Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

DEMS IV > pituitary pathology > Flashcards

pituitary pathology Flashcards

1
Q

Function of T-pit

A

Trxn factor which promotes differentiation of rathe pouch stem cells into corticotrophs which will secrete ACTH. Also involved in ACTH secreting pituitary adenoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Function of Pit-1

A

Trxn factor which promotes differentiation of Rathke pouch stem cells into somatotroph stem cells. Can also be involved in mixed GH/TSH secreting adenomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What do somatotroph stem cells differentiate into

A
  1. Somatotrophs (secrete GH). 2. Thyrotrophs (secrete TSH)- can also convert back into somatotroph stem cells. 3. mammosomatotroph- further differentiates into somatotroph (GH) or latotroph (PRL)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

distribution of cell types in anterior pituitary

A

Corticotrophs (ACTH) and thyrotrophs (TSH) in middle. Lactotrophs (PRL) and somatotrophs (GH) towards the sides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Staining of somatotrophs

A

Acidophilic (orangish) on PAS-orange G staining

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

normal anterior vs posterior pituitary histology

A

anterior: glandular with acidophilic, basophilic and chromophobic staining cells. Posterior: eosinophilic, fibrillar appearance with occasional swollen axonal processes (herring bodies)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Infundibulum histology

A

Congested, thin walled closely juxtaposed hypothalamic-hypophyseal portal system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Causes of pituitary adenomas

A

<5% are familial, the rest are sporadic with an unknown cause.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Genes associated with familial pituitary tumor syndromes

A

MEN1, CDKN1B, PRKAR1A and AIP (GH secreting adenomas)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Features suggesting an inherited pituitary tumor syndrome

A

parathyroid tumors, pancreatic endocrine tumors, atrial myxomas, lentigines, Schwann-cell tumors (Carney complex), family history and young age at onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Pituitary tumor clinical presentation

A
  1. hormone hypersecretion: acromegaly, Cushings, amenorrhea/galactorrhea. 2. Sx from mass effect: headaches, vision loss, piuitary gland dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

pituitary adenoma grade

A

Almost all are WHO grade 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Microadenoma vs macroadenoma of anterior pituitary

A

Micro: 10mm, distorts adjacent tissues such as the dura of the sellar floor or diaphragma sella causing headaches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

pituitary adenomas and diabetes insipidus

A

DI is quite uncommon with pituitary adenomas of any size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Macroadenomas most common growth patterns

A

Most commonly grows directly upwards, compressing the optic chiasm and resulting in bitemporal hemianopsia (loss of lateral visual fields due to compression of medial retinal fields).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Less common growth patterns of macroadenomas of pituitary

A
  1. compression of hypothalamus- hypothalamic dysfunction is rare. 2. Lateral growth outside the sella may compress the medial temporal lobe causing seizures. 3. May compress brain parenchyma but lack ability to infiltrate into brain parenchyma as single cells. 4. May extend laterally and compress the wall of the cavernous sinus, enwrapping the carotid artery (but not compromising) and distorting cranial nerves III, IV, and VI (cranial nerve palsies). 5. May extend into sphenoid sinus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Giant adenomas

A

Invasive adenomas >4cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Imaging of macroadenomas and giant adenomas

A

Often show cysts and hemosiderin pigment in neuroimaging or in tumor specimen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which pituitary tumors are responsive to medical therapy

A

Prolactinomas and GH secreting tumors (after surgical debulking)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Piuitary adenoma histology

A

intraoperative touch preparation shows abundant exfoliation of cytologically monotonous cells. Nuclear pleomorphism is uncommon. Mitoses are rare in microadenomas but occasionally seen in macro.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Histochemical stain for adenomas

A

Reticulin- normal pituitary has a nested pattern whereas adenoma has a disrupted reticulin pattern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Most frequency pituitary adenomas found incidentally at autopsy

A

prolactinoma, followed by null cell/gonadotroph

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

clinical signs of prolactinoma

A

galactorrhea, amenorrhea, infertility, hypogonadism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

prolactinoma histology and immunoreactivity

A

Diffuse growth pattern, monotonous cell population with increased nuclear chromatin content and conspicuous vasculature. Diffuse immunoreactivity for PRL only.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How does the size of a prolactinoma correlate with PRl levels

A

In premenopausal women, size of adenoma parallels serum levels closely. NOT true for men or post menopausal women.

26
Q

Treatment of prolactinomas

A

Medical management with dopamine agonist usually prevents the need for surgery. Surgery is used when pts have low tolerance for meds, tumor doesn’t shrink appropriately with meds, or limited preoperative testing available

27
Q

Histology of prolactinoma after treatment with dopamine agonist

A

If recent and long term treatment, severe cytoplasmic shrinkage with near-naked nuclei that should not be mistaken for lymphocytes. Also often shows fibrosis

28
Q

Clinical signs of gonadotroph cell adenoma/non secretor

A

headaches, visual field defects, cranial nerve palsies (ptosis, diplopia), pituitary hormone deficits, and rarely-seizzures, stroke or CSF leak.Also hypogonadism or clinically silent

29
Q

gonadotroph cell adenoma histology

A

Sheet like architecture, perivascular arrangement of tumor cells, clear cell appearance, can have regions with more abundant oncocytic cytoplasm and regions with more scant cytoplasm.

30
Q

gonadotroph cell adenoma immunohistochem

A

Immunoreactivity with alpha subunit and FSH/LH. Patchy distribution

31
Q

Growth and treatment of non-secretory adenomas including gonadotroph adenomas

A

Slow growing- usually don’t require post operative radiotherapy

32
Q

clinical signs of GH secretion tumor

A

acromegaly- acral enlargement, soft tissu swelling, cardiac hypertrophy, HTN, hyperglycemia, sleep apnea

33
Q

clinical signs of TSH-cell adenoma

A

thyroid goiter, hyperthyroxinemia

34
Q

Clinical signs of corticotroph adenoma

A

Cushings- hypercortisolism, central obesity, striae, hyperglycemia, osteroporosis, hirsutism

35
Q

histology of ACTH adenoma

A

densely granulated ACTH cells growing as sheets of monotonous round cells. Immunoreactivity with ACTH only

36
Q

How do serum levels of ACTH correlate with size of corticotroph cell adenoma

A

They do not correlate at all! A small adenoma may cause profound cushings

37
Q

What is ACTH hyperplasia and how is it diagnosed

A

An uncommon cause of pituitary ACTH excess. Diagnosed by histology showing expansion, rather than destruction, of acini by reticulin stain. Will show larger acini containing relatively homogenous populations of ACTH reactive cells. Look for ectopic source of CRF

38
Q

what is pituitary apoplexy

A

Sudden headache, acute visual changes, ophthalmoplegia (Acute visual loss or inability to move eyes) and altered mental status (confusion) caused by the sudden hemorrhage or infarction of the pituitary gland

39
Q

What cuases pituitary apoplexy

A

Occurs in 10-15% of pituitary adenomas, but of varying degree of severity.Not clearly cell type or size dependent. 65% occur in patients with undiagnosed pituitary tumors. Anterior pituitary dysfunction is common.

40
Q

Pituitary apoplexy treatment

A

ICU care, steroids, surgery sometimes

41
Q

pituitary apoplexy histology

A

necrosis with areas of discernible adenoma

42
Q

Histology of Rathke cleft cyst

A

Ciliated columnar cyst lining, abundant amorphous eosinophilic nucin cyst contents in which are embedded small strips of pseudostratified ciliated columnar epithelium. Also squamous metaplasia (associated with cyst recurrence)

43
Q

What is lymphocytic hypophysitis

A

Inflammatory process involving the pituitary (usually anterior but posterior can be involved). Primary hypophysitis is an autoimmune disorder involving classically affecting young women during late pregnancy or in the early postpartum period. Secondary type is caused by other factors

44
Q

Lymphocytic hyophysitis histology

A

sheets of cytologically bland pure lymphocytic infiltrates

45
Q

testing for lymphocytic hypophysitis

A

anti-pituitary autoantibodies is not reliable test.

46
Q

Primary lymphocytic hypophysitis presentation, diagnosis, treatment

A

Usually presents as a mass lesion of the pituitary gland simulating pituitary adenoma on neuroimaging studies. Diagnosis: histological. Treatment: corticosteroids usually the only treatment needed. Sometimes surgery

47
Q

Causes of secondary lymphocytic hypophysitis

A

TB, sarcoidosis, Wegeners granulomatosis, Sjogren syndrome, Langerhands cell histiocytosis, germ cell tumors, lymphoma, and rarely- pituitary adenoma, craniopharyngioma, or rathke cleft cysts with secondary tissue damage

48
Q

Craniopharyngioma gross anatomy

A

Cystic and solid components.

49
Q

craniopharyngioma histology

A

ghost cells

50
Q

What is a hypothalamic hamartoma

A

Mass of neurons and glial cells. NOT a true neoplasm. fully differentiated neuroglial tissue that closely resembles normal hypothalamus but is jumbled

51
Q

hypothalamic hamartoma presentation

A

Clinical manifestations, if any, are those of endocrine hyperfunction due to overproduction of hypothalamic gonadotropin-releasing hormone that can cause precocious puberty. Also can see convulsive laughter known as gelastic seizures

52
Q

hypothalamic hamartoma treatment

A

surigcal resection alone IF symptomatic

53
Q

most common sellar region mass

A

pituitary adenoma

54
Q

Who usually gets pituitary adenomas

A

young to middle age adults

55
Q

Who usually gets crainpharyngiomas

A

children and adults- often calcified

56
Q

GH tumors recurrence

A

sparsely granulated GH tumors are more aggressive and have increased recurrence

57
Q

complications of GH tumors

A

mortality (increases with increasing levels of GH), DI, CSF leak, meningitis.

58
Q

GH cell adenoma histology

A

monotonous cells, slightly pleomorphic medium sized cells often wth angular profile. Densely granulated with diffuse, strong staining for GH and keratin reactivity. OR sparsely granulated with cells that lack acidophilia and may show more eccentrically place nuclei and perinuclear clearing in cytoplasm.

59
Q

Feature of sparsely granulated GH adenomas

A

often invade bone- will see entrapped bony spicules surrounded by tumor

60
Q

GH cell adenoma treatment

A

Somatostatin analog, radiotherapy- convential, stereotactic (less radiation to surrounding structures), and lmited experience wit gamma knife, LINAC and proton beam

DEMS IV (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions