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Nurs 206 > ENDOCRINE 1 DIABETES > Flashcards

ENDOCRINE 1 DIABETES Flashcards

1
Q

For all types of diabetes mellitus, the main feature is

A

chronic hyperglycemia resulting from problems with glucose regulation that include reduced insulin secretion or reduced insulin action or both.

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2
Q

Type 1 Diabetes (T1DM)

A
  • Beta-cell destruction leading to absolute insuline deficiency
  • autoimmune
  • Idiopathic
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3
Q

Type 2 Diabetes (T2DM)

A
  • Ranges from insulin resistance with relative insulin deficiency to secretory deficit with insulin resistance.
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4
Q

Other Conditions resulting in hyperglycemia

A
  • genetic defects of beta-cell function
  • genetic defects in insulin action
  • pancreatic diseases (pancreatitis, trauma, cancer, cystic fibrosis, hemochromatosis).
  • endocrine problems (acromegaly, Cushing’s disease, hyperthyroidism, aldosteronism)
  • Drug-or chemical-induced hyperglycemia
  • infections: congenital rubella, cytomegalovirus, human immune deficiency virus.
  • genetic syndromes associated with diabetes: down syndrome, klinefelter syndrome, Turner syndrome, Hunting Disease, and others.
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5
Q

Gestational Diabertes Mellitus (GDM)

A
  • glucose intolerance with onset or first recognition during pregnancy. (All pregnant women should be screened).
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6
Q

Islet of langerhans in pancreas, has two types of cells important to glucose regulation.

A

Alpha cells

beta cells

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7
Q

Normal blood glucose control

A
  • blood glucose is controlled by interactions between:
    • gi tract
    • pancrease
    • liver
  • glucose is either used or stored
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8
Q

Fasting Glucose

A

74-106 mg/dL

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9
Q

Hypoglycemia

A

Blood glucose levels less than 74 mg/dl

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10
Q

Hyperglycemia

A

blood glucose levels greater than 106

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11
Q

Pancreas has exocrine functions

A
  • related to digestion and endocrine functions that attempts to maintain blood glucose control.
  • endocrine portion of the pancreas has 1 million islets of langerhans
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12
Q

alpha cells

A

secrete glucagon

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13
Q

beta cells

A

produce insulin and amylin

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14
Q

Characterization of the underlying pathophysiology is more developed in type 1 diabetes

A

than type 2.

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15
Q

Glucose is the main fuel for the

A

central nervous system cells.

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16
Q

Glucagon

A

is a “counterregulatory” hormone that has actions opposite those of insulin. It prevents hypoglycemia by triggering the release of glucose from storage sites in the liver and skeletal muscle.

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17
Q

Insulin prevents

A

hyperglycemia by allowing body cells to take up, use, and store carbohydrate, fat, and protein

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18
Q

Active insulin is a protein made up of

A

51 amino acids.

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19
Q

Insulin is secreted daily into liver circulation in a two-step manner.

A
  • It is secreted at low levels during fasting (basal insulin secretion) and in a two-phase release after eating (prandial).
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20
Q

An early burst of insulin secretion occurs within

A

10 minutes of eating, followed by an increasing release that lasts until the blood glucose level has returned to normal.

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21
Q

Physiologic Response to Insufficient Insulin

A
  • decreased glycogenesis (conversion of glucose to glycogen)
  • increased glycogenolysis (conversion of glycogen to glucose)
  • increased glyconeogenesis (formation of glucose from noncarbohydrate sources such as amino acids and lactate)
  • increased lipolysis (breakdown of triglycerides to glycerol and free fatty acids)
  • increased ketogenesis (formation of ketones from free fatty acids)
  • Proteolysis (breakdown of protein with amino acid release in muscles).
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22
Q

glycogenesis

A

conversion of glucose to glycogen

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23
Q

glycogenolysis

A

conversion of glycogen to glucose

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24
Q

gluconeogenesis

A

formation of glucose from noncarbohydrate sources such as amino acids and lactate

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25
Q

lipolysis

A

breakdown of triglycerides to glycerol and free fatty acids.

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26
Q

ketogenesis

A

formation of ketones from free fatty acids

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27
Q

Proteolysis

A

breakdown of protein with amino acid release in muscles

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28
Q

polydipsia

A

excessive thirst

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29
Q

polyphagia

A

excessive eating

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30
Q

Insulin for glucose regulation is needed to move glucose into the many body tissues.

A

The lack of insulin in diabetes, from either a lack of production or a problem with insulin use at its cell receptor, prevents some cells from using glucose for energy. The body then breaks down fat and protei in an attempt to provide energy and icnreases levels of counterregulatory hormones to make glucose from other sources.

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31
Q

Hyperglycemia disturbs fluid and electrolyte imbalance, leading to the classic symtoms of diabetes

A

polyuria, polydipsia and ployphagia.

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32
Q

Ketone bodies

A

are abnormal breakdown products that collect in the blood when insulin is not available, leading to ACID-BASE Balance problems of metabolic acidosis.

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33
Q

Dehydrations with DM leads to hemoconcentration; hypovolemia; poor tissue perfusion and hypoxia., especially to the brain.

A

Hypoxic cells do not metabolize glucose efficiently, the Kreb’s cycle is blocked, and lactic acid productin increases, causing more acidosis.

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34
Q

The excess acids caused by absence of insulin increase hydrogen ion and carbon dioxide levels in the blood, causing an anion-grap metabolic acidosis.

A

These products trigger the brain to increase the rate and depth of respiration in an attempt to “blow off” carbon dioxide and acids. (Kussmaul respirations) Acetone is exhaled, giving the breath a “rotting citrus fruit” odor. When the lungs can no longer offset acidosis, the blood pH drops.

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35
Q

Insulin lack initially causes potassium depletion. With the increased fluid loss from hyperglycemia, excessive potassium is excreted in the urine, leading to low serum potassium levels.

A

High serum potassium levels may occur in acidosis because of the shift of potassium from inside the cells to the blood.

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36
Q

Three glucose related-emergencies can occur in patients with diabetes (DM):

A
  • diabetic ketoacidosis (DKA) caused by the absence of insulin and generation of ketoacids.
  • hyperglycemia-hyperosmolar state (HHS) caused by insulin deficiency and profound dehydration.
  • Hypoglycemia from too much insulin or too little glucose.

All three require emergency treatment and can be fatal if treatment is delayed or incorrect.

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37
Q

Diabetes mellitus can lead to organ complications and early death because of changes in large blood vessels (macrovascular) and small blood vessels (microvascular) in tissues and organs.

A

These blood vessel changes lead to complication from poor tissue perfusion and cell ischemia.

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38
Q

Macrovascular complications

A
  • coronary heart disease
  • cerebrovascular disease
  • peripheral vascular disease
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39
Q

Microvascular disease

A
  • Nephropathy
  • Neuropathy
  • Retinopathy
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40
Q

Chronic high glucose levels are the main cause of microvascular complications.

A

Additional risk factors contributing to poor health outcomes for adults with DM include smoking, physical activity, obesity, hypertension, and high blood fat and cholesterol levels.

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41
Q

Patients with DM often have the traditional CVD (cardiovascular disease) risk factors of

A

obesity, high blood lipid levels, hypertension, and sedentary lifestyle.

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42
Q

Kidney Disease, indicated by albuminuria (presence of albumin in the urine), and retinopathy are markers of increase risk for coronary heart disease and motality from coronary artery disease.

