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Adult Nursing V > Endocrine > Flashcards

Endocrine Flashcards

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1
Q

What is the endocrine system and what does it do?

A

Glands that regulate the body through hormones
Controls the body’s metabolism, respiration, excretion, and reproduction
Consists of the hypothalamus, anterior and posterior pituitary, adrenal gland, thyroid gland, parathyroid glands, pancreas, ovaries, and testes

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2
Q

Assessment: History

A

Previous diagnosis of endocrine disorders
Changes in appetite, weight, and activity tolerance
Family history of endocrine disorders
Use of drugs, smoking, or alcohol use

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3
Q

Assessment: Physical

A

VS, weight, height, BMI
Behavior and communication
Skin, hair, and nails
Head and neck for contours, symmetry, and masses
Vision
Breasts for male breasts, shape, symmetry, masses, tenderness and discharge
Symmetry of chest expansion, rate and quality of respiration, retractions, accessory muscles, lung sounds
Heart for murmur, extra heart sounds, rate and rhythm
Bowel sounds, palpate the abdomen for masses, tenderness, and pain
Posture changes, joint pain, stiffness, weakness
Genitalia

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4
Q

General diagnostic procedures for all endocrine diseases

A

Measure serum and urine hormone levels
Hormone deficiency expected: stimulation test
Hormone excess expected: suppression test
24 hour urine collection
X-rays, CT scan, or MRI
Nursing responsibilities: teaching about the test i.e. special diet, fasting, med restrictions, special lab test needs

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5
Q

Gerontological Considerations

A

Aging process affects nearly every gland in the endocrine system: Alterations in secretion, circulating levels, metabolism, and biologic activity of hormones
Despite decreased levels, normal aging usually does not lead to a deficiency state

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6
Q

Thyroid Gland

A

Disorders of the thyroid gland are among the most common diseases of the endocrine system
Primary thyroid disease is dysfunction occurring in the thyroid gland
Secondary thyroid disease is dysfunction occurring in the anterior pituitary
Tertiary thyroid disease is dysfunction occurring in the hypothalamus
Consists of a right and left lobe connected by an isthmus
Located anterolateral to the trachea

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7
Q

Thyroid hormone regulations

A

The thyroid gland produces 2 primary hormones: Triiodothyronin (T3) and Thyroxine (T4)
It also produces calcitonin
Function is regulated by the hypothalamic-anterior pituitary-thyroid gland axis
Thyroid-releasing hormone (TRH) is released from the hypothalamus, TRH stimulates the anterior pituitary to release thyroid-stimulating hormone (TSH), TSH stimulates the thyroid to release T3 & T4
Works through a negative feedback loop
T3 & T4 regulate energy metabolism, heat generation, growth & development, cardiovascular function, and reproduction

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8
Q

Hypothyroidism

A

Most frequent in older adults, occurring in about 6% of individuals over 65 years
Most common cause in adults is autoimmune thyroiditis (Hashimoto thyroiditis), where the immune system attacks the thyroid gland
Globally the most common cause is iodine deficiency and iatrogenic issues
Can also be caused by pituitary and hypothalamic disease
Primary hypothyroidism: serum T3 & T4 are low while TSH levels are high
Secondary and tertiary hypothyroidism: serum TSH, T3 & T4 are all low

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9
Q

Hypothyroidism signs and symptoms

A

Tired, weak, cold intolerance, weight gain with poor appetite, bradycardia, dry skin, cold extremities, hair loss, constipation, peripheral edema

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10
Q

Hashimoto thyroiditis

A

genetic immunological disease that causes fibrosis of the thyroid tissue. Clients present with a goiter

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11
Q

Myxedema Coma/Crisis

A

Severe hypothyroidism
Medical emergency
Precipitated by an event such as infection, trauma, surgery , or neurological disorder in a client with hypothyroidism
Signs include: facial edema, thick tongue, confusion, irritability, significant hypothermia and bradycardia, hypotension, muscle weakness

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12
Q

Hypothyroidism Treatment

A

Replacement of thyroid hormone (oral or IV)
Levothyroxine (Synthroid) is the drug of choice
Lifelong treatment
Annual monitoring once stable levels are reached
Should avoid taking levothyroxine along with calcium supplements because calcium alters the absorption of thyroid replacement medications, 4 hours inbetween

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13
Q

Hypothyroidism Teaching

A 
Fatigue prevention
Lifelong commitment to taking medication
Need for annual monitoring
Don’t change brands
Avoid taking hormone replacement with calcium supplements
Signs of a myxedema crisis
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14
Q

Hyperthyroidism

A

Condition in which there is excess production of thyroid hormone
T3 usually increases more than T4
Thyrotoxicosis is an excess amount of circulating thyroid hormone
Severe hypermetabolic condition caused by thyroid hormones

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15
Q

Graves’ disease

A

Graves’ disease accounts for 60-70% of thyrotoxicosis
Graves’ disease is an autoimmune disorder of unknown cause. The body produces antibodies that mimic TSH and stimulate the thyroid
Signs specific to Graves’ disease: Goiter, Exophthalmos (bulging eyes out of orbit), Pretibial myxedema (‘orange peel’ skin)

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16
Q

Hyperthyroidism signs and symptoms

A

Tachycardia, hyperactivity, irritability, heat intolerance, fatigue, weight loss and increased appetite, warm moist skin, thrill &/or bruit over the thyroid gland

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17
Q

Thyroid storm

A

Life-threatening condition characterized by an exacerbation of all of the signs and symptoms of hyperthyroidism
Temp greater than 104, sweating, tachycardia, afib, N&V, diarrhea, tremors, agitation
Can occur when those with Graves’ disease discontinue their antithyroid medications, undiagnosed hyperthyroidism, during surgery, trauma, infection, etc…
Treatment revolves around supportive measures, administration of ATDs, administration of SSKI to block the release of thyroid hormones

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18
Q

Hyperthyroidism treatment

A

Antithyroid drugs: Good choice for older adults and those with comorbidities where surgery is not safe. Not a permanent treatment.
Thyroidectomy: Permanent treatment. Good option for large, painful goiters or malignancy. Risk of surgical complications
Radioactive iodine: Most common treatment and a permanent cure. Safe for those with comorbidities. Requires radiation precautions for several days afterward

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19
Q

Parathyroid Glands

A

Four small glands located behind the thyroid gland
Secrete parathyroid hormone (PTH)
PTH is an important mediator in the regulation of calcium and phosphate
Maintains normal serum calcium concentration
Target areas include intestinal mucosa, kidneys, and bone
Promotes calcium absorption from the intestinal mucosa and kidneys and release from the bone
Promotes phosphate excretion through the urine

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20
Q

Hypoparathyroidism

A

Results from inadequate parathyroid hormone
Most commonly caused by damage or removal of parathyroid glands at the time of parathyroid or thyroid surgery
Causes hypocalcemia and hyperphosphatemia

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21
Q

Hypoparathyroidism signs and symptoms

A

Sign and symptoms are caused by hypocalcemia
Characterized by increased neuromuscular excitability:
Numbness and tingling in the perioral area, fingers, and toes, Muscle cramps, Seizures, Cardiac arrhythmias, Tetany, Chvostek’s sign (tapping cheek and eye squints) and Trousseau’s sign (hand contracts and points up when taking BP)
Some with hypoparathyroidism may be asymptomatic because they have adapted to their calcium levels

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22
Q

Hypoparathyroidism Diagnosis

A

Diagnosis is made through serum sampling
Serum calcium levels will be decreased and serum phosphate levels will be increased
Serum PTH may be low, normal, or undetectable. If normal it is inappropriately low in relation to the level of calcium
Hypocalcemia can also be caused by nutritional deficiencies, renal failure, and intestinal disorders

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23
Q

Hypoparathyroidism Treatment and Education

A

Calcium and vitamin D supplements

Education about: Lifelong treatment, Risk for injury, especially fractures, Modification of the home environment

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24
Q

Hyperparathyroidism

A

An excess of parathyroid hormone in the bloodstream
Primary hyperparathyroidism is caused by enlargement of one or more of the parathyroid glands causing overproduction of PTH (adenomas, hyperplasia, and carcinomas)
Secondary hyperparathyroidism is the result of another disease process that lowers the level of calcium in the body, causing the parathyroid to overwork to compensate (Chronic renal failure, calcium deficiency, Vit D deficiency)

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25
Q

Hyperparathyroidism Signs and Symptoms

A

S&S are wide and varied: weakness, fatigue, depression, poor concentration, peripheral sensory or motor neuropathy, dysrhythmias, kidney stones, pathological fractures, osteopenia, constipation, nausea & vomiting, asymptomatic

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26
Q

Hyperparathyroidism Diagnosis

A

Measure serum PTH and calcium levels
Primary hyperparathyroidism: Increased PTH and calcium levels, Radiological studies may show osteopenia, and osteoporosis which lend support
Secondary hyperparathyroidism: Increased PTH and normal or low calcium levels, Most likely have some diagnosed underlying disorder

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27
Q

Hyperparathyroidism Treatment

A

Definitive treatment for primary hyperparathyroidism is parathyroidectomy: Watch surgical site closely for bleeding, Look behind the neck for pooling, Assess voice for signs of laryngeal nerve damage
Symptom management
Clients that are asymptomatic with mild hypercalcemia may require no treatment
Follow up lab work to monitor calcium levels
Balanced diet with sources of calcium and Vit D

28
Q

Pituitary Gland

A

The hypothalamus and pituitary form a unit that regulates the function of several endocrine glands, including the thyroid, adrenals, ovaries, and testes
The pituitary gland is composed of two parts: Anterior pituitary and Posterior pituitary
Anterior pituitary produces many hormones including thyroid stimulating hormone (TSH) and growth hormone (GH)
Posterior pituitary produces antidiuretic hormone (ADH)

29
Q

Hypersecretion of Growth Hormone

A

Acromegaly is a rare hormonal syndrome caused in at least 90% of cases by a benign GH-secreting pituitary adenoma
The majority are sporadic but may have a genetic factor
This excess GH causes local overgrowth of bone, especially in the skull and mandible
There is no linear growth because the epiphyses of the long bones have fused after puberty. Excess GH before puberty is called gigantism

30
Q

Hypersecretion of Growth Hormone Signs and Symptoms

A 
Signs appear gradually
Clients have course features with large hands and feet 
Thick fingers and toes
Large tongue
Enlarged heart
Excessive sweating
Carpal tunnel syndrome
Fatigue
Joint pain
Weight gain
Sleep apnea
31
Q

Hypersecretion of Growth Hormone diagnosis

A

Glucose suppression test: Drinking 75 to 100 grams of glucose solution lowers blood GH levels in healthy people. In people with GH overproduction, suppression does not occur
CT scan may show a pituitary tumor
X-ray may show enlargement of the sella turcica (bony cavity that houses the pituitary), sinuses, hands, and feet

32
Q

Hypersecretion of Growth Hormone treatment

A

Surgical removal is normally the initial treatment for a small localized mass
Transsphenoidal microsurgery
Through the nose or under the upper lip and through the gum
Radiation may be needed for those who are not a candidate for surgery or when surgery does not remove all of the tumor
Medications can be used to help suppress growth hormone secretion. They are often used to shrink tumors prior to surgery (Octreotide)

33
Q

Nursing management of Hypersecretion of Growth Hormone

A

Assess the client’s perceived body image and offer emotional support
Preoperative teaching
Postoperative care includes: Neurological assessment, Vital signs, Elevate the HOB 30 degrees. Avoid coughing, sneezing, straining
Test nasal drainage for CSF
Oral cares with a sponge rather than toothbrush
Urine output should be measured

34
Q

Diabetes Insipidus

A

Diabetes Insipidus is an inability of the kidneys to concentrate urine due to a lack of circulating ADH
There can also be resistance of the renal tubules to the action of ADH
Can be permanent or transient: Head trauma, surgery, tumor, infection, cerebral edema, renal disease, medications, genetic predisposition

35
Q

Diabetes Insipidus Signs and Symptoms

A

polyuria, polydipsia, severe dehydration, hypernatremia, fever, cardiovascular collapse

