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NSG219 > Endocrine part 2 > Flashcards

Endocrine part 2 Flashcards

1
Q

where does Cushing’s disease and Addison’s disease orginate

A

adrenal cortex

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2
Q

where does hypo/hyperthyroidism originate

A

thyroid

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3
Q

where does hyperparathyroidsm and hypoparathyroidsm originate

A

parathyroid

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4
Q

what does the adrenal cortex secrete

A

glucocorticoids (cortisol) and mineralocorticoids (aldosterone).

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5
Q

what does the medulla secrete

A

catecholamines (epinephrine and norepinephrine).

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6
Q

what does the cortisol do in the adrenal cortex

A

actions include fat, carbohydrate, and protein metabolism, suppression of the immune response, and control of the body’s stress response.

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7
Q

what does aldosterone do in the adrenal cortex

A

promotes sodium and water reabsorption by the kidney and potassium excretion.

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8
Q

what does Epinephrine and norepinephrine do in the adrenal medulla

A

mimics actions of the sympathetic nervous system.

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9
Q

What does the SNS do?

A

Fight or Flight response – prepares body for danger, muscles tighten, pupils dilate, heart rate increases, sweating increases, etc.

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10
Q

what is the cause of adrenal insufficiency

A

may result from destruction of the adrenal glands stemming from autoimmune issues, decreased secretion of adrenocorticotropic hormone (ACTH) from the anterior pituitary gland, decreased secretion of corticotropin-releasing hormone from the hypothalamus, or decreased secretion of glucocorticoids and mineralocorticoids from the adrenal cortex. Other causes include infections, cancers, and traumatic processes that lead to direct insults to the adrenal cortex.

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11
Q

Females are most often affected by adrenal insufficiency, and it has a peaked incidence in people between what age

A

30-50 years old

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12
Q

what does the body do When circulating levels of cortisol and aldosterone fall

A

the hypothalamus and anterior pituitary gland increase secretion of corticotropic hormone and ACTH. Because melanocyte-stimulating hormone and ACTH share an ancestor hormone there is increase in secretion of melanocyte stimulating hormone, leading to darkened skin tone.

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13
Q

The decreased secretion of cortisol and aldosterone lead to ……

A

to weakness, weight loss, fatigue, nausea, abdominal pain, gastrointestinal issues, changes in mood, irritability, inability to concentrate, and decreased pubic and axillary hair due to decreased sex hormones

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14
Q

Hypotension is caused due to

A

water and sodium loss.

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15
Q

what do you expect cortisol to be when diagnosing adrenal insufficiency

A

less then 3mcg/dL

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16
Q

what do you expect glucose to be when diagnosing adrenal insufficiency

A

decreased due to lack of cortisol

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17
Q

what do you expect potassium to be when diagnosing adrenal insufficiency

A

increased due to water loss

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18
Q

what do you expect sodium to be when diagnosing adrenal insufficiency

A

decreased due to hypocortisolism and hypoaldosteronism

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19
Q

when are cortisol levels the highest

A

in the morning so should be measured between 6am-8am

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20
Q

what is an insulin tolerance test

A

uses hypoglycemic stress to induce cortisol production. The peak cortisol response is measured after an insulin challenge of 0.1-0.15 units/kg.

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21
Q

what is a corticotropin simulation test

A

uses a synthetic form of adrenocorticotropic hormone administered intravenously followed by measurement of serum cortisol levels 30-60 minutes later.

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22
Q

what is the definitive treatment for adrenal insufficiency

A

Cortisol replacement

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23
Q

what is the med of choice for adrenal insufficiency

A

Hydrocortisone

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24
Q

Clients with acute adrenal crisis require what

A

emergency stabilization with IV fluids and glucose, along with IV administration of glucocorticoids (cortisol), Solu-Cortef (hydrocortisone), and dexamethasone (Decadron).

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25
Q

Side effects of Solu-Cortef include

A

weight gain, trouble sleeping, increased appetite, dizziness, and menstrual period changes. It should be tapered off. If stopped abruptly acute adrenal insufficiency could occur.

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26
Q

The client receiving cortisol replacements requires close monitoring including

A

frequent VS, neurological assessment (LOC), serum sodium, glucose and potassium levels.

