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Med Surg Nursing > Nursing Assessment of the Endocrine System (Test 2) > Flashcards

Nursing Assessment of the Endocrine System (Test 2) Flashcards

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1
Q

What are lipid soluble hormones also known as?

A

Steroid hormones.

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2
Q

Classifications and functions: lipid soluble hormones- ?

A

Adrenal cortex, sex glands, thyroid

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3
Q

What are water soluble hormones also known as?

A

Protein base.

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4
Q

Classifications and functions- water soluble hormones?

A

All other hormones

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5
Q

What is the third group of hormones?

A

Reproduction/stress/metabolism/growth

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6
Q

Hormone transport

A

Lipid soluble hormones are bound to plasma proteins for transport

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7
Q

What are the 2 types of hormone receptors?

A

Steroid “ “ and Protein “ “

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8
Q

Where is the steroid hormone receptor located?

A

Inside the cell

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9
Q

What does the protein hormone receptor do?

A

Hormone attaches to receptor on cell membrane “first messenger” which stimulates the production of a “second messenger” that activates intracellular activity

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10
Q

What is simple feedback?

A

Gland increase/decreases the secretion of a hormone based on feedback (ex: insulin/glucose)

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11
Q

What is positive feedback?

A

Increases target organ action beyond normal

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12
Q

What is complex feedback?

A

Communication among several glands to regulate hormone secretion (ex: thyroid)

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13
Q

What is nervous system control?

A

Initiated by CNS and implemented by sympathetic nervous system (ex: stress/catecholamines)

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14
Q

What are rhythms?

A

Hormones fluctuate in predictable patterns during 24 hour period (ex: cortisol)

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15
Q

What hormones types make up the hypothalamus?

A

Inhibiting and releasing hormones

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16
Q

What do inhibiting hormones do?

A

Inhibit the secretion of hormones from the anterior pituitary.

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17
Q

What are examples of inhibiting hormone?

A

Somatostatin; prolactin-inhibiting hormone

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18
Q

What do releasing hormones do?

A

Stimulates the secretion of hormones from the anterior pituitary.

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19
Q

What are examples of releasing hormones?

A

Corticotropin-releasing hormone; growth hormone-releasing factor

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20
Q

What hormones are in the anterior pituitary?

A

Tropic hormones, growth hormone, prolactin

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21
Q

What do tropic hormones do?

A

Control the secretion of hormones by other glands

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22
Q

What are examples of tropic hormones?

A

Thyroid-stimulating hormone (TSH); adrenocorticotropic hormone (ACTH); follicle-stimulating hormone (FSH)

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23
Q

What hormones are in the posterior pituitary?

A

Antidiuretic hormone (ADH), and oxytocin

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24
Q

What does ADH do? What is this stimulated by?

A

Regulates fluid volume by stimulating reabsorption of water in the renal tubules. Stimulated by increased plasma osmolality.

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25
Q

ADH also is…?

A

A potent vasoconstrictor.

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26
Q

What does oxytocin do?

A

Stimulates milk secretion and uterine contraction.

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27
Q

What hormones are in the thyroid gland?

A

Thyroxine (T4), triiodothyronine (T3), and calcitonin

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28
Q

What do T4 and T3 do?

A

Regulate metabolic rate of all cells and processes of cell growth

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29
Q

What do low levels of T4 and T3 cause?

A

Stimulate pituitary gland to release TSH

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30
Q

What does calcitonin do?

A

Inhibits calcium loss from bone, increases calcium storage in bone, and increase renal excretion of calcium and phosphorus

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31
Q

What hormone is in the parathyroid gland?

A

Parathyroid hormone (PTH)

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32
Q

What does PTH stimulate?

A

Stimulates bone desorption and inhibits bone formation; stimulates renal conversion of vitamin D

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33
Q

What does PTH increase?

A

Calcium reabsorption and phosphate excretion in kidneys

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34
Q

What 2 things make up the adrenal gland?

A

Adrenal medulla and adrenal cortex

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35
Q

What hormones are in the adrenal medulla?

A

Catecholamines (epinephrine, norepinephrine, dopamine); stress response

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36
Q

What hormones are in the adrenal cortex?

A

Cortisol, aldosterone, adrenal androgens

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37
Q

What does cortisol do?

A

Regulates blood glucose concentration, anti-inflammatory action, promotes metabolism

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38
Q

What does aldosterone do?

A

Maintains extracellular fluid volume, promotes renal reabsorption of sodium and excretion of potassium

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39
Q

What do adrenal androgens?

A

Promotes masculinization in men and growth and sexual activity in women

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40
Q

What hormones are in the pancreas?

A

Glucagon and insulin

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41
Q

What does glucagon do?

A

Increases blood glucose by stimulating glycogenesis, glycogenesis, and ketogenesis

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42
Q

What is insulin stimulated by?

A

Increased blood glucose level

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43
Q

What does insulin facilitate?

A

Glucose transport into cells

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44
Q

Normal aging results in what 4 things?

A

Decreased hormone production and secretion, altered hormone metabolism and biologic activity, decreased responsiveness of target tissue to hormones, alterations in circadian rhythms

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45
Q

*Changes of aging often mimic what?

A

The manifestation of endocrine disorders

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46
Q

What system is less developed at birth than any other system in the body?

A

Endocrine

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47
Q

Hormonal control of many body functions is lacking until when?

A

12-18 months

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48
Q

Infants may manifest what as a result of lack of hormonal development?

A

Imbalances in fluids, electrolytes, amino acids, glucose, and other trace substances as a result of this lack of development

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49
Q

What things are important to know about past health history?

A

Previous or current endocrine abnormalities, abnormal patterns of growth and development

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50
Q

What medications are important to know they are taking?

A

Hormone replacement, insulin, corticosteroids

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51
Q

What is important to know when gathering info about surgery/other treatment?

A

Neck or brain involvement of increased importance

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52
Q

If kids aren’t getting good growth and weigh percentile numbers, it leads us to what?

A

Endocrine problems

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53
Q

ADH is released by what?

A

The pituitary gland

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54
Q

Where is ADH made?

A

Hypothalamus

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55
Q

What does ADH prevent?

A

The production of dilute urine

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56
Q

What is something to remember about COPD patients when gathering medication info?

A

A lot are on long term steroids

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57
Q

In what assessments may you find abnormalities when assessing the system of a person with endocrine problems?

A

Vital signs, height and weight, mental-emotional status, integument, head, neck, thorax, abdomen, extremities, genitalia (esp. hair distribution)

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58
Q

Common assessment abnormalities?

A

Changes in skin texture, exophthalmos, moon face, polyuria/polydipsia, goiter, changes in weight, lethargy, thermoregulation

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59
Q

What are the changes in skin texture caused by?

A

Hypo/hyperthyroidism

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60
Q

What is exophthalmos caused by?

A

Hyperthyroidism

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61
Q

What is moon face caused by?

A

Cushing syndrome

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62
Q

What is polyuria/polydipsia caused by?

A

DM, DI

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63
Q

What are goiters caused by?

A

Hypo/hyperthyroidism

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64
Q

What are changes in weight caused by?

A

Hypo/hyperthyroidism; DM

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65
Q

What is lethargy caused by?

A

Hypothyroidism

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66
Q

What are thermoregulation problems caused by?

A

Hypo/hyperthyroidism

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67
Q

What are MRIs used for?

A

Used to find tumors?, measure tumors, and evaluate for metastasis

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68
Q

What should you inform the patient about MRIs?

A

That the test is painless and noninvasive, and they will need to lie still

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69
Q

What is a computed tomography (CT scan) used for?

A

To identify tumors or cysts

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70
Q

What do you need to tell the patient about the CT scan?

A

They will need to lie still

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71
Q

What should you do if an IV contrast will be used?

A

Check for iodine allergy

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72
Q

Questions to ask for MRIs?

A

Are you claustrophobic? Do you have on any jewelry? Do you have metal implants or staples? Etc.

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73
Q

What do ultrasounds do?

A

Evaluates thyroid nodules to determine if they are cysts or tumors

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74
Q

What do you need to explain about ultrasounds?

A

Explain the painless procedure will take about 15 minutes

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75
Q

Do you need to fast or be sedated for ultrasounds?

A

No

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76
Q

What is the most sensitive diagnostic test for evaluating thyroid dysfunction?

A

TSH

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77
Q

What is the normal range of TSH?

A

0.4-4.2 microunits/milliliter

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78
Q

What should you explain about the TSH test?

A

Explain blood draw procedure to patient

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79
Q

What is a T4 test used for?

