Endocrine Disorders Flashcards

1
Q

What is acromegaly? What are the clinical manifestations?

A

Overproduction of GH, most often caused by a pituitary adenoma.
Will present as:
Overgrowth of bones/soft tissue of face, hands and feet.
Muscle/joint pain
Tongue enlargement
Deep voice
Vision changes
Headaches (very common)
Skin changes to thick, leathery, oily

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2
Q

Treatment for acromegaly

A

Surgery (hypophysectomy)
Drug therapy (Sandostatin)
Radiation
–The damage caused by this will not reverse–

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3
Q

Pituitary adenomas will manifest how?

A

Headaches
Vision changes
Nausea/vomiting
–These are all signs of increased intracranial pressure–
Also, the location of the adenoma will determine the hormone imbalance. This may manifest with breast, growth hormone, sex hormone, thyroid, fluid balance abnormalities.

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4
Q

What does GH naturally antagonize?

A

Insulin
When GH increases insulin decreases which makes glucose levels increase.

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5
Q

How do we care for a patient after a hypophysectomy (pituitary removal)?
—remember this will be a done through nose or mouth—

A

Watch for hematoma at site of pituitary-this will present at vision changes, eye movements, pupil changes.
Watch for CSF leaks from drain. Monitor for headache which may indicate CSF leak.
HOB >30%
No straining, bending, coughing etc.
No brushing teeth for 10 days
Watch for diabetes insipidus

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6
Q

What hormones are secreted by posterior pituitary?

A

ADH
Oxytocin

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7
Q

What are the two problems associated with imbalance of ADH?

A

SIADH-too much
Diabetes insipidus-too little

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8
Q

What are the hallmark signs of SIADH?

A

Fluid retention
Diluted serum and concentrated urine
Hyponatremia and hypochloremia

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9
Q

What is the most common cause of SIADH?

A

Cancer, especially lung cancer
–This is because the cancer cells start to produce their own ADH leading to an overproduction–This is called an ectopic release of ADH–

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10
Q

What population is most at risk of developing SIADH?

A

Geriatric

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11
Q

Nursing care of SIADH

A

Daily weights
I/O’s
VS
Heart and lung sounds
Watch for signs of hyponatremia like: headache, changes to LOC, decreased neuro function, muscle twitching, abdominal cramps, vomiting.
Fluid restriction
Keep HOB <10 degrees
Watch for skin breakdown

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12
Q

What is the only treatment in mild cases of SIADH?

A

Fluid restriction only—
to allow the sodium levels of body to balance slowly.

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13
Q

What meds are used to treat more severe SIADH?

A

Lasix (but this drops sodium levels)
Demeclocycline (blocks effect of ADH)
Conivaptan and tolvaptan (block ADH)
IV hypertonic NS 3%
–Rebalance must be done slowly–

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14
Q

What are hallmark signs of diabetes insipidus?

A

Polyuria
Polydipsia

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15
Q

What labs will be abnormal in DI?

A

Hypernatremia
Dilute urine with low specific gravity
—Remember this is water loss WITHOUT solute loss—

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16
Q

What are clinical manifestations of DI?

A

Drinking»Peeing very dilute urine
Exhaustion from nocturia
Weakness from hypernatremia
Dehydration s/sx
Neuro changes

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17
Q

What are the 3 types of DI?

A

Central (neuro) DI (problem in pituitary, most common)
Nephrogenic DI (problem in kidney as target tissue of ADH)
Primary DI (thirst center or psych disorder)

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18
Q

What replacement fluids are given in DI?

A

Hypotonic solutions (remember they are hypernatremic so need hypotonic solution)
NS 0.45%
D5W

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19
Q

What is first line drug for CENTRAL DI? Other drugs given?

A

1.DDAVP (ADH hormone replacement)
2.—-Pressin drugs (desmo and vaso)

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20
Q

What is treatment for NEPHROGENIC DI?

A

Hormone DDAVP doesn’t work
Low sodium diet
Thiazide diuretics help kidneys slow down.

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21
Q

What is a goiter? Caused by?

A

An enlarged thyroid
Can be caused by hypo or hyper thyroid issues.

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22
Q

What are goitrogens?

A

Goiter causing food/drugs

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23
Q

What is thyroiditis?

