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Malnutrition

The document discusses malnutrition, its causes, and prevention strategies, highlighting issues like undernutrition and obesity. It covers various deficiencies, including protein-energy malnutrition and micronutrient deficiencies, and the respective health consequences. Preventive measures are emphasized, including nutrition education, dietary changes, and community-level interventions to address malnutrition's prevalence and effects.

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Dr. Dalia El-Shafei Assoc. prof., Community Medicine Department, Zagazig University http://www.slideshare.net/daliaelshafei
MALNUTRITION
MALNUTRITION • Poor nutrition due to an insufficient, poorly balanced diet, faulty digestion or poor utilization of foods. (This can result in the inability to absorb foods). • Not only insufficient intake of nutrients. It can occur when an individual is getting excessive nutrients as well.
WHO IS AFFECTED BY MALNUTRITION? Individuals who are dependent on others for their nourishment (infants, children, the elderly, prisoners….etc) Mentally disabled or ill because they are not aware of what to eat. People who are suffering from TB, eating disorders, HIV/AIDS, cancer, or who have undergone surgical procedures “interferences with appetite or food uptake”.
UNDERNUTRITION
CAUSES OF MALNUTRITION • Deficient in energy and /or protein (Kwashiorkor, marasmus) • Deficiency in one or more mineral/ vitamin (e.g. vitamin A, iodine, iron, zinc, calcium, vitamin D) 1ry causes: "Lack of food” • Alteration of normal metabolism (during infection / fever, HIV/AIDS) • Prevention of nutrient absorption (diarrheal infections) • Diversion of nutrients to parasitic agents (hookworms, tapeworms, schistosome worm, Malaria). 2ry causes:
MOST IMPORTANT CAUSES OF MALNUTRITION Poor dietary habits Metabolic abnormalities Improper &or Inadequate food intake Inadequate food absorption Emotional factors Deficient food supply Food faddism Diseases
PREVENTION OF MALNUTRITION • Nutrition education: requirements & values of different kinds of food and needs of individuals. • Promotion of breast feeding Action at the family level • Socioeconomic development • Survey study of malnutrition problem's prevalence. • Study food habits, nutritional knowledge of population to prepare health education programs. • Sanitary environment & improving health conditions. • Prevention & control of infectious diseases. • Supplementation & fortification of foods. Action on community level • Increasing agricultural production & animal husbandry. • Supplementary feeding programs for preschool and school children. • Prevention of nutritional deficiency disease by providing nutritive elements to pregnant &lactating women. • Nutrition intervention programs.as immunization, environment sanitation family planning and management of infectious and parasitic diseases. • Nutritional surveys & early detection of cases of malnutrition. • Fortification of bread with iron, table salt with iodine (most prevalent deficient elements in all population). Action on the national level
TYPES OF UNDER-NUTRITION DISORDERS Protein Energy Malnutrition (PEM or PCM) • Kwashiorkor • Marasmus Micronutrient deficiencies • Vit D & Calcium deficiency • Rickets • Osteomalacia • Osteoporosis • Iron deficiency anemia • Folate deficiency • Pernicious anemia (B12-Folate deficiency Anemia) • Vitamin A • Bribery (Vit.B1 deficiency) • Pellagra (Vit.B3 deficiency) • Scurvy (Vit.C deficiency) • Iodine Deficiency • Zinc Deficiency • Dental caries
Kwashiorkor Marasmus Causes Deficiency in protein with excess carbohydrates. Increased calories more than required. Deficiency in caloric requirement, protein & all other nutrients Age affected 1-4 years Infants 6-8 months C/P Muscle wasting, oedema ‘moon face’ & overweight. Mental retardation, skin lacerations & hair changes. Hypoglycemia & hypoalbuminaemia. Severe muscle wasting (skin over bone), senile look, underweight. No mental changes, flag skin, dry & lusterless hair. Normal sugar & albumin Prognosis Bad (can lead to coma & death) Good Prevention - Health education about breast feeding & proper weaning. - Growth monitoring for early detection. - Nutrition supplements & rehydration.
Prevalence is 25% in developing countries. Affecting children between 6-24 months. Vit.D Deficiency negatively affects absorption, utilization & deposition of Ca & P in bones. Defective calcification of osteoid & epiphyseal cartilage of growing bones Also, it negatively affects the immunity
CONTRIBUTING FACTORS: Lack of sun exposure & excessive wrapping of infants, especially in winter. Cloudy sky, dusty or foggy weather, Suspended dust in air interferes with penetrating power of UV rays. Chronic malnutrition, especially PEM. Recurrent gastroenteritis, prematurity & LBW. Nutrition ignorance of the mother & non supplementation of infant’s diet with vit.D. Low standard of living, poor housing & bad sanitation Repeated unspaced pregnancy, poor supplementation during pregnancy with Ca & vit.D.
