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Endocrine > pituitary and adrenal > Flashcards

pituitary and adrenal Flashcards

1
Q

hormones released by the anterior pituitary gland

A

ACTH, TSH, FSH, LH, GH, prolactin

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2
Q

ACTH

A

secretion of glucocorticoid, mineralocorticoids, and androgens

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3
Q

FSH

A

growth of the reproductive system

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4
Q

LH

A

sex hormone production

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5
Q

GH

A

promotes growth; lipid and cholesterol metabolism

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6
Q

prolactin

A

secretion of estrogens and progesterone; milk production; spermatogenesis; prostate hyperplasia

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7
Q

hormones secreted by the posterior pituitary gland

A

oxytocin and vasopressin

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8
Q

oxytocin

A

uterine contraction and lactation

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9
Q

vasopressin

A

stimulates water retention; raises blood pressure by contracting arterioles

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10
Q

common pituitary disorders

A

panhypopituitarianism, excess in growth hormone, growth hormone deficiency, hyperprolactinemia

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11
Q

panhypopituitarianism

A

deficiency in ACTH, Gn, GH, TSH; excess PRL

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12
Q

primary panhypopituitarianism

A

secretory issue in pituitary gland

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13
Q

secondary panhypopituitarianism

A

hypothalamus or other pituitary stimulus disorder

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14
Q

causes of panhypopituitarianism

A

surgery, trauma, radiation, ischemia, infection

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15
Q

treatment for panhypopituitarianism

A

replace deficient hormones; glucocorticoids, sex hormones, and levothyroxine (occasionally GH)

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16
Q

gigantism

A

excess in GH in children

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17
Q

acromegaly

A

excess in GH in adults

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18
Q

treatment for excessive growth hormone

A

DA agonists
Somatostatin analogues
GH antagonists

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19
Q

DA agonists

A

bromocriptine and cabergoline

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20
Q

somatostatin analogues

A

octreotide and lanreotide

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21
Q

GH antagonists

A

pegvisomant

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22
Q

GHD in adults

A

prior history of GHD as a child, GHD secondary to structural lesion or trauma, idiopathic GHD

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23
Q

GHD in children

A

congenital GHD, acquired GHD

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24
Q

GHD treatment

A

GH analogues and GHRH analogues

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25
Q

hyperprolactinemia etiology

A

prolactin-secreting tumors (prolactinomas), increased TRH, idiopathic, medication induced

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26
Q

medication induced

A

any medication that antagonizes dopamine or increases the release of prolactin

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27
Q

dopamine antagonists

A

phenothiazines, metoclopramide, haloperidol, atypical antipsychotics

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28
Q

prolactin stimulators

A

methyldopa, cimetidine, SSRIs, TCAs, estrogens, progestins, GRH analogues, benzos, MOAIs, opioids

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29
Q

adrenal gland is located

A

on the upper poles of each kidney

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30
Q

adrenal medulla

A

10% of the total gland, responsible for secretion of catecholamines

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31
Q

catecholamines

A

Epi, NE, dopamine

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32
Q

adrenal cortex

A

90% of the total gland, responsible for the secretion of 3 types of hormones, and 3 separate zones

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33
Q

3 zones of adrenal cortex

A

zona glomerulosa, zona fasciculate, zona reticularis

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34
Q

zona glomerulosa

A

15% of cortex, mineralocorticoid production

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35
Q

mineralocorticoid

A

aldosterone

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36
Q

zona fasciculate

A

60% of cortex, basal and stimulated glucocorticoid production

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37
Q

glucocorticoid

A

cortisol

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38
Q

zona reticularis

A

25% of cortex, adrenal androgen production

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39
Q

Cushing’s syndrome

A

excess cortisol in the plasma either by endogenous production or exogenous sources

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40
Q

etiology of Cushing’s

A

exogenous corticosteroids, overproduction of ACTH (70%), ACTH independent causes (18%), ectopic ACTH - secreting tumors and nonneoplastic corticotropin hypersecretion (12%)