A

Patients with DM often have higher levels of C-reactive protein (CRP), an inflammatory marker associated with increased risk for cardiovascular inflammation and death.

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43
Q

Cardiovascular complication rates can be reduced through

A

aggressive management of hyperglycemia, hypertension, and hyperlipidemia.

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44
Q

The American Diabetes Association recommends that BO be measured

A

at every routine visit and confimred on a separate day if elevated.

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45
Q

The ADA also recommends that BO be maintained below 140/90mm Hg, with a target of

A

130/80 in younger adults if that level can be achieved without excess burden.

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46
Q

Lipid profile screening is recommedned at the first diagnosis, at the initial medical evaluations, and/or at the age of 40 years and every 1 to 2 years thereafter.

A

Patients with DM who do not have overt CVD are recommended to maintain low-density lipoprotein (LDL) cholesterol below 100 and patients with indications of CVD are recommended to maintain LDLS at less than 70 mg/dl.

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47
Q

Lifestyle modifications that focus on reducing saturated fat, trans fat, and cholesterol intake; increasing intake of omega-3 fatty acids, fiber, and plant sterols; weight loss (if indicated); and increasing physical activity

A

are recommended to improve the lipid profile for patients with DM.

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48
Q

Cardiovascular Pharmacology Treatment

A

Either an ACE inhibitor or an angiotensi receptor blocker.

Multiple-drug therapy (two or more agents at maximal doses) is generally required to achieve BP targets.

Administer 1 or more antihypertensive medications at bedtime

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49
Q

Achieve low lipid values:

A
  • LDL <70 mg/dl
  • HDL > 50 mg/dl
  • Triglycerides < 150 mg/dl
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50
Q

Patients with blood pressure >120/80 mmHg should be advised on lifestyle changes to reduce blood pressure.

A

Patient’s confirmed with blood pressure higher than 140/80, need lifestype therapy and drug treatment.

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51
Q

Teach patietns to report subtle indications of ischemia,

A

such as dyspnea with or without cough, extreme fatigue, and sudden onset of nausea and vomiting, to their primary health care provider for evaluation.

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52
Q

Peripheral Vascular Disease

A
  • due to poor circulation diabetics are at higher risk of developing:
    • dry cracked skin
    • foot deformities
    • foot ulcers
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53
Q

Diabetes mellitus

A
  • chronic disorder of impaired carbohydrate, protein, and lipid metabolism caused by a deficiency of insulin.
  • an absolute or relative deficiency of insulin results in hyperglycemia.
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54
Q

Type 1 diabetes mellitus ia nearly absolute deficiency of insulin (primary beta cell destruction);

A

if insulin is not given, fats are metabolized for energy for energy, resulting in ketonemia (acidosis).

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55
Q

Type 2 diabetes mellitus is a relative lack of insulin or resistance to the action of insulin;

A

usually, insulin is sufficient to stablize fat and protein metabolism but not carbohydrate metabolism.

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56
Q

metabolic syndrome is also known as syndrome X, and the individual has coexisiting risk factors for developing type 2 diabetes mellitus;

A

these risk factors include abdoninal obesity, hyperglycemia, hypertension, high triglyceride level, and a lower HDL cholesterol level.

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57
Q

Diabetes mellitus can lead to chronic health problems and early death as a result of

A

complications that occur in the large and small blood vessels in tissues and organs,

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58
Q

Macrovascular complications include

A

coronary artery disease, cardiomyopathy, hypertension, cerebrovascular disease, and peripheral vascular disease.

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59
Q

Microvascular complications include

A

retinopathy, nephropathy, and neuropathy.

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60
Q

Infection is a concern

A

because of reduced healing ability.

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61
Q

Male erectile dysfunction can also occur

A

as a result of the disease.

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62
Q

Obesity

A

is a major risk factor for diabetes mellitus.

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63
Q

diabetes signs and symptoms

A
  • polyuria, polydipsia, polyphagia (more common in type 1 diabetes mellitus).
  • hyperglycemia
  • weight loss (common in type 1 diabetes mellitus, rare in type 2 diabetes mellitus).
  • blurred vision
  • slow wound healing
  • vaginal infections
  • weakness and parenthesias
  • signs of inadequate circulation to the feet
  • signs of accelerated atherosclerosis (renal, cerebral, cardiac, peripheral).
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64
Q

The diabertic client’s diet should take into account weight, medication, activity level, and other health problems.

A

Day-to-day consistency in timing and amount of food intake helps control the blood glucose level.

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65
Q

As prescirbed by the PHCP or endocrinologist, the client

A

may be advised to follow the recommendations of the American Diabetic Association diet or the US dietary guideling issued by the US Deptarment of Agriculture and Health and Human Services.

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66
Q

Carbohydrate counting may be a simpler approach for some clients; it focuses on the total grams of carbohydrates eaten per meal.

A

The client may be more compliant with carbohydrate counting, resulting in better glycemic control; it is usually necessary for clients undergoing intense insulin therapy.

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67
Q

Incorporate the diet into the indidual client

A

needs, lifestyle, and cultural and socioeconomic patterns.

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68
Q

Exercise lowers the blood glucose level, encourages weight loss, reduces cardiovascular risks, improves circulation and muscle tone,

A

decreases total cholesterol and trigylceride levels, and decreases insulin resistance and glucose tolerance.

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69
Q

Instruct the client in dietary adjustments when exercising; dietary adjustments are individualized.

A

If the client requires extra food during exercise to prevent hypoglycemia, it need not be deducted from the regular meal plan.

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70
Q

If the blood glucose level is higher than 250 mg/dL and urinary ketones (type 1 diabetes mellitus) are present,

A

the client is instructed not to exercise until the blood glucose level is closer to normal and urinary ketones are absent.

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71
Q

The client should try to exercise at the same time each day

A

and should exercise when insulin or glucose-lowering medications are peaking.

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72
Q

Insulin should not be injected into an area of the body that will be exercised following injection,

A

as exercise speeds absorption.

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73
Q

Instruct the client with diabetes mellitus to monitor the blood glucose level

A

before, during, and after exercising.

74
Q

Oral hypoglycemia medications

A

Oral medications are prescribed for clients with diabetes mellitus type 2 when diet and weight control therapy have failed to maintain satisfactory blood glucose levels.

75
Q

Insulin is used to treat type 1 diabetes mellitus an may be used to treat type 2

A

when diet and and weight control therapy have failed to maintain satisfactory blood glucose levels.

76
Q

Illness, infection, and stress increase the blood glucose level and the need for insulin;

A

insulin should not be withheld during times of illness, infection, or stress because hyperglycemia and diabetic ketoacidosis can result.

77
Q

The peak action time of insulin is important to explain to the client because

A

of the possiblity of hypoglycemic reactions occuring during this time.

78
Q

Regular insulin (U-100 strength) can be administered via IV injection (IV push).

A

Regular insulin (U-100) and the short duration insulins (lispro, aspart, and glulisine) can be administered via IV infusion.

