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Illness and Patho 1 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Patients experiencing acute adrenal insufficiency are most commonly those who are currently receiving or having recently been withdrawn from what kind of therapy?

A

Corticosteroid

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2
Q

Thyroid storm has an abrupt onset and is best categorized as a state of unregulated what?

A

Hypermetabolism

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3
Q

Neurogenic diabetes insipidus results from an insufficiency of which hormone?

A

Antidiuretic

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4
Q

Myxedema coma can occur in pateitns who have an extremely low metabolic state associated with what?

A

Hypothyroidism

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5
Q

Extreme hyperthyroidism with serious signs and symptoms

A

Thyroid storm

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6
Q

Syndrome on inappropriate ADH is associated with low levels of what?

A

Serum sodium

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7
Q

Controls and regulates the metabolic process

A

Hormones

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8
Q

Destruction of the adrenal gland itself

A

Addison’s disease

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9
Q

Which disease results in myxedema

A

Hypothyroidism

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10
Q

In what patients is hyperglycemic hyperosmolar syndome most commonly seen?

A

Newly diagnosed type 2 DM

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11
Q

Results from alterations in insulin secretion, insulin action, or both

A

Diabetes Mellitus

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12
Q

What is the most frequent form of hyperthyroidism?

A

Graves’ disease

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13
Q

What is the preferred energy source for the brain?

A

Glucose

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14
Q

Glucocorticoid and mineralocorticoid deficiency

A

Acute adrenal crisis

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15
Q

Hypersecretion of ADH

A

SIADH

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16
Q

Hypersecretion of cortisol

A

Cushing’s syndrome

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17
Q

Hypersecretion of insulin

A

Hypoglycemia

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18
Q

Hypersecretion of T3 and T4

A

Thyroid Storm

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19
Q

Hyposecretion of ADH

A

Diabetes Insipidus

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20
Q

Hyposecretion of insulin

A

Type 1 DM

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21
Q

Hyposecretion of T3 and T4

A

Myxedema Coma

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22
Q

What would not be a laboratory finding in a patient with SIADH?

A

Low urine sodium

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23
Q

Indicators for primary hyperthyroidism would include what lab values?

A

Low to normal TSH with elevated T3 and T4

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24
Q

What is cortisol released in response to?

A

Anterior pituitary release of ACTH

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25
Q

What often causes the hypothyroid state in secondary hypothyroidism?

A

Pituitary gland dysfunction

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26
Q

Which test can be performed to assess for the presence of adrenal insufficiency?

A

Cortisol stimulation test

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27
Q

What would the assessment findings for a pateint who is in a myxedema coma include?

A

Lethargy, edema, swollen tongue, and abdominal distension

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28
Q

What is the hallmark sign of SIADH?

A

Dilutional Hyponatremia

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29
Q

What is a potential cause of ectopic ADH secretion, causing SIADH?

A

Small cell carcinoma of the lung

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30
Q

What do the pituitary glands regulate?

A

The endocrine system

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31
Q

What does the hypothalamus regulate?

A

Body temperature

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32
Q

What do the gonads regulate?

A

The sex hormones

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33
Q

What do the adrenal glands regulate?

A

Steroids

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34
Q

What does the thyroid regulate?

A

Metabolism

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35
Q

What does the parathyroid regulate?

A

Serum calcium and phosphorus levels

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36
Q

What does the pancreas regulate?

A

Insulin

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37
Q

What steroids does the adrenal cortex make?

A

Mineralocorticoids and corticosteroids

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38
Q

Name a mineralocorticoid

A

Aldosterone

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39
Q

Name a corticosteroid

A

Cortisol

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40
Q

What steroid does the adrenal medulla make?

A

Catecholamines

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41
Q

Name the catecholamines

A

Epinephrine and Norepinepherine

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42
Q

What is the important history to gather when assessing the endocrine system?

A

Energy levels, elimination pattern, sexual and reproductive functions, and physical appearance

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43
Q

Which endocrine disease would cause a prominent forehead or jaw?

A

Acromegaly

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44
Q

Which endocrine disease would cause a round or puffy face?

A

Cushing’s

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45
Q

Which endocrine disorder would cause a dull or flat expression?

A

Hypothyroidism

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46
Q

Which endocrine disorder would cause striae?

A

Cushing’s

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47
Q

Which endocrine disorder would cause hirsutism?

A

Cushing’s

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48
Q

What laboratory testings would have to be done with an assessment of the endocrine system?

A

Stimulation/suppression tests, assays, and urine tests

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49
Q

What would cause primary pituitary dysfunction?

A

There would be a problem with the pituitary itself

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50
Q

What would cause secondary pituitary dysfunction?

A

A hypothalamic disorder

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51
Q

Deficiency of one or more anterior pituitary hormones

A

Hypopituitarism

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52
Q

Partial or total failure of all anterior pituitary hormones

A

Panhypopituitarism

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53
Q

What are the causes of primary pituitary dysfunction?

A

Hypophysectomy, non-secreting pituitary tumor, radiation, infarction, metastatic disease, and trauma

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54
Q

Why does a non-secreting pituitary tumor cause primary pituitary dysfunction?

