Week 2 Flashcards
There is only one hormone/factor known to increase appetite. From where is this factor secreted, and how do circulating levels change after a meal?
Ghrelin is a peptide hormone secreted from the fundic stomach during fasting – levels decrease after meals.
Your patient comes in for his yearly checkup. You note that he has gained a few pounds every year since you started seeing him 5 years ago. Is his basal metabolic rate likely higher or lower today than it was 5 years ago? Is is possible that genetics contribute to this weight gain?
Higher BMR, and yes. BMR has a positive correlation with body mass, likely due to increased fat free mass and increased energy cost of physical activity. Most individuals do not gain weight due to “thrifty” metabolism. There are hundreds of genetic variants associated with high BMI. Obesity reflects complex interplay between genetics and environment and the relative contribution of individual factors varies by each case.
Waist circumference is predictive of likelihood to develop insulin resistance/diabetes mellitus. What causal mechanisms explain this link?
Visceral fat levels are associated with increased circulation of free fatty acids, which can impair insulin action, increased intracellular lipid accumulation (ectopic fat), and altered levels of circulating cytokines which can modify insulin action (TNFa, IL6: levels increased; adiponectin: levels reduced)
Which two hormones are produced by the posterior pituitary? When are they administered clinically?
Vasopressin, oxytocin. Vasopressin (AVP) has vasoconstrictive and antidiuretic properties. AVP is given occasionally in the context of esophageal varices. AVP is more often given in the form of desmopressin (DDAVP), which is a synthetic analogue with high antidiuretic activity relative to pressor activity. Thus DDAVP is used for central diabetes insipidus (insufficient AVP production). Oxytocin acts through Gq receptors to promote smooth muscle contraction, thus oxytocin is given clinically when labor is protracted or arrested.`
Describe the idea behind the Developmental Origins of Health and Disease hypothesis and state a few potential mechanisms at play.
Early life events (including prenatal factors such as maternal nutrition and placental insufficiency) influence later risk of disease development. This may relate to epigenetic factors such as methylation of genes and acetylation of histones.
What metabolic adaptations take place in the context of starvation to lengthen survival? Over what time span does this occur?
Decreased energy expenditure, decreased glucose utilization rate and increased utilization of alternative fuels (FFAs, ketone bodies). Tissues start using less glucose within the first day; ketone bodies become a primary fuel after 2 days (timeline is inexact and dependent on degree of nutrient restriction)
A patient with history of T1DM and CAD presents with paresthesias, palpitations, confusion, and anxiety. What is the first lab value you would like to see, and what (mechanistically) do you hypothesize happened to this patient?
Glucose. Hypoglycemia is a major cause of death in T1DM and must always be considered in a patient with neuroglycopenic sx (behavioral change, confusion, fatigue, etc.), adrenergic sx (palpitations, tremor, anxiety), and/or cholinergic sx (sweating, hunger, paresthesias). Likely, this patient had excess insulin relative to glucose load (extra dose, secretagogue use, insulin-independent glucose uptake with exercise, reduced insulin clearance eg renal failure)
