Protein Energy Malnutrition Flashcards
spectrum of manifestations depends on what 5 factors?
severity duration age cause association w/ other problems
maramus
simple wasting of fat and muscle mass due to energy deficiency
kwashiorkor
- edematous without wasting and is attributed to protein deficiency
- related to metabolic stress and inflammation
marasmic kwashiorkor
combination of chronic energy deficiency with chronic or acute protein deficit manifested as wasting and edema
global burden malnutrition
- poor nutrition causes half of deaths of children under the age of 5
- 1/5 global disease burden attributed to effects of protein energy malnutrition and micronutrient deficiency
FTT
mild protein energy malnutrition
malnutrition occurs in what percentage of hospitalized patients
50%
-is associated with higher rates of morbidity and mortality and longer hospital stays
anorexia nervosa
- represent a successful adaptation to starvation
- less than critical total lean tissue depletion, weight stability, normal plasma albumin, normal peripheral blood total lymphocyte count, intact immune response
- susceptible to abrupt decompensation with minor insult
5 at risk groups for protein energy malnutrition
- 0-12mths: marasmus/severe wasting
- 12-24mths: kwashiorkor/ edematous PEM
- Older children: stunting common; milder wasting
- pregnant/lactating women: PEM
- Elderly: PEM
wasting deficit is represented by what ratio
weight for height
stunting deficit is represented by what ratio
height for age
alternative use of z scores
Stunting:
clinical features
marasmus > kwashiorkor
weight loss
loss of muscle
loss of fat
clinical features that are absent in marasmus
edema
hepatomegaly
skin lesions
+/- in marasmus but present in kwashiorkor
anorexia
hair changes
clinical features
kwashiorkor > marasmus
psychological impairment
infections
+/- in kwashiorkor:
anorexia
hair changes
absent in marasmus:
edema
hepatomegaly
skin lesions
clinical feature
marasmus = kwashiorkor
diarrhea
6 physiologic responses to severe acute malnutrition: marasmus
- decreased energy expenditure (decreased activity, bradycardia, hypothermia)
- decreased Na pump activity
- fuel utilization to mobilization body fat (increased ketones, decreased gluconeogenesis)
- muscle protein catabolism (decreased overall protein turnover)
- decreased inflammatory response/ immune fxn
- impaired GI fxn (dismotility, malnutrition)
hallmarks of adaptation to severe PEM
- loss of functional reserve
2. loss of physiological responsiveness
pathophysiology of kwashiorkor
failure of normal adaptive response of protein sparing normally seen in fasting state
contributing factors to kwashiorkor
infectious stress, cytokine release, relative micronutrient deficiencies, free radical exposure, oxidative damage
-possible role of microbiome
why would some assume that nutritional status is adequate in kwashiorkor?
fat reserves and muscle mass unaltered
Signs of kwashiorkor
- Flaky paint: skin lesions
- Flag sign: hair texture/ color change
- moon facies: generalized edema
5 metabolic derangements associated with kwashiorkor
- hypoalbuminemia & enlarged fatty liver –> edema
- Increased permeability of biological cell membranes –> edema
- impaired Na/K homeostasis (Na excess, K deficiency)
- hypotransferrinemia (anemia)
- Impaired immune system (infection)
things to avoid when resolving life threatening conditions in PEM
over-hydration
excessive Na
hypoglycemia
resolving life threatening conditions in PEM
- restore circulation with enteral
- K+ supplements (+/-) Mg
- treat infections
- small, frequent oral feeds
restore nutritional status
Goal= Maintain
-small, frequent
Nutritional rehabilitation
- advance energy intake to 1.5X normal and 3-4X protein needs
- prolonged restoration of appetite
- familiar foods
- physical activity: recover cardiorespiratory and skeletal function
when to start nutritional rehabilitation
1-2 weeks after initial stabilization
after resolution of edema
3 derangements seen in re-feeding syndrome that can lead to sudden death
Potassium: intracellular
Phosphorus: intracellular
Magnesium
Potassium in re-feeding syndrome
increased insulin secretion --> intracellular glucose and K+ --> decreased serum K+ --> altered nerve/ muscle fxn
phosphorus in re-feeding syndrome
increased insulin secretion --> intracellular P --> Increased intracellular phosphorylated intermediates --> P trapped in intracellular space
magnesium in re-feeding syndrome
increased metabolic rate
–> increased requirement
= cofactor for ATPase