A

Inflammation of thyroid.
Can be caused by bacteria, virus, goiter, autoimmune.
S/Sx=pain, fever, chills, sweats, fatigue

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24
Q

What labs will be abnormal is Hashimoto’s thyroiditis?

A

Low T4, T3 with high TSH
Antithyroid antibodies-called TPO-Ab
(Thyroid peroxidase antibodies)

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25
Q

Who are at risk for thyroid imbalances?

A

Women
20-40 yo
White
Family Hx
Hx of autoimmune disorders

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26
Q

What is Graves disease?

A

Most common cause of hyperthyroidism
The opposite of Hashimoto’s
Antibodies to TSH receptors results in low TSH and high T3, T4
Autoimmune

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27
Q

Clinical manifestations of hyperthyroidism.

A

Think sympathetic NS stimulation of heart, lungs, nerves, mood
But also stimulates GI system and metabolism
Increased metabolism>increased appetite but with weight LOSS

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28
Q

Clinical manifestations of hypothyroidism.

A

Slows down GI, metabolism, mood, heart, mind
Increased cholesterol and triglycerides

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29
Q

What is exophthalmos?

A

Protruding eyes
Classic finding in Graves disease

30
Q

What is thyrotoxicosis?

A

Thyroid storm
Big dump of T3, T4 in system
Emergency
Can be caused by stress, surgery, infection of someone who already has hyperthyroidism
S/sx are: High fever, tachycardia, agitation, delirium, seizures, nausea, vomiting, diarrhea, abdominal pain

31
Q

What is preferred treatment of hyperthyroidism?

A

Radioactive Iodine Therapy (RAI)
Destroys thyroid tissue
Given orally or IV
Not suitable in pregnancy
Causes patient to be radioactive so home precautions necessary to limit exposure to family
Usually results in HYPOthyroidism

32
Q

What are 3 main types of drugs to treat hyperthyroidism?

A

Antithryoid drugs
Iodine (blocks T3, T4 and shrinks thyroid)
Beta adrenergic blockers

33
Q

What are the two antithyroid drugs used?

A

propyl-thio-uracil
methi-ma-zole
–Never abruptly stop–

34
Q

What are some beta adrenergic blockers used to treat hyperthyroidism?

A

These block the effects of the sympathetic NS
Pro-pran-olol
A-ten-olol

35
Q

What type of diet will a patient with hyperthyroidism need?

A

High calorie

36
Q

Post op care of patient after thyroidectomy.

A

Semi Fowlers
Monitor for signs of tracheal compression or hematoma on neck
Monitor airway and have suction
Assess voice
Watch for signs of hypocalcemia and keep IV calcium gluconate available
Monitor thyroid levels
Keep head/neck protected and supported

37
Q

Nursing care of patient with thyrotoxicosis.

A

ICU
IV Fluid replacement from GI losses
Calm, cool environment
Build trust
Artificial tears
Sit upright (if increased ocular pressure)
Dark glasses
Eye muscle ROM exercises

38
Q

What is the difference between primary and secondary hypothyroidism?

A

Primary=problem with thyroid
Secondary=problem with pituitary or hypothalamus

39
Q

What is cretinism?

A

Hypothyroidism that develops in infancy. Child will have physical and mental defects
Newborns are routinely screened

40
Q

What is myxedema?

A

Long standing hypothyroidism has led to facial swelling, deformity.
Mask like look
–Can lead to serious problem and CV collapse, will get IV T3 and T4 replacement

41
Q

What is biggest caution while increasing T3 and T4 levels in hypothyroidism?

A

Cardiac assessment
Monitor heart rate and dysrhythmias

42
Q

What abnormal labs will be present in hyperparathyroidism?

A

Hypercalcemia
Hypophosphatemia

43
Q

What are clinical manifestations of hyperparathyroid?

A

Hypercalcemia s/sx:
Constipation and decreased appetite
Muscle weakness and decreased DTR
Kidney stones and renal failure
Brain fog and emotional lability
Osteoporosis and occult fractures
Dysrhythmias

44
Q

What test is performed for bone density?

A

DEXA scan

45
Q

Important when giving IV calcium.

A

Highly irritating to vein
Give slowly
Monitory EKG and hypotension

46
Q

Tetany is a sign of …

A

Hypocalcemia
Can start as tingling of mouth and hands
Treatment is IV calcium

47
Q

What is the first sign of hyponatremia? (according to NCLEX)

A

Headache

48
Q

What is Graves’ disease?

