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20 Cards in this Set
- Front
- Back
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Simplified glucose homeostasis parts and regulators
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Glucose Production in Liver and Kidneys - add to what eating
Glucose Uptake and utilization by tissues Regulated by insulin and counter-regulatory hormones (glucagon, GH, catecholamines, cortisol) |
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Glucose Production in Liver and Kidneys Normally and during Starvation
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Normal - Endogenous glucose adds to gut absorbed pool via liver (75%) and kidney (25%). Kidney uses most of it's produced so not added much to pool. Also fat and muscle can uptake based on insulin levels
Starvation - a) Short term (hours-days) - glucose production dependent on breakdown of glycogen b) Long term (days) - glucose production based on amino acid breakdown and gluconeogenesis (Liver>kidney) |
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% Disposal by Various Tissues, Hormone role
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100% absorbed by GI tract
Liver gets 30% Muscle gets 27% Fat Tissue - 5% Kidney - 8% Brain -15% 15% circulates or reabsorbed to liver Changes based on state. Post prandial above Post-absorptive - few hours later most is by brain. When sleeping for example more by brain b/c muscles not using Hormones (Glucagon, Epi/Norepi) can induce liver to produce glucose, Insulin can make liver take up more |
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Normal Insulin Physiology, Muscle, Liver, Fat
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Anabolic hormone causing uptake of glucose and amino acids by peripheral tissues (esp skeletal muscle, cardiac muscle and adipose tissue)
Involved in glycogen formation in liver and skeletal muscle, conversion to triglycerides and protein. Some mitogenic functions Muscle - Increased glucose uptake, glycogen synthesis, protein synthesis Fat - increased glucose uptake, lipogenesis, less lipolysis Liver - Less gluconeogenesis, increased glycogen synthesis, and lipogenesis |
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B cell stimulation, Drug target, Insulin Receptor
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Glucose high, enters in GLUT2 transporter, more ATP made, ATP closes K+ channels, K+ accumulates in cell, depolarization, Ca++ enters cell, Insulin released
Sulfonylureas target K+ channel to close which simulatse high glucose and causes insulin release Insulin receptor in periphery has B unit phosphorylation when bound leading to PI-3K pathway activation (GLUT 4 translocation) and MAP kinase signaling |
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Glucagon Secretion
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via alpha cells, induced by LOW GLUCOSE, inhibited by INSULIN, GABA, ZINC, SOMATOSTATIN
Low levels of glucose activate ATP sensitive K+ channels in brain and alpha cells generating action potentials and sodium and calcium currents (inward) to induce glucagon release More paracrine stimulation (insulin, zinc, GABA) than Beta cells so if have beta celll dysfunction will have unregulated glucagon secretion. Can never give enough insulin to suppress alpha cell secretion of glucagon |
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Promotors and Inhibitors of Glucagon and Effect, Receptor
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Promotors - SNS, Secretin, CCK, Amino acids HIGH, Glucose low
Inhibitors - Insulin, PNS Actions - Increase in fatty acids and ketones, inhibit anabolism, more glycogenolysis and gluconeogenesis. PROMOTES insulin release (insulin also inhibits glucagon release) Receptor - Gs(a) and Gs(q) pathways for adenylate cyclase and phospholipase C action |
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Pyruvate, Glucose and Glycogen balance, changes in day
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Pyruvate to Glucose = gluconeogenesis - glucagon stimulates
Glucose to Glycogen = glycogenesis - insulin stimulates Glycogen to glucose = glycogenolysis - glucagon stimulates Glucose to pyruvate = glycolysis - insulin stimulates After a meal insulin dominates, glycogenesis, then blood sugar overshoots and glucagon dominates (glycogenolysis) then switches back. Does this throughout day until next meal waffling on either side of a set point for blood glucose |
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Def of Diabetes Mellitus, Causes, Diagnosis
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Not a single disease but group of metabolic diseases of HYPERglycemia with problems in carb, fat, protein metabolism with long term complications of vessels, kidneys, eyes and nerves
Causes: problems of insulin production, action or both Hyperglycemia is just the end result, metabolic dysfunctions cause Diagnosis - greater than or equal to 126 mg/dL glucose in blood, also use glucose tolerance test showing >200 2hr post prandial level) |
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Types of DM, Categories
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Over 7, Type II is most common
