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NP2:DiabetesMellitus
Prof.Revak-Lutz; Test 3
| Question | Answer |
|---|---|
| Diabetes is | a chronic multisystem disease related to abnormal insulin production,and:or impaired insulin utilization |
| Diabetes is leading cause of | heart disease, stroke, adult blindness, nontraumatic lower limb amputations |
| Glucagon | hormone counterregulatory to insulin. Results in increased blood glucose by stimulating gluconeogenesis |
| Gluconeogenesis | glucose production in the liver from precursors such as lactate and amino acids |
| Glycogen | primary stotage form of glucose in liver and muscle |
| Glycogenolysis | metabolic conversion of glycogen into glucose |
| Counterregulatory hormones | glucagon, cortisol, growth hormone, and epinephrine. These hormones are released in response to hypglycemia, as a stimulus to effect gluconeogensis |
| Normal insulin metabolism | produced by the beta cells in the islets of langherans of the pancreas |
| Normal glucose range | 70-120 mg |
| An increase of insulin after a meal affects | stimulate storage of glucose as glycogen, inhibits glucogenesis: tells the liver to stop releasing glucose, enhances fat deposition in adipose tissue, increases protien synthesis |
| Cause of Type 1 diabetes | autoimmune attack on the beta cells of pancreas causing absolute deficiency of insulin secretion |
| Facts and numbers of Type 1 | most often occurs in people under 30 years of age, ketosis prone (break down of fat), dependent on exogenous insulin, 10% of people with diabetes have type 1 |
| Onset of symptoms of type 1 are | rapid |
| Manifestations develope when pancreas can no longer | produce insulin |
| Symptoms of type 1 include | hx of recent, sudden, weight loss, polydipsia, polyuria, polyphagia |
| PWD Type 1 require | exogenous insulin to live |
| Cause of type 2 diabetes include | combination of insulin resistance at cellular level and live and inadequate insulin secrection |
| Facts and numbers for type 2 | accounts for 90% of pts with diabetes, usually occurs in people over 35 years of age, 80-90% of patients are overweight |
| Symptoms of type 2 | fatigue, recurrent infections (yeast), prolonged wound healing, visual changes |
| Type 2 incidence | prevalance increases with age, genetic basis |
| Highest rate of diabetes in the world amoung ethnic populations are | native americans and alaskan natives |
| in type 2 pancreas continues to produce | some endogenous insulin but it is either insufficient or poorly utilized by tissues |
| Four major metaboli abnormalities of type 2 are | body tissues do not respond to insulin (either unresponsive receptors or insufficient in #), pancreas decrease ability to produce insulin, inappropriate glucose production from liver, alteration in production of hormones and adipokines |
| Adipokines | play a role in glucose and fat metabolism, contribute to pathophysiology of type 2 |
| Main types of adipokines | adiponectin and leptin |
| Onset of type 2 is | gradual |
| Normal FPG | <100 |
| Normal 2-hr after postload glucose | <140 |
| Impaired fasting glucose | FPG >or= 100-125 |
| Impaired glucose tolerance (IGT): 2-hr postload glucose | 140-199 |
| Normal HbA1C | 5.7-6.4% |
| prediabetes is | not high enough diabetes diagnosis, if no preventive measure taken-usually develop type 2 within 10 years |
| Diabetes is present if fasting glucose level is greater than | 126 |
| Diabetes is present if symptoms plus random or casual plasma glucose is greater than or equal to | 200 |
| Diabetes is present if 2-hr OGTT level is greater than or equal to | 200 |
| Diabetes is present if HbA1C is greater than | 6.5% |
| Risk factors for metabolic syndrome | abdominal obesity, athrogenic dyslipidemia, raised bp, insulin resistance, prothrombic and proinflammatory states |
| Etiology of metabolic syndrome | poor nutrition, inadequate physical activity, subsequent increases in body weight |
| Diagnostic criteria: 3 or more criteria met | abdominal obesity, hypertriglyceridemia, low HDL-C, high bp, high fasting glucose |
| Goals of diabetes management | reduce symptoms, promote well-being, prevent acute complications, prevent and delay onset and progression of long-term complications |
| Glycemic control goal of HbA1C | <7% |
| Glycemic control goal of preprandial glucose | 90-130 |
| Glycemic control goal of postprandial glucose | <180 |
| Goal of treatment for bp | <130;80 |
| Goal of treatment for lipids | <100 |
| Goal of treatment for TG | <150 |
| Goal of treatment for HDL | >40 |
| HbA1C test is | average of blood glucose over life span of RBC, in pwd ADA goal is 7% |
| Nutritional therapy for type 1 is | based on the usual food intake and balanced with insulin and exercise patterns |
| Nutritional therapy for type2 is | calorie reduction, and emphasis placed on achieving glucose, lipid, and bp goals |
| Alchohol | high in calories, promotes hypertriglyceridemia and can cause severe hypoglycemia |
| Carbohydrate counting | method incorporated into nutrional therapy for people with type 1 and 2 |
