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Diabetes final exam
| Question | Answer |
|---|---|
| How is diabetes mellitus defined? | A group of metabolic disease characterized by increased glucose (hyperglycemia) resulting from defects in insulin secretion, insulin action or both |
| What are the major sources of glucose for the body? | Ingest food & Formation of glucose by the liver from food |
| How does insulin work? | Regulates the production & storage of glucose |
| How does glycogen work? | Pancreatic hormone secreted by the alpha cells of the pancreas. Stimulates the liver to release stored glucose |
| Glycogenolysis | Glucose production though the breakdown of glycogen |
| Gluconeogenesis | liver forms glucose from the breakdown of non-carbs, including amino acids |
| How do insulin and glucagons work together? | Work together to maintain a constant level of glucose in the blood |
| What other symptoms may a diabetic have? | Fatigue, Weakness, Sudden vision changes. Tingling / numbness in the hands and or feet. Dry skin, Slow healing & Recurrent infections |
| Discuss type 1 diabetes. | Affects 5-10% of people with diabetes. Beta cells are destroyed by an autoimmune response. Result – production of little or no insulin. Insulin is required to control blood glucose levels |
| Describe type 2 diabetes. | Affects 90-95% of people with diabetes Patient experiences:Decreased sensitivity to insulin (insulin resistance) and impaired functioning of the beta cells causing decreased insulin production |
| Discuss basic pathophysiology as related to diabetes | Insulin is needed to open the receptors on the body’s cells. This lets glucose into the cell which is necessary for cellular fuel. Normally insulin keeps pace with the body’s need for fuel. Fasting glucose 70-100 |
| Describe how glucose is locked out of the cell with type 2 diabetes. | Beta cells do their best to increase insulin production in response to increased glucose. Body cells don’t recognize the insulin are resistant to it (glucose doesn’t get into the cell) |
| What happens to the body’s cells as glucose levels rise? | The cells are literally stored for fuel. Over time this labor wears out beta cells (slowing insulin production)End result: Insulin deficiency |
| Why is a persistently high glucose a serious problem? | Persistently high glucose (a serious problem)Blood becomes viscous and flows less readily (thick, sluggish) |
| What are the effects of viscous blood on the body? | Decreased circulation (body is unable to fight infection & heal wounds)WBCs can’t do there job. Platelets tend to clump (clogging tiny capillaries and decrease microcirculation |
| What are 4 special considerations for the patient with nephropathy? | 1 Angiotensin 2 Contrast media can trigger acute renal failure. 3 Caution with nephrotoxic drug reduced dosage 4 Long term BP management necessary - chronically elevated BP levels to decrease renal function |
| CAD | Can lead to acute MI, the # 1 cause of death in patients with type 2 diabetes |
| How is the diagnosis of diabetes confirmed? | 1. Fasting glucose – 126 mg/dL or more 2. Casual or random glucose – greater than 200 (on more than 1 occasion) |
| What is the target for diabetic control? | Tight glycemic control. Preprandial glucose – 90-130. Postprendial glucose – less than 180 |
| What is a glycosylated hemoglobin? | Also called hgb AIC or AIC. Blood test that reflects the overage blood glucose over a period of 2-3 months. Glucose molecules attach to hgb recall RBCs lifespan of 120 days |
| When should urine be tested for glucose / ketones? | Urine testing done in pts that can’t use meters. Urine ketones should be checked if blood glucose is greater than 240 for 2 test in a row & during illness |
| Sulfonylureas | Increased secretion of insulin. Oldest, largest group of oral agents. Glucotrol & Glyburide |
| Alpha – Glucosidase inhibitors | Delays digestion of CHO’s in the GI tract. (take at the beginning of a meal.)Decreased absorption of glucose. Do not alter insulin secretion, do not cause hypoglycemia. Precose & Glyset |
| Biguanide | Increases the use of glucose by muscle and fat cells. Decreases production of glucose. DC 48 hours before Dx tests with iodine (hypaque) r/t potential renal failure and development of lactic acidosis / resumed 48 hours after the test.Glucophage |
