ch 48 DM Flashcards
1
Q
is the leading cause of adult blindness, end-stage renal disease, and nontraumatic lower limb amputations. It is a major contributing factor to heart disease and stroke.
A
Diabetes
2
Q
, singly or in combination, to genetic, autoimmune, and environmental factors (e.g., virus, obesity).
A
causes of diabetes
3
Q
a disorder of glucose metabolism related to absent or insufficient insulin supply and/or poor use of the available insulin.
A
diabetes is primarily
4
Q
2 most common are type 1 and type 2
-2 other classes are gestational diabetes and other specific types of diabetes with various causes.
A
American Diabetes Association (ADA) recognizes 4 different classes of diabetes.
5
Q
is a hormone made by the β cells in the islets of Langerhans of the pancreas.
-continuously released into the bloodstream in small amounts, with increased release when food is ingested
A
Insulin
6
Q
a stable, normal glucose range of about 74 to 106 mg/dL (4.1 to 5.9 mmol/L). The amount of insulin secreted daily by an adult is about 40 to 50 U, or 0.6 U/kg of body weight.
A
Insulin lowers blood glucose and facilitates
7
Q
excess glucose as glycogen.
A
Liver and muscle cells store
8
Q
gluconeogenesis, enhances fat deposition of adipose tissue, and increases protein synthesis. For this reason, insulin is an anabolic, or storage, hormone.
A
rise in plasma insulin after a meal inhibits
9
Q
the release of stored glucose from the liver, protein from muscle, and fat from adipose tissue.
A
fall in insulin level during normal overnight fasting promotes
10
Q
specific receptors for insulin and are considered insulin-dependent tissues.
-Insulin is required to “unlock” these receptor sites, allowing the transport of glucose into the cells to be used for energy
A
Skeletal muscle and adipose tissue have
11
Q
require an adequate glucose supply for normal function. Although liver cells are not considered insulin-dependent tissue, insulin receptor sites on the liver facilitate uptake of glucose and its conversion to glycogen.
A
Other tissues (e.g., brain, liver, blood cells) do not directly depend on insulin for glucose transport but
12
Q
Other hormones (glucagon, epinephrine, growth hormone [GH], cortisol) work against the effects of insulin. They are
A
counterregulatory hormones (work against insulin)
13
Q
(1) stimulating glucose production and release by the liver and (2) decreasing the movement of glucose into the cells. The counterregulatory hormones and insulin work together to maintain blood glucose levels within the normal range by regulating the release of glucose for energy during food intake and periods of fasting.
A
hormones increase blood glucose levels by (counterregulatory hormones)
14
Q
Ifrom its precursor, proinsulin.
A
insulin is synthesized
15
Q
insulin and C-peptide, and the 2 substances are released in equal amounts. Therefore measuring C-peptide in serum and urine is a useful clinical indicator of pancreatic β-cell function and insulin levels.
A
Enzymes split proinsulin to form
16
Q
juvenile-onset diabetes or insulin-dependent diabetes mellitus (IDDM), accounts for about 5% to 10% of all people with diabetes.
-affects people under 40 years of age, although it can occur at any age.
A
Type 1 diabetes, formerly known as
17
Q
the body develops antibodies against insulin and/or the pancreatic β cells that make insulin. This eventually results in not enough insulin for a person to survive
A
Type 1 diabetes is an autoimmune disorder in which
18
Q
genetic predisposition and exposure to a virus are factors that may contribute to the development of immune-related type 1 diabetes.
A
cause Type 1 diabetes
19
Q
to human leukocyte antigens (HLAs)
-HLA types is exposed to a viral infection, the β cells of the pancreas are destroyed, either directly or through an autoimmune process.
A
Predisposition to type 1 diabetes is related
20
Q
HLA-DR3 and HLA-DR4.
A
risk for type 1 diabetes include
21
Q
type 1 diabetes that is strongly inherited and not related to autoimmunity.
A
Idiopathic diabetes is a form of
22
Q
a slowly progressing autoimmune form of type 1 diabetes. It occurs in adults and is often mistaken for type 2 diabetes.
A
Latent autoimmune diabetes in adults (LADA),
23
Q
the person’s pancreas can no longer make enough insulin to maintain normal glucose. Once this occurs, the onset of symptoms is usually rapid. Patients often are initially seen with impending or actual ketoacidosis. The patient usually has a history of recent and sudden weight loss and the classic symptoms of polydipsia (excessive thirst), polyuria (frequent urination), and polyphagia (excessive hunger).
A
Manifestations develop when (type 1)
24
Q
person with type 1 diabetes requires insulin from an outside source (exogenous insulin) to sustain life. Without insulin, the patient will develop diabetes-related ketoacidosis (DKA), a life-threatening condition resulting in metabolic acidosis. Newly diagnosed patients may have a remission, or “honeymoon period,” for 3 to 12 months after starting treatment. During this time, the patient needs little injected insulin because β-cell insulin production is still sufficient for healthy blood glucose levels. Eventually, as more β cells are destroyed and blood glucose levels increase, the honeymoon period ends and the patient will require insulin on a permanent basis.
A
Type 1 DM and severity of no insulin
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, accounts for about 90% to 95% of people with diabetes.
Type 2 diabetes, formerly known as adult-onset diabetes or non–insulin-dependent diabetes mellitus (NIDDM)
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overweight or obese, being older, and having a family history of type 2 diabetes
risk factors of type 2
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a combination of inadequate insulin secretion and insulin resistance.
Type 2 diabetes is characterized by
28
pancreas usually makes some endogenous (self-made) insulin. However, the body either does not make enough insulin or does not use it effectively, or both.
Type 2 diabetes insulin issue
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a condition in which body tissues do not respond to the action of insulin because insulin receptors are unresponsive, are insufficient in number, or both.
first factor is insulin resistance,
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on skeletal muscle, fat, and liver cells.
Most insulin receptors are located
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a marked decrease in the ability of the pancreas to make insulin, as the β cells become fatigued from the compensatory overproduction of insulin or when β-cell mass is lost
- α cells of the pancreas increase production of glucagon.
second factor in the development of type 2 diabetes is
32
which is inappropriate glucose production by the liver. Instead of properly regulating the release of glucose in response to blood levels, the liver does so in a haphazard way that does not correspond to the body’s needs at the time.
This leads to a third factor, type 2 DM
33
s altered production of hormones and cytokines by adipose tissue (adipokines). Adipokines secreted by adipose tissue appear to play a role in glucose and fat metabolism and are likely to contribute to the development of type 2 diabetes
fourth factor for type 2 DM
34
cause chronic inflammation, a factor involved in insulin resistance, type 2 diabetes, and cardiovascular disease (CVD)
adipokines (in adipose tissue)
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adiponectin and leptin.