| Pt requiring insulin use the carbohydrate counting by | carbohydrates eaten and pre-meal glucose determine amount of insulin taken |
| Exercise is an essential part of diabetes management bc | increases insulin receptor sites, lowers blood glucose levels, decreases insulin resistance, and contributes to weight loss |
| Excercise is best done | after meals |
| Self-monitoring of blood glucose (SMBG) allows | pt to make self-managment decisions regarding diet, excercise, and medication |
| Oral agents work to improve | the mechanisms in which insulin and glucose are produced and used by the body |
| Oral agents work on the three defects of type 2 by | increasing insulin production, decreasing insulin resistance, and decreasing hepatic glucose production |
| Oral hypoglycemic agents include | sulfonylureas and meglitinide |
| Oral insulin sensitizers include | biguanides adn thiazolidendiones |
| Sulfonylureas are used to | increase production from pancreas |
| Examples of Sulfonylureas are | Glipizide (Glucotrol), Glimepiride (Amaryl), Glyburide (Diabeta, Micronase, Givnase) |
| Glipizide | Glucotrol; Sulfonylureas (increase insulin production) |
| Glimepiride | Amaryl; Sulfonylureas (increase insulin production) |
| Glyburide | Diabeta, Micronase, Givnase; Sulfonylureas (increase insulin production) |
| Disadvantages of sulfonylureas | weight gain, hypoglycemia |
| Meglitinides (oral) are used to | increase insulin production from pancreas and is more rapid acting than sulfanylureas but has to be taken 30 minutes before each meal |
| If meal skipped should you take a meglitinide? | no |
| Examples of meglitinides include | Repaglinide (prandin), Nateglinide (starlix) |
| Repaglinide | Prandin; meglitinide (increases insulin production) |
| Nateglinide | Starlix; meglitinide (increases insulin production) |
| Biguanides (oral) are insulin senstizers used to | reduce glucose production by liver, enhance sensitivity at tissues, improve glucose transport into cells |
| Example of biguanides is | Metformin hydrochloride (glucophage)(insulin sensatizer) |
| Side effects of biguanides | GI upset, risk of lactic acidosis |
| Biguanides are contraindicated for use with pts with | renal dysfunction (serum creatine levels >1.5 in males; >1.4 in females), CHF, liver dysfunction |
| Oral thiazolidinediones (TZD) are used to | improve insulin sensitivity, transport and utilization at target tissues |
| Metformin hydrochloride | Glucophage; biguanide (insulin senstizer) |
| Examples of TZD's include Rosiglitazone maleate (Avadia, no longer on market), Pioglitazone HCl (Actos) | |
| Rosiglitazone maleata | Avadia, no longer on market; TZD (insulin sensitizer) |
| Pioglitazone HCl | Actos; TZD (insulin sensitizer) |
| Advantages of TZD's (insulin sensitizer) | no hypoglycemia when used alone, can be used in pts with decreased renal function |
| Disadvantages of TZD's (insulin sensitizers) | weight gain (fluid), increased total and LDL cholesterol, not recommended in pts with heart failure, edema and anemia |
| Glucovance (combination) | metformin and gliburide; risk for hypoglycemia |
| Metaglip (combination) | metformin and glipizide; risk for hypoglycemia |
| Avandiament (combination) | metformin and avandia |
| Alpha-glucosidase inhibitors "startch blockers" are used to | slow down absorption of carbohydrate in small intestine |
| Exaples of alpha-glucosidase inhibitors include | Acarbose (precose), Miglitol (Glyset) |
| Acarbose | Precose; alpha-glucosidease inhibitor |
| Miglitol | Glyset; alpha-glucosidase inhibitor |
| Disadvantages of alpha-glucosidase inhibitors | GI side effects, dosed TID with first bite of meal (forget), in combination, hypoglycemia can only be treated with glucose |
| DDP-4 (other agaent)inhibitor is used to | inhibit dipeptidyl pepidase-4, which inactivates incretin hormones (incretines regulate glucose by increasing insulin sythesis and pancreatic release), decrease hepatic glucose release |
| Disadvantages of "other" agaents | only work when glucose present, mainly injectables, used for type 2 besides amylin |
| DDP-4 inhibitor is | glucose dependent |
| Advantages of DDP-4 inhibitors is | decreased risk of hypoglycemia, no weight gain |
| Examples of DDP-4 inhibitors are | Januvia (sitagliptin), Galvus (vildaglipton) |
| Januvia | Sitagliptin; DDP-4 inhibitor |
| Galvus | Vildaglipton; DDP-4 inhibitor |
| Amylin analog is | hormone secreted by beta cells of pancreas, cosecreted with insulin, indicated for type 1 and 2, administered subQ (thigh or abdomen) |
| Amylin acts to | slow gastric empying, reduces postprandial glucagon secretion, increases satiety |
| Example of amylin is | pramlintide (symlin) |
| Pramlintide | Symlin; amylin |
| Incretin mimetic is a synthetic peptide used to | stimulate release of insulin from beta cells and suppresses glucagon secretion, reduces food intake, slows gastric emptying; subcutaneous injection |
| An exmaple of an incretin mimetic is | Byetta |
| Incretin mimetic such as Byetta are not to be used with | insulin |
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stilsl
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