Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Med-Surg > Chapter 47 Diabetes Mellitus > Flashcards

Chapter 47 Diabetes Mellitus Flashcards

1
Q

1) Leading cause of

2) Major contributing factor

A

1) Leading cause of
- Adult blindness
- End-stage kidney disease
- Nontraumatic lower limb amputations
2) Major contributing factor
- Heart disease
- Stroke
- Hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Etiology and Pathophysiology

A
  • Normal insulin metabolism
  • Produced by beta-cells in islets of Langerhans
  • Released continuously into bloodstream in small increments with larger amounts released after food
  • Stabilizes glucose level in range of 70 to 120 mg/dL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Diabetes is the leading cause of?

A

Adult blindness, end-stage renal disease, and nontraumatic lower limb amputations. It is also a major contributing factor to heart disease and stroke.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Type 1 DM, formerly known as “juvenile-onset” or insulin dependent” diabetes, accounts for approximately 5-10% of all cases of diabetes. This type generally affects who?

A

Younger people than 40 years of age, although it can occur at any age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pathophysiology: Type 1 diabetes is an autoimmune disorder in which the body develops antibodies against insulin and/or the pancreatic B-cells that produce insulin. This eventually results in?

A

Insufficient insulin for survival. Autoantibodies to the islet cells cause a reduction of 80-90% of normal function before hyperglycemia and other manifestations occur.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Factors that may contribute to the pathogenesis of immune-related type 1 diabetes

A

Genetic predisposition and exposure to a virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Type 1 diabetes: Clinical manifestations
Once the pancreas can no longer produce sufficient amounts of glucose to maintain normal glucose the onset of symptoms is usually rapid

A

The patient usually has a history of a recent and sudden weight loss and the classic symptoms of polydipsia (excessive thirst), polyuria (frequent urination), and polyphagia (excessive hunger)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

The individual with type 1 diabetes requires a supply of insulin from an?

A

outside source (exogenous insulin) to sustain life. Without insulin, the patient develops diabetic ketoacidosis (DKA), a life-threatening condition resulting in metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Normal Glucose and Insulin Metabolism.
Insulin is a hormone produced by the β-cells in the islets of Langerhans of the pancreas. Under normal conditions, insulin is continuously released into the bloodstream in small increments, with increased release when food is ingested.
- Insulin lowers blood glucose and facilitates a stable, normal glucose range of approximately?
- The average amount of insulin secreted daily by an adult is approximately?

A
  • Insulin lowers blood glucose and facilitates a stable, normal glucose range of approximately 70 to 110 mg/dL (3.9 to 6.1 mmol/L).
  • The average amount of 1insulin secreted daily by an adult is approximately 40 to 50 U, or 0.6 U/kg of body weight
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Normal endogenous insulin secretion. In the first hour or two after meals, insulin concentrations rise rapidly in blood and peak at about 1 hour. After meals, insulin concentrations promptly decline toward pre­prandial values as carbohydrate absorption from the gastrointestinal tract declines. After carbohydrate absorption from the gastrointestinal tract is complete and during the night, insulin concentrations are low and fairly constant, with a slight increase at dawn.

A

.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Insulin promotes glucose transport from the bloodstream across the cell membrane to the cytoplasm of the cell. Cells break down glucose to make energy, and liver and muscle cells store excess glucose as glycogen.

1) The rise in plasma insulin after a meal does what?
2) The fall in insulin level during normal overnight fasting facilitates the release of?

A

1) inhibits gluconeogenesis, enhances fat deposition of adipose tissue, and increases protein synthesis.
2) stored glucose from the liver, protein from muscle, and fat from adipose tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Classes of Diabetes

A
  • Type 1
  • Type 2
  • Gestational
  • Other specific types – Due to various causes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Type 1 Diabetes Mellitus

A
  • Formerly known as juvenile-onset or insulin-dependent diabetes
  • Accounts for 5% of all cases of diabetes
  • Onset in people younger than 40 years
  • Incidence increasing
  • More frequently in younger children
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Type 1 Diabetes Mellitus Etiology and Pathophysiology

A
  • Autoimmune destruction of β-cells
  • Total absence of insulin
  • Genetic predisposition and viral exposure
    • HLA-DR3 and HLA-DR4
  • Idiopathic diabetes
  • Latent autoimmune diabetes in adults (LADA)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Type 2 Diabetes Mellitus Main Points

A
  • Formerly known as adult-onset diabetes (AODM) or non–insulin-dependent diabetes (IDDM)
  • Most prevalent type (90% to 95%)
  • Risk factors: overweight, obesity, advancing age, family history
  • Increasing prevalence in children
  • Greater prevalence in ethnic groups
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Type 2 diabetes mellitus was formerly known as adult-onset diabetes (AODM) or non–insulin-dependent diabetes (NIDDM). Type 2 diabetes is, by far, the most prevalent type of diabetes, accounting for approximately 90% to 95% of patients with diabetes.

