Endocrinology Flashcards

1
Q

Anterior pituitary hormones (6x)

A

GH, PRL, ACTH, TSH, LH, FSH

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2
Q

Posterior pituitary hormones

A

oxytocin, AVP/ADH

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3
Q

ACTH stimulates the ____ to secrete ___

A

adrenal cortex

cortisol

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4
Q

FSH and LH stimulate the ____ to secrete ____

A

ovaries

estrogen and progesterone

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5
Q

TSH stimulates the ____ to secrete ____

A

thyroid gland

T3 and T4

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6
Q

What stimulates the production of prolactin?

What inhibits the production of prolactin?

A

TRH

Dopamine

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7
Q

What inhibts secretion of GnRH?

A

prolactin

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8
Q

what is the target gland of oxytocin?

A

uterus and mammary glands

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9
Q

what is the target of AVP/ADH?

A

kidneys

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10
Q

what is the target of GH?

A

somatomedin

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11
Q

What will be increased and decreased in hypothyroidism?

A

decreased T3 and T4

elevated TRH and TSH

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12
Q

What will be increased and decreased when the there is damage to the thyroid (primary hypothyroidism)?

A

decreased T3 and T4

elevated TSH

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13
Q

In regards to thyroid hormones, what levels will be affected if there is damage to pituitary gland or hypothalamus?

A

decreased TSH and TRH

decreased T3 and T4

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14
Q

In primary thyroid disorder the problem is in the

A

target organ [thyroid]

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15
Q

In secondary thyroid disroder the problem is in the

A

pituitary

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16
Q

In tertiary thyroid disorder the problem is in the

A

hypothalamus

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17
Q

Hormone that stimulates the liver and other organs to synthesize and secrete IGF to stimulate division of progenitor cells located in the growth plates and in skeletal muscles for body growth

A

growth hormone

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18
Q

hormone that promotes mammary gland development

A

prolactin

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19
Q

hormone that maintains structure and stimulates secretion of glucocorticoids and gonadocorticoids by the zonafasciculata and zonarecticularis of the adrenal cortex

A

adrenocorticotropic hormone (ACTH)

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20
Q

hormone that stimulates follicular development in the ovary and spermatogenesis in the testis

A

follicle stimulating hormone (FSH)

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21
Q

hormone that regulates final maturation of ovarian follicle, ovulation and corpus luteum formation; stimulates steroid secretion by follicle and corpus luteum; in males, essential for maintenance of and androgen secretion of the Leydig cells of the testis

A

luteinizing hormone (LH)

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22
Q

hormone that stimulates growth of thyroid epithelial cells; stimulates production and release of thyroglobulin and thyroid hormones

A

Thyrotropic hormone (TSH)

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23
Q

How does elevated levels of prolactin in pregnancy and lactiation cause amenorrhea?

A

prolactin suppresses GnRH → suppresses FSH and LH → amenorrhea

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24
Q

Predominant inhibitory signal of prolactin

A

dopamine

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25
Q

stimulatory signal of prolactin

A

TRH

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26
Q

4 different causes of prolactinemea

A

pituitary tumor of PRL secreting cells (prolactinoma)
hypothyroidism (elevated TRH)
dopamine antagonist therapy
stalk compression (non-functioning pituitary tumor)

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27
Q

clinical manifestation of hyperprolactinemia in women

A

oligomenorrhea or amenorrhea
reduced fertility
reduced libido
galactorrhoea

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28
Q

clinical manifestations of hyperprolactinemia in men

A

ED
reduced fertility
reduced libido
gynecomastia

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29
Q

Gender neutral clinical manifestations of hyperprolactinemia

A

visual field defects (MC is bitemporal)
headache
stunted growth
delayed puberty

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30
Q

how can stalk compression cause high prolactin levels?

A

dopamine effect on prolactin cells is blocked

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31
Q

With a prolactinoma, elevated prolactin levels are based on ____ and are between the range?

A

tumor size [mass effect]

30-200 ng/mL

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32
Q

any kind of endocrine tumor is called

A

adenoma

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33
Q

In regards to pituitary tumors, if the tumor is > 1 cm it is called a ____ and if the tumor is < 1 cm is called ____

A

macroadenoma

microadenoma

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34
Q

Treatment of choice in prolactinoma

A

medical management [dopamine agonist, bromocriptine, cabergoline]

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35
Q

what percentage of brain tumors are pituitary adenomas?