A

To evaluate thyroid function and monitoring thyroid function

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80
Q

What is the normal range of T4?

A

4.6-11.0 micrograms/deciliter

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81
Q

What should you explain about the T4 test?

A

Explain blood draw procedure to patient

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82
Q

What is a T3 test helpful in?

A

Diagnosing hyperthyroidism in T4 levels are normal

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83
Q

What is the normal T3 range for ages 20-50?

A

70-204 nanograms/deciliter

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84
Q

What is the normal T3 range for ages 50 plus?

A

40-181 nonograms/deciliter

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85
Q

What should you explain to the patient about T3 tests?

A

Explain blood draw procedure to patient

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86
Q

What is a thyroid scan used for?

A

To evaluate thyroid nodules

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87
Q

What is given during a thyroid scan?

A

Radioactive isotopes are given orally or IV thyroid is scanned

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88
Q

What does a normal thyroid look like in a scan?

A

Homogenous pattern

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89
Q

What do benign nodules look like in a scan?

A

Appear as warm spots

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90
Q

What do malignant nodules look like in a scan?

A

Appear as cold spots (meaning they won’t absorb meds)

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91
Q

What should you check before doing a thyroid scan?

A

Check for iodine allergy

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92
Q

What should patients not have before a thyroid scan?

A

Shouldn’t have supplemental iodine for several weeks before

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93
Q

For what tests should you minimize salt intake (iodine)?

A

Thyroid scan and radioactive iodine uptake (RAIU)

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94
Q

What do RAIUs provide?

A

Direct measurement of thyroid activity

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95
Q

What is the patient given for a RAIU?

A

Radioactive iodine orally or IV

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96
Q

When is the thyroid scanned during a RAIU?

A

At several time intervals

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97
Q

What should you check for before a RAIU?

A

Check for iodine allergy

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98
Q

What should be avoided before a RAIU?

A

No supplemental iodine for several weeks before the test

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99
Q

What can interfere with RAIU results?

A

Thyroid medications

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100
Q

Which is more common, RAIU or blood draws?

A

Blood draws, RAIUs aren’t used much

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101
Q

What does cortisol evaluate?

A

Adrenal cortex function

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102
Q

What is the normal range of cortisol at 8am?

A

5-23 micrograms/deciliter

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103
Q

What is the normal range of cortisol at 4pm?

A

3-16 micrograms/deciliter

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104
Q

What time is the most accurate cortisol test collected?

A

In the morning

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105
Q

What is important to remember to write on the sample?

A

Mark sample time of specimen vial

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106
Q

What does fasting blood glucose measure?

A

Measures circulating glucose level

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107
Q

What is the normal range for a fasting blood glucose test?

A

70-99 milligrams/deciliter

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108
Q

How long should they fast for a FBG test?

A

4-8 hours

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109
Q

Is water intake allowed for a FBG test?

A

Yes

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110
Q

What should you ensure when giving a FBG test?

A

Ensure no dextrose in IV solution

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111
Q

What is a Glycosylated Hemoglobin test also known as?

A

HGB A 1 C

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112
Q

What does Hgb A1C measure?

A

Glucose control during previous 3 months

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113
Q

What is the normal range for a Hgb A1C test?

A

4-6%

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114
Q

Is fasting necessary for an Hgb A1C?

A

No

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115
Q

What does a ketone test measure?

A

Amount of acetone secreted in urine as result of incomplete fat metabolism

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116
Q

What does a positive ketone result indicate?

A

Can indicate lack of insulin and diabetic acidosis

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117
Q

How is a ketone test done?

A

Completed with freshly voided urine sample

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118
Q

What other test is a ketone test often done with?

A

Glucose test

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119
Q

When do we usually see ketones?

A

In diabetics without insulin

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120
Q

How else can ketones be tested for?

A

Blood

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121
Q

Theories link cause of DM to single/combo of what factors?

A

Genetic, autoimmune, environmental, viral

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122
Q

What are the two most common types of DM?

A

Type 1 and 2

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123
Q

What other types of DM are there?

A

Gestational, prediabetes, secondary diabetes

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124
Q

Normal insulin metabolism is produced by what?

A

The beta cells (weird B looking letter)

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125
Q

What are the beta cells made of?

A

Islets of Langerhans (pancreas)

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126
Q

How is normal insulin released?

A

Released continuously into the bloodstream in small increments with larger amounts released after food intake

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127
Q

What does normal insulin stabilize glucose range to? (Aka what’s the ideal glucose range?)

A

70-120 mg/dl

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128
Q

What is the average daily secretion of normal insulin?

A

0.6 units/kg body weight

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129
Q

What does insulin promote? What does this cause?

A

Glucose transport from bloodstream across cell membrane to cytoplasm of cell. Causes decrease of glucose in the bloodstream.

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130
Q

What does increased insulin after a meal stimulate?

A

Storage of glucose as glycogen in liver and muscle

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131
Q

What does increased insulin after a meal inhibit?

A

Gluconeogenesis

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132
Q

What does increased insulin after a meal enhance?

A

Fat disposition

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133
Q

What does increased insulin after a meal also increase?

A

Protein synthesis

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134
Q

What are insulin dependent tissue examples?

A

Skeletal muscles and adipose tissues

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135
Q

What are non insulin dependent tissue examples?

A

Brain, liver, blood cells

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136
Q

What is the definition of non insulin dependent tissues?

A

Do not depend directly on insulin for glucose support

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137
Q

What do counterregulatory hormones oppose?

A

Oppose effects of insulin

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138
Q

What do counterregulatory hormones increase?

A

Blood glucose levels

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139
Q

What do counter regulatory hormones provide?

A

A regulated release of glucose for energy

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140
Q

What do counter regulatory hormones help?

A

Help maintain normal blood glucose levels

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141
Q

What are examples of counterregulatory hormones?

A

Glucagon, epinephrine, growth hormone, cortisol

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142
Q

What is the incidence rate of DM?

A

15 per 100,000 people in North America

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143
Q

What are the peak ages of onset for females and males?

A

Between 10 and 12 for girls, and 12 to 14 for boys (puberty)

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144
Q

What factor increases the risk for DM?

A

If the child or adolescent has a first degree relative or identical twin with the disease, but it’s not for sure going to happen though

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145
Q

What type of diabetes may show a familial tendency?

A

Type 1

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146
Q

Theories for DM disease development include?

A

Genetic components, environmental influences such as viruses, and an autoimmune response that causes the destruction of insulin-secreting cells of the pancreas in the islets of Langerhans

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147
Q

What is type 1 DM formerly known as?

A

Juvenile onset or insulin dependent diabetes

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148
Q

What age bracket does type 1 usually occur in?

A

Most often occurs in people under 30 years of age

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149
Q

When is the peak onset of type 1?

A

10-14

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150
Q

What do the body’s T cells do?

A

Attack and destroy beta cells which are the source of insulin

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151
Q

What do antibodies to the islet cells cause?

A

80-90% reduction of normal beta cell function leads to hyperglycemia and diagnosis of type 1 DM

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152
Q

What is the onset of disease like for type 1?

A

Long preclinical period

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153
Q

What are present before symptoms occur for type 1?

A

Antibodies present for months to years before symptoms occur

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154
Q

When do manifestations develop for type 1?

A

When pancreas can no longer produce insulin

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155
Q

After manifestations of type 1, what happens?

A

Rapid onset of symptoms and present as ER with ketoacidosis

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156
Q

What does type 1 history include?

A

Recent, sudden weight loss

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157
Q

What are classic symptoms of type 1?

A

Polydipsia, polyuria, polyphagia

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158
Q

What is polydipsia?

A

Excessive thirst

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159
Q

What is polyphagia?

A

Excessive hunger

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160
Q

Does eating more stop the weight loss of type 1 onset?

A

No, even though you eat a lot, you are still losing weight (15-20 pounds)

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161
Q

What does type 1 diabetes require?

A

Exogenous insulin to sustain life

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162
Q

When does DKA occur?

A

Occurs in absence of exogenous insulin (absolutely no insulin)

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163
Q

Is DKA life threatening?

A

Yes

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164
Q

What does DKA result in?

A

Metabolic acidosis

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165
Q

When is prediabetes also known as?

A

Impaired glucose tolerance (IGT) or impaired fasting glucose (IFG)

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166
Q

Fasting blood glucose levels

A

Higher than normal (over 100 mg/dl, but under 126 mg/dl)

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167
Q

Impaired glucose tolerance 2 hour plasma glucose

A

Higher than normal (between 140 and 199 mg/dl)

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168
Q

Why is pre diabetes not just diabetes?