CLINICAL PICTURE Skeletal manifestations • Craniotabes (softening of skull bones, bossing of parietal & frontal bones, delayed closure of anterior fontanel)& delayed teeth eruption. • Enlarged metaphyseal ends of long bones (wrists & ankles). • Deformities of long bones & pelvis. • Chest: rachitic beads of ribs (rickety rosary), pigeon chest & Harrison’s sulcus. Other manifestations • Hypotonia • Tetany & Convulsions “impaired Ca absorption” • Chest infections (due to chest deformity & suppression of immunity)
PREVENTION Good housing & sanitary environment. Health education of mothers highlighting importance of exposing the infant to sunlight daily & increase inter- pregnancy spacing Specific measures • Vita. D “powdered milk or drug”: • Oral drops 400 IU daily. • IM 200,000 IU every 6 months under medical supervision “risk of hypervitaminosis D” (illiterate mothers or far from health service).
CONTROL Early case finding by growth monitoring. TTT of cases with vitamin D (oral or IM), Ca supplement • Health education of the mother for importance of daily exposure to the sun rays.
Osteomalacia Osteoporosis Def. Bone Softening "bone replaced by soft osteoid tissue". Bone Atrophy "significant reduction of bone density & mass more than 2.5 SD " Path. Vit. D or Ca++ & Ph---deficiency → failure to replace bone turnover → demineralized soft osteoid tissue. Bone mass starts to decline after age 40 ys. due to resorption > formation → too little bone but with normal mineral content. RF • Young women with repeated pregnancy. • Indoor living conditions. • Diet deficient in Ca++, Ph--- • Malabsorption & chronic renal failure. • Post menopasual women & Elderly. • Insufficient intake “Ca++, Ph---, vit.D” • Smoking, alcoholism • Sedentary life • Delayed puberty, hypogonadism • Endocrinal diseases as Cushing's syndrome • Drugs “corticosteroids, cytotoxic drugs”. • Malignancy (lymphoma), CRF • Low body weight.
Osteomalacia Osteoporosis C/P • Bone-ache, tenderness • Uneven gait due to muscular weakness • May be a symptomatic • Persistent backache due to progressive compression & collapse of vertebrae • Kyphosis, hip fracture. TTT Ca++ &vit.D supplementation. Early cases: Ca++, vit.D supplementation Late cases: antiresorptive drugs.
IRON DEFICIENCY ANEMIA
• Microcytic, hypochromic anemia. • Decreased HG concentration than standards. • Most prevalent single deficiency state on a worldwide basis. • Important economically “diminishes the capability of individuals to perform physical labor, growth and learning capacity in children”
CAUSES: Decreased intake of animal proteins Bad dietary habits (intake of tea after meals) Parasitic infections Inadequate dietary intake especially when requirements are high “pregnancy, rapid growth”. Impaired iron absorption “low vit C intake, gastric Hypoacidity, iron Precipitation by oxalates & phosphates”. Chronic blood loss.
DIAGNOSIS: C/P Pale skin, loss of appetite & apathy Fatigue ↓ Attention, learning ability, work performance & immune status Dry brittle nails which later become flat & spoon shaped. Haemic murmurs Blood picture Low HG>11gm./dL.(different cut- off(s) in different ages) Decreased RBCs. Small color index 0.5-0.7
PREVENTION & CONTROL: Adequate dietary intake. Dietary supplementation “dry milk & bread” Prevention & control of parasitic diseases & pathological conditions associated with blood loss. Early detection by lab testing.
(B12-Folate deficiency Anemia) PERNICIOUS ANEMIA
MACROCYTIC MEGALOBLASTIC ANEMIA Deficiency of vitamin B12 & Folic acid arrests the development of erythrocytes in the bone marrow at the stage of megaloblasts.
AT RISK GROUPS: Pregnant & lactating women “↑ demand” Vegetarians “diet lacks vit B12” Gastrectomy “lacking of intrinsic factor needed for absorption of B12” Diphyllobothrium latum infestation “consumes B12” Malabsorption syndrome Medications that treat DM, acid reflux & peptic ulcers
CLINICAL PICTURE: GIT, NS, and CVS. CVS: Chest pain or heart palpitations CNS: Confusion, memory loss, Depression or dementia GIT: Constipation, Pale skin or jaundice, poor appetite, sore mouth & tongue and weight loss. Developmental delays & failure to thrive. Fatigue or weakness Numbness or coldness of hands & feet.