36
Q

Diabetes Insipidus Diagnosis and Treatment

A

Diagnosed with the water deprivation test
Treatment:
For central DI: DDAVP and replacing fluids
For nephrogenic DI: low sodium diet, fluid replacement, treat underlying cause

37
Q

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

A

due to an excess of ADH and results in reduced urinary output and fluid volume expansion
Can be caused by shock, trauma, stress, surgery, pulmonary infections, medications
A high percentage of those with SIADH have a malignant tumor, usually of the lung, that secretes ADH

38
Q

SIADH signs and symptoms

A

Due to the resulting hyponatremia and include: fatigue, headache, nausea, altered LOC, seizure, coma, death, or asymptomatic

39
Q

SIADH diagnosis

A

high urine osmolality, low plasma osmolality, increased urinary sodium, and euvolima

40
Q

SIADH treatment

A

fluid restriction, hypertonic IV solutions, meds include declomycin and lithium

41
Q

Nursing care of SIADH

A

I&O, vital signs, daily weights, monitoring electrolytes, LOC, ECG, skin integrity, reducing injury risk, coping, education, follow up

42
Q

Adrenal Gland

A

Located on the superior poles of each kidney

Consists of two divisions: adrenal medulla and adrenal cortex

43
Q

Adrenal medulla

A

inner portion
Produces catecholamines epinephrine and norepinephrine which increase HR, CO, vasoconstriction, and BP. They also have an effect on metabolism stimulating gluconeogensis, glycogenolysis, and lipolysis

44
Q

Adrenal cortex

A

Outer portion
Produces aldosterone which works on the kidney to promote sodium and water reabsorption and potassium and hydrogen excretion, cortisol which increases gluconeogensis and lipolysis, inhibits bone formation, anti-inflammatory, alters mood, stimulates RBC production, and androgen precursors

45
Q

Pheochromocytoma

A

Catecholamine producing tumors located in adrenal or extra-adrenal sites (retroperitoneal, pelvic, and thorax)
2 to 8 out of 1 million people per year
No defined cause but 25% carry a gene mutation

46
Q

Pheochromocytoma signs and symptoms

A

headache, excessive sweating, palpitations, tachycardia, episodic or sustained hypertension, anxiety, panic attacks
Episodic hormone release lasts usually less than an hour and is characterized by palpitations and tachycardia. May be precipitated by surgery, pregnancy, medications

47
Q

Pheochromocytoma diagnosis

A

Plasma and urinary catecholamines and CT or MRI to locate the tumor

48
Q

Pheochromocytoma Treatment and Nursing Management

A

Treatment includes tumor removal
Nursing Management:
Pre-operatively the client will most likely be hyperglycemic and hypertensive
Monitor the client’s blood sugar and blood pressure
Administer alpha and beta blockers for hypertension
Post-operatively monitor for hypoglycemia and hypotension
Administer fluids to prevent hypotension
Basic post operative cares

49
Q

Adrenocortical Hypofunction

A

Primary adrenal insufficiency is caused by dysfunction of the adrenal cortex, which results in deficiency of adrenocortical hormones- aldosterone, cortisol, androgens
Secondary adrenal insufficiency is caused by dysfunction of the anterior pituitary leading to a loss of adrenocorticotropic hormone (ACTH), which results in a deficiency of adrenocortical hormones

50
Q

Addison’s disease

A

Autoimmune adrenalitis is the primary cause of primary adrenocortical insufficiency, accounting for 80% of cases
Other causes of primary adrenocortical insufficiency include: infection, surgical removal, tumor
There is gradual destruction so signs are not apparent until severe damage has occurred

51
Q

Addison’s disease signs and symptoms

A

Signs & symptoms are related to the decrease in aldosterone, cortisol, and androgens: fatigue, weakness, weight loss, hypotension, dehydration, hypoglycemia, hyponatremia, hyperkalemia, acidosis
Pigmentation changes from increased ACTH
Freckling, darkening of the skin
Bluish-black patches on the mucous membranes