A

The pressure of the tumor destroys the pituitary gland

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55
Q

Why does an infarction cause primary pituitary dysfunction?

A

It causes hypertrophy of the pituitary gland

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56
Q

Which metastatic disease is likely to cuase primary pituitary dysfunction?

A

Small cell carcinoma of the lung

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57
Q

What kind of trama causes primary pituitary dysfunction?

A

Closed head injury that puts pressure on the pituitary

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58
Q

What are the causes of secondary hypopituitarism?

A

Infection, trauma, tumors, congenital defects, and infiltrative processes

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59
Q

What infection generally causes secondary hypopituitarism?

A

Meningitis

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60
Q

What type of infiltrative processes generally causes secondary hypopituitarism?

A

Scaroidosis

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61
Q

What disorders are associated with hypopituitarism?

A

Sterility, loss of libido and secondary sex characteristics, ammenhorhea, decrease of spermatogenesis, and testicular atrophy

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62
Q

What is the second most common cause of hypopituitarism?

A

Growth hormone deficiency

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63
Q

What do you have to screen for before giving replacement growth hormone?

A

Cancer

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64
Q

What are the interventions for patients with hypopituitarism?

A

Improve body image

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65
Q

Why are females with hypopituitarism given estrogen and progesterone?

A

To replace lost LH and FSH

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66
Q

When can females with hypopituitarism not be given estrogen or progesterone?

A

Before puberty and the closure of the epiphyseal plates

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67
Q

What do females on estrogen and progesterone replacement need to ovulate?

A

Clomid

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68
Q

What are the side effects of estrogen and progesterone replacement therapy?

A

Blood clots and hypertension

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69
Q

What does testosterone given to males with hypopituitarism treat?

A

Gynocomastia, baldness, chest hair, high pitched voice, low muscle mass, poor libido and small peens

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70
Q

When should growth hormone be given?

A

Prior to the closal of the epiphyseal plates

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71
Q

What is a side effect of somatropin?

A

Bone pain

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72
Q

Over secretion of one or more pituitary hormones

A

Hyperpituitarism

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73
Q

What is the cause of primary hyperpituitarism?

A

Benign adenoma

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74
Q

Disease caused by the over secretion of growth hormone in children

A

Giantism

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75
Q

Disease caused by the over secretion of growth hormone in adults

A

Acromegaly

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76
Q

What disease is caused by excess ACTH?

A

Cushing’s

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77
Q

What drug treats hyperpituitarism?

A

Parlodel

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78
Q

How does parlodel work?

A

Suppresses the secretion of prolactin

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79
Q

What are the risks of radiation of the pituitary gland?

A

Hypopituitarism and optic nerve damage

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80
Q

What are the symptoms of hyperpituitarism?

A

Hyperpolactinemia

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81
Q

Removal of the pituitary gland or microadenoma?

A

Hypophysectomy

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82
Q

What are the nursing interventions for a patient who is post op with a transsphenoidal hypophysectomy?

A

No toothbrushing, dental flossing, or mouthwash for 1-2 weeks; avoid nasotracheal suctioning; no blowing nose, sneezing or coughing; avoid straining bowel movements; check for a CSF leak; and monitor for signs and symptoms of meningitis

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83
Q

What is the hallmark characteristic of acromegaly?

A

Large facial features

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84
Q

What is the purpose of the posterior pituitary?

A

Promotes water reabsorption

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85
Q

What is the pathophysiology of SIADH?

A

Excess ADH causes the reabsorption of water from the renal tubules, causing dilutional hyponatremia

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86
Q

What are the treatments for hyperpituitarism?

A

Drugs, radiation, or surgical management

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87
Q

Which condition causes an increase in milk production, gynecomastia, and altered sexual function

A

Hyperpolactinemia

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88
Q

What can cause SIADH?

A

Oat cell cancer metastasis, thymomas, non-malignant pulmonary problems, CNS disorders, and various drugs

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89
Q

Which disorders of the CNS causes SIADH?

A

CVA or infection

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90
Q

Which drugs cause SIADH?

A

Anesthesia, narcotics, or tricyclic antidepressants

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91
Q

Which disorder can produce ectopic ADH?

A

Non-malignant pulmonary problems

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92
Q

What are the clinical manifestations of SIADH?

A

Water retention, GI disturbances, edema, increased heart rate, hypothermia, increased urine Na levels, increased urine specific gravity, low serum Na, low plasma osmolarity, changes in LOC, seizures, coma, and sluggish deep tendon reflexes

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93
Q

Tumors behind the breast bone that make cells identical to ADH

A

Thymomas

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94
Q

What are the nursing interventions for patients with SIADH?

A

Restrict fluid intake to 500-600 mL/day, administer diuretic, maintain strict I/Os, take daily weights, and monitor for LOC changes

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95
Q

What is the pathophysiology for diabetes insipidus?

A

Decreased ADH causes decreased water reabsorption in the renal tubules, resulting in hypernatremia and excessive urine output

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96
Q

What can cause diabetes insipidus?