2 main adipokines thought to affect insulin sensitivity are
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type 2 diabetes
brain, kidneys, and gut have roles in the development of
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increased glucose levels, abdominal obesity, high BP, high levels of triglycerides, and decreased levels of high-density lipoproteins (HDLs)
-person with 3 of the 5 components is considered to have metabolic syndrome
Metabolic syndrome has 5 components: (develop type 2 DM)
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50% to 80% of β cells are no longer secreting insulin
-average person has had type 2 diabetes for 6½ years.
signs and symptoms of hyperglycemia develop when about
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impaired glucose tolerance (IGT), impaired fasting glucose (IFG), or both.
Prediabetes is defined as
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the 2-hour oral glucose tolerance test (OGTT) values are 140 to 199 mg/dL (7.8 to 11.0 mmol/L).
diagnosis of IGT is made if
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fasting blood glucose levels are 100 to 125 mg/dL (5.56 to 6.9 mmol/L).
IFG is diagnosed when
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such as fatigue, frequent infections, or slow-healing wounds.
symptoms of diabetes
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pregnancy and occurs in about 2% to 10% of pregnancies in the United States
Gestational diabetes develops during
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cesarean delivery, and their babies have increased risk for perinatal death, birth injury, and neonatal complications.
Women with gestational diabetes have a higher risk for
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at 24 to 28 weeks of gestation
Women with an average risk for gestational diabetes are screened using an OGTT
46
6 weeks postpartum.
Most women with gestational diabetes have normal glucose levels within
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of developing type 2 diabetes within 16 years.
Women with a history of gestational diabetes have up to a 63% chance
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Cushing syndrome, hyperthyroidism, recurrent pancreatitis, cystic fibrosis, hemochromatosis, and parenteral nutrition.
-Common drugs that can induce diabetes include corticosteroids (prednisone), thiazides, phenytoin (Dilantin), and atypical antipsychotics (e.g., clozapine [Clozaril]).
other medical issues cause DM (causes abnormal blood glucose)
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are polyuria, polydipsia, and polyphagia
classic symptoms of type 1 DM
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is a result of cellular malnourishment when insulin deficiency prevents cells from using glucose for energy.
Polyphagia (TYPE 1 DM)
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the body cannot get glucose and instead breaks down fat and protein to try to make energy.
Weight loss may occur because (TYPE 1 DM)
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more common manifestations associated with type 2 diabetes are fatigue, recurrent infections, recurrent vaginal yeast or candida infections, prolonged wound healing, and vision problems.
-polyuria, polydipsia, and polyphagia
common symp type 2 DM
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. A1C of 6.5% or higher
2. Fasting plasma glucose (FPG) level of 126 mg/dL (7.0 mmol/L) or greater. Fasting is defined as no caloric intake for at least 8 hours
3. A 2-hour plasma glucose level of 200 mg/dL (11.1 mmol/L) or greater during an OGTT, using a glucose load of 75 g
4. In a patient with classic symptoms of hyperglycemia (polyuria, polydipsia, unexplained weight loss) or hyperglycemic crisis, a random plasma glucose level of 200 mg/dL (11.1 mmol/L) or greater
diagnosis of diabetes is made using 1 of the following 4 methods:
54
recent severe restrictions of dietary carbohydrate, acute illness, drugs (e.g., contraceptives, corticosteroids), and restricted activity, such as bed rest. A patient with impaired gastrointestinal (GI) absorption or who has recently taken acetaminophen may have false-negative results.
factors that can falsely elevate values include
55
glycosylated hemoglobin (Hgb) as a percentage of total Hgb.
-glucose stays attached to the red blood cell (RBC) for the life of the cell (about 120 days).
A1C measures the amount of
56
a measurement of blood glucose levels over the previous 2 to 3 months, with increases in the Hb A1C reflecting elevated blood glucose levels.
A1C provides
57
greater convenience, since fasting is not needed. Diseases affecting RBCs (e.g., iron deficiency anemia, sickle cell anemia) can influence the A1C and should be considered when interpreting results.
A1C has several advantages over the FPG, including
58
The eAG = 28.7 × A1C − 46.7. For example, an A1C of 8.0% is equivalent to a glucose level of 183 mg/dL.
estimated average glucose (eAG) can be determined from the A1C.
59
It is formed by a chemical reaction of glucose with plasma protein. It reflects glycemia in the previous 1 to 3 weeks. Fructosamine levels may show a change in blood glucose levels before A1C does. It is used for people with hemoglobinopathies, or for short-term measurement of glucose levels, for instance, after a change in medication or during pregnancy.
Fructosamine is another way to assess glucose levels.
60
primarily done to help distinguish between autoimmune type 1 diabetes and diabetes from other causes. Autoantibodies can develop to 1 or several autoantigens, including GAD65, IA-2, or insulin.
Islet cell autoantibody testing is
61
insulin, oral agents (OAs), and noninsulin injectable agents.
3 major types of glucose-lowering agents (GLAs) used in the treatment of diabetes are
62
n to survive. They often use multiple daily injections of insulin (often 4 or more) or continuous insulin infusion via an insulin pump to adequately manage blood glucose levels.
type 1 diabetes require exogenous insuli
63
common bacteria (e.g., Escherichia coli) or yeast cells using recombinant deoxyribonucleic acid (DNA) technology
- insulin was extracted from beef and pork pancreases.
insulin is derived from
64
their onset, peak action, and duration
Insulins differ by
65
as rapid-acting, short-acting, intermediate-acting, and long-acting insulin
insulin is categorized
66
insulin approach that most closely mimics endogenous insulin production is the
basal-bolus plan (often called intensive or physiologic insulin therapy).
67
consists of multiple daily insulin injections (or an insulin pump) together with frequent self-monitoring of blood glucose (or a continuous glucose monitoring system).
-Injections include rapid- or short-acting (bolus) insulin before meals and intermediate- or long-acting (basal) background insulin once or twice a day.
basal-bolus plan (often called intensive or physiologic insulin therapy).
68
achieve a glucose level as close to normal as possible, as much of the time as possible. This is referred to as “.”
time in range
69
aspart (NovoLog), glulisine (Apidra), and lispro (Humalog), have an onset of action of about 15 minutes.
-should be injected within 15 minutes of mealtime.
-most closely mimic natural insulin secretion in response to a meal.
Rapid-acting synthetic insulin analogs, which include
70
has an onset of action of 30 to 60 minutes. It is injected 30 to 45 minutes before a meal to ensure that the insulin is working at the same time as meal absorption.
-more likely to cause hypoglycemia because of a longer duration of action.
Short-acting regular insulin
71
a long- or intermediate-acting basal (background) insulin to maintain blood glucose levels in between meals and overnight.
-Without 24-hour background insulin, people with type 1 diabetes are more prone to developing DKA
mealtime insulin, people with type 1 diabetes use
72
adequately manage blood glucose levels.
people with type 2 diabetes who use OAs will need basal insulin to
73
degludec (Tresiba), detemir (Levemir), and glargine (Lantus, Toujeo, Basaglar).