1) Many risk factors contribute to the development of type 2 diabetes, including?
2) Although the disease is seen less frequently in children, the incidence is increasing due to?
3) Type 2 diabetes is more prevalent in some ethnic populations.

A

1) being overweight or obese, being older, and having a family history of type 2 diabetes.
2) the increasing prevalence of childhood obesity.
3) African Americans, Asian Americans, Hispanics, Native Hawaiians or other Pacific Islanders, and Native Americans have a higher rate of type 2 diabetes than whites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Etiology and Pathophysiology.

1) Type 2 diabetes is characterized by a combination of?
2) The pancreas usually?
3) major distinction between type 1 and type 2 diabetes

A

1) inadequate insulin secretion and insulin resistance.
2) produces some endogenous (self-made) insulin. However, the body either does not produce enough insulin or does not use it effectively, or both.
3) The presence of endogenous insulin is a major distinction between type 1 and type 2 diabetes. (In type 1 diabetes, there is an absence of endogenous insulin.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Type 1 diabetes mellitus role of the pancreas

A
  • Autoimmune destruction of B-cells
  • Autoantibodies present for months to years before clinical symptoms
  • Insufficient production of insulin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Type 2 diabetes mellitus role of the pancreas, liver, adipose tissue, muscle

A

1) Pancreas:
- Defective B cell secretion of insulin
- Insulin resistance stimulates increase in insulin secretion
- Eventual exhaustion of B cells in many people
- Increase glucagon secretion
2) Liver
- Excess glucose production
- Inappropriate regulation of glucose production
3) Adipose Tissue
- Decrease adiponectin and Increase leptin
- Results in altered glucose and fat metabolism
4) Muscle
- Defective insulin receptors
- Insulin resistance
- Decreased uptake of glucose by cells resulting in hyperglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Type 2 Diabetes Mellitus Etiology and Pathophysiology Main Points

A
  • Pancreas continues to produce some endogenous insulin
  • Insulin insufficient or poorly utilized
  • Multiple etiologic factors
  • Obesity is greatest risk factor
  • Genetic component increases insulin resistance and obesity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Type 2 Diabetes Mellitus Etiology and Pathophysiology

Four major metabolic abnormalities

A
  • Insulin resistance
  • Decreased insulin production by pancreas
  • Inappropriate hepatic glucose production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Type 2 Diabetes: Genetic mutations that lead to insulin resistance and a higher risk for obesity have been found in many people with type 2 diabetes. Individuals with a first-degree relative with the disease are 10 times more likely to develop type 2 diabetes. Four major metabolic abnormalities play a role in the development of type 2 diabetes

A

1) The first factor is insulin resistance, which describes a condition in which body tissues do no respond to the action of insulin because insulin receptors are unresponsive, insufficient in number, or both. Entry of glucose into the cell in impeded, resulting in hyperglycemia
2) A second factor is a marked decrease in the ability of the pancreas to produce insulin as the B-cells become fatigue from the compensatory overproduction of insulin or when B-cell mass is lost
3) A third factor 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
4) A fourth factor is alteration in the production of hormones and cytokines by adipose tissue (adipokines). Adipokines play a role in glucose and fat metabolism and likely contribute to the pathophysiology of type 2 diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Individuals with metabolic syndrome are at an increased risk for the development of type 2 diabetes. Overweight indidivuals with metabolic syndrome can reduce their risk for diabetes by?

A

through a program of weight loss and regular physical activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Disease onset in type 2 diabetes is usually gradual, with signs and symptoms of hyperglycemia developing when about 50% to 80% of B-cells no longer secrete insulin. Many people are diagnosed on?

A

routine laboratory testing or when they undergo treatment for other conditions and elevated glucose or glycosylated hemoglobin (A1C) levels are found

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

1) The fasting blood glucose level of a patient with prediabetes may range from?
2) The normal blood glucose level ranges from?
3) A blood glucose level of what indicates hypoglycemia?
4) A blood glucose level of what indicates hyperglycemia?