A

Generally head trauma, but also surgery or destruction of the proximal pituitary

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97
Q

How much can patients with diabetes insipidus void daily?

A

Up to 3 liters

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98
Q

What would the sodium levels of a patient with diabetes insipidus be?

A

Greater than 145 mEq/L

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99
Q

What are the clinical symptoms of diabetes insipidus?

A

Extreme thirst and dehydration, hypovolemia, tachycardia, poor skin turgor, low PA pressures, and low urine specific gravity

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100
Q

What is the treatment of diabetes insipidus?

A

Vasopressin or Desmopressin, maintain adequate hydration, monitor strict I/Os, administer IV and oral fluids, teach for life long med administration, and have the patient wear a medic alert band

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101
Q

What is vasopressin?

A

A potent vasoconstrictor

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102
Q

What is desmopressin?

A

A nasal spray that does not have the potency of vasopressin but has a longer lasting anti-diuretic effect

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103
Q

What kind of IV and fluids should a patient with diabetes insipidus be given?

A

Normal saline through two large bore IVs

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104
Q

What do patients newly diagnosed with diabetes insipidus need to be taught?

A

To always have their meds with them and always wear a med alert bracelet

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105
Q

What would the serum osmolality of a patient with diabetes insipidus be?

A

Greater than 295

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106
Q

What would the urine osmolarity of a patient with diabetes insipidus be?

A

Less than 100

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107
Q

What would the urine specific gravity of a patient with diabetes insipidus be?

A

Less than 1.005

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108
Q

What would the serum osmolarity of a patient with SIADH be?

A

Less than 280

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109
Q

What are the symptoms of Cushing’s syndrome?

A

Moon face, buffalo hump, decreased ability to fight infection and heal, weight gain, and increased glucose levels

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110
Q

Which steriods regulate the metabolism and increase blood sugar in response to physiologic stress?

A

Glucocoritcoids

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111
Q

Which steroids balance sodium and potassium?

A

Mineralocoritcoids

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112
Q

What does androgen contribute to?

A

Growth and development in both genders and sexual activity in women

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113
Q

What do androgens increase the instance of?

A

Myocardial infarctions

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114
Q

What is the leading endogenous cause of Cushing’s syndrome?

A

ACTH-secreting pituitary tumors

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115
Q

What are the clinical manifestations of Cushing’s syndrome?

A

Hyperglycemia, protein wasting, loss of collagen, mood disturbances, insomnia, irrationality, psychosis, hypertension, and acne

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116
Q

What causes Cushing’s syndrome?

A

Excess corticosteroids, particularly glucocorticoids

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117
Q

Who is Cushing’s disease most common in?

A

Women 20-40 years old

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118
Q

Why do patients with Cushing’s exhibit muscle wasting?

A

Cortisol has catabolic effects

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119
Q

Why do patients with Cushing’s exhibit hypertension?

A

Mineralocorticoids cause fluid retention, causing hypertension

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120
Q

What do the excess adrenal androgens seen in patients with Cushing’s syndrome cause?

A

Pronounced acne, virilization in women, and feminization in men

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121
Q

Why is hyperglycemia a clinical manifestation of Cushing’s syndrome?

A

Glucose intolerance is associated with cortisol-induced insulin resistance and there is increased gluconeogenesis by the liver

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122
Q

How is Cushing’s syndrome diagnosed?

A

24-Hour urine collection looking for free cortisol or a CT and MRI of the the pituitary and adrenal glands

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123
Q

What levels of free cortisol in urine indicate Cushing’s syndrome?

A

50-100 mcg/day

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124
Q

What indicates ACTH-dependent Cushing’s disease?

A

High or normal ACTH levels

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125
Q

What is the primary goal in treating Cushing’s syndrome?

A

Normalize hormone secretion

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126
Q

What imbalances are seen in patients with ectopic ACTH syndrome and adrenal carcinoma?

A

Hypokalemia and alkalosis

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127
Q

What is the treatment for Cushing’s caused by a pituitary adenoma?

A

Surgical removal of tumor and/or radiation and drug therapy

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128
Q

What conditions can lead to false positives in the diagnostic tests for Cushing’s syndrome?

A

Depression, stress, and alcoholism

129
Q

What indicates an adrenal or exogenous etiology of Cushing’s disease?

A

Low or undetectable ACTH levels

130
Q

What is the treatment for Cushing’s caused by an adrenal tumor or hyperplasia?

A

Adrenalectomy and drug therapy

131
Q

What is the treatment for Cushing’s caused by ectopic ACTH-secreting tumors?

A

Treatment of the primary neoplasm and drug therapy

132
Q

Suppresses cortisol production, alters peripheral metabolism of cortisol, and decreases plasma and urine corticosteroid levels

A

Mitotane (Lysodren)

133
Q

Which drugs inhibit cortisol synthesis?

A

Metyrapone, ketoconazole, and aminoglutethimide

134
Q

What are the side effects of drug therapy for Cushing’s syndrome?

A

Anorexia, nausea and vomiting, GI bleeding, depression, vertigo, skin rashes, and diplopia

135
Q

What should you do if Cushing’s develops during use of corticosteroids?

