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ABSN NUR 326 > Week 5: Endocrine > Flashcards

Week 5: Endocrine Flashcards

1
Q

What are the 2 adrenocortical hormone disorders?

A

Addison’s and Cushing

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2
Q

What is Cushing Syndrome?

A

hypercortisolism (too much cortisol)

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3
Q

What can cause hypercortisolism?

A

Primary= disease of the adrenal cortex (Cushing SYNDROME)
Secondary= disease of the anterior pituitary (Cushing DISEASE)
Exogenous steroids= long term steroid use for other diseases (Cushing’s SYNDROME)

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4
Q

What are the s/s of Cushing syndrome?

A
  1. CNS- mood swings, insomnia, loss of libido
  2. Suppression of immune- impaired wound healing and risk for infection
  3. protein breakdown - muscle wasting, muscle weakness, thinning of skin, bone pain, thinning hair
  4. maintain vascular system - HTN, capillary friability
  5. increased glucose availability - glucose intolerance and hyperglycemia
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5
Q

What is the treatment for Cushings?

A

treat the cause; take out tumor, or stop steroids

drugs; aminoglutethimide and ketoconazole

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6
Q

MOA of aminoglutethimide

A

blocks the synthesis of all adrenal steroids

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7
Q

indication for aminoglutethimide

A

temporary therapy to decrease cortisol

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8
Q

S/E of aminoglutethimde

A

drowsiness, nausea, anorexia, and rash

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9
Q

MOA of ketoconazole

A

antifungal drug that also inhibits glucocorticoid synthesis

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10
Q

Indication for ketoconazole

A

adjunct therapy to surgery or radiation for Cushing Syndrome

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11
Q

S/E of ketoconazole

A

severe liver damage

do NOT take with ETOH, drugs, or while pregnant

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12
Q

What is Addison Disease?

A

disease of the adrenal cortex that causes HYPOsecretion of ALL 3 adrenocortical hormones

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13
Q

The lack of which hormone causes the most severe effects of Addisons?

A

Cortisol

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14
Q

What is the etiology of Addisons?

A

idiopathic, autoimmune, or other

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15
Q

Pathogenesis of Addisons?

A

adrenal gland is destroyed, most symptoms don’t show until 90% non-functional causing adrenocorticotropic hormone (ACTH) and melanocyte-stimulating hormone (MSH) are secreted in large amounts

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16
Q

Early s/s of Addison Disease

A

anorexia, weight loss, weakness, malaise, apathy, E- imbalances, and skin hyperpigmentation

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17
Q

Late s/s of Addison disease

A

Think Na and water retention problems

-hypotension, decreased cardiac output, salt craving, hyponatremia, hyperkalemia, hypoglycemia, weakness and fatigue, hyperpigmentation

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18
Q

What are complications of Addisons?

A

Addisonian (Adrenal) crisis

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19
Q

What causes an Addisonian crisis?

A

sudden loss of adrenal gland OR sudden increase in stress OR suddenly stopping steroid therapy

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20
Q

What is the pharmacotherapy of Addison disease?

A

-glucocorticoid (sometimes mineralocorticoid)

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21
Q

What considerations with the drug therapy of Addisons?

A

NEVER abruptly stop steroid therapy, take higher doses during stress, always have an emergency supply, and wear a medic alert bracelet

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22
Q

What is pheochromocytoma?

A

rare tumor of the adrenal medulla that produces excessive catecholamines (epinepherine and norepinepherine)

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23
Q

r/f for pheochromocytoma

A

young to middle age

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24
Q

S/S of pheochromocytoma

A

headache, diaphoresis, and tachycardia

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25
Q

What is the treatment for pheochromocytoma

A

preferred= surgery
drugs= alpha-adrenergic blockers (used for inoperable tumors and preop HTN)

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26
Q

What alpha-adrenergic is taken with pheochromocytoma?

A

phenoxybenzamine

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27
Q

What is the MOA of phenoxybenzamine?

A

long-lasting IRREVERSIBLE blockage of alpha adrenergic receptors

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28
Q

s/e of phenoxybenzamine

A

lowers blood pressure ,nasal congestion, reflex tachycardia, sexual s/e for men (remember IRREVERSIBLE)

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29
Q

What are the two Antidiuretic hormone disorders?

A

Diabetes Insipidus and SIADH

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30
Q

What is SIADH?

A

“Syndrome of Inappropriate AntiDiuretic Hormone”

-an abnormal production or sustained secretion of ADH

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31
Q

Characterization of SIADH

A

fluid retention, low serum osmolality, hyponatremia, concentrated urine

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32
Q

Etiology of SIADH

A

-Malignant tumors (e.g. small cell carcinoma of the lungs)
-CNS disorders (e.g. head trauma, stroke, brain tumor)
-drug therapy (e.g. morphine, SSRIs, chemo)
-Miscellaneous conditions (e.g. hypothyroidism, infection)

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33
Q

What is osmolality with SIADH?

A

Serum= LOW
NA+=LOW
UO=LOW
weight=GAIN
Urine SG= HIGH

34
Q

SIADH s/s

A

dyspnea, fatigue, confusion, lethargy, muscle twitching, convulsions, impaired taste, anorexia, vomiting, cramps,

SEVERE= Na<100-115 causes possible irreversible neurological damage

35
Q

what is the treatment of SIADH

A

treat the cause first
second line = demeclocycline

36
Q

What class is demeclocycline?

A

tetracycline

37
Q

MOA for demeclocycline

A

interferes with renal response to ADH

38
Q

S/E of demeclocycline

A

photosensitivity, teeth staining, and nephrotoxic

39
Q

What is Diabetes Insipidus (DI)?