PREVENTION: Balanced diet with considerable intake of animal food. B12 & Folic acid Supplementation “pregnant, lactating women & vegetarians”. Atrophic gastric mucosa or who had gastrectomy should be given intrinsic factor.
FOLATE DEFICIENCY
C/p: If deficiency during pregnancy Regulates the nerve cells of the embryonic development. Neural tube defect & Spina bifida Anencephaly LBW Preterm delivery Anemia
PREVENTION: ↑ Consumption of Liver, Kidney, Fish, Green leafy vegetables&Beans. Folic acid supplementation if needed.
VITAMIN A DEFICIENCY
Most important cause of blindness in developing countries.
MANIFESTATIONS: Delayed growth ↓ Iron utilization Follicular keratosis of the skin ↑ Susceptibility to respiratory & urinary tract infections (anti- infection vit.). Night blindness: nyctalopia or day sight. Conjunctival xerosis “affection of the lacrimal gland” Bitot spots in the cornea Xerophthalmia, Corneal ulceration and keratomalacia Blindness
PREVENTION : Nutritional education M.C.H. Services • Mothers after labor (200 000IU) • Infants as drops at 9th month (100 000IU) & another dose at 18th month (200 000IU) Fortification of foods with vitamin A • Margarines • vegetable oils • Dried skimmed milk
Thiamine (vitamin B1) deficiency “BERIBERI”
Common in South East Asia where many diets consist solely of white rice. Affects nervous & circulatory system C/P: muscle wasting & nerve damage. Prevention: foods such as pork, beef and whole grain (unrefined) breads and grains.
Niacin or Vit B3 (or Tryptophan) Deficiency PELLAGRA “ROUGH SKIN"
 Prevention: Broccoli, Eggs, Dates, Beef, Salmon, Seeds & Peanuts.
Vitamin C deficiency “SCURVY”
 In bottle fed infants, pregnant, elderly, workers in desert who consumed canned food.  C/P: General weakness Muscle & joint pain Swelling of gums Bleeding Blepharitis Anemia “↓ iron absorption” Stomatitis, Gingivitis Impaired healing of wounds. Hge under skin & joints provoked by slight trauma
PREVENTION: ↑ Intake of fresh vegetables & fruits. (vit.C is heat labile, easily oxidized & destroyed by storage) Nutrition education Supplying infant during weaning by orange & tomato juice Dietary supplementation by food rich in vit C for the high-risk groups in camps or isolated communities
IODINE DEFICIENCY
Most important cause of preventable brain damage & mental retardation in babies. Lower IQ by 10-15%. Deficiency gives hypothyroidosis & goitre. Stillbirth & miscarriage. Cretinism: mental retardation, stunted, hypothyroidism, deaf-mutism. Prevention: Iodising salt, Sea fish, sea plants (vegetables grown on iodized soil).
DENTAL CARIES
Def in Ca, ph, vitamin D, and fluorine. Ingestion of carbohydrates, sugars, & soft drinks with neglecting oral hygiene.
ZINC DEFICIENCY
 C/P: Growth retardation & increased susceptibility to infections especially skin & eye lesions.  Prevention: Consumption of foods as: Whole-grain cereals, Legumes, Meat, Chicken and fish.
Obesity “OVERNUTRITION”
Definition: it is excess adipose tissue in different parts in the body due to excess storage of fat. The ability to store fat is unlimited but if the amount of fat to be stored exceeds the ability of the fat cells to expand (50 times its size), the body forms new adipose cells. With weight loss, fat cells decrease in size but NOT in number. Once a fat cell formed, it exists for life.
ETIOLOGY (OF SIMPLE OBESITY): Imbalance between energy intake & energy expenditure for long periods of time.
Obesity RF Non-modifiable Biological Genetics Age Sex Modifiable Behavioral Diet Physical inactivity Psychological & emotional disorders Environmental Family Work Advanced technology Foods advertisements
A. Biological factors (Non-modifiable): 1. Genetics: Brown adipose tissue (BAT): interscapular adipose tissue and along the aorta. Thin persons have more brown adipose tissue, so that fat oxidized more than stored.
Leptin “satiety factor” It is a hormone secreted from adipocytes with central control from hypothalamus. Suppress appetite, deplete fat stores & ↑ energy expenditure. In obesity there is a state of leptin resistance at cell level with hyperleptinaemia → complications as CVDs.
Gremlin hormone Hormone produced in the stomach. Its secretion stimulated by adrenaline & nor-adrenaline which are released in response to hypoglycemia where it promotes the appetite.
2. Age: Obesity may appear at any age but obesity in childhood is predictive to obesity later on adulthood. 3. Sex: Both sexes are exposed. Pregnancy causes ↑ in mother weight by 4-6 pounds over her pre-pregnancy weight. Menopause represents a risk period for extra weight gain and redistribution of fat towards visceral regions.
