TBL-Obesity and Nutrition Flashcards
Primary malnutrition
Carbs, fats, proteins, vitamins and/or minerals are missing from the diet
Secondary malnutrition
Nutrient supply is adequate, but malnutrition is due to insufficient intake, malabsorption, impaired utilization/storage, excess loss or increased need for nutrients
6 common causes for malnutrition
1) Poverty 2) Infection 3) Illness 4) Alcoholism 5) Ignorance 6) Self-imposed dietary restriction
Definition of a malnourished child. What could this definition possibly be masked by?
< 80% normal weight. May be masked by generalized edema. Fat stores, muscle mass and serum proteins can provide a better picture in this setting.
A child presents with recurrent infections, emaciated extremities and his head appears too large for his body. He below 60% normal weight for his age group. What nutritional deficiency is causing his condition? What would you expect to see on labs of serum albumin, leptin, cortisol and CBC?
Marasmus. This is caused by depletion of the somatic protein compartment and fat stores. Serum albumin will be normal, leptin will be low, cortisol high and CBC will show anemia and leukopenia, particularly T-cells.
A child presents with a recurrent infections, swollen abdomen, apathy, listlessness and loss of appetite. On physical exam you note the skin has a flaky paint appearance, alternating bands of pale and darker hair and spared subcutaneous fat and muscle mass. What is likely causing this child’s condition?
Kwashiorkor. Protein depravation associated with a strictly carbohydrate-only diet causes severe loss of the visceral protein compartment, hypoalbuminemia and generalized edema. This can also be caused by chronic diarrhea, nephrotic syndrome and extensive burns.
You visit an 89 year old bedridden patient complaining of recurrent infections and impaired wound healing. On physical exam you note depletion of subcutaneous fat in the arms, chest, shoulders and metacarpal regions. Muscle is wasted in the quadriceps and deltoid muscles. She has ankle edema. What is likely causing her symptoms and how do you assess her nutritional status?
She has secondary protein-energy malnutrition (PEM). You can assess her nutritional status with the Mininutritional assessment (MNA).
Kwashiorkor liver
Enlarged and fatty
Why infants with kwashiorkor initially do not respond well to milk-based diets
Small bowel loss of villi and intestinal enzymes due to decreased mitotic activity.
Why is the bone marrow hypoplastic in kwashiorkor and marasmus?
Decreased red cell precursors from iron, folate and/or protein deficiency. It could also be due to anemia of chronic disease from chronic parasitic or worm infection.
CNS effects of kwashiorkor
Cerebral atrophy, reduced neurons, impaired myelinization
Conditions that present with cachexia
AIDS, GI, pancreatic and lung cancers
A patient with a history of HIV presents with 20 pound weight loss in the past 2 months and fatigue. Physical exam shows muscle atrophy, anorexia and edema. Labs reveal anemia. What is likely causing his condition? What is a common cause of mortality associated with this condition?
Cachexia is common w/AIDS. Proteolysis-inducing factor (PIF found in urine) and pro-inflammatory cytokines (TNF, IL-2 & IL-6) produced by tumors activate NF-kB signaling to activate the muscle-specific ubiquitin ligases that degrade the myosin heavy chain.
A patient presents with amenorrhea, cold intolerance, bradycardia, constipation, changes in skin/hair, dry/scaly skin, decreased bone density, anemia, lymphopenia and hypoalbuminemia. What is causing her condition? What is a common cause of mortality associated with this condition?
Anorexia: decreased gonadotropin-releaseing hormone -> decreased LH -> decreased FSH, which causes amenorrhea and is diagnostic for anorexia. Thyroid hormone decrease -> cold intolerance, bradycardia, constipation and changes in skin/hair. Electrolyte abnormalities -> dry/scaly skin. Low estrogen levels -> decreased bone density. Cardiac arrhythmia is common cause of sudden death due to hypokalemia electrolyte imbalance.
A patient presents with cardiac arrhythmias, aspiration pneumonia and gastric cardiac rupture. What is likely causing this patient’s condition?
Bulimia.
What are the components of the peripheral afferent systems in regulation of satiety, energy expenditure and hunger?
Leptin/adiponectin from fat cells. Ghrelin from stomach, peptide YY from ileum/colon and insulin from pancreas.
What efferent neurohormonal signals are generated by the arcuate nucleus in the hypothalamus?
