Diabetes Mellitus
February 6, 2017 | Author: Manish Chandra Prabhakar | Category: N/A
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Description
Barbara S. Hays Winter, 2006
Inside CNS
◦ Brain uses glucose as primary fuel ◦ Brain cannot store/produce glucose
Outside CNS
◦ Fatty acids: stored as
Glycogen (liver/muscles) Triglycerides (fat cells)
Outside CNS, continued ◦ Endocrine portion of pancreas: Islets of Langerhans Alpha cells make glucagon “counterregulatory”, acts opposite of insulin
Beta cells make insulin Allows body cells to store and use carbohydrate, fats, and protein
When blood glucose becomes high ◦ INSULIN allows glucose to enter cells Liver Production /storage of glycogen Inhibits glycogen breakdown Increased protein & fat synthesis (VLDL formation)
Muscles Promotes protein and glycogen synthesis
Fat cells Promotes storage of triglycerides
Drowsy Flushed Thirsty
Glucagon: causes release of glucose from liver ◦ “glycogenolysis (breakdown of glycogen to glucose) ◦ “glyconeogenesis of glucose not available Lipolysis (breakdown of fat) Proteolysis (breakdown of amino acids)
Weak, sweaty Confused/irritable/ disoriented
Major health problem US/worldwide Complications [lousy blood vessels] ◦ ◦ ◦ ◦ ◦
Blindness Renal failure Amputations [heart attacks and strokes] [OB/neonatal complications]
The good news: ◦ Blood glucose control reduces complications of Diabetes!
Absence (or ineffectiveness of ) insulin Cellular resistance Cells can’t use glucose for energy ◦ Starvation mode Compensatory breakdown of body fat/protein Ketone bodies from faulty fat breakdown Metabolic acidosis, compensatory breathing (Kussmal’s breathing)
HYPERGLYCEMIA: fluid/electrolyte imbalance. ◦ Polyuria Sodium, chloride, potassium excreted
◦ Polydipsia from dehydration ◦ Polyphagia: cells are starving, so person feels hungry despite eating huge amounts of food. Starvation state remains until insulin is available.
Complications of chronic hyperglycemia ◦ Macrovascular complications Cardiovascular disease (heart attack) Cerebrovascular disease (strokes)
◦ Microvascular
Blindness (retinal proliferation, macular degeneration) Amputations Diabetic neuropathy (diffuse, generalized, or focal) Erectile dysfunction
Type I Diabetes: autoimmune ◦ Beta cell destruction in genetically susceptible person ◦ Some viral infections
Type II Diabetes ◦ Reduction in ability of most cells to respond to insulin ◦ Poor control of liver glucose output ◦ Decreased beta-cell function (eventual failure)
Major risk factors
◦ Family history ◦ Obesity ◦ Origin (Afro-American, Hispanic, Native American, Asian-American) ◦ Age (older than 45) ◦ History of gestational diabetes ◦ High cholesterol ◦ Hypertension
Prevention of effects: combination approach ◦ Increased exercise
Decreases need for insulin
◦ Reduce calorie intake
Improves insulin sensitivity
◦ Weight reduction
Improves insulin action
Diet
Medication ◦ Oral hypoglycemics ◦ Insulins
Exercise
Exercise ◦ Under physician supervision ◦ Check glucose prior
Diet ◦ Lower calorie ◦ Fewer foods of “high glycemic index” ◦ Spread meals evenly
Anti-Diabetic medications
◦ Oral hypoglycemic agents (“Easy” p 297)
Sulfonylureas Thiazolidinediones Biguanides Alpha-glucosidase inhibitors D-phenylalinine derivatives Combinations
◦ Insulins (“Easy” Prototype Pro p 393)
Stimulate pancreas to secrete insulin ◦ Glyburide (Diabeta) [Prototype Pro p 393] Glucotrol (Glipizide) Diabenese (chlorpropamide)
Adverse reactions
◦ Hypoglycemia ◦ Water retention/edema ◦ Photosensitivity
May need to add insulin in times of stress
Decreases liver production of glucose Decreases intestinal absorption of glucose Improves cell sensitivity to insulin
Example: Metformin
◦ GI upset, flatulence ◦ Cardiac (CHF, MI)
Increase cellular sensitivity to insulin ◦ Pioglitazone (Actos) ◦ Rosiglitazone (Avandia)
Client should have liver enzymes checked periodically
Nateglinide (Starlix)
Rapid onset, short half-life ◦ Good for those with rapid post prandial rise in blood glucose
Glucovance ◦ Glyburide and Metformin
Avandamet ◦ Avandia and Metformin
[come tell me when you run into this question…]
Made in beta cells of the pancreas Moves glucose into cells (thus acts like growth hormone in a way) Moves potassium into cells (can buy time in emergencies)
Rapid acting (lispro, asparte) Short acting (regular) Intermediate acting (NPH) Long acting ◦ Ultralente ◦ [Glargine/Lantus]
Onset of action
Peak (blood glucose will be lowest then)
Duration
Lispro (Humolog, Novolog Aspart) ◦ Onset of action “15-30” minutes [may come on in 5 minutes…]
◦ Peak of action 1 - 2 hours
◦ Duration 3 – 4 hours
Regular (clear so can be given IV) ◦ Onset of action 0.5 to 1 hour
◦ Peak of action 2 – 4 hours
◦ Duration of action 6 – 8 hours
NPH, Lente (chemicals added. Cloudy) ◦ Onset of action 1 – 4 hours
◦ Peak of action 4 – 12 hours
◦ Duration of action 18 – 24 hours
Ultralente ◦ Onset of action 4 – 8 hours
◦ Peak of action 18 hours
◦ Duration of action 24 – 36 hours
Glargine/Lantus ◦ Cannot be diluted or mixed in syringe with any other insulin ◦ Slow, steady release ◦ Daily dosing [usually at bedtime] ◦ Refrigerated or tosses every 14 days
70/30 (70% NPH and 30% regular) Humolog 70/30 (Humolog and regular) Fewer injections Rotate sites to decrease lipodystrophy
Byetta for type II Diabetics taking sulfonylureas or combination ◦ Mimics physiologic glucose control Inhances insulin secretion only in presence of hyperglycemia Insulin secretion decreases as blood glucose approaches normal
Neutontin for Diabetic nerve pain
Insulin moves potassium into cells ◦ Good for emergency situations ◦ Dangerous if potassium level already low
HHNK (Hyperglycemic Hyperosmolar NonKetotic Coma). Also called ◦ HHNK ◦ HNKS [syndrome] Like dibetic ketoacidosis, without the ketones Type II diabetic, makes enough insulin to avoid ketones, but sugar guilds up to dangerous levels -> cellular dehydration
Dawn Phenomenon vs Somogi’s effect ◦ Dawn phenomenon Blood sugar rises in early morning
◦ Somogi’s (rebound) effect Blood sugar rise in morning as reaction to hypoglycemic time during the night
Diabetic foot care ◦ Dry, cracked skin + poor circulation could = loss of a limb ◦ For the most part nurses don’t trim nails of diabetic clients. Refer to Podiatrist.
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