STUDY - Technical - New Dacian's Medicine
Protein-Caloric
Malnutrition
Translation Draft
Insufficient intake of proteins and energy factors cause both decreasein body mass and body fat, and may predominate one or the other. Protein-calorie malnutrition (MMP) occurs in particular in two situations: in populations in developing areas, where it may be present in endemic form, and in famine conditions, when malnutrition can reach 25% among the population.
The first step of malnutrition occurs when socio-economic factors limit the quantity and quality of nutrition and a particular problem occurs when plant proteins with low biological value are the major components of the diet and when the incidence of infectious diseases is high.
This problem is accentuated when energy intake is insufficient, thus causing the use of proteins in the diet for energy production rather than for the synthesis of new proteins. In children in developing countries, two MPM syndromes are distinguished: 1. marasm, manifested by stopping growth, loss of fat, general loss of protein mass, without edema, which appears to be a combination of the effects of protein and energy malnutrition and 2. koshiokor, manifested by insufficient growth, edema, hypoalbuminemia, fatty loading of the liver and preservation of subcutaneous fat, which appears to be a selective protein malnutrition.
Mixed forms are common in both children and adults, and the difference between pure protein malnutrition and MMP has minor clinical significance. In populations in developed areas, MMP occurs, in particular, as a secondary condition in people with poor nutrition and developing malnutrition in association with a subacute or chronic disease.
Predisposing traits include anorexia, hypermetabolism, malabsorption, drug abuse, drugs and alcohol, and in old age, depression, isolation and low material income may play a certain role. Almost half of elderly patients hospitalized are malnourished upon admission or develop a nutritional deficiency during admission. Synergism of primary and secondary causes is common in individuals with low protein and energy reserves, who develop clinical MCAN much faster than ill-fed patients when changes in metabolism, anorexia, infections or other catabolic conditions occur.
From an epidemiological point of view, the relevance of malnutrition in a given population can be assessed by measuring the subcutan cell tissue, the muscle area at the half arm or the ratio of urinary creatinine over 24 hours to height. The importance of this problem around the world is very high. In the 1980s, the World Health Organization estimated that more than 300 million children were delayed in secondary malnutrition, the consequences for mortality, cognitive function, social organization and economic development being large but impossible to quantify (especially since this figure has steadily increased, exceeding 400 million in the 2000s).
Pre-school children in developing areas are particularly susceptible due to their diet dependence on others, increased protein and energy needs and increased susceptibility to infections, especially as a result of unhygienic conditions. Gastrointestinal infections frequently precipitate a clinical MPC due to the association of diarrhea, anorexia, vomiting, increased metabolic needs and decreased intestinal absorption (parasitosis plays a major role in malnutrition in many parts of the world).
In developed countries, protein deficiency in adults tends to be low and subclinical, but poor nutrition is not limited only to the poor adult population. In a study focused on low material income (in some areas of developed regions), 22-35% of children between 2 and 6 years of age had a sharp weight loss and a below-normal height (age-appropriate). In hospitalized patients, both mild and severe deficiencies are quite common. Furthermore, the nutritional status of patients deteriorates frequently during hospitalization, and the occurrence of postoperative infections, the time needed to heal surgical wounds and the duration of hospitalization are increased in certain individuals. Processes that affect the state of nutrition can be both preventable and reversible.
From a physiopathological point of view, when energy intake falls below the minimum requirement, the body's response, in order of physiological adaptation, involves the hormones of energy metabolism, which stimulate the mobilization of free fatty acids from the fat tissue and amino acids in the muscles, which thus provide the energy of the oxidative needs of the body and mainly of the brain. Amino acids are divided between gluconeogenesis and oxidation, protein synthesis is reduced, metabolism rate decreases, and muscle mass and fat tissue decrease.
