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Endo/Repro 2 Final > 2. Robbins: Pituitary Gland > Flashcards

2. Robbins: Pituitary Gland Flashcards

1
Q

Embryonic development of the pituitary gland

A
  1. Infundibular process => posterior pituitary, which connects directly to the hypothalamus.
  2. Rathke’s pouch (oral ectoderm) => anterior pituitary, which makes the hypophyseal portal circulation.
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2
Q
  1. Neurohypophysis => _____ pituitary gland.
  2. Adenohypophysis => _____ pituitary gland.
A
  1. Neurohypophysis => posterior pituitary gland.
  2. Adenohypophysis => anterior pituitary gland.
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3
Q

Histology of the Anterior Pituitary

A
  • Made up of: nests and glands.
  • Cytoplasm is made up of
    • 1. Acidophils (eosinophillic cytoplasm) => secrete GH and prolactin
    • 2. Basophils (basophillic cytoplasm) => secrete TSH, LH/FSH, ACTH
    • 3. Chromophobes (poor staining cytoplasm) => secrete anything
    • *but any of these can secrete anything
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4
Q

Histology of the Posterior Pituitary

A
  • Looks like brain tissue
    • - Axonal neurons
    • - Supportive pituicytes (neuroglial cells)
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5
Q

AP contains 6 cells. What do they secrete?

  1. Somatotrophs
  2. Mammosomatotrophs
  3. Lactotrophs
  4. Corticotrophs
  5. Thyrotrophs
  6. Gonadotrophs
A
  1. Somatotrophs => GH
  2. Mammosomatotrophs => GH and prolactin
  3. Lactotrophs => prolactin
  4. Corticotrophs => ACT, POMC (pro-opiomelanocortin), MSH (melanocyte-stimulating hormone)
  5. Thyrotrophs => TSH (thyroid-stimulating hormone)
  6. Gonadotrophs => FSH and LH
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6
Q

What are the functions of LH and FSH?

A
  • LH => causes ovulatation and formation of corpora lutea in ovary.
  • FSH => forms graafian follicle in ovary
  • Both regulate spermatogenesis and testosterone production in males
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7
Q

How does pituitary pathology come to attention?

A
  1. Hyperpituitarism (usually due to adenoma)
  2. Hypopituitarism
  3. Mass effect
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8
Q

What is mass effect?

A
  • Non-functioning adenomas (those without clinical symotoms of hormone excess) can get large, protrude from sella turcica and cause mass effect
    • 1. Increased intracranial pressure (ICP) => HTN, HA, N/V bradycardia, shallow breathing, papilledema*
    • 2. Bilateral temporal hemianopsia => loss of lateral FOV due to compression of the optic chiasm
    • 3. Pituitary apoplexy => hemorrage into adenoma, a surgical MRGNC that can cause death.
      1. Underproduction of pituitary hormones (bc encroach on adjacent AP parenchyma) and OVERproduction of prolactin
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9
Q

What is pituitary apoplexy?

A

Hemorrage into the adenoma caused by mass effect of a non-functioning adenoma

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10
Q

Mass effect can cause an overproduction of one hormone. What is that hormone and why?

A
  • Overproduction of prolactin, because DA (which inhibits prolactin) cannot bind.
  • DA cannot bind => cannot prevent prolactin secretion => hyperprolactinemia.
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11
Q

Hyperpituitarism:

  • Most common cause:
  • Other causes:
A
  • Adenoma in the AP
  • Hyperplasia, carcinoma, secretion from non-pituitary tumors, certain hypothalamic disorders.
    *
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12
Q
  • Microadenoma => ____
  • Macroadenoma => ____
  • Giant adenoma => ____
A
  • Microadenoma => less than 1cm
  • Macroadenoma => 1-4cm
  • Giant adenoma => bigger than 4cm
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13
Q

Pituitary Adenoma

  • MC in who?
  • Types?
  • Sporadic or familial?
  • Histologically, a typical pituitary adenoma is made up of what type of cells and how are they arranged?
A
  1. 35-60 YO
  2. Functional (secrete excess hormones) vs non-functional (do not have clinical sx of too much hormone)
  3. Majority are sporadic, but 5% are familial.
  4. Uniform, polygonal cells arranged in sheets or cords
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14
Q

What 2 morphological features of pituitary adenomas distinguish them from non-neoplastic anterior pituitary parenchyma?