A

Autoimmune
Thyroid enlargement
Excess T3, T4
Most common cause of hyperthyroidism

49
Q

What is acropachy?

A

Sign of Graves disease.
Swelling of hands and clubbing of fingers

50
Q

What are two types of iodine meds and how do they work?

A

Potassium iodine (SSKI)
Lugol’s solution
–Usually given to shrink and decrease vascularity of thyroid before surgery–
Blocks T3, T4 and shrinks thyroid

51
Q

Most common type of endocrine cancer.

A

Thyroid

52
Q

S/Sx of thyroid cancer.

A

Fullness of neck
Dysphagia
Hoarseness
Painless
Enlarged thyroid
Normal T3, T4

53
Q

What is MEN stand for?

A

Multiple Endocrine Neoplasm
–Inherited, benign (but can become malignant) growths on multiple endocrine glands. Affects hormone balance of several types

54
Q

What is main hormone of salt control?

A

Aldosterone

55
Q

What are clinical manifestations of Cushings?

A

Weight gain through trunk
Moon face with redness
Hirsutism (Her-si-tism)
Buffalo hump
Weak thin extremities with edema
Increased BP
Hyperglycemia
Thin, easily bruised skin
Poor wound healing
Purple red striae

56
Q

Who are most at risk of developing Cushings?

A

Patients on long term corticosteroids
–Must taper these down slowly–

57
Q

Nursing goals in Cushings.

A

Relief of symptoms
Prevent or treat any complicating conditions (hyperglycemia, hypernatremia, infection, CVD)
Emotional support

58
Q

Treatment for Cushings.

A

Find the cause
Options include:
Removing any pituitary or adrenal tumors
Adrenalectomy
Meds like ketoconazole (Nizoral) and mitotane
(these meds suppress cortisol production, but they are highly toxic)

59
Q

What hormones are hypo in Addison’s disease?

A

Too little:
Cortisol
Aldosterone
Androgens

60
Q

What is primary cause of Addison’s?

A

Autoimmune

61
Q

S/Sx of Addison’s.

A

Hypoglycemia
Hyponatremia, dehydration» hypovolemia»Low BP
Muscle weakness, anorexia, weight loss
Bronzing
–this is a slow progression–

62
Q

What brings on an Addisonian crisis?

A

Emotional Stress
Physical stress
Surgery
In an already hypoadrenal patient

63
Q

What does an Addisonian crisis look like?

A

Signs of hypovolemic shock:
Acute hypotension
High fever
Cyanosis
Headache
Nausea/diarrhea
Confusion, restlessness

64
Q

Treatment for Addisons.

A

Hydrocortisone
Fludrocortisone
DHEA
IV fluid replacement

65
Q

Nursing care for Addisons.

A

Watch for:
Signs of shock
Monitor BP closely
Monitor I/O’s carefully
Protect from infection
Protect from stressors

66
Q

What is Conn syndrome?

A

Hyperaldosteronism
Results in too much salt and too low potassium
Results in high BP and hypokalemic alkalosis

67
Q

What is pheochromocytoma?

A

Rare
Tumor in adrenal medulla
Makes too much epi and norepinephrine
Severe HTN, headache, tachycardia, chest pain
–Don’t palpate the abdomen–

68
Q

Side effects of corticosteroid therapy.

A

Delayed wound healing and increased risk for infection
Suppressed inflammatory response
Pathologic fx, muscle weakness and atrophy
Hard on stomach»Peptic ulcer
Hyperglycemia, hypernatremia
Hypokalemia, hypocalcemia
Hypertension
Mood/behavior changes

69
Q

Number one thing to teach patients about corticosteroids?

A

Never stop abruptly

70
Q

What are signs of Conn syndrome?

A

Hypertension
Headache
Hypokalemia
–We should suspect this in patients with these 3 signs who are NOT on diuretics–

71
Q

Treatment for Conn syndrome.

A

Adrenalectomy
Spironolactone (K+ sparing)
Antihypertensives
Sodium restrictions

72
Q

What is classic triad of symptoms in patients with pheochromocytoma?

A

Severe pounding headache
Tachycardia
Profuse sweating
—This will occur in young to mid age adults–