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M6 13-005
Exam 13: Diabetes Mellitus
| Term | Definition |
|---|---|
| Diabetes Mellitus (DM) | Systemic metabolic disorder that involves improper metabolism of carbohydrates, fats and proteins. |
| Diabetes: Problem with insulin | ↓ or absolute lack of insulin production by the beta cells of the “islets of Langerhans” -Body’s insulin supply is either absent or deficient. ↓ activity of the insulin that is secreted. -Target cells in the body resist action of insulin. |
| Diabetes: Diagnosis (Clinical Manifestations) | Polyuria. Polydipsia. Polyphagia. |
| Polyuria | Increased urine output |
| Polydipsia | Increased thirst |
| Polyphagia | Increased appetite |
| 200mg/dl | Random blood glucose over _______. Warrants further investigation |
| Glycosuria | Glucose in the urine |
| Ketonuria | Ketones in the urine |
| Diabetes Mellitus: Causes | Unknown. Genetic predisposition. Viruses: -Coxsackie virus B. -Rubella. -Mumps. Aging process. Diet & lifestyle. Ethnicity. Obesity. Auto-immune process attacking the B cells. |
| Diabetes Mellitus: Dx Pt Hx | Hunger. Thirst. Nausea. Nocturia. Weakness. Fatigue. Blurred vision. Appearance of halos around lights. Headache. |
| Normal metabolism | After digestion glucose, fatty acids, glycerol, & amino acids are absorbed into venous circulation. -Carried to the liver: --For storage (as glycogen). --Immediate use by the body. |
| Liver | Changes glycerol and fatty acids into glucose. Changes glucose into triglycerides as needed Stores glucose in the form of glycogen. -Can be converted back to glucose when needed for energy. |
| By products of fatty acid synthesis are | ketones bodies and acetone. Serve as fuel for body muscles and brain when no glucose is accessible. |
| Brain and Kidney | ONLY organs that can use free serum glucose without insulin |
| IMPORTANT!!! | Insulin must be present to enable muscle cells and other cells of the body to use glucose. |
| Diabetes | Lack insulin. Body does not use insulin correctly. Result: -Body does not use glucose correctly. -Excessive glucose accumulates in the blood – causes hyperglycemia. |
| glycosuria caused by | Body attempts to rid itself of the excess glucose by excreting it in to the urine |
| Polyuria caused by | To excrete the increased glucose, the kidneys require extra water for dilution |
| polydipsia caused by | the kidneys require extra water, the client develops excessive thirst |
| dehydration caused by | often unable to drink enough fluids to compensate for volume loss |
| Despite excessive glucose in blood stream, it can not be used by body without | Insulin |
| Body’s fat and protein sources are broken down for | energy |
| Insulin Dependent Diabetes Mellitus (IDDM) | Type I- Little or no endogenous insulin produced. -Requires injections of insulin |
| Insulin Dependent Diabetes Mellitus (IDDM): Causes | Progressive destruction of beta cell function: -Autoimmune process -Viral -Genetic predisposition -Chemical agents |
| Non-Insulin Dependent Diabetes Mellitus (NIDDM, Type II): Causes | Decrease tissue responsiveness to insulin: -Caused by receptor defects. -Insulin resistance. Decrease secretion of insulin from beta cells. Abnormal hepatic regulation. |
| NIDDM Type II: Etiology | Strong genetic component. Associated with obesity. -80% are overweight. Ethnic association. -African-American, Hispanic, American Indian. Approximately 90% of diabetic clients are Type II. Primarily in adults > 30 years old Require insulin injectio |
| Question: What are the cardinal manifestations of diabetes? | Gycosuria, polyuria, polydipsia, and polyphagia |
| IDDM Type I: Clinical Manifestations | Abrupt onset. Hyperglycemia. 3 classic symptoms: -Polyuria. -Polydipsia. -Polyphagia. Mobilization of protein and fat stores: -Muscle wasting and weight loss. -Thin clients. Ketone formation from breakdown of fat. |
| IDDM Type I: Subjective Data | Headache. Hunger. Nausea, vomiting. Nocturia, dehydration, hypovolemia. Blurred vision, halo around lights. |
| NIDDM Type II: Clinical Manifestations (Ojective Data) | May have Type I signs and symptoms. Slow wound healing. Pruritus. Boils or other skin infections. Vaginal infections. Skin thin and shiny. Legs & feet cold to touch. ↓ sensation to pain and temp in feet and hands. |
| Diagnostic Test for DM | Random blood glucose > 200 mg/dl Requires further testing Client self monitoring. Glucose Monitoring tool of choice. .Provides an accurate picture of current blood glucose levels. |
| Urine testing for ketones | Determines DKA. Performed in lab or with urine dipstick. |
| Fasting blood glucose | After an 8 hour fast. Normal: 60 – 120 mg/dl. > 126 mg/dl is considered abnormal. |