A

Gradually discontinue therapy

136
Q

What happens if you stop corticosteroid therapy too suddenly?

A

Life-threatening adrenal insufficiency

137
Q

What nursing diagnoses should be implemented for a patient with Cushing’s syndrome?

A

Risk for infection, imbalanced nutrition related to decreased appetite, disturbed self-esteem related to altered body image, and impaired skin integrity

138
Q

What are the goals for patients with Cushing’s syndrome?

A

Experience relief of symptoms, have no serious complications, maintain positive self-image, and actively participate in the therapeutic plan

139
Q

What nursing interventions should be implemented for patients with Cushing’s syndrome?

A

Health promotion, acute intervention, patient monitoring, emotional support, preoperative care, postoperative care and home care

140
Q

What is diplopia?

A

Double vision

141
Q

What should the nurse monitor for a patient with Cushing’s syndrome?

A

Vital signs, daily weights, glucose, infection, signs and symptoms of abnormal thromboembolic phenomena

142
Q

What needs to be controlled tightly pre-op for patients with Cushing’s syndrome?

A

Hypertension, hyperglycemia, and hyperkalemia

143
Q

What preoperative care needs to be performed on a patient with Cushing’s syndrome?

A

Nasogastric tube, urinary catheter, IV therapy, central venous pressure monitoring, and leg compression devices

144
Q

Why is the risk of hemorrhage increased post-op for patients with Cushing’s?

A

High vascularity of the adrenal glands

145
Q

Why are the blood pressure, fluid balance, and electrolyte levels of a post-op patient with Cushing’s unstable?

A

Manipulation of the glandular tissues may release hormones into circulation

146
Q

What should be reported to the doctor about post-op patients with Cushing’s?

A

Blood pressure, respirations, heart rate, skin, circulation, and infection

147
Q

What should be closely monitored post-op for patients with Cushing’s?

A

Fluid intake and output, circulatory instability, and urine levels of cortisol

148
Q

What is the critical period for circulatory instability post-op for patients with Cushing’s?

A

24-48 hours

149
Q

What are the indications of hypocortisolism post-op for patients with Cushing’s?

A

Vomiting, increased weakness, dehydration, and profound hypotension

150
Q

What are the side effects of surgery for patients with Cushing’s syndrome?

A

Painful joints, pruritus, peeling skin, and severe emotional disturbances

151
Q

How long should the post-op patient with Cushing’s be on bed rest?

A

Until the blood pressure is stabilized

152
Q

What should post-op patients with Cushing’s be taught to avoid?

A

Stress, extremes of temperature, and infections

153
Q

What indicates that surgery for patients with Cushing’s has been successful?

A

They have no signs or symptoms of infection, attain weight appropriate for height, increase acceptance of appearance and maintain intact skin

154
Q

What is Addison’s disease caused by?

A

Adrenocortical insufficiency

155
Q

Which classes of adrenal corticosteroids are decreased in Addison’s disease?

A

Glucocorticoids, mineralocorticoids, and androgens

156
Q

What are the possible causes of Addison’s disease?

A

Autoimmune disease, TB, infarction, fungal infection, AIDS, or metastatic cancer

157
Q

Who does Addison’s disease most often affect?

A

Women younger than 60

158
Q

When does Addison’s disease become evident?

A

When 90% of the adrenal cortex is destroyed

159
Q

What are the primary features of Addison’s disease?

A

Progressive weakness, fatigue, weight loss, anorexia, and skin hyperpigmentation

160
Q

Why does Addison’s manifest the symptoms it does?

A

Low androgens

161
Q

Where is hyperpigmentation generally manifest in patients with Addison’s?

A

Areas exposed to the sun, at pressure points, over joints, in skin and especially palmar creases

162
Q

What are the clinical manifestations for patients with Addison’s?

A

Orthostatic hypotension, hyponatremia, hyperkalemia, nausea and vomiting, and diarrhea

163
Q

How can primary Addison’s be distinguished from secondary Addison’s?

A

Secondary lacks hyperpigmentation

164
Q

What triggers a life-threatening Addisonian crisis?

A

Sudden, sharp decrease in adrenocortical hormones caused by stress from infection, surgery, trauma, hemorrhage, psychological distress or sudden withdrawal of corticosteroid replacement therapy

165
Q

What are the manifestations of glucocorticosteroid and mineralocorticoid deficiencies in patients with Addison’s?

A

Hypotension, tachycardia, dehydration, hyponatremia, hyperkalemia, hypoglycemia, fever, weakness, and confusion

166
Q

What can the hypotension associated with Addison’s lead to?

A

Shock and circulatory collapse

167
Q

Which diagnostic study indicates Addison’s disease?

A

Cortisol levels fail to rise over basal levels with ACTH stimulation

168
Q

What abnormal laboratory findings would a patient with Addison’s exhibit?

A

Hyperkalemia, hypochloremia, hyponatremia, hypoglycemia, anemia, increased BUN and low urine cortisol levels

169
Q

What would the ECG of a patients with Addison’s exhibit?

