Diabetes Mellitus Barbara S. Hays Winter, 2006. Blood Glucose (normal serum level 65 – 105 mg)...
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Transcript of Diabetes Mellitus Barbara S. Hays Winter, 2006. Blood Glucose (normal serum level 65 – 105 mg)...
Blood Glucose(normal serum level 65 – 105
mg)
• 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)
Blood glucose, cont.
• 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
Hyperglycemia
• 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
Hypoglycemia
• 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)
Diabetes Mellitus(problem with glucose
metabolism)• Major health problem US/worldwide• Complications [lousy blood vessels]
– Blindness– Renal failure– Amputations– [heart attacks and strokes]– [OB/neonatal complications]
Diabetes Mellitus
• 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)
Diabetes Mellitus
• 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.
Diabetes Mellitus
• 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
Classifying Diabetes Mellitus
• Type I Diabetes: autoimmune– Beta cell destruction in genetically
susceptible person
– Some viral infections
Classifying Diabetes Mellitus
• 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)
Diabetes Mellitus
• 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
Diabetes Mellitus
• Prevention of effects: combination approach– Increased exercise
• Decreases need for insulin
– Reduce calorie intake• Improves insulin sensitivity
– Weight reduction• Improves insulin action
Diabetes treatment
• 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)
Sulfonylureas
• 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
Biguanides
• Decreases liver production of glucose• Decreases intestinal absorption of
glucose• Improves cell sensitivity to insulin
• Example: Metformin– GI upset, flatulence– Cardiac (CHF, MI)
Thiazolidinediones
• Increase cellular sensitivity to insulin– Pioglitazone (Actos)– Rosiglitazone (Avandia)
Client should have liver enzymes checked periodically
D-Phenylalanine derivatives
• Nateglinide (Starlix)
• Rapid onset, short half-life– Good for those with rapid post prandial
rise in blood glucose
Combinations
• Glucovance– Glyburide and Metformin
• Avandamet– Avandia and Metformin
[come tell me when you run into this question…]
Insulin
• 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)
Insulin preparations (“Easy” p 390)
given ONLY with syringes marked in “units”
• Rapid acting (lispro, asparte)
• Short acting (regular)
• Intermediate acting (NPH)
• Long acting– Ultralente– [Glargine/Lantus]
Rapid acting insulin
• 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
Short acting insulins
• 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
Intermediate acting insulins
• NPH, Lente (chemicals added. Cloudy)– Onset of action
• 1 – 4 hours
– Peak of action• 4 – 12 hours
– Duration of action• 18 – 24 hours
Long acting insulins
• Ultralente– Onset of action
• 4 – 8 hours
– Peak of action• 18 hours
– Duration of action• 24 – 36 hours
Once a day insulin
• 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
Combination insulins
• 70/30 (70% NPH and 30% regular)• Humolog 70/30 (Humolog and
regular)
• Fewer injections• Rotate sites to decrease
lipodystrophy
Miscellaneous
• 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
Some things to know
• Insulin moves potassium into cells– Good for emergency situations– Dangerous if potassium level already
low
Some things to know…
• HHNK (Hyperglycemic Hyperosmolar Non-Ketotic 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
Some things to know…
• 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
Some things to know…
• 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.