11th Part
Q Prevention of PEM in a community ( short notes) 5
A Some of the measures are -
1 Prevention of PEM should start with the mother of the child. The main reason for low birth weight is maternal malnutrition i.e. the mother of the child consumes inadequate quantities of energy and protein during her pregnancy. Therefore, one must ensure that a pregnant woman consumes extra food to meet the additional needs of pregnancy.
2 Mother's milk is the best food for an infant. Lactating mothers should be encouraged to breastfeed their children as long as possible. By the age of about 6 months, however, the mother's milk alone is not adequate for the child. Supplementary food should be provided to the children by the age of six months, in addition to breast milk.
3 Children should be fed 5-6 times a day. As Indian diets are quite bulky and unless the child is fed frequently it cannot meet the energy and protein requirements.
4 Infections like diarrhoea and respiratory infections increase the risk of PEM. Prompt treatment of these infections is necessary to help to prevent PEM. In addition, during diarrhoea and any other infection, food should not be restricted. The child should be fed as usual.
5 Protection of children against diseases like tuberculosis or measles, whooping cough by immunization is another important aspect in the prevention of PEM.
Q Discuss the main causative factors of protein-energy malnutrition in children. 5
Q Causative factors of PEM 7
A Some of the causes of PEM are :
a) Poverty: PEM occurs in poor Indian communities. It is commonly seen in families of landless agricultural labor, and tribal communities without any regular earnings among others. In India, PEM is seen in backward communities of Harijans, nomadic tribes, and children in urban slums. These communities are poor, illiterate, and generally have large families.
b) Maternal malnutrition: The nutritional status of the mother determines the state of nutrition of the child to be born. The main reason for low birth weight is maternal malnutrition i.e. the mother of the child consumes inadequate quantities of energy and protein during her pregnancy.
c) Infections and poor hygiene: Infections like diarrhoea and respiratory infections increase the risk of PEM. The mothers may follow unsound and unhygienic methods of feeding the child. Feeding bottles may not be properly sterilized. Flies may be allowed to sit on the nipple of the feeding bottle. This may lead to frequent diarrhoea and lead to marasmus.
d) Ignorance: Both the forms of PEM occur as a result of ignorance of the mother, in addition to poverty. The mother, due to ignorance;.delays the introduction of supplementary food (in addition to breast milk), even up to the age of 1 year. This has serious consequences because mother's milk alone is not enough for the child by the age of 6 months. The infant should be given supplementary foods in addition to breast milk. Moreover, the mothers restrict the diet when the child is suffering from infections such as diarrhoea, measles, and common fevers. This practice is not good since such a dietary restriction leads to PEM in children who are underfed.
e) Wrong child feeding practices: The child is usually given the same diet as taken by the adults. The typical Indian diet is based on cereals and is quite bulky for a small child. This would mean that the child can consume only smaller amounts of food at one time. As a result, the child does not get adequate food. Consequently, the child cannot get enough energy, protein which is the major cause of PEM in India.
Q PEM (Define) 5
A PEM can be defined as a range of pathological conditions arising from the deficiency of protein and energy and is commonly associated with infections. Protein-energy malnutrition (PEM) is widely prevalent among young children (0-6 years), however, it is also observed among adolescents and adults, mostly lactating women, especially during periods of famine or other emergencies. PEM has serious consequences for the health of individuals particularly children and can even result in death.
Clinical features of PEM -
PEM is a condition characterized by two forms:
a) Marasmus
b) Kwashiorkor
The symptoms of are Marasmus - very low body weight for age, loss of fat (fat under the skin), gross muscle wasting. It is observed more frequently in infants and very young children.
Kwashiorkor, on the other hand, is a condition characterized by oedema (excessive accumulation of fluid in the intercellular spaces of tissue) and very low body weight for age. The syndrome is most frequently observed in children aged 1-3 and is precipitated by an infection or by a series of infections.
Enumerate the clinical features and measures for the control of the following disorders :
(a) PEM 5
A Marasmus -
(How to identify a child suffering from Marasmus?)
Some common clinical features of marasmus include :
i) Muscle Wasting: The characteristic sign of marasmus is the extensive wasting of muscle with little or no fat under the skin. The ribs are clearly visible. Because of the absence of fat, the skin starts dangling with a number of folds, particularly on the buttocks. The child with marasmus, thus, can be described as a combination of skin and bones.
ii) Failure to thrive: The child suffering from marasmus usually is irritable and fretful. In fact, the child is often so weak that the cry of the child cannot even be heard.
iii) Growth failure: Failure to grow is another important feature of the disease. The children often weigh about 50 percent or less of normal children for their age. For example, a healthy normal one-year-old child weighs about 10 kg, whereas, a marasmic child would weigh only about 5 to 6 kg.
Iv) Deficiency& Infections - The child may also suffer from frequent watery diarrhoea associated with dehydration (loss of fluids). The child may also have other deficiencies particularly, vitamin A deficiency.
Kwashiorkor
(How to identify a child suffering from Kwashiorkor?)
