malnutrition Flashcards
- describe its environmental and biological causes & clinical consequences.
Causes of the problem:
Social and economic factors: poverty, ignorance, inadequate breastfeeding and weaning practices
Biologic factors: maternal malnutrition (low birthweight infants), infectious diseases
Environmental factors: overcrowded &/or unsanitary living conditions, agricultural patterns, droughts, floods, wars
There are major ties between infection and malnutrition.
Measles- predisposes to blindness from vitamin A deficiency
diarrhea- is a major factor in the pathogenesis of PEM.
Malnutrition-impairs the function of the immune system and the function of the gastrointestinal tract. => vicious circles can be established between malnutrition, infection, and diarrhea.
In the United States, the effects of malnutrition due to nutrient deficiencies are often not so dramatic as in developing countries. Nevertheless, they are a frequent occurrence, especially in hospitalized patients. Many hospitalized infants and young children have some evidence of growth faltering or “failure to thrive” (FTT), a term used in this country to denote mild protein-energy malnutrition. Malnutrition secondary to chronic disease or to the acute effects of surgery, trauma, sepsis, etc. is estimated to occur in up to 50% of hospitalized patients. Numerous studies have documented higher rates of morbidity and mortality, and longer hospital stays in patients with evidence of malnutrition. Individuals with anorexia nervosa represent, in an otherwise healthy person, a “successful adaptation” to starvation, with less than critical total lean tissue depletion, weight stability, normal plasma albumin, normal peripheral blood total lymphocyte count, and intact immune response. They manifest the adaptations to starvation/marasmus noted below, and are susceptible to abrupt decompensation in response to minor insult.
Several reports have been published of infants in the U.S. presenting with classic kwashiorkor secondary to parents’ or physicians’ perceptions of milk allergy, intentional use of fad or unorthodox diets. Whether FTT is attributable to “non-organic” causes such as inadequate parenting, or to organic illness (e.g. malabsorption, chronic illness, etc), protein energy malnutrition is the final common pathway.
- Compare and contrast energy and substrate metabolism in short term and long term starvation.
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compare and contrast features of marasmus and kwashiorkor.
CLINICAL FEATURES
MARASMUS KWASHIORKOR
Weight Loss ++++ ++
Loss of Muscle ++++ +
Loss of Fat ++++ +
Edema — ++++
Psych Impairment ++ ++++
Anorexia +/- ++++
Hepatomegaly — ++
Ass. Infections ++ ++++
Diarrhea +++ +++
Skin Lesions — ++
Hair Changes +/- ++
- Identify likely physical exam findings associated with the two major types of undernutrition.
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- Describe general appropriate treatment approaches to PEM.
Resolving life-threatening conditions
Cautious restoration of circulation – enteral preferred; avoid over-hydration
Potassium supplements ± Mg++; avoid excessive Na+
Treatment of infections (signs/symptoms may be mild/absent)
Avoid hypoglycemia (preferably by small, frequent oral feeds)
Restoring nutritional status without abruptly disrupting homeostasis*
Begin slowly (pt is adapted to malnourished state)
Small frequent (≤ q 4 hr) feeds, liquid oral or via nasogastric tube
Initial goal = maintenance protein and energy requirements (ie, not catch-up amounts)
Diet should be high biologic quality protein, high fat
Replete specific micronutrient deficiencies (especially K, Mg, P, Zn, Vitamin A )
Ensuring nutritional rehabilitation
Gradually advance energy intakes to 1.5x normal and 3-4x protein needs;
Usually begins 1-2 wk after initial stabilization – after resolution of edema
Restoration of appetite may be prolonged, especially in kwashiorkor
Introduction of familiar foods
Emotional & physical stimulation, including physical activity to enhance recovery of cardiorespiratory and skeletal function.
- Describe metabolic derangements associated with “refeeding syndrome.”
Refeeding a starved person may result in predictable metabolic derangements, esp due to acute shifts from extracellular to intracellular spaces. Most common & potentially dangerous: K+, P, & Mg++
Potassium: ↑ insulin secretion (in response to feeding) → intracellular glucose & K+ → ↓ serum K+ → altered nerve/muscle function
Phosphorus: ↑ insulin secretion → intracellular P; ↑ intracellular phosphorylated intermediates; P “trapped” in intracellular space;
Magnesium: ↑ requirements w/ ↑ metabolic rate (= co-factor for ATPase)
Thiamine
Marasmus
refers to severe wasting of fat and muscle mass, due primarily to energy deficiency; it is most equivalent to “simple” starvation
Kwashiorkor
edema, hypoalbuminemia
Moon facies
Flag sign of hypo pigmented hair
Hepatomegaly, flaky paint skin (can be pallagroid)
refers to edematous PEM, without wasting and classically attributed to “protein deficiency”; now clear related to metabolic stress & inflammation .
Marasmic kwashiorkor
is a combination of chronic energy deficiency and chronic or acute protein deficit, and is manifested clinically with evidence of both wasting and edema.
- Describe the pathophysiology and adaptive responses Marasmus
The “normal” physiologic response to starvation includes:
Reduction in energy expenditure ( ↓ physical activity, bradycardia, hypothermia)
Decreased activity of sodium pump
Shift in fuel utilization to mobilization of body fat (↑ ketones, ↓ gluconeogenesis)
Muscle protein catabolism (but w/ ↓ overall protein turnover)
Decreased inflammatory response & impaired immune function
Impaired function of G-I tract (dysmotility, malabsorption)
(Reduced body mass)
While these and other responses result in decreased nutrient demands and achieve a new equilibrium, if the nutritional deprivation persists, the patient is less able to adapt to complications, such as an infectious insult. As reserves are depleted, the individual is susceptible to injury that a normal host could withstand with little repercussion: ie, loss of functional reserve and loss of physiological responsiveness to stress are the hallmarks of the adaptation to severe PEM.
- Describe the pathophysiology and adaptive responses Kwashiorka
The etiologic mechanisms of kwashiorkor are not completely understood, it is generally considered a failure of the normal adaptive response of protein sparing that is normally seen in a fasting state. As noted above, classically protein deficiency in the face of adequate energy intake was thought to be etiologic, but clearly this is an oversimplification. Contributing factors include infectious stress, cytokine release, relative micronutrient deficiencies and possibly free radical exposure and oxidative damage. Potential role of the enteric microbiome recently highlighted (NEJM, 2013). Fat reserves and muscle mass tend to be unaltered; this may lead to the assumption that nutritional status is adequate. Other characteristic clinical findings include skin lesions (“flaky paint”), hair texture and pigmentation changes (“flag sign”), and generalized edema (“moon facies”). The list below indicates some of the metabolic derangements seen in kwashiorkor, which is associated with a relatively higher mortality than marasmus.
Hypoalbuminemia & enlarged fatty liver → edema
Increased permeability of biological cell membranes → edema
Impaired sodium/potassium homeostasis (sodium excess, potassium deficiency)
Hypotransferrinemia (anemia)
Impairment of immune system (infection)
What’s most common PEM in infants?
Marasmus, severe wasting
What’s most common PEM in children
Kwashiorkor, voluntary restrictive alternative feeding
What causes acute weight loss
Social deprivation
Anorexia nervosa
Barbaric surgery
Underweight