79
Q

Local allergic reactions

A
  • redness, swelling, tenderness, and induration or a wheal at the site of injecgtion may occur 1 to 2 hours after administration.
  • Reactions usually occur during the arly stages of insulin therapy.
  • Instruct the client to cleanse the skin with alcohol before injection.
80
Q

Insulin lipodystrophy

A
  1. the development of fibrous fatty masses at the injection site caused by repeated use of an injection site; use of human insulin prevents this.
  2. Instruct the client to avoid injecting insulin into affected sites.
  3. Instruct the client the importance of rotating insulin injection sites. Systematic rotation with 1 anatomical area is recommended to repvent lipodystrophy; the client should be instructed not to use the same site more than once in a 2- to 3-week period. Injections should be 1.5 inches apart within the same anatomical area.
81
Q

Dawn Phenomenon

A
  1. Dawn phenomenon is characterized by hyperglycemia upon morning awakening that results from excessive early morning release of GH and cortisol.
  2. Treatment requires an increase in the client’s insulin dose or a change in the time of insulin administration.
82
Q

Somogyi phenonmenon

A
  1. Normal or elevated blood glucose levels are present at bedtime; hypoglycemia occurs at about 2 to 3 a.m., which causes an increase in the production of counterregulatory hormones.
  2. By about 7 am, in reponse to counterregulatory hormones, the blood glucose rebounds significantly to the hyperglycemic range.
  3. Treatment includes a decrease in the client’s insulin dose or increase in the bedtime snack, or both.
  4. clients experiencing the Somogyi phenomenon may complain of early morning headaches, night sweats, or nightmares caused by the early morning hypoglycemia.
83
Q

The combination of factors leading to the nerve damage in diabetic neuropathy are:

A
  1. Hyperglycemia, long duration of DM, hyperlipidemia.
  2. Damaged blood vessels leading to reduced neuronal oxygen and other nutrients.
  3. Autoimmune neuronal inflammation.
  4. Increased genetic susceptibility to nerve damage.
  5. Smoking and alchohol use.
84
Q

Proliferative diabetic retinopathy

A

a form of retinopathy assocaited with diabetes mellitus in which a network of fragile new blood vessels develops, leaking blood and protein into the surrounding tissue. The new blood vessels are stimulated by retinal hypoxia that results from poor capillary perfusion of the retinal tissues. New blood vessels grow in the retina, onto the iris, and into the back of the vitreous. The vitreous contracts and pulls away from the retina, causing blood vessels to break and bleed into the vitreous.

85
Q

Diabetic Peripheral Neuropathy

A

A progressive deterioration of nerves that results in loss of nerve function (sensory Perception). A common complication of diabetes, it often involves all parts of the body

86
Q

Distal symmetric polyneuropathy

A
  1. Diffuse neuropathy
  2. sensory alterations: paresthesias: burning/tingling sensations, starting in toes and moving up legs; dysesthesias: burning,stinging, or stabbing pain; and anesthesia: loss of sensation.
  3. Motor alterations in intrinsic muscles of foot: Foot deformatives; high arch, claw toes, hammertoes; shift of weight bebearing to metatarsal heads and tips of toes.
87
Q

Autonomic neuropathy

A
  1. Diffuse neuropathies
  2. Anhidrosis : dry, cracking of the skin
  3. Gastrointestinal: Delayed gastric emptying, gastric retention, early saiety, bloating, nausea, vomiting, anorexia, constipation, diarrhea, diffuse sweating while eating, nocturnal diarrhea
  4. Nueorgenic bladder: atonic bladder, urinary retention
  5. Impotence: erectile dysfunction
  6. Cardiovascular autonomic neuropathy: early fatigue, weakness with exercise, orthostatic hypotension
  7. Defective counterregulation: Loss of warning signs of hypoglycemia.
88
Q

Focal ischemia

A
  1. Focal Neuropathy
  2. Thoracolumbar readiculopathy with sensory and reflex loss: pain radiating across back, side, and front of chest or abdomen.
  3. Cranial nerve palsies, third and sixth nerves: Sudden diplopia or ptosis; eye pain.
  4. Amyotrophy: pain; asymmetric weakness; wasting of iliopsoas, quadriceps, and adductor muscles.
89
Q

Focal neuropathies

A

in DM affect a single nerve or nerve group and usually are caused by an acute ischemic event that leads to nerve damage or nerve death. Occur when blood supply to a nerve or nerve group is disrupted. Symptoms begin suddenly, affect only one side of the body area, and are self-limiting. The most common neuropathies affect the nerves that control the eye muscles. Symptoms begin with pain on one side of the face near the affected eye. The eye muscles become paralyzed, resulting in double vision. The problem usually resolves in 2 to 3 months.

90
Q

Diffuse Neuropathies

A

are the most common neuropathies in DM and involve widespread nerve function loss and sensory perception loss. The onset is slow, affects both sides of the body, involves motor and sensory nerves, progresses slowly, and is permanent. Late complications include foot ulcers and deformaties.

91
Q

Nephropathy

A

is a pathologic change in the kidey that reduces kidney function and leads to kidney failure.

92
Q

Type 1 Diabetes

A
  1. Former names: Juvenile-onset diabetes; ketosis-prone diabetes; insulin dependent diabetes mellitus (IDDM)
  2. Age at onset: usually younger than 30 yr
  3. Symptoms: abrupt onset, thirst, hunger, increased urine output, weight loss
  4. Etiology: viral infections, autoimmunity
  5. Pathology: Pancreatic beta-cells destruction
  6. Antigen Patterns: HLA-DR, HLA-DQ
  7. Antibodies: Present at diagnosis
  8. Endogenous Insulin and C-peptide: None
  9. Inhertiance: Complex
  10. Nutritional Status: Usually nonobese
  11. Insulin: All dependent on insulin
  12. Medical Therapy: Mandatory
93
Q

Type 2 Diabetes

A
  1. Former names: Adult-onset diabetes; Ketosis-resistant diabetes; Non-insulin-dependent diabetes mellitus (NIDDM)
  2. Age at onset: May occur at any age in adults.
  3. Symptoms: Frequently none; thirst, fatigue, blurred vision, vascular or neural complications.
  4. Etiology: Not known
  5. Pathology: Insulin resistance; difunctional pancreatic beta cell.
  6. Antigen patterns: none
  7. Antibodies: none
  8. Endogenous insulin and C-peptide: low, normal, or high.
  9. Inheritance: Autosomal-dominant, multifactorial
  10. Nutritional Status: 60 to 80% obese
  11. Insulin: Required for 20% to 30%
  12. Medical Therapy: Mandatory
94
Q

Type 1 Diabetes

A
  • Possible environmental trigger
  • Genetic predisposition: HLA-DR & HLA-DQ
  • the patient produces little to no insulin
  • insulin producing pancreatic beta cells are destroyed by an autoimmune process
  • acute onset any age, usually before 30
95
Q

Metabolic syndrome

A
  • is the simultaneous presence of metabolic factors known to increase risk for developing type 2 DM and cardiovascular disease
96
Q

Features of Metabolic syndrome

A
  • Abdominal obesity: waist circumference of 40 inches or more for men and 35 inches or more for women.
  • Hyperglycemia: fasting blood glucose level of 100mg/dl or more or on drug treatment for elevated blood glucose levels.
  • hypertension: systolic BP of 130 mm Hg or more or diastolic BP of 85 mm Hg or more or on drug treatment for hypertension.
  • Hyperlipidemia: triglyceride level of 15 mg/dl or more or on drug treatment for elevated triglycerides; HDL cholesterol less than 40 mg/dl for men and less than 50 mg/dl for women.
97
Q

Risk for type 1 DM is determined by inheritance of genes coding for the HLA-DR and HLA-DQ mand DQB tissue types. However, inheritance of these genes only increases the risk, and mot people with these genes do not develop type 1 DM.

