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Endocrine > Bone and PThyroid Path (15/16) > Flashcards

Bone and PThyroid Path (15/16) Flashcards

1
Q

understand normal apperance of pituitary gland

A

pituitary

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2
Q

how does the anterior pituitary stain if it’s growth hormone positive

A

has a brown immunostain

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3
Q

What does normal posterior pituitary histology look like?

A

contains pituicytes and axons; secretes antidiuretic hormone (ADH) & oxytocin

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4
Q

What do we see in the anterior pituitary when we perform a reticulin stain?

A

delinateds small clusters of cells that are held together by extracellular framework.

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5
Q
  • 10-15% of all intracranial neoplasms
  • Women > men
  • 3 rd to 6th decades
A

Pituitary adenomas

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6
Q

What is the most common hormal secreation of Pituitary adenomas?

A

Prolactin is most common: (30%)

its a lactotroph/acidophil!!

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7
Q

What is the second most common pituitary adenoma?

A

Non-secreating (null) cell!

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8
Q

What does a pituitary adenoma look like and how do you resect it?

A

well circumscribed

via trans-spenoid resection

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9
Q

what is a defining characteristic of pituitary adenoma on HE?

A

Has dominantly ONE cell type

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10
Q

What do we see with a reticulin stain of a pituitary adenoma?

A

Destruction of normal pattern of reticulin occurs in adenomas

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11
Q

what does an immunostain look like with pituiatary adenoma?

A

would expect speckling all over, now with adenoma just have one dominant cell type

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12
Q
  • Postpartum ischemic necrosis of pituitary gland
  • Pituitary gland enlarges in pregnancy (increased lactotrophs)

– More susceptible to ischemia – Obstetrical hemorrhage or shock – Results in hypopituitarism (anterior, not posterior)

A

Sheehan syndrome

**of ANTERIOR

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13
Q
  • Slight elevation in prolactin level
  • Result of lack of inhibitory hypothalamic influence on prolactin
  • Caused by a mass/destructive lesion pressing on stalk or hypothalamus-not a prolactinsecreting adenoma
A
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14
Q

Rathke Cleft Cyst location:

A

• Sella or suprasellar location

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15
Q

• May produce symptoms or may be asymptomatic (found at autopsy) • Columnar to cuboidal cells with cilia and occasionally mucin, lining a thin walled cyst

A

Rathkes cleft cyst

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16
Q

what is the devo origin of rathkes cleft cyst

A

Developmental origin: remnant of Rathke’s cleft pouch

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17
Q
  • Benign tumors
  • Usually suprasellar, may be within sella, third ventricle or rarely pineal region
A

Craniopharyngioma

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18
Q

When do craniopharyngiomas usually present?

A

• Two age peaks – Children (5 to 14yrs): usually adamantinomatous type – Adults (65 to 74 yrs): usually papillary type

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19
Q

What are the presenting symptoms with craniopharnygiomas?

A

– Visual abnormalities (chiasm)

– Hypopituitarism

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20
Q

– Misplaced odontogenic epithelium

– Vestigal remnants of Rathke’s pouch

A

possible histogenesis of craniopharnygiomas

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21
Q

– Cysts filled with dark brown fluid (motor oil) and cholesterol crystals – Basally palisading squamous epithelium

– Abundant keratin

– Local invasion of brain with chronic inflammation

A

Adamantinomatous type

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22
Q

Your 10 yr old pt recently has a tumor biopsied from the suprasellar region. The tumor has abundant keritin and basaly palisading sq epithelium. Dx?

A

Craniopharnygioma adamantinomatous type

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23
Q

Describe papillary type craniopharnygioma and who do we see it in?

A

Papillary type

– Papillary architecture

– No keratin formation

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24
Q

Why is recurrence common in craniopharngiomas?