A

Not high enough for diabetes diagnosis

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169
Q

What does having pre diabetes increase your risk for?

A

Type 2

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170
Q

If no preventative measure is taken about the pre diabetes, what usually happens?

A

Develop diabetes within 10 years

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171
Q

Does damage occur with pre diabetes?

A

Long term damage already occurring to heart and blood vessels

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172
Q

How does pre diabetes appear?

A

Usually present with no symptoms

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173
Q

What do you need to do with a patient that has pre diabetes?

A

Must watch for diabetes symptoms

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174
Q

What is the most prevalent type of diabetes?

A

Type 2

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175
Q

What is the percentage of patients with type 2 of all diabetes types?

A

Over 90%

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176
Q

What age bracket does type 2 usually occur in?

A

Over 35

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177
Q

How many patients with type 2 are overweight?

A

80-90%

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178
Q

Type 2 prevalence increases with…?

A

Age

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179
Q

What type of basis does type 2 have?

A

Genetic basis

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180
Q

What ethnic populations have an increased rate of type 2?

A

African Americans, Asian Americans, Hispanic Americans, and Native Americans

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181
Q

What ethnic populations have the highest rate of diabetes in the world?

A

Native Americans and Alaskan Natives

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182
Q

What are HCPs finding more and more of?

A

Children with type 2 diabetes, a disease usually diagnosed in adults aged 40 years and older

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183
Q

What may be major contributors to the increase in type 2 diabetes during childhood or adolescence?

A

The epidemics of obesity and the low level of physical activity among young people

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184
Q

Why is type 2 difficult in children?

A

It can go undiagnosed for a long time and children often have mild/no symptoms

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185
Q

In type 2 what does the pancreas do?

A

Continues to produce some endogenous insulin

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186
Q

The insulin produced in a patient with type 2 is…?

A

Is either insufficient or poorly utilized by tissues

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187
Q

What is the most powerful risk factor for type 2?

A

Obesity (abdominal/visceral)

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188
Q

???What genetic mutations are related to type 2?

A

Lead to insulin resistance and increased risk for obesity

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189
Q

What are the 4 major metabolic abnormalities r/t type 2?

A

Insulin resistance, pancreas’ decreased ability to produce insulin, inappropriate glucose production from liver, and alteration in production of hormones and adipokines

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190
Q

What happens in insulin resistance?

A

Body tissues don’t respond to insulin and insulin receptors are either unresponsive or insufficient in number

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191
Q

What happens when pancreas has decreased ability to produce insulin?

A

Beta cells are fatigued from compensating and beta cells mass lost

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192
Q

What happens from inappropriate glucose production from liver?

A

Liver’s response of regulating release of glucose is haphazard, and it is not considered a primary factor in development in type 2

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193
Q

What does alteration in production of hormones and adipokines do?

A

Play a role in glucose and fat metabolism and contribute to pathophysiology of type 2; two main adipokines- adiponectin and leptin

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194
Q

What kind of onset is type 2?

A

Gradual onset

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195
Q

A person may go with with undetected..?

A

Hyperglycemia

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196
Q

What from hyperglycemia may become severe?

A

Osmotic fluid/electrolyte loss or hyperosmolar coma

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197
Q

What is probably the number one way people get diagnosed as type 2?

A

Improper wound healing

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198
Q

What are clinical manifestations of type 2?

A

Nonspecific conditions (may have classic symptoms of type 1), fatigue, recurrent infections, recurrent vaginal yeast or candida infections, prolonged wound healing, visual changes

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199
Q

When does gestational diabetes develop?

A

During pregnancy

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200
Q

When is gestational diabetes detected?

A

At 24 to 28 weeks

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201
Q

Usually normal glucose levels at…?

A

6 weeks postpartum

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202
Q

What does GD increase risk for?

A

Increased risk for C section, perinatal (baby) death, and neonatal complications

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203
Q

Why do these increased risks exist?

A

Because these babies grow at much faster rates and causes those risks

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204
Q

After having GD, it increases risk for what?

A

Risk for developing type 2 in 5 to 10 years

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205
Q

What is therapy for GD?

A

1st nutritional, 2nd insulin

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206
Q

What puts you at higher risk for GD?

A

Excessive weight gain and family diabetes history

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207
Q

Secondary diabetes results from what?

A

Another medical condition: Cushing syndrome, hyperthyroidism, pancreatitis, parenteral nutrition, cystic fibrosis, hematochromatosis, corticosteroids (Prednisone), thiazides, phenytoin (Dilantin, which is a long term antiseizure)

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208
Q

When does secondary diabetes resolve?

A

Usually resolves when underlying condition is treated

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209
Q

Diagnosing diabetes- Hgb A1C level

A

over 6.5%

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210
Q

Diagnosing diabetes- fasting plasma glucose level

A

Over 126 mg/dl

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211
Q

Diagnosing diabetes- OGTT 2 hour plasma glucose level

A

200 mg/dl

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212
Q

Diagnosing diabetes- random plasma glucose level

A

Over 200 mg/dl in a patient with classic symptoms of hyperglycemia

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213
Q

Nursing history type of assessment for DM patients?

A

Past health history (viral infections, medications (esp. steroids, antibiotics, etc.), recent surgery), positive health history, obesity

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214
Q

If a patient with DM is obese, what will the doctor probably do?

A

Probably start yearly fasting glucose checks and more often if they have a family history

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215
Q

Stress and sugar relationship?

A

Stress of illness or injury makes sugar levels increase, if you keep it between 70-120 mg/dl it helps wound healing

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216
Q

What do you say if a patient asks why they are getting fingersticks and they’re not diabetic?

A

Stress of illness or injury makes sugar levels increase, if you keep it between 70-120 mg/dl it helps wound healing

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217
Q

What do we assess during physical assessment for DM patients?

A

Weight loss, thirst, hunger, poor healing, Kussmaul respirations (rapid breathing and a sign of DKA)

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218
Q

Nursing diagnoses for DM?

A

Ineffective therapeutic regimen management, risk for injury, risk for infection, powerlessness, imbalanced nutrition: more than body requirements

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219
Q

What is important to remember about DM as a nurse?

A

Managing diabetes takes a lot of discipline, so put yourself in your shoes before you judge

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220
Q

What are overall goal examples during the planning period for DM?

A

Active patient participation (and family and SO’s if applicable), few or no episodes of acute hyperglycemic emergencies or hypoglycemia, maintain normal blood glucose levels, prevent or delay chronic complication, lifestyle adjustments with minimal stress

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221
Q

Health promotion for implementation phase for DM?

A

Identify those at risk, routine screening for overweight adults over age 45 (FPG is preferred method in clinical settings

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222
Q

Acute intervention for implementation phase for DM?

A

Hypoglycemia, DKA, Hyperosmolar hyperglycemic nonketotic syndrome

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223
Q

Acute intervention for stress of illness and injury for DM?

A

Increase blood glucose level, continue regular meal plan, increase intake of noncaloric fluids, continue taking oral agents and insulin, frequent monitoring of blood glucose at least every 4 hours and ketone testing if glucose is over 240 mg/dl

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224
Q

Patients undergoing surgery or radiologic procedures requiring contrast medium should…?

A

Hold their metformin (glucophage) day of surgery and 48 hours, (begun after serum creatinine has been checked and is normal???)

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225
Q

What is the overall goal of ambulatory and home care?

A

To enable patient or caregiver to reach an optimal level of independence

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226
Q

When implementing insulin therapy and oral agents in ambulatory and home care what do you need to do?

A

Provide education of proper administration, adjustment, and side effects; assessment of patient’s response to therapy

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227
Q

When implementing personal hygiene in ambulatory or home care what do you need to do?

A

Regular bathing with emphasis on foot care, and daily brushing/flossing (dentist should be informed about diabetes diagnosis*)

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228
Q

What is important about medical identification and travel card for DM patients?

A

Must carry id indicating diagnosis of diabetes

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229
Q

What is important about patient and family teaching for DM?

A

Educate on disease process, physical activity, medications, monitoring blood glucose, diet, resources; enable patient to become most active participant in his/her care

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230
Q

What is exogenous insulin?

A

Insulin from an outside source

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231
Q

Who may take exogenous insulin?

A

Required for type 1, prescribed for type 2 who can’t control blood glucose by other means

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232
Q

What is the only type of insulin used today?

A

Human insulin

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233
Q

How is human insulin prepared?

A

Prepared through genetic engineering- common bacteria (Escherichia coli) and yeast cells using recombinant DNA technology

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234
Q

Insulins differ in regard to what 4 things?