A

Development of DM is an interactive effect of genetic predisposition and exposure to certain environmental factors. When assessing adults, always ask whether any family members have been diagnosed with either type 1 or type 2 diabetes.

98
Q

Indications for Testing People for Type 2 Diabetes

A
  • Testing for diabetes is considered at any age in adults with a BMI greater than 25 kg/m3 with one or more of these additional risk factors:
    • Have a first degree relative with diabetes
    • are physically inactive
    • are members of a high risk ethnic population (African Americans, Hispanic Americans, American Indian, or Pacific Islander)
    • Have a baby weighing more than 9 lb or have been diagnosed with GDM.
    • Are hypertensive (>140/90 mmHg)
    • Have a HDL cholesterol level less than 35 mg/dL and/or a triglyceride level greater than 250 mg/dL.
    • Have polycystic ovary syndrome
    • Have A1C greater than 6.5% or IFG or IGT on previous testing
    • Have a history of vascular disease
  • If the tested adult has normal glucose values at this time but other conditions and risk factors remain the same, testing should be treated at 3-year intervals.
99
Q

Classification of Diabetes

A
  • Diabetes mellitus associated with other dieases or medications
  • Type 1 diabetes
  • Prediabetes
  • Type 2 diabetes
  • Gestational diabetes
100
Q

PreDiabetes

A
  • People say “I have a bit of suagr.” no longer called Borderline diabetes.
  • They have impaired glucose tolerance
  • Associated with abdominal or visceral obesity, dyslipidemia, triglycerides, low HDL, cholesterol and high BP.
  • Progression to type 2 can be prevented or delayed.
101
Q

Main Symptom of Diabetes

A
  • Central Nervous System: polydipsia, polyphagia, (lethargy, stupor type 1).
  • Systemic: weight loss, type 1
  • Respiratory: Kussmaul breathing (hyperventilation) type 1
  • Eyes: blurred vision
  • Breath: smell of acetone , type 1
  • Gastric: Nausea, vomiting, abdominal pain , type 1
  • Urinary: polyuria, glycosuria
102
Q

Metabolic syndrome

A
  • Syndrome x
    • metabolic factors that are known to increase risk for developing Type 2 Diabetes
      • Overweight
      • BMI>= 25kg/m3
      • begins at age 45
103
Q

Type 2 Diabetes

A
  • People have decresed sensitivity to insulin and impaired beta cell functioning resulting in decreased insulin production
  • more common in peope
    • > 30 years of age and obese
  • due to growing obesity, this type of diabetes is increasing
104
Q

Type 2 Diabetes

A
  • Treatment is intially treated with diet and exercise
  • if persists, diet and exercise are supplemented with oral agents.
  • If blood glucose levels are not controlled insulin injections are required.
  • Insulin may be needed during acute physiologic stress (illness or surgery)
105
Q

Microvascular: Nephropathy

A
  • Pathological change in the kidney that reduces kidney function
  • Begin:
    • Ace inhibitor or angiotensin REceptor Blocker
106
Q

Diabetic Neuropathy

A
  • Progessive deterioration of nerves that results in loss of nerve function.
  • Symptoms vary according to class of sensory fibers involved.
  • Involves all part of the body
107
Q

Retinopathy

A
  • Optimize BP control to reduce risk or slow progression of retinopathy
  • legal blindness
    • blockage of retinal blood vessels
    • causes vessels to leak
    • leading to retinal hypoxia
  • Risk Factors:
    • 10-15 year history of diabetes.
    • Diabetic retinopathy
    • poor blood glucose control
    • uncontrolled hypertension
    • genetic predisposition
108
Q

Retinopathy

A
  • Adults with type 1 screened within 5 years of onset of diabetes by opthalmaologist of optometrist.
    • if no evidence of retinopathy for one or more eye exams, then exams every 2 years.
    • if retinopaty for type 1 or type 2, annual exams.
109
Q

Insulin pumps

A
  • Continuous subcutaneous insulin infusion is administered by an externally worn device that contains a syringe and pump; different types of pumps are available and the one selected is based on the client’s needs.
  • The client inserts the needle or Teflon catheter into the sucutaneous tissue (usually on the abdomen or upper arm) and secures it with tape or a transparent dressing; the needle or Teflon catheter is changed at least every 2 to 3 days.
  • A continuous basal rate of insulin infuses; in addition, on the basis of blood glucose level, the anticipated food intake, and the activity level, the client delivers a bolus of insulin before each meal.
  • Both rapid-acting and regular short-acting insulin (buffered to prevent the precipitation of insulin crystals within the catheter) are appropriate for use in these pumps.
110
Q

Criteria for the diagnosis of Diabetes

A

A1C> 6.5%. The test should be performed in a laboratory using a method that is NGSP certified and standardized to the DCCT assay

or

Fasting blood glucose greater than or equal to 126 mg/dL. Fasting is defined as no calorie intake for at least 8 hours.

or

Two-hour blood glucose equal to or greater than 200 mg/dL during oral glucose tolerance test. The test should be performed using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water.

or

in a patient with classic manifestations of hyperglycemia or hyperglycemic crisis, a random blood glucose concentration greater than 200 mg/dL. Casual is defined as any time of the day without regard to time since last meal. The classic symptoms of diabetes include polyuria, polydipsia, and unexplained weight loss. Note: In the absence of unequivocal hyperglycemia, the first three criteria should be confirmed by repeat testing.

111
Q

Insulin pump and skin

A
  • A skin sensor device can be used that monitors the client’s blood glucose continuously; the information is transmitted to the pump, which determines the need for insulin, and then the insulin is injected.
  • The pump holds up to a 3-day supply of insulin and can be disconnected easily if necessary for certain activities such as bathing.
112
Q

Pancreas Transplants

A
  • The goal of pancreatic transplantation is to halt or reverse the complications of diabetes mellitus.
  • Transplantations are performed on a limited number of clients (in general, these are clients who are undergoing kidney transplantation simultaneously).
  • Immunosuppressive therapy is prescribed to prevent and treat rejection.
113
Q

Self-Monitoring of blood glucose level

A
  • self-monitoring provides the client with the current blood glucose level and information to maintain good glycemic control.
  • monitoring requires a finger prick to obtain a drop of blood for testing.
  • alternative site testing (obtaining blood from the forearm, upperarm, abdomen, thigh or calf) is available, using specific measurement devices.
  • Tests must be used with caution in clients with diabetic neuropathy
114
Q

Client Instructions: Self-Monitoring of Blood glucose Levels

A
  • Use the proper procedure to obtain the sample for determining the blood glucose level.
  • Perform the procedure precisely to obtain accurate results.
  • Follow the manufacturer’s instructions for the glucometer.
  • Wash hands before and after performing the procedure to prevent infection.
  • If needed, calibrate the monitor as instructed by the manufacturer.
  • Check the expiration date on the test strips.
  • If the blood glucose level results do not seem reasonable, reread the instructions, reassess technique, check the expiration date of the test strips, and perform the procedure again to verify results.
115
Q

