.html). Vitamin A, found in foods that come from animal sources, is called preformed vitamin A. Some carotenoids found in colorful fruits and vegetables are called provitamin A; they are metabolized in the body to vitamin A. Among the carotenoids, beta-carotene, a retinol dimer, has the most significant provitamin A activity.
[Show full text]
Vitamin a Information Vitamin a Deficiency (VAD) Is the Leading
Vitamin A Information Vitamin A deficiency (VAD) is the leading cause of preventable blindness in children. Xerophthalmia, which is abnormal dryness of the conjunctiva and cornea of the eye, is associated with VAD and when left untreated can lead to blindness. The World Health Organization estimates that worldwide there are “at least 254 million children under the age of five that are at-risk in terms of their health and survival”. An estimated 250,000 to 500,000 vitamin A deficient children become blind each year. Half of these children die within 12 months of losing their sight. Although this problem is most prevalent in Africa and South East Asia, it is certainly existent throughout the developing nations. According to UNICEF, “Of 82 countries deemed ‘priorities’ for national-level vitamin A supplementation programs, 57 had coverage estimates available for 2014. Half of these 57 countries achieved the recommended coverage of 80 percent.” As a result, half did not receive the 80 percent level, and for those that did, a significant number of children remained untreated. While the problem is most prevalent in Africa and South East Asia, central American countries are also at risk. “About 40% of Mexican children in rural areas had deficient values of plasma vitamin A” (Rosado, 1995). Furthermore, it was noted as far back as 1989 that vitamin A deficient Guatemalan children grow poorly, are more anemic, have more infections and are more likely to die than their peers (Sommer, 1989). The World Health Organization recommends that all children between the ages of six months and six years in developing nations that are at risk receive vitamin A supplementation.
[Show full text]
About Thiamine (B1) and Thiamine Deficiency
NLOSS North London Obesity Surgery Service About Thiamine (B1) and Thiamine Deficiency What does thiamine do? Thiamine (vitamin B1) is an important nutrient for taking energy from food and turning it into energy for your brain, nerves and heart. It is needed by the body to process carbohydrates, fats, and proteins – but it is most important for how we process carbohydrates (sugars and starches). What happens if my thiamine is low/if I don’t get enough thiamine? Your body stores very little thiamine, so deficiency can happen very quickly – especially if you are not eating much or if you are vomiting for any reason. Thiamine deficiency may be called Beriberi or Wernicke’s Encephalopathy depending on how it presents. When you don’t get enough thiamine, you may first have nausea, vomiting, loss of appetite, fatigue and difficulty concentrating. You may also have weakness, sleepiness, changes in personality and memory, leg and foot cramping, burning feet, headache, constipation, and cramping. If thiamine deficiency is severe, serious problems can result including loss of hearing, permanent nerve damage, coma, permanent brain damage, heart damage, liver damage, and death. What are other symptoms? Other symptoms of thiamine deficiency include: • Blurred or double vision • Difficulty urinating • Difficulty taking/swallowing • Numb/painful hands/feet • Facial weakness • Foot drop, leg weakness • Amnesia, memory loss, dementia • Clumsiness, loss of balance, • Rapid heartbeat falling • Faintness on standing up • Loss of muscle • Leg swelling Where can I get thiamine? Thiamine is found throughout the diet, but fortified cereals, beans/peas, nuts and pork are very good sources. Other sources are also milk, cheese, fresh and dried fruit, and eggs.