A

Onset, peak, action, and duration

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235
Q

What are insulins characterized as?

A

Rapid, short, intermediate, and long acting

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236
Q

Different types in insulin may be used for…?

A

Combination therapy

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237
Q

Examples of rapid acting insulin?

A

Lispro (Humalog), Aspart (Novolog), and glulisine (Apirdra)

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238
Q

Examples of short acting insulin?

A

Regular

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239
Q

Examples of intermediate acting insulin?

A

NPH (cloudy)

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240
Q

Examples of long acting insulin?

A

Glargine (Lantus), detemir (Levemir)

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241
Q

What is a basal-bolus regimen?

A

Closely mimics endogenous insulin production

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242
Q

What is given for a basal-bolus?

A

Long acting (basal) once a day and rapid/short acting (bolus) before meals

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243
Q

How are rapid acting (bolus) prepared/onset?

A

Injected 0-15 minutes before meals, onset of action 15 minutes

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244
Q

How are short acting (bolus) prepared/onset?

A

Injected 30-45 minutes before meal, onset of action 30-60 minutes

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245
Q

Do patients have to wait to eat after getting insulin?

A

No????

246
Q

How are long acting (basal) prepared/peak action?

A

Injected once a day at bedtime or morning, no peak action

247
Q

What insulin cannot be mixed with any other insulin or solution?

A

Long acting (basal)

248
Q

How may insulin be stored?

A

In use vials may be left at room temp up to 4 weeks, Lantus only for 28 days, extra insulin should be refrigerated

249
Q

How should insulin not be stored?

A

Do not heat/freeze, avoid exposure to direct sunlight

250
Q

Study graph on page 13

A

Study graph on page 13

251
Q

Are oral agents insulin?

A

No!

252
Q

What are oral agents?

A

Work to improve mechanisms by which insulin and glucose are produced and used by the body

253
Q

What do oral agents work on?

A

Insulin resistance, decreased insulin production, increased hepatic glucose production

254
Q

What are examples of oral agents?

A

Sulfonylureas, meglitinides, biguanides, alpha-glucosidase inhibitors thiazolidinediones

255
Q

What do sulfonylureas do to insulin production?

A

Increase production from pancreas

256
Q

What do Sulfonylureas do to chance of prolonged hypoglycemia?

A

Decrease chance

257
Q

How many experience decreased effectiveness after prolonged use of Sulfonylureas?

A

10%

258
Q

What are examples of Sulfonylureas?

A

glipizide (glucotrol), glimepiride (amaryl)

259
Q

What do Meglitinides do to insulin production?

A

Increase production from pancreas

260
Q

When are Meglitinides taken?

A

30 minutes before each meal up to time of meal

261
Q

When should Meglitinides not be taken?

A

If meal is skipped

262
Q

What are examples of Meglitinides?

A

Repaglinide (Prandin), Nateglinide (Starlix)

263
Q

What do Biguanides do to glucose production?

A

Reduce glucose production by liver

264
Q

What do Biguanides do to insulin sensitivity?

A

Enhance it at tissues

265
Q

What do Biguanides do to glucose transport?

A

Improve glucose transport into cells

266
Q

Why are Biguanides popular?

A

Do not promote weight gain

267
Q

What is an example of Biguanides?

A

Metformin (Glucophage)

268
Q

What are Alpha-Glucosidase Inhibitors also called?

A

“Starch blockers”

269
Q

What do AGIs do?

A

Slow down absorption of carbohydrates in small intestines

270
Q

What is an example of AGI?

A

Acarbose (Precose)

271
Q

What are Thiazolidinediones most effective with?

A

In those with insulin resistance

272
Q

What do Thiazolidinediones improve?

A

Improves insulin sensitivity, transport, and utilization at target tissues

273
Q

What are examples of Thiazolidinediones?

A

Pioglitazone (Actos), Rosiglitazone (Avandia)

274
Q

What is Amylin analog secreted by?

A

Hormone secreted by beta cells of pancreas

275
Q

What is Amylin analog cosecreted with?

A

Insulin

276
Q

What is Amylin analog indicated for?

A

Type 1 and 2

277
Q

How is Amylin analog administered?

A

Subq in thigh or abdomen

278
Q

What does Amylin analog do to GI related things?

A

Slows gastric emptying, reduces postprandial glucagon secretion, increases satiety (fullness)

279
Q

What is an example of Amylin analog?

A

Pramlintide (Symlin)

280
Q

What does post prandial mean?

A

After meals

281
Q

What is Incretin mimetic?

A

Synthetic peptide

282
Q

What does Incretin mimetic stimulate?

A

Release of insulin from beta cells

283
Q

How is Incretin mimetic administered?

A

Subq injection

284
Q

What does Incretin mimetic suppress?

A

Glucagon secretion

285
Q

What does Incretin mimetic reduce?

A

Food intake

286
Q

What does Incretin mimetic slow?

A

Gastric emptying

287
Q

Can Incretin mimetic be used with insulin?

A

No

288
Q

What is an example of Incretin mimetic?

A

Byetta

289
Q

What happened to a lot of people while taking Incretin mimetic?

A

Lost weight

290
Q

What do Beta Adrenergic blockers mask?

A

Symptoms of hypoglycemia

291
Q

What do Beta Adrenergic blockers prolong?

A

Hypoglycemic effects of insulin

292
Q

What can Thiazide/loop diuretics do?

A

Potentiate hyperglycemia by inducing potassium loss

293
Q

What is an example of Thiazide/loop diuretics?

A

Lasix

294
Q

What is pancreas transplantation used for?

A

Patients with type 1 who also have end stage renal disease and had/plan to have a kidney transplant

295
Q

How are pancreas transplants usually done?

A

With kidney transplants, alone is rare

296
Q

What does a pancreas transplant eliminate the need for? What else can it also eliminate?

A

Exogenous insulin; can eliminate hypoglycemia and hyperglycemia

297
Q

What is the cornerstone of care for a diabetes patient?

A

Nutritional therapy

298
Q

What is the most challenging part of therapy for many people?

A

Nutritional therapy

299
Q

Who is recommended to be part of a diabetic’s team?

A

Recommended that diabetes nurse educator and registered dietitian with diabetes experience be members of team

300
Q

What do American Diabetes Association (ADA) guidelines indicate?

A

That within context of an overall healthy eating plan, person with diabetes can eat same food as person who doesn’t have diabetes

301
Q

What is the ADA’s overall goal?

A

Assist people in making changes in nutrition and exercise habits that will lead to improved metabolic control

302
Q

What is type 1’s meal plan?

A

Based on individual’s usual food intake and is balanced with insulin and exercise patterns

303
Q

Type 1 insulin regimen?

A

Managed day to day

304
Q

What is type 2’s emphasis on?

A

Based on achieving glucose, lipid, and blood pressure goals

305
Q

What is a focus on for type 2’s?

A

Calorie reduction

306
Q

What is essential for a diabetic diet?

A

Nutrient balance

307
Q

What should be balanced for a type 2?

A

Nutritional energy intake should be balanced with energy output

308
Q

How much should carbohydrates and monosaturated fats provide of total energy intake?

A

45-65%

309
Q

What kind of diet is not recommended for diabetics?

A

Decreased carb diet

310
Q

What does the Glycemic Index term used to describe?

A

Rise in blood glucose levels after consuming carb containing food

311
Q

What should be considered when formulating a meal plan?

A

The GI

312
Q

What diet systems are based on the GI?

A

Nutrisystem, weight watcher’s

313
Q

How much fat should make up a meal plan’s total calories for a diabetic?

A

No more than 25-30%

314
Q

How much of the total fat comes from saturated fats?

A

7%

315
Q

How much protein should contribute the total energy consumed?

A

Less than 10%

316
Q

What kind of intake should be significantly less than the general population?

A

Protein intake

317
Q

Does alcohol have any nutritive value?

A

No

318
Q

What does alcohol promote?

A

Hypertrigylceridemia

319
Q

What does alcohol have a detrimental effect on?

A

Liver

320
Q

What can alcohol cause?

A

Severe hypoglycemia

321
Q

Who initially provides diet teaching?

A

Dietician

322
Q

What should be included during diet teaching?

A

Family and SO’s

323
Q

What is an appropriate basic teaching tools for diabetics?

A

USDA MyPyramid Guide

324
Q

What is the plate method?

A

Helps patient visualize the amount of vegetable, starch, and meat that should fill a 9 inch plate

325
Q

What is an essential part of diabetes management?

A

Exercise

326
Q

What does exercise do to insulin receptor sites?

