Diabetes Mellitus

Barbara S. HaysWinter, 2006

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

Hyperglycemia

• Drowsy• Flushed• Thirsty

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)

Hypoglycemia

• Weak, sweaty• Confused/irritable/

disoriented

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

The good news:– Blood glucose control reduces

complications of Diabetes!

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

Triad of Treatment

• Diet

• Medication– Oral hypoglycemics– Insulins

• Exercise

Diabetes treatment

• Exercise– Under physician supervision– Check glucose prior

Diabetes treatment

• Diet– Lower calorie– Fewer foods of “high glycemic index”– Spread meals evenly

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]

Your learning

• Onset of action

• Peak (blood glucose will be lowest then)

• Duration

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.

Typical diabetic foot ulcer