malnutrition Flashcards
Marasmus
Severe wasting of fat and muscle mass, due primarily to energy deficiency; slower onset, better adaptation. it is most equivalent to “simple” starvation
Kwashiorkor
edematous Protein energy malnutrition, without wasting and classically attributed to “protein deficiency”; rapid onset, mal-adaptation. now clearly related to metabolic stress & inflammation
Marasmic kwashiorkor
combination of chronic energy deficiency and chronic or acute protein deficit, and is manifested clinically with evidence of both wasting and edema.
starvation
pure caloric deficiency- organism adapts to conserve lean body mass and increase fat metabolism
Cachexia
associated with inflammatory or neoplastic conditions. Not reversed by feeding
Sarcopenia
subnormal amount of skeletal muscle w/out weight loss
social/economic causes of malnutrition
poverty, ignorance, inadequate breastfeeding and weaning practices
biologic causes of malnutrition
maternal malnutrition (low birthweight infants), infectious diseases
environmental causes of malnutrition
Overcrowded &/or unsanitary living conditions, agricultural patterns, droughts, floods, wars
failure to thrive
mild protein energy malnutrition
Malnutrition in hospitalized patients
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.
Who is most at risk for PEM
infants, acute weight loss, chronic illness, elderly
What type of malnutrition is most common in 0-12 month olds
marasmus/severe wasting most common form of PEM, but stunting also very common, and often starts during first year of life
What type of malnutrition is most common in 12-24 month olds
kwashiorkor/edematous PEM more common
What type of malnutrition is most common in older children
stunting common; typically degree of wasting is milder;
What type of malnutrition is most common in pregnant/lactating women
w/ PEM, effects primarily on fetus, neonates, and infants
Malnutrition in elderly
tend to suffer from PEM
Which groups have lowest rates of PEM
adolescents, adult men and non-pregnat/non lactating women
What is wasting
decreased weight relative to length
define severe vs mild wasting
severe : 65% IBW. Mild: 83% IBW
compare clinical features of Marasmus vs kwashiorkor
marasmus: Mostly weight loss, loss of muscle, loss of fat, diarrhea. NO edema, hepatomegaly or skin lesions. Kwashiorkor: Mostly edema, psychological impairment, anorexia, infections, diarrhea, and hepatomegaly
Pathophys of marasmus
Normal response to starvation. Muscle: utilize triglycerides and fatty acids. Brain: increase ketone utilization, decrease glucose. Liver: decrease gluconeogenesis. Muscle: decrease protein degradation. Liver/kideny: decrease urea production and excretion. Result: utilize fat stores, minimize muscle wasting, decrease basal metabolic rate
Endocrine changes in response to starvation
decrease insulin, decrease thyroid, increase epi and corticosteroids.
How does blood sugar change with starvation
it stays in normal range due to gluconeogensis
How does GI tract change with starvation
mucosal atrophy, decreased secretions, decreased motility
how does Heart change with starvation
myocardial atrophy, decreased cardiac output
Pathophys of kwashiorkor
abnormal adaptive response to protein deficiency. Hypoalbuminemia, edema, increased insulin, decreased lipolysis, increased hepatic fatty acid synthesis (enlarged liver). Erythematous hyperpigmentation, and dry brittle depigmented hair (flag sign)
Treatment of severe PEM
Especially for kwashiorkor- go slowly. Resolve infections, restore nutritional status w/out abruptly disrupting homeostasis.
Refeeding syndrome
Broad range of metabolic consequences occurring due to rapid reinstitution of nutrients (& energy/substrate) in pt w/ PEM; can result in sudden death
Pathophys of refeeding syndrome
Going from catabolic to anabolic state results in fluid shifts and heart failure. Requires E, nutrients, enzymes. K, P, Mg and thiamine often get deranged
potassium in refeeding syndrome
Increased insulin secretion in response to feeding results in intracellular glucose and K, leading to decreased serum K and altered nerve/muscle function
Phosphorus in refeedig syndrome
Increased insulin secretion leads to intracellular P and phosphorylated intermediates, such as glucose. Decreased serum P causes altered nerve and muscle function
Mg in refeeding syndrome
increased requirement with increased metabolic rate (co Factor for ATPase)
Thiamine in refeeding syndrome
rapid depletion due to being a co factor in glycolysis leads to cardiomyopathy +/- encephalopathy
