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HCC Diabetes
| Question | Answer |
|---|---|
| Diabetes Mellitus(DM) | Common chronic disease of adults. No cure, lifelong lifestyle/health condition changes. Diabetes(Greek)-siphon. Mellitus(Latin)-sweet. |
| Innapropriate Hyperglycemia(DM) | Caused by a relative or absolute deficiency of insulin. Increased resistance to insulin uptake. |
| Cardiovascular Complications | Main cause of death in DM |
| Prevalence of DM | 2X more common in African, 2.5X More common in Hispanic, 5X more common in Native American. Type I-Males. Type II-Females. |
| Diseases Caused by DM | Endstage renal, newly diagnosed blindness, non-traumatic amputation. |
| Diabetes Origin | Egyptian doctor discovered it. About 3500 years old, one of the oldest diseases. Cause still not understood. |
| Microscope | Advanced the diagnosis and treatment of DM. |
| 1921 | Removed insulin from a pancreas, called it insulin, and shortly devised a way of detecting blood glucose levels. Then injected, it resulted in a decline in blood glucose level. |
| 5TH LEADING CAUSE OF DEATH | It's not the diabetes that kills, it's the complications as a result from diabetes. |
| Elderly | DMII |
| Insulin | beta cells. Reduces blood glucose levels, inhibits breakdown of stored lipids, moves amino acids into cells for protein synthesis. |
| The Car | Insulin is the car that drives the glucose into the cells. |
| alpha Cells | Produce/secrete glucagon which decreases glucose oxidation = increased blood glucose. |
| beta cells | Produce/secrete insulin which reduces blood glucose levels. |
| delta cells | Produce/secrete somatostatin which inhibits production of glucagon/insulin. |
| Glucagon | Counter-regulatory hormone. Result of either glycogenolysis or gluconeogenesis. "Called in" when blood glucose falls below 70 mg/dL |
| Body Systems | All require constant supply of glucose, but not all require insulin for absorption. Brain, liver, intestines, and renal tubules. |
| Blood Glucose Parameters | Normal <110(65-99), Pre-diabetes >110-126, Diabetes >126. |
| Type I | Formerly IDDM/Juvenile-Onset. 5-10% of all DM. |
| Type II | Formerly NIDDM/Adult-Onset. 90-95% of all DM. |
| Obese | 80% of clients with diabetes are obese. |
| Non-obese | 20% of clients with diabetes are not obese. |
| Gestational Diabetes | Lifelong or just during pregnancy. |
| Pre-diabetes | Increased risk for type II. Will have diabetes within 10 years if not prevented. Lose wt., exercise regularly, eat healthy. |
| Epinephrine | From medulla cortex of adrenal gland as a response to a drop in blood glucose levels-stress-GAS-increase in epinephrine-increase blood sugar level. |
| GAS | General Adaptation Syndrome. An adaptive hormone. |
| Cortisol | From adrenal cortex in response to drop in blood glucose levels-raises blood glucose levels-works during fasting/between meals. |
| Growth Factor | From anterior pituitary increases blood glucose levels. Anti-insulin effect. |
| Metabolic Syndrome | Umbrella cluster. Increased risk for type II. |
| Characteristics of Metabolic Syndrome | Increased insulin resistance, elevated glucose levels, high triglycerides, low HDL's, high LDL's, hypertension. |
| Risk for Metabolic Syndrome | Central obesity, sedentary lifestyle, ethnicities, urbanization/westerniztion(poor eating) |
| Type I Pathophysiology | Usually before 30. Inappropriate hyperglycemia, breakdown of body fats & proteins, and development of ketosis. |
| Ketone Bodies | Result from breakdown or oxidation of fatty acids. |
| beta cell destruction | Genetic predisposition, viral or toxic chemical agents, and autoimmune attack. |
| DMI Stage 1 | Genetic predisposition |