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27
Q

Adrenal crisis is a life-threatening emergency that leads to

A

severe hypovolemia and hypotension. Because of the decrease in aldosterone and cortisol the client loses sodium and fluid. Hyperkalemia and hypoglycemia are associated with lack of both mineralocorticoids and glucocorticoids

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28
Q

what is another name for adrenal insufficiency

A

addisons disease

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29
Q

what do you expect to find for addisons disease

A 
autoimmune destruction 
abdominal pain 
dark skin 
salt craving 
low sodium and cortisol 
stress 
high potassium
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30
Q

what is the cause of adrenal cortex hyperfunction

A

may be secondary to excessive secretion of glucocorticoids (hypercortisolism) or excessive secretion of aldosterone (hyperaldosteronism).
It is typically caused by excessive hormone production due to a pituitary tumor causing excess adrenocorticotropic hormone (ACTH) secretion or a tumor on the adrenal cortex. However, it can be medication induced.

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31
Q

Hypercortisolism signs and symptoms include

A

hyperglycemia, fluid retention, hypokalemia, abnormal fat distribution, and decreased muscle mass. The maldistribution of fats and changes in muscle are related to the effects that glucocorticoids have on fat and protein metabolism

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32
Q

what is cushings disease

A

describes a condition caused by excess cortisol production.

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33
Q

what gender and age is more likely to get cushings

A

femal 25-40

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34
Q

how do you diagnose cushings

A

client presentation and confirmed with serum cortisol levels, results of suppression tests, and serum electrolyte levels. 24-hour urine cortisol levels should be used, as cortisol levels fluctuate throughout the day.

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35
Q

what is the focus for hypercortisolism or cushings

A

The focus is to prevent complications associated with fluid overload, changes in immune system, skin integrity, and changes in body structure.

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36
Q

what does aminoglutethimide do and what does it treat

A

is an example of a medication that interferes with cortisol production in the adrenal cortex
cushings

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37
Q

what should be monitored when taking aminoglutethimide

A

The nurse should monitor for s/s of adrenal suppression including hypoglycemia and hyponatremia.

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38
Q

what does cyproheptadine do and what does it treat

A

impacts ACTH production.

cushings

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39
Q

what should be monitored when taking cyproheptadine

A

Monitor for s/s of adrenal suppression including hypoglycemia and hyponatremia.

40
Q

what does pasireotide (Signifor) do and what does it treat

A

is a subcutaneous somatostatin used to inhibit release of corticotropin in patients with Cushing’s secondary to a pituitary adenoma.

41
Q

what is the surgical management for cushings

A

Transsphenoidal hypophysectomy or adrenalectomy

Radiation and stereotactic radiosurgery of pituitary gland may be used.

42
Q

what is the physical appreance of someone with cushings

A 
buffalo hump 
thin arms and legs 
extra body hair 
moon face 
round body 
thinning hair
43
Q

what is Hyperaldosteronism

A

over secretion of aldosterone.

44
Q

Hyperaldosteronism signs and symptoms include

A

sodium and water reabsorption and potassium excretion (elevated sodium and low potassium), elevated BP, edema, and cardiac irregularities caused secondary to hypokalemia.

45
Q

what is Conn’s syndrome

A

describes a condition associated with excess aldosterone production.

46
Q

who is more at risk for Conn’s syndrome.

A

Females and African Americans

47
Q

how do you diagnosis hyperaldosteronism

A

made through evaluation of serum electrolytes as well as imaging studies. Serum aldosterone levels as well as hypokalemia and hypernatremia are observed.

48
Q

what if the focus of medical management for hyperaldosteronism

A

controlling hypertension and managing hypokalemia.

49
Q

what is the surgical management for hyperaldosteronism

A

include removing hypersecreting tumors of the adrenal cortex.

50
Q

what is the diet for someon with hyperaldosteronism

A

high potassium, low sodium diet if needed.