A
  1. Cellular monomorphism
  2. Absence of a reticulin (CT) network, making them soft (bc no CT/reticulin)
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15
Q

Which genetic mutation is seen in many pituitary adenomas, especially somatotroph cell adenomas (40%); leads to what signaling effects?

A

GNAS mutations —> α subunit of Gs loses GTPase activity—> GTP stays bound and GDP does NOT shut off pathway => ↑↑↑ cAMP => cellular proliferation

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16
Q

GNAS mutations are not seen in what type of adenomas?

A
  1. Thyrotroph
  2. Lactotroph
  3. Gonadotroph
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17
Q

Some pituitary adenomas can secrete 2 hormones, what is the most common combination?

A

GH and prolactin = Bihormonal mammosomatotroph adenoma

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18
Q

Functional vs. Non-functional adenomas: which are most likely to come to be diagnosed as macroadenomas?

A

Non-functional adenomas, because they are most likely to come to attention at a later stage.

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19
Q

Large pituitary adenomas, particularly nonfunctioning ones, may cause hypopituitarism how?

A

By encroaching on and destroying adjacent anterior pituitary parenchyma

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20
Q

Gross morphology of a typical pituitary adenoma?

A

Soft and well-circumscribed

  • Small => confined to the sella turica. If expands, erodes sella turcica.
  • Large => extend through diaphragm sella and compress optic chiasm and adjacent structures.
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21
Q

Gross morphology of a invasive adenoma

A
  • Not grossly encapsulated and infiltrate neighboring tissue
  • Hemorrhage and necrosis = more common.
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22
Q

Atypical adenomas have a higher propensity for aggressive behavior and are associated with mutations in which gene?

A

TP53

23
Q

What is the most common secretory pituitary adenoma?

A

Lactotroph adenoma

24
Q

What is the 2nd most common pituitary adenoma?

A

Somatotroph adenoma (secretes GH)

25
Q

What is the most common cause of Cushing syndrome?

A

Iatrogenic Cushing syndrome due to glucocorticoid administration (giving a patient long-term steroids)

26
Q

Corticotroph adenomas stain positively with what stain due to the presence of POMC?

A

PAS

27
Q

What are the 3 major types of cancer associated with paraneoplastic secretion of ACTH or ACTH-like substance leading to Cushing Syndrome?

A
  1. - Small-cell carcinoma of lung
  2. - Pancreatic carcinoma
  3. - Neural tumors
28
Q

If Cushings syndrome is diagnosed, how do we find out the etiology?

A
  • Check ACTH levels
    1. Low ACTH => ACTH-independent: problem with adrenal glands (adrenal Cushings)
      1. CAT scan/MRI
        1. => Adrenal adenoma or adrenal cancer
        2. => Bilateral adrenal hyperplasia
    2. High ACTH => ACTH-dependent: problem with AP/ectopic source
      1. Inferior petrosal sinus sampling and MRI of brain
        1. Pituitary tumor (Cushings disease)
        2. Ectopic ACTH source
29
Q

Non-functioning pituitary adenomas are often called what?

A

Silent or null-cell adenomas because they are not noticed till large and presenting with mass effect.

30
Q

Pituitary carcinoma

  • How common and dangerous?
  • Essential conditions for prescence: _______ and ______
  • Most are functional/non-functional
  • Most commonly secrete ________
A
  • RARE and can metastasize, spread through brain
  • Craniospinal or systemic metastases
  • Functional
  • Prolactin and ACTH
31
Q

Which mutation is associated with familial pituitary adenomas, causing pituitary adenoma predisposition (PAP) syndrome?

A

LOF of AIP, most commonly in somatotroph adenomas

32
Q

What are the most common mutations seen in somatic/sporadic pituitary adenomas?

A
  1. GNAS
  2. USP8 (in 36-62% of corticotroph adenomas)
    1. => upregulation of EGFR
33
Q

Where are AIP mutations more common?

A

Ireland/Irish

34
Q

Causes of hypopituitarism (which can be d/t hypothalamus or pituitary)

A
  1. Tumors and mass lesions in sella
  2. TBI and subarachnoid hemorrhage => MCC*
  3. Pituitary surgery or radiation
  4. Pituitary apoplexy
  5. Ischemic necrosis of pituitary and Sheehan syndrome
  6. Rathke cleft cyst
  7. Empty sella syndrome
  8. Hypothalamic lesion (craniopharyngioma and metastasis from breast and lung cancer)
35
Q

What are 2 other AP neoplasias (derived from AP epithelium?