In the first week of fasting, 4 to 5 kg of body weight is lost, with losses accounting for almost 25% in body fat, 35% in extracellular fluids and 40% in protein. Over the coming weeks, losses continue, but at a slower pace. The different compartments shrink in different proportions: the skeletal muscles faster than the heart muscle, the gastrointestinal tract and the liver are faster than the kidneys. The mobilisation of amino acids in the muscles ensures the synthesis of a certain amount of albumin and, therefore, hypoalbuminemia develops over time.
Protein intake may be much lower than energy intake when low biological value proteins (especially vegetable proteins) are the major protein components of the diet or when glucose is the only organic nutrient in the intravenous diet in patients who cannot eat. The consequence, in both cases, is an increase in insulin secretion, which delays lipolysis in fat tissue, preserving its mass, and inhibits the mobilization of amino acids in the muscle.
The plasma concentration of amino acids decreases, and the synthesis of albumin and other proteins is impaired (hypoalbuminemia and edema are characteristic features and fatty infiltration of the liver occurs). As mentioned above, these traits are typical for kwashirkor. The distribution of minerals is, in part, due to a decrease in body mass and extracellular fluids, but potassium and magnesium can be lost in addition as a result of leaving intracellular deposits. Low mineral intake (as in patients with intravenous glucose is the only source of energy) and increased losses (diuresis, diarrhoea, butts, etc.) can worsen their deficiency.
Simple starvation, as described above, does not rapidly lead to death, but induces a gradual metabolic adaptation, which involves changes in metabolism in the central nervous system, with oxidation of fatty acids and ketones of the body for energy and marked decrease in the rate of metabolism, which leads to the preservation of the remaining protein reserves. Starvation in the context of physical exertion is considerably more harmful.
The extent to which the effects of a particular stress are given by the direct metabolic consequences of inflammation, infection, fever and wound healing, compared to the indirect consequences of the release of inflammatory cytokines, such as the alpha tumor necrosis factor, interleukin 2 and interleukin 6 is not clear, but adding stress to starvation increases metabolic rate and accelerates weight loss , nitrogen compounds and microelements. For this reason, a severe MPV occurs when malnutrition and stress are present. A particular interest in this regard is mPL as a strong feature in AIDS, when we think that this is the consequence of anorexia (and decreased in intake), fever and diarrhoea.
Let's move on to clinical manifestations, from mild to moderate MMP. Children have a weight and height deficiency (adults generally lose weight, although edema can mask these losses). if the individual was obese, the loss of protoplasm may be hidden from residual fat. Increased skin fold in the triceps and muscle surface half arm are diminished. In the absence of kidney disease, the ratio of 24-hour urinary creatinine to height is a sensitive indicator of protein malnutrition and should be measured at weekly intervals.
Serum levels of albumin, transferin and prealbumin may be low. Serum triiodothyronine is low, the level of triiodothyronine lost is high, and the metabolic rate is low. Peripheral lymphopenia may be present and glucose tolerance may be low. Heart size tends to shrink. Severe MPL is characterized by profound impairment of the body's composition and laboratory data. The decrease in muscle mass is evident on the objective examination, being indicated by the retraceability of intercostal spaces, with decreased temporal muscles and extremities, and the subcutan cell tissue is low or absent.
The presence of placidity, fatigue, feeling cold, dry and slapped skin, ailing facies and skin and hair depigmentation are common aspects. Skin ulcers of decubit occur in advanced stages. Blood pressure is low, the heart rate is low, and the temperature may be low. There is a global decrease in the body's functions. Let's see what the changes in the cardiovascular system, kidneys and lungs are! Fan response to hypoxia is weak. During malnutrition, the heart and kidneys lose mass in proportion to the loss of muscle mass, and the decrease in the rate of metabolism, as well as heart rate and the rate of glomerular filtration, is made according to body mass size and metabolic status.
However, heart failure may occur during vigorous nutritional and volemy rebalancing in infections and in various physical stresses. Blood volume, hematocrit, serum albumin, transferin and the number of lymphocytes are low. Anemia is normochrome, normocytic and is usually given by decreased production of erythrocytes, as a result of the general decrease in protein biosynthesis. Iron, folate and pyridoxine deficiency can contribute to anemia. In the absence of fever, the rate of basal metabolism decreases, and hypothermia is present, possibly as a consequence of the decrease in triiodothyronine levels and the loss of the insulating layer of subcutan cell tissue.
Hypoglycaemia may be present in the terminal stages. Atrophy of the gastrointestinal tract involves both intestinal villosities and exocrine and endocrine functions of the pancreas, and bacterial exacerbation may occur in the small intestine. Malabsorption and lactose intolerance may be present. Gastrointestinal manifestations may occur, at least some of them, as a result of decreased oral nutrition, rather than starvation, since similar changes occur in patients fed entirely parenterally. From the point of view of the immune system, cell-mediated immunity is low, as indicated by all standard tests, whereas the response of humoral immunity is generally unaltered.
Infections with common germs or opportunistic germs can lead to an increase in morbidity and mortality. Pneumonia is common. All wounds and incisions heal much more slowly with MPL. Wound dehiscence is common. In terms of reproductive function, almost every aspect of reproduction is affected in women with MBC, including implantation of the fertilized egg, fetal growth, lactation and parturithia (act of birth), and newborns are stopped in development and may have decreased cognitive functions if they survive.
The hypothetical evolution of malnutrition has the following route: the month interval 0-1 occurs slowing growth (in children - that is, usually the first manifestation), the interval month 1-2 occurs hypoalbuminemia then the loss of cell-mediated immunity that predisposes to infections (including anemia and amenorrhea), the interval month 2-3 appears poor healing of the wounds (hypermetabolism and anorexia from infections accelerates the cheesexia), interval month 3-4 appears aspiration pneumonia and towards the end of the period the individual becomes too weak to walk, range month 4-5 appear urinary tract infections and towards the end the individual becomes too weak to stand, in the range of month 5-6 appear decubit escares and over this period of 6 months occurs death. It should be noted that in advanced MPM, the subcutaneous cell layer in the middle of the arm decreases greatly, and the creatinine/height ratio is less than 60% of normal and is associated with fatal infections.
In terms of other deficits, MMP rarely appears as an isolated phenomenon. Usually, nutritional deficiencies coexist, which include those for folic acid, thiamine, riboflavin, nicotinic acid, pyridoxine and vitamin A (in children with MCOP, vitamin A deficiency is a fluke). As MPL worsens and protoplasmic proteins are consumed, intracellular potassium, phosphorus, magnesium are excreted in parallel with nitrogen compounds, so that total deficiencies of the body may occur after refueling.
Let's get to the treatment! In the case of a mild or moderate MMP, any precipitating event should be removed and the ingestion of protein and energy (depending on the ideal weight) should be increased sufficiently to allow the deficiencies to be covered. It is appropriate to take multivitamins in all these patients. It is also essential that during rebalancing, the administration of minerals and trace elements is appropriate to prevent the development of hippopotasemia, hypomagnesemia, hypophosphatemia, life-threatening disorders. Most patients who can eat and swallow can be treated orally. However, if anorexia is an important problem or if the patient is edentated, the diet should be supplemented with liquid formulas either per bone or by assisted enteral feeding.
Treatment of a severe MPM is much more urgent and more complicated for several reasons: 1. Precipitating diseases tend to be much severe and more difficult to treat and may not be able to restore the balance of nitrogen compounds until the infection and fever are controlled; 2. The degree of malnutrition itself may prevent recovery from associated life-threatening conditions, so early intervention with assisted enteral nutrition or parenteral nutrition may be urgently necessary; 3. The introduction of nutritional factors into the gastrointestinal tract may in itself cause diarrhea due to atrophy of the intestinal mucosa and the decrease of pancreatic and intestinal enzymes, and parenteral nutrition may also be necessary 4. Associated deficient situations are common and care should be taken when administering multivitamins, trace elements and all essential minerals so that this is in an efficient/sufficient quantity to restore the body's reserves. Recovery in adults may be slow and limited, but in children it is between 3 and 4 months. Complete nutrition education, psychosocial stimulation and rehabilitation programs should be established in all cases.
