Download Free Medical Deficiency Disorders PowerPoint Presentation

Deficiency Disorders PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : This medical presentation is on malnutrition (improper nutrition) and deals with over nutrition, under nutrition (PEM) and deficiencies of essential nutrients. The presentation provides information on diseases caused by the deficiency of protein, fat, carbohydrates, minerals and vitamins.

Tags : malnutrition, improper nutrition, over nutrition, under nutrition, PEM, deficiencies of essential nutrients, diseases, disease, deficiency, protein, fat, carbohydrates, minerals, vitamins

Published on : Apr 21, 2021 | Views : 5357 | Downloads : 16

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Deficiency Disorders Dr.K.V BEENA DISTRICT PROGRAMME MANAGER NRHM, Ernakulam
Slide 2-

ppt slide no 2 content not found
Slide 3-

Protein Fat Carbohydrates Minerals Vitamins Diseases caused by the deficiency of
Slide 4-

Protein Energy Malnutrition
Slide 5-

ACUTE AND CHRONIC ENERGY DEFICIENCY
Slide 6-

OVERVIEW OF PEM Protein calorie malnutrition is one of the most important public health problems in many developing countries including India, South East Asia and Africa.
Slide 7-

OVERVIEW OF PEM It is a wide spread deficiency disease among children in low socio economic group Lack of food & clean water, poor sanitation, infection & social unrest lead to LBW & PEM Malnutrition is implicated in >50% of deaths of <5 children (5 million/yr) Those who survive may suffer from impaired growth and perhaps mental retardation
Slide 8-

PRECIPITATING FACTORS LACK OF FOOD (famine, poverty) Inadequate breast feeding Wrong concepts about nutrition Diarrhoea & malabsorption INFECTIONS (worms, measles, T.B)
Slide 9-

CLASSIFICATION A. CLINICAL ( WELLCOME ) Parameter: weight for age + oedema Reference standard (50th percentile) Grades: 80-60 % without oedema is under weight 80-60% with oedema is Kwashiorkor < 60 % with oedema is Marasmus-Kwash < 60 % without oedema is Marasmus
Slide 10-

KWASHIORKOR Cecilly Williams, a paediatrician ,working in west africa had introduced the word Kwashiorkor to the medical literature in 1933. The word is described as displaced child meaning the sickness which a child develops when the next baby is born and the older one is deprived of breast milk
Slide 11-

KWASHIORKOR
Slide 12-

ppt slide no 12 content not found
Slide 13-

Definitions of Malnutrition Kwashiorkor: protein deficiency Marasmus: energy deficiency Marasmic/ Kwashiorkor: combination of chronic energy deficiency and chronic or acute protein deficiency
Slide 14-

The effect of protein deficiency in adults may show itself in the form of loss of weight, reduced subcutaneous fat Anaemia Great susceptibility to infection Frequent loose stools General lethargy Inability to do sustained hard work Delay in healing of wounds and oedema
Slide 15-

ETIOLOGY Kwashiorkor can occur in infancy but its maximal incidence is in the 2nd yr of life following abrupt weaning. Kwashiorkor is not only dietary in origin. Infective, psycho-socical, and cultural factors are also operative.
Slide 16-

CONSTANT FEATURES OF KWASHIORKAR Oedema – starts with feet and lower legs Psychomotor changes – no interest in suroundings, cheerless, no appetite Growth retardation – body wt deminished to 11-40% Muscle wasting – unable to hold the head when gently pulled from a lying to the sitting position
Slide 17-

USUALLY PRESENT SIGNS Moon face – oedema leads to full well rounded face Hair changes – red hair, puckability of hair Skin depigmentation – dry rough, scaly skin Loose stools – due to gastro intestinal disturbances
Slide 18-

OCCASIONAL FEATURES Fatty liver - Assosiated vitamin deficiency – occurance of keratomalacia and angular stomatisis Susceptibilty to infection – more prone to infectious diseases
Slide 19-

MARASMUS The term marasmus is derived from the Greek marasmos, which means wasting. Marasmus involves inadequate intake of protein and calories and is characterized by emaciation. Marasmus represents the end result of starvation where both proteins and calories are deficient.
Slide 20-

ppt slide no 20 content not found
Slide 21-

EPIDEMIOLOGY & ETIOLOGY Seen most commonly in the first year of life due to lack of breast feeding and the use of dilute animal milk. Poverty or famine and diarrhoea are the usual precipitating factors Ignorance & poor maternal nutrition are also contributory
Slide 22-

Clinical Features of Marasmus Severe wasting of muscle & s/c fats Severe growth retardation Dehydration occurs due to watery diarrhoea No edema or hair changes The abdomen may be shrunken or distendend with gas Continued feeling of hunger The eyes become large in size and give the appearnace of staring
Slide 23-

