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Chapter 46
Diabetes Mellitus and
Hypoglycemia
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Diabetes Mellitus
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Pathophysiology
• Chronic disorder of impaired metabolism with
vascular and neurologic complications
• Key feature is elevated blood glucose, called
hyperglycemia
• Blood glucose level normally regulated by insulin, a
hormone produced by beta cells in the islets of
Langerhans located in the pancreas
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Type 1
• Absence of endogenous insulin
• Formerly called juvenile-onset diabetes because it most
commonly occurs in juveniles and young adults
• An autoimmune process, possibly triggered by a viral
infection, destroys beta cells, the development of
insulin antibodies, and the production of islet cell
antibodies (ICAs)
• Affected people require exogenous insulin for the rest
of their lives
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Type 2
• Inadequate endogenous insulin and body’s inability to
properly use insulin
• Beta cells respond inadequately to hyperglycemia;
results in chronically elevated blood glucose
• Continuous high glucose level in the blood
desensitizes the beta cells; they become less
responsive to the elevated glucose
• More common in adults; increasing in children
• Controlled by diet and exercise; may require oral
hypoglycemic agents or exogenous insulin
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Role of Insulin
• Glucose
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Insulin stimulates active transport of glucose into cells
If insulin absent, glucose remains in the bloodstream
Blood becomes thick, which increases its osmolality
Increased osmolality stimulates the thirst center
Increased fluid does not pass into body tissues; high serum
osmolality retains fluid in the bloodstream
• As blood passes through the kidneys, some glucose
eliminated
• Osmotic force created by glucose draws extra fluid and
electrolytes with it, causing abnormally increased urine volume
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Role of Insulin
• Fatty acids
• Promotes fatty acid synthesis and conversion of fatty acids into
fat, which is stored as adipose tissue
• Also spares fat by inhibiting breakdown of adipose tissue and
mobilization of fat and by inhibiting the conversion of fats to
glucose
• Without adequate insulin, fat stores break down and increased
triglycerides are stored in the liver
• Increased fatty acids in the liver can triple the production of
lipoproteins; promotes atherosclerosis
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Role of Insulin
• Protein
• Enhances protein synthesis in tissues and inhibits the
conversion of protein into glucose
• Amino acids are admitted into cells; enhances rate of protein
formation while preventing protein degradation
• Without adequate insulin, protein storage halts; large amounts
of amino acids dumped into the bloodstream
• High levels of plasma amino acids place people with diabetes
at risk for development of gout
• Changes in protein metabolism lead to extreme weakness and
poor organ functioning
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Etiology
• An autoimmune malfunction may cause
complete destruction of the islets of
Langerhans in the pancreas, creating type 1
diabetes
• Islet cell antibodies are identified in more than
80% of all people with type 1 diabetes at the
time of diagnosis
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Figure 46-1
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Risk Factors
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Obesity
Sedentary lifestyle
Family history of diabetes
Age 40 years and older
History of gestational DM
History of delivering infant weighing more than 10 lb
African American (33% higher risk for type 2 DM)
Latin American/Hispanic (>300% higher risk for type 2 DM)
American Indians (33%-50% higher risk for type 2 DM)
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Risk Factors
• Metabolic syndrome
• Thought to be a precursor to diabetes
• Impaired glucose tolerance, high serum insulin, hypertension,
elevated triglycerides, low HDL cholesterol, altered size and
density of LDL cholesterol
• Believed that metabolic syndrome is a chronic low-grade
inflammatory process affecting endothelial tissue
• Long-term effects: atherosclerosis, ischemic heart disease, left
ventricular hypertrophy, type 2 DM
• Research directed at learning how to detect this syndrome
early and what interventions might slow or arrest the progress
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Long-Term Complications
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Microvascular Complications
• Retinopathy
• Pathological changes in the retina that are
associated with DM
• Nephropathy
• Kidney damage
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Macrovascular Complications
• Accelerated atherosclerotic changes in the
person with diabetes
• Associated with coronary artery disease (CAD),
cerebral vascular accidents (CVA or stroke),
and peripheral vascular disease (PVD)
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Long-Term Complications
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Neuropathic Complications
• Neuropathy: pathologic changes in nerve
tissue
• Mononeuropathy affects a single nerve or group of
nerves
• Polyneuropathy involves both sensory and
autonomic nerves
• Autonomic neuropathy affects the sympathetic and
parasympathetic nervous systems
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Hypoglycemic Unawareness
• The usual symptoms of tachycardia,
palpitations, tremor, sweating, and
nervousness may be absent
• Patient may suddenly have changes in mental