A

1) 100 to 125 mg/dL.
2) 70 to 130 mg/dL.
3) A blood glucose level less than 70 mg/dL indicates hypoglycemia.
4) A blood glucose level greater than 200 mg/dL indicates hyperglycemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

A patient is admitted with diabetic ketoacidosis. Which signs/symptoms would the nurse expect to find upon physical examination?

Blood sugar 200 mg/dL and bradypnea

Hypotension and blood sugar 68 mg/dL

Diaphoresis and extreme hunger

Dry skin and ketonuria

A

Dry skin and ketonuria

In diabetic ketoacidosis, the lungs try to compensate for the acidosis by blowing off volatile acids and carbon dioxide. This leads to a pattern of Kussmaul respirations, which are deep and nonlabored. The patient also will present with dry, loose skin. Blood pressure will not be low and respiratory rate will be increased, not decreased.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Which hormone regulates the normal blood glucose level in the body?

Insulin

Glucagon

Epinephrine

Growth hormone

A

Insulin

Insulin is a hormone secreted by beta cells in the Islet of Langerhans of the pancreas. It helps in regulating the blood glucose level. Glucagon is a hormone secreted by the alpha cells of the Islet of Langerhans. It increases the blood glucose level by counteracting the mechanism of insulin. Epinephrine is a hormone secreted by the adrenal gland. It may not be helpful in maintaining the blood glucose level. Growth hormone is secreted by the pituitary gland and it helps in growth of all tissues and bones in the body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

The nurse is preparing an educational session on Type 2 diabetes for the public. Which symptoms of type 2 diabetes would the nurse include in the presentation? Select all that apply.

Fatigue

Polyuria

Weight loss

Visual changes

Recurrent infections

A

Fatigue
Polyuria
Visual changes
Recurrent infections

The onset of type 2 diabetes usually is delayed, resulting in chronic complications having already manifested. The patient will have slower wound healing and infection healing, fatigue, and visual changes as a result of the disease progression. Some patients with type II diabetes may have polyuria. Weight loss is typically seen with type I diabetes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Which is an insulin-dependent tissue?

Brain

Kidney

Skeletal muscle

Red blood cells

A

Skeletal muscle

Skeletal muscles have specific receptors that are activated by insulin that permit the transportation of glucose into the cells. The brain, kidney, and red blood cells do not have receptors; instead they require only a specific amount of glucose for normal functioning.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Which conditions may cause a patient to develop diabetes mellitus? Select all that apply.

Glaucoma

Astigmatism

Cystic fibrosis

Hyperthyroidism

Hemochromatosis

Recurrent pancreatitis

A

Cystic fibrosis
Hyperthyroidism
Hemochromatosis
Recurrent pancreatitis

Diabetes may occur due to some other medical conditions. Cystic fibrosis, hyperthyroidism, hemochromatosis, and recurrent pancreatitis result from destruction, damage, interference, or injury to pancreatic cell function and can result in diabetes. Glaucoma and astigmatism are not related to pancreatic cell dysfunction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the clinical manifestations of type 1 diabetes mellitus? Select all that apply.

Fatigue

Excessive thirst

Frequent urination

Recurrent infections

Unexplained weight loss

A

Excessive thirst
Frequent urination
Unexplained weight loss

Excessive thirst, frequent urination, and unexplained weight loss are clinical symptoms of both type 1 and type 2 diabetes mellitus. Fatigue and recurrent infections are clinical manifestations of type 2 diabetes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Diabetes is the leading cause of?

A

Adult blindness, end-stage renal disease, and nontraumatic lower limb amputations. It is also a major contributing factor to heart disease and stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Type 1 Diabetes Mellitus formerly known as?

A

Juvenile-onset or insulin dependent diabetes, accounts for approximately 5-10% of all cases of diabetes. This type generally affects people younger than 40 yrs of age, although it can occur at any age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Patho for diabetes type 1

A

-Autoimmune disorder in which the body develops antibodies against insulin and/or the pancreatic B-cells that produce insulin. This eventually results in insufficient insulin for survival. Autoantibodiesto the islet cells cause a reduction of 80-90% of normal function before hyperglycemia and other manifestations occur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What factors may contribute to diabetes type 1?

A

A genetic predisposition and exposure to a virus are factors that may contribute to pathogenesis of immune-related type 1 diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Diabetes type 1: Once the pancreas can no longer produce sufficient amounts of glucose to maintain normal glucose, what happens?