[Show full text]
A Retrospective Case Series of Thiamine Deficiency in Non
Journal of Clinical Medicine Article A Retrospective Case Series of Thiamine Deficiency in Non-Alcoholic Hospitalized Veterans: An Important Cause of Delirium and Falling? Elisabeth Mates 1,2,* , Deepti Alluri 3, Tailer Artis 2 and Mark S. Riddle 1,2 1 Medicine Department, Veterans Affairs Sierra Nevada Healthcare System, Reno, NV 89502, USA; [email protected] 2 School of Medicine, University of Nevada, Reno, NV 89502, USA; [email protected] 3 Sound Physicians, Lutheran Hospital, Fort Wayne, IN 46804, USA; [email protected] * Correspondence: [email protected] Abstract: Thiamine deficiency (TD) in non-alcoholic hospitalized patients causes a variety of non- specific symptoms. Studies suggest it is not rare in acutely and chronically ill individuals in high income countries and is underdiagnosed. Our aim is to demonstrate data which help define the risk factors and constellation of symptoms of TD in this population. We describe 36 cases of TD in hospitalized non-alcoholic veterans over 5 years. Clinical and laboratory data were extracted by chart review +/− 4 weeks of plasma thiamine level 7 nmol/L or less. Ninety-seven percent had two or more chronic inflammatory conditions (CICs) and 83% had one or more acute inflammatory conditions (AICs). Of possible etiologies of TD 97% had two or more of: insufficient intake, inflammatory stress, or increased losses. Seventy-five percent experienced 5% or more weight loss. Ninety-two percent had symptoms with the most common being weakness or falling (75%) followed by neuropsychiatric Citation: Mates, E.; Alluri, D.; Artis, manifestations (72%), gastrointestinal dysfunction (53%), and ataxia (42%). We conclude that TD is T.; Riddle, M.S.
[Show full text]
Micronutrient Malnutrition – Detection, Measurement and Intervention: a Training Package for Field Staff Handouts for Group Tr
Micronutrient Malnutrition – Detection, Measurement and Intervention: A Training Package for Field Staff Compiled by the Institute of Child Health Handouts for Group Training For UNHCR Version 1 2003 ICH/UNHCR Handout Contents Section 1: Section 2: Section 3: Important Micronutrient Detection Nutrition Concepts Deficiency Diseases and Prevention 1. Food and Nutrition 1. Anaemia 1. Detection of Deficiencies 2. Nutritional Requirements 2. Vitamin A Deficiency 2. Intervention 3. Nutritional Deficiencies 3. Iodine Deficiency Disorders 4. Micronutrient Deficiency Disease 4. Beriberi 5. Nutritional Assessments 5. Ariboflavinosis 6. Causes of Malnutrition 6. Pellagra 7. Scurvy 8. Rickets ICH/UNHCR Handout 2 Section 1 Food and Nutrition • All people and animals need food to live, grow and be healthy. • Food contains different types of nutrients. • Food contains certain nutrients called macronutrients: – Fat – Carbohydrate – Protein • Food also contains nutrients called micronutrients: – Vitamins – Minerals • A good diet is made up of foods that contain all these types of nutrients – macronutrients and micronutrients. ICH/UNHCR Handout 3 Section 1 Nutritional Requirements For people to be healthy and productive they need a certain amount of nutrients. This is called their nutritional requirement. • The amount of energy that people get from their food is measured in kilo calories (kcal). • The average person needs about 2100 kcal each day • 17-20 % of this energy should come from fat • At least 10 % of this energy should come from protein • People also need certain amounts of vitamins and minerals • For example the average person should have at least 12 mg of the B vitamin niacin, 28 mg of vitamin C, and 22 mg of iron each day.
[Show full text]
Infantile Thiamine Deficiency: New Insights Into an Old Disease
R E V I E W A R T I C L E Infantile Thiamine Deficiency: New Insights into an Old Disease MUDASIR NAZIR1, ROUMISSA LONE2 AND BASHIR A HMAD CHAROO3 From Departments of Pediatrics; 1Shri Mata Vaishno Devi Narayana Hospital, Kakryal; 2Government Medical College Jammu, and 3Sher-I-Kashmir Institute of Medical Sciences Hospital, Srinagar; Jammu & Kashmir, India. Correspondence to: Dr Mudasir Nazir, Department of Pediatrics and Neonatology, Shri Mata Vaishno Devi Narayana Hospital, Kakryal, Jammu, Jammu & Kashmir 182 320, India. [email protected]. Context: The wide spectrum of clinical presentation in infantile thiamine deficiency is difficult to recognize, and the diagnosis is frequently missed due to the lack of widespread awareness, and non-availability of costly and technically demanding investigations. Evidence acquisition: The topic was searched by two independent researchers using online databases of Google scholar and PubMed. We considered the related studies published in the last 20 years. The terms used for the search were ‘thiamine’, ‘thiamine deficiency’, ‘beri- beri’, ‘B-vitamins’,‘micronutrients’, ‘malnutrition’, ‘infant mortality’. ‘Wernicke’s syndrome’,‘Wernicke’s encephalopathy’, and ‘lactic acidosis’. Results: In the absence of specific diagnostic tests, a low threshold for a therapeutic thiamine challenge is currently the best approach to diagnose infantile thiamine deficiency in severe acute conditions. The practical approach is to consider thiamine injection as a complementary resuscitation tool in infants with severe acute conditions; more so in presence of underlying risk factors, clinically evident malnutrition or where a dextrose-based fluid is used for resuscitation. Further, as persistent subclinical thiamine deficiency during infancy can have long-term neuro-developmental effects, reasonable strategy is to treat pregnant women suspected of having the deficiency, and to supplement thiamine in both mother and the baby during breastfeeding.