Urine Testing

A
  1. Urine testing for glucose is not a reliable indicator of the blood glucose levvel and is not used for monitoring purposes.
  2. Instruct the client in the procedure for testing urine ketones.
  3. The presence of ketones may indicate impending ketoacidosis.
  4. Urine ketone testing should be performed during illness and whenever the client with type 1 diabetes mellitus has persistently elevated blood glucosed levels (higher than 250 mg/dL or as prescribed for 2 consecutive testing periods.)
116
Q

Hypoglycemia

A
  1. Hypoglcemia occurs when the blood glucose level falls below 70mg/dL or when the blood glucose level drops rapidly from an elevated level.
  2. Hypoglycemia is caused by too much insulin or too arge an amount of an oral hypoglycemic agent, too little food, or excessive activity.
  3. The client needs to be instructed in ways to carry some form of fast-acting carbohydrate with him or her.
  4. If the client has a hypoglycemic reaction and does not have any of the recommended emergency foods available, any available food should be eaten, high-fat foods slow absorption of glucose, and hypoglycemic symptoms may not resolve quickly.
  5. Clients who experience frequent episodes of hypoglycemia, older clients, and clients taking B-adrenergic blocking agents may not experience the warning signs of hypoglycemia until the blood glucose level is dangerously low; this phenomenon is termed hypoglycemia unawareness.
117
Q

simple carbohydrates to treat hypoglycemia

15 g

A
  • commercially prepared glucose tablets (3-4 tablets) or 1 tube glucose gel
  • 4-6 life savers or hard candy
  • 3 tsp of sugar
  • 4 sugar cubes
  • 1-2 tbsp of honey or syrup
  • 4 oz of fruit juice or 6 oz regular (nondiet) soft drink
  • 1/2 tube of cake mate
  • 8 oz of lowfat milk
  • 6 saltine crackers
  • 3 graham crackers.
118
Q

mild hypoglycemia: The client remains fully awake but displays adrenergic symptoms, the blood glucose level is lower than 70 mb/dl

A
  • hunger
  • shakiness (tremor)
  • weakness
  • paleness
  • blurry vision
  • increased heart rate or palpitations (tachycardia)
  • sleepiness changed behavior
  • sweating
  • anxiety (nervousness)
  • dilated pupils
119
Q

Moderate hypoglycemia: the client displays symptoms of worsening hypoglycemia; the blood glucose level is usually lower than 39 mg/dL.

A
  • confusion
  • double vision
  • drowsiness
  • emotional changes
  • headache
  • impaired cooridination
  • inability to concentrate
  • irrational or combative behavior
  • lightheadedness
  • numbness of the lips and tongue
  • slurred speech
120
Q

Sever hypoglycemia: the client displays severe neuroglycemia symptoms; the blood glucose level is usually lower than 20mg/dL.

A
  • difficulty arousing
  • disoriented behavior
  • loss of consciousness
  • seizures
121
Q

Hypoglycemia : moderate to severe symptoms

A
  • yawning
  • irritability/frustration
  • extreme tiredness/fatigue
  • inability to swallow
  • sudden crying
  • confusion
  • restlessness
  • dazed appearance
  • unconsciousness/coma
  • seizures
122
Q

Interventions for Suspected Hypoglycemic Reaction (the 15/15 rule)

A
  1. I f a blood glucose monitor is readily available, check the client’s blood glucose level. If the client is experiencing symptom suggestive of hypoglycemia such as diaphoresis, hunger, pallor, and shakiness, and a blood glucose monitor is not readily available, assume hypoglycemia and treat accordingly.
  2. For the client whose blood glucose is below 70mg/dL or for the client with an unknown blood glucose who is exhibiting signs of hypoglycemia, administer 15 g of a simple carbohydrate such as 1/2 cup of fruit juice or 15 g of glucose gel.
  3. Recheck the blood glucose in 15 minutes.
  4. If the blood glucose remains below 70 mg/dL administer another 15 g of a simple carbohydrate.
  5. Recheck the blood glucose level in 15 minutes; if still below 70 mg/dl, treat with additional 15 g of a simple carbohydrate.
  6. Recheck the blood glucose level in 15 minutes; if still below 70mg/dL, treat with 25 to 50 mL of 50% dextrose intravenously or, if no intravenous (IV) equipment is present, treat with 1 mg of glucagon subcutaneously or intramuscularly.
  7. After the blood glucose level has recovered, have the client ingest a snack that includes a complex carbohydrate and a protein.
  8. Document the client’s complaints, actions taken, and outcome.
  9. Explore the precipitating cause of the hypoglycemia with the client.
  10. If the client is experiencing an altered level of consciousness, bypass oral treatment and start with injectible glucagon or 50% dextrose. If the client is at home and does not have access to injectible glucagon, the client should seek immediate medical care.
123
Q

Do not attempt to administer oral food or fluids to the client experiencing a sever hypoglycemia reaction who is semiconscious or unconscious and is unable to swallow.

A

This client is at risk for aspiration. For this client, an injection of glucagon is administered subcutaneously or intramuscularly. In the hospital or emergecy department, the client may be treated with an IV injection of 25 to 50 ml of 50% dextrose in water.

124
Q

Body’s response to absence of Insulin

A
  • Hyperglycemia
    • polyuria
    • polydipsia
    • polyphagia
    • ketone bodies
  • Dehydration causes:
    • hemoconcentration
    • hypovolemia
    • hyperviscosity
    • hypoxia.
125
Q

Hypoglycemia treatment

A
  • Glucose (15-20 g) is the preferred treatment for the conscious individual with hypoglycemia, although any form of carbohydrate that contains glucose may be used.
  • Glucagon should be prescribed for all individuals at significant risk of severe hypoglycemia
  • A glucagon kit requires a prescription
    • care should be taken to ensure that glucagon kits are not expired.
126
Q

Severe Hypoglycemia Treatment

A
  • Rare, but life threatening, if not treated promptly:
    • Place client on his or her side
    • lift chin to keep airway open
    • inject glucagon
    • Never give food or put anything in client’s mouth
    • call 911
    • client should respond in 10 to 20 minutes
    • remain with individual until help arrives
127
Q

Hypoglycemia Prevention

A
  • Physical activity, insulin, eating, checking BG, per schedule.
  • Keep a quick-acting sugar source with the client
  • ALWAYS
    • treat at onset of symptoms
    • ensure insulin dosing matches food eaten.
128
Q

Normal Lab values

A
  • A1C (HbA1c) <5.7%

or

fasting plasma glucose (FPG) < 100mg/dl

or

oral glucose tolerance test glucose < 140 mg/dl during an OGTT

129
Q

Diabetes diagnosis

A

FBG >= 126 mg/dl

Random Plasma Glucose >= 200 mg/dl plus symptoms

OGTT 2 hr >= 200 mg/dL

A1C >= 6.5 %

130
Q

Prediabetes diagnosis

A
  • Impaired fasting glucose >= 100 mg/dl to 125
  • Impaired glucose tolerance test: 2 hr PG 140 mg/dL to 199 mg/dL
  • A1C 5.7% to 6.4%
131
Q

A1C to Average Blood Glucose (ADA)

A

6 = 126

6.5=140

7=154

7.5=169

8=183

9=212

9.5=226

10=240

132
Q

Urine Ketones

A
  • Hyperketonuria indicates severe lack of insulin
  • hyperketonuria in the presence of hyperglycemia is a medical emergency
133
Q

Oral Glucose Tolerance Testing (OGTT)

