Diabetes Mellitus

Barbara S. Hays
Winter, 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