A

The onset of symptoms is usually rapid
-Pt usually has history of recent and sudden weight loss and classic symptom of polydipsia (excessive thirst), polyuria (frequent urination), and polyphagia (excessive hunger)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Environmental factors for type 1 and type 2 diabetes

A

Type 1: Virus, toxins

Type 2: Obesity, lack of exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Primary defect for type 1 and type 2 diabetes

A
  • Type 1: Absent or minimal insulin production

- Type 2: Insulin resistance, decreased insulin production over time, and alterations in production of adipokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Endogenous insulin for type 1 and type 2 diabetse

A
  • Type 1: Absent

- Type 2: Initially increased in response to insulin resistance. Secretion diminishes over time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Symptoms of type 1 and type 2 diabetes

A
  • Type 1: Polydipsia, polyuria, polyphagia, fatigue, weight loss without trying
  • Type 2: Fatigue, recurrent infections, may also experience polyuria, polydipsia, and polyphagia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Those with type 1 diabetes requires?

A

A supply of insulin from an outside source (exogenous insulin) to sustain life. Without insulin the pt will develop diabetic ketoacidosis (DKA), a life-threatening condition resulting in metabolic acidosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Type 1 diabetic have to give insulin but on a sliding scale. So if they are sick and not eating and they have?

A

high blood sugar because being sick can raise your blood surgar so you still have to check blood sugar and give them insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Normal insulin metabolism

A
  • Produced by b-cells in islets of Langerhans
  • Released continuously into bloodstream in small increments with larger amounts released after food
  • Stabilizes glucose level in range of 70 to 120 mg/dL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Type 1 Diabetes Mellitus Etiology and Pathophysiology

A
  • Autoimmune destruction of β-cells
  • Total absence of insulin
  • Genetic predisposition and viral exposure
    • HLA-DR3 and HLA-DR4
  • Idiopathic diabetes
  • Latent autoimmune diabetes in adults (LADA)
45
Q

Type 2 Diabetes Mellitus Main Points

A
  • Formerly known as adult-onset diabetes (AODM) or non–insulin-dependent diabetes (IDDM)
  • Most prevalent type (90% to 95%)
  • Risk factors: overweight, obesity, advancing age, family history
  • Increasing prevalence in children
  • Greater prevalence in ethnic groups
46
Q

Patho for diabetes type 2

A

-Pancreas usually continues to produce some endogenous (self made) insulin. However, the body either does not produce enough insulin or does not use it effectively, or both. The presence of endogenous insulin is the major pathophysiologic distinction between type 1 and type 2 diabetes

47
Q

Diabetes Type 2: Genetic mutations that lead to insulin resistance and a higher risk for obesity have been found in many people with type 2 diabetes.

A

-Individuals with a first degree relative with the disease are 10 times more likely to develop type 2 diabetes.

48
Q

Four major metabolic abnormalities play a role in the development of type 2 diabetes

A

1) Insulin resistance: Condition in which body tissues do not respond to the action of insulin because insulin receptors are unresponsive, insufficient in number, or both. Entry of glucose into the cell is impeded, resulting in hyperglycemia
2) Marked decrease in ability of pancreas to produce insulin as the B-cells become fatigued from the compensatory overproduction of insulin or when B-cell mass is lost
3) 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
4) Alteration in the production of hormones and cytokines by adipose tissue (adipokines). Adipokines play a role in glucose and fat metabolism and likely contribute to the pathophysiology of type 2 diabetes

49
Q

Individuals with metabolic syndrome are at an increased risk for?

A

the development of type 2 diabetes. Overweight individuals with metabolic syndrome can reduce their risk for diabetes through a program of weight loss and regular physical activity

50
Q

Disease onset of type 2 diabetes is?

A

Usually gradual, with s/s of hyperglycemia developing when about 50-80% of B-cells no longer secrete insulin. Many people are diagnosed on routine laboratory testing or when they undergo Tx for other conditions and elevated glucose or glycosylated hemoglobin (A1C) levels are found

51
Q

Prediabetes: Individuals diagnosed with prediabetes are at increased risk for the development of?

A

Type 2 diabetes.
-Prediabetes is an intermediate stage between normal glucose homeostasis and diabetes, is defined as impaired glucose tolerance (IGT), impaired fasting glucose (IFG), or both

52
Q

Prediabetes: A diagnosis of Impaired glucose tolerance (IGT) is made if?
-IFG is diagnosed how?