Next time we talk about obesity...
Insufficient intake of proteins and energy factors cause both decreasein body mass and body fat, and may predominate one or the other. Protein-calorie malnutrition (MMP) occurs in particular in two situations: in populations in developing areas, where it may be present in endemic form, and in famine conditions, when malnutrition can reach 25% among the population.
The first step of malnutrition occurs when socio-economic factors limit the quantity and quality of nutrition and a particular problem occurs when plant proteins with low biological value are the major components of the diet and when the incidence of infectious diseases is high.
This problem is accentuated when energy intake is insufficient, thus causing the use of proteins in the diet for energy production rather than for the synthesis of new proteins. In children in developing countries, two MPM syndromes are distinguished: 1. marasm, manifested by stopping growth, loss of fat, general loss of protein mass, without edema, which appears to be a combination of the effects of protein and energy malnutrition and 2. koshiokor, manifested by insufficient growth, edema, hypoalbuminemia, fatty loading of the liver and preservation of subcutaneous fat, which appears to be a selective protein malnutrition.
Mixed forms are common in both children and adults, and the difference between pure protein malnutrition and MMP has minor clinical significance. In populations in developed areas, MMP occurs, in particular, as a secondary condition in people with poor nutrition and developing malnutrition in association with a subacute or chronic disease.
Predisposing traits include anorexia, hypermetabolism, malabsorption, drug abuse, drugs and alcohol, and in old age, depression, isolation and low material income may play a certain role. Almost half of elderly patients hospitalized are malnourished upon admission or develop a nutritional deficiency during admission. Synergism of primary and secondary causes is common in individuals with low protein and energy reserves, who develop clinical MCAN much faster than ill-fed patients when changes in metabolism, anorexia, infections or other catabolic conditions occur.
From an epidemiological point of view, the relevance of malnutrition in a given population can be assessed by measuring the subcutan cell tissue, the muscle area at the half arm or the ratio of urinary creatinine over 24 hours to height. The importance of this problem around the world is very high. In the 1980s, the World Health Organization estimated that more than 300 million children were delayed in secondary malnutrition, the consequences for mortality, cognitive function, social organization and economic development being large but impossible to quantify (especially since this figure has steadily increased, exceeding 400 million in the 2000s).
Pre-school children in developing areas are particularly susceptible due to their diet dependence on others, increased protein and energy needs and increased susceptibility to infections, especially as a result of unhygienic conditions. Gastrointestinal infections frequently precipitate a clinical MPC due to the association of diarrhea, anorexia, vomiting, increased metabolic needs and decreased intestinal absorption (parasitosis plays a major role in malnutrition in many parts of the world).
In developed countries, protein deficiency in adults tends to be low and subclinical, but poor nutrition is not limited only to the poor adult population. In a study focused on low material income (in some areas of developed regions), 22-35% of children between 2 and 6 years of age had a sharp weight loss and a below-normal height (age-appropriate). In hospitalized patients, both mild and severe deficiencies are quite common. Furthermore, the nutritional status of patients deteriorates frequently during hospitalization, and the occurrence of postoperative infections, the time needed to heal surgical wounds and the duration of hospitalization are increased in certain individuals. Processes that affect the state of nutrition can be both preventable and reversible.
From a physiopathological point of view, when energy intake falls below the minimum requirement, the body's response, in order of physiological adaptation, involves the hormones of energy metabolism, which stimulate the mobilization of free fatty acids from the fat tissue and amino acids in the muscles, which thus provide the energy of the oxidative needs of the body and mainly of the brain. Amino acids are divided between gluconeogenesis and oxidation, protein synthesis is reduced, metabolism rate decreases, and muscle mass and fat tissue decrease.
In the first week of fasting, 4 to 5 kg of body weight is lost, with losses accounting for almost 25% in body fat, 35% in extracellular fluids and 40% in protein. Over the coming weeks, losses continue, but at a slower pace. The different compartments shrink in different proportions: the skeletal muscles faster than the heart muscle, the gastrointestinal tract and the liver are faster than the kidneys. The mobilisation of amino acids in the muscles ensures the synthesis of a certain amount of albumin and, therefore, hypoalbuminemia develops over time.