[Show full text]
Nutrition Journal of Parenteral and Enteral
Journal of Parenteral and Enteral Nutrition http://pen.sagepub.com/ Micronutrient Supplementation in Adult Nutrition Therapy: Practical Considerations Krishnan Sriram and Vassyl A. Lonchyna JPEN J Parenter Enteral Nutr 2009 33: 548 originally published online 19 May 2009 DOI: 10.1177/0148607108328470 The online version of this article can be found at: http://pen.sagepub.com/content/33/5/548 Published by: http://www.sagepublications.com On behalf of: The American Society for Parenteral & Enteral Nutrition Additional services and information for Journal of Parenteral and Enteral Nutrition can be found at: Email Alerts: http://pen.sagepub.com/cgi/alerts Subscriptions: http://pen.sagepub.com/subscriptions Reprints: http://www.sagepub.com/journalsReprints.nav Permissions: http://www.sagepub.com/journalsPermissions.nav >> Version of Record - Aug 27, 2009 OnlineFirst Version of Record - May 19, 2009 What is This? Downloaded from pen.sagepub.com by Karrie Derenski on April 1, 2013 Review Journal of Parenteral and Enteral Nutrition Volume 33 Number 5 September/October 2009 548-562 Micronutrient Supplementation in © 2009 American Society for Parenteral and Enteral Nutrition 10.1177/0148607108328470 Adult Nutrition Therapy: http://jpen.sagepub.com hosted at Practical Considerations http://online.sagepub.com Krishnan Sriram, MD, FRCS(C) FACS1; and Vassyl A. Lonchyna, MD, FACS2 Financial disclosure: none declared. Preexisting micronutrient (vitamins and trace elements) defi- for selenium (Se) and zinc (Zn). In practice, a multivitamin ciencies are often present in hospitalized patients. Deficiencies preparation and a multiple trace element admixture (containing occur due to inadequate or inappropriate administration, Zn, Se, copper, chromium, and manganese) are added to par- increased or altered requirements, and increased losses, affect- enteral nutrition formulations.
[Show full text]
From Vitamin a to Zinc: Addressing Micronutrient Malnutrition 3
CHAPTER 3 3 From Vitamin A to Zinc: Addressing Micronutrient Malnutrition USAID's SPRING Project Micronutrients, or vitamins and minerals needed in small quantities, are Attention to Micronutrients in USAID’s Early Years essential for good nutrition, proper growth and development, and overall (1967-1975) 8 health. Their deficiency contributes to extensive health problems and death throughout low-income countries, afecting millions of people globally each An early set of initiatives USAID undertook at the start of nutrition 9 year. The negative impacts of these deficiencies, however, are not easily programming in the late 1960s and into the 1970s, in collaboration with perceived because clinical signs appear only under extreme situations. The USDA, was developing and testing low-cost food fortification technology term “hidden hunger” is ofen used to characterize the dificulty in timely options. Trials included tea with vitamin A in Pakistan, wheat with vitamin 10 detection of the consequences of micronutrient deficiencies. A in Bangladesh and with iron in Egypt, monosodium glutamate (MSG) with vitamin A in Indonesia, and salt with iodine in Pakistan.12 A USAID For decades, USAID has been a leader in addressing micronutrient nutrition program in India in the 1960s supported fortifying wheat bread and deficiencies, primarily through the targeted distribution of micronutrient atta (whole wheat meal used to make chapatis, the flatbread staple) with supplements, food fortification and social and behavior change. Since the multiple micronutrients and lysine (an essential amino acid to boost protein 1960s, three micronutrients—vitamin A, iron and iodine—have been the focus quality). The program also experimented with fortifying salt with iron of USAID support because they are most ofen deficient; they also profoundly and iodine (called double fortified salt).
[Show full text]