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| Pancreas location | under the stomach in the C curve of the duodenum
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| The pancreas is a __ gland; what does that mean related to the pancreas specifically? | heterocrine; has both endocrine (1%) and exocrine (99%) function
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| 4 anatomical features of the pancreas; name the 3 segments and 2 visible ducts; which segment sits in the C-curve? | 8-10 in long, flat, pale yellow, nodular; head, body, tail; pancreatic and accessory ducts; head
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| The pancreatic and accessory ducts release __ into the __; action regulated by the __. This is part of the pancreas' __ function. | pancreatic juice, duodenum, sphincter of Oddi, exocrine
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| __ cells make up 99% of pancreas histology. They make __ containing __. | Acini, pancreatic juices, digestive enzymes
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| The structures that house the endocrine cells of the pancreas are called? It has four cell types:__ and what does each secrete? | Islets of Langerhans; Alpha-glucagon, Beta-insulin, Delta-hGHIH (somatostatin), F cell-pancreatic polypeptide
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| All hormones released by the pancreas are __ | P&Ps
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| Glucagon __, mainly by __ in the __. It's potent: 1 glucagon results in the release of __ glucose molecules. | increases blood glucose, glycogenolysis, liver; 100,000,000
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| Pancreatic __ and __ cells are unique because they __. They are __; other hormones that affect blood glucose will affect their release; why? | alpha, beta, monitor and control glucose levels without NS or hormonal control, highly sensitive; energy balance in the body is crucial
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| Glucagon release is stimulated by __, and inhibited by __ and __. | hypoglycemia, hyperglycemia, hGHIH
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| Insulin acts to __ by __; it also stimulates __ for __, and __ to absorb __(x3) for storage as triglycerides | decrease blood glucose, priming cells to take up glucose, amino acid absorption, protein synthesis, adipocytes; glucose, fatty acids, glycerol
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| The process of converting glucose to glycogen is called __; it's stimulated by __. | glycogenesis, insulin
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| When glucose enters cells, it is either __ or __. | used immediately for ATP production, converted to glycogen and stored
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| Organ/tissue cells without insulin receptors:__ (x4). Why? | kidneys, brain, RBCs, GI lining; they absorb and use glucose without insulin stimulation
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| Insulin release is stimulated by __ and inhibited by __ and __. | hyperglycemia, decreased glucose, hGHIH
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| Delta cells release __; its 2 main functions:__ | hGHIH (somatostatin); inhibit glucagon and insulin to create balance, and slows exocrine activity of pancreas (which slows nutrient absorption and enzyme secretion)
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| F cells secrete __, which stimulates __ production in __ cells, ultimately increasing __ | pancreatic polypeptide; pancreatic juice, acini, nutrient absorption from GI
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| Which diabetes is insulin dependent (IDDM)? Which isn't (NIDDM)? What are the approximate ages of onset? | Type II, Type II, Type 1 is juvenile, Type 2 is after 35
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| What are the three cardinal signs of DM? Which one is absent in DI? | polydipsia, polyphagia, polyuria, polyphagia is absent in DI
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| Three possible causes of Type I diabetes | genetic (congenital beta cell damage), viruses like chicken pox (damages beta cells), auto-immune response (T-cells target beta cells)
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| The cause of DM is auto-immune __% of the time. Describe the mechanism. | 80%, T-cells make antibodies that target GAD on beta cells, mistaking it for the P69 protein displayed by infected beta cells
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| DI results from __ and DM is associated with __ | decreased ADH, decreased insulin and/or increased blood glucose
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| What's the role of GAD? GABA? | Converts glutamate to GABA, which is a messenger between neurons and pancreatic cells
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| Normally,__ protein receptors on cell membranes are primed by __ so that they may __ via __. How is this process altered in DM T1 and T2? | glut4, insulin, take up glucose, passive facilitated transport; in T1, there is no insulin to "prime the pump", in T2 there is plenty of insulin but few receptors
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| The immediate effects of increased serum glucose are __ and __; this change causes a cascade of negative effects throughout the body. Name some the major body systems/organs affected. | increased blood volume, B/P; kidneys, heart, brain, blood vessels, eyes
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| What are the effects of elevated B/P on the heart and vasculature? | myocardial dilation/hypertrophy/cell damage/heart failure; contributes to atherosclerosis and vessel damage
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| How does high B/P affect the kidneys? | renal damage/disease/failure from damage to the endothelial capsular membrane of the glomerulus
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| Explain why atherosclerosis is a risk factor, and what it puts pts at risk of | further increases B/P and puts pt at risk for embolism, CAD, cardiac ischemia, MI, cerebral ischemia, stroke, coma, PVD w/necrosis/gangrene/ulceration, further damage to kidneys
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| Atherosclerosis causes __, or narrowing of the arteries. This results in __, or insufficient blood delivery | stenosis, ischemia
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| In DM, since cells can't use glucose for energy, the body increases __, causing __ (increased fat circulating in the blood), resulting in __(x3) | lipolysis, lipidemia, weight loss, atherosclerosis, ketone body formation
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| What is the most simple test to distinguish DM from DI? | urinalysis for glucose levels
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| What are ketone bodies? Why are they bad (2 main reasons)? | negatively charged bodies that pull Na and K out in the urine; cause ketoacidosis which can lead to coma; depleted Na and K result in diabetic neuropathy (palsies, paresthesia, ANS dysfunction)
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| Treatments for T1DM? What is the preferred delivery method for the more common treatment? Why is the transplant treatment rarely done? | insulin replacement, rarely Islet transplant, cyclosporin in PTDM (immunosuppressive); insulin pump; stem cell controversy
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| In T2DM, what's going on with beta cells? Insulin? What's responsible for the hyperglycemia in T2? | beta cells are making insulin, insulin levels are normal, there are fewer insulin receptors (glut4 receptors) on cells
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| What are the two main risk factors for developing T2DM? Why/how are glut4 receptors down-regulated in T2DM? | genetic predisposition and obesity; adipose tissue produces "tumor necrosis factor alpha" which decreases glut4 production
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| Treatment for T2DM? What are the drug actions? | diet, exercise, oral antidiabetic meds; metformin reduces glucose synthesis and release by liver, glyburide stimulates insulin secretion to better prime cells
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| What are the two causes of hyperinsulinism? Which is more common? How are these corrected? | benign beta cell tumor, overdose of insulin; 2nd is more common; tumor removal, consuming glucose (e.g. juice)
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| What are the effects of hyperinsulinism? | hypoglycemia, anxiety, nervousness, tremors, weakness, disorientation, unconsciousness
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