-type of insulin is released steadily and continuously.
-does not have a peak of action bc they lack peak action time, the risk for hypoglycemia from this type of insulin is greatly reduced.
long-acting insulins include
74
often given twice daily
detemir is (long-acting insulins )
75
diluted or mixed with any other insulin or solution in the same syringe.
Glargine and detemir must not be
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basal insulin. It has a duration of 12 to 18 hours.
Intermediate-acting insulin (NPH) can be used as a
77
it has a peak ranging from 4 to 12 hours, which can result in hypoglycemia. NPH can be mixed with short- and rapid-acting insulins. It should never be given IV.
The disadvantage of NPH is that
78
NPH, lispro protamine, and aspart protamine.
-They are cloudy because they contain a protein called protamine, which makes them work longer.
All insulins are clear solutions except
79
with intermediate-acting insulin in the same syringe. This allows the patient to have both mealtime and basal coverage without having to give 2 separate injections.
For those who want to use only 1 or 2 injections per day, a short- or rapid-acting insulin is mixed
80
convenience to patients, who do not have to draw up and mix insulin from 2 different vials. This is especially helpful to those who lack the visual, manual, or cognitive skills to mix insulin themselves.
Premixed formulas offer
81
and can make it less effective. Insulin vials and pens in use may be left at room temperature for up to 4 weeks unless the room temperature is higher than 86° F (30° C) or below freezing (less than 32° F [0° C]).
-Store unopened insulin vials and pens in the refrigerator.
Extreme temperatures alter the insulin molecule
82
stable for up to 1 week when stored in the refrigerator.
Prefilled syringes with 2 different insulins are
83
stable up to 30 days.
-store syringes in a vertical position with the needle pointed up to avoid clumping of suspended insulin in the needle.
Syringes with only 1 type of insulin are
84
Before injection, gently roll prefilled syringes between the palms 10 to 20 times to warm the insulin and resuspend the particles.
-Some insulin combinations cannot be prefilled and stored because the mixture can alter the onset, action, and/or peak times of either insulin.
Rules for insulin
85
- given subcutaneous injection
-given IV when immediate onset of action is desired
-Insulin is not taken orally because it is inactivated by gastric fluids.
- avoid injecting insulin IM because rapid and unpredictable absorption could result in hypoglycemia.
-Caution the patient about injecting into a site that is to be exercised=This could increase the rate of insulin absorption and speed the onset of action, resulting in hypoglycemia.
-patients to rotate the injection within and between sites.= better absorption
- Injections are rotated systematically across the board, with each injection site at least ½ to 1 inch away from the previous injection site. It can be helpful to inject fast-acting insulin into faster-absorbing sites and slow-acting insulin into slower absorbing sites.
Administration of insulin
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the abdomen, followed by the arm, thigh, and buttock.
fastest subcutaneous absorption is from
87
U100. This means that 1 mL contains 100 U of insulin. U100 insulin must be used with a U100-marked syringe.
Most commercial insulin is available as
88
1.0, 0.5, and 0.3 mL.
Disposable plastic insulin syringes are available in a variety of sizes, including
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doses of 50 U or less.
0.5-mL size may be used for
90
30 U or less
-0.5- and 0.3-mL syringes are in 1-unit increments. This provides more accurate delivery when the dose is an odd number.
0.3-mL syringe can be used for doses of
91
50 U of insulin. The 1.0-mL syringe is in 2-unit increments
1.0-mL syringe is necessary for patients who inject more than
92
6 mm (¼ in), 8 mm (5⁄16 in), and 12.7 mm (½ in).
Insulin syringe needles come in 3 lengths:
93
28, 29, 30, and 31.
-higher the gauge number, the smaller the diameter, thus resulting in a more comfortable injection
needle gauges available are
94
a 90-degree angle. For extremely thin or muscular patients in the hospital, perform injections at a 45-degree angle. At home, patients inject at a 90-degree angle using the shortest needle desired.
-Pinching up of the skin to avoid IM injection is no longer done because of the use of short needles.
Insulin injections are typically given at
95
4 mm (5⁄32 in), 5 mm (3⁄16 in), 8 mm (5⁄16 in), and 12.7 mm (½ in) and in 3 gauges: 29, 31, and 32.
Pen needles are available in lengths of
96
delivers a continuous subcutaneous insulin infusion through a small device worn on the belt, in a pocket, or under clothing.
-rapid-acting insulin
insulin pump
97
an insulin pump that is a tubing-free system
Insulet Corporation has
98
All insulin pumps are programmed to deliver a continuous infusion of rapid-acting insulin 24 hours a day, known as thebasal rate
basal rate
99
increased or decreased based on carbohydrate intake, activity changes, or illness. Pump users need different basal rates at different times of the day.
Basal insulin can be temporarily
100
is the potential for keeping blood glucose levels in a tighter range with a goal of eliminating both high and low glucose.
major advantage of the insulin pump
101
infection at the insertion site, an increased risk for DKA if the insulin infusion is disrupted, the cost of the pump and supplies, and being attached to a device.11
Potential challenges of insulin pump therapy include
102
hypoglycemia, allergic reactions, lipodystrophy, hypertrophy, and the Somogyi effect.
Problems associated with insulin therapy include
103
the same injection sites are used frequently. The use of human insulin has significantly reduced the risk for lipodystrophy.
Lipodystrophy (loss of subcutaneous fatty tissue) may occur if (infusion pump issue)
104
which is uncommon, is the wasting of subcutaneous tissue and presents as indentations in injection sites
Atrophy,
105
happens more often and is a thickening of the subcutaneous tissue. It eventually regresses if the patient does not use the site for at least 6 months. Injecting into a hypertrophied site may result in erratic insulin absorption.
Hypertrophy (infusion pump issue)
106
Hyperglycemia in the morning may be due to the
Somogyi effect
107
high dose of insulin causes a decline in blood glucose levels during the night. As a result, counterregulatory hormones (e.g., glucagon, epinephrine, GH, cortisol) are released. They stimulate lipolysis, gluconeogenesis, and glycogenolysis, which in turn cause rebound hyperglycemia.
Somogyi effect
108
= is also characterized by hyperglycemia that is present on awakening.
-Two counterregulatory hormones (GH and cortisol), which are excreted in increased amounts in the early morning hours, may be the cause of this phenomenon.
- most severe when GH is at its peak in adolescence and young adulthood.
dawn phenomenon
109
a bedtime snack, reducing the dose of insulin, or both
treatment for Somogyi effect is
110
is an increase in insulin or an adjustment in administration time.
treatment for dawn phenomenon
111
is a rapid-acting inhaled insulin
- given at the beginning of each meal or within 20 minutes after starting a meal
-must be used in combination with long-acting insulin in patients with type 1 diabetes. It should not be used to treat diabetic ketoacidosis.
