Recovery
What are F-100 and F-75
F-100 and F-75 (also known as Formula 100 and Formula 75) are therapeutic milk products designed to treat severe malnutrition. F-75 is considered the "starter" formula, and F-100 the "catch-up" formula. The designations mean that the product contains respectively 75 and 100 kcals per 100 ml. Both are very high in energy, fat, and protein, and provide a large amount of nutrients. Ingredients include concentrated milk powder, food oil (sometimes grease), and dextrin vitamin complexes. The formulas may be prepared by mixing with the local water supply. Sometimes Plumpy'nut is substituted for F-100. F-75 may be cereal-based in place of milk. F-75 provides 75 kcal and 0.9 g protein per 100 mL, while F-100 provides 100 kcal and 2.9 g protein There are other variants like Low Lactose F-75 and Lactose Free F-75, which are used in case of persistent diarrhea in severe acute malnutrition.
Appetite differences between marasmus and kwashiokor
Children with marasmus tend to have voracious appetites while children with kwashiorkor tend to have a loss of appetite
The meaning of the word Kwashiokor
"The sickness the baby gets when the new baby comes"- derived from the Ga language of Ghana
Cause of kwashiorkor vs marasmus
Kwashiorkor is caused by sufficient calorie intake but severely inadequate protein intake.
Marasmus is caused by severe malnutrition (inadequate calorie/protein intake)
What are the 3 sources of amino acids for the body
Food, de novo synthesis, and protein degradation
Describe the effects of kwashiorkor and a carbohydrate-only diet on vitamin levels and how this affects vision
Decreased apolipoprotein production → inhibited lipid transport from the liver → decreased transport of fat-soluble vitamins → decreased vitamin levels
Vitamin A, which plays a large role in vision, is fat-soluble. There will be an issue getting it to the eyes if we lack apolipoproteins
Where does the body get protein in a pt with kwashiorkor vs marasmus?
From a functional standpoint, there are two protein compartments in the body: the somatic compartment, represented by proteins in skeletal muscles, and the visceral compartment, represented by protein stores in the visceral organs, primarily the liver.
The somatic compartment (skeletal muscle) is affected more severely in marasmus, and the visceral compartment (primarily the liver) is depleted more severely in kwashiorkor.
What metabolic processes are happening in kwashiorkor in the fed state?
We still have carbs and so we are in an insulin dominant state meaning glycolysis and glycogenesis can occur normally. Fatty acid synthesis is happening but to a lesser extent since tissues can't receive TG as much, so it uses adipose tissue as a source of TG
Symptoms and complications marasmus can cause (name 5)
What are the external signs of marasmus? (name 5)
Long-term consequences of protein-energy malnutrition (kwashiorkor) and prolonged starvation (marasmus) even after successful treatment.
Stunted growth slowed brain development, and repeated infections.
Long term consequences of kwashiorkor (try to name at least 5)
Fatty liver + hepatomegaly
Mental defects (lethargy and listlessness) - due to the lack of essential amino acids in the diet (ex: tryptophan which is important for neurotransmitter synthesis)
Edema/ascites
Poor immune system- due to lack of micro/macro nutrients (ex: vitamin E)
Loss of ability to make proteins if you reach the point of no return.
Stunted growth
What is an emaciated appearance and which pathology is it seen in?
This is seen in marasmus
Main fuel source in marasmus and what it leads to physically
Beta oxidation- leads to decreased subcutaneous fat
What leads to ascites/edema formation in kwashiorkor pts?
Reduced protein intake leads to hypoalbuminemia. Less albumin in the blood → oncotic pressure falls and water leaks out of the blood vessels into the tissues, resulting in edema.
Describe treatment of kwashiokor according to WHO regulations
During the early phase, children with kwashiorkor are given a liquid therapeutic “F75”-formulated diet to fulfill daily requirements (100 kcal/kg/day) and other micronutrient supplements while preventing excesses of sodium and proteins. When the child is stabilized and expresses an appetite/able to eat, either “F100”-concentrated milk diet or ready-to-use-therapeutic food (RUTF) are given for a minimum caloric intake of ∼175 kcal/kg/day during the maintenance phase. RUTF is a diet enriched with high levels of lipid, protein, multivitamins, and micronutrients. Children with kwashiorkor with no clinical signs and symptoms can be directly treated with RUTF from the beginning if they express an appetite and able to consume the daily recommended calories.
