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Endocrine M2T2 > 4. Pituitary And Adrenal Gland Path > Flashcards

4. Pituitary And Adrenal Gland Path Flashcards

1
Q

CDKN1B gene product is what. Mutation causes what.

A

Cell cycle checkpoint regulator. Causes MEN like syndromes

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2
Q

PRKAR1A mutation causes what syndrome and what is the MOA

A

Carneys syndrome. Loss of function causes inappropriate activation of cAMP –> pituitary neoplasms

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3
Q

AIP mutations cause what

A

GH adenomas and acromegaly in younger age groups

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4
Q

What four genetic abnormalities in pituitary tumors are associated with aggressive adenomas

A

Over expression of cyclin D
P53 mutation
Epigenetic silencing of retinoblastoma gene RB1
Activation of HRAS oncogene (rare carcinomas)

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5
Q

Histological characteristics of pituitary adenomas

A

Cellular monomorphism

Absence of reticulin network

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6
Q

Atypical pituitary adenomas genetic changes

A

Mitotic activity
P53 mutations
Ki-67 mutations

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7
Q

What are psamomma bodies and why do they occur? In what condition do you see them in in terms of pituitary pathology

A

Psamomma bodies are calcium deposits occurring in damaged/necrotic tissue
DOES NOT need elevated Calcium (aka this is dystrophic calcification.
This occurs in PROLACTINOMA

N.B. Calcium deposition occurring from elevated serum calcium levels would be called metastatic calcification

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8
Q

PROLACTINOMA characteristics: histology, clinical, epidemiology, tx

A

Most common hyper functioning endocrine tumor of pituitary
Amyloid deposition
Dystrophic calcification + psamomma bodies
Peri-nuclear crescent pattern on IHC

Causes amenorrhea, galactorrea, loss of libido, impotence
More common in women 40-60 but evens out as you age

Tx: surgery or bromocriprine

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9
Q

Clinical features of cushings syndrome

A

Htn
Weight gain esp trunk
Moon face
Buffalo hump
Dec muscle mass atrophy of type 2 m fibers
Prox limb weakness
Hyperglycemia, glucosuria, polydypsia (inc GNG, dec glucose uptake)
Striae
Osteoporosis
Inc risk of ifx (glucocorticoids dec immune response)
Hirsutism, menstrual abnormalities
Mental disturbances: depression, personality changes, fatigability

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10
Q

Difference between nodular and macronodular hyperplasia of adrenal cortex

A

Nodular: seen with ACTH-dependent cushings
Macronodular: seen with ACTH-independent cushings, tumor is in adrenal gland due to overexpression of receptors that bind GIP, LH, ADH, 5HT

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11
Q

Craniopharyngiomas general characteristics: epidemiology, location, remnant of ____, clinical findings

A 
Arise in supra stellar region
Bi-modal age distribution 
Headaches and visual problems
Remnant of rathke pouch
Benign with good prognosis
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12
Q

Adamantinomatous craniopharyngioma most common in ___, histology

A

Children
Calcifications, nests and cords of stratified squamous epi in reticular background
Cysts have cholesterol rich thick brown fluid
Pallisading squamous epi
Compact lamellar keratin
Fibrosis, cyst formation, chronic inflammation

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13
Q

Papillary craniopharyngioma

A

Solid sheets and papillae lined with squamous cells

No keratin, calcifications, pallisading

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14
Q

Dexamethasone relationship to Cushings (pituitary, adrenal, ectopic)

A

Pituitary- high lvls Dex suppress ACTH
Adrenal - no effect, ACTH already low
Ectopic - high ACTH not suppressed by Dex

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15
Q

Epidemiology of Conn Syndrome

A

Middle aged life. Women

Hyperaldosteronism

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16
Q

Spironolactone bodies and in what condition are they seen in?

A

Spironolactone treatment causes laminated cytoplasmic inclusions called spironolactone bodies in aldosterone secreting adenomas

Seen in hyperaldosteronism

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17
Q

What is MEN1, and mutation in it causes what?

A

Multiple endocrine neoplasm 1 gene, mutation causes Multiple endocrine neoplasm syndrome type 1

18
Q

What is secondary hyperaldosteronism due to?

A

activation of RAAS system due to arteriolar nephrosclerosis and renal artery stenosis –> inc levels of plasma renin –> inc aldosterone

19
Q

What enzyme does hyperaldosteronism effect, and how does that lead to oxidative stress?

A

Effects glucose 6 phosphate dehydrogenase, causing decreased levels of the enzyme. Leads to endothelial dysfunction and decreased production of NO –> oxidative stress

20
Q

What is adrenogenital syndrome?

A

Abnormal production of androgens

21
Q

Most common enzyme deficiency that causes adrenogenital syndrome

A

21 hydroxylase deficiency

Results in increased secretion of DHEA, decreased production of cortisol and aldosterone

22
Q

What other electrolyte besides sodium is effected by hyperaldosteronism? What happens to that electrolyte’s level?

A

K+

hypokalemia

23
Q

What is Waterhouse-friderichsen syndrome caused by? What are symptoms?

A

Neisseria meningitidis septicemia (can also be pseudomonas, pneumococci, h flu)
Rapidly progressing hypotension and shock
DIC
Adrenocortical insufficiency

24
Q

What is Addison’s disease? List some common symptoms

A

Primary Chronic adrenocortical insufficiency
Hyperpigmentation due to increased ACTH release–> stimulates melanocytes
Hyponatermia, hyperkalemia, hypovolemia, hypotension

25
Q

What is secondary hyperaldosteronism due to?

A

activation of RAAS system due to arteriolar nephrosclerosis and renal artery stenosis –> inc levels of plasma renin –> inc aldosterone

26
Q

What enzyme does hyperaldosteronism effect, and how does that lead to oxidative stress?

A

Effects glucose 6 phosphate dehydrogenase, causing decreased levels of the enzyme. Leads to endothelial dysfunction and decreased production of NO –> oxidative stress

27
Q

What is adrenogenital syndrome?

A

Abnormal production of androgens

28
Q

Most common enzyme deficiency that causes adrenogenital syndrome

A

21 hydroxylase deficiency

Results in increased secretion of DHEA, decreased production of cortisol and aldosterone

29
Q

What other electrolyte besides sodium is effected by hyperaldosteronism? What happens to that electrolyte’s level?

A

K+

hypokalemia

30
Q

For pheochromocytoma, what is the rule of 10’s?

A

10% sporadic
10% malignant
10% extra-adrenal
10% nonhypertension

31
Q

Clinical features of pheochromocytoma

A 
HTN
Headaches
Tachycardia
Urinary excretion of VMAs
MI
CVA
32
Q

What tumor is zellbellen associated with and what is it?

A

Zellbellen- nests of tumor cells bound by fibrovascular stroma (German for ball of cells)

Pheochromocytoma

33
Q

In what condition do you see homer-wright pseudorosettes? What are they?

A

H-WP: cells gathered around tangled eosino fibrils

Neuroblastoma

34
Q

What locations in the body do you see neuroblastomas?

A

Adrenal/retroperitoneal

Posterior mediastinum

35
Q

For pheochromocytoma, what is the rule of 10’s?

A

10% sporadic
10% malignant
10% extra-adrenal
10% hypertension

36
Q

Clinical features of pheochromocytoma

A 
HTN
Headaches
Tachycardia
Urinary excretion of VMAs
MI
CVA
37
Q

What tumor is zellbellen associated with and what is it?

A

Zellbellen- nests of tumor cells bound by fibrovascular stroma (German for ball of cells)

Pheochromocytoma

38
Q

In what condition do you see homer-wright pseudorosettes? What are they?

A

H-WP: cells gathered around tangled eosino fibrils

Neuroblastoma

39
Q

What locations in the body do you see neuroblastomas?

A

Adrenal/retroperitoneal

Posterior mediastinum

40
Q

Differentiate ganglioneuroblastoma from ganglioneuroma

A

Ganglioneuroblastoma: ganglion cells in diff stages of development, malignant, neuroblasts
Ganglioneuroma: differentiated mature ganglion cells, benign, no neuroblasts

Endocrine M2T2 (16 decks)

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