Some common clinical features of Kwashiorkor include:
i) Oedema: Oedema is the excessive accumulation of fluid in the intercellular spaces of the tissues. Oedema is usually observed on the lower limbs, but it may also be distributed all over the body including the face. We can detect oedema by pressing the skin of the leg with your fingers. Because of the accumulation of fluid under the skin, when you press there will be a depression at the place where the pressure is applied.
ii) Failure of growth: Children with kwashiorkor weigh only about 60per cent of the weight of normal children for their age. For example, a three-year-old healthy normal boy weighs about 13.5 kgs. whereas, another boy of the same age but suffering from kwashiorkor may only weigh 60 % i.e about 8 kg. In other words, they are very much lighter than healthy normal children of their age.
iii) Irritability: The child suffering from kwashiorkor is generally irritable and has no interest in his/her surroundings.
iv) Skin Changes; The skin of the child may peel off easily leaving behind cracks or sores.
v) Hair Changes: The hair may become sparse and can be easily pulled off. The hair usually loses its black colour and appears reddish-brown.
vi) Moon Face: The face of the child suffering from kwashiorkor may appear puffy with the cheeks sagging. This condition is normally known as a moon face.
vii) Associated deficiencies: The children may have signs of other deficiencies like those of vitamin A and B-complex deficiencies.
viii) Associated diseases: The child is often suffering from watery diarrhoea (frequent loose motions) or severe respiratory infection (cough). The children may be suffering from measles, a childhood disease.
Q Xerophthalmia 2
Q Briefly describe the clinical features of xerophthalmia. 5
Q Causative factors of Xerophthalmia 4
A Xerophthalmia refers to the eye manifestations (signs) because of vitamin A deficiency. Blindness as a result of xerophthalmia is an important public health problem in India.
Clinical features of xerophthalmia. -
a) Night Blindness: One of the earliest manifestations of xerophthalmia is night blindness. Individuals suffering from night blindness cannot see in dim light or around dusk. The child will be unable to see even the meal plate kept in front of him/her in dim light.
b) Conjunctival Xerosis: Xerosis means dryness. In the normal eyes, the membrane covering the white portion of the eye (i.e.conjunctiva) is bright, white, and moist. In the case of xerophthalmia, it becomes discolored (muddy coloured), dry, and loses its brightness. This is known as conjunctival xerosis.
C Bitot spots: In addition to xerosis, dry foamy, triangular spots may appear on the conjunctiva. These are known as Bitot's spots. If they are neglected, the changes may continue to progress affecting the cornea of the eye and may lead to irreversible blindness.
d) Corneal xerosis: When the deficiency of vitamin A becomes severe, the cornea becomes dry and dull and appears like ground glass. This condition is called corneal xerosis which means dryness of the cornea. This condition should be treated as an emergency. If it is not treated immediately with vitamin A, the child can develop ulcers in the cornea. Corneal ulcers when healed leave white scars known as leucoma that interferes with normal vision.
e) keratomalacia: The most dangerous form of xerophthalmia is known as keratomalacia. In this condition, the cornea becomes very soft and raw and easily infected. It leads to the destruction of the eye. In other words, the eye gets completely melted and destroyed. This condition leads to irreversible blindness.
The causative factors of Xerophthalmia -
a) Dietary inadequacy of vitamin A: The primary cause of xerophthalmia is the deficiency of vitamin A in our diet. In the villages and urban slums, among the low-income groups, the intake of vitamin A is less than a quarter of the Recommended Dietary Intakes (RDI).
b) Maternal Malnutrition: Indian children from very poor rural families are born with low stores of vitamin A in the liver it is because their mothers are also deficient in vitamin A. Due to inadequate consumption of vitamin A, the child develops xerophthalmia.
c) Infections and Infestations: Diarrhoea and respiratory infections and worm infestations like roundworm disease are very common in children. These are known to decrease the absorption of vitamin A and lead to deficiency. Measles, one of the childhood infections, is another important cause of xerophthalmia.
Q Clinical features of Vitamin A deficiency 6
A Above
Q How to prevent Vitamin A deficiency?
A Consume Vitamin A rich diet: the most rational method of prevention of vitamin A deficiency is to make sure that communities consume foods rich in vitamin A regularly. Inexpensive foods like green leafy vegetables (palak, amaranth, etc.), yellow vegetables (yellow pumpkin and carrots) and fruits (papaya and mango) are good sources of beta carotene.
Periodic administration of Vitamin A: It is possible to build up sufficient vitamin A stores in a child by giving large doses of vitamin A periodically. Under the program, the children between the ages of one and five years are given a massive oral dose of vitamin A (200.000 IU) once every six months. The distribution of vitamin A is carried out by the village level health workers like health workers of the State Governments.
