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54 Cards in this Set
- Front
- Back
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Structure and blood supply? of pancreas
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B Cells in middle sourrounded by A cells in periphery. Blood flow from pancreaticoduodenal aa goes from middle to outside so insulin can inhibit glucagon. Blood goes to splenic vein and into portal vein
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Percentage of islets that must be lost to lose endocine function?
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70%
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Describe synth and secretion of insulin?
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preprohormone made by ribosomes go into ER, cleaved into prohormone which go to Golgi to be processed and secreted. In golgi, proinsulin is cleaved into insulin and C-peptide
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What peptides are secreted by the B cells?
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insulin, C-peptide, and uncleaved proinsulin
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What causes insulin release?
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glucokinase action on glucose to form G6P is sensor.
ATP produce blocks K efflux; depolarization and Ca entry triggers exocytosis of granules |
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Effect of Insulin?
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activates Tyrosine Kinase (Tyrone probably has diabetes and needs insulin) to amplify downstream signals to eventually add GLUT4 transporter to cells
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What is special about B cell glucose transportrs?
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they allow bidirectional glucose transport to create equilibrium
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Insulin receptors are present where?
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liver, muscle, fat, and other nonclassic target tissues
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Insulin released during ingestion of what nutrients?
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glucose and amino acids
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Synthesis of what is carrier molecule is increased with insulin release?
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VLDL so that TAG can be delivered to tissues for storage
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Which tissue uptake of glucose is NOT regulated by insulin?
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liver
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Insulin effects on fat cell?
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1) stimulation of liproprotein lipase to liberate TAG from VLDL for fat storage.
2) Also, increases GLUT4 transporter so glycerol phosphates made from glucose can be incorporated into fatty acids 3) Lipolysis is inhibited. |
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HAlf life of insulin
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2-5 minutes
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first pass metabolism of insulin?
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50%
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Major inhibitors of insulin secretion?
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somatostatin, catecholamines
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HAlf life of glucagon?
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3-6 minutes
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Glucagon secretion stimulated by?
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amino acids, cortisol, catecholamines
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Glucagon secretion inhibited by?
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fatty acids, ketones, and glucose
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Effect of glucagon?
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Liver (some muscle) Gs activation to cause activation via phosphorylation to certain proteins
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Somatostatin synthesized where?
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hypothalamus, GI, pancreas
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What is octreotide?
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longer half life than somatostatin used for excess GH release
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Somatostatin effects?
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Activates Gi to inhibit B and A cell release, retard nutrient absorption/gut motility, and inhibit GH
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What occurs during fasting state?
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glucagon release to increase glycogenolysis.
Gluconeogenesis, lipolysis, ketogenesis at low levels due to a little insulin |
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Prolonged fasting state?
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higher glucagon, lower insulin.
Switch from gluconeogenesis to ketones |
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Kidneys produce what?
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20% of glucose during fasting, only by gluconeogenesis.
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Definition of diabetes?
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fasting > 126 mg/dL
2) symptoms plus random >200 3)glucose >200 after 75g glucose |
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Type 1 DM presentation?
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polydipsia, weight loss, and ketoacidosis before 30
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When does gestational diabetes usually occur?
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2nd half of gestation due to increasing levels of hormones with counterregulatory anti-insulin effects.
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Antigens in DMI?
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glutamic acid, thyrosine phosphatase, and insulin antibody (Abs agains insulin itself instead of B cells!)
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GAD shares homology with?
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coxsackie protein
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Elevations in VLDL in DM due to?
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increased production (insulin promotes liver synth) and decreased clearance due to decrease in liporptotein lipase
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Hyperglycemia due to?
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linability to incorporate glucose into tissues due to relative insulin deficiency
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polyuria caused by?
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osmotic diuresis
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polyphagia caused by?
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loss of calories in the form of glucose that causes decreased satiety in hypothal
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polydipsia due to?
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dehydration from glucosurial osmotic diuresis
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Weight loss due to?
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dehydration and loss of calories from glucose loss/muscle wasting
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Osmolar damage seen in?
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retina to cause blurred vision, nerve cell to cause decreased conduction,
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HbA1c is?
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nonenzymatic glycation of HbA which should be ___?
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AGE on macrophages?
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advanced glycation endproducts cause cytokine release from macrophages which affect vascular proliferation
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Increased electron donors in hexosamine pathway cause what?
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hyperglycemia induced oxidative stress
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Retinopathy stages?
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nonprolif and proliferative
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Microaneurysms of retinopathy caused by?
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loss of pericytes that support capillary walls
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what causes cotton wool spots in preproliferative stages?
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ischemia with axonoplasmic debris
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Proliferative retinopathy?
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abnormal neovascularization as a reaction to ischemia resulting in grwoth factor release...may hamorrhage or detatch retina
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Diabetic nephropathy occurs more frequently in?
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Type 1 but there is just so much more type 2 prevalance
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cause of diabetic nephropath?
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glomerulosclerosis with kimmelstiel-wilson nodules
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Type 1 course of nephropathy?
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hyperfiltration and microalbuminuria due to decreased heparan sulfate content of BM that causes loss of negative charge
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What preceeds nephropathy?
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retinopathy
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Diabetic individual with proteinuria and no retinopathy?
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MUST rule out other causes of proteinuria vecause retinopathy usually preceds nephropathy
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Type 1 vs Type 2 htn acquisition?
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Type 1 usually after nephropathy, Type 2 - HTN usually seen as a comorbidity
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metabolic syndrome?
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obesity, diabetes,?
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what accompanies peripheral neuropathy more frequently in tpe 1 DM?
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autonomic neuropathy (like a ganglionic block effect)
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asymmetric focal neuropathies due to?
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vascular occlusion and ischemia causing pain
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#1 cause of preventable amupation?
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diabetes - gangrene from ischemia due to macrovascular disease
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