Pituitary Pathology Flashcards by Zach Visinoni

What symptoms/processes occur due to the mass effect of pituitary lesions? (5)

Increased intracranial pressure - HA, N/V, HTN, bradycardia, papilledema.

Visual field disturbances - BL temporal hemianopsia.

Pituitary apoplexy - hemorrhage into the adenoma.

Underproduction of pituitary hormones.

Hyperprolactinemia

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Sizes of the following pituitary adenomas:

< 1 cm
1-4 cm
> 4 cm

< 1 cm: microadenoma
1-4 cm: macroadenoma
> 4 cm: giant adenoma

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What is the most common secretory pituitary adenoma (30%)?

Lactotroph adenoma (prolactinoma)

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Lactotroph adenoma (prolactinoma) presentation in women (5) vs. men (3)

Women: menstrual irregularities (responsible for >20% of cases of amenorrhea), galactorrhea, diminished libido, infertility and mass effect.

Men: decreased libido, decreased sperm count, mass effect.

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What are the 2 classifications of lactotroph adenomas? Which is more common?

Sparsely granulated - most common

Densely granulated - rare

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What is the progression of lactotroph adenomas?

Stromal hyalinization w/ psammoma bodies (calcifications) can progress to dense calcifications and eventually a pituitary stone.

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What are the 2 major treatments for lactotroph adenomas?

Dopamine agonists - Bromocriptine, Cabergoline

Surgery

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What can cause Hyperprolactinemia in the absence of adenoma? (5)

Pregnancy

Lactation/nipple stimulation

Loss of DA -> lactotroph hyperplasia (damage to neurons (stroke, trauma, etc.), drugs, mass effect.

Renal failure (increased production and decreased clearance of PRL.

Hypothyroidism (increased TSH can stimulate PRL production)

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What 2 diseases will somatotroph adenomas lead to?

Gigantism and Acromegaly

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What are some features of Acromegaly?

Enlargement of the face and hands
Protruding jaw
Enlarged nose
Thickened lips

Joint pain/limited mobility
Enlarged viscera
Shortened lifespan (due to CV complications)

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How is Acromegaly diagnosed?

How is it treated? (3)

Elevated serum levels of IGF-1 prompts an oral glucose tolerance test for GH response.

Somatostatin analogs
GH receptor antagonists
Surgical excision

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What type of growth is characteristic of all pituitary adenomas?

What helps confirm a diagnosis?

Diffuse growth

Confirmation made w/ GH immunochemistry

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What is the pathological findings of somatotroph adenomas?

Can be sparsely or densely granulated. May be mixed with PRL-secreting cells.

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What occurs as a result of a corticotroph adenoma?

ACTH induces hypercortisolism - Cushing’s syndrome

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What is difference between Cushing syndrome and Cushing’s disease?

Cushing syndrome - obesity, DM, hirsutism, adrenal hyperplasia (basically anything that can occur due to hypercortisolism).

Cushing’s disease - derives from pituitary ACTH (Corticotroph adenoma).

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Which 3 malignancies can cause Cushing syndrome as a paraneoplastic feature?

Small-cell lung carcinoma

Pancreatic carcinomas

Neural tumors

What is the most common cause of Cushing syndrome?

Iatrogenic Cushing syndrome - due to corticosteroid administration.

What happens on the high-dose dexamethasone suppression test in a corticotroph adenoma?

What happens during the CRH stimulation test?

Suppression of ACTH

There is an elevated response, meaning they retain their responsivity to CRH.

What is the treatment for a Corticotroph adenoma? (3)

Somatostatin agalogs
DA agonists (Bromocriptine)
Surgical excision

What is Nelson’s syndrome?

Nelson’s syndrome is a rare disorder and occurs in patients who have had both adrenal glands removed owing to Cushing syndrome

What type of adenoma are Gonadotroph adenomas considered?

How do they present?

Non-functioning - “silent” or “null cell” adenomas

Present w/ mass effect. They typically show minimal function.

What genetic change is associated with pituitary adenomas? What changes as a result?

Is it somatic or familial?

Which adenoma is it most commonly seen in? Which one is it rarely seen in?

GNAS - makes the alpha subunit of Gs lose its GTPase activity. The signaling cascade is not turned off, so there is constant cAMP-driven cell proliferation.

Somatic

Exists in 40% of Somatotroph adenomas and rarely in Corticotroph adenomas.

What mutation occurs in Corticotroph adenomas?

Somatic or familial?

USP8 - mutation results in EGFR upregulation.

Somatic

What mutation often effects Somatotroph adenomas?

Somatic or familial?

AIP (FIPA)
PAP - pituitary adenoma predisposition

Familial

What is the morphology of a pituitary adenoma generally? What happens in aggressive adenomas?

Well circumscribed, may erode bone, may bleed. Aggressive adenomas are poorly circumscribed and may invade brain if they get big enough.

What is a Rathke's cleft cyst? What can occur as a result?

Cystic mass derived from Rathke's pouch. Can expand and compress a normal pituitary. It can rupture and result in inflammation of the pituitary or meningitis.

Two groups of Craniopharyngiomas: Kids (5-15 y/o) Adults (>65 y/o)

Kids (5-15 y/o): most often adamantinomatous craniopharyngiomas. GR results from the hypopituitarism. Adults (>65 y/o): papillary craniopharyngiomas. Signs of increased intracranial pressure or hypopituitarism.

What are Craniopharyngiomas derived from? What are 3 histological findings?

Rathke's pouch remnants. Squamous epithelium "Wet" keratin Calcified cyst

What is the cause of primary empty sella syndrome? What is the cause of secondary empty sella syndrome?

Primary - CSF leaks into the sella and compresses the pituitary. Secondary - the pituitary expands and infarcts within the sella, leaving an empty space.

What are symptoms of anterior hypopituitarism? (5)

Loss of GH - increased fat, decreased muscle, reduced strength. Loss of gonadotropins - (men) poor libido/impotence, infertility, reduced facial/body hair; (women) amenorrhea, dyspareunia, infertility, breast atrophy. Loss of TSH - fatigue, constipation, weight gain. Loss of ACTH - weakness, fatigue, hypoglycemia. Loss of PRL - lactation failure.

What is Sheehan's syndrome?

Post-partum necrosis of the pituitary gland.

Which 2 hormones are secreted by the posterior pituitary?

Oxytocin and ADH

Diabetes insipidus = What are 3 features a patient might notice?

Decreased reclaimation of free water from the renal collecting system. Increased serum Osm (hypernatremia) Dilute, excessive urinate Polyuria

What happens when DDAVP is given to patients with central DI vs. nephrogenic DI?

Central DI - kidneys respond w/ increased water retention and increased urine Osm/Na+. Nephrogenic DI - no response by the kidneys.

What occurs in SIADH? What are 3 features a patient might notice? What are 3 major causes?

Inappropriate ADH secretion; increased reclaimed free water from renal collecting system. ``` Decreased serum Osm (hyponatremia) Concentrated urine (hypernatriuria) Mental status changes, muscle weakness, seizures ``` Causes: - small cell lung carcinoma - traumatic brain injury/subarachnoid hemorrhage - drugs (SSRIs)