B. Behavioral factors (modifiable factors): Diet: Eat more than need in Quality & Quantity: ↑Sweets, fats, snacks & soft drinks . Nibbling in between meals. Evening overeating. Physical inactivity: Sedentary occupations, preferring indoor life & with least activity. Psychological & emotional disorders: Anxiety, Stress & Depressive illness “emotional relieve”.
C. Environmental factors (modifiable factors): Family lifestyle & feeding pattern Work problems & unemployment Advanced technology Foods advertisements
ASSESSMENT OF OBESITY
Assessment of obesity Qualitative Pear-shaped obesity (Gynacoid). Apple-shaped obesity (Android) Quantitative Body mass index (BMI) Skinfold thickness Relative (RW) Waist/hip ratio (WHR) Arm Fat Area (AFA) Hydrostatic water weighing (densitometry)
A. QUALITATIVE ASSESSMENT: Fat distribution in the body which is of morbid significance: Pear-shaped obesity (gynacoid) Females “fat in hips & thighs”. Apple-shaped obesity (android) Males “fat around waist & abdomen”.
B. QUANTITATIVE ASSESSMENT: 1. BMI is not a sensitive index (BMI > 30)
2. Skinfold thickness.
3. Relative weight: (RW=body weight "kg"/desirable body weight "kg" x 100) • RW is supposed to be 100%. • Desirable body weight for each height is obtained from special tables. • RW > 120% is considered obesity.
4. Waist/hip ratio (WHR): if > 85%: android obesity “more health hazards as cardiovascular problems”. If <85% : gynacoid obesity.
5. Arm Fat Area (AFA): It is a measure of total body fat (fat weight) and calculated from mid-arm circumference and triceps skin fold thickness by certain equation as : AFA = Arm area - Arm muscle area.
6. Hydrostatic water weighing (densitometry): It is comparing of body weight on standard scale with the weight underwater. By assuming that adipose tissue is less dense than lean tissue (muscles & bones), so the more adipose tissue in a body, the less its underwater weight (the more it tends to float). It is an accurate method for estimating the total body fat.
Management of obesity
Management of obesity Lifestyle modification Diet Physical activity Behavioral modification Medications Surgery
I) Lifestyle modification: Diet: decreasing caloric intake by about 500 Kcal./day to achieve a weight loss of 450 gm/week. Because of the way the body uses fuel from carbohydrates, fats and protein, a more rapid weight loss will compel the body to use protein (muscles) instead of fat for energy. This will decrease muscle mass with each dieting attempt and fat percentage will increase. Other principles of healthy eating relevant to weight loss: Eat plenty of food rich in starch and fibers. Eat plenty of fruits and vegetables. Avoid eating too much fat and sugars. Not skip meals “suppress metabolism”.
2. Physical activity:  Walking or swimming are safe exercise for all persons.  Those who are bed ridden or are in wheel-chairs can use upper arm exercises.  Aerobic exercises require more air & tend to use the highest % of body fat for fuel. ↓ body fat while helping to preserve muscles tissue tone. Manage mental stress. ↑ energy levels Control of appetite Improve blood sugar control in diabetes. ↓ Blood pressure. ↑Amounts of HDL-C. Improve bone density where weight-bearing exercises can slow down bone loss after menopause or even ↑ bone density.
3. Behavioral modification: By focusing on small, gradual behavioral changes, the individual learns to gain control on eating behaviors with the goal of permanent changes in eating habits. Some basic strategies can be useful in promoting behavior changes for sustained weight loss include: Self-monitoring Behavioral contracting Stimulus control (precedes eating) Cognitive restructuring Stress management Social support Physical activity Relapse prevention
II) Medications: • Control obesity “appetite suppression or prevention of fat absorption”. • Supplementation of vitamins & minerals • Management of obesity complications.
III) Surgery: It is used in cases of morbid obesity (BMI > 40) or in cases of failure of other methods to control of obesity.
Complications of obesity
Cardiovascular “Main cause of death in obese” • Coronary heart disease: Hyper-insulinaemia (insulin resistance)& Hypertriglyceridemia (dyslipidemia). • Hypertension ↑ renal sodium retention & catecholamines release. Diabetes mellitus • Insulin resistance syndrome: due to defect in the insulin receptors at the cell level leading to inability of the body cells to utilize blood sugar to give the needed energy Other complications • Musculoskeletal disorders, gout, • Cancer (colon, breast) • Gall stones, hernias & Menstrual irregularities
Malnutrition

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Malnutrition

  • 1.