A

The 2-hour oral glucose tolerance test (OGTT) values are 140 to 199 mg/dL (7.8 to 11.0 mmol/L).
-IFG is diagnosed when fasting blood glucose levels are 100 to 125 mg/dL (5.56 to 6.9 mmol/L)

53
Q

prediabetes: People with prediabetes usually do not have symptoms. However, long term damage to the?

A

Body, especially the heart and blood vessels, may already by occuring. It is important for patients to undergo screening and understand risk factors for diabetes

54
Q

prediabetes teaching

A
  • Encourage those with prediabetes to have their blood glucose and A1C tested regularly and to self monitor for symptoms of diabetes, such as polyuria, polyphagia, and polydipsia
  • Maintaining a healthy weight, exercising regularly, and eating a healthy diet reduce the risk of developing overt diabetes in people with prediabetes
55
Q

Clinical manifestations for diabetes type 1

A
  • Onset is rapid
  • Initial manifestations are usually acute
  • Osmotic effect of glucose produces polydipsia and polyuria
  • Polyphagia is a consequence of cellular malnourishment when insulin deficiency prevents use of glucose for energy.
  • Weight loss, weakness, and fatigue
56
Q

Clinical manifestations for diabetes type 2

A
  • Often nonspecific
  • Fatigue
  • Recurrent infections
  • Prolonged wound healing
  • Visual changes
  • Polydipsia, polyuria, and polyphagia may also occur
57
Q

Acute complications arise from events associated with?

A

Hyperglycemia and hypoglycemia (insulin reaction). It is important for the HCP to distinguish between hyperglycemia and hypoglycemia because hypoglycemia worsens rapidly and constitutes a serious threat if action is not immediately taken

58
Q

Type 2 Diabetes Mellitus Etiology and Pathophysiology

A
  • Pancreas continues to produce some endogenous insulin
  • Insulin insufficient or poorly utilized
  • Multiple etiologic factors
  • Obesity is greatest risk factor
  • Genetic component increases insulin resistance and obesity
59
Q

Metabolic syndrome increases risk for type 2 diabetes

A
  • Elevated glucose levels
  • Abdominal obesity
  • Elevated blood pressure
  • High levels of triglycerides
  • Decreased levels of HDLs
60
Q

Prediabetes

Individuals at risk for type 2 diabetes

A
  • Impaired glucose intolerance (IGT)
    Two-hour oral glucose tolerance test (OGTT): 140 to 199 mg/dL
  • Impaired fasting glucose (IFG)
    Fasting glucose level: 100 to 125 mg/dL
61
Q

Prediabetes
Asymptomatic but long-term damage already occurring
- Patient teaching important

A
  • Undergo screening
  • Manage risk factors
  • Monitor for symptoms of diabetes
  • Maintain healthy weight, exercise, healthy diet
62
Q

Clinical Manifestations Type 1 Diabetes Mellitus

A
  • Classic symptoms
  • Polyuria (frequent urination)
  • Polydipsia (excessive thirst)
  • Polyphagia (excessive hunger)
  • Weight loss
  • Weakness
  • Fatigue
63
Q

Clinical Manifestations Type 2 Diabetes Mellitus

A
  • Nonspecific symptoms
  • Classic symptoms of type 1 may manifest
  • Fatigue
  • Recurrent infection
  • Recurrent vaginal yeast or candidal infection
  • Prolonged wound healing
  • Visual changes
64
Q

Diabetic Ketoacidosis (DKA) is caused by?

A

A profound deficiency of insulin and is characterized by hyperglycemia, ketosis, acidosis, and dehydration. Precipitating factors include illness and infection, inadequate insulin dosage, undiagnosed type 1 diabetes, poor self management, and neglet

65
Q

DKA is most likely to occur in?

A

Type 1 diabetes but may be seen in type 2 during severe illness or stress when the pancreas cannot meet the extra demand for insulin. If it is left untreated, death is inevitable

66
Q

Manifestations of DKA include?

A

Dehydration signs (poor skin turgor, dry mucous membranes), tachycardia, orthostatic hypotension with a weak and rapid pulse, vomiting, Kussmaul respirations, and a sweet fruity odor of acetone on the breath

67
Q

DKA laboratory findings

A

Blood glucose level of 250 mg/serum bicarbonate level less than 16 mEq/L (16 mmol/L), and moderate to large amount of ketones in the urine or serum.