A

Recurrence occurs due to difficulty in completely resecting

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25
Q

Pituitary adenomas are proliferations of_____ cells without a_____ network

A

monomorphic

reticulin

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26
Q

Pituitary adenomas are classified based on

A

immunostain

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27
Q

_______cell adenoma is the most common pituitary adenoma

A

Prolactin

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28
Q

Large pituitary adenomas can cause

A

bitemporal hemianopsia

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29
Q

Arise from the pharyngeal pouches

– Inferior and thymus –____ pharyngeal pouch

– Superior –____ pharyngeal pouch

A

third

fourth

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30
Q
  • Are normally located in proximity of upper and lower poles of the thyroid gland
  • May be ectopically located in thymus, anterior mediastinum, carotid sheath
A

parathyroid glands

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31
Q
  • Yellow, brown ovoid nodule
  • 30 - 45 mg
  • Composed primarily of chief cells and some oxyphil cells
A

Parathyroid glands

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32
Q

Parathyroid

In adults there is a large amount of _______

•______ cells secrete parathyroid hormone

A

intervening stromal fat 30 – 70%

Chief

33
Q

Parathyroid gland histology

A

encapsulated ovoid cells with purpule nuclei

can be in sheets and look simular to pituitary and can be dispersed w/in gland itself

34
Q

be able to identify chief cells and oxyphillic cells

A

chief and oxyphillic cells

35
Q
  • Parathyroid Hyperplasia
  • Parathyroid Adenoma
  • Parathyroid Carcinoma

all cause what?

A

Parathyroid hyperfunction

36
Q

What are some causes of hypofunction of parthyroid abnormalities

A
  • Congenital (DiGeorge syndrome)
  • Iatrogenic (surgical)
  • Familial
  • Autoimmune
37
Q

Primary Hyperparathyroidism etiology

A
  • Annual incidence: 25 per 100,000
  • F:M = 3:1
  • Middle age to older adults
  • Causes: – Adenoma: 75% - 80% – Primary hyperplasia: 10% - 15% – Parathyroid carcinoma: <5%
38
Q

– Erosion of bone matrix by osteoclasts

– Grossly thinned cortex

– Fibrosis of marrow with hemorrhage and cyst formation

A

Osteitis fibrosa cystica

39
Q

– Osteoclasts, reactive giant cells, hemorrhage

– Morphologically identical to giant cell tumor of bone

A

Brown tumor

40
Q
  • Composed of sheets of chief cells with decrease in stromal fat
  • Oxyphil cells may also be present
  • May show a rim of normal parathyroid at the periphery
A

Parathyroid Adenoma

41
Q
  • Solitary nodule arising in a single parathyroid gland
  • 0.5 – 5.0 grams
  • Other glands are either normal or atrophic
A

Parathyroid Adenoma

42
Q
  • Classically all four glands are involved; however, there may be relative sparing of 1 or 2 glands
  • Morphologically there is chief cell hyperplasia just as in adenomas
  • May be difficult to distinguish histologically from adenoma
A

Parathyroid Hyperplasia

43
Q
  • Exceedingly rare
  • Difficult to distinguish from adenomas in parathyroid
  • Usually not diagnosed until they become clearly invasive and/or metastatic
A

parathyroid carcinoma

44
Q

What features do we expect to see in parathyroid carcinoma?

A

• Cellular atypia is not a reliable feature of malignancy • Mitotic activity, fibrous bands, and capsular/vascular invasion

45
Q

Why are parathyroid carncinomas difficult to remove?

A

• Difficult to remove from surrounding structures at the time of surgery due to fibrous adhesions

46
Q

is the most common cause of primary hyperparathyroidism

A

Parathyroid adenoma

47
Q

Parathyroid adenomas have a rim of normal parathyroid tissue at the periphery while _______ will not

A

(parathyroid hyperplasia will not)

48
Q

Parathyroid carcinoma is diagnosed be demonstrating

A

invasion into surrounding tissues or metastasis

49
Q

Bone manifestations of hyperparathyroidism result from osteoclast activation and include

A

osteitis fibrosa cystica and Brown tumors

50
Q

• CORTEX:

  • Zona glomerulosa (G): Mineralocorticoids (aldosterone) =
  • Zona fasciculata (F): Glucocorticoids (cortisol) =
  • Zona reticularis (R): Sex steroids (estrogens and androgens) =
A

“Salt”

“Sugar”

“Sex”

51
Q

In the medulla what type of cells release catecholamies?