A

Increase

327
Q

What does exercise do to blood glucose levels?

A

Lowers

328
Q

What contributes to weight loss?

A

Exercise

329
Q

What can be taken during exercise?

A

Several small carbohydrate snacks can be taken every 30 minutes during exercise to prevent hypoglycemia

330
Q

When is exercise best done?

A

After meals

331
Q

When should exercise plans be started?

A

After medical clearance and slowly with gradual progression

332
Q

What should exercise be?

A

Individualized

333
Q

When should blood glucose levels be monitored r/t exercise?

A

Before, during, and after

334
Q

Why do people not follow their glucose plan?

A

Most don’t because of cost

335
Q

What does self monitoring of blood glucose (SMBG) enable?

A

Enables patient to make self management decisions regarding diet, exercise, and medication

336
Q

What is SMBG important for?

A

Detecting episodic hyperglycemia and hypoglycemia

337
Q

What is crucial for SMBG?

A

Patient training

338
Q

What does SMBG supply?

A

Immediate info about blood glucose levels

339
Q

What is more common than diabetes in elderly? (???)

A

Hypoglycemia unawareness

340
Q

What must you consider for the elderly?

A

Patient’s own desire for treatment and coexisting medical problems

341
Q

What elderly limitations must you recognize?

A

Physical activity, manual dexterity, and visual acuity

342
Q

What could interfere with treating hypoglycemia in the elderly?

A

Presence of delayed psychomotor function

343
Q

What should education for the elderly be based on?

A

Their individual needs, using slower pace

344
Q

What main things do you need to do for pediatric DM illness management?

A

Continue insulin treatment, stay close to the meal plan, give plenty of liquids, choose meds wisely, check blood glucose and ketone levels frequently

345
Q

What does illness often do to diabetic kids?

A

Increase the amount of insulin the body needs

346
Q

What should you instruct parents?

A

Insulin should never be withheld

347
Q

What should you do if the child has an upset stomach and can’t eat?

A

Give clear liquids that contain carbohydrates (sports drinks, juices, gelatin, broth, frozen fruit bars, regular pop)

348
Q

What should you encourage the child to do?

A

Drink as much water and other non-caffeinated beverages as possible (caffeine dehydrates you

349
Q

Many OTC meds contain what?

A

Sugar and alcohol

350
Q

What in meds can rapidly add up?

A

Glucose

351
Q

What should parents look for in meds? What if that’s unavailable?

A

Parents should look for a glucose free version of the medication. If unavailable, carbs must be accounted for in the meal plan.

352
Q

What can meds that contain alcohol do? What should you ensure?

A

Lower blood glucose levels; ensure the child eats something to prevent hypoglycemia

353
Q

What medicines are better?

A

Alcohol free rather than including it

354
Q

Many decongestants can do what?

A

Raise blood glucose levels

355
Q

What should you check frequently?

A

Blood glucose and ketone levels

356
Q

What becomes a danger when the child is sick?

A

DKA

357
Q

To prevent DKA or catch it early, what should you do?

A

Check the child’s blood glucose levels often (every few hours) while sick

358
Q

How often should you check ketones for kids? When do you need to do it more often?

A

Check urine several times a day; more for when vomiting or diarrhea is present

359
Q

5 facts about infants?

A

Very rapid growth, trusting relationship with the parents, erratic eating habits (food can become a power struggle), erratic sleep patterns, treatment schedule is difficult to keep

360
Q

Why is a treatment schedule difficult to keep for infants?

A

Because of erratic feeding and sleeping patterns

361
Q

When do peer issues begin to emerge?

A

Preschool age

362
Q

When can kids begin to understand rules?

A

Preschool

363
Q

What can preschool kids do about care?

A

Can perform more self care, including blood tests under parental supervision

364
Q

Preschool eating behavior is…?

A

Less erratic

365
Q

Preschoolers are at risk for what? Because?

A

Hypoglycemia because they are very energetic

366
Q

How are preschoolers’ sleeping patterns?

A

Regular

367
Q

What is a challenge when dealing with preschoolers and food?

A

May be more challenging to provide snacks and meals that match what siblings and friends eat

368
Q

What do school age kids fear?

A

Being different from other kids

369
Q

What can school age kids do?

A

Can perform most self care, including blood tests and insulin injections

370
Q

What are school age kids eager to do?

A

Learn

371
Q

What are school age kids beginning to do?

A

Understand consequences of their actions

372
Q

What do school age kids test?

A

Independent decision making

373
Q

Where is most of school age kids’ time spent?

A

Away from home

374
Q

When is puberty well under way?

A

Adolescence

375
Q

What are adolescents concerned with?

A

Physical appearance

376
Q

What do adolescents have a clearer sense of than school age kids?

A

Clearer sense of self (can set goals)

377
Q

What is increased in adolescence?

A

Autonomy

378
Q

What are diabetic related adolescent risk taking behaviors?

A

Not taking insulin and not performing blood sugar tests

379
Q

What is unpredictable about adolescents?

A

Many social activities are unpredictable

380
Q

What counseling do adolescents need?

A

Regarding contraception, alcohol, and smoking

381
Q

What is DKA caused by?

A

Profound deficiency of insulin

382
Q

What is DKA characterized by?

A

Hyperglycemia, ketosis, acidosis, dehydration

383
Q

In what type does DKA most likely occur?

A

Type 1

384
Q

What are precipitating factors of DKA?

A

Illness, infection, inadequate insulin dosage, undiagnosed type 1, poor self management, neglect

385
Q

What happens when supply of insulin is insufficient?

A

Glucose cannot be properly used for energy and body breaks down fat stores

386
Q

What are ketones?

A

By products of fat metabolism

387
Q

What do ketones/fat metabolism affect?

A

Alters pH balance which causes metabolic acidosis, ketone bodies excreted in urine, electrolytes become depleted

388
Q

What are signs and symptoms of DKA?

A

Lethargy/weakness, dehydration, abdominal pain, Kussmaul respirations

389
Q

What are the early symptoms of DKA?

A

Lethargy/weakness

390
Q

What does dehydration lead to/cause?

A

Poor skin turgor, dry mucous membranes, tachycardia, orthostatic hypotension

391
Q

What are related to the abdominal pain symptom of DKA?

A

N/V

392
Q

What do Kussmaul respirations include?

A

Rapid deep breathing, attempt to reverse metabolic acidosis, sweet fruity odor

393
Q

They may or may not need hospitalization depending on what?

A

Signs and symptoms

394
Q

Laboratory findings of DKA: blood glucose-

A

Over 300 mg/dl

395
Q

Laboratory findings of DKA: arterial blood pH-

A

Below 7.30

396
Q

Laboratory findings of DKA: serum bicarbonate level-

A

Under 15 mEq/l

397
Q

Laboratory findings of DKA: What’s the 4th finding?

A

Ketones in blood and urine

398
Q

What may be included in treatment of DKA and signs and symptoms

A

Airway management- oxygen administration

399
Q

What IV will be used to correct fluid/electrolyte imbalance for DKA? What does it do?

A

0.45% or 0.9% NaCl; Restore urine output and raise blood pressure

400
Q

When blood glucose levels approach what, what do you do?

A

When they approach 250 mg/dl, 5% dextrose is added to regimen and the point is to prevent hypoglycemia

401
Q

What electrolyte needs to be replaced?

A

Potassium

402
Q

When do patients with DKA need sodium bicarbonate?

A

If it less than 7

403
Q

What insulin therapy is used with DKA?

A

Withheld until fluid resuscitation has begun, bolus followed by insulin drip

404
Q

Is Hyperosmolar hyperglycemic syndrome (HHS) life threatening?

A

Yes

405
Q

Which is more common, HHS or DKA?

A

DKA

406
Q

In what patient type does HHS often occur in?

A

Over 60 with type 2

407
Q

Does ketoacidosis occur in HHS? Why?

A

Patient has enough circulating insulin so ketoacidosis doesn’t occur

408
Q

HHS earlier stages have…?

A

Less symptoms

409
Q

Why do neurologic manifestations occur in HHS?

A

Due to increased serum osmolality

410
Q

HHS patients usually have a history of what?

A

Inadequate fluid intake, increasing mental depression, polyuria

411
Q

HHS laboratory values: blood glucose-

A

Over 400 mg/dl

412
Q

HHS laboratory values: What is increased?

A

Serum osmolality

413
Q

HHS laboratory values: What is absent/minimal?

A

Ketone bodies

414
Q

What administrations of DKA and HHS patients should be closely monitored?