Hormonal - Any endocrinopathy of hormone excess can cause (GH, cortisol, TH, Epi, Glucagon, Aldosterone Pancreatic disease - neoplasia, pancreatitis, cystic fibrosis, hemachromatosis Drugs Genetic mutations |
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Type II DM Pathogenesis, RF, Pathophysiology, Other Factors
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Risk Factors - smoking, obesity (MAIN ONE), other environmental agents
Pathogenesis - genetic susceptibility or risk factors leads to defects of beta cell function (less insulin or done in disrupted pulses with disrupted communication) and insulin resistance (decreased ability of peripheral tissue to respond to insulin) Pathophysiology - Impaired secretion from pancreas leads to increased glucose production in periphery, decreased uptake and increased lypolysis. leads to further hyperglycemia, high fatty acids in blood, insulin resistance and beta cell dysfunction Other Factors - adipokines, inflammation, hyperglycemia, free fatty acids promote insulin resistance and beta cell dysfunction. Salicylates can improve insulin resistance |
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Natural History of DM II
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Beta cell function steadily declines from prediabetes through DM II course
Insulin secretion and resistance steadily increase till DM II diagnosis, then resistance flattens while secretion drops (B-cell dysfunction) Postprandial glucose and fasting glucose slowly rise till DM II diagnosis then take off due to less insulin and more resistance Eventually produce no insulin and become totally dependent |
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Causes of Hyperglycemia in DM II by organ
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Pancrease - decreased insulin secretion
Kidneys - increased glucose reabsorption Brain - neurotransmitter dysfunction Adipose - increased lipolysis Digestive system - decreased incretin effect Liver - increased gluoconeogenesis and decreased uptake Muscle - decreased uptake Alpha cells - increased glucagon secretion |
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Complications of DM II, Most prevalent ones
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From hyperglycemia
Retinopathy - cataracts glaucoma Neuropathy - stocking glove Nephropathy - glcomerulosclersosis, pyelnonephritis, arteriosclerosis Also get HTN, MI, brain hemorrhage, atherosclerosis, vasular atherosclerosis in periphery leading to gangrene Most prevalent Main cause of adult blindness - retinopathy in 70% over 20 years which can be delayed or avoided if treat Main cause of non-traumatic amputations in US Main cause of kidney failure in US 2/3 die of heart disease or stroke |
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US diabetes prevalence, Cost
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Increases after age 20, continue to rise. Expected to be 30% by 2050.
In hospitals 40% have DM, 35% of admissions ahve hyperglycemia or diabetes, cost more and more mortality |
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Non-medication Treatment in DM II
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Education - Most important w/ therapy, MUST correctly check blood sugar and correctly take meds. Counseling - Education of pt and family MOST IMPT PART OF TREATMENT
Nutrition - used to have ADA diet, but not anymore b/c no consensus. Well balanced diet best, Ultimately for Obese pts (most) centers on WEIGHT CONTROL. In non-obese don't have to restrict calories but MUST watch CARBS (50-55%), 20% (at least 10-20%) protein, 30% fat (less saturated fats [<8-9%], less polyunsaturated fat [<8-9%], more olive oil), limit cholesterol to <300mg/day. and time meals, snacks, etc Exercise - Increases sensitivity to insulin, increases carb and fat utilization, can cause hypoglycemia or hyperglycemia (strenuous due to SNS activation) so must educate pts on how works with system. Best is INTERVAL TRAINING for short time periods to bring up blood glucose, prevent dropping and prevent need to eat right after work out |
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Carbs and DM II
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Carbs cause more hyperglycemia, hyperlipidemia. In DM II obese pts weight control more impt but if not obese must try to lower carbs
Substitute |
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Physical Exercise recommendations ADA
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>150 min week (30min day/ 5 days)
Moderate intensity (50-70% HR max) Resistance training 3x week if have no contraindications (eg no significant retinopathy which can lead to retinal detachment due to blood vessel bursting from pressure) |
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Main things to control to prevent diabetes complications long term
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Blood sugar
Blood pressure Lipid control Preventative care for eyes, kidneys, feet, teeth, gums Aspirin, ACEi and statins EDUCATION |
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Blood glucose targets normal and diabetics
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Normal - 60-100 btw meals, <140 post prandial
Diabetics - 70-130 btw meals, <180 post prandial |