Afrezza
112
must be used in combination with long-acting insulin in patients with type 1 diabetes. It should not be used to treat diabetic ketoacidosis. Patients with chronic lung disease, such as asthma or COPD, or who smoke, should not use Afrezza because bronchospasm can occur. Other common adverse reactions are hypoglycemia, cough, and throat pain or irritation.
Afrezza (inhaled insulin)
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improve the mechanisms by which the body makes and uses insulin and glucose.
OAs and noninsulin injectable agents work to
114
primarily work on 3 defects of type 2 diabetes: (1) insulin resistance, (2) decreased insulin production, and (3) increased hepatic glucose production
OAs and noninsulin injectable agents primarily work on 3 defects of type 2 diabetes:
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metformin. It is the only drug in the biguanide class
most widely used OA is
116
is the most effective first-line treatment for type 2 diabetes
Metformin
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Glucophage (immediate release), Glucophage XR (extended release), Fortamet (extended release), and Riomet (liquid).
Forms of metformin include
118
to reduce glucose production by the liver. It enhances insulin sensitivity at the tissue level and improves glucose transport into the cells. It also has beneficial effects on plasma lipids.
primary action of metformin is
119
prevent type 2 diabetes in those with prediabetes who are younger than age 60 and have risk factors, such as hypertension or a history of gestational diabetes.
Metformin also ised
120
Patients who are undergoing surgery or radiologic procedures that involve the use of a contrast medium need to temporarily discontinue metformin before surgery or the procedure.
-should not resume the metformin until 48 hours afterward, once their serum creatinine has been checked and is normal.
Metformin ALERT
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the dose before each meal based on the current blood glucose level and the carbohydrate content of the meal.
Patients using rapid-acting insulin can adjust
122
, such as multiple daily injections or the use of an insulin pump, allows considerable flexibility in food selection and can be adjusted for changes from usual eating and exercise habits.
Intensified insulin therapy
123
usual food intake and preferences balanced with insulin and exercise patterns.
People with type 1 diabetes base their meal planning on
124
achieving glucose, lipid, and BP goals. Modest weight loss has been associated with improved insulin sensitivity.
Nutrition therapy in type 2 diabetes emphasizes
125
Monitoring blood glucose levels, A1C, lipids, and BP gives feedback on how well the goals of nutrition therapy are being met.
goals of nutrition therapy are being met. type 2
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sugars, starches, and fiber. They are an important source of energy, fiber, vitamins, and minerals and needed by all people, including those with diabetes.
Carbohydrates include
127
whole grains, fruits, vegetables, and low-fat dairy are part of a healthy meal plan.
Foods containing carbohydrate from
128
the sugar substitutes saccharine, aspartame, sucralose, stevia, neotame, and acesulfame-K
Nonnutritive sweeteners include
129
energy, transports fat-soluble vitamins, and provides essential fatty acids.
Dietary fat provides
130
plants, such as olives, nuts, and avocados.
Healthy fats are those that come from
131
gluconeogenesis (breakdown of glycogen to glucose) by the liver.
- can cause severe hypoglycemia in patients on insulin or OAs that increase insulin secretion
Alcohol inhibits
132
eating carbohydrates when drinking alcohol.
patient can reduce the risk for alcohol-induced hypoglycemia by
133
sweetened mixers and can increase blood glucose levels.
mixed drinks often contain
134
sugar-free mixes and drinking dry, light wines.
To decrease the carbohydrate content, recommend using
135
is a meal planning technique used to keep track of the amount of carbohydrate eaten with each meal and per day.
Carbohydrate counting
136
blood glucose levels, age, weight, activity level, patient preference, and prescribed medications.
amount of total carbohydrate per day depends on
137
15 g
-typical adult usually starts with 45 to 60 g of carbohydrate per meal
-(e.g., 1 U/15 g carbohydrate, 2 U/25 g carbohydrate).
serving size of carbohydrate is
138
are another method for meal planning.
-Instead of counting carbohydrate, the person is given a meal plan with specific numbers of helpings from a list of exchanges for each meal and snack.
Diabetes exchange lists
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starches, fruits, milk, meats, vegetables, fats, and free foods.
exchanges are (Diabetes exchange lists)
140
-This method may be easier for some patients than carbohydrate counting
-helps the patient limit portion sizes and overall food intake, an important part of weight management.
Advantage of Diabetes exchange lists
141
represent national nutrition guidelines for people with or without diabetes.
-simple method helps the patient see the amount of vegetables, starch, and meat that fills a 9-in plate.
-each meal has half of the plate filled with nonstarchy vegetables, one fourth filled with a starch, and one fourth filled with a protein
-8-oz glass of nonfat milk and a small piece of fresh fruit complete the meal.12
MyPlate
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at least 150 min/wk (30 minutes, 5 days/week) of a moderate-intensity aerobic physical activity
ADA recommends that people with diabetes engage in
143
resistance training 3 times a week unless contraindicated
ADA encourages people with type 2 diabetes to perform
144
have a direct effect on lowering blood glucose levels. It contributes to weight loss, which further decreases insulin resistance.
Exercise decreases insulin resistance and can
145
triglyceride and low-density lipoprotein (LDL) cholesterol levels, increase HDL, reduce BP, and improve circulation.
Regular exercise may also help reduce
146
hypoglycemia when they increase physical activity, especially if they exercise at the time of peak drug action or eat too little to maintain adequate blood glucose levels. This can also occur if a normally sedentary patient with diabetes has an unusually active day.
Patients who use insulin, sulfonylureas, or meglitinides are at increased risk for
147
hypoglycemia should exercise about 1 hour after a meal or have a 10- to 15-g carbohydrate snack and check their blood glucose before exercising. It is preferable not to increase caloric intake for exercise. If needed, they can eat small carbohydrate snacks every 30 minutes during exercise to prevent hypoglycemia
-always carry a fast-acting source of carbohydrate, such as glucose tablets or hard candies, when exercising.
Patients who use drugs that can cause
148
eat a 15-g carbohydrate snack. After 15 to 30 min, recheck blood glucose levels. Delay exercise if <100 mg/dL.
Before exercise, if blood glucose ≤100 mg/dL,
149
and ketones are present, delay vigorous activity until ketones are gone. Drink fluids.
Before exercise, if blood glucose ≥250 mg/dL in a person with type 1 diabete
150
a stress, causing a release of counterregulatory hormones and a temporary elevation of blood glucose. Teach these patients to delay activity if the blood glucose level is over 250 mg/dL and ketones are present in the urine.
The body can perceive strenuous activity as
151
worsen these conditions.
-If hyperglycemia is present without ketosis, it is not necessary to postpone exercise
In a person with type 1 diabetes who has hyperglycemia and ketones, exercise can
152
provides patients with a tool for achieving and maintaining specific glycemic goals. It is recommended for all patients who use insulin to manage their diabetes.
