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Endocrine > Anterior And Posterior Pituitary Pathology > Flashcards

Anterior And Posterior Pituitary Pathology Flashcards

1
Q

Hormones that act by binding to cell surface receptors

A

Two sub groups

1) peptides
- includes GH and insulin

2) small molecules non peptide
- includes epinephrine, TH

  • *both sub groups bind to cell surface receptors and increase intracellular second messengers such as cAMP, ionized calcium and IP3**
  • all three increase PK activity which upregulates DNA transcription
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2
Q

Hormones that act by binding to intracellular receptors

A

Mainly comprised of lipid-soluble hormones, which diffuse through plasma membrane and interacts with receptors in the cytosol or nucleus. Binds to regulatory elements in DNA and increases/decreases expression of genes
- includes all steroids and retinoids

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3
Q

Pituitary anatomy

A

Resides in sella turcica of the ethmoid bone and is connected directly to the hypothalamus via the infundibulum stalk

Stalk contains hypothalamic-hypophyseal tracts that extend from super optic/paraventricular nuclei into the pars nervosa of the posteriorpituitary

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4
Q

Anterior primary hormones

A

TSH

Prolactin (PRL)

Follicle stimulating hormone (FSH)

Lutenizing hormone (LH)

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5
Q

Trophic hormones that are released by hypothalamus

A

Inhibiting:

  • PIH
  • GIH

Releasing

  • TRH
  • PRH
  • GnRH
  • CRH
  • GHRH
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6
Q

Hormones secreted from posterior pituitary

A

primarily GH and adrencorticotrophic hormone (ACTH)

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7
Q

Anterior (adenohypophysis) pituitary anatomy

A

Develops during the 3rd week forms from the hypophyseal (Rathke) pouch from the primitive pharynx and extends upwards to meet with the neurohypophyseal bud that extends down words from the primitive diencephalon

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8
Q

Two main inhibitory hormones for the pituitary that are released from the hypothalamus

A

Somatostatin

Dopamine

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9
Q

Hyperpitutiarism

A

Excessive secretion of trophic hormones
- most common cause = anterior pituitary adenoma

Pituitary adenomas are subclassified into nonfunctional or functional and based on size

  • microadenoma = <1cm
  • macroadenoma = >1cm

Symptoms depend on what hormone is excessively produced

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10
Q

Hypopituiarism

A

Caused by deficiency of trophic hormone release from antihero pituitary

  • common causes = ischemia, surgery, radiation treatments and chronic/acute inflammation
  • rarely = NONfunctional pituitary adenomas (functional ALWAYS produces hyperpituitism)
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11
Q

Most common local mass effect of pituitary disorders/masses

A

Often damages/impinges the optic nerves

  • this is because the pituitary is located near the optic chiasm
  • classically produces “bitemporal hemianopsia” also referred to as “binocular vision”

Others:

  • headaches/ new onset migraines
  • insomnia/somnolence
  • pituitary apoplexy
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12
Q

What technique is used to differentiate functional pituitary adenomas?

A

IHC staining

- shows that hormones the neoplasm produces excess of. Confirms it

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13
Q

Assuming a functional pituitary adenoma is secreting two different hormones, what is the most common combo seen?

A

Growth hormone and prolactin

Results in:

  • gigantism/acromegaly
  • galactorrhea and amenorrhea
  • sexual dysfunction
  • infertility
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14
Q

What is the most common genetic mutation in pituitary adenomas?

A

G-protein mutations in the GNAS gene
- plays a role in signal transduction to cell surface receptors

Most commonly eliminates GTPase activity and leads to constitutive activation of Gsa proteins and generation of cAMP

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15
Q

What are the 4 genes associated with familial pituitary adenomas?

A

MEN1, CDKN1B, PRKAR1A and AIP

*only makes up 5% of all pituitary adenomas

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16
Q

What are the most common mutations in pituitary adenomas that signal aggressive behavior/metastasis?

A

Overexpression of cyclin D1
- promotes very rapid G1 -> S phase in cells

Mutations in TP53 gene
- normal TP53 = initiates cell arrest if DNA damage occurs/hypoxia

Epigenetic silencing retinoblastoma gene (RB)

17
Q

Morphology of pituitary adenomas

A

70% = well encapsulated and soft masses

30% of cases = are nonencapsulated and infiltrate adjacent bone dura
- even less of these can be hemorrhagic

Cell morphology = uniform/polygonal cells in sheet/cord structure

  • NO/SPARSE reticulum and reticular fibers
  • can stain acidiophilic/basophilic or chromophobic
18
Q

What is the most frequent type of hyper-functioning pituitary adenoma?

A 
Lactotroph adenoma (prolactin-secreting) 
- makes up roughly 30%

Range in size and mass effect potential

Produce galactoherra/amenorrhea/sexual dysfunction/ infertility
- much more obvious in premenopausal women and are diagnosed earlier in females

Can also be seen secondarily in:

  • pregnancy
  • renal failure
  • hypothyroidism
  • dopamine/estrogen therapies
  • hypothalamic lesions

IHC staining = “dot-like” staining pattern near nuceli

19
Q

What is the second most common functional pituitary adenoma?