| Thiazolidinediones | Increases the effectiveness of circulating insulin. Decreases insulin resistance. Stimulates muscle receptors (restores effectiveness of body’s insulin)Actos & Avandia |
| Meglitidides | Stimulates release of insulin from the beta cells. Short half life (about an hour)Take before each meal. Prandin & Starlix |
| Short acting insulin, type and peak time | regular insulin peaks in 2-3 hours |
| intermediate acting insulin, type and peak time | NPH & Lente peaks in 8-12 hours |
| Long acting insulin, type and peak time | ultralente peaks in 10-30 hours |
| What are 3 acute complications of diabetes? | 1. Hypoglycemia 2. DKA 3. HHNS (hyperglycemia hyperosmolar nonketotic syndrome) |
| What is hypoglycemia and its cause? | Insulin reaction. BS falls below 50-60 Causes: 1. Too much insulin or oral agent 2. Not enough food 3. Excessive physical activity |
| Name adrenergic symptoms of hypoglycemia | Tachycardia, Tremor, Palpitations, Sweating, Nervousness Hunger |
| What are 3 complications of diabetic ketoacidosis? | Hyperglycemia. Dehydration / electrolyte loss, Acidosis |
| . Be familiar with the pathophysiology related to DKA. | 1. Glucose can’t get in to the cell 2. Liver increases glucose production 3. Kidneys eliminate glucose, water * lytes (na &K) 4. Excessive urination 5. Breakdown of fatty acids 6. Ketone bodies are acids-metabolic acidosis |
| What are 3 possible causes of DKA? | Missed dose of insulin, illness / infection, undiagnoses / untreated diabetes |
| How does the pt in DKA present? | Polyuria, polydipsia, Blurred vision, weakness, headache, Orthostatic hypotension; weak, rapid pulse, Acidosis, ketosis (GI symptoms, N/V, anorexia, abd pain, Acetone breath, Hyperventilation, Alert, lethargic, comatose |
| Discuss the diagnostic findings or a DKA work up | Glucose 300-800. Metabolic acidosis on ABG Na / K (low, normal, high depending on the level of dehydration, Increased creatinine, BUN, hgb, hct |
| How can an individual with diabetes prevent DKA? | Take insulin despite n/v, Small frequent consumption of carbs (juices, sodas, gelatin)Fluids every hour to prevent dehydration. Call dr if unable to keep fluids down |
| List 3 components of DKA treatment. | Re-hydrate, Restore lytes, Reverse acidosis |
| How is IV insulin properly administered? | When mixing an insulin drip flush the insulin through the entire IV infusion set & discard the 1st 50mL of fluid. Insulin sticks to the inner surface of the infusion set. The initial fluid may contain a decrease concentration of insulin |
| What is hyperosmolar nonketotic syndrome? | Lack of insulin – persistent hyperglycemia – osmotic diuresis & loss of water & lytesAlternations in LOC, Ketosis: absent / minimal |
| What are symptoms of HHNS? | Polyuria, Polydipsia, No GI symptoms, Profound dehydration, Hypotension, Tachycardia, Neurologic signs (altered sensorium, seizures, hemiporesis |
| Discuss diagnostic work up finding with HHNS. | Glucose 600-1200. High osmolality – greater than 350. Lab studies – severe dehydration postural hypotension, Nuero changes (cerebral dehydration from hyperosmolarity |
| How is HHNS managed? | Fluids 0.9 or 0.45% NS. Correct lytes: lab/EKG determine K replacementInsulin continuous low rate Goal 250-300Once through crisis diet & oral agents |
| What are reasons for hyperglycemia during hospitalization? | Decreased activity, increased food, decreased insulinMedications (steroids)IV dextrose (main IV or IVPB)Over vigorus treatment of decreased BS, Poor timing of insulin & meals (regular insulin immediately before or after eating |
| What are possible causes of hypoglycemia during hospitalization? | Overuse of sliding scale insulin, Lack of dosage change (when pt is NPO), vigorous treatment of hyperglycemia (use of regular insulin too frequently, before the peak is reached), Delayed meals |
| NPO | Anticipate half usual intermediate dose / elimination of regular |
| Clear liquid diet | Receives simple carbs: juice / gelatin |
| Enteral tube feedings | More simple carbs, increased glucose |
| Parenteral nutrition | regular insulin in the TPN & SQ if needed |
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angie030104
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