Self-monitoring of blood glucose (SMBG)
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the patient’s glycemic goals, type of diabetes, medication regimen, patient’s ability to check blood glucose independently, access to supplies and equipment, and patient’s willingness and ability to do so.
frequency of SMBG depends on several factors. These include
154
their blood glucose 4 to 8 times each day.
recommendation for patients who use multiple insulin injections or insulin pumps is to monitor
155
rapidly changing blood glucose readings, during pregnancy, or when symptoms of low blood glucose are present.
Alternative site use is not recommended with
156
are another route for monitoring glucose. More people with type 1 diabetes are using CGMs. These systems are slowly being used by people with type 2 diabetes as well
-lags behind blood glucose by 5 to 10 minutes.
-patient inserts the sensor using an automatic insertion device. Data are sent from the sensor to a transmitter, which displays the glucose value on either an insulin pump or a pager-like receiver
-used with or without an insulin pump
Continuous glucose monitoring (CGM) systems
157
is another option. It allows users to wave a reader over a subcutaneous sensor and get glucose readings at any time
-systems display glucose values that are updated every 1 to 5 minutes.
Flash glucose monitoring
158
may be an option for patients with type 2 diabetes, especially if the diabetes or associated co-morbidities are hard to manage with lifestyle and drug therapy.
Bariatric surgery
159
s an option for select patients with type 1 diabetes. Usually it is done for patients who have end-stage renal disease (ESRD) and have had or plan to have a kidney transplant.
Pancreas transplantation i
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done together, or a pancreas may be transplanted after a kidney transplant.
Kidney and pancreas transplants are often
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(1) a history of frequent, acute, and severe metabolic complications (e.g., hypoglycemia, hyperglycemia, ketoacidosis) requiring medical attention; (2) clinical and emotional problems with the use of exogenous insulin therapy that are so severe as to be incapacitating; and (3) consistent failure of insulin-based management to prevent acute complications.
If renal failure is not present, the ADA recommends that pancreas transplantation be considered only for patients who exhibit these 3 criteria:
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eliminating the need for exogenous insulin and frequent blood glucose measurements. Transplantation can eliminate acute complications experienced by patients with type 1 diabetes (e.g., hypoglycemia, hyperglycemia).
Successful pancreas transplantation can improve quality of life, primarily by
163
patient will need lifelong immunosuppression to prevent rejection of the organ. Complications can result from immunosuppressive therapy.
disadvantage of pancreas transplantation
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islets are harvested from the pancreas of a deceased organ donor. Most recipients need the use of 2 or more pancreases.
-pain and recovery time are less than with whole pancreas transplants.
Pancreatic islet cell transplantation
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a cost-effective approach. Current recommendations for primary prevention include lifestyle modifications for at-risk people. A modest weight loss of 5% to 7% of body weight and 150 minutes of physical activity a week lowered the risk for developing type 2 diabetes by 34% to 58%
Primary prevention is
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hypoglycemia, DKA, and hyperosmolar hyperglycemic syndrome (HHS).
Acute situations involving the patient with diabetes include
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hyperglycemia. Even common illnesses, such as a viral upper respiratory tract infection or the flu, can cause this response
-Encourage patients with diabetes to check blood glucose at least every 4 hours during times of illness.
Acute illness, injury, and surgery may evoke a counterregulatory hormone response, resulting in
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check urine for ketones every 3 to 4 hours.
Teach acutely ill patients with type 1 diabetes and a blood glucose greater than 240 mg/dL (13.3 mmol/L) to
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over 300 mg/dL twice in a row or urine ketone levels are moderate to high
contact the HCP when glucose levels are
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continue to take OAs, noninsulin injectable agents, and/or insulin as prescribed while supplementing food intake with carbohydrate-containing fluids. Examples include low-sodium soups, juices, and regular, sugar-sweetened decaffeinated soft drinks
When illness causes patients to eat less than normal, they can
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patient is given IV fluids and insulin (if needed) just before, during, and after surgery when there is no oral intake.
During the intraoperative period
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signs of hypoglycemia, such as sweating, tachycardia, and tremors. Frequent monitoring of blood glucose can prevent episodes of severe hypoglycemia.
caring for an unconscious surgical patient receiving insulin, be alert for
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syringe magnifiers, vial stabilizers, and dosing aids for the visually impaired
Assistive devices for self-administration of insulin include
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daily brushing and flossing and regular dental visits.
Because of the susceptibility to periodontal disease, encourage (DM)
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educational approach that facilitates informed decision making by the patient is advocated. We call this the empowerment approach to education.
empowerment approach
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eliminating messages that are judgmental and negative and replacing them with empowering, person-centered, and strengths-based language.
empowerment approach includes
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aloe, ginger, cinnamon, St. John’s wort, garlic, and ginseng.
herbs that lower BG
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when there is not enough insulin working.
Hyperglycemia (high blood glucose) occurs
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when there is too much insulin working.
Hypoglycemia (low blood glucose) occurs
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a profound deficiency of insulin.
Diabetes-related ketoacidosis (DKA) is caused by
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t is characterized by hyperglycemia, ketosis, acidosis, and dehydration. It is most likely to occur in people with type 1 diabetes.
Diabetes-related ketoacidosis (DKA) characterized by
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unresponsive because of hypoglycemia.
use glucagon if patient becomes
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acidic by-products of fat metabolism that can cause serious problems when they become excessive in the blood.
Ketones are
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the pH balance, causing metabolic acidosis to develop.
Ketosis alters
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ketone bodies are excreted in the urine. During this process, electrolytes that are cations are also excreted with the anionic ketones to try to maintain electrical neutrality.
Ketonuria is a process that occurs when (electrolytes affected)
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excessive protein degradation. This results in nitrogen losses from the tissues.
Insulin deficiency impairs protein synthesis and causes
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in the liver and leads to further hyperglycemia.
Insulin deficiency stimulates the production of glucose from amino acids (from proteins)
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corticosteriods, illness and infections
cause of hyperglycemia
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severe depletion of sodium, potassium, chloride, magnesium, and phosphate
if DK not treated
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Dehydration occurs in DKA with manifestations of dry mucous membranes, tachycardia, and orthostatic hypotension. Early symptoms may include lethargy and weakness. As the patient becomes severely dehydrated, the skin becomes dry and loose, and the eyes become soft and sunken. Abdominal pain may be present and accompanied by anorexia, nausea, and vomiting. Acetone is noted on the breath as a sweet, fruity odor.
Kussmaul respirations (rapid, deep breathing associated with dyspnea) are the body’s attempt to reverse metabolic acidosis through the exhalation of excess CO2.
signs/symp of DKA
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a blood glucose level of 250 mg/dL (13.9 mmol/L) or greater, arterial blood pH less than 7.30, and serum bicarbonate level less than 16 mEq/L (16 mmol/L). Moderate to large ketones are present in the urine or serum.