1st order neurons: pro-opiomelanocortin/ cocaine and amphetamine-regulated transcripts (POMC/CART) and neuropeptide Y/Agouti-related peptide (NPY/AgRP). 2nd order neurons that communicate w/POMC and CART carry signals to control food intake and regulate energy expenditure from the hypothalamus.
How do POMC/CART neurons enhance energy expenditure and weight loss?
The induce production of alpha-melanocyte-stimulating hormone (MSH) and activate melanocortin receptors (MC3/4) in second order neurons
How do POMC/CART neurons promote food intake and weight gain?
Activation of Y1/5 receptors on secondary neurons.
What genetic conditions can cause disorders of leptin?
Ob gene (leptin) or db gene (leptin receptor)
What stimulates leptin secretion? What effect does leptin have on the body?
Abundant fat stores. Leptin stimulates physical activity, heat production and energy expenditure. It also mediates thermogenesis, hematopoiesis and lymphopoiesis.
How does leptin increase energy expenditure and inhibit hunger?
Stimulation of POMC/CART neurons to produce MSH. Inhibit NPY/AgRP neurons.
Mutations responsible for 5% of obese patients
MC4R. This results in no signaling of satiety. Note that leptin mutations are rare.
Mutation that causes obesity associated with Wilm’s tumor, anuria, genitourinary defects and mental retardation (WAGR syndrome)
Brain-derived neurotrophic factor (BDNF)
What does adiponectin do?
Binding to AdipoR1/R2 stimulates fatty acid oxidation in muscle, decreases influx of fatty acids to liver, decreases glucose production in liver (increasing insulin sensitivity) and inactivates acetyl CoA carboxylase (inactivating fatty acid synthesis). Note that decreased levels of adiponectin in obese people contributes to hyperinsulinemia and insulin insensitivity.
Why do obese people struggle with sub-clinical inflammatory states?
Adipose tissue secretes cytokines (TNF, IL-6, IL-1, IL-18), chemokines and steroid hormones.
Why might genetics make it difficult to maintain healthy weight after losing weight?
of adipocytes remains the same.
Where does ghrelin come from and what does it do?
Produced in stomach and hypothalamus. Binds to growth hormone secretagogue receptor in hypothalamus and pituitary. Stimulates NPY/AgRP neurons to increase food intake. Note that these levels rise before meals and fail to fall after meals in obese patients.
Where does PYY come from and what does it do? What syndrome is it associated with?
Produced in ileum and colon. It reduces energy intake by stimulating POMC/CART neurons and is associated with hyperphagia and obesity in patients with Prader-Willi syndrome (has low levels of PYY)
Where does amylin come from and what does it due?
Comes from pancreas. Reduces food intake and weight gain by stimulating POMC/CART neurons.
Metabolic syndrome
Adiposity, insulin resistance, hyperinsulinemia, glucose intolerance, HTN, hypertriglyceridemia and low HDL.
What causes hypertension in obese patients?
Insulin resistance/hyperinsulinemia
Why are obese patients at risk for coronary artery disease?
Hypertriglyceridemia and low HDL levels
Liver disease w/obesity
Non-alcoholic fatty liver disease
Why are obese patients at risk for cholelithiasis?
Increased total body cholesterol
Why are obese patients at risk for right-sided heart failure?
Hypoventilation (pickwickian) syndrome. Apnea -> polycythemia -> right-sided heart failure.
Obese male cancer associations
Esophageal adenocarcinoma, thyroid, colon and kidney cancers.
Obese female cancer associations
Esophageal adenocarcinoma, endometrial, gallbladder and kidney cancers.
Why can obesity be a significant risk factor for cancer?
Hyperinsulinemia can activate cell growth pathways. It also increases insulin-like growth factor-1 (IGF-1) and inhibits IGF-binding proteins (IGFBP-1 and IGFBP-2). IGF-1 is mitogenic and anti-apoptotic and is expressed in many tumors. In addition to activating many insulin receptors that stimulate cell growth, it also increases production of VEGF.
How does obesity specifically increase risk for breast and uterine cancers?
Increases synthesis of estrogen from androgen precursors in adipose tissue. Insulin increases androgen synthesis and enhances estrogen availability by inhibiting the production of sex-hormone-binding globulin (SHBG) in the liver.
