Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Pancreas Bio162
Note that some of the cards are INCORRECT based on materials provided by instruc
| Question | Answer |
|---|---|
| Pancreas location | under the stomach in the C curve of the duodenum |
| The pancreas is a __ gland; what does that mean related to the pancreas specifically? | heterocrine; has both endocrine (1%) and exocrine (99%) function |
| 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 |
| 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 |
| __ cells make up 99% of pancreas histology. They make __ containing __. | Acini, pancreatic juices, digestive enzymes |
| 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 |
| All hormones released by the pancreas are __ | P&Ps |
| 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 |
| 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 |
| Glucagon release is stimulated by __, and inhibited by __ and __. | hypoglycemia, hyperglycemia, hGHIH |
| 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 |
| The process of converting glucose to glycogen is called __; it's stimulated by __. | glycogenesis, insulin |
| When glucose enters cells, it is either __ or __. | used immediately for ATP production, converted to glycogen and stored |
| Organ/tissue cells without insulin receptors:__ (x4). Why? | kidneys, brain, RBCs, GI lining; they absorb and use glucose without insulin stimulation |
| Insulin release is stimulated by __ and inhibited by __ and __. | hyperglycemia, decreased glucose, hGHIH |
| 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) |
| F cells secrete __, which stimulates __ production in __ cells, ultimately increasing __ | pancreatic polypeptide; pancreatic juice, acini, nutrient absorption from GI |
| 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 |
| What are the three cardinal signs of DM? Which one is absent in DI? | polydipsia, polyphagia, polyuria, polyphagia is absent in DI |
| 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) |
| 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 |
| DI results from __ and DM is associated with __ | decreased ADH, decreased insulin and/or increased blood glucose |
| What's the role of GAD? GABA? | Converts glutamate to GABA, which is a messenger between neurons and pancreatic cells |
| 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 |
| 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 |
| 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 |
| How does high B/P affect the kidneys? | renal damage/disease/failure from damage to the endothelial capsular membrane of the glomerulus |
| 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 |
| Atherosclerosis causes __, or narrowing of the arteries. This results in __, or insufficient blood delivery | stenosis, ischemia |
| 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 |
| What is the most simple test to distinguish DM from DI? | urinalysis for glucose levels |
| 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) |
| 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 |
| 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 |
| 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 |
| 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 |
| 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) |
| What are the effects of hyperinsulinism? | hypoglycemia, anxiety, nervousness, tremors, weakness, disorientation, unconsciousness |
Created by:
rakalilla
Popular Anatomy sets