68
Q

Hyperglycemia manifestations

A
  • Elevated blood glucose
  • Increase in urination
  • Increase in appetite followed by lack of appetite
  • Weakness, fatigue
  • Blurred vision
  • HA
  • Glycosuria
  • N/V
  • Abdominal cramps
  • Progression to DKA or HHS
69
Q

Hypoglycemia manifestations

A
  • Blood glucose <70 mg/dL (3.9 mmol/L)
  • Cold, clammy skin
  • Numbness of fingers, toes, mouth
  • Rapid heartbeat
  • Emotional changes
  • HA
  • Nervousness, tremors
  • Faintness, dizziness
  • Unsteady gait, slurred speech
  • Hunger
  • Changes in vision
  • Seizure, coma
70
Q

Hyperglycemia causes

A
  • Illness, infection
  • Corticosteroids
  • Too much food
  • Too little or not diabetes medication
  • Inactivity
  • Emotional, physical stress
  • Poor absorption of insulin
71
Q

Hypoglycemia causes

A
  • Alcohol intake w/out food
  • Too little food-delayed, omitted, inadequate intake
  • Too much diabetes medication
  • Too much exercise w/out adequate foot intake
  • Diabetes medication w/out food taken at wrong time
  • Loss of weight w/out change in medication
  • Use of B-adrenergic blockers interfering with recognition of symptoms
72
Q

Hyperglycemia Tx

A
  • Get medical care
  • Continue diabetes medication as prescribed
  • Check blood glucose frequently and check urine for ketones; record results
  • Drink fluids at least on an hourly basis
  • Contact HCP regarding ketonuria
73
Q

Hypoglycemia Tx

A
  • Conscious person: give 15 g of a simple (fast acting) carbohydrate (fruit juice or regular soft drink). Recheck the blood glucose 15 minutes later. If value is still below 70 mg/dL, have the patient ingest 15 g more of carbohydrate and recheck the blood glucose in 15 minutes. Have the patient ingest a complex carbohydrate after recovery to prevent rebound hypoglycemic attack. If no significant improvement occurs after 2 or 3 doses of 15 g of simple carbohydrate, contact HCP
  • Worsening symptoms or unconscious patient. Subcutaneous or IM injection of 1 mg glucagon, or IV administration of 25-50 mL of 50% glucose
74
Q

Hyperglycemia preventive measures

A
  • Take prescribed dose of medication at proper time
  • Accurately administer insulin, noninsulin injectables, and/or OAs.
  • Make healthy food choices
  • Follow sick day rules when ill
  • Check blood glucose routinely
  • Wear or carry diabetes ID
75
Q

Hypoglycemia preventive measures

A
  • Take prescribed dose of medication at proper time
  • Accurately administer insulin, noninsulin injectables, OAs
  • Coordinate eating with medications
  • Eat adequate food intake needed for calories for exercise
  • Be able to recognize and know symptoms and treat them immediately
  • Carry simple carbohydrates
  • Educate family and caregivers about symptoms and treatment
  • Check blood glucose routinely
  • Wear or carry diabetes ID
76
Q

Diagnostic Studies

A
  • Hemoglobin A1C level: 6.5% or higher
  • Fasting plasma glucose level: higher than 126 mg/dL
  • Two-hour plasma glucose level during OGTT: 200 mg/dL (with glucose load of 75 g)
  • Classic symptoms of hyperglycemia with random plasma glucose level of 200 mg/dL or higher
77
Q

Hemoglobin A1C test

A
  • Glycosylated hemoglobin: reflects glucose levels over past 2 to 3 months
  • Used to diagnose, monitor response to therapy, and screen patients with prediabetes
  • Goal: less than 6.5% to 7%
78
Q

Hyperosmolar Hyperglycemic Syndrome (HHS) is a?

A

Life threatening syndrome that can occur in the patient with DM who is able to produce enough insulin to prevent DKA but not enough to prevent severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion

79
Q

The main difference between HHS and DKA is that the patient with HHS usually?

A

Has enough circulating insulin so that ketoacidosis does not occur. Because HHS produces fewer symptoms in the earlier stages, blood glucose levels can climb quite high before the problem is recognized. The higher blood glucose levels increase serum osmolality and produce more severe neurologic manifestations, such as somnolence, coma, seizures, hemiparesis, and aphasia

80
Q

HHS is less common than DKA. It often occurs in patients greater than?