    Dr. Dalia El-Shafei Assoc.prof., Community Medicine Department, Zagazig University http://www.slideshare.net/daliaelshafei
  • 2.
  • 3.
    MALNUTRITION • Poor nutritiondue to an insufficient, poorly balanced diet, faulty digestion or poor utilization of foods. (This can result in the inability to absorb foods). • Not only insufficient intake of nutrients. It can occur when an individual is getting excessive nutrients as well.
  • 5.
    WHO IS AFFECTEDBY MALNUTRITION? Individuals who are dependent on others for their nourishment (infants, children, the elderly, prisoners….etc) Mentally disabled or ill because they are not aware of what to eat. People who are suffering from TB, eating disorders, HIV/AIDS, cancer, or who have undergone surgical procedures “interferences with appetite or food uptake”.
  • 6.
  • 7.
    CAUSES OF MALNUTRITION •Deficient in energy and /or protein (Kwashiorkor, marasmus) • Deficiency in one or more mineral/ vitamin (e.g. vitamin A, iodine, iron, zinc, calcium, vitamin D) 1ry causes: "Lack of food” • Alteration of normal metabolism (during infection / fever, HIV/AIDS) • Prevention of nutrient absorption (diarrheal infections) • Diversion of nutrients to parasitic agents (hookworms, tapeworms, schistosome worm, Malaria). 2ry causes:
  • 8.
    MOST IMPORTANT CAUSESOF MALNUTRITION Poor dietary habits Metabolic abnormalities Improper &or Inadequate food intake Inadequate food absorption Emotional factors Deficient food supply Food faddism Diseases
  • 12.
    PREVENTION OF MALNUTRITION •Nutrition education: requirements & values of different kinds of food and needs of individuals. • Promotion of breast feeding Action at the family level • Socioeconomic development • Survey study of malnutrition problem's prevalence. • Study food habits, nutritional knowledge of population to prepare health education programs. • Sanitary environment & improving health conditions. • Prevention & control of infectious diseases. • Supplementation & fortification of foods. Action on community level • Increasing agricultural production & animal husbandry. • Supplementary feeding programs for preschool and school children. • Prevention of nutritional deficiency disease by providing nutritive elements to pregnant &lactating women. • Nutrition intervention programs.as immunization, environment sanitation family planning and management of infectious and parasitic diseases. • Nutritional surveys & early detection of cases of malnutrition. • Fortification of bread with iron, table salt with iodine (most prevalent deficient elements in all population). Action on the national level
  • 13.
    TYPES OF UNDER-NUTRITIONDISORDERS Protein Energy Malnutrition (PEM or PCM) • Kwashiorkor • Marasmus Micronutrient deficiencies • Vit D & Calcium deficiency • Rickets • Osteomalacia • Osteoporosis • Iron deficiency anemia • Folate deficiency • Pernicious anemia (B12-Folate deficiency Anemia) • Vitamin A • Bribery (Vit.B1 deficiency) • Pellagra (Vit.B3 deficiency) • Scurvy (Vit.C deficiency) • Iodine Deficiency • Zinc Deficiency • Dental caries
  • 17.
    Kwashiorkor Marasmus Causes Deficiencyin protein with excess carbohydrates. Increased calories more than required. Deficiency in caloric requirement, protein & all other nutrients Age affected 1-4 years Infants 6-8 months C/P Muscle wasting, oedema ‘moon face’ & overweight. Mental retardation, skin lacerations & hair changes. Hypoglycemia & hypoalbuminaemia. Severe muscle wasting (skin over bone), senile look, underweight. No mental changes, flag skin, dry & lusterless hair. Normal sugar & albumin Prognosis Bad (can lead to coma & death) Good Prevention - Health education about breast feeding & proper weaning. - Growth monitoring for early detection. - Nutrition supplements & rehydration.
  • 29.
    Prevalence is 25%in developing countries. Affecting children between 6-24 months. Vit.D Deficiency negatively affects absorption, utilization & deposition of Ca & P in bones. Defective calcification of osteoid & epiphyseal cartilage of growing bones Also, it negatively affects the immunity
  • 30.
    CONTRIBUTING FACTORS: Lack ofsun exposure & excessive wrapping of infants, especially in winter. Cloudy sky, dusty or foggy weather, Suspended dust in air interferes with penetrating power of UV rays. Chronic malnutrition, especially PEM. Recurrent gastroenteritis, prematurity & LBW. Nutrition ignorance of the mother & non supplementation of infant’s diet with vit.D. Low standard of living, poor housing & bad sanitation Repeated unspaced pregnancy, poor supplementation during pregnancy with Ca & vit.D.
  • 31.