A

Low voltage, vertical QRS axis, and peaked T waves

170
Q

What is most commonly used as replacement therapy for patients with Addison’s disease?

A

Hydrocortisone

171
Q

What is the most important teaching for patients with Addison’s disease?

A

Glucocorticoid dosage must be increased during times of stress to prevent an Addisonian crisis

172
Q

What is the treatment for patients in Addisonian crisis?

A

Administer large volumes of NSS and 5% dextrose

173
Q

What are the nursing interventions for patients with Addison’s?

A

Frequent assessment, monitoring vitals, daily weights, diligently administer corticosteroid therapy, protect against infection, assist with daily hygiene, and protect from extreme light, noise, and temperature

174
Q

How often do the vitals of patients with Addison’s need to be taken?

A

Every 30 minutes to 4 hours for the first 24 hours

175
Q

What is the priority nursing intervention for people with Addison’s?

A

Administer corticosteroid therapy diligently

176
Q

Why do patients with Addison’s disease need to avoid extreme light, noise, and temperature?

A

They don’t have the physiological ability to cope with stress

177
Q

Why do patients with Addison’s need to have their vitals monitored so closely?

A

To check for signs of fluid and electrolyte imbalance

178
Q

Why do mineralocorticoids need to be given in the morning?

A

To reflect the normal circadian rhythm and decrease the side effects like GI irritaion

179
Q

What indicates a need for corticosteroid dose adjustment?

A

Fever, influenza, tooth extraction, and physical exertion

180
Q

What symptoms indicate an Addisonian crisis?

A

Vomiting and diarrhea

181
Q

What is the discharge teaching for a patient with Addison’s disease?

A

Teach for signs and symptoms of corticosteroid deficiency and excess, always wear a medical alert bracelet, teach when to increase glucocorticoids, instruct how to take BP, carry emergency kit, teach how to give IM injections

182
Q

What are the expected side effects of corticosteroid therapy?

A

Altered anti-inflammatory action, altered immunosuppression, inability to maintain normal BP, and altered carbohydrate and protein metabolism

183
Q

What is the pathophysiology of hyperadolsteronism?

A

Excessive aldosterone secretion, causing sodium retention, hypokalemia, and extra hydrogen ion excretion

184
Q

What is the hallmark of hyperaldosteronism?

A

Hypertension with hypokalemic alkalosis

185
Q

What causes primary hyperaldosteronism?

A

Adrenocorticoid adenoma

186
Q

What causes secondary hyperaldosteronism?

A

Renal artery stenosis, renin-secreting tumors, and chronic kidney disease

187
Q

What does elevated aldosterone do to electrolytes?

A

Sodium retention and elimination of potassium, leading to hypernatremia, hypertension, and headache, and hypokalemia causing muscle weakness, fatigue, and cardiac dysrhythmias

188
Q

What laboratory levels of a patient with hyperaldosteronism would be off?

A

Increased plasma aldosterone levels, increased sodium levels, decreased potassium levels, and decreased renin activity

189
Q

What is the preferred treatment of primary hyperaldosteronism?

A

Surgical removal of the adenoma

190
Q

What do patients with hyperaldosteronism need pre-surgery?

A

Low sodium diet, potassium sparing diuretic, antihypertensive agents, normal blood pressure and fluid electrolyte balance

191
Q

What is pheochromocytoma caused by?

A

A tumor of the adrenal medulla producing catecholamines

192
Q

Who is most susceptible to pheochromocytomas?

A

Young to middle aged women

193
Q

What is the hallmark of pheochromocytoma?

A

Severe hypertension

194
Q

How is pheochromocytoma generally diagnosed?

A

Blood pressure screenings

195
Q

What can untreated pheochromocytoma lead to?

A

Diabetes mellitus, cardiomyopathy, and death

196
Q

What are the clinical manifestations of pheochromocytoma?

A

Severe, episodic hypertension, severe, pounding headache, tachycardia with palpitations, profuse sweating, and abdominal or chest pain

197
Q

What is the best diagnostic test for pheochromocytoma?

A

Measurement of urinary fractionated metanephrines and catecholamines in a 24 hour collection

198
Q

How is a pheochromocytoma treated?

A

Surgical removal of the tumor, calcium channel blockers, sympathetic drugs and beta blockers

199
Q

What do calcium channel blockers do for patients with pheochromocytoma?

A

Controls blood pressure

200
Q

What do sympathetic blocking agents do for patients with pheochromocytoma?

A

Lower blood pressure and decrease the symptoms of catecholamine excess

201
Q

What do beta blockers do for patients with pheochromocytoma?

A

Decrease dysrhythmias

202
Q

What are the nursing interventions for patients with pheochromocytoma?

A

Monitor blood pressure and glucose closely and make the patient as comfortable as possible

203
Q

Why do patients with pheochromocytoma need a lot of nourishment?

A

They are in a hyper metabolic state

204
Q

Over activity of one or more the the parathyroid glands

A

Hyperparathyroidism

205
Q

What are the classifications hyperparathyroidism?

A

Primary, secondary or tertiary

206
Q

Who is hyperparathyroidism most common in?

