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44 Cards in this Set
- Front
- Back
Cortisol as a glucose counter regulatory hormone
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under normal conc. cortisol effects carb metabolism but barely. It helps adjustment to fasting.
cortisol maintains enzymes required for gluconeogenisis and lipolysis |
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Glucose counter reulatory hormones
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glucagon (main one)
symp system cortisol GH |
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GH primary responsiblity
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stimulates protein synthesis and bone growth
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GH affects on carb and lipid metabolism
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GH has minor effects on carb and lipid metabolsim. GH affects carbs and lipid metabolism when plasma levels are hi or lo. At hi levels GH has anti insulin effects and it makes adipocyes for sensitive to lipolytic stimuli and increases gluconeogenisis by liver and decreases muslce and adipocytes sensitivy to insulin.
it overall decreases glucose uptake by cells |
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hormone levels during fasting
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insulin is lo (decreases)
glucagon hi (increase) GH hi (increase) cortisol normal |
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what happens to glycogen during fasting
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glycogen stores in liver and muscle are depleted so plasma glucose declines
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during fasting what do metabolic substrate shift to?
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lipolysis products
fa glycerol ketones |
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describe glucose uptake by liver, adipocytes, muscle, and brain during fasting
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glucose uptake by liver, adipocytes, and skeltal m. decreases
glucose uptake by brain remains normal |
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what happens during fasting
5 main things |
1. glucose uptake by liver, adipocytes, muscle decreases but brain glucose uptake remains constant
2. glycolysis is decreased in liver and skeletal m. 3. lipolysis increases. tissue shift to use fa for metabolism 4. breakdown protein 5. glycerol from lipolysis and aa (alanine) from protein catabolism undergo gluconeogenisis |
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what happens after 3days of fasting?
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1. decrease in insulin MORE
2. use more fa 3. increase ketone conc. for brain bc no more glucose left. increase ketones decrease protein catabolism bc now brain is using ketones. |
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Problem with ketone synthesis
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can cause metabolic acidosis
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how long can fat stores provide body with metabolic substrate
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60 days then death occurs
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hypoglycemia
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lo blood sugar in postabsorptive state
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sympotoms of hypoglycemia
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due to lack of glucose in brain
headaches confusion dizziness incoordination slurred speech convulsions coma if below 40 mg/dL |
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effects of symp stimulation due to lo blood glucose (hypoglycemia)
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tachycardia
trembling nervousness sweating anxiety |
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2 things that can cause hypoglycemia
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increased blood insulin
defect in glucose counter regulatory systems |
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how can blood insulin be increased to cause hypoglycemia
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insulin secreting tumors
drugs causing insulin secretion overdose of insulin drugs (beta adrenergic, ethanol) |
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how can pt get a defect in glucose counter regulatory systems to cause hypoglycemia
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inadequate glycogenolysis or gluconeogenisis due to liver disease
glucagon defiency cortisol defiency |
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criteria for diagnosis of diabetes
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fasting plasma glucose of more than 140 mg/dL or plasma glucose over 200 mg/dl 2 hrs after glucose meal
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% of people with Type I diabets
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9%
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2 peaks of incidence for diabetes I
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first at puberty
second peak around 40 |
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Type I diabetes
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lack of insulin due to destruction of pancreatic beta cells
autoimmune disease |
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plasma glucose with type I diabetes
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plasma glucose is 300-400 mg/dl but could be up to 1000 mg/dl. since glucose does not enter the cell, the cell thinks its starving so it increases lipolysis, making fa, glycerol and ketones
ketones cause diabetic ketoacidosis with leads to problems w/ neural function |
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what is seen with type I diabetes pts.
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see hi glucose levels, hi triacylglyceride levels due to lipolysis and lo insulin
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what is in Type I diabetes pts urine?
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glucose and ketones bc saturation of renal transporters
glycosurea |
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polyuria
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seen with type I and II diabetes
when osmotic diuresis and loss of electrolytes and nutrients cause dehydration |
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polydipsia
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seen mainly with type I diabetes
it is excessive thirst bc increase urine flow and lossof water |
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why do you see wieght loss in people with Type I diabetes although polyphagia is occuring?
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due to loss of glucose and nutrients in the urine
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therapy for type I diabetes
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insulin injection
insulin pump insulin pump/glucoe monitor insulin inhalation |
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who are main pts who get diabetes type II
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90% are overwieght and 80% are obese
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type II diabetes
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insulin is made BUT target tissue is unresponsive to insulin. cells decrease glucose uptake and decrease glycogen synthesis. This is due to obesity
some loss of insulin occurs bc beta cells are not as sensitive to glucose |
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why do pts w/type II diabetes not lose wieght?
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bc not enough glucose is excreted in urine
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only time ketosis occurs in type II diabetes
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stress or trauma from infections
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symptoms of type II diabetes
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polyuria,thirst,blurred vision, parethsis, and fatigue
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therapy for type II diabete
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excercise
drugs |
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how does excersice help type II diabetes pts?
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weight reduction w/excercise. insulin responsiveness increases w/ excercise. excercise increases the number of glucose transporters in skeletal m.
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non insulin dep. diabetes
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Type II
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drugs to treat type II diabetes
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sulfonylureas
biguanides GLP-1 agonist amylin agonist |
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how does sulfonylureas help Type II diabetes
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stimulates secretion of insulin from pancrease by closing K channel
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how does biguanides help type II diabetes pts?
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inhibits hepatic gluconeogenisis so more glucose wont be released
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how does GLP-1 agonist help diabetes II pt?
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enhances glucose stimulated insulin release and decrease release of nutrients from tummy
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symptoms of type I diabetes
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polydipsia
weightloss polyphagia blurred vision polyuria |
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effects of chronic elevated glucsoe levels
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atherosclerosis bc lipid circulation
kidney failure peripherial vascualr disease neuropathies infection retinopathies cause blindness |
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what causes chronic abnormalities of diabetes mellitus
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due to non enzymatic glycoslyation of proteins caused by chronic elevated gllusoe levels
mainly due to damage to vasculature and narrowing of caps |