Laboratory findings of DKA include
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Other factors to consider when deciding where the patient is managed include the presence of fever, nausea, vomiting, and diarrhea; altered mental status; the cause of the ketoacidosis;
if DKA severe and needs hospitalization
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pneumonia or a urinary tract infection (UTI) usually need admitted to the hospital.
Patients with DKA who have an illness such as
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Typically, the initial fluid therapy involves an IV infusion of 0.45% or 0.9% NaCl at a rate to raise BP and restore urine output to 30 to 60 mL/hr. When blood glucose levels approach 250 mg/dL (13.9 mmol/L), 5% to 10% dextrose is added to prevent hypoglycemia and a sudden drop in glucose that can be associated with cerebral edema.
DKA Tx (IV infusion)
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f the patient is hypokalemic, giving insulin will further decrease potassium levels, making early potassium replacement essential.
Obtain a serum potassium level before starting insulin. I
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hyperglycemia and hyperketonemia
IV insulin therapy is given to correct
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rapid drop in plasma osmalilty.
cerebral edema occurs from
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is a life-threatening syndrome that can occur in the patient with diabetes who is able to make enough insulin to prevent DKA, but not enough to prevent severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion
Hyperosmolar hyperglycemia syndrome (HHS)
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UTIs, pneumonia, sepsis, any acute illness, and newly diagnosed type 2 diabetes.
Common causes of HHS are
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impaired thirst sensation and/or a functional inability to replace fluids.
HHS is often related to
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that the patient with HHS usually has enough circulating insulin so that ketoacidosis does not occur
main difference between HHS and DKA is
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severe neurologic manifestations, such as somnolence, coma, seizures, hemiparesis, and aphasia (resemble stroke)
higher blood glucose levels increase serum osmolality and cause more (HHS SIGN/SYMP)
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a blood glucose level greater than 600 mg/dL (33.33 mmol/L) and a marked increase in serum osmolality. Ketone bodies are absent or minimal in both blood and urine.
Laboratory values in HHS include
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includes immediate IV administration of insulin and either 0.9% or 0.45% NaCl.
****When blood glucose levels fall to about 250 mg/dL (13.9 mmol/L), IV fluids containing dextrose are given to prevent hypoglycemia.
Tx HHS
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IV fluids containing dextrose are given to prevent hypoglycemia.
When blood glucose levels fall to about 250 mg/dL (13.9 mmol/L),
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, although fluid losses may result in milder potassium deficits that require replacement
Hypokalemia is not as significant in HHS as it is in DKA
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there is too much insulin in proportion to available glucose in the blood. This causes the blood glucose level to drop to less than 70 mg/dL
Hypoglycemia, or low blood glucose, occurs when
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Suppression of insulin secretion and production of glucagon and epinephrine provide a defense against hypoglycemia.
When glucose drops below 70 mg/dL, counterregulatory hormones are released and the autonomic nervous system is activated.
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shakiness, palpitations, nervousness, diaphoresis, anxiety, hunger, and pallor.
Epinephrine release causes manifestations that include (hypoglycemia counterregulatory hormones)
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are difficulty speaking, visual changes, stupor(near unconscious), confusion, and coma.
-( Because the brain needs a constant supply of glucose in sufficient quantities to function properly, hypoglycemia can affect mental functioning)
“neuroglycopenia” manifestations (hypoglycemia)
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alcohol intoxication. Untreated hypoglycemia can progress to loss of consciousness, seizures, coma, and death.
Manifestations of hypoglycemia can mimic
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is a condition in which a person does not have the warning signs and symptoms of hypoglycemia until the glucose level reaches a critical point. (person may become incoherent and combative or lose consciousness. )
Hypoglycemia unawareness
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cause person to become incoherent and combative or lose consciousness.
result of diabetes-related autonomic neuropathy that interferes with the secretion of counterregulatory hormones
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those who have had repeated episodes of hypoglycemia, older adults, and patients who use β-adrenergic blockers. Using intensive treatment to lower blood glucose levels in patients who have or are at risk for hypoglycemia unawareness may not be an appropriate goal.
Patients at risk for hypoglycemia unawareness include
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a mismatch in the timing of food intake and the peak action of insulin or OAs that increase endogenous insulin secretion. The balance between blood glucose and insulin can be disrupted by giving too much insulin or medication, ingesting too little food, delaying the time of eating, and performing unusual or unexpected exercise
Causes of hypoglycemia are often related to
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ex: short acting insulin (takes 30-60 mins to kick in )cause hypoglycemia
longer duration of action of these drugs.(cause hypoglycemia)
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a very high blood glucose level falls too rapidly (e.g., a blood glucose level of 300 mg/dL [16.7 mmol/L] falling quickly to 150 mg/dL [10 mmol/L]).
-(lowering high blood glucose levels for the first time, or lowering blood glucose with insulin after a long period of hyperglycemia can cause this situation.)
Symptoms of hypoglycemia may occur when
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-value less than 70 mg/dL is treated by ingesting 15 g of a simple (fast-acting) carbohydrate, such as 4 to 6 oz of fruit juice or a regular soft drink. (Commercial products, such as gels or tablets containing specific amounts of glucose, are convenient for carrying in a purse or pocket to be used in such situations)
-Recheck the blood glucose 15 minutes later
-still less than 70 mg/dL, ingest 15 g more of carbohydrate and recheck the blood glucose in 15 minutes
-If no significant improvement occurs after 2 or 3 doses of 15 g of simple carbohydrate, contact the HCP.
Tx for hypoglycemia (Rule of 15) conscious pt
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the patient may need a snack with carbohydrate and protein if the next meal is more than an hour away or if they are being active.
After an acute episode of hypoglycemia,
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Subcutaneous or IM injection of 1 mg glucagon or IV administration of 20–50 mL of 50% glucose.
* Turn the patient on the side to prevent aspiration.
Tx of hypoglycemic unconcious pt
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fat, such as candy bars, cookies, whole milk, and ice cream. The fat in those foods will slow the absorption of the glucose and delay the response to treatment.
-Do not overtreat with large quantities of quick-acting carbohydrates because a rapid fluctuation to hyperglycemia can occur.
Avoid treatment with carbohydrates that contain (Tx hypoglycemia)
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20 to 50 mL of 50% dextrose IV. If the patient is not alert enough to swallow and no IV access is available, another option is to give 1 mg of glucagon by IM or subcutaneous injection.
acute care setting, patients with hypoglycemia Tx may be given
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to give 1 mg of glucagon by IM or subcutaneous injection.
- IM injection in a site such as the deltoid muscle will result in a quicker response.