A

Females older than 60

207
Q

What is the pathophysiology of primary hyperparathyroidism?

A

Severity of hypercalcemia reflects the quantity of hyperfunctioning parathyroid tissue

208
Q

Where does the excess serum calcium come from in patients with hyperparathyroidism?

A

Intestines, kidneys, and bones

209
Q

What problems result from hyperparathyroidism?

A

Kidney stones, bone demineralization, myopathy, and hypercalcemia

210
Q

What does hypercalcemia cause?

A

Hypergastinemia, abdominal pain peptic ulcer disease, pancreastitis and constipation

211
Q

What causes primary hyperparathyroidism?

A

Adenoma or hyperplasia of the parathyroid gland

212
Q

What causes secondary hyperparathyroidism?

A

The parathyroid glands are hyper plastic because of another organ’s dysfunction

213
Q

Which patients are at risk for secondary hyperparathyroidism?

A

Patients with renal failure, Paget’s disease, multiple myeloma, or carcinoma with bony metastasis

214
Q

What is the pathophysiology of secondary hyperparathyroidism?

A

Chronic renal failure hyperphosphatemia caused by a decrease in GFR

215
Q

What are the clinical manifestations of hyperparathyroidism?

A

Back pain, joint pain, pathological fractures, polyuria, polydipsia, hypertension, thirst, nausea, anorexia, constipation, listlessness, depression, paranoia, and hypercalcemia

216
Q

What would the labs of a patient with hyperparathyroidism be?

A

Serum calcium elevated, serum phosphate levels decreased, urine calcium and phosphate levels are high, and alkaline phosphatase is high

217
Q

How is hyperparathyroidism treated?

A

Lower calcium levels, administer NSS, administer loop diuretics, administer anti-reabsorption agents, phosphates, calcitonin,and glucocorticosteriods

218
Q

What should the diet of a patient with hyperparathyroidism be?

A

Low calcium and vitamin D

219
Q

What are the nursing diagnoses for patients with hyperparathyroidism?

A

Risk for injury and altered nutrition

220
Q

What is the surgical treatment for hyperparathyroidism?

A

Parathyroidectomy

221
Q

What are the possible complications of parathyroidectomies?

A

Hypocalcemia and respiratory distress

222
Q

What should parathyroidectomy patients be loaded with post-op?

A

Calcium

223
Q

Hyposecretion of the parathyroid glands produce the reverse syndrome of hyperparathyroidism

A

Hypoparathyroidism

224
Q

What are the clinical manifestations of hypoparathyroidism caused by?

A

Low serum calcium levels, elevated pH and alkalosis

225
Q

What are the signs of acute hypoparathyroidism?

A

Tetany, Chvostek’s sign, and Trousseasu’s sign

226
Q

What are the symptoms of chronic hypoparathyroidism?

A

Lethargy, thin, patchy hair, brittle nails, dry, scaly skin, personality changes, calcifications in eyes and basal ganglia and eventual cardiac problems

227
Q

What findings diagnose hypoparathyroidism?

A

Chvostek’s sign, trousseaus’s signs, hyperactive deep tendon reflexes, circumoral paresthesia, numbness and tingling of the fingers, low calcium, low PTH, high phosphorous, decreased urine calcium, and opthalmic exam

228
Q

What would a opthalmic exam of a patient with hypoparathyroidism reveal?

A

Cataracts

229
Q

How should hypoparathyroidism be treated?

A

Administer calcium gluconate, vitamin D, PTH hormone, and treat seizures and laryngeal spasms

230
Q

What should always be in the room of a patient with hypoparathyroidism?

A

Trach tray

231
Q

Touching the facial nerve causes it to twitch

A

Chvostek’s sign

232
Q

One of the most common medical disorders in the US affecting 10% of women and 3% of men over 65 years old, resulting from insufficient circulating thyroid hormone

A

Hypothyroidism

233
Q

Hypothyroidism related to the destruction of thyroid tissue or defective hormone synthesis

A

Primary hypothyroidism

234
Q

What is the most common cause of hypothyroidism?

A

Iodine deficiency, then atrophy of the gland

235
Q

What is atrophy of the typhoid gland the end result of?

A

Hashimoto’s thyroiditis and Graves’ disease

236
Q

What drugs can produce hypothyroidism?

A

Amiodarone and lithium

237
Q

Hypothyroidism related to pituitary disease with lowered TSH secretion or hypothalamic dysfunction

A

Secondary hypothyroidism

238
Q

Blood pressure cuffs makes arm pronate

A

Trousseau’s sign

239
Q

Caused by thyroid hormone deficiencies during fetal or neonatal life

A

Cretinism

240
Q

What do the clinical manifestations of hypothyroidism depend on?

A

Severity, duration, and age of onset

241
Q

What are the cardiovascular symptoms associated with hypothyroidism?

A

Decreased cardiac output, decreased cardiac contractility, anemia, cobalamin, iron, and folate deficiencies, and increased serum cholesterol and trigylcerides

242
Q

What are the respiratory symptoms associates with hypothyroidism?