A

10-15%

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36
Q

what type of pituitary adenoma causes hypopituitarism?

A

nonfunctioning pituitary adenoma

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37
Q

pituitary adenomas secrete

A

prolaction → MC

GH and ACTH

38
Q

Why does GH excess cause gigantism in children?

A

epiphysis is not closed → bone growth longitudinally

39
Q

excess GH after the closure of epiphyses is termed

A

acromegaly → “extremity enlargement”

40
Q

MC cause of acromegaly

A

pituitary adenoma → macroadenoma

41
Q

signs and symptoms of acromegaly

A
large, doughy, moist hands
carpal tunnel syndrome
coarse facial features
hypertension and cardiomegaly 
weight gain 
visual field defects 
arthralgia
insulin resistance
42
Q

Patient has pituitary adenoma that is causing hypofunctioning of the pituitary gladn but they are asymptomatic. What can cause them to be symptomatic?

A

crisis precidpitated by infection or surgery

43
Q

Three main classes of hormones produced by the adrenal cortex

A

mineralocorticoids [aldosterone]
glucocorticoids [cortisol]
adrenal androgens [testosterone and DHEA]

44
Q

what detects and responds to changes in solute concentrations of the blood?

A

hypothalmic osmoreceptors

45
Q

What does the hypothalamus synthesize when solute concentration is high? What is the effect?

A

ADH/AVP

inhibits urine formation

46
Q

When are ADH levels the highest in the body?

A

11pm to midnight

47
Q

If not enough ADH is made/release, what results?

Symptoms?

A

diabetes insipidus

huge urine output and intense thirst

48
Q

ADH hypersecretion due to neurosurgery, trauma, or cancer cell secretion causes

A

Syndrome of Inappropriate ADH Secretion [SIADH]

49
Q

6 criteria for diagnosing diabetes insipidus

A
hypotonic polyuria
24 hr urine volume >50 
urine specific gravity < 1.010 
urine osmolarity < 300 
absense of solute diuresis
normal thyroid and cortisol
50
Q

Causes of central diabetes inspidus

A

complete or partial ADH deficiency from posterior pituitary
head trauma
post-surgery
tumors
infections [TB, syphilis, toxoplasmosis, encephalitis, meningitis, sarcoidosis]
cerebrovascular disease

51
Q

what occurs in nephrogenic diabetes insipidus?

A

ADH/AVP receptors on the kidneys are unresponsive to ADH

52
Q

Abnormal electrolyte levels in nephrogenic diabetes insipidus?

A

hypercalcemia and hypokalemia

53
Q

MC cause of nephrogenic diabetes insipidus

A

drug toxicity → lithium, NSAID, demeclocycline

54
Q

How do you differentiate central vs nephrogenic diabetes insipidus?

A

water deprivation test

55
Q

Results from water deprivation test in a patient with central DI

A

urine osmolarity after fluid deprivation → < 300

urine osmolarity after desmopressin → > 800

56
Q

Results from water deprivation test in a patient with nephrogenic DI

A

urine osmolarity after fluid deprivation → < 300

urine osmolarity after desmopressin → < 300

57
Q

Results from water deprivation test in a patient with primary polydipsia

A

urine osmolarity after fluid deprivation → > 800

urine osmolarity after desmopressin → > 800

58
Q

Treatment for central diabetes insipidus

A

desmopressin (DDAVP) → hormone replacement

59
Q

Treatment for nephrogenic diabetes insipidus

A

treat underlying cause
encourage fluid intake
hydrochlorthiazide or amiloride [excrete more salt]

60
Q

What is most problamatic in a patient with SIADH?

A

dilutional problem → hyponatremia

61
Q

clinical presentation of SIADH

A

depend on degree of hyponatremia and how rapidly it develops

62
Q

SIADH etiologies

A

CNS → bleed/hemorrhage, CVA, DTs, trauma, hydrocephalus, infection, tumor
Drugs
neoplasms [ectopic ADH section] → lungs, prostate, duodenum, etc

63
Q

Serum levels of sodium < 125 in a patient with SIADH will display what symptoms?

A

muscular weakness, nausea, headache, lethargy, ataxia, psychosis to cerebal edema, increase ICP, seizures, coma

64
Q

diagnostic criteria for SIADH

A

plasma hypoosmolality
urine concentration inappropriate for hypoosmolality [>100]
clinical euvolemia
absent renal sodium convervation [urine sodium > 30]
normal thyroid, adrenal, renal function!!

