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(OMS2) ENRP Exam 2 > Pituitary pathology > Flashcards

Pituitary pathology Flashcards

1
Q

What is the most common form of primary endocrine hyperfunction?

A

Neoplasia (except thyroid)

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2
Q

What are the results of mass effect of pituitary lesions

A
  1. Increased intracranial pressure
  2. Visual field disturbances
  3. Pituitary apoplexy
  4. Underproduciton of pituitary hormones
  5. Hyperprolactinemia
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3
Q

Most important PE finding of increased intracranial pressure

A

Papilledema

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4
Q

What is the visual field disturbance associated with pituitary mass effect?

A

Bilateral temporal hemianopsia

From compression of the optic chiasm

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5
Q

What are the 2 classes of pituitary adenomas?

A
  1. Functional: hormone excess

2. Non-functional: mass effect

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6
Q

What are the types of cells in the pituitary?

What do they secrete?

A
  1. Lactotroph – prolactin
  2. Somatotroph – growth hormone
  3. Corticotroph – ACTH
  4. Thyrotroph – TSH
  5. Gonadotroph – LH/FSH
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7
Q

What is the most common secretory pituitary adenoma?

A

Lactotroph adenoma

prolactinoma

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8
Q

When is a prolactinoma generally discovered in males?

A

With mass effect

Decreased libido and sperm count isn’t likely to get males to seek help

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9
Q

Prolactinoma presentation in females

A 
Menstrual irregularities
◦ Responsible for >20% of cases of
amenorrhea
Galactorrhea
Diminished libido
Infertility
Mass effect
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10
Q

How are prolactinomas treated?

A

Dopamine agonists – Bromocriptine, Cabergoline

Surgery

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11
Q

Causes of hyperprolactinemia in the absence of adenoma

A
  1. Pregnancy
  2. Lactation/nipple stimulation
  3. Loss of dopamine –> Lactotroph hyperplasia
  4. Renal failure (increased production and decreased clearance of PRL)
  5. Hypothyroidism (increased TRH can stimulate PRL production)
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12
Q

What is the Lactational Amenorrhea Method?

A

Relies on elevations of prolactin levels from breastfeeding to maintain ovulation

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13
Q

What are the results of a somatotroph adenoma?

A

Gigantism (pre-epiphysial plate closure)

Acromegaly (post-closure)

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14
Q

Features of acromegaly

A
  1. Enlargement of the face and hands (spade like)
  2. Protruding jaw
  3. Enlarged nose
  4. Thickened lips
  5. Joint pain/limited mobility
  6. Enlarged viscera
  7. Shortened lifespan (typically due to
    cardiovascular complications)
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15
Q

Is it possible to have both gigantism and acromegaly?

A

yes (andre the giant)

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16
Q

How do you diagnose a somatotroph adenoma?

A

Serum levels of IGF-1

If elevated, do oral glucose test for GH (IGF-1) response

Levels decrease if normal

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17
Q

Treatment of somatotroph adenoma

A
  1. Somatostatin analogs or GH receptor antagonists

2. surgical excision

18
Q

Distinguish between cushing syndrome and cushing’s disease

A

Cushing syndrome:
◦ Obesity (central), diabetes, hirsutism, adrenal hyperplasia
(original 1912 description)
◦ Modern definition: Hypercortisolism and all it brings with it

Cushing’s disease:
◦ From the original description by Harvey Cushing
◦ Derives from pituitary ACTH
◦ CORTICOTROPH ADENOMA!

19
Q

Signs of hypercortisolism

A 
Centripetal obesity
Moon facies
Striae
Thin skin
Hirsutism
20
Q

What is the most common cause of Cushing syndrome

A

Glucocorticoid administration

21
Q

What is the first step in the work-up of hypercortisolism

A

Determine of ACTH dependedent or independent

22
Q

How do corticotroph adenomas respond to high dose dexamethasone suppression testing?

To CRH stimulation test?

A
  1. Suppression of ACTH on high dose dexamethasone suppression test
  2. Elevated response to CRH stimulation test
23
Q

Treatment of corticotroph adenomas

A

Somatostatin analogs, bromocriptine, or surgical excision

Corticotroph adenomas can express dopamine receptors and somatostatin receptors

24
Q

What is nelson syndrome?

A

insert later

25
Q

What are the ‘silent’ or ‘null cell’ adenomas?

How do they typically present?

A
  1. Non-functioning and gonadotroph adenomas
  2. present with mass effect

Gonadotroph adenomas typically show minimal function

26
Q

What transcription factor are most functioning pituitary adenomas associated with?

What is the exception?

A
  1. PIT-1

2. Corticotroph adenoma is associated with TPIT

27
Q

What SOMATIC mutations are associated with pituitary adenomas?

A

GNAS

USP8 - corticotroph

28
Q

What FAMILIAL mutation is associated with pituitary adenomas?

A 
AIP (FIPA)
◦ Pituitary Adenoma Predisposition
(PAP)
◦ Most commonly Somatotroph
adenomas

Commonly results in familial gigantism

29
Q

What is a rathke’s cleft cyst?

What makes it clinically significant?

A
  1. Cystic mass derived from Rathke’s pouch
    Can expand and compress normal pituitary
  2. Can rupture and result in inflammation of the pituitary or meningitis
30
Q

Which form of craniopharingioma most commonly manifiests in kids (5-15)

How does it present?

A
  1. Adamantinomatous craniopharyngiomas

2. Growth retardation from hypopituatarianism

31
Q

Which form of craniopharingioma most commonly manifiests in adults (>65)

How does it present?

A

Papillary craniopharyngiomas

◦ Signs of increased intracranial pressure or
hypopituitarism

32
Q

Histology of craniopharyngiomas

A

Derived from Rathke’s pouch remnants:
squamous epithelium
Wet keratin
Calcified cyst

33
Q

What is the etiology of primary empty sella syndrome?

Secondary?

A

Primary: CSF leaks into the sella and compresses the pituitary

Secondary: The pituitary expands and infarcts within the sella, leaving an empty space

34
Q

What is sheehan syndrome?

Most notable symptom?

A
  1. post-partum necrosis of the anterior pituitary

2. Failure of lactation

35
Q

What is the result of ADH deficiency?

excess?

A

Deficiency: diabetes insipidus

Excess: SIADH

36
Q

What symptom is present in both DI and SIADH?

Explain why for each

A

Thirst

DI: a legit need to replace fluids –> polydipsia

SIADH: direct effect of ADH on the brain results in inappropriate thirst

37
Q

WHat is the difference between central and nephrogenic DI?

A

Central: ADH deficiency

Nephrogenic: Reduced response to endogenous ADH

38
Q

How do you test to determine central vs nephrogenic DI?

A

Administer DDAVP (desmopressin)

Does the kidney respond with increased water
retention and increased urine sodium/osmolality?
Yes – Central DI
No – Nephrogenic DI

39
Q

Causes of SIADH

A 
◦ Small cell carcinoma of the lung
◦ OTHER MALIGNANCIES AS WELL
◦ Traumatic Brain Injury/Subarachnoid
hemorrhage
◦ Drugs (SSRIs)
40
Q

Diabetes insipidus

edit

A 
Decreased reclaimed free water from
renal collecting system
◦ Increased serum osmolality, hypernatremia
◦ Dilute, excessive urine
◦ Polyuria
41
Q

SIADH

edit

A

Increased reclaimed free water from renal
collecting system
◦ Decreased serum osmolality (hyponatremia)
◦ Concentrated urine (hypernatriuria)
◦ Mental status changes, muscle weakness, seizures

(OMS2) ENRP Exam 2 (9 decks)

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