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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
What is the treatment for pheochromocytoma
preferred= surgery drugs= alpha-adrenergic blockers (used for inoperable tumors and preop HTN)
26
What alpha-adrenergic is taken with pheochromocytoma?
phenoxybenzamine
27
What is the MOA of phenoxybenzamine?
long-lasting IRREVERSIBLE blockage of alpha adrenergic receptors
28
s/e of phenoxybenzamine
lowers blood pressure ,nasal congestion, reflex tachycardia, sexual s/e for men (remember IRREVERSIBLE)
29
What are the two Antidiuretic hormone disorders?
Diabetes Insipidus and SIADH
30
What is SIADH?
"Syndrome of Inappropriate AntiDiuretic Hormone" -an abnormal production or sustained secretion of ADH
31
Characterization of SIADH
fluid retention, low serum osmolality, hyponatremia, concentrated urine
32
Etiology of SIADH
-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)
33
What is osmolality with SIADH?
Serum= LOW NA+=LOW UO=LOW weight=GAIN Urine SG= HIGH
34
SIADH s/s
dyspnea, fatigue, confusion, lethargy, muscle twitching, convulsions, impaired taste, anorexia, vomiting, cramps, SEVERE= Na<100-115 causes possible irreversible neurological damage
35
what is the treatment of SIADH
treat the cause first second line = demeclocycline
36
What class is demeclocycline?
tetracycline
37
MOA for demeclocycline
interferes with renal response to ADH
38
S/E of demeclocycline
photosensitivity, teeth staining, and nephrotoxic
39
What is Diabetes Insipidus (DI)?
a deficiency of ADH or a decreased renal response to ADH, characterized by excessive loss of water in urine
40
What two forms of DI?
Neurogenic, Nephrogenic
41
Etiology of Neurogenic DI
hypothalamus or pituitary gland damage Sometimes associated with stroke, TBU, brain surgery or cerebral infections
42
Is Neurogenic DI onset sudden or slow?
SUDDEN
43
Is Neurogenic DI permanent?
Usually
44
What is the etiology of Nephrogenic DI?
loss of kidney function, often drug related (e.g Lithium for bipolar)
45
Is nephrogenic DI onset sudden or slow?
SLOW
46
Is nephrogenic DI acute or progressive?
progressive
47
What is the osmolality for DI?
serum= HIGH sodium=HIGH UO=HIGH Urine SG= LOW Weight= LOSS
48
s/s of DI
polyuria, polydipsia, dehydration, electrolyte imbalance, hypovolemic shock
49
Treatment for NEUROgenic DI
synthetic ADH replacement
50
Treatment for NEPHROgenic DI
thiazide diuretics
51
What drug is a synthetic ADH?
Desmopressin
52
S/E of desmopressin
small dose= none nasal spray=irritation large dose= hyponatremia, water intoxication
53
What does thyroxine (T4) do?
regulate the bodies metabolism that influences almost every body system
54
What is the flow for the release of thyroxine?
hypothalamus | (TRH) anterior pituitary | (TSH ) thyroid gland | increased thyroxine
55
What does thyroxine inhibit?
the hypothalamus from releasing TRH, and the anterior pituitary from releasing TSH *Negative Feedback*
56
What are the most common thyroid disfunctions?
primary thyroid disorders
57
What can occur with thyroid disorders?
goiter (thyroid enlargement)
58
What is hypothyroidism?
insufficient levels of thyroid hormones (T3 and T4)
59
What happens in primary hypothyroidism?
increase in release of TSH from pituitary
60
What is the most common cause of hypothyroidism?
Hashimoto's thyroiditis (an autoimmune disorder)
61
R/F for hypothyroidism
female, age>50, Caucasian, pregnancy, hx of autoimmune disorder, family hx, medications, treatments for hyperthyroidism
62
Early hypothyroidism s/s
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
Late hypothyroidism s/s
below normal temp, bradycardia, weight gain, decreased LOC, thickened skin, and cardiac complications
64
How does hypothyroidism affect the body?
-raises cholesterol -raises carotene levels (yellow skin) -causes anemia -decreased filtration by kidney (risk of med toxicity) -can cause hoarse voice)
65
What are the labs with a primary hypothyroidism diagnosis?
-high TSH levels -Low T3 and T4
66
What are the labs associated with a secondary hypothyroidism diagnosis?
-high TSH levels -high T# and T4
67
What is the MOA of levothyroxine?
T4-synthetic thyroid hormone, that is converted to T3 in the body
68
What are the three types of hyperthyroidism?
1. Primary = thyroid problem 2. Secondary= pituitary problem 3. Tertiary = hypothalamus problem
69
R/F for hyperthyroidism
family hx of graves, age>40, women, Caucasian, medications, excessive iodine intake, pregnancy
70
What is graves' disease
autoimmune disorder causing excess levels of T3 and T4
71
S/S of Graves' disease
nervousness, insomnia, sensitivity to heat, weight loss, thyroid is enlarges, an audible bruit over thyroid, afib, myexedma, exophthalmos
72
What is exophthalmos?
a wide eyed stare associated with increased sympathetic tone and infiltration of the extraocular area with lymphocytes and mucopolysaccharides
73
labs for diagnosis of Graves' disease?
low TSH high T3 and T4
74
Treatments for Graves' disease
antithyroid hormone medication (propythiouracil), radioactive iodine, or surgery (and then used levothyroxine)
75
What considerations are needed when taking propylthiouracil?
hepatotoxic and only used in 1st trimester with caution
76
What is a thyrotoxic crisis or thyroid storm?
overwhelming release of thyroid hormones that exerts an intense stimulus of metabolism life threatening
77
What typically triggers a thyrotoxic crisis?
surgery, trauma, or infection
78
What causes all the symptoms of hypoparathyroidism?
hypocalcemia from insufficient PTH
79
S/S of hypocalcemia
muscle cramps, irritability, tetany, convulsions
80
What is the treatment for hypoparathyroidism?
replace PTH, normalize Ca and Vitamin D level, possible surgery (PTH are then lifelong)
81
S/S of hyperparathyroidism (high Ca)
muscle weakness, poor concentration, neuropathies, HTN, kidney stones, metabolic acidosis, osteopenia, fractures, constipation, depression, confusion, or subtly cognitive defects
82
treatment of hyperparathyroidism
reduce levels of calcium, diuretics, calcitonin, bisphosphonates, Vitamin D, and surgical interventions

ABSN NUR 326 (10 decks)

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