A

60 yrs with type 2 diabetes. Common causes of HHS are urinary tract infections, pneumonia, sepsis, and any acute illness. HHS is more common among patients with newly diagnosed type 2 diabetes

81
Q

HHS lab values

A

-Blood glucose level above 600 mg/dL (33.33 mmol/L) and a marked increase in serum osmolatity. Ketone bodies are absent or minimal in both blood and urine

82
Q

Hypoglycemia, or low blood glucose, occurs when?

A

There is too much insulin in proportion to available glucose in the blood. This causes the blood glucose level to drop below 70 mg/dL.

  • Manifestations include: shakiness, palpitations, nervousness, diaphoresis, anxiety, hunger, and pallor.
  • Untreated hypoglycemia can progress to loss of consciousness, seizures, coma, and death
83
Q

Chronic complication so DM

A
  • Primarily those of end-organ disease arising from damage to the blood vessels from chronic hyperglycemia
  • Angiopathy (blood vessel disease) is one of the leading causes of diabetes-related deaths. These chronic blood vessel problems are divided into two categories: Macrovascular complications and microvascular complications
84
Q

Chronic Complications: Macrovascular complications and Microvascular complications

A

1) Macrovascular Complications: Diseases of the large and medium sized blood vessels that occur with greater frequency & an earlier onset in people with diabetes.
- Risk factors: obesity, smoking, HTN, high fat intake, & sedentary lifestyle. Can be reduced
- Insulin resistance plays a role in development of CVD and implicated in pathogenesis of essential HTN and dyslipidemia
2) Microvascular Complications: Result from thickening of vessel membranes in capillaries and arterioles in response to chronic hyperglycemia.
- Although microangiography can be found throughout the body, the areas most noticeably affected are the eyes (retinopathy), kidneys (nephropathy), and nerves (neuropathy)

85
Q

Microvascular Complications: Diabetic retinopathy

A

Most common cause of new cases of adult blindness

86
Q

Microvascular Complications: Nonproliferative retinopathy

A

Most common form, partial occlusion of small blood vessels in the retina causes microaneurysms to develop in capillary walls. Capillary fluid leaks out, causing retinal edema and eventually hard exudates or intraretinal hemorrhages. Vision may be affected if the macula is involved

87
Q

Microvascular Complications: Proliferative retinopathy

A

More severe and involves retina and vitreous
-when retinal capillaries become occluded, new fragile blood vessels are formed. Eventually light does not reach the retina as vessels tear and bleed. A tear or retinal detachment may then occur. If the macular is involved, vision is lost. Tx involves laser photocoagulation

88
Q

Microvascular Complication: Diabetic Nephropathy

A

Associated w/damage to small blood vessels that supply the glomeruli of the kidney.

  • leading cause of end-stage renal disease in US
  • Tight blood glucose control is critical in prevention/delay of diabetic nephropathy
  • HTN accelerates progression of disease. Aggressive BP management indicated for all patients with diabetes
89
Q

Patients with diabetes are screened for nephropathy annually with a random spot urine collection to assess for albuminuria and measure the albumin-to-creatine ratio. Serum creatinine is also measured to provide?

A

as estimation of the glomerular filtration rate and thus degree of kidney function

90
Q

Neuropathy is?

A

Nerve damage that occurs because of the metabolic alterations associated with diabetes. About 60-70% of pt’s w/diabetes have some degree of this.

  • more than 60% of nontraumatic amputations in the US are done for people w/diabetes
  • Screening for neuropathy should begin at the time of diagnosis in patients with type 2 diabetes and 5 years after diagnosis of type 1
91
Q

Two major categories of diabetes-related neuropathy are?

A

sensory neuropathy, which affects the peripheral nervous system and is the more common type of neuropathy, and autonomic neuropathy, which can affect nearly all body systems

92
Q

Most common form of sensory neuropathy is distal symetric neuropathy, which affects the hands or feet bilaterally. Characteristics include?

A

loss of sensation, abnormal sensations, pain, paresthesias. The pain, often described as burning, cramping, crushing, or tearing, is usually worse at night. The paresthesias may be associated with tingling, burning, and itching sensations

93
Q

Autonomic neuropathy can lead to?

A

hypoglycemia unawareness, bowel incontinence and diarrhea, and urinary retention. Delayed gastric emptying (gastroparesis), a complication of autonomic neuropathy, can produce nausea, vomiting, gastroesophageal reflux, and persistent feelings of fullness. Cardiovascular abnormalities, such as postural hypotension, painless MI, and resting tachycardia can occur

94
Q

What is the Tx of diabetic neuropathy?