52
Q

Addison’s disease diagnosis

A

Diagnosis can be difficult because adrenocortical hormone serum levels may be normal
Measure serum ACTH and cortisol levels
Rapid ACTH stimulation test
Measurement of the cortisol in the client’s blood before and 60 minutes after an ACTH injection

53
Q

Addison’s disease treatment

A

hormone replacement: Hydrocortisone and Fludrocortisone
Maintain adequate intake of sodium
Some physicians may prescribe androgen replacement to improve mood and sexuality
DHEA

54
Q

Addison’s disease nursing management

A

Education regarding lifelong treatment and how to take prescribed medications
Stress and illness will increase their need for hydrocortisone
Flu like symptoms should never be ignored because they could signal an adrenal crisis

55
Q

Adrenal Crisis

A

Life-threatening complication characterized by dehydration, fever, hyponatremia, hyperkalemia, vascular collapse, and death
Occurs in clients with chronic adrenocortical insufficiency and is precipitated by stress such as trauma or infection

56
Q

Adrenal Crisis Treatment & Management

A

IV infusion of hydrocortisone, normal saline, and vasopressors (if needed)
Monitor electrolytes
Treat underlying problem
Watch for complications such as seizures, changes of LOC, ECG changes

57
Q

Secondary Adrenal Insufficiency

A

One of the most common causes is chronic use of corticosteriods such as prednisone
Increases the serum concentration of cortisol and suppresses ACTH secretion
Can also be caused by damage to the pituitary
When prednisone is taken long term the adrenals can atrophy from lack of ACTH stimulation

58
Q

Secondary Adrenal Insufficiency signs & symptoms

A

Signs & symptoms are similar to primary adrenal insufficiency except there are no pigmentation changes and aldosterone is still produced (due to RAAS), electrolyte levels should be normal and hypotension is less prevalent

59
Q

Adrenal Hyperfunction/Cushing’s

A

Cushing syndrome, results from chronic exposure to excessive circulating levels of cortisol
Those with Cushing syndrome also have varied degrees of hyperaldosteronism and adrenal androgens
ACTH-dependent which results from excess production of ACTH from pituitary or ectopic sites (tumor)
ACTH-independent which results from an adrenal cortex tumor or use of medications such as prednisone

60
Q

Cushing’s signs and symptoms

A

Upper body obesity, Thin arms and legs, Moon face, Buffalo hump, Acne, Hirsutism (abnormal growth of hair), Purple striae, Fatigue, Depression, Hyperglycemia, Hypertension, Water retention, Poor wound healing

61
Q

Cushing’s diagnosis

A

24- hour urinary free cortisol collection measures the total amount of free cortisol excreted into the urine in a 24-hour period
Low-dose dexamethasone suppression test. Dexamethasone is a synthetic steroid similar to cortisol, which suppresses ACTH secretion in healthy people. Therefore, giving dexamethasone should reduce ACTH levels, resulting in decreased cortisol levels.
Plasma ACTH may help to distinguish between ACTH-dependent or independent causes
CT or MRI can locate tumors

62
Q

Cushing’s treatment

A

Surgery to remove tumor
Radiation
Mitotane is a medication used to decrease the size of adrenal tumors and reduce symptoms
For those on long-term corticosteroids, they will need gradual withdrawal or reduction
Corticosteroids cannot be withdrawn abruptly or it may trigger an adrenal crisis

63
Q

Hyperaldosteronism

A

Primary aldosteronism is an excess aldosterone production by the adrenal cortex
Two main causes are adenoma or bilateral idiopathic adrenocortical hyperplasia

64
Q

Hyperaldosteronism signs and symptoms

A

hypertension that is often long standing and refractory to multiple medications, muscle weakness, polydipsia, polyuria, headache, fatigue
Any client that has hypokalemia despite potassium supplement should be assessed for hyperaldosteronism

65
Q

Hyperaldosteronism diagnosis

A

Diagnosis is made through elevated plasma and urine aldosterone levels with suppressed plasma renin activity (renin from the kidney stimulates aldosterone production), CT or MRI for tumor location

66
Q

Hyperaldosteronism treatment

A

Removal of the tumor or administration of spironolactone (aldactone)

Adult Nursing V (4 decks)

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