Protein intake may be much lower than energy intake when low biological value proteins (especially vegetable proteins) are the major protein components of the diet or when glucose is the only organic nutrient in the intravenous diet in patients who cannot eat. The consequence, in both cases, is an increase in insulin secretion, which delays lipolysis in fat tissue, preserving its mass, and inhibits the mobilization of amino acids in the muscle.
The plasma concentration of amino acids decreases, and the synthesis of albumin and other proteins is impaired (hypoalbuminemia and edema are characteristic features and fatty infiltration of the liver occurs). As mentioned above, these traits are typical for kwashirkor. The distribution of minerals is, in part, due to a decrease in body mass and extracellular fluids, but potassium and magnesium can be lost in addition as a result of leaving intracellular deposits. Low mineral intake (as in patients with intravenous glucose is the only source of energy) and increased losses (diuresis, diarrhoea, butts, etc.) can worsen their deficiency.
Simple starvation, as described above, does not rapidly lead to death, but induces a gradual metabolic adaptation, which involves changes in metabolism in the central nervous system, with oxidation of fatty acids and ketones of the body for energy and marked decrease in the rate of metabolism, which leads to the preservation of the remaining protein reserves. Starvation in the context of physical exertion is considerably more harmful.
The extent to which the effects of a particular stress are given by the direct metabolic consequences of inflammation, infection, fever and wound healing, compared to the indirect consequences of the release of inflammatory cytokines, such as the alpha tumor necrosis factor, interleukin 2 and interleukin 6 is not clear, but adding stress to starvation increases metabolic rate and accelerates weight loss , nitrogen compounds and microelements. For this reason, a severe MPV occurs when malnutrition and stress are present. A particular interest in this regard is mPL as a strong feature in AIDS, when we think that this is the consequence of anorexia (and decreased in intake), fever and diarrhoea.
Let's move on to clinical manifestations, from mild to moderate MMP. Children have a weight and height deficiency (adults generally lose weight, although edema can mask these losses). if the individual was obese, the loss of protoplasm may be hidden from residual fat. Increased skin fold in the triceps and muscle surface half arm are diminished. In the absence of kidney disease, the ratio of 24-hour urinary creatinine to height is a sensitive indicator of protein malnutrition and should be measured at weekly intervals.
Serum levels of albumin, transferin and prealbumin may be low. Serum triiodothyronine is low, the level of triiodothyronine lost is high, and the metabolic rate is low. Peripheral lymphopenia may be present and glucose tolerance may be low. Heart size tends to shrink. Severe MPL is characterized by profound impairment of the body's composition and laboratory data. The decrease in muscle mass is evident on the objective examination, being indicated by the retraceability of intercostal spaces, with decreased temporal muscles and extremities, and the subcutan cell tissue is low or absent.
The presence of placidity, fatigue, feeling cold, dry and slapped skin, ailing facies and skin and hair depigmentation are common aspects. Skin ulcers of decubit occur in advanced stages. Blood pressure is low, the heart rate is low, and the temperature may be low. There is a global decrease in the body's functions. Let's see what the changes in the cardiovascular system, kidneys and lungs are! Fan response to hypoxia is weak. During malnutrition, the heart and kidneys lose mass in proportion to the loss of muscle mass, and the decrease in the rate of metabolism, as well as heart rate and the rate of glomerular filtration, is made according to body mass size and metabolic status.
However, heart failure may occur during vigorous nutritional and volemy rebalancing in infections and in various physical stresses. Blood volume, hematocrit, serum albumin, transferin and the number of lymphocytes are low. Anemia is normochrome, normocytic and is usually given by decreased production of erythrocytes, as a result of the general decrease in protein biosynthesis. Iron, folate and pyridoxine deficiency can contribute to anemia. In the absence of fever, the rate of basal metabolism decreases, and hypothermia is present, possibly as a consequence of the decrease in triiodothyronine levels and the loss of the insulating layer of subcutan cell tissue.