A
  • is a sensitive test for the diagnosis of diabetes
  • two or more of the venous plasma levels must be met or exceeded for a positive diagnosis
  • test is inconvenient, costly, and time consuming as compared with fasting blood glucose measures.
134
Q

Hypoglycemia Acronym

A

TIRED

T- TACHYCARDIA

I- IRRITABILITY

R- RESTLESSNESS

E- EXCESSIVE HUNGER

D- DIAPHORESIS/DEPRESSION

135
Q

ADA Recommendations: Hypoglycemia

A
  • Hypoglycemia unawareness or one or more episodes of severe hypoglycemia should trigger re-evaluation of the treatment regimen.
  • Insulin-treated patients with hypoglycemia unawareness or an episode of severe hypoglycemia.
    • advised to raised glycemic targets to strictly avoid hypoglycemia for at least several weeks.
    • Goal is to partially reverse hypoglycemia unawareness, and to reduce risk of future episodes.
136
Q

Fasting blood glucose test

A
  • Normal range <100 mg/dL older adults: levels rise 1 mg/dL per decade of age
  • Levels >100mg/dL but <126 mg/dL indicate impaired fasting glucose.
  • Levels >126mg/dL obtained on at least two occasions are diagnostic of diabetes, even in older adults..
137
Q

Glucose tolerance test (2 hr post-load result)

A
  • <140 mg/dL
  • Levels >140 mg/dL and <200 mg/dL indicate impaired glucose tolerance
  • Levels >200 mg/dL indicate provisional diagnosis of diabetes.
138
Q

Glycosylated hemoglobin (A1C) test

A
  • 4%-6% normal range
  • levels of 5.7% to 6.4% indicate increased risk for development of diabetes.
  • levels >6.5% indicate diabetes.
  • levels >8% indicate poor diabetes control and need for adherence to regimen or changes in therapy.
139
Q

To avoid drug interactions, teach the patient who is taking an antidiabetic drug

A

to consult with his or her PHCP or pharmacist before using any over-the-counter drugs.

140
Q

Metformin can cause lactic acidosis in patients with kidney inpairment and should not be used by anyone with kidney disease.

A

To prevent lactic acidosis and acute kidney injury, the drug is withheld before and after using contrast medium or any surgical procedure requiring anesthesia until adequate kidney function is established.

141
Q

Do not confuse Actos with Actonel.

A

Actos is an oral antidiabetic drug from the thiazolidinedione class, and Actonel is a drug that prevents calcium loss from bones.

142
Q

Insulin Stimulators (Secretagogues)

Second Generation Sylfonylurea Agents (Oral)

  • Glipizide (Glucotrol)
  • Glyburide (Diabeta, Micronase)
  • Glimepiride (Amaryl)

Meglitinide Analogs (Oral)

  • Repaglinide (Prandin)
  • Nateglinide (Starlix)
A
  • These drugs lower blood glucose levels by triggering the release of preformed insulin from beta cells.
  • Teach patients the signs and symptoms of hypoglycemia (Hunger, headache, tremors, sweating, confusion) because these drugs lower blood glucose levels even when hyperglycemia is not present.
  • Instruct patients to take these drugs with or just before meals to prevent hypoglycemia.
  • Instruct patients taking sulfonylurea to check with his or her primary health care provider or a pharmacist before taking any over the counter drug or supplement because these drugs interact with many other drugs.
  • Warn patients that nausea, headache, and weight gain are common side effects of these drugs because knowing the expected side effects decreases anxiety when they appear.
143
Q

Biguanides

  • Metformin (Glucophage)
A
  • These drugs lower blood glucose levels by inhibiting liver glucose production, decreasing intestinal absorption of glucose, and increasing insulin sensitivity.
  • Instruct patients not to drink alchoholic beverages while taking this drug to reduce the risk for lactic acidosis.
  • Remind patients that this drug may be discontinued before certain imaging tests using contrast agents and not started again for 48 hours after testing because of the increased risk for kidney damage and lactic acidosis.
  • Warn patients that diarrhea, nausea, flatulence, indigestion, and abdominal pain are common side effects of this drug class because knowing the expected side effects decreases anxiety when they appear.
144
Q

Insulin Sensitizers

Thiazolidinediones (TZDs) (Oral)

  • Pioglitazone (Actos)
  • Rosiglitazone (Avandia)
A
  • These drugs lower blood glucose levels by decreasing liver glucose production and improving the sensitivity of insulin receptors.
  • Teach patients with any cardiovascular disease to weigh themselves daily and report a weight gain of more than 2 lb in one day or 4 lb in a week to the PHCP because this class of drugs increases the risk for heart failure. These drugs carry a black box warning from the FDA and are not to be given to anyone with symptomatic heart failure.
  • Instruct patients to report vision changes immediately because these drugs increase the risk for macular edema.
  • Warn women about an increased risk for bone fractures because these drugs decrease bone density in women.
  • Warn patients that weigh gain and peripheral edema are common side effects of this drug class because knowing the expected side effects decreases anxiety when they appear.
145
Q

Alpha-Glucodisase Inhibitors

  • Acarbose (Precose)
  • Miglitol (Glyset)
A
  • These oral drugs prevent after-meal hyperglycemia by inhibiting enzymes in the intestinal tract from breaking down starches into glucose. This action delays the digestion of starches and the absorption of glucose from the small intestine.
  • Teach patients to take these drugs with only a meal because the action is in the intestinal tract. If a meal is skipped, so is the drug.
  • Warn patients that abdominal discomfort and bloating, flatulence, nausea, diarrhea, and indigestion are common side effects of this drug class because knowing the expected side effects decreases anxiety when they appear.
146
Q

Incretin Mimetics (GLP-1 Agonists)

  • Albiglutide (Tanzeum)
  • Dulaglutide (Trulicity)
  • Exenatide (Byetta)
  • Exenatide Extended-release (Bydureon)
  • Liraglutide (Victoza)
  • Lixisenatide (Adlyxin)
A
  • The drugs act like the natural “gut” hormones that work with insulin to lower blood glucose levels by reducing pancreatic glucagon secreation; reducing liver glucose production; and delaying gastric emptying, which slows the rate of nutrient absorption into the blood.
  • Teach patients the signs and symptoms of hypoglycemia (hunger, headache, tremors, sweaating, confusion) because these drugs lower blood glucose levels even when they are not elevated.
  • Instruct patients how to inject themselves because these drugs are only available as subcutaneous formulations.
  • Teach patients to inspect injection site for redness, warmth, or hard nodules because injection site reactions are common.
  • Instruct patients to read exenatide, albiglutide, and dulaglutide pens carefully because extended-release form is only injected weekly (compared with others given at least daily). Injecting the extended-release form daily will cause serious harm.
  • Teach patients to report persistent abdominal pain and nausea to the health care provider because these drugs increase the risk for pancreatitis.
147
Q

Do not attempt to administer oral food or fluids to the client experiencing a severe hypoglycemic reaction who is unconscious or semiconscious and is unable to swallow.

A

The client is at risk for aspiration. For this client, an injection of glucagon is administered subcutaneously or intramuscularly. In the hospital or emergecy department, the client may be treated with an IV injection of 25 to 50 ml of 50% dextrose in water.