Q Explain the causative factors and preventive measures for anaemia. 8
Q Preventive measures of Iron deficiency 5
Q Discuss in detail how nutritional anemia can be prevented. 7
A Causes - Anaemia occurs due to iron deficiency or folic acid and vitamin B12 deficiency. The various causes of iron deficiency anaemia are -dietary deficits or less absorption of iron and loss of iron from the body.
a) Dietary inadequacy: The deficiency of iron in the body can be due to two reasons - low dietary intake of iron or reduced (low) absorption of iron in the body. The iron requirement is high in the body in certain physiological conditions especially in infants, children & women in reproductive years(as a result of menstruation, pregnancy & lactation). If iron intake during these periods is not adequate, it may result in anaemia. Iron absorption problem
b) Losses of Iron: The second major cause of anaemia is increased loss of iron from the body. In adult women of reproductive age, loss of iron occurs due to menstrual loss, loss of iron occurs during pregnancy, delivery, and lactation. If proper care of women is not taken during these periods, it can lead to anaemia. Iron losses from the body are also more in the case of people suffering from hookworm and other worm infestations. Heavy loss of iron from the body in conditions of surgery or accident can also lead to anaemia.
Folic acid and Vitamin B12 deficiency: Anaemia can also occur due to the deficiency of folic acid and vitamin B12 as they play a major role in blood formation. People who are strict vegetarians but avoid green leafy vegetables or eat no animal products are prone to it.
Preventive measures for anaemia -
a) Dietary measures: The most rational method of prevention of anaemia is to ensure the consumption of diets by the population that is rich in iron. The women should be particularly encouraged to consume iron-rich foods regularly. Inexpensive sources of iron are green leafy $vegetables (palak, amaranth, etc), whole wheat flour, rice flakes, other vegetables like (lotus stem), groundnuts, apple, jaggery, amla. These foods should be consumed as they are rich sources of iron, care should be taken that enough vitamin C-rich and protein-rich foods are consumed along with them (as they enhance absorption of iron).
b) Fortification of foods: Certain food items that are consumed on a regular basis are fortified with iron to improve the iron content in them and subsequently increased consumption of iron by vulnerable sections of the population. Baby foods are fortified with iron to protect infants from anaemia, today many food items are fortified with iron like biscuits, wheat flour.
c) Distribution of iron and folic acid tablets: By consuming iron tablets, the hemoglobin levels in the blood can be raised. For over the last 20 years, iron (60 mg) and folic acid (500pg) tablets are distributed among the vulnerable sections of the community (those who are more prone to deficiency disorders) women, pregnant and lactating women, and children (1-5 years).
Q Prevention and control of IDD 5
Q Give any two clinical features of Iodine deficiency disorder. 2
Q Spectrum of iodine deficiency disorders 5
Q Give the clinical manifestations of iodine deficiency disorder. 4
A Causes - In mountainous and hilly regions, iodine deficiency occurs because of the washing down of the soil from iodine content due to heavy rains and glaciers. In the case of plains, repeated floods deplete the iodine content in soil and water. As a result, all animal and vegetable foods dependent on the soil and water are deficient in iodine. Thus, when these foods which are deficient in iodine are consumed, it leads to iodine deficiency.
Apart from this, certain chemical substances called goitrogens (goiter producing substances) interfere with the utilization of iodine by the thyroid gland. Foods like cabbage and radish are contained goitrogens. Consumption of these foods in large quantities in some cases may lead to iodine deficiency.
Two clinical features of Iodine deficiency disorder - Goitre and cretinism
The clinical manifestations of both goitre and cretinism are -
Goitre - Iodine is essential for the normal functioning of an endocrine gland known as the thyroid gland. The thyroid gland secretes a hormone called thyroxine, which is very important for normal human development and health. Iodine helps in the formation of thyroxine. When iodine is inadequate, the thyroid gland enlarges in an attempt to produce thyroxine for the body's needs. Due to the deficiency of iodine in the body, the thyroid gland enlarges in order to trap more iodine (whatever is available). The swelling or enlargement can vary in size depending on the severity of the goitre. The word goitre means swelling/or enlargement of the thyroid gland.
Cretinism: It is the most severe manifestation of IDD. Cretinism refers to the adverse effects of iodine deficiency on the infant and young child. Iodine deficiency interferes with the brain development of the foetus. This means it can cause irreversible brain damage even before birth. If an infant is born to an iodine-deficient mother, he or she is likely to suffer from hypothyroidism. If this condition of iodine deficiency or hypothyroidism continues further even after the birth of the child, the child may suffer from a series of disorders which may include mental retardation, growth failure, speech and hearing defects, neuromuscular disorders, paralysis.
Prevention and Control - Control: Since IDD is due to reduced intake of iodine, the rational method is to ensure a sufficient intake of iodine by the population living in areas where IDD is common. A few methods to increase the iodine intake of people residing in endemic regions include:
1) Use of Iodized salt: The oldest and the most extensively used method is fortification (enrichment) of common salt with iodine (Potassium iodate). For 10 g of common salt about 150ug iodine is added. The iodized salt (common salt to which iodine is added) smells, tastes and even looks exactly like the common salt.
2) Use of tablets of sodium or potassium iodide: The intake of sodium/potassium iodate tablets to school children in areas where goitre and cretinism are severe. The addition of iodine to the drinking water supply has been tried in some countries.
3) Use of Iodized oil: During the last decade, injection of oil, to which iodine has been added is given in areas where goitre and cretinism is severe. The advantage is that an injection of a 1 ml dose of iodized oil can provide protection to an individual for 3-5 years.
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