51
Q

what are some complications for hypercortisolism

A

Osteoporosis may develop due to cortisol effects on bone density.
If due to exogenous therapy, abrupt withdrawal may occur. Elevated glucose and GI bleeding may also occur due to release of hydrochloric acid released secondary to cortisol secretion.
Cortisol is a stress hormone – when it’s elevated, s/s mirror stress – HTN, increased HR, elevated glucose

52
Q

what are some complications of hyperaldosteronism

A

Complications usually related to severe hypokalemia or hypertension. BP can lead to MI and stroke. Dysrhythmias are associated with hypokalemia.

53
Q

what is Pheochromocytoma

A

rare catecholamine-secreting tumors of the adrenal medulla and 50% are diagnosed only on autopsy.

54
Q

Because of excessive catecholamine secretion, pheochromocytomas may cause

A

life threatening hypertension and cardiac arrhythmias leading to sudden death

55
Q

what race is mostly affected by Pheochromocytoma

A

white

56
Q

how do you diagnosis Pheochromocytoma

A

Classic presentation is sudden elevated BP accompanied by other manifestations of catecholamine release. Severe headache, tachycardia, and severe hypertension in excess of 250/140 can be observed.

57
Q

A 24-hour urine is required to accurately measure catecholamine metabolites. Prior to testing the client is asked to avoid

A

avoid bananas, chocolate, vanilla, tea and coffee and any other foods high in amines.

58
Q

Urine and plasma levels of catecholamines are measured. Direct measurements of plasma catecholamines require patient preparation to prevent elevations of circulating catecholamines. The client should be

A

lying supine and be at rest at least 30 mins prior to testing.

59
Q

Medical management includes what for pheochromocytoma.

A

treating hypertension, tachycardia and other symptoms of pheochromocytoma. The client will need cardiac monitoring and ICU placement. The client should be on bedrest with HOB elevated. Beta blockers and calcium channel blockers may be given to decrease BP and HR.

60
Q

what is the surgical managment for pheochromocytoma.

A

include an adrenalectomy, typically performed through bilateral abdominal incisions.

61
Q

what is the pre op care before surgical management of pheochromocytoma.

A

Client preparation focuses on control of BP and HR. Treatment with alpha adrenergic blockers is started 7-10 days prior to the scheduled procedure. A goal BP of 120/80 or lower should be accomplished prior to the procedure. In the event of hypertension during the procedure, sodium nitroprusside (Nipride) is administered.

62
Q

Clients with bilateral adrenalectomy will require adrenal cortex hormone ….

A

replacements for life. These clients will take cortisol daily and may require additional doses during episodes of stress.

63
Q

Metabolic activity and rate are primarily controlled by two hormones released from the thyroid glands, ….

A

T3 and T4

64
Q

what does t3 do

A

increases metabolic rate- targets all cells

65
Q

what does t4 do

A

increases the bodies response to catecholamines

66
Q

The release of T3 and T4 are “triggered” by the

A

anterior pituitary gland secreting thyroid-stimulating hormone (TSH) and the hypothalamus secreting thyrotropin-releasing hormone (TRH

67
Q

Serum calcium levels are controlled through the release of

A

thyrocalcitonin(calcitonin) from the thyroid gland and parathyroid hormone (PTH) from the parathyroid glands.

68
Q

Thyrocalcitonin decreases …..

A

breakdown of bone, decreases reabsorption of calcium in renal tubules, and decreases reabsorption of calcium in the intestines. It helps maintain healthy calcium levels

69
Q

what is Hashimoto’s thyroiditis

A

is the most common type of hypothyroidism and is caused by an autoimmune response that leads to destruction of the thyroid gland.

70
Q

what are the ss of Hashimoto’s thyroiditis

A

Decreased metabolism is the hallmark of hypothyroidism. Decreased metabolism causes decreased energy, increased sleep, fatigue, weight gain, decreased appetite, hair loss, lack of sweating, and susceptibility to cold temperatures.

71
Q

what is Myxedema

A

a condition causing non pitting edema in the face. Cardiac alterations, enlargement, and effusions can occur due to lack of T3 and T4.

72
Q

Goiter or enlargement of the thyroid gland (hypertrophy) occurs

A

when the thyroid works hard to compensate for low levels of T3 and T4 due hypothyroidism.

73
Q

Hypothyroidism occurs most often in ….