A
  1. Rathkes Cleft Cyst
  2. Craniopharyngioma
36
Q

Pituitary apoplexy in its most dramatic presentation produces sudden onset of what sx’s?

A
  1. - Excruciating HA
  2. - Diplopia
  3. - Hypopituitarism
37
Q

What is the most common form of clinically significant ischemic necrosis of the anterior pituitary?

A

Sheehan syndrome aka postpartum necrosis

38
Q

List some conditions which may be associated with pituitary necrosis

A
    • DIC
    • Sickle cell anemia
    • ↑ ICP
    • Traumatic injury
    • Shock
39
Q

What are Rathke cleft cysts lined with and how can they lead to hypopituitarism?

A

Ciliated cuboidal epithelium w/ some goblet cells and anterior pituitary cells

=> Hypopituitarism

  1. Accumulate proteinaceous fluid and expand=> compress NL pituitary.
  2. If rupture => inflammation of pituiary and meningitis.
40
Q

Craniopharyngiomas may be seen in which 2 age groups;

  • Types and dysfunction caused in each?
A
  • Kids (5-15 y/o) = adamantinomatous craniophryngiomas that cause [growth retardation from hypopituitarism]
  • Adults (>65 y/o) = papillary craniopharyngiomas that cause [↑ ICP or hypopituitarism]
41
Q

Gross craniopharyngiomas

A

Usually cystic and multiloculated

42
Q

4 histological findings of adamantinomatous craniopharyngiomas?

A
  1. Nests/cords of stratified squamous epithelium embedded in spongy “reticulum” w/ “palisading” at the periphery
  2. “Wet”/lamellar keratin formation = DIAGNOSTIC FEATURE
  3. Dystrophic calcification => calcified cyst
  4. Cholesterol-rich, thick brownish yellow fluid (“machine oil”)
43
Q

What do the papillary type of craniopharyngiomas lack histologically?

A

Usually lack keratin, calcification, and cysts

44
Q

What occurs in primary empty sella syndrome?

A

Defect in diaphragma sella causes arachnoid mater + CSF to leak into sella => expand the sella => compress the pituitary

45
Q

Primary empty sella syndrome is most commonly seen in whom?

A

Obese women w/ a hx of multiple pregnancies

46
Q

How do individuals with primary empty sella syndrome commonly present?

A

Visual field defects and occasional endocrine abnormalities such as hyperprolactinemia

47
Q

What occurs in secondary empty sella syndrome?

A

Pituitary adenoma enlarges the sella and is then either surgically removed or undergoes infarction –> loss of pituitary function + empty space

48
Q

Anterior hypopituitarism =>

  1. ↓ GH
  2. ↓ gonadotropin
  3. ↓ TSH
  4. ↓ prolactin
A
  1. ↓ GH
    1. Increase body fat, ↓ muscle and strength
  2. ↓ gonadotropin
    1. M: ↓ sex drive, facial and body hair and infertility
    2. W: amenorrhea, dysparenia, infertility, breast atrophy
  3. ↓ TSH
    1. ↓ NRG, hypoglycemia and tiredness
  4. ↓ prolactin
    1. cannot lactate
49
Q

What is an example of an inflammatory disorder and infection which can involve the hypothalamus and cause deficiencies of anterior pituitary hormones and diabetes insipidus?

A
  1. - Sarcoidosis
  2. - Tuberculous meningitis
50
Q

What is Sheehan syndrome (post-partum necrosis)?

A

NL, during pregnancy, AP grows 2x size, however, BS and space does not increase => compressed and relative hypoxia => ischemia and infarctaion during labor and delivery.

51
Q

What does posterior pituitary secrete?

A
  1. ADH
  2. Oxytocin
52
Q

What are hypothalamic suprasellar tumors and what can they cause?

A

Gliomas and craniopharyngiomas.

Cause: hypofunction/hyperfunction, of AP, DI or a combination of both.

53
Q

How do craniophargiomas come to attention?

A
  • Children: growth retardation due to hypopituitarism and GH deficiency
  • Adults: HA/visual disturbances.

Endo/Repro 2 Final (11 decks)

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