A

Low exercise tolerance and shortness of breath on exertion

243
Q

What are the neurological symptoms associated with hypothyroidism?

A

Fatigued and lethargic, personality and mood changes, impaired memory, slowed speech, decreased initiative and somnolence

244
Q

What are the GI symptoms associated with hypothyroidism?

A

Decreased motility, achlorhydria common, and constipation

245
Q

What are the integumentary symptoms associated with hypothyroidism?

A

Cold intolerance, hair loss, dry/coarse skin, brittle nails, hoarseness, muscle weakness and swelling, and weight gain

246
Q

What are the reproductive symptoms associated with hypothyroidism?

A

Menorrhagia

247
Q

Accumulation of hydrophilic mucopolysaccharides in the dermis and other tissues causing puffiness, periorbital edema and a mask like effect

A

Myxedema

248
Q

What are the compilations of myxedema?

A

Mental sluggishness, drowsiness, and lethargy

249
Q

What are the characteristics of myxedema?

A

Subnormal temperature, hypotension, and hypoventilation

250
Q

What precipitates a myxedema coma?

A

Infection, drugs, cold, or a trauma

251
Q

How is a myxedema coma treated?

A

IV thyroid hormone replacement

252
Q

What would the diagnostics labs of a patient with hypothyroidism show?

A

Elevated serum TSH, elevated free T4, lowered serum T3, lowered serum T4, and increased cholesterol, triglycerides and anemia

253
Q

What should the diet of a patient with hypothyroidism be?

A

Low calorie

254
Q

What drug to patients take to treat hypothyroidism?

A

Synthroid

255
Q

What has to be monitored when a patient is on synthroid?

A

Angina and cardiac dysrhythmias

256
Q

What are the nursing diagnoses for patients with hypothyroidism?

A

Imbalanced nutrition, activity intolerance, and disturbed thought process

257
Q

What acute nursing care does a patient with myxedema coma require?

A

Mechanical respiratory support, cardiac monitoring, aspiration precautions, IV thyroid hormone replacement, and monitoring of core temperature

258
Q

What discharge teaching is needed for a patient with hypothyroidism?

A

Prevent skin breakdown, emphasize the need for a warm environment, avoid sedatives, minimize constipation

259
Q

What are the signs of a synthroid overdose?

A

Orthopnea, dyspnea, rapid pulse, palpitations, nervousness, and insomnia

260
Q

How often should patients with diabetes and hypothyroidism check their blood glucose?

A

At least daily

261
Q

What leads to thyroid cancer?

A

Hormones in food, lack of sun, and pollution

262
Q

A sustained increase in the synthesis and release of thyroid hormones by the thyroid gland

A

Hyperthyroidism

263
Q

Who is hyperthyroidism most common in?

A

Women 20-40 years old

264
Q

What most commonly causes hyperthyroidism?

A

Graves’ disease, and then thyroiditis, toxic nodular goiter, exogenous iodine excess, pituitary tumors, and thyroid cancer

265
Q

Physiological effects/clinical syndrome of hyper metabolism resulting from increased circulating levels of T3 and T4

A

Thyrotoxicosis

266
Q

Autoimmune disease of unknown etiology caused by diffused thyroid enlargement and excessive thyroid hormone secretion

A

Graves’ disease

267
Q

What percentage of hyperthyroidism results from Graves’ disease?

A

75%

268
Q

What does Graves’ disease lead to?

A

Thyrotoxicosis

269
Q

Thyroid hormone-secreting nodules independent of TSH

A

Toxic nodular goiters

270
Q

What are the hallmark clinical manifestations of thyroid hormone excess?

A

Increased metabolism, increased tissue sensitivity to stimulation by sympathetic nervous system, ophthalmopathy, and intolerance to heat

271
Q

What are the cardiovascular symptoms of hyperthyroidism?

A

Bruit over the thyroid gland, systolic hypertension, increased cardiac output, dysrhythmias, cardiac hypertrophy, and atrial fibrillation

272
Q

What are the GI symptoms of hyperthyroidism?

A

Increased appetite, increased thirst, weight loss, diarrhea, splenomegaly, and hepatomegaly

273
Q

What are the integumentary symptoms of hyperthyroidism?

A

Warm, smooth, moist skin, thin, brittle nails, hair loss, clubbing of fingers, diaphoresis, vitiligo

274
Q

Protrusion of the eyeballs from the orbits

A

Exophthalmos

275
Q

What causes exophthalmos?

A

Increased fat and edema in retroorbital tissues and impaired drainage from the orbit

276
Q

What are the musculoskeletal symptoms of hyperthyroidism?

A

Fatigue, muscle weakness, proximal muscle wasting, dependent edema, and osteoporosis

277
Q

What are the neurological symptoms of hyperthyroidism?

A

Fine tremors, insomnia, delirium, hyperreflexia of tendon reflexes, and inability to concentrate

278
Q

What are the reproductive symptoms of hyperthyroidism?

A

Menstrual irregularities, amenorrhea, decreased libido, impotence, gynecomastia, and decreased fertility

279
Q

Acute, rare, and life threatening condition in which all manifestations of hyperthyroidism are heightened

A

Thyrotoxic crisis

280
Q

What is the cause of thyrotoxic crisis?

