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N2
Unit 3: Nutrition - Altered Glucose Metabolism
| Question | Answer |
|---|---|
| Describe the role of insulin in the metabolism of carbohydrates, fats, and amino acids. | An anabolic hormone made in beta cells of the islets of Langerhans in the pancreas, plays a key role in allowing body cells to 'store and use' carbohydrates, fat and protein |
| DM on Glucose metabolism | The lack of insulin affects metabolism of carbohydrates,proteins, and fat and leads to long-term complicationsthroughout the body. |
| DM on Fat metabolism | The lack of insulin affects metabolism of carbohydrates,proteins, and fat and leads to long-term complicationsthroughout the body. |
| DM on Protein metabolism | The lack of insulin affects metabolism of carbohydrates,proteins, and fat and leads to long-term complicationsthroughout the body. |
| Type 1 diabetes mellitus (Insulin Dependent) | is an autoimmune disorder caused by primarybeta-cell destruction, leading to absolute insulin deficiency. |
| Type 2 diabetes mellitus | Characterized by a reduction in the ability of most of the cells to respond to insulin (insulin resistant), poor control of liver glucose output and decreased beta cell function |
| Explain the cause for the difference in symptoms, onset and complications of, | (blank) |
| Describe the role of genetic and environmental influence on the development of | (blank) |
| Describe the rationale for the increased incidence and prevalence of Type 2 diabetes | (blank) |
| Explain the fasting blood glucose parameters that are diagnostic of Type 2 diabetes. | >126 ON 2 SEPARATE OCCASIONS THE PERSON IS A DIABETIC. |
| Explain the fasting blood glucose parameters that are diagnostic of Type 2 diabetes. | >126 ON 2 SEPARATE OCCASIONS THE PERSON IS A DIABETIC. |
| Insulin resistance | (blank) |
| Metabolic syndrome | (blank) |
| Fasting blood glucose | (blank) |
| Capillary glucose testing | (blank) |
| Glycosylated hemoglobin (hemoglobin A1c) | IT IS CALLED THIS AS HEMOGLOBIN ATTRACTS GLUCOSE AND OVER TIME THE GLUCOSES INCREASES AND REMAINS ATTACHED TO THE HEMOGLOBIN MOLECULE. IT IS THERE FOR 120 DAYS. MEASURE OF OVERALL GLUCOSE CONTROL OVER 120 DAYS AS RBC’S DIE AFTER 120 DAYS. THE LOWER THE |
| Glycosylated serumproteins and albumin | MEASURES CONTROL OVER 14 DAYS. |
| Oral glucose tolerance | (blank) |
| Serum glucose level | (blank) |
| Urine analysis for glucose and acetone | WILL SHOW KETONES. IF ALBUMIN OR MICROALBUMIN CELLS ARE IN THE URINE IT IS INDICATIVE OF DAMAGE TO THE KIDNEYS. |
| Differentiate between oral hypoglycemic agents and insulin in the management of | (blank) |
| Discuss the reason for sliding scale administration of short acting insulin which is | (blank) |
| Discuss the nutritional management of DM. | (blank) |
| Explain the American Diabetes Association average premeal blood glucose | (blank) |
| Describe how exercise, alcohol consumption, surgery, and/or illness may | Exercise increases the body’s ability to utilize caloriesand decreases the need for insulin. The combined effectof these two actions is that the diabetic client may havea hypoglycemic episode due to having too much exogenousinsulin or insuffi cient glycog |
| Type 1 DM: Dawn phenomenon | A fasting hyperglycemia thought to result from nocturnal release of growth hormone secretion that may cause blood glucose elevations around 5 to 6 am and is treated by providing more insulin for the overnight period |
| Type 1 DM: Somogyi phenomenon | A morning hyperglycemia resulting from effective counter regulatory response to nighttime hypoglycemia, that is treated by ensuring adequate dietary intake at bedtime and evaluating insulin dose and excercise program. |
| nephropathy | renal failure |
| neuropathy | damage to peripheral and autonomic nerves |
| retinopathy | ocular complications leading to blindness |
| cardiovascular disease | (blank) |
| cerebrovascular disease | (blank) |
| S/O: Hypoglycemia | • Diaphoresis Fatigue• Agitation Diplopia• Confusion Hunger• Weakness Tachycardia• Irritability Pallor• Trembling Palpitations• Headache Coma |
| S/O: Diabetic ketoacidpsis (DKA) | (blank) |
| S/O: Hypoglycemia | Blood glucose = 50 mg/dl or lower; (too much insulin or too little glucose |
