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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
Pituitary adenomas are proliferations of\_\_\_\_\_ cells without a\_\_\_\_\_ network
monomorphic reticulin
26
Pituitary adenomas are classified based on
immunostain
27
\_\_\_\_\_\_\_cell adenoma is the most common pituitary adenoma
Prolactin
28
Large pituitary adenomas can cause
bitemporal hemianopsia
29
Arise from the pharyngeal pouches – Inferior and thymus –\_\_\_\_ pharyngeal pouch – Superior –\_\_\_\_ pharyngeal pouch
third fourth
30
* Are normally located in proximity of upper and lower poles of the thyroid gland * May be ectopically located in thymus, anterior mediastinum, carotid sheath
parathyroid glands
31
* Yellow, brown ovoid nodule * 30 - 45 mg * Composed primarily of chief cells and some oxyphil cells
Parathyroid glands
32
Parathyroid In adults there is a large amount of \_\_\_\_\_\_\_ •\_\_\_\_\_\_ cells secrete parathyroid hormone
intervening stromal fat 30 – 70% Chief
33
Parathyroid gland histology
encapsulated ovoid cells with purpule nuclei can be in sheets and look simular to pituitary and can be dispersed w/in gland itself
34
be able to identify chief cells and oxyphillic cells
chief and oxyphillic cells
35
- Parathyroid Hyperplasia - Parathyroid Adenoma - Parathyroid Carcinoma all cause what?
Parathyroid hyperfunction
36
What are some causes of hypofunction of parthyroid abnormalities
- Congenital (DiGeorge syndrome) - Iatrogenic (surgical) - Familial - Autoimmune
37
Primary Hyperparathyroidism etiology
* 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
– Erosion of bone matrix by osteoclasts – Grossly thinned cortex – Fibrosis of marrow with hemorrhage and cyst formation
Osteitis fibrosa cystica
39
– Osteoclasts, reactive giant cells, hemorrhage – Morphologically identical to giant cell tumor of bone
Brown tumor
40
* 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
Parathyroid Adenoma
41
* Solitary nodule arising in a single parathyroid gland * 0.5 – 5.0 grams * Other glands are either normal or atrophic
Parathyroid Adenoma
42
* 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
Parathyroid Hyperplasia
43
* Exceedingly rare * Difficult to distinguish from adenomas in parathyroid * Usually not diagnosed until they become clearly invasive and/or metastatic
parathyroid carcinoma
44
What features do we expect to see in parathyroid carcinoma?
• Cellular atypia is not a reliable feature of malignancy • Mitotic activity, fibrous bands, and capsular/vascular invasion
45
Why are parathyroid carncinomas difficult to remove?
• Difficult to remove from surrounding structures at the time of surgery due to fibrous adhesions
46
is the most common cause of primary hyperparathyroidism
Parathyroid adenoma
47
Parathyroid adenomas have a rim of normal parathyroid tissue at the periphery while _______ will not
(parathyroid hyperplasia will not)
48
Parathyroid carcinoma is diagnosed be demonstrating
invasion into surrounding tissues or metastasis
49
Bone manifestations of hyperparathyroidism result from osteoclast activation and include
osteitis fibrosa cystica and Brown tumors
50
• CORTEX: - Zona glomerulosa (G): Mineralocorticoids (aldosterone) = - Zona fasciculata (F): Glucocorticoids (cortisol) = - Zona reticularis (R): Sex steroids (estrogens and androgens) =
“Salt” “Sugar” “Sex”
51
In the medulla what type of cells release catecholamies?
chromaffin cells!
52
• Bilateral thickening of the adrenal cortex Can be: Diffuse or Nodular * Predominantly fasciculata cells : Clear cells * Microscopically resembles adrenocortical adenoma
Adrenocortical Hyperplasia
53
Adrenocortical Hyperplasia represenets what microscopically?
adrenocortical hyperplasia
54
what does adrenocortical hyperplasia multinodular pattern look like?
see image
55
what are the genral features of a adrenocortical adenoma?
• Yellow • Encapsulated • 1-2 cm •
56
are adrenocortical adenomas funcitonal or non-functional?
Functional or non-functional – Cannot be determined by histology – Most are non-functional
57
where in the adrenal gland do we see the most hyperplasia in adrenocortical adenoma?
Predominantly zona fasciculata cells – like hyperplasia – Solitary encapsulated lesion
58
Found in the adrenals, • Rare • \>200-300 grams • Usually \>5 cm diameter
adrenocortical carcinoma
59
What are key features that differentiate adrenocortical carcinoma from adenoma
Invasive, with effacement of normal structures Necrosis and hemorrhage
60
Where do adrenocortical carcinomas invade?
Tendency to invade adrenal vein and vena cava • Lymph node metastasis
61
Describe histology of adrenocortical carcinoma
can be well to poorly differentiated see increased mitotic activity may appear simular to adenoma but have INVASIVE behavior
62
What features will we more likely see in adrenocortical carcinoma over adenoma
• Large size (\>5 cm) • Capsular and vascular invasion • Necrosis • Increased mitoses • Cellular pleomorphism
63
• Hypercortisolism: depends on cause – Exogenous glucocorticoids →
Cortical atrophy
64
• Hypercortisolism: depends on cause: – Increased ACTH →
Bilateral hyperplasia from Pituitary adenoma
65
• Hypercortisolism: depends on cause: – ACTH independent hypercortisol →
Adrenocortical adenoma or carcinoma
66
* Hypercortisolism: depends on cause: * Hyperaldosteronism:
– Usually adrenal cortical adenoma (Conn syndrome)
67
* Hypercortisolism: depends on cause: * Congenital Adrenal Hyperplasia (CAH) –
Bilateral hyperplasia
68
Classic triad seen with pheochromocytoma
Headaches, palpitations, diaphoresis
69
Neoplasms composed of adrenal medullary chromaffin cells
Pheochromocytoma
70
Are Pheochromocytoma usually bening or malignant, how can you tell?
IG bening, only sign of malignancy is METASTASIS
71
See Zellballen architecture with a tons of neuroendocrine markers Dx
72
Describe cytoplasm seen in pheochromocytoma
abundant; granular and basophilic may see nuclear pleomorphism
73
what expands in a pheochromocytoma?
the MEDULLA, not the cortex
74
Extra adrenal pheochromocytoma • Almost all are non-functional
Paraganglioma
75
How is a paraganglioma simular to a pheochromocytoma?
Similar morphology to pheochromocytoma – Zellballen
76
Common sites of paraglangliomas
– Jugulotympanic – Carotid body – Vagal – Aorticopulmonary
77
What is the rule of 10s for pheochromocytomas
10% bilateral 10% maligant 10% arise in childhood 10% extra-adrenal (paraganglioma) 10% from familial sydromes
78
Bilateral hyperplasia is most common finding associated with
endogenous Cushing (↑ACTH)
79
Adrenocortical adenomas are mostly \_\_\_\_\_\_ • Adrenocortical carcinoma is diagnosed by finding \_\_\_\_\_\_
non-functional invasion or metastasis

Endocrine (20 decks)

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