What metabolic processes are happening in kwashiorkor in the fasted state?
less gluconeogenesis compared to normal due to decreased amino acids.
Beta oxidation can still occur
What states are pt's in kwashiorkor vs marasmus in? (fed, fasted, starved)
Kwashiorkor: Body is not in the starved state because there is adequate amounts of carbohydrates in diet for glucose to be made, used and stored as fat the only thing missing is the proteins
Marasmus: permanent prolonged starved state, so increased beta oxidation and muscle wasting occurs to have baseline glucose for the brain to use even though muscle wasting is decreased. Fatty acids and ketones are the main fuel source of energy (usually deficient in most vitamins).
What is nitrogen balance, why do we care about it and when do we see a positive vs negative nitrogen balance?
Nitrogen balance: the amount of nitrogen incorporated in the body in a day equals the amount excreted. In normal adults, nitrogen intake matches nitrogen excreted (nitrogen equilibrium).
The state of protein nutrition can be determined by the nitrogen balance.
Positive nitrogen balance: excess of ingested over excreted nitrogen.
ex: growth, pregnancy
Negative nitrogen balance: output exceeds intake.
May follow surgery, advanced cancer, and nutritional disorders kwashiorkor and marasmus.
What causes fatty liver and hepatomegaly in kwashiorkor pts?
Fatty acids are synthesized in the liver and there is a lack of apolipoproteins and VLDL so the triglycerides and cholesterol cannot be packaged and shipped out of the liver allowing them to accumulate in the liver.
This is made worse by lipolysis during the fasted state by adipose tissue because the fatty acids keep coming and this leads to hepatomegaly.
Due to the predisposition of undernourished kids, what is typically given to children in addition to nutrition for treatment?
Undernourished children are more predisposed to infections, while chronic or repeated infections damage the digestive system impairing its ability to absorb nutrients, thus further aggravating malnutrition. RUTF combined with antibiotics treatment is an internationally accepted standard therapeutic approach that was shown to increase body weight and reduce the mortality in malnourished children.
Why might pts with kwashiorkor have delayed malnutrition diagnosis?
Patients with kwashiorkor have edema that can mask true growth failure due to the weight of the edema, delaying the diagnosis of malnutrition.
Explain the progression to muscle wasting in prolonged starvation
After utilization of glucose and glycogen stores, fatty acids for beta-oxidation and production of ketone bodies, the body must use glucogenic amino acids to keep blood sugar levels high enough for survival.
In prolonged fasting, the glycogen stores are first depleted and gluconeogenesis is turned on and non essential proteins in muscle, lactate, and glycerol are used as substrates for gluconeogenesis. If the body is not fed, fatty acid oxidation takes over as the primary source of fuel and the body will decrease its use of amino acids for gluconeogenesis in order to spare the muscle. Then the body turns to ketone bodies.
What are the "muscle sparing" mechanisms normally?
Usually, non essential amino acids like alanine are used as a substrate for gluconeogenesis. At some point the body decreases usage of non essential amino acids to spare the muscle.
Ketone body synthesis and utilization happens in prolonged fasting after beta oxidation. High amounts of ketones can inhibit the breakdown of proteins in muscle in order to spare the muscle. As you continue to use ketones in the starved state even though you produce a lot of ketones you are using a lot more so there are less ketones to inhibit the breakdown of muscle so you still get that muscle break down.
What metabolic processes aren't happening in pts with marasmus and why?
Constant glucagon-dominant state meaning no glycolysis, glycogenesis in the liver and no other insulin-dependent processes.
Also can't properly do gluconeogenesis in the liver because:
there is no protein feeding into it so muscle breakdown begins for fuel when beta oxidation and fat stores are depleted
lack of carb intake to replenish glycogen stores
relies on glycerol from lipolysis to feed into gluconeogenesis