A

a deficiency of ADH or a decreased renal response to ADH, characterized by excessive loss of water in urine

40
Q

What two forms of DI?

A

Neurogenic, Nephrogenic

41
Q

Etiology of Neurogenic DI

A

hypothalamus or pituitary gland damage

Sometimes associated with stroke, TBU, brain surgery or cerebral infections

42
Q

Is Neurogenic DI onset sudden or slow?

A

SUDDEN

43
Q

Is Neurogenic DI permanent?

A

Usually

44
Q

What is the etiology of Nephrogenic DI?

A

loss of kidney function, often drug related (e.g Lithium for bipolar)

45
Q

Is nephrogenic DI onset sudden or slow?

A

SLOW

46
Q

Is nephrogenic DI acute or progressive?

A

progressive

47
Q

What is the osmolality for DI?

A

serum= HIGH
sodium=HIGH
UO=HIGH
Urine SG= LOW
Weight= LOSS

48
Q

s/s of DI

A

polyuria, polydipsia, dehydration, electrolyte imbalance, hypovolemic shock

49
Q

Treatment for NEUROgenic DI

A

synthetic ADH replacement

50
Q

Treatment for NEPHROgenic DI

A

thiazide diuretics

51
Q

What drug is a synthetic ADH?

A

Desmopressin

52
Q

S/E of desmopressin

A

small dose= none
nasal spray=irritation
large dose= hyponatremia, water intoxication

53
Q

What does thyroxine (T4) do?

A

regulate the bodies metabolism that influences almost every body system

54
Q

What is the flow for the release of thyroxine?

A

hypothalamus
| (TRH)
anterior pituitary
| (TSH )
thyroid gland
|
increased thyroxine

55
Q

What does thyroxine inhibit?

A

the hypothalamus from releasing TRH, and the anterior pituitary from releasing TSH

Negative Feedback

56
Q

What are the most common thyroid disfunctions?

A

primary thyroid disorders

57
Q

What can occur with thyroid disorders?

A

goiter (thyroid enlargement)

58
Q

What is hypothyroidism?

A

insufficient levels of thyroid hormones (T3 and T4)

59
Q

What happens in primary hypothyroidism?

A

increase in release of TSH from pituitary

60
Q

What is the most common cause of hypothyroidism?

A

Hashimoto’s thyroiditis (an autoimmune disorder)

61
Q

R/F for hypothyroidism

A

female, age>50, Caucasian, pregnancy, hx of autoimmune disorder, family hx, medications, treatments for hyperthyroidism

62
Q

Early hypothyroidism s/s

A

cold intolerance, WEIGHT GAIN, lethargy, fatigue, memory deficits, poor attention span, increased cholesterol, muscle cramps, raises carotene levels, constipation, decreased fertility, puffy face, hair loss, and brittle nails

63
Q

Late hypothyroidism s/s

A

below normal temp, bradycardia, weight gain, decreased LOC, thickened skin, and cardiac complications

64
Q

How does hypothyroidism affect the body?

A

-raises cholesterol
-raises carotene levels (yellow skin)
-causes anemia
-decreased filtration by kidney (risk of med toxicity)
-can cause hoarse voice)

65
Q

What are the labs with a primary hypothyroidism diagnosis?

A

-high TSH levels
-Low T3 and T4

66
Q

What are the labs associated with a secondary hypothyroidism diagnosis?

A

-high TSH levels
-high T# and T4

67
Q

What is the MOA of levothyroxine?

A

T4-synthetic thyroid hormone, that is converted to T3 in the body

68
Q

What are the three types of hyperthyroidism?

A
  1. Primary = thyroid problem
  2. Secondary= pituitary problem
  3. Tertiary = hypothalamus problem
69
Q

R/F for hyperthyroidism

A

family hx of graves, age>40, women, Caucasian, medications, excessive iodine intake, pregnancy

70
Q

What is graves’ disease

A

autoimmune disorder causing excess levels of T3 and T4

71
Q

S/S of Graves’ disease

A

nervousness, insomnia, sensitivity to heat, weight loss, thyroid is enlarges, an audible bruit over thyroid, afib, myexedma, exophthalmos

72
Q

What is exophthalmos?

A

a wide eyed stare associated with increased sympathetic tone and infiltration of the extraocular area with lymphocytes and mucopolysaccharides

73
Q

labs for diagnosis of Graves’ disease?

A

low TSH
high T3 and T4

74
Q

Treatments for Graves’ disease

A

antithyroid hormone medication (propythiouracil), radioactive iodine, or surgery (and then used levothyroxine)

75
Q

What considerations are needed when taking propylthiouracil?

A

hepatotoxic and only used in 1st trimester with caution

76
Q

What is a thyrotoxic crisis or thyroid storm?

A

overwhelming release of thyroid hormones that exerts an intense stimulus of metabolism

life threatening

77
Q

What typically triggers a thyrotoxic crisis?

A

surgery, trauma, or infection

78
Q

What causes all the symptoms of hypoparathyroidism?

A

hypocalcemia from insufficient PTH

79
Q

S/S of hypocalcemia

A

muscle cramps, irritability, tetany, convulsions

80
Q

What is the treatment for hypoparathyroidism?

A

replace PTH, normalize Ca and Vitamin D level, possible surgery (PTH are then lifelong)

81
Q

S/S of hyperparathyroidism (high Ca)

A

muscle weakness, poor concentration, neuropathies, HTN, kidney stones, metabolic acidosis, osteopenia, fractures, constipation, depression, confusion, or subtly cognitive defects

82
Q

treatment of hyperparathyroidism

A

reduce levels of calcium, diuretics, calcitonin, bisphosphonates, Vitamin D, and surgical interventions

ABSN NUR 326 (10 decks)

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