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ENRP Exam II > Pituitary Pathoglogy Singh > Flashcards

Pituitary Pathoglogy Singh Flashcards

1
Q

Mass Effect of pituitary lesions?

A
  • Inc. ICP
    • ha, n/v, bradycardia, htn,papilledema
  • Hyperprolactinemia
  • underproduction of hormones
  • Pituitary apoplexy
  • b/l temporal hemianopsia
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2
Q

What is Pituitary apoplexy

A

Hemorrhage into an adenoma

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3
Q

If a pituitary lesion is compressing the stalk, what hormone is going to be overproduced?

A

Prolactin as dopamine can no longer inhibit its release from the anterior pituitary

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4
Q

Lactotroph?

A

secretes prolactin

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5
Q

Somatotroph?

A

growth hm secreting

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6
Q

Corticotroph?

A

ACTH secreting

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7
Q

Thyrotroph?

A

TSH secreting

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8
Q

Gonadotroph?

A

LH/FSH secreting

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9
Q

How does a lactotroph adenoma (prolactinoma) present in females vs males?

A

Female:

  • Menstrual irregularites
  • galactorrhea
  • diminished libido
  • infertility
  • mass effect

Male:

  • Mass effect
  • diminished libido and sperm count
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10
Q

What is the most common secretory pituitary adenoma?

A

Lactotroph adenoma

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11
Q

How do you stain for a suspected lactotroph adenoma?

A

PRL stain, + for procatin

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12
Q

How do lactotroph adenomas progress?

A

Stromal hyalinization with psammoma bodies leading to a pituitary stone

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13
Q

How do you treat lactotroph adenomas?

A
  • Dopamine or somatostatin analogs
  • surgery
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14
Q

What can cause hyperprolactinemia in the absence of an adenoma?

A
  • pregnancy, lactation/nipple stimulation
  • loss of dopamine
  • renal failure
  • hypothyroidism
    • inc. TRH can stimulate PRL production
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15
Q

How can a somatotroph adenoma cause both acromegaly and gigantism?

A
  • If the somatotroph adenoma is present before the epiphyseal plates close it releases GH causing the bones to grow leading to gigantism
  • If the adeoma is present after the growth plates have closed it causes the bones to thicken rather than lengthen
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16
Q

Features of acromegaly?

A
  • Enlargement of hands and face
  • protruding jaw, nose, thickened lips
  • Joint pain and limited mobility
  • shortened life due to CV issues
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17
Q

How do you diagnose a somatotroph adenoma?

A
  • Check serum levels of IGF-1
  • If it is elevated give oral glucose tolerance test for GH response
    • normally glucose would inhibit GH release which would decrease IGF-1 levels
    • in an adenoma the IGF-1 levels remain high
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18
Q

How do you treat somatotroph adenomas?

A
  • somatostatin analogs
  • GH receptor antagonists
  • surgery
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19
Q

Whta is unique about corticotroph adenomas?

A
  • They can have a very small size but they are also very functional and can induce cushing disease
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20
Q

Differentiate between Cushing’s syndrome and disease.

A
  • Syndrome is hypercortisolism and all of the sx associated with it
  • Disesase is derived from the pituiutary ACTH → Corticotroph adenoma
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21
Q

What is the most common cause of Cushing Syndrome?

A

Iatrogenic CUshing syndrome → we cause it with glucocorticoid administration

22
Q

If we have cushing syndrome and ACTH is high, what could cause this and what does it mean?

A
  • If ACTH is high it is an ACTH dependent process
  • This can be caused by a pituitary tumor (Cushing’s Disease) OR an Ectopic ACTH producing tumor
23
Q

If we have a patient with Cushing Syndrome and low ACTH, what does this mean and what can cause it?

A
  • It is an ACTH independent process (adrenal cushings)
  • Caused by an adrenal adenoma/cancer OR b/l adrenal hyperplasia
24
Q

If you have an ACTH dependent hypercortisolism how do you test to figure out the cause?

A
  • Dexamethasone suppression test → if you give a high enough dose, pituitary adenomas will eventually decrease production
  • If there is no response it is NOT a pituitary adenoma and you need to look into a small cell carcinoma
25
Q

What is inferior petrosal sinus sampling?

A
  • thread a catheter up through jugular vein into the sinus and collect a sample to ID if there is secretion of a pitutary hormone into the sinus
    • can be done if you suspect the problem is pituitary but you can’t see it on imaging
26
Q

How do you treat a corticotroph adenoma?

A
  • Somatostatin analog
  • bromocriptine
  • surgery
27
Q

What is Nelson Syndrome?

A
  • Occurs when you remove the adrenal glands due to a pituitary adenoma that you can’t remove
  • give exogenous cortisol for physiologic needs, but it fails to inhibit pituitary turmor and ACTH secretion
  • results in increased pigmentation and relief of cushing syndrome
28
Q

What are the “silent” or “null cell” adenomas?

A
  • Non functioning and Gonadotroph adenomas
  • NF typically present with a mass effect
  • GA show minimal functioning
29
Q

What is the TF that is associated with most functioning pituitary adenomas?

A

PIT-1

30
Q

Most Functioning pituitary adenomas are associated with the TF ____. The exception is _____ adenoma which is associated with _____.

A

Most Functioning pituitary adenomas are associated with the TF PIT-1**. The exception is **Corticotroph** adenoma which is associated with **TPIT.

  • “TPIT or not TPIT, that is the Cushing”
31
Q

What somatic mutations are associated with pituitary adenomas?

A
  • GNAS
  • USP8
    • corticotroph (32-62%)
    • mutation upregulates EGFR
32
Q

What are the familial germline mutations that causes pituitary adenomas?

A
  • AIP
    • Somatotroph pituitary adenoma predisposition
33
Q

Describe the GNAS mutation associated with pituitary adenomas.

A
  • Mutation of GNAS makes the alpha subunit of Gs lose its GTPase activity
    • GDP isn’t there to turn off the cascade, so GTP initiates cascade with cAMP
  • normally GTPase activity favors GTP to GDP
    • GDP turns off the cascade
34
Q

Compare pituitary adenomas and Aggressive adenomas.

A
35
Q

What is Rathke’s Cleft Cyst? What is the histilogical makeup?

A
  • Cystic mass derived from Rhathke’s pouch
  • This can expand and compress the normal pituitary
  • Can also rupture and result in inflammation of pituitary or meningitis
  • Comes from oral ectoderm, which makes up respiratory epithelium
36
Q

What is a craniopharyngioma?

A
  • Kids (5-15 yo)
    • most often adamantinomatous and causes growth retardation from hypopituitarism
      • adamantinomatous=calcified tough external shell
  • Adults (>65 yo)
    • papillary craniopharyngioma
    • signs of increased ICP or hypopituitarism
37
Q

What makes up the histology of craniopharyngioma?

A
  • derived from remnants of Rathke’s pouch
    • made of squamous epithelium
    • wet keratin
    • calcified cyst
38
Q

What can cause hypopituitarism?

A
  • Tumors/mass lesions
  • TBI/hemorrhage
  • Surgery/radiation
  • Apoplexy
  • Ischemic necrosis/Sheehan syndrome
  • Inflammatory disorders
  • Genetic defects

All of these occur via three mechanisms→ “squashed”, “killed off”, or “bled into”

39
Q

What is primary empty sella syndrome?

A
  • CSF leaks into sella and compresses the pituitary
40
Q

What is secondary empty sella syndrome?

A

Pituitary expands and infarcts within the sella leaving an empty space

41
Q

What results from anterior hypopituitarism GH?

A

Incr. body fat, decreased muslce, reduced strength

42
Q

What results from anterior hypopituitarism gonaddotropins?

A
  • Men: poor libido/impotence, infertility, reduced facial/body hair
  • Women: amenorrhea, dyspareunia, infertilty, breast atrophy
43
Q

What results from anterior hypopituitarism TSH

A

Decreased energy constipation weight gain

44
Q

What results from anterior hypopituitarism ACTH?

A

Weakness tiredness and hypoglycemia

45
Q

What results from anterior hypopituitarism prolactin

A

Lactation failure

46
Q

what is Sheehan syndrome?

A
  • Postpartum necrosis
  • ischemia and infarction can occur during labor and delivery due to a rapid enlargement of the pituitary outgrowing the sella and compressing the vessels supplying it
    • results in secondary empty sella
  • initial result of this is lack of ability to nurse baby
47
Q

Posterior pituitary ADH deficiency and excess?

A

Deficiency results in diabetes insipidus and excess results in SIADH

48
Q

Diabetess Insipidus?

A
  • Decreaed reclaimed free water from renal collecting duct
    • incerased serum osmolality and hypernatremia
    • dilute excessive urine
    • polyuria
  • Can be caused centrally or nephrogenic
    • central: kidneys respond with inc. water retention and increased urine Na/osmolality to DDAVP
    • Nephrogenic: no response to DDAVP
49
Q

SIADH and sx? What is the msot common cause of it?

A
  • Increased reclaimed free water from renal collecting duct
    • decreased serum osmality
    • concentrated urine
    • mental status changes, mm weakness, seizures
  • Small cell carcinoma of the lung is mc cause
    • also TBI and subarachnoid hemorrhage and SSRI’s can cause
50
Q

Compare DI and SIADH.

A

ENRP Exam II (9 decks)

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