TBL: Nutrition Robbins Flashcards
This deck just deals with the objectives of the session, which are covered by the few assigned Robbins pages. Not reading 12 pages of Mark’s.
:)
Murasmus
Marasmus is a form of severe malnutrition characterized by energy deficiency. A child with marasmus looks emaciated. Body weight is reduced to less than 60% of the normal (expected) body weight for the age.
Loss of muscle mass, looks like a skeleton
Kwashiorkor Disease
a form of malnutrition caused by protein deficiency in the diet, typically affecting young children in the tropics.
We see edema in these patients due to increased water retention, which masks the loss in weight
Cachexia
Protein energy malnutrition in advanced AIDS and cancer patients
Discuss the mechanism behind Leptin
Leptin plays a key role in energy balance. Its output from adipose tissue is regulated by the abundance of fat stores. Leptin binding to its receptors in the hypothalamus increases energy consumption by stimulating POMC/CART neurons and inhibiting NPY/AgRP neurons
Discuss the basic regulation of energy balance
It’s complex.
Three main components:
- Afferent signals, provided mostly by Insulin, Leptin, ghrelin, and peptide YY
- Central hypothalamic system: Integrates afferent signals and triggers efferent signals
- Efferent signals which control energy balance
Discuss POMC/CART neurons
Enhance energy expenditure and weight loss through the production of Melanocyte Stimulating Hormone and activating melanocortin receptors 3 and 4 in second order neurons, which in turn upregulate TSH and CRH to increase our base metabolic rate and anabolic metabolism, favoring weight loss.
Discuss NPY/AgRP neurons
Promote food intake and weight gain by activating Y1/5 receptors in secondary neurons, which then release melanin concentrating hormone to stimulate appetite
Where do we find leptin, PYY and ghrelin
Leptin - Adipose
PYY - Intestines
Ghrelin - Stomach
What is the cause of mortality in cachexia patients?
Atrophy of the diaphragm and respiratory muscles
Two tumor/immunosuppressive factors related to cachexia
- Proteolysis-inducing factor - a glycosylated polypeptide excreted in the urine of weight-losing patients with pancreatic, breast, colon, and other cancers
- Lipid mobilizing factor - Increases fatty acid oxidation and proinflammatory cytokines like TNF (originally called cachectin) and IL-6
How do proteolysis-inducing factor and inflammatory cytokines break down skeletal muscle?
Through the Nf-kappa B induced activation of the ubiquitin proteasome pathway which induces myosin heavy chain breakdown via ubiquitin ligases that are muscle specific.
Lab values/Clinical Signs Anorexia vs. Bulimia
Anorexia - Similar to PEM
- Amenorrhea - Decreased secretion of gonadotropin releasing hormone, with subsequent decreased LH and FSH secretion
- Common findings because of decreased thyroid function: Cold intolerance, bradycardia, constipation
- Decreased bone density due to low estrogen
With both diseases we worry about arrhythmias and sudden death
Bulimia
- Amenorrhea in less than 50% - Gonadotropin and weight remain relatively normal
- Most effects secondary to laxatives and diuretics like hypokalemia, pulmonary aspiration of stomach contents and esophageal rupture.
What part of the hypothalamus is involved in satiety and hunger?
Arcuate nucleus
Adiponectin
Found to be decreased in the obese. “Gaurdian angel against obesity,” this guy directs fatty acids to muscle for oxidation and decreases what is sent to the liver to reduce blood TG levels.
It floats around in monomer aggregates and binds AdipoR1 and R2, which are everywhere, but highest in skeletal muscle and the liver.
Binding causes a cAMP dependent protein kinase, which in turns acetylates (inactivates) Acetyl Coenzyme A carboxylase, a key enzyme required for fatty acid synthesis.
