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HCC Diabetes

QuestionAnswer
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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