A

IV fluids, insulin therapy, electrolytes

415
Q

What assessments of DKA and HHS patients should be closely monitored?

A

Renal status, cardiopulmonary status, level of consciousness

416
Q

What else should the patient be closely monitored for?

A

Signs of potassium imbalance, cardiac monitoring, vital signs

417
Q

Does HHS have a low mortality rate?

A

No, high

418
Q

What is HHS therapy similar to?

A

DKA therapy, except HHS requires greater fluid replacement

419
Q

Hypoglycemia is…?

A

Low blood glucose

420
Q

Hypoglycemia occurs when?

A

Too much insulin in proportion to glucose in the blood and blood glucose level is less than 70 mg/dl

421
Q

Hypoglycemia common manifestations?

A

Confusion, irritability, diaphoresis, tremors, hunger, weakness, visual disturbances, and can mimic alcohol intoxication

422
Q

Untreated hypoglycemia can progress to what?

A

Loss of consciousness, seizures, coma, and death

423
Q

What is hypoglycemia unawareness?

A

Person does not experience warning signs/symptoms, increasing risk for decreased blood glucose levels, and this is related to autonomic neuropathy

424
Q

Causes of hypoglycemia?

A

Mismatch in timing- food intake and peak action of insulin or oral hypoglycemic agents

425
Q

At first sign of hypoglycemia what should you do?

A

Check blood glucose

426
Q

Blood glucose level actions-

A

If under 70 mg/dl begin treatment, if over 70 investigate further for cause of signs/symptoms

427
Q

What should done if blood glucose monitoring equipment is not available and there is a sign of hypoglycemia?

A

Treatment should be initiated

428
Q

What is used for treatment of hypoglycemia?

A

If alert enough to swallow, 15 to 20 grams of a simple carb (ex: pb on graham crackers) with 4-6 ounces of fruit juice or regular soft drink

429
Q

What food should be avoided with a hypoglycemic patient?

A

Foods with fat, it decreases absorption of sugar

430
Q

Important things to do/remember about hypoglycemic treatment:

A

Do not overtreat, recheck blood sugar 15 min after treatment, repeat until blood sugar is under 70 mg/dl, patient should eat regularly scheduled meal/snack to prevent rebound hypoglycemia, check blood sugar again 45 min after treatment

431
Q

If no improvement after 2 or 3 doses of simple carbohydrate or patient not alert enough to swallow, what treatment should you use?

A

Administer 1 mg of glucagon IM or subq

432
Q

What side effect does glucagon have?

A

Rebound hyperglycemia

433
Q

After recovery of hypoglycemia, what should you have the patient do?

A

Ingest a complex carb after recovery

434
Q

In acute care settings what would you use for treatment?

A

25-50 ml of 50% dextrose IV push

435
Q

What is macrovascular disease?

A

Diseases of large and medium sized blood vessels

436
Q

Macrovascular disease and diabetes relationship?

A

Occurs with greater frequency and with an earlier onset in diabetics

437
Q

What is macrovascular disease development promoted by?

A

Altered lipid metabolism common to diabetes

438
Q

What can tight glucose control do for macrovascular disease?

A

May delay atherosclerotic process

439
Q

Risk factors for macrovascular disease?

A

Obesity, smoking, hypertension, high fat intake, sedentary lifestyle

440
Q

What should patients with diabetes be screened for?

A

Dyslipidemia at diagnosis of macrovascular disease

441
Q

What does microvascular disease result from? In response to what?

A

Result from thickening of vessel membranes in capillaries and arterioles; in response to chronic hyperglycemia

442
Q

Which is specific to diabetes: microvascular or macro vascular?

A

Microvascular is specific

443
Q

Areas most noticeably affected by microvascular?

A

Eyes (retinopathy), kidneys (nephropathy), skin (dermopathy)

444
Q

When do clinical manifestations of microvascular appear?

A

Usually after 10-20 years of diabetes

445
Q

What is diabetic retinopathy?

A

Microvascular damage to retina, result of chronic hyperglycemia

446
Q

What is diabetic retinopathy the most common cause of?

A

New cases of blindness in people ages 20 to 74

447
Q

What is the most common form of diabetic retinopathy?

A

Nonproliferative

448
Q

What is non pro. DR?

A

Partial occlusion of small blood vessels in retina

449
Q

What does non pro. DR cause?

A

Causes development of microaneurysms

450
Q

What happens in non pro. DR?

A

Capillary fluid leaks out, which leads to retinal edema and eventually hard exudates or intraretinal hemorrhages occur

451
Q

What is the most severe form of DR?

A

Proliferative

452
Q

What does pro. DR involve?

A

Retina and vitreous

453
Q

When does pro. DR occur?

A

When retinal capillaries become occluded

454
Q

What happens when retinal capillaries become occluded?

A

Body forms new blood vessels, vessels are extremely fragile and hemorrhage easily (produces vitreous contraction), and retinal detachment can occur

455
Q

The earliest and most treatable stages of DR often?

A

Often produces no changes in vision

456
Q

People with DR must get what yearly?

A

Annual dilated eye exams

457
Q

Treatment types for DR?

A

Photocoagulation, Cryotherapy, Vitrectomy

458
Q

What is photocoagulation?

A

Most common, laser destroys ischemic areas of retina which prevents further visual loss

459
Q

What is Cryotherapy?

A

Used to treat peripheral areas of retina, probe creates frozen area until reaches specific point on retina

460
Q

What is Vitrectomy?

A

Aspiration of blood, membrane, fibers from inside eye through small incision

461
Q

When is Vitrectomy used?

A

Vitreal hemorrhage doesn’t clear in 6 months and/or threatened or actual retinal detachment

462
Q

What is diabetic neuropathy associated with?

A

Damage to small blood vessels that supply the glomeruli of the kidney

463
Q

What is the leading cause of end stage renal disease?

A

Diabetic neuropathy

464
Q

What are critical factors for prevention/delay of diabetic neuropathy?

A

Tight glucose control, blood pressure management, and yearly screening

465
Q

What is involved in blood pressure management?

A

Angiotensin-converting enzyme (ACE inhibitors) (used even when not hypertensive), and angiotensin II receptor antagonists

466
Q

What is the yearly screening for diabetic neuropathy consist of?

A

Microalbuminuria in urine and serum creatinine

467
Q

How many patients with diabetes have some degree of neuropathy?

A

60-70%

468
Q

What is diabetic neuropathy related nerve damage due to?

A

Metabolic derangements of diabetes

469
Q

Which is more common- sensory or autonomic neuropathy?

A

Sensory

470
Q

What is a part of sensory neuropathy?

A

Distal symmetric

471
Q

What does sensory neuropathy affect?

A

Hands and/or feet bilaterally

472
Q

Characteristics of sensory neuropathy?

A

Loss of sensation, abnormal sensations, pain, and paresthesias

473
Q

When is sensory neuropathy usually worse?

A

At night

474
Q

What can occur with sensory neuropathy?

A

Foot injury and ulcerations can occur without feeling pain

475
Q

What is the treatment for sensory neuropathy?

A

Tight glucose control and drug therapy

476
Q

What does drug therapy for sensory neuropathy include?

A

Topical cream, Tricyclic antidepressants, Selective serotonin and norepinephrine reuptake inhibitors, and antiseizure meds

477
Q

What can autonomic neuropathy affect?

A

Nearly all body systems

478
Q

What complications can be caused by autonomic neuropathy?

A

Gastroparesis (delayed gastic emptying), cardiovascular abnormalities, sexual functions, neurogenic bladder

479
Q

What is the most common cause of hospitalization in diabetes?

A

Foot complications

480
Q

What do foot complications result from?

A

Combination of microvascular and macro vascular disease

481
Q

What are risk factors for foot complications?

A

Sensory neuropathy and peripheral artery disease

482
Q

Other contributors to foot complications are?

A

Smoking, clotting abnormalities, impaired immune function, autonomic neuropathy

483
Q

What integumentary complications can occur with diabetes?

A

Acanthosis nigricans and necrobiosis lipoidica diabeticorum

484
Q

What is acanthosis nigricans?

A

Dark, coarse, thickened skin

485
Q

What is necrobiosis lipoidica diabeticorum associated with?

A

Type 1

486
Q

What does necrobiosis lipoidica diabeticorum appear as?

A

Red yellow lesions and skin becomes shiny, revealing tiny blood vessels

487
Q

Diabetics are more susceptible to what?

A

Infections

488
Q

What is the definition of infection?

A

Defect in mobilization of imflammatory cells and impairment of phagocytosis by neutrophils and monocytes

489
Q

What may loss of sensation cause?