| DMI Stage 2 | Environmental trigger |
| DMI Stage 3 | Active autoimmunity |
| DMI Stage 4 | Progressive beta cell destruction |
| DMI Stage 5 | Overt DM(cause unkown) |
| Manifestations of DMI | Sleepiness, malaise, fatigue, blurred vision. |
| Renal Threshold | 180 for blood glucose then spills over into urine. |
| Polydipsia | Decreased intracellular volume/increased urine output->dry mouth->increased thirst->polydipsia. |
| Polyphagia | Decreased energy production->increased hunger->polyphagia->wt. loss(lost water/protein & fat breakdown) |
| DCCT | Diabetes and Control and Complications Trial. 10 year tracking of clients keeping blood glucose WNL's = reduced complications. |
| DKA | Diabetic Ketoacidosis. MEDICAL EMERGENCY! |
| DKA Metabolic Process 1 | Hyperosmolarity from hyperglycemia and dehydration. |
| DKA Metabolic Process 2 | Metabolic acidosis from accumulation of ketoacids. |
| DKA Metabolic Process 3 | Extracellular volume depletion from osmotic diuresis. |
| DKA Metabolic Process 4 | Electrolyte imbalances from osmotic diuresis. |
| DKA Dehydration | Intense thirst, decreased turgor, warm dry skin, soft eye balls, dry mucous membranes, decreased BP, increased weak pulse. |
| DKA Acidosis | N&V, Ketone breath, lethargy, coma. |
| DKA S&S | Abdominal pain, Kussmaul's respirations, blood glucose in excess of 300, pH <7.3, plasma bicarb <10, serum ketones, urine ketones & glucose, haywire electrolytes. |
| Kussmaul's respirations | Increased rate and depth of respirations. Blows off carbon dioxide(acid). |
| Treatment of DKA | Lower blood glucose, balance F&E, correct pH. IV fluids, electrolytes, and insulin. |
| Hypoglycemia | TIRED. Tachycardia, Irritability, Restlessness, Excessive hunger, Diaphoresis/Depression. |
| DM Type II | Some avail indogenous insulin. More/more treated w/insulin. Sufficient insulin so non-ketotic form of DM. |
| Apple Shape | Type II. Tend to have insulin receptor abnormalities. |
| DM Type II S&S | Slow onset. Numbers not as high as type I. Polyuria/Polydipsia often(polyphagia/wt. loss uncommon). Blurred vision, parasthesias, frequent skin infections. |
| Diabetes Prevention Program Research Group | Very preventable w/lifestyle changes(non-pharmacologically). |
| HHNS | Hyperglycemic Hyperosmolar Nonketotic Syndrome. Metabolic Complication of DMII. Serum osmolarity of 340+. |
| HHNS Complications | Greatly increased BGL's in excess of 600-1000+. Altered LOC, MED EMERGENCY, higer mortality than DKA. |
| HHNS Treatment | IV F&E, insulin, maintain BGL's. |
| HHNS S&S | Very dry skin and mucous membranes, altered LOC, Hyperthermia, Motor skill impairment, postive Babinski's, seizures. |
| HHNS Path | Altered LOC->lethargy->coma->death. |
| Dawn Phenomenon | A rise in BG between 4-8am that is not a response to hypoglycemia. Cause unknown. |
| Somogyi Phenomenon | A rise in the BG in the morning iin response to nocturnal hypoglycemia(rebound). |
| Management of Altered BGL's | Careful self monitoring of BG, regular healthy bedtime snacks, careful assessment of tremors, night sweats, nightmares, HA, stomach aches. |
| BGL's | Blood Glucose Levels |
| 3 Changes in Diabetic Neuropathies | Thickening of blood vessel walls, demyelinization of the Schwann cells, formation and accumulation of sorbital. |
| Thickening of Blood Vessel Walls | Interferes w/nutrient delivery. |
| Demyelinization of Schwann Cells | Impairs/slows nerve conduction(without the insulation the electrical impulse doesn't travel as fast). |
| Formation and Accumulation of Sorbital | Buildup of sorbital damages Schwann cells. |
Created by:
mande747
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