A

chromaffin cells!

52
Q

• Bilateral thickening of the adrenal cortex

Can be: Diffuse or Nodular

  • Predominantly fasciculata cells : Clear cells
  • Microscopically resembles adrenocortical adenoma
A

Adrenocortical Hyperplasia

53
Q

Adrenocortical Hyperplasia represenets what microscopically?

A

adrenocortical hyperplasia

54
Q

what does adrenocortical hyperplasia multinodular pattern look like?

A

see image

55
Q

what are the genral features of a adrenocortical adenoma?

A

• Yellow • Encapsulated • 1-2 cm •

56
Q

are adrenocortical adenomas funcitonal or non-functional?

A

Functional or non-functional – Cannot be determined by histology – Most are non-functional

57
Q

where in the adrenal gland do we see the most hyperplasia in adrenocortical adenoma?

A

Predominantly zona fasciculata cells – like hyperplasia – Solitary encapsulated lesion

58
Q

Found in the adrenals, • Rare • >200-300 grams • Usually >5 cm diameter

A

adrenocortical carcinoma

59
Q

What are key features that differentiate adrenocortical carcinoma from adenoma

A

Invasive, with effacement of normal structures

Necrosis and hemorrhage

60
Q

Where do adrenocortical carcinomas invade?

A

Tendency to invade adrenal vein and vena cava • Lymph node metastasis

61
Q

Describe histology of adrenocortical carcinoma

A

can be well to poorly differentiated

see increased mitotic activity

may appear simular to adenoma but have INVASIVE behavior

62
Q

What features will we more likely see in adrenocortical carcinoma over adenoma

A

• Large size (>5 cm) • Capsular and vascular invasion • Necrosis • Increased mitoses • Cellular pleomorphism

63
Q

• Hypercortisolism: depends on cause

– Exogenous glucocorticoids →

A

Cortical atrophy

64
Q

• Hypercortisolism: depends on cause:

– Increased ACTH →

A

Bilateral hyperplasia from Pituitary adenoma

65
Q

• Hypercortisolism: depends on cause:

– ACTH independent hypercortisol →

A

Adrenocortical adenoma or carcinoma

66
Q
  • Hypercortisolism: depends on cause:
  • Hyperaldosteronism:
A

– Usually adrenal cortical adenoma (Conn syndrome)

67
Q
  • Hypercortisolism: depends on cause:
  • Congenital Adrenal Hyperplasia (CAH) –
A

Bilateral hyperplasia

68
Q

Classic triad seen with pheochromocytoma

A

Headaches, palpitations, diaphoresis

69
Q

Neoplasms composed of adrenal medullary chromaffin cells

A

Pheochromocytoma

70
Q

Are Pheochromocytoma usually bening or malignant, how can you tell?

A

IG bening, only sign of malignancy is METASTASIS

71
Q

See Zellballen architecture with a tons of neuroendocrine markers

Dx

A
72
Q

Describe cytoplasm seen in pheochromocytoma

A

abundant; granular and basophilic

may see nuclear pleomorphism

73
Q

what expands in a pheochromocytoma?

A

the MEDULLA, not the cortex

74
Q

Extra adrenal pheochromocytoma

• Almost all are non-functional

A

Paraganglioma

75
Q

How is a paraganglioma simular to a pheochromocytoma?

A

Similar morphology to pheochromocytoma

– Zellballen

76
Q

Common sites of paraglangliomas

A

– Jugulotympanic – Carotid body – Vagal – Aorticopulmonary

77
Q

What is the rule of 10s for pheochromocytomas

A

10% bilateral

10% maligant

10% arise in childhood

10% extra-adrenal (paraganglioma)

10% from familial sydromes

78
Q

Bilateral hyperplasia is most common finding associated with

A

endogenous Cushing (↑ACTH)

79
Q

Adrenocortical adenomas are mostly ______

• Adrenocortical carcinoma is diagnosed by finding ______

A

non-functional

invasion or metastasis

Endocrine (20 decks)

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