A

Control of blood glucose is the only Tx. It is effective in many but not all cases. Drug therapy may be used to treat neuropathic symptoms, particuarly pain

95
Q

Diagnostic Studies: The diagnosis of diabetes can be made through one of the following four methods. In the absence of unequivocal hyperglycemia, criteria 1 to 3 should be confirmed by repeat testing

A

1) A1C level of 6.5% or greater
2) Fasting plasma glucose (FPG) level at or above 126 mg/dL (7.0 mmol/L). Fasting is defined as no caloric intake for at least 8 hours
3) Two-hour plasma glucose level at or above 200 mg/dL (11.1 mmol/L) during an OGTT, using a glucose load of 75g
4) In a patient with classic symptoms of hyperglycemia (polyuria, polydipsia, unexplained weight loss) or hyperglycemia crisis, a random plasma glucose of at least 200 mg/dL (11.1 mmol/L)

96
Q

Interprofessional Care: The major types of glucose lowering agents (GLAs) used in the Tx of diabetes are?

A

Insulin and oral and noninsulin injectable agents

97
Q

Goals of diabetes management

A
  • Decrease symptoms
  • Promote well-being
  • Prevent acute complications
  • Delay onset and progression of long-term complications
  • Need to maintain blood glucose levels as near to normal as possible
98
Q

Patient teaching

A
  • Nutritional therapy
  • Drug therapy
  • Exercise
  • Self-monitoring of blood glucose
  • Diet, exercise, and weight loss may be sufficient for patients with type 2 diabetes
  • All patients with type 1 require insulin
99
Q

Insulin Exogenous

A
  • Insulin from an outside source
  • Required for type 1 diabetes
  • Prescribed for patients with type 2 diabetes who cannot control blood glucose by other means or during periods of severe stress and illness or surgery
100
Q
  • Human insulin

- Categorized according to onset, peak action, and

A 
- Human insulin
Genetically engineered in laboratories
- Categorized according to onset, peak action, and duration
 * Rapid-acting
 * Short-acting
 * Intermediate-acting
 * Long-acting
101
Q

Insulin Regimens

A
  • Basal-bolus regimen
  • Most closely mimics endogenous insulin production
  • Rapid- or short-acting (bolus) insulin before meals
  • Intermediate- or long-acting (basal) background insulin once or twice a day
  • Less intense regimens can also be used
102
Q

Mealtime Insulin (Bolus) Insulin preparations

A
  • Rapid-acting (bolus)
  • Lispro, aspart, glulisine
  • Onset of action 15 minutes
  • Injected within 15 minutes of mealtime
  • Short-acting (bolus)
  • Regular with onset of action 30 to 60 minutes
  • Injected 30 to 45 minutes before meal
  • Onset of action 30 to 60 minutes
  • In addition to mealtime insulin, those with type 1 diabetes must also use a long or intermediate acting (background) insulin to control blood glucose levels between meals and overnight.
103
Q

(Basal) Background Insulin

- Long-acting (basal)

A
  • Used to control glucose levels in between meals and overnight
  • Long-acting (basal)
  • Insulin glargine (Lantus) and detemir (Levemir)
  • Released steadily and continuously with no peak action
  • Administered once or twice a day
  • Do not mix with any other insulin or solution
104
Q

(Basal) Background Insulin

- Intermediate-acting insulin

A
  • NPH
  • Duration 12 to 18 hours
  • Peak 4 to 12 hours
  • Can mix with short- and rapid-acting insulins
  • Cloudy; must agitate to mix
105
Q

Combination Insulin Therapy

A
  • Can mix short- or rapid-acting insulin with intermediate-acting insulin in same syringe
  • Provides mealtime and basal coverage in one injection
  • Commercially premixed or self-mix
106
Q

Administration of insulin

A
  • Typically given by subcutaneous injection
  • Regular insulin may be given IV
  • Cannot be taken orally
107
Q

Insulin pump

A
  • Continuous subcutaneous infusion
  • Battery-operated device
  • Connected to a catheter inserted into subcutaneous tissue in abdominal wall
  • Program basal and bolus doses that can vary throughout the day
  • Potential for tight glucose control
  • Insertion site is changed every 2-3 days
108
Q

Problems with insulin therapy

A
  • Hypoglycemia
  • Allergic reaction
  • Lipodystrophy – using the same injection site frequently.

Med-Surg (32 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions