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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
What are the 'silent' or 'null cell' adenomas? How do they typically present?
1. Non-functioning and gonadotroph adenomas 2. present with mass effect Gonadotroph adenomas typically show minimal function
26
What transcription factor are most functioning pituitary adenomas associated with? What is the exception?
1. PIT-1 | 2. Corticotroph adenoma is associated with TPIT
27
What SOMATIC mutations are associated with pituitary adenomas?
GNAS USP8 - corticotroph
28
What FAMILIAL mutation is associated with pituitary adenomas?
``` AIP (FIPA) ◦ Pituitary Adenoma Predisposition (PAP) ◦ Most commonly Somatotroph adenomas ``` Commonly results in familial gigantism
29
What is a rathke's cleft cyst? What makes it clinically significant?
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
Which form of craniopharingioma most commonly manifiests in kids (5-15) How does it present?
1. Adamantinomatous craniopharyngiomas | 2. Growth retardation from hypopituatarianism
31
Which form of craniopharingioma most commonly manifiests in adults (>65) How does it present?
Papillary craniopharyngiomas ◦ Signs of increased intracranial pressure or hypopituitarism
32
Histology of craniopharyngiomas
Derived from Rathke's pouch remnants: squamous epithelium Wet keratin Calcified cyst
33
What is the etiology of primary empty sella syndrome? Secondary?
Primary: CSF leaks into the sella and compresses the pituitary Secondary: The pituitary expands and infarcts within the sella, leaving an empty space
34
What is sheehan syndrome? Most notable symptom?
1. post-partum necrosis of the anterior pituitary | 2. Failure of lactation
35
What is the result of ADH deficiency? excess?
Deficiency: diabetes insipidus Excess: SIADH
36
What symptom is present in both DI and SIADH? Explain why for each
Thirst DI: a legit need to replace fluids --> polydipsia SIADH: direct effect of ADH on the brain results in inappropriate thirst
37
WHat is the difference between central and nephrogenic DI?
Central: ADH deficiency Nephrogenic: Reduced response to endogenous ADH
38
How do you test to determine central vs nephrogenic DI?
Administer DDAVP (desmopressin) Does the kidney respond with increased water retention and increased urine sodium/osmolality? Yes – Central DI No – Nephrogenic DI
39
Causes of SIADH
``` ◦ Small cell carcinoma of the lung ◦ OTHER MALIGNANCIES AS WELL ◦ Traumatic Brain Injury/Subarachnoid hemorrhage ◦ Drugs (SSRIs) ```
40
Diabetes insipidus edit
``` Decreased reclaimed free water from renal collecting system ◦ Increased serum osmolality, hypernatremia ◦ Dilute, excessive urine ◦ Polyuria ```
41
SIADH edit
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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