| S/O: Hyperglycemic hyperosmolar nonketotic syndrome (HHNS) | insulin defi ciency and profound dehydration) |
| Int: Hypoglycemia | (blank) |
| Int: Diabetic ketoacidosis (DKA) | DEVELOPS IF LEFT UNTREATED. KETOACIDOSIS IS AN ACCUMULATION OF KETONES. KETONES ARE KETONE ACETONES. |
| Int: Hyperglycemic hyperosmolar nonketotic syndrome (HHNS) | Very serous complications. Onset comes slowly. The mortality rate is > 50%. Happens to more elderly people. Related to a period of Hyperglycemia. The older person does not take in enough fluids and their thirst mechanism does not work as well. Then |
| Explain why older individuals are at greater risk for developing hyperglycemichyperosmolar | (blank) |
| acid-base balance: Blood gas analysis | (blank) |
| acid-base balance: Compensatory and non-compensatory mechanisms | (blank) |
| acid-base balance: Subjective and objective assessment | (blank) |
| acid-base balance: Treatment | (blank) |
| Classification: Parenteral antidiabetic – Insulin / Prototype: Rapid acting: Humalog (Lispro) or Novolog (Insulin Aspart) | Necessary for type 1 diabetes & for moderate to severe type 2 diabetes |
| Classification: Oral antidiabetic – Sulfonylurea / Prototype: First generation – Chlorpropamide (Diabinese) | These agents are appropraite only for clients with pancratic beta cell function; hypoglycemia is the most serious complication; other side effects include hematologic reactions, allergic skin reactions and GI effects |
| Classification: Oral antidiabetic – Meglitinides / Prototype: Repaglinide (Prandin) | Action & Side effects are similar to sulfonylura agents. Adverse effects include hypoglycemia, GI disturbance, Upper resp infections, athrlagia, back pain and headache |
| Classification: Oral antidiabetic – D – phenylalanines / Prototype: Nateglinide (Starlix) | Derivatives lower blood glucise by triggering insulin secretion via interaction with teh ATP sensitive potassium channel on pancreatic beta cells |
| Classification: Oral antidiabetic – Alpha-glucosidase inhibitors / Prototype: Arcarbose (Precose) | Reduce postprandial hyperglycemia by slowing digestion and absorption of carbohydrate within the intestine. Side effects include abdominal discomfort r/t undigested carbohydrate in the intestinal tract. |
| Classification: Oral antidiabetic – Biguanides / Prototype: Metformin (Glucophage) | only available in US & can cause lactic acidosis in clients with renal insufficiency |
| Classification: Oral antidiabetic – Thiazolidinediones (glitazones) / Prototype: Rosiglitazone maleate (Avandia) | Enhance Insulin action, promoting glucose utilization in peripheral tissue. Liver function studies should be done at the start of therapy and at regular intervals while on therapy |
| Classification: Oral antidiabetic – Combination agents / Prototype: Glucovance (Metformin & glyburide) | These are combnations from two different classes of medications |
| Classification: Pancreatic hormone / Prototype: Glucagon (GlucaGen) | (blank) |
| Explain the procedure and rationale for mixing insulins | (blank) |
| Continuous subcutaneous infusion | (blank) |
| Implanted insulin pump | (blank) |
| Injection devices | (blank) |
| Nebulized | (blank) |
| Transdermal | (blank) |
| Evaluate the success of whole-pancreas and human islet cell transplantation. | (blank) |
| Develop a teaching plan for exogenous insulin administration | (blank) |
| Develop a teaching plan for capillary glucose monitoring | (blank) |
| Lipoatrophy | (blank) |
| Lipohypertrophy | THICKENING OF THE SITE. INSULIN WILL NOT ABSORBG AS WELL WHEN SKIN IS ATROPHIED. |
| Develop a teaching plan for preventing, or living with, the possible long term complications | (blank) |
| Develop a plan to teach Sick-Day Rules to a patient with either Type 1 or Type 2 diabetes mellitus | o Take insulin/oral drugs as usual o Test BG q4ho Test urine ketoneso Prevent dehydrationo Eato Report N/V (nausea/vomiting), diarrheao Rest |
| Identify tasks that can be delegated to assistive personnel when caring for a patient with diabetes | (blank) |
| Urine testing for DM | Urine testing for glucose is less precise than blood testing.Fluid intake, urine concentration, time since lastvoiding, and certain drugs affect the results. |
Created by:
littlemina