A

May delay detection of infection

490
Q

Treatment of infections in diabetics must be what?

A

Prompt and vigorous

491
Q

What is acromegaly caused by?

A

Caused by an overproduction of growth hormone usually caused by a benign pituitary tumor

492
Q

What does acromegaly present as?

A

Presents as a thickening of bone and soft tissue

493
Q

How many people have acromegaly?

A

Very rare, 3 out of 1 million in US

494
Q

What is the onset of acromegaly?

A

Gradual onset, 7 to 9 years between onset of symptoms and final diagnosis

495
Q

What are clinical manifestations of acromegaly?

A

Enlargement of hands and feet, joint pain, thick leathery oily skin, visual disturbances, headaches

496
Q

What is the treatment of choice for acromegaly? What will the patient need?

A

Hypophysectomy (removal of pituitary gland) and the patient will require hormone supplements for life

497
Q

What may a large tumor require?

A

Radiation or drug therapy in addition to hypophysectomy

498
Q

Bone growth and soft tissues r/t acromegaly

A

Bone growth can usually be stopped and soft tissue hypertrophy reversed

499
Q

What does SIADH stand for?

A

Syndrome of Inappropriate Antidiuretic Hormone

500
Q

When does SIADH occur?

A

When ADH is released despite normal or low plasma osmolarity

501
Q

What are causes of SIADH?

A

Most common is malignancy, the rest is on table 50-1

502
Q

What does SIADH lead to?

A

Fluid retention, serum hypoosmolality, hyponatremia, hypochloremia, and concentrated urine

503
Q

Pathophysiology map of SIADH?

A
  1. Increased diuretic hormone leads to 2. increased water reabsorption in renal tubules which leads 3. to increased intravascular fluid volume which leads 4. to dilution hyponatremia and decreased serum osmolality
504
Q

What are clinical manifestations of SIADH?

A

Muscle cramping, pain, and weakness (caused by hyponatremia); decreased urinary output; increased body weight; and lethargy, seizures, and coma (severe, late stage)

505
Q

How is SIADH diagnosed?

A

Through measurement of urine and serum osmolality

506
Q

Nursing and collaborative management for SIADH (Table 50-2, p. 1260)?

A

Restrict fluid intake to no more than 1000 mL a day (includes IV fluids too), position head of bed to flat, seizure precautions, and frequent oral care

507
Q

What is diabetes insipidus?

A

Decrease in ADH production, secretion, or renal response

508
Q

What are the 3 types of diabetes insipidus?

A

Central, nephrogenic, and primary

509
Q

What is central diabetes insipidus caused by?

A

Caused by lesion of the hypothalamus or pituitary (most common cause)

510
Q

What is nephrogenic diabetes insipidus? What is it caused by?

A

There is adequate ADH but the kidneys do not respond appropriately. Caused by meds (ex: Lithium which is long term usually)

511
Q

What is primary diabetes insipidus associated with?

A

Associated with excessive water intake

512
Q

What are clinical manifestations of diabetes insipidus?

A

Polydipsia and polyuria (5-20 L/day)

513
Q

What is the diagnostic study for diabetes insipidus?

A

Water restriction test

514
Q

What nursing and collaborative management is needed for diabetes insipidus?

A

Fluid and hormone replacement

515
Q

What does DI fluid and hormone replacement include?

A

IV fluid titrated to replace urinary output (0.45% NS; D5W) and desmopressin acetate (DDACP)- chemical replacement for ADH

516
Q

How many thyroid nodules are benign?

A

95%

517
Q

What are clinical manifestations of thyroid cancer?

A

Painful, palpable nodule in an enlarged thyroid gland

518
Q

What are diagnostic studies for thyroid cancer?

A

Ultrasound, Cat Scan or MRI

519
Q

Nursing and Collaborative management for thyroid cancer?

A

Surgical removal of the tumor with or without radiation treatment (and the thyroid gland?) and monitor patient for hypocalcemia after surgery

520
Q

Is true thyroid cancer common?

A

No it’s rare

521
Q

What is hyperthyroidism?

A

Increase in synthesis and release of T3, T4, or both

522
Q

Does hyperthyroidism occur more often in males or females?

A

Females

523
Q

What age is the highest frequency of hyperthyroidism?

A

20-40 years old

524
Q

What is the most common type of hyperthyroidism?

A

Grave’s Disease

525
Q

What is Grave’s Disease?

A

Autoimmune disease of unknown etiology; patient develops antibodies to TSH receptors. The antibodies then attach to the receptors and stimulate the thyroid gland to secrete T3, T4, or both

526
Q

Clinical manifestations of hyperthyroidism?

A

Table 50-5 pg. 1264, increased appetite, weight loss, hair loss, thin brittle nails, fatigue, insomnia, menstrual irregularities

527
Q

Complications of hyperthyroidism?

A

Thyrotoxic crisis

528
Q

What is thyrotoxic crisis?

A

(When it releases way too much hormone?) It is life threatening and can cause serve tachycardia, heart failure, shock, hyperthermia, and coma

529
Q

Why do we especially not palpate thyroids as student nurses?

A

We can cause thyrotoxic crisis

530
Q

Diagnostic studies of hyperthyroidism?

A

Decreased TSH levels, and increased free T4 levels

531
Q

Collaborative care for hyperthyroidism?

A

Antithyroid meds, radioactive iodine therapy, subtotal thyroidectomy (common), nutritional therapy

532
Q

What does hyperthyroidism nutritional therapy include?

A

High calorie diet (4000-5000 calories a day) may be needed to satisfy hunger and prevent tissue breakdown

533
Q

Nursing implementation for hyperthyroidism?

A

Elevate HOB to promote fluid drainage from periorbital area

534
Q

Nursing implementation after thyroidectomy?

A

Assess patient every 2 hours for first 24 hours for signs of hemorrhage or tracheal compression, position patient’s head to avoid tension on the suture line, monitor vital signs, monitor of signs and symptoms of hypocalcemia, control post op pain

535
Q

Why does hypothyroidism occur?

A

Insufficient circulating thyroid hormones

536
Q

How many people does hypothyroidism affect?

A

Approximately 1 in 50 women and 1 in 300 men

537
Q

Clinical manifestations of hypothyroidism?

A

Onset of symptoms may occur over months to years, fatigue, lethargy, impaired memory, cold intolerance, muscle weakness, weight gain

538
Q

Diagnostic studies for hypothyroidism?

A

High TSH indicates a defect in the thyroid gland, low TSH indicates a defect in the pituitary or hypothalamus

539
Q

Collaborative care for hypothyroidism?

A

Levothyroxine (Synthroid) is very common, they are started on a low dose and increased every 4 to 6 weeks as needed and they need to have blood work checked

540
Q

What is hyperparathyroidism?

A

Oversecretion of PTH

541
Q

What is hyperparathyroidism most commonly caused by?

A

A benign tumor in the parathyroid gland

542
Q

What does hyperparathyroidism lead to?

A

Hypercalcemia and hypophosphatemia

543
Q

Clinical manifestations of hyperparathyroidism?

A

Muscle weakness, loss of appetite, constipation, fatigue, shortened attention span

544
Q

What are diagnostic studies for hyperparathyroidism?

A

Elevated PTH and calcium levels

545
Q

Collaborative care for hyperparathyroidism?

A

Surgical removal of parathyroid gland or nonsurgical therapy

546
Q

What does hyperparathyroidism non surgical therapy include?

A

Fosamax- normalizes calcium levels; oral phosphate replacement

547
Q

What is hypoparathyroidism?

A

Inadequate levels of PTH

548
Q

What does hypoparathyroidism lead to?

A

Hypocalcemia and hyperphosphatemia

549
Q

What are clinical manifestations of hypoparathyroidism?

A

Irritability, abdominal cramps, fatigue, weakness

550
Q

What are hypoparathyroidism diagnostic studies?

A

Low PTH and calcium levels

551
Q

What are hypoparathyroidism nursing and collaborative management?

A

Treat complications such as tetany, IV calcium may be needed, instruct patient on management of long term drug therapy and nutrition

552
Q

What is Cushing Syndrome?

A

Spectrum or abnormalities caused by an excess of corticosteroids

553
Q

What is the most common cause of Cushing Syndrome?

A

Administration of exogenous corticosteroids (ex: Prednisone)

554
Q

What can Cushing Syndrome also be caused by?

A

ACTH secreting tumor

555
Q

What are clinical manifestations of Cushing Syndrome?