    CLINICAL PICTURE Skeletal manifestations • Craniotabes(softening of skull bones, bossing of parietal & frontal bones, delayed closure of anterior fontanel)& delayed teeth eruption. • Enlarged metaphyseal ends of long bones (wrists & ankles). • Deformities of long bones & pelvis. • Chest: rachitic beads of ribs (rickety rosary), pigeon chest & Harrison’s sulcus. Other manifestations • Hypotonia • Tetany & Convulsions “impaired Ca absorption” • Chest infections (due to chest deformity & suppression of immunity)
  • 33.
    PREVENTION Good housing & sanitary environment. Healtheducation of mothers highlighting importance of exposing the infant to sunlight daily & increase inter- pregnancy spacing Specific measures • Vita. D “powdered milk or drug”: • Oral drops 400 IU daily. • IM 200,000 IU every 6 months under medical supervision “risk of hypervitaminosis D” (illiterate mothers or far from health service).
  • 34.
    CONTROL Early case finding by growth monitoring. TTTof cases with vitamin D (oral or IM), Ca supplement • Health education of the mother for importance of daily exposure to the sun rays.
  • 37.
    Osteomalacia Osteoporosis Def. BoneSoftening "bone replaced by soft osteoid tissue". Bone Atrophy "significant reduction of bone density & mass more than 2.5 SD " Path. Vit. D or Ca++ & Ph---deficiency → failure to replace bone turnover → demineralized soft osteoid tissue. Bone mass starts to decline after age 40 ys. due to resorption > formation → too little bone but with normal mineral content. RF • Young women with repeated pregnancy. • Indoor living conditions. • Diet deficient in Ca++, Ph--- • Malabsorption & chronic renal failure. • Post menopasual women & Elderly. • Insufficient intake “Ca++, Ph---, vit.D” • Smoking, alcoholism • Sedentary life • Delayed puberty, hypogonadism • Endocrinal diseases as Cushing's syndrome • Drugs “corticosteroids, cytotoxic drugs”. • Malignancy (lymphoma), CRF • Low body weight.
  • 38.
    Osteomalacia Osteoporosis C/P •Bone-ache, tenderness • Uneven gait due to muscular weakness • May be a symptomatic • Persistent backache due to progressive compression & collapse of vertebrae • Kyphosis, hip fracture. TTT Ca++ &vit.D supplementation. Early cases: Ca++, vit.D supplementation Late cases: antiresorptive drugs.
  • 40.
  • 41.
    • Microcytic, hypochromicanemia. • Decreased HG concentration than standards. • Most prevalent single deficiency state on a worldwide basis. • Important economically “diminishes the capability of individuals to perform physical labor, growth and learning capacity in children”
  • 42.
    CAUSES: Decreased intake ofanimal proteins Bad dietary habits (intake of tea after meals) Parasitic infections Inadequate dietary intake especially when requirements are high “pregnancy, rapid growth”. Impaired iron absorption “low vit C intake, gastric Hypoacidity, iron Precipitation by oxalates & phosphates”. Chronic blood loss.
  • 44.
    DIAGNOSIS: C/P Pale skin, lossof appetite & apathy Fatigue ↓ Attention, learning ability, work performance & immune status Dry brittle nails which later become flat & spoon shaped. Haemic murmurs Blood picture Low HG>11gm./dL.(different cut- off(s) in different ages) Decreased RBCs. Small color index 0.5-0.7
  • 46.
    PREVENTION & CONTROL: Adequatedietary intake. Dietary supplementation “dry milk & bread” Prevention & control of parasitic diseases & pathological conditions associated with blood loss. Early detection by lab testing.
  • 47.
  • 49.
    MACROCYTIC MEGALOBLASTIC ANEMIA Deficiencyof vitamin B12 & Folic acid arrests the development of erythrocytes in the bone marrow at the stage of megaloblasts.
  • 50.
    AT RISK GROUPS: Pregnant& lactating women “↑ demand” Vegetarians “diet lacks vit B12” Gastrectomy “lacking of intrinsic factor needed for absorption of B12” Diphyllobothrium latum infestation “consumes B12” Malabsorption syndrome Medications that treat DM, acid reflux & peptic ulcers
  • 51.
    CLINICAL PICTURE: GIT, NS,and CVS. CVS: Chest pain or heart palpitations CNS: Confusion, memory loss, Depression or dementia GIT: Constipation, Pale skin or jaundice, poor appetite, sore mouth & tongue and weight loss. Developmental delays & failure to thrive. Fatigue or weakness Numbness or coldness of hands & feet.
  • 53.
    PREVENTION: Balanced diet with considerable intake ofanimal food. B12 & Folic acid Supplementation “pregnant, lactating women & vegetarians”. Atrophic gastric mucosa or who had gastrectomy should be given intrinsic factor.