CLINICAL ASSESSMENT Interrogation & physical exam including detailed dietary history. Anthropometric measurements Team approach with involvement of dieticians, social workers & community support groups.
Slide 24-

Investigations for PEM Full blood counts Blood glucose profile Septic screening Stool & urine for parasites & germs Electrolytes, Ca, Ph & ALP, serum proteins CXR & Mantoux test Exclude HIV & malabsorption
Slide 25-

Complications of P.E.M Hypoglycemia Hypothermia Hypokalemia Hyponatremia Heart failure Dehydration & shock Infections (bacterial, viral & thrush)
Slide 26-

TREATMENT Correction of water & electrolyte imbalance Treat infection & worm infestations Dietary support: 3-4 g protein & 200 Cal /kg body wt/day + vitamins & minerals Prevention of hypothermia Counsel parents & plan future care including immunization & diet supplements
Slide 27-

KEY POINT FEEDING Continue breast feeding Add frequent small feeds Use liquid diet Give vitamin A & folic acid on admission With diarrhea use lactose-free or soya bean formula
Slide 28-

Cereal pulse combination Khichadi Green gram payasam Puffed rice Idli Dosa Cereal, Pulse vegetable porridge Ragi, dhal roti Paushtic ladoo
Slide 29-

PROGNOSIS Kwashiorkar & Marasmus- Kwashiorkar have greater risk of morbidity & mortality compared to Marasmus and under weight Early detection & adequate treatment are associated with good outcome Late ill-effects on IQ, behavior & cognitive functions are doubtful and not proven
Slide 30-

Prevention and Control Nutrition education of the correct feeding practices Promotion of breast feeding Development of low cost yet nutritive weaning foods Control of infections Promotion of food hygiene and personnel hygiene
Slide 31-

Prevention and Control Detection an treatment of hook worm and other parasitic infestation Provision of a mineral, multi vitamin supplementation
Slide 32-

ppt slide no 32 content not found
Slide 33-

ppt slide no 33 content not found
Slide 34-

ppt slide no 34 content not found
Slide 35-

Micronutrients: Those required in small quantity; i.e, mg/mcg Trace elements: Those present in very small quantity in the body; i.e, <0.01% or 0.1 mg/g ash weight MDD- Micronutrient deficiency disorders MNM- Micronutrient Malnutrition Hidden Hunger- Subclinical MNM Definitions
Slide 36-

Associated with blindness and signs of “toad skin” & Mobidity and mortality (Ophthalmologist Sommers noted that in populations with eye signs of VAD, the children had very high levels of mortality and morbidity) Surface protection- Vit A, SIgA Eye signs were dryness, clouding, corneal clouding, and liquefaction and extrusion of lens Increased deaths from infection; especially pneumonia, diarrhea, measles Body barriers to infection damaged (i.e., skin, all mucous membranes, eye covering); immune function impaired Fat soluble Vitamin deficiency in liver diseases VITAMIN A DEFICIENCY
Slide 37-

Vitamin A deficiency Lack of intake of vitamin A - containing fruits and vegetables, milk and organ meat Beta carotene – GYOR Blindness leading cause- Preventable Night blindness (6 mo – 6 yrs)> 1% in community- VAD-Public Health problem Corneal impression cytology, S, retinol, S RBP
Slide 38-

Eye diseases due to VAD (WHO) Night blindness (XN) Conjunctival xerosis (X1A) Bitot’s spots (X1B) Corneal xerosis (X2) Corneal ulceration/keratomalacia <1/3 of cornea(X3A) Corneal ulceration/keratomalacia >1/3 of cornea(X3B) Corneal scar (XS) Xerophthalmic fundus (XF)
Slide 39-

BITOTS SPOTS-VITAMIN A DEFICIENCY
Slide 40-

Bitot Spots
Slide 41-

Keratomalacia
Slide 42-

Approaches- VAD Nutrition education, cultivation of vitamin A-rich fruits and vegetables (sweet potato, carrots, tomatoes, green leafy vegetables) GYOR- Rainbow Revolution Food fortification Prophylaxis: high-dose vitamin A capsule/ concentrate distribution to children under five years of age every six months, low doses to pregnant women and also to nursing mothers 0.5 L to < 6 mo, < 1yr. 1 L, >1 yr- 2 L 9 megadoses – integrated with immunisation.
Slide 43-

2 doses on consecutive days and then after 1 mo, every 6 months PEM- repeat monthly till PEM resolves Aquasol A- Water Soluble & No Storage Hypervitaminosis- Gulf syndrome Hypervitaminosis A- Pseudotumor cerebri/ Benign intracranial hypertension 1 ml/2 ml spoon Vs 1-2 ml syringe Vitamin A Deficiency (VAD)
Slide 44-

