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Clinical Medicine 2 > Exam 4: Pituitary Disorders > Flashcards

Exam 4: Pituitary Disorders Flashcards

1
Q

What does ACTH do?

A

Stimulates production and release of cortisol by the adrenal cortex

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2
Q

What does LH do in females?

A

Triggers ovulation and development of the corpus luteum

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3
Q

What does LH do in males?

A

Stimulates Leydig cell production of testosterone

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4
Q

What does FSH do in females?

A

Stimulates growth of ovarian follicles

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5
Q

What does FSH do in males?

A

Stimulates formation of secondary spermatocytes

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6
Q

What does GH do?

A

Stimulates growth, cell reproduction, and cell regeneration

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7
Q

What does prolactin do in males?

A

Works with LH and Testosterone to increase reproductive function

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8
Q

What two hormones does the posterior pituitary release?

A

ADH and oxytocin

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9
Q

What does ADH do?

A

Causes the kidneys to reabsorb solute free water, resulting in concentrated urine and reduced urine volume

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10
Q

What does oxytocin do?

A
  • In a positive feedback loop, increases uterine contractions and promotes stretching of the cervix and uterus during labor
  • in breastfeeding women, it also stimulates the contraction of cells around the milk ducts causing milk to be released
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11
Q

What does the intermediate pituitary do?

A

Synthesizes and secretes melanocytes stimulating hormone, which controls skin pigmentation

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12
Q

Which part of the pituitary does no synthesize hormones, but just holds and secretes them?

A

The posterior pituitary does not synthesize any hormones

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13
Q

What is the most common place to get a sellar mass?

A

The sella Turcica

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14
Q

What is the clinical presentation of a sellar mass?

A

Visual impairment, diplopia, and headaches

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15
Q

Why do visual disturbances commonly happen with sellar masses?

A

Occurs as a result of suprasellar extension of the adenoma, leading to compression of the optic chiasm
-Commonly causes bitemporal hemianopsia

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16
Q

Are pituitary adenomas, craniopharyngioma, and meningioma usually benign or malignant?

A

Benign

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17
Q

What cancers are most likely to metastasize to the brain?

A

Breast and lung cancer

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18
Q

What accounts for over 60% of all pituitary adenomas?

A

Prolactinoma

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19
Q

What constitutes as a microadenoma?

Macro adenoma?

A

Micro: <1cm
Macro: >1cm

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20
Q

How are sellar masses diagnosed?

A
  • MRI

- check labs for hormonal hypersecretion (serum prolactin, serum IGF, 24 hours urine cortisol, and T3/T4/TSH

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21
Q

What results from GH excess?

A

Gigantism and acromegaly

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22
Q

What results from GH deficiency?

A

Short stature, adult deficiency

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23
Q

What are the clinical features of a prolactinoma in premenopausal women?

A
  • Infertility
  • Amenorrhea
  • Galactorrhea
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24
Q

What are the clinical features of prolactinoma in postmenopausal women?

A
  • Headache
  • impaired vision
  • Galactorrhea
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25
Q

What is the clinical presentation of prolactinoma in men?

A

Decreased libido, impotence, infertility, gynecomastia, and galactorrhea

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26
Q

How is a prolactinoma diagnosed in premenopausal women?

A

Serum prolactin >30ng/mL

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27
Q

How is a prolactinoma diagnosed in postmenopausal women and men?

A

Serum prolactin >20ng/mL

28
Q

What are the possible causes of hyperprolactinemia?

A

Pregnancy, lactation, stress, exercise, drugs (phenothiazine, haloperidol, and benzos), or pathologic (prolactinoma and hypothyroid)

29
Q

How is a prolactinoma treated?

A

Pharmacologic: Bromocriptine, cabergoline

Surgical: transsphenoidal resection, radiotherapy

30
Q

What is the most common etiology of growth hormone excess?

A

Benign pituitary macroadenoma

31
Q

Increase in GH causes an increase in ** from the liver.

A

Insulin like growth factor (IGF-1)

32
Q

What are the clinical features of GH excess?

A
  • occurs in adults, enlargement/elongation of hands, feet, and jaw
  • increased risk of DM, HTN, and CAD
33
Q

How is growth hormone excess diagnosed?

A
  • serum IGF
  • serum prolactin
  • 2 hour oral glucose tolerance test
  • MRI will reveal pituitary tumor in 95% of patients
34
Q

What is the gold standard to diagnose GH excess and what will it show?

A

-2 hour oral glucose tolerance test, will show failure of GH to decrease to less than 2mcg

*** random serum GH is not accurate as levels fluctuate

35
Q

How is GH excess treated?