  • 54.
  • 55.
    C/p: If deficiencyduring pregnancy Regulates the nerve cells of the embryonic development. Neural tube defect & Spina bifida Anencephaly LBW Preterm delivery Anemia
  • 57.
  • 58.
  • 59.
    Most important causeof blindness in developing countries.
  • 61.
    MANIFESTATIONS: Delayed growth ↓Iron utilization Follicular keratosis of the skin ↑ Susceptibility to respiratory & urinary tract infections (anti- infection vit.). Night blindness: nyctalopia or day sight. Conjunctival xerosis “affection of the lacrimal gland” Bitot spots in the cornea Xerophthalmia, Corneal ulceration and keratomalacia Blindness
  • 63.
    PREVENTION : Nutritional education M.C.H. Services •Mothers after labor (200 000IU) • Infants as drops at 9th month (100 000IU) & another dose at 18th month (200 000IU) Fortification of foods with vitamin A • Margarines • vegetable oils • Dried skimmed milk
  • 64.
  • 65.
    Common in South EastAsia where many diets consist solely of white rice. Affects nervous & circulatory system C/P: muscle wasting & nerve damage. Prevention: foods such as pork, beef and whole grain (unrefined) breads and grains.
  • 67.
    Niacin or VitB3 (or Tryptophan) Deficiency PELLAGRA “ROUGH SKIN"
  • 69.
     Prevention: Broccoli, Eggs,Dates, Beef, Salmon, Seeds & Peanuts.
  • 70.
  • 71.
     In bottlefed infants, pregnant, elderly, workers in desert who consumed canned food.  C/P: General weakness Muscle & joint pain Swelling of gums Bleeding Blepharitis Anemia “↓ iron absorption” Stomatitis, Gingivitis Impaired healing of wounds. Hge under skin & joints provoked by slight trauma
  • 73.
    PREVENTION: ↑ Intake of fresh vegetables& fruits. (vit.C is heat labile, easily oxidized & destroyed by storage) Nutrition education Supplying infant during weaning by orange & tomato juice Dietary supplementation by food rich in vit C for the high-risk groups in camps or isolated communities
  • 74.
  • 77.
    Most important causeof preventable brain damage & mental retardation in babies. Lower IQ by 10-15%. Deficiency gives hypothyroidosis & goitre. Stillbirth & miscarriage. Cretinism: mental retardation, stunted, hypothyroidism, deaf-mutism. Prevention: Iodising salt, Sea fish, sea plants (vegetables grown on iodized soil).
  • 79.
  • 80.
    Def in Ca,ph, vitamin D, and fluorine. Ingestion of carbohydrates, sugars, & soft drinks with neglecting oral hygiene.
  • 81.
  • 82.
     C/P: Growthretardation & increased susceptibility to infections especially skin & eye lesions.  Prevention: Consumption of foods as: Whole-grain cereals, Legumes, Meat, Chicken and fish.
  • 83.
  • 84.
    Definition: it isexcess adipose tissue in different parts in the body due to excess storage of fat. The ability to store fat is unlimited but if the amount of fat to be stored exceeds the ability of the fat cells to expand (50 times its size), the body forms new adipose cells. With weight loss, fat cells decrease in size but NOT in number. Once a fat cell formed, it exists for life.
  • 87.
    ETIOLOGY (OF SIMPLEOBESITY): Imbalance between energy intake & energy expenditure for long periods of time.
  • 90.
    Obesity RF Non-modifiable Biological Genetics Age Sex Modifiable Behavioral Diet Physicalinactivity Psychological & emotional disorders Environmental Family Work Advanced technology Foods advertisements
  • 91.
    A. Biological factors(Non-modifiable): 1. Genetics: Brown adipose tissue (BAT): interscapular adipose tissue and along the aorta. Thin persons have more brown adipose tissue, so that fat oxidized more than stored.
  • 96.
    Leptin “satiety factor” Itis a hormone secreted from adipocytes with central control from hypothalamus. Suppress appetite, deplete fat stores & ↑ energy expenditure. In obesity there is a state of leptin resistance at cell level with hyperleptinaemia → complications as CVDs.
  • 97.
    Gremlin hormone Hormone producedin the stomach. Its secretion stimulated by adrenaline & nor-adrenaline which are released in response to hypoglycemia where it promotes the appetite.
  • 98.
    2. Age: Obesitymay appear at any age but obesity in childhood is predictive to obesity later on adulthood. 3. Sex: Both sexes are exposed. Pregnancy causes ↑ in mother weight by 4-6 pounds over her pre-pregnancy weight. Menopause represents a risk period for extra weight gain and redistribution of fat towards visceral regions.