A

women between the ages of 30 and 60, and the incidence increases with age. Women are affected 7-10 times more often than men.

74
Q

what should be drawn if suspecting Hashimoto’s

A

Antithyroid antibodies should be drawn

75
Q

what is the primary treatment for hypothyroidsm

A

Replacement of thyroid hormone is the primary treatment

76
Q

what is the most common med for hypothyroidism

A

Synthroid (levothyroxine).

77
Q

how does administration for for Synthroid (levothyroxine).

A

started at a low dose and increased as needed to treat symptoms of hypothyroidism. The medication is to be taken in the morning since it affects metabolism. It should be taken on an empty stomach, at least one hour before other medications. Medications are lifelong and should be taken at the same time every day.

78
Q

what are some complications of hypothyroidism

A

Myxedema coma is characterized by hypoxia and carbon dioxide retention secondary to hypoventilation. Intubation may need to be performed.

79
Q

Hyperthyroidism can be present at any age but is most common in

A

in women between the ages of 20 and 40 years old. It is 10 times more prevalent in women

80
Q

what are the ss of hyperthyroidism

A

: Accelerated metabolism is characteristic of hyperthyroidism. Elevated HR, heat intolerance, weight loss, fatigue, nervousness, insomnia, hair loss, absent or light menses, and increased appetite. Exophthalmos is characteristic of hyperthyroidism and results in visual changes. Goiter can be present due to hyperplasia of the gland in response to the action of TSH on thyroid tissue.

81
Q

how do you diagnosis hyperthyroidism

A

based on elevated T3, T4, and decreased TSH. Antibodies to TSH are evaluated and high titers indicate Graves disease.

82
Q

what is graves disease

A

is an autoimmune disease that stimulates your thyroid to create too much thyroid hormone. Graves’ disease is a hereditary condition. It’s more common in people assigned female at birth.

83
Q

Graves’ disease is the most common cause of

A

hyperthyroidsm

84
Q

what does Propylthiouracil (PTU) do and what does it treat

A

inhibits synthesis of thyroid hormone by diverting iodine pathways. Teach patient to monitor weight 2-3 times per week.
hyperthyroidsm

85
Q

what is the teaching for Propylthiouracil (PTU)

A

s/s of hypothyroidism, monitor WBC’s, and take at the same time each day.

86
Q

what does Topazole do and what does it treat

A

Inhibits synthesis of thyroid hormone by blocking combination of iodine with a protein called thyroglobulin.
Hyperthyroidism

87
Q

what is the teaching for topazole

A

Take at the same time each day, monitor weight 2-3 times per week, s/s of hypothyroidism.

88
Q

what does Lithium carbonate do and what does it treat

A

Interferes with thyroid hormone synthesis

89
Q

what is the teaching for Lithium carbonate

A

Teach client to monitor for signs of toxicity including vomiting diarrhea, drowsiness, and lack of coordination. Drink at least 2-3 L of fluid each day.

90
Q

what may be the cause of a Thyroid storm

A

may develop with poorly managed hyperthyroidism.

91
Q

what are the ss of thyroid storm

A

include tachycardia, fever, systolic hypertension, abdominal pain, tremors, and changes in level of consciousness. Thyroid storm can be caused by palpation/manipulation.

92
Q

what are the priorities of a thyroid storm

A

airway and fluid resuscitation

93
Q

what are the ss of Hypoparathyroidism

A

numbness and tingling around mouth or in hands and feet, severe muscle cramps, spasms in hands or feet, and tetany.

94
Q

Chvostek’s and Trousseau’s signs are associated with an increased risk

A

risk of tetany that can result in laryngospasm and airway compromise.

95
Q

what are some foods to treat hypoparathyroidism

A

fruit and fruit juices that are fortified with calcium and vit D
dark green leafy veggies
soy products

96
Q

what foods should be avoided for hypoparathyroidism

A

high in phosphorus like organ meats and dairy.

97
Q

what are the ss of Hyperparathyroidism

A

polyuria, anorexia, constipation, cardiac changes, prolonged PR interval and shortened QT, abdominal pain, lethargy, confusion, muscle weakness, fatigue, and generalized bone pain and bone weakness

NSG219 (11 decks)

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