Boiled egg, Egg Custard Coriander and mint chutney with chapathi Carrot halwa, Carrot salad, Carrot kheer, Carrot Juice Papaya Orange juice, Tomato Juice, Mango Juice Green leafy vegetable with dhal Suggested recipes for Vitamin A deficiency
Slide 45-

Vitamin D Deficiency Rickets is the term signifying a failure (defective) in the mineralization of growing bone or osteoid tissue (ends of long bones) Osteomalacia- defective mineralisation in the adult
Slide 46-

What are the various forms of Vitamin D Two forms of vit D are of practical importance D2 or calciferol –available as irradiated ergosterol & fish liver oil D3-available synthetically.naturally present in human skin in pro vitamin stage as 7 dehydrocholestrol.
Slide 47-

Rickets (VDD)-Knock Knees
Slide 48-

Rickets – causes softening and weakening of bones.
Slide 49-

RICKETS
Slide 50-

Sources of Vit D Sunlight Breastmilk(4-100 IU/liters) Cows milk(5-40IU/liters) Egg yolk(3-10mcg) RDA of vit D 400 IU/day (1mcg = 40 IU)
Slide 51-

Vitamin C - Scurvy Age - 6m to 2yr Gradual onset Irritability, generalised tenderness, excruciating pain, resents examination Frog like position of legs, due to pain Spongy swelling gums X-ray- knee is characteristic (white line. Pencil line cortex, zone of degeneration)
Slide 52-

ppt slide no 52 content not found
Slide 53-

Iron Deficiency Most prevalent deficiency globally, next to energy (calories) Many functional impairments: Cognitive function, activity and attention - may not be completely reversible Poor work capacity and performance (iron in muscle (myoglobin) Impaired immune function Anemia - mild to severe, with poor oxygenation of tissues; late manifestation Neurotransmitters may be impaired
Slide 54-

Causes of deficiency Decreased intake Decreased absorption Increased demands Those fed on pure milk diet likely to develop anemia. Periodic deworming Anemia
Slide 55-

Neural tube defect & Folic acid Periconceptional foloc acid for primary prevention of NTD Primary prevention of CHD- conotruncal defects
Slide 56-

Endemic Iodine Deficiency Disorder (IDD)
Slide 57-

Geographic distribution — Grading of Goitre Urinary iodine >100 mcg/L- N < 20 –severe UIS- 15 ppm K iodate Double fortified salt Pregnancy: increased wastage, severely retard affected child born (cretin), with irreversible mental and physical retardation Goiter common In lesser forms and older children and adults, mentally dull, short, poor ability to work and earn Iodine deficiency disease
Slide 58-

Calcium Most abundant mineral 99% in bones and teeth Involved in blood clotting process, nerve conduction, muscle stimulation, parathyroid function Milk, milk products, millet (ragi) –Requirement Infants 400 to 600 mg/day Children 500 to 800 mg/day Puberty 1000 to 1200 mg/day Deficiency: tetany, rickets, osteoporosis
Slide 59-

Iron Folic acid- Anemia prophylaxis among children, adolescents, pregnant & Lactating women. Vitamin A supplementation- Preventable Blindness – setbacks Universal iodisation of salt Double fortification of salt- Iron & iodine Other priorities- Calcium, zinc in priority groups Available Programmes
Slide 60-

A- 1500 IU D- 400 IU E- 5-15 IU/mg C- 40 mg B1,2,6- 0.5-15 mg B 3- 5-15 mg 11 – 10-150 mcg 12- 0.5-1.5 mcg Ca- 500-100 mg P- 800-1000 mg Mg- 200-300 mg Fe- 10-20 mg Io- 50-150 mcg Cu- 1-2 mg Zn- 5-15 mg Fl, Mn- 1-5 mg Se- 100 mcg Cr- 10 mcg RDA- Requirements
Slide 61-

Genetic Environmental Illness < 1% Evaluation Pathological obesity – short Endogenous obesity – tall for age Diet therapy Exercise Behavioural modification Lifestyle modification. Obesity
Slide 62-

OVERWEIGHT AND OBESITY Genetic &Metabolic syndromes Endocrine
Slide 63-

Want to confirm to the ideal body image. More in young women Anorexia nervosa in women Various social, economic and ethnic back grounds. Association between eating disorders and low self esteem Dieting behavioural support by friends and commercial adventisements. Dieting leads to decreased dietary intake leading on to iron deficiency anaemia, osteoporosis (later in life), amenorrhea. develop further eating disorders. Healthy mind in a healthy body. ANOREXIA / DIETING
Slide 64-

ppt slide no 64 content not found
Slide 65-

Thank You