  • 99.
    B. Behavioral factors(modifiable factors): Diet: Eat more than need in Quality & Quantity: ↑Sweets, fats, snacks & soft drinks . Nibbling in between meals. Evening overeating. Physical inactivity: Sedentary occupations, preferring indoor life & with least activity. Psychological & emotional disorders: Anxiety, Stress & Depressive illness “emotional relieve”.
  • 100.
    C. Environmental factors(modifiable factors): Family lifestyle & feeding pattern Work problems & unemployment Advanced technology Foods advertisements
  • 101.
  • 102.
    Assessment of obesity Qualitative Pear-shaped obesity (Gynacoid). Apple-shapedobesity (Android) Quantitative Body mass index (BMI) Skinfold thickness Relative (RW) Waist/hip ratio (WHR) Arm Fat Area (AFA) Hydrostatic water weighing (densitometry)
  • 103.
    A. QUALITATIVE ASSESSMENT: Fatdistribution in the body which is of morbid significance: Pear-shaped obesity (gynacoid) Females “fat in hips & thighs”. Apple-shaped obesity (android) Males “fat around waist & abdomen”.
  • 105.
    B. QUANTITATIVE ASSESSMENT: 1.BMI is not a sensitive index (BMI > 30)
  • 106.
  • 107.
    3. Relative weight: (RW=bodyweight "kg"/desirable body weight "kg" x 100) • RW is supposed to be 100%. • Desirable body weight for each height is obtained from special tables. • RW > 120% is considered obesity.
  • 108.
    4. Waist/hip ratio(WHR): if > 85%: android obesity “more health hazards as cardiovascular problems”. If <85% : gynacoid obesity.
  • 110.
    5. Arm FatArea (AFA): It is a measure of total body fat (fat weight) and calculated from mid-arm circumference and triceps skin fold thickness by certain equation as : AFA = Arm area - Arm muscle area.
  • 111.
    6. Hydrostatic waterweighing (densitometry): It is comparing of body weight on standard scale with the weight underwater. By assuming that adipose tissue is less dense than lean tissue (muscles & bones), so the more adipose tissue in a body, the less its underwater weight (the more it tends to float). It is an accurate method for estimating the total body fat.
  • 113.
  • 114.
  • 115.
    I) Lifestyle modification: Diet:decreasing caloric intake by about 500 Kcal./day to achieve a weight loss of 450 gm/week. Because of the way the body uses fuel from carbohydrates, fats and protein, a more rapid weight loss will compel the body to use protein (muscles) instead of fat for energy. This will decrease muscle mass with each dieting attempt and fat percentage will increase. Other principles of healthy eating relevant to weight loss: Eat plenty of food rich in starch and fibers. Eat plenty of fruits and vegetables. Avoid eating too much fat and sugars. Not skip meals “suppress metabolism”.
  • 116.
    2. Physical activity: Walking or swimming are safe exercise for all persons.  Those who are bed ridden or are in wheel-chairs can use upper arm exercises.  Aerobic exercises require more air & tend to use the highest % of body fat for fuel. ↓ body fat while helping to preserve muscles tissue tone. Manage mental stress. ↑ energy levels Control of appetite Improve blood sugar control in diabetes. ↓ Blood pressure. ↑Amounts of HDL-C. Improve bone density where weight-bearing exercises can slow down bone loss after menopause or even ↑ bone density.
  • 117.
    3. Behavioral modification: Byfocusing on small, gradual behavioral changes, the individual learns to gain control on eating behaviors with the goal of permanent changes in eating habits. Some basic strategies can be useful in promoting behavior changes for sustained weight loss include: Self-monitoring Behavioral contracting Stimulus control (precedes eating) Cognitive restructuring Stress management Social support Physical activity Relapse prevention
  • 118.
    II) Medications: • Controlobesity “appetite suppression or prevention of fat absorption”. • Supplementation of vitamins & minerals • Management of obesity complications.
  • 119.
    III) Surgery: It isused in cases of morbid obesity (BMI > 40) or in cases of failure of other methods to control of obesity.
  • 120.
  • 122.
    Cardiovascular “Main causeof death in obese” • Coronary heart disease: Hyper-insulinaemia (insulin resistance)& Hypertriglyceridemia (dyslipidemia). • Hypertension ↑ renal sodium retention & catecholamines release. Diabetes mellitus • Insulin resistance syndrome: due to defect in the insulin receptors at the cell level leading to inability of the body cells to utilize blood sugar to give the needed energy Other complications • Musculoskeletal disorders, gout, • Cancer (colon, breast) • Gall stones, hernias & Menstrual irregularities