If the patient is not alert enough to swallow and no IV access is available, another option is (unconscious hypoglycemic pt Tx)
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a strong hepatic response to convert glycogen to glucose and makes glucose rapidly available.
Glucagon stimulates
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Nausea is a common reaction after glucagon injection.
-To prevent aspiration if vomiting occurs, turn the patient on the side until they are alert.
SE of glucagon Injection
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alcohol-related hepatic disease, starvation, and adrenal insufficiency
Patients with minimal glycogen stores will not respond to glucagon includes patients with
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primarily those of end-organ disease from damage to blood vessels (angiopathy) from chronic hyperglycemia
Chronic complications associated with diabetes are
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,of diabetes-related deaths with about 68% of deaths caused by CVD and 16% caused by strokes for those ages 65 or older.19
Angiopathy is a leading cause
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macrovascular complications and microvascular complications.
chronic blood vessel dysfunctions are divided into 2 categories:
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(1) the accumulation of damaging by-products of glucose metabolism, such as sorbitol, which is associated with damage to nerve cells; (2) the formation of abnormal glucose molecules in the basement membrane of small blood vessels, such as those that circulate to the eyes and kidneys; and (3) a derangement in RBC function that leads to a decrease in oxygenation to the tissues.
how and why chronic hyperglycemia damages cells and tissues Possible causes include
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keeping blood glucose levels as near to normal as possible for as much of the time as possible (tight or intensive therapy).
risk for microvascular complications could be significantly reduced in patients with type 1 diabetes by
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retinopathy and nephropathy,
common microvascular complications.
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developing diabetes-related eye, kidney, and neurologic problems.
intensive treatment of type 2 diabetes significantly lowered the risk for
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diseases of the large and medium-size blood vessels that occur with greater frequency and with an earlier onset in people with diabetes.
Macrovascular complications are
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cerebrovascular, cardiovascular, and peripheral vascular disease.
Macrovascular diseases include
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as obesity, smoking, hypertension, high fat intake, and sedentary lifestyle.
Patients with diabetes can decrease several risk factors associated with macrovascular complications, such
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Insulin resistance is important in the development of CVD and implicated in the pathogenesis of essential hypertension and dyslipidemia.
Insulin resistance is important in the development of CVD
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CVD and renal disease
Optimizing BP control in patients with diabetes is significant in preventing
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a decrease in macrovascular and microvascular complications.
Treating hypertension in those with diabetes results in
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thickening of the vessel membranes in the capillaries and arterioles (small vessels) in response to conditions of chronic hyperglycemia.
Microvascular complications result from
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the eyes (retinopathy), kidneys (nephropathy), and nerves (neuropathy)
microangiopathy can be found throughout the body, the areas most noticeably affected are
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to the process of microvascular damage to the retina because of chronic hyperglycemia, nephropathy, and hypertension in patients with diabetes
Diabetes-related retinopathy refers
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of new cases of adult blindness.
Diabetes-related retinopathy is the leading cause
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as nonproliferative or proliferative
classify retinopathy as
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partial occlusion of the small blood vessels in the retina causes microaneurysms to develop in the capillary walls. The walls of these microaneurysms are so weak that capillary fluid leaks out, causing retinal edema and eventually hard exudates or intraretinal hemorrhages. This may cause mild to severe vision loss, depending on which parts of the retina are affected. If the center of the retina (macula) is affected, vision loss can be severe.
nonproliferative retinopathy, the most common form,
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involves the retina and vitreous
Proliferative retinopathy, the most severe form,
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When retinal capillaries become occluded, the body compensates by forming new blood vessels to supply the retina with blood, a pathologic process known as neovascularization. These new vessels are extremely fragile and hemorrhage easily, producing vitreous contraction. Eventually light is prevented from reaching the retina as the vessels break and bleed into the vitreous cavity. The patient sees black or red spots or lines. If these new blood vessels pull the retina while the vitreous contracts, causing a tear, partial or complete retinal detachment will occur. If the macula is involved, vision is lost.
Proliferative retinopathy, the most severe form,
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because of the occlusion of the outflow channels from neovascularization. This type of glaucoma is hard to treat and often results in blindness
Glaucoma occurs (DM vision problem)
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at an earlier age and progress more rapidly in people with diabetes.
Cataracts develop (DM vision problem)
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an ophthalmologist or a specially trained optometrist at the time of diagnosis and annually thereafter for early detection and treatment.
type 2 diabetes to have a dilated eye examination by
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5 years after the onset of diabetes and then annually.
type 1 diabetes need to have a dilated eye examination within
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the risk for vision loss in patients with proliferative retinopathy or macular edema and, sometimes, nonproliferative retinopathy.
Laser photocoagulation therapy can reduce (Tx for vision)
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ischemic areas of the retina that make growth factors that encourage neovascularization.
Laser photocoagulation destroys the (Tx for vision)
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undergo vitrectomy.
patient who develops vitreous hemorrhage and retinal detachment of the macula may need to
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is the aspiration of blood, membrane, and fibers from the inside of the eye through a small incision just behind the cornea
Vitrectomy
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is used to treat retinopathy.
fluocinolone acetonide intravitreal implant (Iluvien)
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an injectable microinsert that provides sustained treatment through continuous delivery of corticosteroid fluocinolone acetonide for 36 months. Iluvien is injected in the back of the patient’s eye with an applicator that uses a 25-gauge needle, which allows for a self-sealing wound.
fluocinolone acetonide intravitreal implant (Iluvien)
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plays a key role in the development of diabetes-related retinopathy.
Vascular endothelial growth factor (VEGF)
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is a microvascular complication associated with damage to the small blood vessels that supply the glomeruli of the kidney
-leading cause of ESRD
Diabetes-related nephropathy
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hypertension, genetic predisposition, smoking, and chronic hyperglycemia.
Risk factors Diabetes-related nephropathy include
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a random spot urine collection to assess for albuminuria and measure the albumin-to-creatinine ratio.
screened for nephropathy annually with
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measured to give an estimate of the glomerular filtration rate and the degree of kidney function.
Serum creatinine is
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either ACE inhibitor drugs (e.g., lisinopril [Prinivil, Zestril]) or angiotensin II receptor blockers (e.g., losartan [Cozaar]).
-(delay the progression of nephropathy in patients with diabetes)
Patients with diabetes who have albuminuria receive (Tx)
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is nerve damage that occurs because of the metabolic imbalances associated with diabetes
Diabetes-related neuropathy
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sensory neuropathy. This can lead to the loss of protective sensation in the lower extremities.
most common type affecting persons with diabetes is
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metabolic, vascular, and autoimmune factors.
-persistent hyperglycemia leads to an accumulation of sorbitol and fructose in the nerves that causes damage.
Theories cause neuropathy include
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sensory neuropathy, which affects the peripheral nervous system, and autonomic neuropathy
2 major categories of diabetes-related neuropathy are
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distal symmetric polyneuropathy, which affects the hands and/or feet bilaterally.
most common form of sensory neuropathy is aka stocking-glove neuropathy.
