Care of Patients with
Diabetes Mellitus
Chapter 64
Diabetes
• Chronic metabolic disease
• Requires lifelong changes
• Multiple complications
• Hypertension
• Behavioral
• Hyperlipidemia
• Lifestyle
• Blindness
• Renal disease
• Limb amputations
Pathophysiology
• Chronic hyperglycemia resulting from:
• Problem with insulin secretion
• Inadequate insulin action
• Classified by underlying problem
• Type I (lack of insulin)
• Type II (insulin deficiency)
Pancreas
Endocrine
• Related to blood glucose control
• Has approx. 1 million glands (islets of
Langerhans)
• Alpha
• Secrete glucagon
• Beta
• Produce insulin and amylin
Exocrine
• Related to digestion
• Breaks down enzymes
Glucagon
• “Counterregulatory” hormone
• Actions opposite of insulin
• Prevents hypoglycemia (low blood
sugar)
• Triggers release of glucose from
cell storage sites
Insulin
• Prevents hyperglycemia by allowing
body to absorb or “take up”, use and
store carbohydrate, fat and protein
• Daily secretion is roughly 40-50 units
directly to liver circulation via two
separate steps
• Main metabolic effects:
• Stimulate glucose uptake in skeletal and
heart muscle
• Suppress liver production of glucose
• Fasting-secretion suppressed
• Low level
• Basal insulin secretion
• Prandial
• Increased after eating
• Early burst occurs within 10 minutes of
eating
• Increased release until blood glucose
reaches normal level
Insulin continued…
• Needed to move glucose into most
body tissues
• Lack of insulin prevents some cells
from using glucose for energy
• Body breaks down fat and protein to
provide energy
• Increases levels of counterregulatory
hormones to attempt to make glucose
from other sources
• Glucagon
• Epinephrine
• Norepinephrine
• Growth hormone
• Cortisol
Insulin (See Table 64-8 on pg. 1314)
• Rapid-Acting
• Onset = 15 min
• Peak = 1-3 hours
• Duration = 3-5 hours
• Short acting
• Onset = 30 min
• Peak = 2-5 hours
• Duration = 5-8 hours
• Intermediate acting
• Onset = 15 min-1.5 hours
• Peak = 4-12 hours
• Duration = 5-24 hours
• Long acting (Lantus)
• Onset = 2-4 hours
• Peak = NONE
• Duration = 24 hours
Absence of Insulin
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Hyperglycemia- high blood glucose level
Polyuria- Frequent/excessive urination
Polydipsia – excessive thirst
Polyphagia – excessive eating
Ketones- Abnormal breakdown products of
fatty acids
• Hemoconcentration- Increased blood
concentration due to dehydration
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Hypovolemia- decreased blood volume
Hyperviscosity- thick, concentrated blood
Hypoxia- poor tissue oxygenation
Kussmaul respiration- even, deep, rapid
Hypokalemia- Low potassium level
Hyperkalemia- High potassium level
Glucose
• Main fuel for central nervous system
cells (CNS)
• Stored inside cells as glycogen in liver
and muscles
• Free fatty acids stored as triglyceride in
fat cells
• After illness or prolonged fast,
proteins broken down and converted
into glucose
• Brain needs continuous supply to
prevent neuro dysfunction and cell
death
• Brain cannot produce or store glucose
Glucose Homeostasis
• Fasting state = stomach empty, glucose
maintained between 60-150 mg/dL
• Balanced by:
• Glucose uptake by cells
• Glucose production by liver
• Insulin allows glucose in blood to
move into cells which in turn creates
energy
• Starts by biding to insulin receptors on
cell membranes
• Glucose level falls=insulin secretion
stops, glucagon released which triggers
release of glucose from liver
Hemoglobin A1c
• Test that measures how much
glucose permanently attaches to
specific area of hemoglobin
molecule
• Tests glucose levels over a period
of 3 months
• The higher the glucose level over
time, the higher A1c will be
• Highly standardized
• Level >6.5% is diagnostic of
diabetes mellitus
• Normal for adults is 5.6 or less
Hypoglycemia
• Blood glucose level <60
• Manifestations
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Weakness
Fatigue
Confusion
Difficulty thinking
Behavior changes
Hungry
Thirsty
Death
• Manifestations continued
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Emotional instability
Seizures
Loss of consciousness
Brain damage
Shaky
Nervous
Heart pounding
Sweaty
Diabetic Ketoacidosis (DKA) Patho
• Characterized by uncontrolled
hyperglycemia, metabolic acidosis and
increased production of ketones
• Results from combination of insulin
deficiency and increase in
counterregulatory hormone release.
• Hormonal changes lead to increased
liver and kidney glucose production
and decreased glucose use in
peripheral tissues.
• Increased production of
counterregulatory hormones leads to
production of ketoacids with resultant
ketonemia and metabolic acidosis
• Hyperglycemia leads to osmotic
diuresis with dehydration and
electrolyte loss.
DKA Labs
• Serum glucose >300
• Serum ketones = Positive at 1:2
dilutions
• Serum pH <7.35
• Serum HCO3 = <15 mEq/L
• Serum Na = Low, normal or high
• BUN = >30; elevated because of
dehydration
• Creatinine = >1.5; elevated because
of dehydration
• Urine ketones = positive
DKA Order Prioritization
• Monitor for manifestations of
DKA
• Assessment of airway, pt. fluid
balance, daily weight, hypertension
• Fluid therapy
• Assess cardiac, kidney and mental
status
• Labs
• ABGs
• Drug therapy
ABG Analysis for DKA
• Ph <7.35
• Serum HCO3 <15
• Increased anion gap (calculated by subtracting the sum of chloride and
bicarbonate concentration from the sodium concentration) Normal anion
gap is between 7-9. Anion gap greater than 10-12 indicates metabolic
acidosis
DKA Drug Therapy
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Potassium replacement
Bicarbonate is used only for severe acidosis (pH <7 or serum barcobonate is <5)
Fluid replacement
IV Insulin therapy
• Bolus given at start of IV infusion (0.1 unit/kg)
• IV infusion of 0.1 unit/kg/hour
• Subcutaneous insulin started when pt. can take oral fluids and ketosis has stopped
Glyburide
• Mechanism of action: Causes B-cells in pancreas to release insulin,
leading to drop in blood glucose level. May improve insulin binding to
insulin receptors with prolonged administration. May also reduce basal
hepatic glucose secretion. Not effective is patient lacks functioning B-cells
Glyburide Pt. Education
• Teach pt. to check for symptoms of
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cholestatic jaundice
Teach patient to check capillary blood
glucose level
Teach patient symptoms of
hypoglycemia/hyperglycemia
Must be continued on a daily basis
Caution pt. to avoid OTC medications
unless approved by prescriber
• Teach pt. that diabetes is a life-long
illness; glyburide is not a cure
• Instruct pt. to wear sunscreen or stay
out of the sun to prevent burns
• Instruct pt. to take 30 min before
breakfast. If large dose is required,
may be divided into 2.
• Can be taken with meals to decrease
GI upset and provide best absorption