65
Q

Treatment of SIADH

A

correct low sodium → not too fast!!
Treat underlying cause
restrict fluid, oral salt tablets
demeclocycline

66
Q

What is the role of aldosterone?

A

regulates salt and water homeostasis via renin/angiotensin

67
Q

what is the role of cortisol?

A

carbohydrate metabolism and chronic stress response

68
Q

Clinical manifestations of excessive cortisol levels

A
hypertension
hypokalemia 
central obesity 
skinny limbs [breakdown of skeletal muscle]
thin skin and purple striae 
bruise easily 
interscapular fat pad "buffalo hump"
osteoporosis 
simple carb cravings → boost insulin and promote fat storage [cortisol is appetite stimulant]
menstrual irregularity and ED
69
Q

Cushings syndrome vs Cushings disease

A

Disease → ACTH and cortisol are both elevated

syndrome → high cortisol and low ACTH

70
Q

Cushings Disease is the result of

A

too much ACTH from the pituitary

71
Q

Cushings Syndrome is the result of

A

non pituitary source → adrenal tumor, excess intake of corticosteroids

72
Q

1 cause of ectopic production of ACTH

A

small cell carcinoma of lung

73
Q

What will be elevated in ectopic ACTH production?

A

ACTH and cortisol

74
Q

In diagnosing hypercortisolism, you need documentation of cortisol excess by at least 1 of the following mechanisms

A

24 hour urine free cortisol levels → on 2 occasions
midnight/diurnal salivary cortisol levles → on 2 occasions
dexamethasone suppression test → 8-9am cortisol < 1.8

75
Q

What test do you use to confirm the pituitary gland is the source of hypercortisolism?

A

high dose Dexamethasone suppresion test → give dex @ 11pm & measure ACTH and cortisol → repeat at 8-9 am the next day → decrease of cortisol by >69%

76
Q

What size of pituitary adenoma warrants surgical removal?

A

> 8 mm

77
Q

Management of Cushings Disease

A

trans-sphenoid surgery

radiation + surgery [dural/cavernous sinus invasion]

78
Q

Management if Cushings Syndrome is secondary to adrenal gland disease

A

unilateral or bilateral adrenalectomy

79
Q

Management of Cushings Syndrome secondary to an ectopic source

A

surgical removal of culprit tumor

80
Q

Medical management in hypercortisolism patient if surgery ineffective or not an option

A

steroid blocking agents → ketoconazole, metyrapone, mitotane, etomidate

81
Q

Clinical manifestations of adrenal insufficiency

A

low blood sugar [due to decrease cortisol] → malaise and weight loss, fatigue, weakness
hyponatremia and hyperkalemia
decreased BP
increased ACTH and MHS secretion → increased pigmentation of lips, freckles, buccal mucosa, skin creases!!

82
Q

What test confirms diagnosis of adrenal insufficiency?

A

8 am cortisol < 3

normal 10-20

83
Q

How do you determine if adrenal insufficiency is primary or secondary?

A

look at ATCH
ACTH is elevated → primary AI
ACTH is suppressed → secondary AI

84
Q

In the ACTH stimulation test, what are you tring to stimulate?

A

trying to stimulate the adrenal gland to make cortisol with high concentration of ACTH

85
Q

What value in ACTH stimulation test will rule out AI?

A

cortisol > 18 at 60 min

86
Q

Management of primary adrenal insufficiency

A

replacing corticosteroids and mineralocorticoids

87
Q

Management of secondary adrenal insufficiency

A

replacing corticosteroids

88
Q

In treating AI, how should hydrocortisone be dosed?

A

highest given in the morning → early afternoon (2 dose) or at lunch → afternoon (3 dose)

89
Q

What is it important to counsel a patient with AI on with their hormone replacement?

A

increase the dose if get fever (>38→double; >39→triple)
increase for mild/mod surgery stress
increase for major surgery requiring sedation

90
Q

Management of adrenal crisis

A

rapid infusion of NS or D5N5

IV HC → taper to PO when tolerate

91
Q

Who do you refer to endocrinologist?

A

early cases of acromegaly, functional pituitary adenoma, Cushings Syndrome, all hyperfunctioning cases