| Oral Glucose Tolerance Test (OGTT) | Client fasts for 8 hours. Blood and urine samples collected for baseline. Client ingests an oral glucose solution. Blood is drawn periodically. -30 min, 1 hour, 2 hour, 3 hour. Urine collected at the same times. |
| OGTT: Non-diabetic vs. Diabetic | Non-diabetic client: -Blood glucose levels return to normal in 2 – 3 hours. -Urine is negative for glucose Diabetic client: -Blood glucose levels return to normal slowly. -Urine is positive for glucose. |
| Postprandial blood sugar (PPBS) | Blood drawn 2 hours after completion of oral intake. Blood glucose > 160 mg/dl indicates DM. |
| Glycosylation | Glucose binding to hemoglobin. Occurs constantly during the 120 day lifespan of the RBC. Test shows effectiveness of diabetic therapy for the preceding 8 – 12 weeks. |
| Glycosylated hemoglobin (HbgA1c) | Measures the amount of glucose bound to hemoglobin within the RBC. Reported in % of total Hgb: Normal 4 – 6 % To reduce complications, critical to keep value below 7% > 8% = average blood glucose level of approximately 200 mg/dl |
| normal blood glucose level | Normal 60-110 trying to achieve... < 126 mg/dl |
| Management of Diabetes: Meal Planning | Quantitative. Qualatative. |
| What are 2 goals for diabetic clients? | Helping achieve normal blood glucose level < 126 mg/dl. Prevention and treatment of acute complications. |
| Management of Diabetes: Exercise | Improves circulation. Metabolize carbohydrates, ↓ insulin requirements. Lowers cholesterol and triglyceride levels. ↓ blood pressure. Helps control weight. Prevents wide fluctuations in glucose levels. ↑ activity may require different food and insul |
| Diabetic Medications: Insulin | Necessary for all clients with Type I DM. Used for the client with Type II whose condition can not be controlled by diet, exercise, or oral hypoglycemics alone. Must be injected subcutaneously. |
| Insulin: Types | Beef and pork. Biosynthetic: -Replaced Beef and Pork. -More identical action to that of human insulin. |
| Insulin: Formulas | Short acting (regular, Humulin or Novolin insulin). Intermediate acting (NPH, insulin). Long acting (Lantus insulin). Each as different onset, peak, action and duration. |
| Only insulin that be given IV | Short/rapid acting insulin. |
| Long acting insulin | Ultralente, Humulin U Onset: 4 – 8 hours Peak: 16 – 19 hours Duration: 36 hours |
| Insulin lispro | Humalog. Recent human insulin formula. Takes effect in less than ½ the time of regular, fast acting insulin. Onset: 15 minutes. Used in insulin pumps. |
| LANTUS | Long acting synthetic insulin. Administered once a day. Regular insulin is used during the day to control hyperglycemia. |
| Premixed insulin combinations | Used for clients with stable insulin needs. Combination 70/30: 70% NPH and 30% Regular. Combination 50/50: -50% NPH and 50% Regular. Combination 75/25: -75% lispro protamine {NPH} and 25% lispro Humalog {rapid acting}). |
| Insulin delivery systems | Automatic injectors. Needless injector. Uses high pressure and rapid speed. -No needle. Decrease pain. Increased cost. Continuous subcutaneous Insulin infusion. |
| Continuous subcutaneous Insulin infusion | External infusion pump. Cannula inserted into subcutaneous tissue. Capable of delivering basal rate and boluses. Provides better control. |
| signs of hypoglycemia | Faintness. Sudden weakness. Diaphoresis. Irritability. Hunger. Palpitations. Trembling. Drowsiness. |
| Insulin - Nursing interventions | U100: -Each 1ml contains 100U of insulin. -Syringe contains total of 1ml. -Marked in 2 unit increments. Gauge 25 – 32: Smaller gauge = less tissue trauma. |
| Oral Hypoglycemics | Compounds that stimulate the beta cells to produce insulin. -Not a substitute for insulin. Client must have some functioning insulin production for these medications to be effective. |
| Sulfonylureas | Stimulate beta cells to produce insulin. Improves use of insulin at receptor sites. Increases the effectiveness of existing insulin. Can NOT be used in clients with little or no pancreatic activity. |
| Sulfonylureas: Examples | Tolbutamide (Orinase), Chlorpropanamide (Diabinese), Glipizide (Glucotrol), Gylburide (Micronase) |
| Non-sulfonylureas | Precose (Acarbose). Glucovance. Actos (Pioglitazone HCL). |
| Precose (Acarbose) | Acts by delaying the digestion of ingested carbohydrates. Results in smaller rise of blood glucose after a meal. Used alone or in conjunction with sulfonylureas. |
| Glucovance | combined glyburide/metformin, recently been approved by the FDA. |
| Actos (Pioglitazone HCL) | effective for the treatment of insulin resistive patients. |