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41
Q

is Cushing’s more common in men or women

A

women

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42
Q

90-100 prevalence of these symptoms in cushings

A

central obesity, moon face, facial plethora, decreased libido

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43
Q

tests that establish the presence of hypercortisolism

A

24 hour urine free cortisol, midnight plasma cortisol, low-dose dexamethasone suppression test (LDDST)

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44
Q

tests that differentiate between etiologies

A

high dose DST; plasma ACTH measured by radioimmunoassay (RIA) or immunoradiometric assay (IRMA); CT/MRI of adrenal, chest, of abdominal area; CRH stimulation test; inferior petrosal sinus sampling; MRI of pituitary gland

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45
Q

clinical suspicion for cushings

A

increased urinary free cortisol, lack of cortisol suppression after dexamethasone, increased late evening salivary cortisol

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46
Q

treatment of cushings

A

surgical resection if tumor is present, inhibitors of steroid production, neuromodulators of ACTH release, and spironolactone

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47
Q

advantages of surgical resection of tumor

A

preservation of pituitary function, low complication rate, and high clinical improvement rate

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48
Q

inhibitors of steroid production are used when

A

patients are not surgical candidates

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49
Q

inhibitors of steroid productions

A

metyrapone, aminoglutethimide, ketoconazole, mitotane, mifepristone

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50
Q

MOA metyrapone

A

inhibits 11-hydroxylase activity thereby interfering with cortisol and corticosterone synthesis

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51
Q

ADR of metyrapone

A

NV, vertigo, HA, GI discomfort, allergic rash, hypotonia

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52
Q

metyrapone

A

mostly used as a diagnostic agent, compensatory increase in endogenous ACTH occurs due to a sudden decrease in cortisol

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53
Q

aminoglutethimide

A

1) causes serum cortisol levels to decrease by 50%
2) as monotherapy - short term use in inoperable cases with ectopic ACTH syndrome as etiology
3) may decrease effect of warfarin

54
Q

MOA aminoglutethimide

A

blocks the conversion of cholesterol to pregnenolone = reduction in all hormonally active steroids

55
Q

ADR aminoglutethimide

A

sever sedation, nausea, ataxia, skin rash, myalgias

56
Q

ketoconazole

A

high doses are need to inhibit steroid production

57
Q

MOA ketoconazole

A

potent, non-selective inhibitor of adrenal and gonadal steroid synthesis

58
Q

ADR ketoconazole

A

gynecomastia, GI upset, HA, increase in LFTs (reversible)

59
Q

mitotane

A

hospitalization is required for administration due to the extreme reduction in cortisol production

60
Q

MOA mitotane

A

cytotoxic to the adrenal gland thereby reducing the synthesis of cortisol and corticosterone

61
Q

ADR mitotane

A

lethargy, somnolence, GI upset, change of taste, neuropsychiatric symptoms

62
Q

mifepristone

A

1) binds to the glucocorticoid receptor 18x that of cortisol
2) effect is dose dependent
3) may block negative feedback of glucocorticoid on the HAP axis leading to increase in ACTH and cortisol

63
Q

MOA mifepristone

A

glucocorticoid receptor antagonist

64
Q

ADR mifepristone

A

uterine cramping, HA, dizziness, GI upset, fatigue

65
Q

neuromodulators of ACTH release MOA

A

regulate neurotransmitters that control the HPA axis

66
Q

neuromodulators of ACTH release

A

no agent has been shown to be very effective

cyproheptadine, valproic acid, bromocriptine, ritanserin, octreotide

67
Q

spironolactone and cushings

A

provides symptomatic relief of HTN and hypokalemia

68
Q

ectopic ACTH nondrug treatment

A

surgery, chemotherapy, irradiation

69
Q

ectopic ACTH drug treatment

A

metyrapone, aminoglutethimide

70
Q

pituitary dependent nondrug treatment

A

surgery, irradiation

71
Q

pituitary dependent drug treatment

A

cyproheptadine, mitotane, metyrapone

72
Q

adrenal adenoma non drug treatment

A

surgery, postoperative replacement

73
Q

adrenal adenoma drug treatment

A

ketoconazole

74
Q

adrenal carcinoma nondrug treatment

A

surgery

75
Q

adrenal carcinoma drug treatment

A

mitotane

76
Q

monitoring in cushings

A

24 hour urine free cortisol and serum cortisol level. steroid replacement as needed

