NUR 133
Dyslipidemia
Assessment and Management of
Patients With Diabetes
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Copyright © 2018 Wolters Kluwer · All Rights Reserved
Dyslipidemia Treatment
Prevention is key:
o Maintain healthy weight – BMI<26
o Regular physical activity – 30 min 5+ days/week
o Maintain diet low in saturated fats <7% of calories/d
Limit red meat, low fat dairy;
o Maintain diet low in cholesterol <200 mg/d
o Smoking cessation
o Increase dietary fiber 20 – 30 gm/d
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Pharmacologic Therapy: Dyslipidemia
Several classes of medications:
o ↓ Total cholesterol
↓ LDL cholesterol
↑ HDL cholesterol
o ↓ Triglycerides
Statins- HMG CoA Reductase Inhibitors: Atorvostatin
o Side effects: Myopathy, rhabdomyolysis, liver
toxicity
Monitor for: muscle pain, abdominal pain,
jaundice
Lab surveillance: CPK, LFTs
Interactions: grapefruit juice; Fibrates
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Antilipemics: Rhabdomyolysis
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Diabetes
A group of diseases characterized by hyperglycemia
caused by defects in insulin secretion, insulin action, or
both
Affects nearly 25.8 million people in the United States;
one third of the cases are undiagnosed
Prevalence is increasing
Minority populations and older adults are
disproportionately affected
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Classifications of Diabetes
Type 1 diabetes
Type 2 diabetes
Latent autoimmune diabetes of adults (LADA)
Gestational diabetes
Diabetes associated with other conditions or syndromes
Refer to Table 46-1
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Functions of Insulin
Transports and metabolizes glucose for energy
Stimulates storage of glucose in the liver and muscle as
glycogen
Signals the liver to stop the release of glucose
Enhances storage of dietary fat in adipose tissue
Accelerates transport of amino acids into cells
Inhibits the breakdown of stored glucose, protein, and fat
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Insulin: Necessary for Cellular Glucose
Uptake
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Type 1 Diabetes
Insulin-producing beta cells
in the pancreas are
destroyed by a combination
of genetic, immunologic,
and environmental factors
Results in decreased insulin
production, unchecked
glucose production by the
liver and fasting
hyperglycemia
Affects 5% of adults with
diabetes
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Type 2 Diabetes
Insulin resistance and
impaired insulin
secretion
Affects 95% of adults
with diabetes, onset
over age 30 years,
increasing in children
r/t obesity
Slow, progressive
glucose intolerance
and may go
undetected for years
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Pathogenesis of Type 2 Diabetes
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Latent Autoimmune Diabetes of Adults
(LADA)
Subtype of diabetes in which progression of autoimmune
beta cell destruction in the pancreas is slower than in
types 1 and 2 diabetes
Not insulin dependent in the initial 6 months of disease
onset.
Clinical manifestation of LADA shares the features of
types 1 and 2 diabetes
Emerging subtype has led some to propose the diabetes
classification scheme should be revised to reflect changes
in the beta cells in the pancreas
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Risk Factors
Type 1: early-onset, Type 2: obesity, age, previous
familial, genetic identified impaired fasting
predisposition, possible glucose or impaired glucose
immunologic or tolerance, hypertension
environmental (viral or ≥140/90 mm Hg, HDL ≤35
toxins) factors mg/dL or triglycerides ≥250
Refer to Chart 46-1 mg/dL, history of gestational
diabetes or babies over 9
pounds
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Clinical Manifestations
Depends on the level of hyperglycemia
“Three Ps”
o Polyuria
o Polydipsia
o Polyphagia
Fatigue, weakness, vision changes, tingling or numbness
in hands or feet, dry skin, skin lesions or wounds that are
slow to heal, recurrent infections
Type 1 may have sudden weight loss
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Diagnostic Findings
Fasting blood
glucose 126
mg/dL or more
Casual glucose
exceeding 200
mg/dL
Refer to Chart 51-
2 for ADA
diagnostic criteria
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Medical Management of Diabetes
Main goal is to normalize insulin activity and blood
glucose levels to reduce the development of
complications.