| Diabetic Surgical Treatment: Pancreas transplant | Candidate – Type I diabetic with renal failure. Usually transplant kidney as well. Requires life long immunosuppressive therapy. Type II: -Not recommended for this therapy. -Transplant will not change their insulin resistance. |
| Diabetic Surgical Treatment: Islet Call Transplant | Islet cells are harvested from human donors and pigs. Injected into the client’s peritoneum. Begin producing insulin. Require immunosuppressives. Many clients require little or no exogenous insulin therapy. |
| Skin and foot education for Pt with DM | Proper skin care is Essential because poor circulation can lead to development of skin problems. Foot Care important because Poor circulation and decreased nerve sensation (neuropathy) increases ulcer development. Can lead to gangrene. No barefoot! |
| vascular disturbance Education for Client with DM | Teach/Assess understanding of vascular disturbances and manifestations. Prone to circulatory disturbances. Arteriosclerosis is accelerated. Affects peripheral blood vessels. Especially lower extremities, kidneys, heart and eyes. |
| Vascular disturbances | Arteriosclerosis leads to increased: CAD, HTN, PVD. MI (2X higher). CVA (2-6x higher). Orthostatic hypotension. Bowel/bladder dysfunction. Impotence, premature ejaculation. Increased cholesterol levels. |
| Glycosylated hemoglobin is | Stickier: Clumps/clots occlude small vessels in brain, heart, kidneys and eyes |
| Capillary changes contribute to | renal sclerosis: Often progresses to end stage renal disease (ESRD). May require hemodialysis or peritoneal dialysis. |
| Decreased blood supply to the skin and peripheral nerves result in: | Decreased ability to fight infection. Delayed wound healing. Cramping. |
| Neuropathy | Any abnormal condition characterized by inflammation and degeneration of the peripheral nerves |
| Neuropathy & DM | Legs most frequently affected: Bilaterally and symmetrically. Pain and parathesias at night may be relieved by walking. Complete or partial loss of sensitivity to touch and temperature. |
| Neuropathy affecting the autonomic nervous system may also result in | Gastrophy: Delayed gastric emptying that can produce anorexia, nausea, vomiting, early satiety, persistent feelings of fullness. |
| Education for Client with DM: Visual changes/ Diabetic Retinopathy | Microvascular changes affect retinal capillaries: Tend to develop multiple tiny aneurysms accompanied by small points of hemorrhage and exudate. Scarring results from repeated hemorrhages. |
| Diabetic retinopathy | May lead to blindness: DM causes more blindness than any other disease. Increased risk of cataracts and retinal detachment. |
| Diabetic Ketoacidosis | Occurs in Type I, IDDM clients: -Often occurs due to an acute illness. Blood glucose levels are elevated, but no insulin present to promote glucose entry into cells. |
| Diabetic Ketoacidosis: Etiology | Body compensates by: Using fats & proteins for energy: -Produces ketones. Ketones accumulates in the blood: -pH decreases. Hypovolemia & electrolyte imbalances occur due to the elevated blood glucose. |
| Diabetic Ketoacidosis: Diagnosis | Based on symptoms. High blood glucose levels (300 –800 mg/dl) and blood ketones. Urine test positive for glucose and ketones. Hyponatremia, hyperkalemia, hypochloremia, decreased bicarbonate. Serum pH: 6.8 – 7.3. |
| Diabetic Ketoacidosis: Early Symptoms | -Weakness -Drowsiness -Vomiting -Thirst -Abdominal pain -Dehydration -Hot, dry skin -Flushed cheeks -Dry mouth |
| Diabetic Ketoacidosis: LAte Symptoms | -Kussmaul’s breathing -Sweetish odor on breath -Acetone -Hypotension -Rapid weak pulse -Restlessness -Stupor, coma, Death |
| Diabetic Ketoacidosis: Medical management | Reduction of elevated blood glucose levels and decrease acidosis. -IV Insulin infusion to maintain BG 200 – 250mg/dl. |
| Hypoglycemia | Low blood glucose level. Glucose level falls below 60 mg/dl. |
| Hypoglycemia: Causes | Overdose of insulin or oral hypoglycemic agent. Inadequate food intake; delayed meal. Excessive physical activity. |
| Hypoglycemia: Initial Symptoms | Faintness. Sudden weakness. Diaphoresis. Irritability. Hunger. Palpitations. Trembling. Drowsiness. Pallor. Headache. Nausea/vomiting. Personality changes. |
| Hypoglycemia: Intermediate Symptoms | Dizziness. Confusion. Loss of speech. Unable to control body movements. Diplopia, blurred vision. |
| Hypoglycemia: Late Symptoms | Convulsions. Unconscious. Brain damage. Death. |
| Hypoglycemia: Treatment (Conscious) | Restore Glucose Level. -Oral administration of simple CARB. |
| Hypoglycemia: Treatment (Unconscious) | IV bolus of 20 ml of 50% glucose or 50 ml of 20 % glucose. Glucagon: -IV or IM. D10 or D20 at 100ml/hr to follow initial treatment. |
Created by:
jtzuetrong
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