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12 Cards in this Set
- Front
- Back
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How is BMI calculated?
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weight (kg) / (height (m) squared)
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What are the BMI criteria for normal weight, overweight, obesity and morbid (extreme) obesity?
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normal: 18.5-24.9
overweight: 25-29.9 obese I: 30-34.9 obese II: 35-39.9 morbidly obese: >40 |
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How does the body respond to return to its weight set point when you're trying to lose weight?
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decreased energy use
decreased basal metabolic rate decreased SNS tone |
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What are some medical complications of obesity?
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Type 2 diabetes
decreased life expectancy increased CV risk, HTN, hyperCE, atherosclerosis gallstones endocrine dysfunctions (amenorrhea, PCOS) cancers of GI and reproductive system hypoventilation, sleep apnea osteoarthritis, degenerative heart disease |
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How does the adipose distribution affect health?
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visceral adiposity is bad (omental and deep subcutaneous, "apple-shaped"). It has more adverse metabolic effects and does not release adiponectin.
subcutaneous adiposity (superficial storage depot, especially hips, thighs and buttocks, "pear-shaped") is no atherogenic and does secrete adiponectin |
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How does adipose tissue affect insulin action?
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-FFA and TNF-alpha secreted by fat induces insulin resistance.
-adiponectin secreated by fat enhances insulin sensitivity and is vascular protective (only secreted by subcutaneous fat) |
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How is metabolic syndrome defined?
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glucose intolerance/diabetes (fasting glucose > 100 mg/dL)
hypertension (>130/85) waist size (men > 40in, women > 35 in) high TG (>150) low HDL (men <40, women <50) small dense LDL abnormal thrombolysis (decreased plasminogen activator inhibitor 1) endothelial dysfunction (inflammatory changes) |
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What's acanthosis nigrans?
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A clinical sign of insulin resistance.
hyperpigmented, hypertrophic change in axilla or neck folds, thought to be from epidermal thickening due to insulin binding to IGF-1 receptors to enhance skin growth |
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What's the pathogenesis of type 2 diabetes?
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1. obesity-related insulin resistance
2. inadequate beta-cell secretion after an initial increase to try to keep up. Due to glucotoxicity (impairs insulin secretion), lipotoxicity (FFA in pancreas impairs release, in muscle/liver impairs insulin action), deficient incretins. 3. excessive secretion of glucagon by alpha-cells (causes increased hepatic glucose production. |
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What are incretins and what do they do?
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GLP-1: from ileal/colonic L cells, increases glucose-dependent insulin secretion after a meal, decreases glucagon, slows food passage, decreases appetite and weight.
GIP: from duodenal K cells, stimulates glucose-dependent insulin secretion after a meal This explains the difference between blood glucose after ingested glucose vs IV glucose. Degraded by DPP-4. Incretins are decreased in type 2 diabetes --> post-meal abnormalities. |
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What does amylin do?
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Co-secreted with insulin from beta cells.
-suppresses inappropriate glucagon -decreases gastric emptying -decreases appetite and caloric intake -reduces blood glucose peak after meals Deficient in type 1 and type 2 diabetes. |
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What are the criteria for diabetes?
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fasting hyperglycemia (>126) or
failed OGTT (>200 after 2 hrs) or random glucose > 200, with symptoms or HbA1c > 6.5 % |