A
  • somatostatin analogs are inhibitory and may decrease tumor size
  • transsphenoidal microsurgery is most successful in patients with GH levels below 50 and pituitary tumors <2cm
  • IGF should be measured every 3-6 months, as this is directly linked to morbidity and mortality
36
Q

Is gigantism or acromegaly more common in adults?

A

Acromegaly

37
Q

What is the most common etiology of GH deficiency?

A

Pituitary adenoma

38
Q

What is the rare etiology of GH deficiency?

A

Sheehan syndrome

39
Q

What are the clinical features of GH deficiency?

A

Decrease in lean body mass, decrease in bone mineral density, decrease in QOL, increase in fat mass, increase in rate of fractures, increase in mortality

40
Q

What is the #1 cause of GH deficiency in adults?

A

Tumors

41
Q

What is the recommended therapy for GH deficiency in patients who have childhood onset of GH deficiency?

A

GH therapy

42
Q

What are the side effects of supplemental GH therapy?

A

Peripheral edema, arthralgia, paresthesias, and worsening of glucose tolerance

43
Q

What is the difference between primary and secondary hypogonadism?

A

Primary: due to failure of the testes
Secondary: due to defects in the HPT axis

44
Q

What will labs show in primary hypogonadism?

A

Low testosterone, high FSH and LH

45
Q

What will labs show in secondary hypogonadism?

A

Low testosterone, low to normal FSH and LH

46
Q

What are the clinical features of secondary hypogonadism?

A

ED, hot flashes, gynecomastia, infertility, decreased energy, libido, muscle mass, and body hair

47
Q

How is secondary hypogonadism diagnosed?

A

Free and total serum testosterone, LH, and FSH

  • prolactin, TSH, CBC, CMP, possibly semen analysis
  • MRI
48
Q

What are the testosterone treatment options for secondary hypogonadism?

A
  • IM injections Q 2 weeks
  • Transdermal cream/gel/patch applied daily
  • pellets placed SC Q3 months
49
Q

Before initiating treatment for secondary hypogonadism, what should be done?

A

-DRE and PSA as history of prostate cancer is contraindicated in testosterone therapy

50
Q

What should be done to monitor treatment for secondary hypogonadism?

A

-Free and total testosterone, CBC (risk of erythrocytosis, free estradiol, and annual DRE and PSA

51
Q

What is it called when a patient has global anterior pituitary dysfunction, resulting in decreased anterior pituitary hormones?

A

Pan hypopituitarism

52
Q

What are the etiologies of Pan-hypopituitarism?

A

Radiation therapy, pituitary tumors, Sheehan syndrome, and extrapituitary syndrome

53
Q

What is Sheehan syndrome?

A

Postpartum pituitary gland necrosis, due to blood loss and hypovolemia shock during and after childbirth

54
Q

What is the most common initial symptom of Sheehan syndrome?

A

Agalactorrhea/ difficulties with lactation

55
Q

How is pan-hypopituitarism diagnosed?

A

Extensive history and physical exam, full hormone work up, brain MRI, and stimulation tests as indicated to exclude primary disease

56
Q

What is the treatment for pan-hypopituitarism?

A
  • Extensive hormone replacement for life (Levothyroxine, dexamethasone, testosterone, estrogen-progestin, and GH)
  • 1500 mg Ca with 800 IU of Vit D per day to protect the bones
57
Q

What are the two disorders of the posterior pituitary?

A

Central DI, and SIADH

58
Q

What is it called when there is decreased release of ADH from the posterior pituitary?

A

Central DI

59
Q

What are the common etiologies of central DI?

A
  • Most are idiopathic

- second most common is tumor of the posterior pituitary

60
Q

What is the clinical presentation of Central DI?

A
  • Overly dilute urine and polyuria
  • dehydration
  • polydipsia
  • ice water craving
  • nocturnal/enuresis
  • hypernatremia in late stages
61
Q

How is central DI diagnosed?

A
  • 24 hour urine collection
  • serum electrolytes
  • simultaneous serum and urine osmolality
  • glucose
62
Q

What will the urine osmolality be in central DI?

A

<250 mOsm/kg

63
Q

What is the treatment for central DI?

A

-Desmopressin (available intranasal)

64
Q

What is it called when there is inappropriately high release of ADH from the posterior pituitary?

A

SIADH

65
Q

What is the clinical presentation of SIADH?

A
  • Overly concentrated urine and decreased urine volume
  • increase urine osmolality
  • decreased serum osmolality
  • hyponatremia
66
Q

How is SIADH diagnosed?

A
  • 24 hour urine collection
  • serum electrolytes
  • simultaneous serum and urine osmolality
67
Q

What is the treatment for SIADH?

A
  • focused on correcting the hyponatremia
  • fluid restriction to <800mL/day
  • consider oral salt intake
  • consider vasopressin receptor antagonist

Clinical Medicine 2 (22 decks)

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