A

Somatotropin adenoma

  • secretes excess growth hormone which hyper stimulates hepatic insulin-like growth factor (IGF1) secretion
  • far more subtle

Causes gigantism or acromegaly

IHC staining = growth hormone within cytoplasm or neoplastic-like cells

20
Q

Acromegaly features

A

Enlargement of the jaw and protrusion

Separation of front teeth

Enlarged hands/feet with “sausage-like” fingers

21
Q

Extra pituitary manifestations of somatotrophic adenomas

A 
#1 = diabetes mellitus Type 2
- caused by chronic exposure of IGF1 which increases peripheral insulin resistance

Others:

  • gonadal dysfunction
  • muscle weakness (general)
  • new onset HTN
  • arthritis
  • CHF
  • increased risk of GI cancers
22
Q

Corticotroph adenomas

A

Caused by excessive production of ACTH and ultimately causes Cushing syndrome (hypercortisolism)

Stain (+) with PAS stains and show accumulation of glycosylation ACTH on IHC stains

23
Q

Why do patients with cushings have hyperpigmentation skin?

A

Increased ACTH also increases production of melanocyte stimulating hormone (MSH)

24
Q

Gonadotroph adenoma

A

Produces excess LH and FSH

Very difficult to recognize early since they secrete hormones inefficiently and variably
- typically only found once they have gotten big enough to cause mass effect symptoms

IHC = neoplastic cells show reactivity to gonadotrophic a-subunit and specific B-FSH/LH subunits
- also consists of chromophobe cells

25
Q

Thyrotroph adenoma

A

Accounts for 1% of all pituitary adenomas and is a super rare cause of hyperthyroidism

26
Q

Pituitary carcinomas

A

Exceedingly rare carcinoma that always metastasis

- determined by complete erosion of the sella turcica floor

27
Q

How much of the anterior pituitary parenchyma must be loss to show clinically significant hypopituitatism?

A

75% or greater

Almost never congenital and almost always acquired

  • most common is tumor
  • can be iatrogenic in nature = ablation of pituitary via surgery or radiation.

if hypopituitarism + diabetes insipidus is present = hypothalamic lesion should be suspected

28
Q

Sheehan syndrome

A

Also called “postpartum necrosis”

Caused by anterior pituitary enlargement during pregnancy (due to increase need for prolacitn) WITHOUT subsequent angiogenesis of blood supply

Causes the enlarged gland to be vulnerable to ischemic injuries (especially if the pregnant female is already hypotensive before pregnancy)

29
Q

Potential symptoms of hypopituitarism

A

Depends on specific hormones effected

GH = dwarfism

FSH/LH = amenorrhea and infertility in women; impotence and loss of pubic/axillary hair in men

TSH/ACTH = hypothyroidism and hypoadrenalism

Prolacitin = failure of postpartum lactation

also usually produces hypopigmentation

30
Q

Two hormones posterior pituitary produces

A

ADH/vasopressin

  • predominantly synthesized in the supraoptic nucleus
  • acts on collecting tubules to promote resorption of free water
  • is released in response to exercise, emotions, plasma osmotic pressure increases

Oxytocin:
- synthesis is directly in posterior pituitary- functions to stimulate contraction of uterine and lactiferous duct smooth muscles in a positive feedback mechanism

31
Q

Diabetes insipidus

A

ADH deficiency causes this and leads to:

  • polydipsia
  • inability to concentrate ursine
  • low specific gravity of urine
  • serum sodium and osmolalitity are increased which leads to excessive thirst

Two types

1) central:
- damage to the head/posterior pituitary in anyway
2) nephrogenic:
- damage or unresponsive ness of the the CD cells to ADH

32
Q

SIADH

A

Syndrome of inappropriate ADH leads to the exact opposite of DI

Too much ADH leads to excessive free water reabsoption and results in primarily hyponatremia, cerebral edema and its symptoms
- there is NO PERIPHERAL EDEMA. (This is because as blood volume increases, body moves volume from plasma -> intracellular spaces. Then ANP provides the “escape” mechanism to keep blood volume from getting to edematous levels

Causes:

  • malignant neoplasms (especially small-cell lung)
  • COPD and other non neoplastic diseases of the lungs
  • injury to hypothalamus or neurohypophysis
33
Q

How does insulin differ in effects of patients with acromegaly vs diabetes mellitus type 2

A

Diabetes mellitus type 2

  • insensitivity of cells to insulin
  • insulin shows impaired glucose uptake in both muscles and liver cells and also impairs gluconeogenesis
  • enhances glucose release into blood stream

Acromegaly

  • excessive IGF-1 which leads to “anti-insulin” effects and insulin resistance
  • impairs glucose uptake in muscle and liver cells but increases gluconeogenesis in liver
34
Q

What effects does exercise have on insulin release?

A

Stimulates its release since it muscle cells need more intracellular glucose to work better

Endocrine (46 decks)

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