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loss of sensation, abnormal sensations, pain, and paresthesias. The pain, which patients describe as burning, cramping, crushing, or tearing, is usually worse at night and may occur only at that time. The paresthesias may be associated with tingling, burning, and itching sensations. The patient may report a feeling of walking on pillows or numb feet. The skin can become so sensitive (hyperesthesia) that the patient cannot tolerate even light pressure from bed sheets. Complete or partial loss of sensitivity to touch and temperature is common. Foot injury and ulcerations can occur without the patient ever having pain (
-cause atrophy of the small muscles of the hands and feet, causing deformity and limiting fine movement.
Characteristics sensory neuropathy is aka stocking-glove neuropathy. include
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include topical creams (e.g., capsaicin [Zostrix]), tricyclic antidepressants (e.g., amitriptyline), selective serotonin and norepinephrine reuptake inhibitors (e.g., duloxetine [Cymbalta]), and antiseizure drugs (e.g., gabapentin [Neurontin], pregabalin [Lyrica]).
Drug Tx for sensory neuropathy aka stocking-glove neuropathy.
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is a moderately effective topical cream made from chili peppers.
-depletes the accumulation of pain-mediating chemicals in the peripheral sensory neurons.
-The cream is applied 3 or 4 times a day.
Capsaicin
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nearly all body systems and lead to hypoglycemia unawareness, bowel incontinence and diarrhea, and urinary retention.
Autonomic neuropathy can affect (type of neuropathy)
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autonomic neuropathy that can cause anorexia, nausea, vomiting, gastroesophageal reflux, and persistent feelings of fullness.
Gastroparesis (delayed gastric emptying) is a complication of
274
delaying food absorption.
Gastroparesis can trigger hypoglycemia by
275
postural hypotension, resting tachycardia, and painless MI.
Cardiovascular abnormalities associated with autonomic neuropathy are
276
Erectile dysfunction (ED) in men with diabetes is well recognized and common, often being the
first manifestation of autonomic neuropathy.
277
vascular disease, elevated blood glucose levels, endocrine disorders, psychogenic factors, and medications. Decreased libido is a problem for some women with diabetes. Candida and nonspecific vaginitis are common
ED is common with other disease, including
278
sensation in the inner bladder wall decreases, causing urinary retention.
neurogenic bladder may develop as the
279
may be used.with neurogenic bladder (urinary retnetion)
Cholinergic agonist drugs, such as bethanechol (Urecholine),
280
a combination of microvascular and macrovascular diseases that place the patient at risk for injury and serious infection
development of diabetes-related foot complications can be the result of
281
foot complications
Sensory neuropathy and peripheral artery disease (PAD) are risk factors for
282
being aware that a foot injury has occurred. Improper footwear and injury from stepping on foreign objects while barefoot are common causes of undetected foot injury in the person with LOPS
Loss of protective sensation (LOPS) often prevents the patient from
283
This is done by applying a thin, flexible filament to several spots on the plantar surface of the foot and asking the patient to report if it is felt. Insensitivity to a monofilament greatly increases the risk for foot ulcers that can lead to amputation.
annual screening using a monofilament
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a reduction in blood flow to the lower extremities. With decreased blood flow, oxygen, white blood cells (WBCs), and vital nutrients are not available to the tissues. Wounds take longer to heal, and the risk for infection increases.
PAD increases the risk for amputation by causing
285
intermittent claudication, pain at rest, cold feet, loss of hair, delayed capillary filling, and dependent rubor (redness of the skin that occurs when the extremity is in a dependent position)
Signs of PAD include
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history, ankle-brachial index (ABI), and angiography.
PAD is diagnosed by
287
. Casting can redistribute the weight on the plantar surface of the foot. Wound care for the ulcer can include debridement, dressings, advanced wound healing products (becaplermin [Regranex]), vacuum-assisted closure, ultrasound, hyperbaric O2, and skin grafting.
Several forms of treatment can be used for ulcer
288
debridement, dressings, advanced wound healing products (becaplermin [Regranex]), vacuum-assisted closure, ultrasound, hyperbaric O2, and skin grafting.
Wound care for the ulcer can include
289
in ankle and foot changes that lead to joint dysfunction and footdrop.
Neuropathic arthropathy, or Charcot’s foot, results
290
reddish brown, round or oval patches.
Diabetes-related dermopathy, the most common skin lesion, is characterized by
291
initially are scaly, then they flatten out and become indented. The lesions appear most often on the shins but can occur on the front of the thighs, forearm, side of the foot, scalp, and trunk.
Diabetes-related dermopathy,
292
is a manifestation of insulin resistance.
-appear as a velvety light brown to black skin thickening, mainly on flexures, axillae, and the neck.
Acanthosis nigricans
293
usually appears as red-yellow lesions, with atrophic skin that becomes shiny and transparent, revealing tiny blood vessels under the surface
-appear before other signs and symptoms of diabetes.
-mainly young women
Necrobiosis lipoidica diabeticorum
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of a defect in the mobilization of WBCs and an impaired phagocytosis by neutrophils and monocytes.
person with diabetes is more susceptible to infections because
295
in the undiagnosed patient often lead the HCP to suspect diabetes
Recurring or persistent infections, such as Candida albicans, boils, and furuncles
296
bladder infections, especially patients with a neurogenic bladder.
Persistent glycosuria may predispose patients to
297
or delay the immune response
Decreased circulation resulting from angiopathy can prevent
298
practicing good hand hygiene, avoiding exposure to persons who have a communicable illness, and getting an annual influenza vaccine and pneumococcal vaccine.
prevent infection by
299
self-care, feelings of helplessness related to chronic illness, and poor outcomes
Depression contributes to diminished diabetes
300
anorexia, bulimia, binge eating, excessive restriction of calories, and intense exercise.
Disordered eating behaviors (DEBs) (occur in type 1 &2)
301
Patients may intentionally decrease their dose of insulin or omit the dose. This is called “diabulimia.” It leads to weight loss, hyperglycemia, and glycosuria because the food ingested cannot be used for energy without adequate insulin.
diabulimia
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retinopathy, neuropathy, lipid abnormalities, DKA, and death.26
Insulin omission and DEBs can have serious consequences, including
303
a reduction in β-cell function, decreased insulin sensitivity, and altered carbohydrate metabolism.
aging is associated with
304
Aging is also associated with conditions that are more likely to be treated with drugs that impair insulin action (e.g., corticosteroids, antihypertensives, phenothiazines).
drugs that impair insulin actions
305
low energy levels, falls, dizziness, confusion, and chronic UTIs.
Undiagnosed and untreated diabetes is more common in older adults, partly because many of the normal physiologic changes of aging resemble those of diabetes, such as