77
Q

primary aldosteronism

A

abnormality is within the adrenal cortex

78
Q

causes of primary aldosteronism

A

adrenal adenoma (60%), idiopathic adrenocortical hyperplasia

79
Q

other rare causes of primary aldosteronism

A

adrenal cortex carcinoma, primary adrenocortical hyperplasia, renin-responsive adrenocortical adenoma, and genetic mutations

80
Q

clinical presentation of hyperaldosteronism

A

women age 30-50 yo
HTN, muscle weakness, fatigue, headache, metabolic alkalosis
tetany/paralysis, polydipsia, nocturnal polyuria
impaired glucose tolerance in 25% of patients

81
Q

in hyperaldosteronism there is a decrease in

A

potassium, renin, magnesium

82
Q

in hyperaldosteronism there is an increase in

A

aldosterone, sodium, bicarbonate

83
Q

diagnosis for hyperaldosteronism

A

1) serum potassium < 3.5 with a urinary potassium > 30 per 24 hours
2) PA:PRA > 25

84
Q

in hyperaldosteronism you have to differentiate between

A

aldosterone producing adenoma (APA) and bilateral adrenal hyperplasia (BAH)

85
Q

APA

A

2/3 of cases

  • more severe HTN
  • profound hypokalemia
  • higher plasma and urinary aldosterone levels
86
Q

BAH

A

1/3 of cases

  • similar to APA, but not as severe
  • pts with this condition are able to maintain control of RAAS system with little effect following doses of ACTH
87
Q

treatment of APA

A

surgical resection of adrenal adenoma and spironolactone as needed

88
Q

treatment of BAH

A

spironolactone, amiloride, eplerenone

89
Q

spironolactone and BAH

A

inhibits aldosterone binding to the MR, high doses are needed. low doses can be given to prevent ADR but may need additional agents for BP

90
Q

amiloride and BAH

A

DOC in men. even at high doses not effective at achieving BP control

91
Q

eplerenone and BAH

A

like spironolactone but has less progestational and antiandrogenic side effects

92
Q

secondary aldosteronism

A

stimulation of the zona glomerulosa by a stimulus outside of the adrenal gland, such as RAAS

93
Q

secondary aldosteronism causes

A

excessive potassium intake, oral contraceptives, pregnancy, menses, CHF, cirrhosis, renal artery stenosis, barter’s syndrome

94
Q

lab changes in secondary aldosteronism

A

increase in serum renin

95
Q

treatment of secondary aldosteronism

A

remove extra-adrenal sources and spironolactone should be used until etiology is known

96
Q

addisons disease

A

primary adrenal insufficiency

97
Q

addisons

A

destruction of all regions of the adrenal cortex, deficiencies seen with cortisol, aldosterone, and various androgens

98
Q

______ of the adrenal cortex must be destroyed before symptoms occur

A

about 90%

99
Q

______ of the cases are due to autoimmune disorders

A

about 70%

100
Q

secondary adrenal insufficiency

A

exogenous steroid use leading to suppression of HPA axis, cushing’s, decrease release of ACTH = impairment of androgen and cortisol production BUT NOT aldosterone

101
Q

prednisone can block

A

the release of CRH and ACTH, CRH level swill drop and the pituitary no longer is stimulated to release ACTH therefore adrenals fail to secrete sufficient amounts of cortisol

102
Q

symptoms of addisons disease

A

hyperpigmentation, aldosterone secretion is lost, plasma ACTH levels after ACTH stimulation are elevated, weight loss, dehydration, hyponatremia, hyperkalemia, elevated BUN, salt craving