The ADA now recommends HgbA1c less than 7%
Diabetes management has five components:
o Nutritional therapy
o Exercise
o Monitoring
o Pharmacologic therapy
o Education
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Dietary Management Goals
Control of total caloric intake to attain or maintain a
reasonable body weight
Control of blood glucose levels
Normalization of lipids and blood pressure to prevent
heart disease
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Role of the Nurse
Be
Knowledgeabl Be knowledgeable about dietary management
e
Communicate important information to the dietician or other management
Communicate specialists
Reinforce Reinforce patient understanding
Support Support dietary and lifestyle changes
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Meal Planning
Consider food preferences, lifestyle, usual eating times,
and cultural and ethnic background
Review diet history and need for weight loss, gain, or
maintenance
Caloric requirements and calorie distribution throughout
the day; exchange lists
o Carbohydrates: 50% to 60% carbohydrates;
emphasize whole grains
o Fat: 30%, limiting saturated fats to 10% and <300 mg
cholesterol
o Nonanimal sources of protein (e.g., legumes, whole
grains) and increase fiber
Refer to Table 46-2 for exchange list
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Glycemic Index
Combining starchy foods with protein and fat slows
absorption and glycemic response
Raw or whole foods tend to have lower responses than
cooked, chopped, or pureed foods
Eat whole fruits rather than juices; this decreases
glycemic response because of fiber (slowing absorption)
Adding food with sugars may produce lower response if
eaten with foods that are more slowly absorbed
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Other Dietary Concerns
ALCOHOL NUTRITIVE AND MISLEADING FOOD
NONNUTRITIVE LABELS
SWEETENERS
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Exercise
Lowers blood sugar
Aids in weight loss,
easing stress, and
maintaining a
feeling of well-being
Lowers
cardiovascular risk
Refer to Chart 46-4
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Exercise Precautions
Exercise elevates blood sugar levels; insulin must be
adjusted
Insulin normally decreases with exercise; patients on
exogenous insulin should eat a 15-g carbohydrate snack
before moderate exercise to prevent hypoglycemia
Potential postexercise hypoglycemia: refer to Chart 46-5
Need to monitor blood glucose levels
Gerontologic considerations
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Insulin Therapy
Blood glucose monitoring:
o Cornerstone of diabetes management
o Self-monitoring of blood glucose (SMBG) levels has
dramatically altered diabetes care
Categories of insulin: refer to Table 46-3
o Rapid acting
o Short acting: regular insulin
o Intermediate acting: NPH insulin
o Very long acting: “Peakless”
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Insulin Regimen
Varies from 1 to 4 injections per day
Combination of a short-acting insulin and a longer-acting
insulin
Table 46-4 describes several insulin regimens and the
advantages and disadvantages of each
Two general approaches to insulin therapy:
o Conventional
o Intensive
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Complications of Insulin Therapy
Local allergic reactions
Systemic allergic
reactions
Insulin lipodystrophy
Resistance to injected
insulin
Morning hyperglycemia
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Methods of Insulin Delivery
Traditional subcutaneous
injections
Insulin pens
Jet injectors
Insulin pumps
Future: Implantable
insulin pumps
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Educating Patients in Insulin Self-
Management
Use and action of
insulin
Symptoms of
hypoglycemia and
hyperglycemia
o Required actions
Blood glucose
monitoring
Self-injection of
insulin
Insulin pump use
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Oral Antidiabetic Agents
Used for patients with type 2 diabetes who require more
than diet and exercise alone
Combinations of oral drugs may be used
Major side effect: hypoglycemia
Nursing interventions: monitor blood glucose for
hypoglycemia and other potential side effects
Patient education
Table 46-5
o Sulfonylureas, Biguanides, TZDs
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Sites of Action of Oral Antidiabetic Agents
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Acute Complications of Diabetes
Hypoglycemia
DKA
Hyperglycemic hyperosmolar syndrome (HHS)
Comparison of DKA and HHS: refer to Table 46-6 & ATI
p.537
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Hypoglycemia
Abnormally low blood glucose level (below 50 to 60
mg/dL); too much insulin or oral hypoglycemic agents,
excessive physical activity, and not enough food
Adrenergic symptoms: sweating, tremors, tachycardia,
palpitations, nervousness, hunger
Central nervous system symptoms: inability to
concentrate, headache, confusion, memory lapses,
slurred speech, drowsiness
Severe hypoglycemia: disorientation, seizures, loss of
consciousness, death
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Management of Hypoglycemia
Give Retest Provide
Give 15 g of Retest blood Provide a snack
fast-acting, glucose in 15 with protein and
concentrated minutes; retreat carbohydrate
carbohydrate if ‹70 mg/dL or if unless the
• Three or four symptoms patient plans to
glucose tablets persist more eat a meal
• 4 to 6 oz of juice or than 10 to 15 within 30 to 60
regular soda (not minutes and minutes
diet soda)
testing is not
possible
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Emergency Measures
If the patient cannot
swallow or is
unconscious:
o Subcutaneous or
intramuscular
glucagon (1 mg)
o 25 to 50 mL of
50% dextrose
solution IV
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Diabetic Ketoacidosis (DKA)
Absence or inadequate
amount of insulin
resulting in abnormal
metabolism of
carbohydrate, protein,
and fat
Clinical features
o Hyperglycemia
o Dehydration
o Acidosis
Refer to Figure 46-7
“Sick day rules”: refer to
Chart 46-9
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Assessment of DKA
Blood glucose levels >300 to 1000
Severity of DKA not only due to blood glucose level
Ketoacidosis is reflected in low serum bicarbonate, low
pH; low PCO2 reflects respiratory compensation (Kussmaul
respirations)
Ketone bodies in blood and urine
Electrolytes vary according to degree of dehydration;
increase in creatinine, Hct, BUN
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Treatment of DKA
Rehydration with IV fluid
IV continuous infusion of regular insulin
Reverse acidosis and restore electrolyte balance
Note: rehydration leads to increased plasma volume and
decreased K; insulin enhances the movement of K+ from
extracellular fluid into the cells
Monitor blood glucose, renal function and urinary output,
ECG, electrolyte levels, VS, lung assessments for signs of
fluid overload
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Hyperglycemic Hyperosmolar Syndrome
Hyperosmolar hyperglycemia is
caused by a lack of sufficient
insulin; ketosis is minimal or absent
Hyperglycemia causes osmotic
diuresis, loss of water and
electrolytes, hypernatremia, and
increased osmolality
Manifestations include
hypotension, profound dehydration,
tachycardia, and variable
neurologic signs caused by cerebral
dehydration
High mortality rate
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Treatment of HHS
Rehydration
Insulin administration
Monitor fluid volume and
electrolyte status
Prevention
o BGSM
o Diagnosis and
management of
diabetes
o Assess and promote
self-care
management skills
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Long-Term Complications of Diabetes
Macrovascular: accelerated
atherosclerotic changes,
coronary artery disease,
cerebrovascular disease, and
peripheral vascular disease
Microvascular: diabetic
retinopathy (refer to Figure 46-8),
and nephropathy
Neuropathic: peripheral
neuropathy, autonomic
neuropathies, hypoglycemic
unawareness, neuropathy, sexual
dysfunction
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Neuropathic Ulcers – Diabetes
Complications
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