148
Q

Diabetic Ketoacidosis

A
  • diabetic ketoacidosis is a life-threatening complication of type 1 diabetes mellitus that develops when a sever insulin deficiency occurs.
  • The main clinica manifestations include hyperglycemia, dehydration, ketosis, and acidosis
149
Q

DKA interventions

A
  • Restoring circulating blood volume and protect against cerebral, coronary, and renal hypoperfusion.
  • treat dehydration with rapid iv infusions of 0.9% NS or 0.45% NS as prescribed; dextrose is added to IV fluids when the blood glucose level reaches 250 to 300 mg/dL. Too rapid administration of IV fluids; use of incorrect types of IV fluids, particularly hypotonic solutions; and correcting the blood glucose level too rapidly can lead to cerebral edema.
  • Treat hyperglycemia with insulin administered intravenously as prescribed.
  • Correct electrolyte imbalances (potassium level may be elevated as a result of dehydration and acidosis).
  • Monitor potassium level closely, because when the client receives treatment for the dehydration and acidosis, the serum postassium level will decrease and potassium replacement may be required.
  • Cardiac monitoring should be in place for the client with DKA due to risks associated with abnormal serum levels.
150
Q

Insulin IV administration

A
  • Use short-duration insulin only.
  • An IV bolus dose of short-duration regular U-100 insulin (usually 5-10 units) may be prescribed before a continuous infusion is begun.
  • The prescribed IV dose of insulin for continuous infusion is prepared in 0.9% or 0.45% NS as prescribed.
  • Always place the insulin infusion on an IV infusion controller.
  • Insulin is infused continuously until subcutaneous administration resumes, to prevent a rebound of the blood glucose level.
  • Monitor vital signs.
  • Monitor urinary tract output and monitor for signs of fluid overload.
  • Monitor potassium and glucose levels and for signs of increased intracranial pressure.
  • The potassium level will fall rapidly within the first hour of treatment as the dehydration and acidosis are treated.
  • Potassium is administered intravenously in a diluted solution as prescribed; ensure adequate renal function before administering potassium.
151
Q

DKA Client Education: Guidelines During Illness

A
  • take insulin or oral antidiabetic medications as prescribed.
  • Determine the blood glucose level and test the urine for ketones every 3 to 4 hours.
  • If the usualy meal plan cannot be followed, substitute soft foods 6 to 8 times a day.
  • If vomiting, diarrhea, or fever occurs, consume liquids every 30 to 60 minutes to prevent dehydration and to provide calories.
  • Notify the PHCP if vomiting, diarrhea, or fever persists; if blood glucose levels ar ehigher than 250 to 300 mg/dL; when ketonuria is present for more than 24 hours; when unable to take food or fluids for a period of 4 hours; or when illness persists for more than 2 days.
152
Q

Monitor the client being treated for DKA closely for signs of increased intracranial pressure.

A

If the blood glucose level falls too fast or too far before the brain has time to equilibrate, water is pulled from the blood to the cerebrospinal fluid and the brain, causing cerebral edema and increased intracranial pressure.

153
Q

Hyperosmolar hyperglycemic Syndrome

A
  • Extreme hyperglycemia occurs without ketosis or acidosis.
  • The syndrome occurs most often in individuals with type 2 diabetes mellitus.
  • the major difference between HHS and DKA is that ketosis and acidosis do not occur with HHS; enough insulin is present with HHS to prevent the breakdown of fats for energy this preventing ketosis.
154
Q

Diabetic ketoacidosis Signs and Symptoms

A
  • onset is sudden
  • precipitating factors: infection, other stressors, inadequate insulin dose
  • manifestations: ketosis: kussmaul’s respiration, “fruity” breath, nausea, abdominal pain, dehydration or electrolyte loss: polyuria, polydipsia, weight loss, dry skin, sunken eyes, soft eyeballs, lethargy, coma
  • serum glucose: >300 mg/dL
  • osmolarity: variable
  • serum ketones: postive at 1:2 dilution
  • serum pH: <7.35
  • serum HCO3 <15 mEq/L
  • serum Na low, normal or high
  • Serum K normal; elevated with acidosis, decreases following hydration
  • BUN >20 mg/dL
  • creatinine >1.5 mg/dL; elevated because of dehydration
  • urine ketones: positive
155
Q

Hyperosmolar Hyperglycemia Syndrome

A
  • Onset: gradual
  • Precipitating factors: infection, other stressors, poor fluid intake, altered central nervous system function with neurological symptoms, dehydration or electrolyte loss: polyuria, polydipsia, weight loss, dry skin, sunken eyes, soft eyeballs, lethargy, coma
  • SErum glucose: >800 mg/dL
  • osmolarity >350 mOsm/kg
  • Serum ketones: negative
  • Serum pH: >7.4
  • Serum HCO3: >20 mEq/L
  • Serum Na normal or low
  • Serum K Normal or low
  • BUN elevated
  • creatinine elevated
  • urine ketones negative
156
Q

Hyperosmolar hyperglycemic syndrome (HHS)

Interventions

A
  • similar to that for DKA
  • Treatment includes fluid replacement, correction of electrolyte imbalances, and insulin administration.
  • Fluid replacement in the older adult client must be done very carefully because of the potential for heart failure.
  • Insulin plays a less critical role in the treatment of HHS than it does in the treatment of DKA because ketosis and acidosis do not occur, rehydration alone may decrease glucose levels.
157
Q

Diabetic retinopathy

A
  • chronic and progressive impairment of the retinal circulation that eventually causes hemorrhage.
  • permanent vision changes and blindness can occur.
  • The client has difficulty with carrying out the daily tasks of blood glucose testing and insulin injections.
158
Q

diabetic retinopathy assessment

A
  • a change in vision is caused by the rupture of small microaneurysms in retinal blood vessels.
  • blurred vision results from macular edema
  • Sudden loss of vision results from retinal detachment
  • cataracts results from lens opacity
159
Q

diabetic retinopathy interventions

A
  • maintain safety
  • early prevention via the control of hypertension and blood glucose levels.
  • Photocoagulation (laser therapy) may be done to remove hemorrhagic tissue to decrease scarring and prevent progression of the disease process.
  • Vitrectomy may be done to remove vitreous hemorrhages and thus decrease tension on the retina, preventing detachment.
  • cataract removal with lens implantation improves vision.
160
Q

diabetic nephropathy

A
  • Progressive decrease in kidney function.
  • assessment:
    • microalbuminuria
    • thirst
    • fatigue
    • anemia
    • weight loss
    • signs of malnutrition
    • frequent urinary tract infections
    • signs of neurogenic bladder
  • Interventions
    • early prevention measures include the control of hypertension and blood glucose levels
    • assess vital signs
    • monitor intake and output
    • monitor the blood urea nitrogen, creatinine, and urine albumin levels.
    • restrict dietary protein, sodium, and potassium intake as prescribed.
    • avoid nephrotoxic medications
    • prepare the client for dialysis procedures if planned.
    • prepare the client for kidney transplant if planned.
    • prepare the client for pancreas transplant if planned
161
Q

Diabetic Neuropathy

A
  • general deterioration of the nervous system throughout the body
  • complications include the development of nonhealing ulcers of the feet, gastric paresis and erectile dysfunction.
162
Q