103
Q

symptoms of secondary adrenal insufficiency

A

aldosterone secretion is preserved, plasma ACTH levels are stimulation are normal to low, hyponatremia not responsive to saline

104
Q

symptoms of hypofunction of adrenal gland

A

depression, anxiety, fatigue, NVD, anorexia, orthostatic hypertension

105
Q

treatment of hypoaldosteronism

A

prednisone, hydrocortisone, cortisone. doses are in the PM because replacement is trying to mimic bodys normal rhythm. fludrocortisone acetate in secondary aldosterone insufficiency

106
Q

adverse effects of fludrocortisone acetate

A

GI upset, edema, HTN, hypokalemia, insomnia, excitability, DM

107
Q

endpoint of therapy in hypoaldosteronism

A

reduction in excess pigmentation is a good clinical marker, stop therapy if cushings syndrome symptoms begin

108
Q

treatment of secondary hypoaldosteronism vs. addisons

A

treatment is the same except fludrocortisone acetate is not necessary

109
Q

patients with adrenal insufficiency

A

should wear a MedicAlert bracelet or necklace and they should have easy access to injectable hydrocortisone or glucocorticoids suppositories in case times of physical stress or illness

110
Q

acute adrenal insufficiency

A

true endocrine emergency, adrenal crisis or Addisonian crisis

111
Q

precipitating factors of adrenal crisis

A

chronic use of glucocorticoids with abrupt withdrawal, surgery, infection, stress, trauma

112
Q

early symptoms of adrenal crisis

A

malaise, myalgia, anorexia, weakness

113
Q

late symptoms of adrenal crisis

A

fever, hypotension, vomiting, hypoglycemia, hypercalcemia, hyponatremia

114
Q

treatment in adrenal crisis

A

fluid replacement and IV glucocorticoids

115
Q

fluid replacement

A

D5NS at a rate to support BP

116
Q

IV glucocorticoids

A

hydrocortisone continue IV infusion for 24-48 hours then switch to oral

117
Q

metabolism of glucocorticoids

A

stimulate gluconeogenesis, mobilize amino acids to serve as substrates for gluconeogenesis in the liver, stimulate fat breakdown in adipose tissue to glycerol and fatty acids, inhibits glucose intake in the muscle and fat

118
Q

inflammation and glucocorticoids

A

potent anti-inflammatory and immunosuppressive properties that vary based on which glucocorticoid given

119
Q

potency of glucocorticoids

A

least to most

cortisone, hydrocortisone, prednisone, prednisolone, triamcinolone, methylprednisolone, betamethasone, dexamethasone

120
Q

complications of glucocorticoid administration

A

osteoporosis, Cushing’s syndrome, increased risk of infection, cataracts, hypokalemia, hypomagnesemia, seizures, edema, steroid myopathy, HPA pathway suppression

121
Q

glucocorticoids and NSAIDs

A

peptic ulcer disease

122
Q

major concern in steroid tapering

A

HPA suppression, much more concerning at high doses of steroid and/or long duration of therapy

123
Q

how to test HPA function

A

ACTH test - if normal test results then daily steroid dose is not necessary

124
Q

monitoring in glucocorticoid therapy

A

glucose concentrations, electrolytes, ophthalmologic exams, growth and development

125
Q

counseling with glucocorticoid therapy

A
  • take with food
  • never DC medication on your own
  • carry or wear ID
  • dosage increase at times of stress
  • take ASAP if missed dose
126
Q

complications in early therapy of steroid use

A

insomnia, enhanced appetite, weight gain

127
Q

common in patients with underlying risk factors and steroid use

A

HTN, DM, PUD

128
Q

long-term intense treatment of steroids

A

cushingoid habitus, HPA suppression, impaired wound healing

129
Q

delayed and insidious complications from steroid use

A

cataracts and atherosclerosis

130
Q

rare and unpredictable complications from steroid use

A

psychosis, glaucoma, and pancreatitis

Endocrine (7 decks)

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