status as the first sign of hypoglycemia
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Long-Term Complications
• Foot complications of diabetes
• May have foot problems associated with neuropathy,
inadequate blood supply, or a combination
• Mechanical irritation
• Thermal injury
• Chemical irritation
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Long-Term Complications: Prevention
• Diabetes Control and Complications Trial
(DCCT): intensive treatment of type 1 DM
delayed the onset or slowed the progress of
diabetic retinopathy, nephropathy, and
neuropathy
• Outcome of United Kingdom Prospective
Diabetes Study (UKPDS): similar benefits of
tight control with type 2 DM
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Long-Term Complications: Prevention
• ADA recommends
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Blood pressure: <130 systolic, <80 diastolic
Total cholesterol: <200 mg/dL
LDL: <100 mg/dL
HDL: >45 mg/dL for men (>55 mg/dL for women)
Triglyceride: <150 mg/dL
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Acute Emergency Complications
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Acute Hypoglycemia
• Dangerous drop in blood glucose
• Causes
• Taking too much insulin, not eating enough food or not eating
at the right time, an inconsistent pattern of exercise
• Gastroparesis, renal insufficiency, and certain drugs including
aspirin and beta-adrenergic blockers
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Acute Hypoglycemia
• Signs and symptoms
• Adrenergic: shakiness, nervousness, irritability, tachycardia,
anxiety, lightheadedness, hunger, tingling or numbness of the
lips or tongue, and diaphoresis
• Neuroglucopenia: drowsiness, irritability, impaired judgment,
blurred vision, slurred speech, headaches, and mood swings
progressing to disorientation, seizures, and unconsciousness
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Acute Hypoglycemia
• Treatment
• Give patient 10 to 15 g of quick-acting
carbohydrates
• Repeat every 15-30 minutes until blood glucose is
>70 mg/dL for adults, 80 to 100 mg/dL for older
adults and children
• If patient is unable to swallow, an IM or
subcutaneous injection of 1 mg of glucagon or an IV
dose of 50 mL of 50% dextrose should be given as
ordered or per protocol
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Diabetic Ketoacidosis (DKA)
• Life-threatening emergency caused by a relative or
absolute deficiency of insulin
• Early signs and symptoms
• Anorexia, headache, and fatigue
• As condition progresses, classic symptoms of polydipsia,
polyuria, and polyphagia develop
• If untreated, patient becomes dehydrated, weak, and
lethargic with abdominal pain, nausea, vomiting, fruity
breath, increased respiratory rate, tachycardia, blurred
vision, and hypothermia
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Diabetic Ketoacidosis (DKA)
• Late signs
• Air hunger (Kussmaul’s respirations), coma, and
shock
• Death can result without prompt medical care
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Diabetic Ketoacidosis (DKA)
• Treatment aimed at correction of three main
problems
• Dehydration
• Electrolyte imbalance
• Acidosis
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Hyperglycemic Hyperosmolar
Nonketotic Syndrome
• Patient goes into a coma from extremely high glucose
levels (>600 mg/dL)
• There is no evidence of elevated ketones
• Pancreas produces enough insulin to prevent breakdown of
fatty acids and formation of ketones, but not enough to prevent
hyperglycemia
• Persistent hyperglycemia causes osmotic diuresis,
resulting in loss of fluid and electrolytes
• Dehydration and hypernatremia develop
• May be caused by the same factors that trigger
ketoacidosis
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Medical Diagnosis
• One or more of the following criteria on two separate
occasions is considered DM
• Polyuria, polydipsia, polyphagia, unexplained weight loss plus
random glucose level >200 mg/dL
• Fasting serum glucose level >126 mg/dL (after at least an 8hour fast)
• Two-hour postprandial glucose level >200 mg/dL during oral
glucose tolerance test (OGTT) under specific guidelines. Test
must use a glucose load of 75 g of anhydrous glucose
dissolved in water
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Medical Diagnosis
• Prediabetes
• Individuals with impaired fasting glucose (IFG)
and/or impaired glucose tolerance (IGT)
• Individuals should receive education on weight
reduction and increasing physical activity
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Medical Diagnosis
• Oral glucose tolerance test
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Diet of 150 to 300 g carbohydrate for 3 days before test
Night before test, patient fasts after midnight
Morning of test, blood drawn for fasting serum glucose
Patient then given a drink (Glucola) containing 75 g of
carbohydrates and instructed to remain quiet
• Blood drawn at 30 minutes and 1 hour after the ingestion of
glucose. After these two samples, blood is drawn at hourly
intervals until the test is completed
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Medical Treatment
• Nutritional management
• Medical nutrition therapy (MNT) is an important part
of diabetes management; should be included in
diabetes self-management education
• Because of complexity of nutritional management, a
registered dietitian should be part of the diabetes
management team, and the individual with diabetes should
be included in decision making
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Medical Treatment
• Exercise
• Effective adjunct for people with diabetes
• Aids in weight loss, improves cardiovascular
conditioning, improves insulin sensitivity, and
promotes a sense of well-being
• Exercising muscle uses glucose at 20 times the rate
of a muscle at rest and does not require insulin
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Insulin Therapy
• All patients with type 1 disease need insulin injections;
some patients with type 2 disease may eventually need
insulin
• Insulins classified by source and course of action
• Source: human, pork, or beef (beef is being phased
out)
• Course of action: rapid acting, short acting,
intermediate acting, and long acting
• All rapid-acting and short-acting insulins are clear
• The other insulins are cloudy
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Figure 46-2
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Insulin Therapy
• Route
• Oral: insulin cannot be given orally because it is rendered
useless in the gastrointestinal tract
• Subcutaneously: all insulins can be given subcutaneously
• Intravenously: ONLY regular insulin can be given intravenously
• Inhalation: a form of insulin that can be taken by inhalation has
recently been approved, but it is not yet widely used
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Insulin Therapy
• Concentrations
• U-100 insulin has 100 units/mL
• Most commonly used
• U-500 insulin has 500 units/mL
• Used only in emergencies and for patients who are
extremely insulin resistant
• U-40 insulin has 40 units/mL
• Not available in the United States
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Insulin Therapy
• Premixed insulin products
• Contain both Regular and NPH insulin
• 70% NPH and 30% Regular insulin
• 50% NPH and 50% Regular insulin
• 75% NPH and 25% Lispro
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Insulin Therapy
• Dosing schedules
• Conventional therapy
• Typically uses a combination of a short-acting and an
intermediate- or long-acting insulin
• Intensive therapy
• To achieve tight control; may require 3 or 4 injections daily
• Continuous subcutaneous insulin infusion
• Patient has indwelling subcutaneous catheter connected to
an external portable infusion pump; pump delivers Regular
insulin continuously
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Insulin Therapy
• Insulin mixing
• Two types can be mixed in one syringe to avoid two injections
• Insulin injection
• Site rotation helps prevent lipohypertrophy or lipoatrophy
• Absorption rate varies with different body sites
• American Diabetes Association recommends rotating sites
within one anatomic area rather than moving among all areas
• See Figure 46-3
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Figure 46-3
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Insulin Therapy
• Insulin pump
• Needle is inserted subcutaneously in an appropriate
part of the anatomy
• Pump is programmed to deliver a steady trickle of
insulin throughout the day and can provide a bolus
of insulin at mealtimes
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Figure 46-4
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Insulin Therapy
• Intranasal route
• Only 10% of the drug is absorbed through the nasal mucosa,
making it relatively expensive to use
• Nasal irritation is a frequent side effect
• Only Regular insulin is given intranasally
• Insulin catheter
• Indwelling subcutaneous catheters may be placed in the
abdomen to permit repeated insulin injections without repeated
needlesticks
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Oral Hypoglycemic Agents
• If patients with type 2 DM unable to control blood
glucose with nutrition and exercise, physician may
prescribe oral hypoglycemics
• Sulfonylureas (three generations), alpha-glucosidase
inhibitors, biguanides, thiazolidinediones, Dphenylalanines, meglitinides
• Combination oral medications
• ACTOplus met (pioglitazone and metformin), Avandamet
(rosiglitazone and metformin), Avandaryl (rosiglitazone and
glimepiride), Glucovance (glyburide and metformin), Metaglip
(glipizide and metformin)
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Self-Monitoring of Blood Glucose
• Allows patients to monitor blood glucose levels
to regulate their diet, exercise, and medication
regimens to remain euglycemic
• Portable electronic glucose meters have
largely replaced other methods of selfmonitoring
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lycosylated Glucose Levels
• Glycosylated hemoglobin (HbA1c) reflects
glucose levels over the past few months
• Fructosamine levels reflect those over several
weeks
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Complications of Therapy
• Hypoglycemia
• A person injects too much insulin, does not eat enough, eats at
the wrong time, or exercises inconsistently: glucose levels may
suddenly drop
• Somogyi phenomenon
• Rebound hyperglycemia in response to hypoglycemia
• Dawn phenomenon
• An increase in fasting blood glucose levels between 5 and 9 AM
that is not related to hypoglycemia
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Assessment
• Ketoacidosis: ketonuria, Kussmaul’s
respirations, orthostatic hypotension,
hypertension, nausea, vomiting, lethargy, or
change in level of consciousness
• Hypoglycemic patient: expect to find
tachycardia, anxiety, trembling, and decreasing
level of consciousness
• Be alert for indications of hyperosmolar
nonketotic coma
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Assessment
• Attempt to determine the following
• Type of diabetes
• Hypoglycemic agents: name, dosage, when last
dose was taken
• Food and fluid intake for the past 3 days
• Relevant laboratory values: blood glucose, blood pH,
bicarbonate levels, electrolytes, and osmolality and
urine osmolality
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Health History
• Chief complaint and history of present illness
• Signs/symptoms that prompted patient to seek medical care
• Past medical history
• Type and duration of DM
• Name and dosage of prescribed medications and when they
were last taken
• If patient monitors blood glucose, record type of equipment
used, testing schedule, recent test results
• Family history
• Diabetes, heart disease, stroke, hypertension, hyperlipidemia
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Health History
• Review of systems
• Description of the patient’s general health
• Changes in skin moisture or turgor
• Inquire whether the patient has had floaters, diplopia (double
vision), or blurred vision, or has seen white halos around
objects
• Abdominal symptoms: diarrhea, abdominal bloating, and gas
• Problems passing or holding urine
• If any pain in the legs, note when it occurs
• Numbness, tingling, or burning in the extremities
• Changes in mental alertness or seizures
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Health History
• Functional assessment
• Explore factors that can affect patient’s ability to perform
self-care, including literacy, financial resources such as
health insurance, and family support
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Health History
• Physical examination
• Level of consciousness, posture and gait, and apparent wellbeing
• Vital signs, height, and weight
• Skin color, warmth, turgor, and lesions noted
• Inspect eye grounds for evidence of diabetic retinopathy or
cataracts
• Be alert for a sweet, fruity odor to the patient’s breath that is
common with ketoacidosis
• Carefully assess the feet
• Test gait, balance, and motor coordination
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Interventions
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Ineffective Health Maintenance
Ineffective Therapeutic Regimen Management
Risk for Deficient Fluid Volume
Risk for Injury
Activity Intolerance
Chronic Pain
Disturbed Sensory Perception or Impaired Skin
Integrity
• Disturbed Thought Processes
• Ineffective Coping
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Hypoglycemia
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Pathophysiology
• Develops when the blood glucose level falls to
less than 45 to 50 mg/dL
• Symptoms occur at different blood levels
according to individual tolerances and how
rapidly the level falls
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Causes
• Exogenous hypoglycemia
• Results from outside factors acting on the body to
produce a low blood glucose
• Include insulin, oral hypoglycemic agents, alcohol,
or exercise
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Causes
• Endogenous hypoglycemia
• Occurs when internal factors cause an excessive
secretion of insulin or an increase in glucose
metabolism
• These conditions may be related to tumors or
genetics
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Causes
• Functional hypoglycemia
• From a variety of causes, including gastric surgery,
fasting, or malnutrition
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Signs and Symptoms
• Glucose level falls rapidly, causes epinephrine, cortisol,
glucagon, and growth hormone to be secreted in an
attempt to increase glucose levels
• Symptoms: weakness, hunger, diaphoresis, tremors, anxiety,
irritability, headache, pallor, and tachycardia
• A blood glucose level that falls over several hours:
symptoms attributed to lack of essential glucose to
brain tissue
• Symptoms: confusion, weakness, dizziness, blurred or double
vision, seizure, and in severe cases, coma
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Medical Diagnosis
• The diagnosis of hypoglycemia not associated with
diabetes can be based on fasting blood glucose, OGTT,
intravenous glucose tolerance test, and 72-hour
inpatient fasting
• Whipple’s triad
• The presence of symptoms
• Documentation of low blood glucose when symptoms occur
• Improvement of symptoms when blood glucose rises
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Medical Treatment
• In an unconscious patient who has diabetes,
hypoglycemia should be suspected until it is ruled out
• 50 mL of 50% glucose solution should be administered
immediately
• The patient with a milder form of hypoglycemia
• Treated with 15 g carbohydrate
• If the patient’s condition does not improve, another
15 g of carbohydrate should be given after 10 minutes
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Medical Treatment
• Prevention of hypoglycemia by proper food intake
• The diet is directed by the underlying cause
• If overproduction of insulin after carbohydrate ingestion, a lowcarbohydrate, high-protein diet
• Restriction of carbohydrates to no more than 100 g/day is
recommended
• Simple sugars avoided; complex carbohydrates encouraged
• Patients may tolerate smaller, more frequent meals. Alcohol
should be avoided
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Assessment
• Present illness: shakiness, nervousness, irritability,
tachycardia, anxiety, lightheadedness, hunger, tingling
or numbness of the lips or tongue, nightmares, and
crying out during sleep
• Note when episodes occur in relation to meals and
particular food intake
• The past medical history documents diabetes, previous
gastric surgery, abdominal cancer, or adrenal
insufficiency
• Medications, paying particular attention to
hypoglycemic agents
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Assessment
• Note hypoglycemic agents, prescribed dose,
and the time last dose taken
• Functional assessment: information about
current diet, exercise, alcohol intake, and the
effects of symptoms on daily activities
• Important aspects of the physical examination
include general behavior, appearance, pulse,
and blood pressure
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Interventions
• Deficient Knowledge
• Risk for Injury
• Impaired Adjustment
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