Classifications of Diabetic neuropathy

A
  • focal neuropathy or mononeuropathy: involves a single nerve or a group of nerves, most frequently cranial nerves III (oculomotor) and VI (abducens), resulting in diplopia.
  • Sensory or peripheral neuropathy: Affects distal portion of nerves, most frequently in the lower extremities.
  • autonomic neuropatju: symptoms vary according to the organ system involved.
  • Cardiovascular: cardiac denervation syndrome (heart rate does not respond to changes in oxygenation needs) and orthostatic hypotension occur.
  • Pupillary: Pupil does not dilate in response to decreased light.
  • gastric: decreased gastric emptying (gastroparesis)
  • urinary: neurogenic bladder
  • skin: decreased sweating
  • adrenal: hypoglycemic unawareness
  • reproductive: impotence (male), painful intercourse (female)
163
Q

diabetic neuropathy assessment

A
  • findings depend on the classification.
  • paresthesias
  • decreased or absent reflexes
  • decreased sensation to vibration or light touch
  • pain, aching, and burning in the lower extremities.
  • poor peripheral pulses
  • skin breakdown and signs of infection
  • weakness or loss of sensation in cranial nerves III (oculomotor), IV (trochlear), V (trigeminal), and VI (abducens)
  • dizziness and postural hypotension
  • nausea and vomiting
  • diarrhea or constipation
  • incontinence
  • dyspareunia
  • impotence
  • hypoglycemic unawareness.
164
Q

diabetic neuropathy interventions

A
  • early prevention measures incluse the control of hypertension and blood glucose levels.
  • careful foot care is required to prevent trauma.
  • administer medications as prescribed for pain relief.
  • initiate bladder training programs
  • instruct in the use of estrogen-containing lubricants for women with dyspareunia
  • prepare the male client with impotence for penile injections or other possible treatment options as prescribed.
  • prepare for surgical decompression of compression lesions related to the cranial nerves as prescribed.
165
Q

Preventative Foot care Measures

A
166
Q

DPP-4 Inhibitors

  • Alogliptin (Nesina)
  • Linagliptin (Tradjenta)
  • Sacaglyptin (Onglyza)
    • Sitagliptin (Januvia)
A
  • DPP-4 is an enzyme that breaks down the natural gut hormones (GLP-1 and GIP). DPP-4 inhibitors are oral agents that prevent the enzyme DPP-4 from breaking down the natural gut hormones, which then allows these natural substances to work with insulin to lower glucagon secretion from the pancreas, leading to reduced liver glucose production. These oral drugs also reduce blood glucose levels by delaying gastric emptying, slowing the rate of nutrient absorption in the blood and reducing food intake.
  • Teach patients the signs and symptoms od hypoglycemia (hunger, headache, tremors, sweating, confusion) because these drugs lower blood glucose levels even when hyperglycemia is not present.
  • Instruct patients to be alert and observe for rash or other sign of allergic reaction because this class of drugs is associated with a moderate incidence of drug allergy.
  • teach patients to report persistent abdominal pain and nausea to the PHCP because these drugs increase the risk for pancreatitis.
167
Q

Amylin Analogs

Pramlintide (Symlin)

A
  • These drugs are similar to amylin, a naturally occuring hormone from beta cells in the pancreas that is co-secreted with insulin and lowers blood glucose levels by decreasing endogenous glucagon, delaying gastric emptying, and triggering satiety.
  • Teach the patient signs and symptoms of hypoglyemia (tremors, hunger, headache, sweating, confusion) because these drugs lower glucose even when hyperglycemia is not present.
  • Instruct the patients how to inject themselves because these drugs are only available as subcutaneous formulations.
  • Teach patients to inspect injection sites for redness, warmth, or hard nodules because injection site reactions are common.
  • Warn patients that nausea and vomiting are common side effects of this drug class because knowing the expected side effects decreases anxiety when they appear.
168
Q

Sodium-Glucose Contransport Inhibitors

Canagliflozin (Invokana)

Dapagliflozin (Farxiga)

Empagliflozin (Jardiance)

A
  • These oral drugs lower blood glucose levels by preventing kidney reabsorption of glucose and sodium that was filtered from the blood into the urine. This filtered glucose is excreted in the urine rather than moved back into the blood.
  • Teach patients the signs and symptoms of hypoglcemia because these drugs lower blood glucose levels even when they are not elevated.
  • Teach patients the signs and symptoms of dehydration (increased thirst, light headedness, dry mouth and mucous membranes, orthostatic hypotension) because these drugs increase sodium excretion.
  • Teach patients the signs and symptoms of of urinary tract infection (frequency, pain and burning on urination, foul urine odor) because the increased glucose in the urinary tract predisposes to infection.
  • Instruct women to be alert for genital itching and vaginal discharge because these drugs increase the risk for genital yeast infection.
169
Q

Combination Products

A
  • Many fixed combinations of oral drugs are available. Each ingredient has the sam mechanism of action and nursing implications as the parent drug class. When a drug that has the side effect of hypoglycemia is combined with a drug that does not alone produce hypoglycemia, the development of hypoglycemia is still very much a risk for the combination agent.
170
Q

Albiglutide (Tanzeum), extended-release exenatide (Bydureon), and dulaglutide (Trulicity)

A

are administered subcutaneously once weekly.

171
Q

DPP-4 inhibitors and the incretin mimetics may be associated with an increased risk for pancreatitis. Warn patients taking these drugs to

A

immediately report signs of jaundice; sudden onset of intense abdominal pain that radiates to the back, left flank, or left shoulder; or gray-blue discoloration of the abdomen or periumbilical area to the PHCP.

172
Q

Do not mix pramlintide and insulin in the same syringe

A

because the pH of the two drugs is not compatible.

173
Q

The FDA has issued a warning that the use of empagliflozin

A

increases the risk for acute kidney injury and inpaired renal function.

174
Q

Do not mix any other insulin type

A

with insulin glargine (Lantus), insulin detemir (Levemir) or any of the premixed insulin formulations such as Humalog MIx 75/25.

175
Q

Rapid-Acting Insulin Analogs

A
  • Insulin aspart (novolog)
  • Human lispro injection (Humalog)
  • “15 mins feels like an hour during 3 rapid responses.”
  • onset 15 minutes
  • peak 1 hr
  • duration 3 hrs
176
Q

Short Acting Insulin

A
  • regular humulin (humulin R)
  • “Short staffed nurses went from 30 patients 2 eight patients.”
  • onset 30 minutes
  • peak 2 hours
  • duration 8 hours
177
Q

Intermediate Acting Insulin

A
  • NPH , Humulin N and Novolin N.
  • “Nurses play hero 2 eight 16 year olds”
  • onset 2 hrs
  • peak 8 hrs
  • duration 16 hrs
178
Q

Long Acting Insulin

A
  • Insulin glargine (Lantus)
  • Insulin detemir (Levemir)
  • “The two long nursing shifts never peaked but lasted 24 hours.”
  • Onset 2 hrs
  • Peak none
  • Duration 24 hrs
179
Q

Because of the potenial for alcohol-induced delayed hypoglycemia,

A

instruct the patient with DM to ingest alcohol only with or shortly after meals.

180
Q

Subcutaneous Insulin Administrations

with vial and syringe

A
  • wash your hands
  • inspect the bottle for the type of insulin and the expiration date.
  • Gently roll the bottle of the intermediate-acting insulin in the palms of your hands to mix the insulin.
  • Clean the rubber stopper with an alcohol swab.
  • remove the needle cover and pull back the plunger to draw air into the syringe. The amount of air should be equal to the insulin dose

Nurs 206 (4 decks)

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