A

Additional stressors

281
Q

What are the clinical manifestations of a thyrotoxic crisis

A

Tachycardia, heart failure, shock, hyperthermia, restlessness, agitation, seizures, abdominal pain, nausea, vomiting, diarrhea, delirium, and coma

282
Q

What is the treatment of thyrotoxic crisis?

A

Decrease thyroid hormone levels and treat symptoms

283
Q

How is hyperthyroidism generally diagnosed?

A

Radioactive iodine uptake levels

284
Q

Which laboratory studies are done to diagnose hyperthyroidism?

A

TSH, Free T4, and total T3 and T4

285
Q

What are the primary treatment options for hyperthyroidism?

A

Antithyroid medications, radioactive iodine therapy, and subtotal thyroidectomy

286
Q

What types of drug therapy are patients with hyperthyroidism on?

A

Antithyroid drugs, iodine, and beta adrenergic blockers

287
Q

Why are patients with hyperthyroidism given beta adrenergic blockers?

A

To decrease the arrhythmias, tachycardia, and hypertension

288
Q

How long do patients have to be on antithyroid hormones to have good results

A

4-8 weeks

289
Q

What are the antithyroid medications?

A

Propylthiouracil (PTU) and methimazole (tapazole)

290
Q

How does propylthiouracil work?

A

Blocks the conversion of T4 to T3

291
Q

Used with other antithyroid drugs in preparation for thyroidectomy or treatment of a crisis

A

Iodine

292
Q

How does iodine work to lower thyroid levels?

A

Decreases the vascularity of the thyroid gland

293
Q

What are the types of iodine drugs?

A

Saturated solution of potassium iodine, and Lugol’s solution

294
Q

When does the maximal effect of iodine occur?

A

1-2 weeks

295
Q

Symptomatic relief of thyrotoxicosis resulting from beta adrenergic receptor stimulation

A

Beta adrenergic blockers

296
Q

What are the beta adrenergic blockers?

A

Propranolol

297
Q

What is the treatment of choice for non pregnant adults with hyperthyroidism?

A

Radioactive iodine therapy

298
Q

How long does radioactive iodine therapy take to work?

A

2-3 months

299
Q

What is the drug used to treat hypopituitarism?

A

Somatropin

300
Q

What is the drug used to treat hyperpituitarism?

A

Parlodel

301
Q

Why is it okay for radioactive iodine therapy to cause hypothyroidism?

A

Because it is easy to control and replace them

302
Q

When is surgical therapy indicated for hyperthyroidism?

A

When the condition is unresponsive to drug therapy or there is tracheal compression or if there is a possible malignancy

303
Q

What is the preferred surgical procedure to treat hyperthyroidism?

A

Subtotal thyroidectomy

304
Q

How much of the thyroid has to be removed for a subtotal thyroidectomy to be effective?

A

90%

305
Q

What needs to be achieved before a subtotal thyroidectomy can take place?

A

A euthyroid state

306
Q

What are the post op complications of a subtotal thyroidectomy?

A

Hypothyroidism, hyperparathyroidism, damage of the parathyroid glands, hemorrhage, injury to laryngeal nerve, thyrotoxic crisis, and infection

307
Q

What should the diet of a hyperthyroid patient be like?

A

High calorie, avoidance of caffeine, highly seasoned foods, and high-fiber foods, and a protein allowance of 1-2 g/kg

308
Q

What are the nursing diagnoses or patients with hyperthyroidism?

A

Activity intolerance, risk for injury, imbalanced nutrition, anxiety, and insomnia

309
Q

What are the goals for patients with hyperthyroidism?

A

Relief of symptoms, maintain nutritional balance, and control therapeutic pain

310
Q

Where does treatment for hyper and hypothyroidism generally take place?

A

Outpatient settings

311
Q

What should the environment of a patient with thyrotoxicosis be?

A

Calm, quiet, and cool room with light bed coverings

312
Q

What should the nurse do for a patient with thyrotoxicosis?

A

Administer medications to block thyroid hormone production, administer IV fluids, ensure adequate oxygenation, monitor for cardiac dysrhythmias and decompensation, assist with exercise, apply artificial tears, elevate head of bed, restrict salt, and dark glasses

313
Q

What pre-op teaching should be done for patients with hyperthyroidism?

A

Coughing, deep breathing, and leg exercises, range of motion for neck

314
Q

How often should patients post-op subtotal thyroidectomy be checked for hemorrhage and tracheal compression?

A

Every 2 hours for 24 hours

315
Q

What are the signs and symptoms of tracheal compression post-op subtotal thyroidectomy?

A

Irregular breathing, neck sweeping, frequent swallowing, and choking

316
Q

What position should patients post-op subtotal thyroidectomy be in?

A

Semi-fowlers with head supported

317
Q

When is hoarseness acceptable post-op subtotal thyroidectomy?

A

3-4 days

318
Q

What are the side effects of radioactive iodine therapy?

A

Dryness and irritation of the mouth

Illness and Patho 1 (12 decks)

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