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Exocrine Duct system carries juices and enzymes to the small intestine
Endocrine Consists of Islets of Langehans (makes hormons), that are absorbed into the blood
Islets of Langerhans contain Alpha and Beta tissues
PNS stimulation occurs when immediately after a meal to increase insulin stim
SNS Stimulation occurs hours after a meal to increase glucagon stimulation (alpha cells)
Insulin increases when when glucose levels increase
Alpha cells release Glucagon
Beta cells release Insulin
Delta cells release Somatostatin
Exocrine hormones Lipase and amylase
Endocrine releases Alpha and beta cells
Glycogenolysis Glucagon stimulates liver to change glycogen to glucose
Gluconeogenesis Amino acids/fatty acids change to glucose Glucagon converts fats and excess amino acids into energy allowing normal blood glucose levels
Lipolysis Lipid breakdown by glucagon into glucose
Insulin Secreted by b cells in islets of Langehans in pancreas
Glucagon hyperglycemic agent, doesnt work good on alcoholics
Growth Hormone makes sugars rise-insulin antagonist, secretion triggered by hypoglycemia
Somatostatin Lowers sugars, secreted when BG is high, suppresses secretion of growth hormone
DMI Type 1 Autoimmune Disease,lifelong insulin needed s/s polydipsia,weight loss
DMI Type 2 Hereditary-moderate decline in insulin production and fewer insulin receptor sites-insulin resistant
Prediabetes 100-125 mg/dl
Secondary DMI result of being on certain medications like steroids, pancreatitis
Gestational DMI
Oral Meds
Stimulators stimulates insulin release, increases insulin receptor sites-IE.sulfonylureas,diabinese,tolinase,orinase,glucotrol
Sensitizers increases binding copacity of receptor sites ie.glucophage, actos, avandia (metformin)
Slow absorbers of carbs prevents post meal spike in glucose levels-Precose,glycet
Acanthosis Nigricans Skin disorder where skin gets darker and thick, caused by insulin resistances
Insulin humalog/novalog 15-30 Regular-30-60 NPH/Lente-1-3hr ultralente insulin-6-8 hrs Lantus-24hr
Hypoglycemia Sudden onset,s/s-AMS,diaphoretic,hypotension,coma
hyperglycemia without Ketones gradual onset->120-150 mg, causes=too little insulin
DKA no insulin or glucagon activity, BG >250-300 with presence of ketones,causes metabolic acidosis
Hyperglycemic Hyperosmolar NonKetotic Acidosis (HHNK) associated with Type 2 DMI, insulin and glucagon activity present, coma develops when sustained hyperglycemia causes osmotic diuresis to cause dehydration and when water intake is inadequate BG >1000 mg-common death from clot
Created by: rebeccabelleth