PhclB
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- 4 islet cell hormones and what they produce
- 1. alpha- glucagon 2. beta-insulin and amylin 3. delta-somatostatin (GHIH) 4. F/PP cells-pancreatic polypeptide (stimulates digestion)
- 3 functions of insulin
- 1. lowers blood glucose 2. promotes glu utilization by skeletal muscle and fat 3. supress glucose production by liver
- 2 fxn of glucagon
- 1. rasie blood glucose 2. Promotes glucose production
- 7 things that stimulate insulin secretion
- 1. glucose 2. aa 3. glucagon 4. gastrin 5. beta agonists 6. alpha blockers 7. sulfonylureas
- 4 things that inhibits insulin secretion
- 1. alpha agonists 2. somatostatin 3. prostaglandins-mostly E class 4. Diazoxide
- What stimulates glucagon secretion (3)
- 1. decrease in blood glucose 2. aa 3. sympathetic nerve stimulation
- What inhibits glucagon secretion (3)
- 1. increase in blood glucose 2. somatostatin 3. fatty acids
- 4 main things that oppose insulin in response to low blood glucose levels
- 1. glucagon 2. Beta agonists 3. glucocorticoids 4. GH; diabetogenic
- Where are most insulin degraded?
- Liver
- GI hormones that stimulate pancreas to produce insulin
- Incretins/GLP-1
- Summarize insulin secretion and action; start from stimulus of intestine
- 1. Glu from intestine stimulates the beta cell of pancreas to produce insulin 2. insulin acts on liver to cause inhibition of hepatic glucose production and degrade 50-90% of insulin 3. Insulin that survives liver degradation will increase glucose utilization of skeletal muscle and fat
- What happens when there's no inuslin?
- Then the liver can't inhibit hepatic glucose production and glucose production will continue. Since no insulin, muslce/fat can't utilize it resulting in hyperglycemia
- 4 regulatory mechanisms that protect against hypoglycemia
- As glucose levels decrease, these will increase: 1. Glucagon 2. EPI 3. Cortisol 4. GH
- How does alpha cell regulate insulin secretion?
- As insulin decrease, alpha cell produces glucagon to act on liver to increase glu production
- How does adrenal medulla regulate insulin secretion?
- As insulin decrease, sympathetic nervous system kicks in and adrenal medulla produces EPI to act on liver to increase glu production
- How does adrenal cortex regulate insulin secretion?
- As insulin decrease, adrenal cortex produces cortisol to act on liver to increase glu production
- How does pituitary regulate insulin secretion?
- As insulin decrease, pituitary produces GH to decrease the rate of glucose utilization
- Difference between DMI & DMII: Age of onset
- DM1: <30 ; DM2: >40 (but lower now)
- Difference between DMI & DMII: Body weight
- DM1: nonobese ; DM2: obese
- Difference between DMI & DMII: Genetics % for identical twins
- DM1: 40-50% ; DM2: 95-100%
- Difference between DMI & DMII: Ketoacidosis
- DM1: susceptible ; DM2: rare
- Difference between DMI & DMII: Chronic Complications
- DM1: neuropathy, retinopathy, nephorpathy, PVD, cornary heart disease; DM2: Same as DM1
- Difference between DMI & DMII: Causes
- DM1: autoimmune destruction of beta cells/complete loss of islet B-cells; DM2: insufficient glucose-induced insulin secretion and/or pheripheral insulin resistance
- Difference between DMI & DMII: Circulating Insulin and C-peptide levels
- DM1: none or little circulating insulin/C-peptide; DM2: have circualting insulin/C-peptide
- Difference between DMI & DMII: Tx options
- DM1: only insulin; DM2: diet, exercise, anti-diabetic agents and insulin
- Define metabolic characteristics of diabetic state
- It is the over production and under utilization of glucose resulting in hypergycemia
- What is lipogenesis?
- synthesis of fatty acid and trigs
- What is lipolysis?
- breakdown of trigs to fatty acids
- What happens in lipid metabolism in diabetic state?
- Decreased lipogenesis and increased lipolysis leading to hyperlipidemia and ketoacidosis
- What happens in protein metabolism?
- Diminished protein synthesis and enhanced proteolysis leading to gluconeogenesis and aminoacidemia
- How does ketoacidosis occur?
- Usually in DM1 caused by large maounts of ketone bodies such as beta-hydroxybutyrate and acetoacetate; May be due to stimulation of lipolysis by glucagon
- In ER situations, 2 tx DM ketoacidosis
- 1. regular insulin IV 2. isotonic saline and KCl
- Ketone body affect on blood pH
- Decreases pH in blood
- What is normal fasting glu level?
- 80-90mg/dl
- Dx of DM fasting plasma glu level
- >126mg/dl for 2 occassions
- Dx of DM casual plasma glucose level (anytime)
- >200mg/dl and with symptoms
- Dx of DM oral glucose tolerance test value
- >200mg/dl at 2 hrs
- What level is IGT (impaired glucose tolerant)
- Plasma glu bewtween 140-200mg/dl at 2 hours of OGTT
- What does insulin bind to and what does it cause?
- Binds to tyrosine insulin receptor causing translocation of GLUT4 transporter in insulin sensitive tissues from internal membrane vesicales to plasma membrane to allow glucose to flow into cell for metabolism and storage
- Which insulin pathway stimulates GLUT4 to translocate to plasma membrane?
- PI3-kinase
- Two ways to stimulate PI3 kinase
- Activated directly from insulin receptor or off of IRS (insulin receptor substrate)
- Short and long term goals of DM?
- Short=relieve and prevent hyperglycemia and ketoacidosis; Long=prevent long term complications associated w/heart, kidney, eye and nervous system
- For non-diabetics, what is the A1C goal vs a diabetic
- Non-diabetic=5.5%; Diabetic<7.0%
- In diabetics, what is the goal for preprandial blood glu?
- 70-130mg/dl
- In diabetics, what is the goal for postprandial blood glu?
- <180mg/dl
- What effect does exercise have on insulin?
- Exercise lowers insulin requirements
- T/F-Conventional insulin therapy for DM1 may provide better glycemic control than intensive insulin therapy (multiple daily regimen)
- False, intensive therapy better
- T/F-Diet and exercise alone in some cases is adequate to control DM2 without any drugs
- TRUE
- 4 types of oral hypoglycemic agents
- 1. sulfonylureas 2. biguanides 3. thiazolidinediones 4. alpha-glucosidase inhibitors
- Which is first line therapy for DM2: Oral or insulin
- Oral; insulin only for pts failing in other therapies
- 2 types of DM2 therapy for pregant women
- 1. insulin 2. sulfonylureas
- How does regular insulin formulation come and how to get it absorbed?
- As hexamers complexed with Zn and must dissociate to monomer in skin in order for it to be absorbed into blood
- For regular insulin: 1. when do monmers enter blood 2. when is their peak absorption 3. duration of action
- 1. enter blood 30-60 min after injection 2. peak absorption at 2-3 hours after injection 3. duration 8-10 hrs