Hypoglycaemia may be present in the terminal stages. Atrophy of the gastrointestinal tract involves both intestinal villosities and exocrine and endocrine functions of the pancreas, and bacterial exacerbation may occur in the small intestine. Malabsorption and lactose intolerance may be present. Gastrointestinal manifestations may occur, at least some of them, as a result of decreased oral nutrition, rather than starvation, since similar changes occur in patients fed entirely parenterally. From the point of view of the immune system, cell-mediated immunity is low, as indicated by all standard tests, whereas the response of humoral immunity is generally unaltered.
Infections with common germs or opportunistic germs can lead to an increase in morbidity and mortality. Pneumonia is common. All wounds and incisions heal much more slowly with MPL. Wound dehiscence is common. In terms of reproductive function, almost every aspect of reproduction is affected in women with MBC, including implantation of the fertilized egg, fetal growth, lactation and parturithia (act of birth), and newborns are stopped in development and may have decreased cognitive functions if they survive.
The hypothetical evolution of malnutrition has the following route: the month interval 0-1 occurs slowing growth (in children - that is, usually the first manifestation), the interval month 1-2 occurs hypoalbuminemia then the loss of cell-mediated immunity that predisposes to infections (including anemia and amenorrhea), the interval month 2-3 appears poor healing of the wounds (hypermetabolism and anorexia from infections accelerates the cheesexia), interval month 3-4 appears aspiration pneumonia and towards the end of the period the individual becomes too weak to walk, range month 4-5 appear urinary tract infections and towards the end the individual becomes too weak to stand, in the range of month 5-6 appear decubit escares and over this period of 6 months occurs death. It should be noted that in advanced MPM, the subcutaneous cell layer in the middle of the arm decreases greatly, and the creatinine/height ratio is less than 60% of normal and is associated with fatal infections.
In terms of other deficits, MMP rarely appears as an isolated phenomenon. Usually, nutritional deficiencies coexist, which include those for folic acid, thiamine, riboflavin, nicotinic acid, pyridoxine and vitamin A (in children with MCOP, vitamin A deficiency is a fluke). As MPL worsens and protoplasmic proteins are consumed, intracellular potassium, phosphorus, magnesium are excreted in parallel with nitrogen compounds, so that total deficiencies of the body may occur after refueling.
Let's get to the treatment! In the case of a mild or moderate MMP, any precipitating event should be removed and the ingestion of protein and energy (depending on the ideal weight) should be increased sufficiently to allow the deficiencies to be covered. It is appropriate to take multivitamins in all these patients. It is also essential that during rebalancing, the administration of minerals and trace elements is appropriate to prevent the development of hippopotasemia, hypomagnesemia, hypophosphatemia, life-threatening disorders. Most patients who can eat and swallow can be treated orally. However, if anorexia is an important problem or if the patient is edentated, the diet should be supplemented with liquid formulas either per bone or by assisted enteral feeding.
Treatment of a severe MPM is much more urgent and more complicated for several reasons: 1. Precipitating diseases tend to be much severe and more difficult to treat and may not be able to restore the balance of nitrogen compounds until the infection and fever are controlled; 2. The degree of malnutrition itself may prevent recovery from associated life-threatening conditions, so early intervention with assisted enteral nutrition or parenteral nutrition may be urgently necessary; 3. The introduction of nutritional factors into the gastrointestinal tract may in itself cause diarrhea due to atrophy of the intestinal mucosa and the decrease of pancreatic and intestinal enzymes, and parenteral nutrition may also be necessary 4. Associated deficient situations are common and care should be taken when administering multivitamins, trace elements and all essential minerals so that this is in an efficient/sufficient quantity to restore the body's reserves. Recovery in adults may be slow and limited, but in children it is between 3 and 4 months. Complete nutrition education, psychosocial stimulation and rehabilitation programs should be established in all cases.
Next time we talk about obesity...
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Dorin, Merticaru