A

Truncal obesity, “moon face”, purplish red striae on abdomen, hirsutism in women, menstrual disorders, hypertension, unexplained hypokalemia, buffalo hump, and increase in axillary, chest, etc. hair in abnormal places

556
Q

What are diagnostic studies for Cushing Syndrome?

A

Plasma cortisol levels may be increased, 24 hour urine for free cortisol is often done

557
Q

What is collaborative care for Cushing Syndrome?

A

Treatment depends on underlying cause and medication adjustments may be necessary if caused by corticosteroids by decreasing dose and alternate day dosing

558
Q

What is Addison’s Disease?

A

Caused by a lack of adrenal corticosteroids (glucocorticoids, mineral corticoids, androgens)

559
Q

What is Addison’s Disease most commonly caused by?

A

An autoimmune response

560
Q

In what population is Addison’s Disease most common?

A

White females under 60

561
Q

Addison’s Disease is often (blank) before diagnosis is made?

A

Advanced

562
Q

Clinical manifestations of Addison’s Disease?

A

Progressive weakness, fatigue, weight loss, anorexia, skin hyper pigmentation (especially around joints of arms, legs and knuckles and it looks like a bad self tanner)

563
Q

Complications of Addison’s Disease?

A

Addisonian crisis- acute adrenal insufficiency

564
Q

Diagnostic studies for Addison’s Disease?

A

Decreased cortisol levels

565
Q

Collaborative care for Addison’s Disease?

A

Replacement therapy with hydrocortisone usually through IV, increased salt in diet, increase in hydrocortisone dose during periods of high stress (surgery; hospitalization)

566
Q

Effects of Corticosteroids?

A

Anti-inflammatory action, immunosuppression, maintenance of normal BP, carbohydrate and protein metabolism

567
Q

Side effects of Corticosteroids?

A

Table 50-20 pg. 1283

568
Q

Patient teaching guide for Corticosteroids?

A

Table 50-21 pg. 1283 (delayed wound healing, infections, can increase BP and blood sugar)

569
Q

What is hyperaldosteronism?

A

Excessive secretion of aldosterone causing sodium retention and potassium excretion

570
Q

What is hyperaldosteronism most commonly cause by?

A

Adrenocortical tumor in adrenal cortex

571
Q

What are clinical manifestations of hyperaldosteronism?

A

Hypertension, headache, muscle weakness, cardiac dysrhythmias

572
Q

What is Pheochromocytoma?

A

Excessive catecholamine production due to tumor of the adrenal medulla

573
Q

What are clinical manifestations of Pheochromocytoma?

A

Severe hypertension, pounding headache, tachycardia with palpitations, profuse sweating, chest pain

574
Q

Treatment for Pheochromocytoma includes what?

A

Surgical removal of the tumor and good BP management

575
Q

When does Growth Hormone Deficiency occur?

A

WHen GH is absent or produced in inadequate amounts

576
Q

What is hypopituitarism?

A

If other pituitary hormones are lacking + GHD

577
Q

What is an important part of determining normal growth?

A

The child’s growth pattern

578
Q

When can GHD occur?

A

At any age

579
Q

What are signs of GHD?

A

Growth of less than 2 inches per year between the ages of 2 and 11 years in girls or 2 and 13 years in boys; leveling off and slowing of growth progress; growth below the 5th percentile on standardized growth charts

580
Q

Etiology of GHD?

A

Can be congenital, acquired, or idiopathic; tends to run in families but may occur with no family history,

581
Q

What may congenital GHD be associated with?

A

An abnormal pituitary gland or be a part of another syndrome

582
Q

What are acquired GHD causes?

A

Brain tumors (or other disorders), cranial irradiation, infections, trauma (head)

583
Q

What are clinical manifestations of GHD?

A

Short height for child’s age, increased amount of fat around waist and in face, emotional feelings about height or weight, younger appearance than children of same age, decreased muscle mass, delayed skeletal maturation, delayed onset of puberty, delayed tooth development, hypoglycemia

584
Q

What are GHD diagnostic studies?

A

Thyroid panal, serum electrolytes, blood urea nitrogen, creatinine, complete blood count, insulin-like growth factor 1, insulin-like growth factor binding protein 3, karotyping (form of genetic testing), bone density scan

585
Q

Management of GHD?

A

If the cause is a tumor, surgical removal or radiation therapy may be indicated. Replacement of deficient hormones is often required even after successful treatment of a pituitary tumor

586
Q

What kind of injection is GH?

A

Most children receive subq injection

587
Q

How often are GH injections given?

A

Daily or 3 to 4 times per week and have increased growth velocity at bedtime

588
Q

Does GH need refrigerated?

A

Yes

589
Q

How does growth need to be monitored?

A

Close monitoring of growth with endocrinology visits every 3 to 4 months and pediatric follow up

590
Q

How long is GH replacement therapy given?

A

Continued until the child achieves an acceptable height or growth velocity drops to less than 1 inch per year

591
Q

Nursing implications for GHD?

A

Assess compliance with medication regimen, assess and address issues of self esteem, monitor growth (accurate is impt), teach the child and family about the disorder, teach proper technique for administering meds (shots), educational resources for parents

592
Q

What are educational resources for parents about GHD?

A

Magic Foundation www.magicfoundation.org/wwww, Human Growth Foundation www.hgfound.org, Child Growth Foundation www.childgrowthfoundation.org/ghd.htm

593
Q

When is the onset of precocious puberty?

A

Before age 7 or 8 and before age 9 in boys

594
Q

What is precocious puberty accompanied by?

A

The appearance of secondary sexual characteristics, advanced growth rate, and bone maturation

595
Q

What does precocious puberty cause?

A

Short stature as an adult from premature closure of epiphyseal ends of the long bones

596
Q

What is the etiology for precocious puberty?

A

Hormone-secreting tumors, brain injury caused by head trauma, infection, thyroid dysfunction, ovarian dysfunction, idiopathic

597
Q

What is the most common etiology for precocious puberty?

A

Idiopathic

598
Q

Clinical manifestations of precocious puberty in females?

A

Females: breast development, axillary hair, pubic hair, adult body odor, onset of menses, acne, deepening voice

599
Q

Clinical manifestations of precocious puberty in males?

A

Testicular enlargement, acne, penile enlargement, axillary and chest hair, pubic hair, adult body odor, facial hair

600
Q

Diagnostic studies for precocious puberty?

A

Bone density scan, gonadotropin0releasing hormone simulation test, pelvic and abdominal ultrasound, computed tomographic scan or MRI, Blood work of testosterone levels and estrogen fraction test

601
Q

What is the treatment for precocious puberty?

A

Involves the suppression of puberty

602
Q

What are clinical manifestations of Congenital Hypothyroidism?

A

Large for age despite having poor feeding habits and increased birth weight, puffy face, swollen tongue, hoarse cry, poor muscle tone, cold extremities, persistent constipation, bloated or full to the touch, lack of energy and sleeps most of the time, appears tired even when awake, little to no growth, often appears perfectly normal at birth

603
Q

Why is screening forCongenital Hypothyroidism vital at birth?

A

They often appear perfectly normal at birth

604
Q

What are Congenital Hypothyroidism diagnostic studies?

A

State required screening of TSH and T4 for every baby born, Low T4, elevated TSH, or both indicate hypothyroidism, positive test results ay be followed by scan for bone age, blood tests before 48 hours after birth may be falsely interpreted because of the rise in TSH immediately after birth

605
Q

What indicates hypothyroidism in babies?

A

Low T4, elevated TSH, or both

606
Q

What should you monitor in an infant with Congenital Hypothyroidism?

A

Monitor growth and development of the infant (serial measurements of height, weight, and head circumference and screens for developmental milestones)

607
Q

What should you assess for in children with Congenital Hypothyroidism?

A

Assess for retarded physical growth and slow intellectual development, if cognitive impairment has occurred then provide support to the family

608
Q

What should you teach the family about Congenital Hypothyroidism?

A

Teach importance of daily admin of meds, drug therapy is needed for life

609
Q

When do we stop measuring head circumference?

A

18 months to 2 years because fontanelles close around 18 months

610
Q

How can meds for infants with Congenital Hypothyroidism be prepared?

A

Crushed and added to a small amount of formula, food, or water, or can be offered mixed with formula through a syringe or a nipple

611
Q

How must meds for infants never be prepared?

A

Never put in a full bottle of formula in case they don’t finish it

612
Q

What should you include instructions of about Congenital Hypothyroidism in kids?

A

Include instructions on taking pulse in the teaching plan to monitor for signs of drug overdose

Med Surg Nursing (7 decks)

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