Pituitary and Intro Endocrine Flashcards

1
Q

What are the 3 broad classifications of endocrine disease?

A
  1. Impaired synthesis or release
  2. Abnormal Interaction (hormone & target)
  3. Abnormal response (by target)

OR

hyper / hypo / mass lesions

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2
Q

What’s the normal size and weight of pituitary gland?

A

1 cm and about 5 gm pumpkin shaped organ

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3
Q

What is this? And how is it sectioned?

A

normal pituitary

3 sections: adeno, neuro, intermediate

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4
Q

What makes up the adenohypophysis component of the pituitary gland? (the cell type and the hormone associated)

A

80% of gland, from Rathke’s pouch (oral ectoderm); five cell types

  1. Somatotrophs (GH),
  2. Lactotrophs (PRL) {both Acidophilic – red}
  3. Thyrotrophs (TSH),
  4. Corticotrophs (ACTH & MSH),
  5. Gondaotrophs (LH & FSH) {all Basophilic – blue}
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5
Q

What makes up the neurohypophysis component of the pituitary gland? (the cell type and the hormone associated)

A

An extension of CNS, contains Pituicytes (modified glia), secretion is from Herring Bodies (Oxytocin & ADH, which are made in Hypothalamus but released here)

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6
Q

Where are ADH and Oxytocin released?

A

at neurohypophysis from hypothalamus via hypothalamohypophyseal tract

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7
Q

Where does the superior hypophyseal artery brings blood?

A

to Primary Plexus, which connects to the Secondary Plexus via the Hypophyseal Portal Veins (this whole connection brings blood and releaseing hormones to the adenohypophysis)

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8
Q

Where does inferior hypophyseal a. provides blood?

A

to the neurohypohysis; from there, both sides flow to the systemic circuit

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9
Q

List and rank by frequency the 4 main causes of hyperpituitarism.

A
  1. adenoma in the anterior lobe
  2. hyperplasia and carcinoma of anterior lobe
  3. extra-pituitary tumor secretion (secretes trophic hormones)
  4. hypothalamic disorders (excess releasing hormones)
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10
Q

List and rank by frequency the 4 main causes of hypopituitarism

A
  1. ischemic injury
  2. surgery or radiation
  3. inflammatory reaction
  4. non-functional adenoma encroaching on normal tissue
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11
Q

How does pituatary adenoma lead to hypopituitarism?

A

the adenoma grows and compresses good tissue leading to reduced or loss of function

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12
Q

What’s the frequency of incidental pituitary adenomas at autopsy?

A

25% of routine autopsies

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13
Q

What’s the percentage of intracranial neoplasms that are pituitary adenomas?

A

10% of intracranial neoplasms

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14
Q

What’s the difference in size between microadenoma vs macroadenoma?

A

micro <1cm; macro > 1cm

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15
Q

Are pituitary adenomas normally monoclonal or polyclonal?

A

monoclonal

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16
Q

What are the different functions of pituitary adenomas?

A

non-functional; monohormonal; plurihormonal (esp. GH &PRL together)

17
Q

List and rank by frequency the types of pituitary adenoma.

A
  1. prolactinoma (most common - 20-30%)
  2. GH cell (2nd most common)
  3. Null cell (20%; nonfunctional)
  4. ACTH cell (10-15%)
  5. Plurihormonals other than GH/PRL (10%)
  6. Gonadotroph cell (5%)
  7. GH/PRL cell (5%)
  8. TSH cell (1%)
18
Q

What microscopically distinguishes a pituitary adenoma from non-neoplastic anterior pituitary parenchyma?

A

cellular monomorphism and lack of significant reticulin network

19
Q

What’s the classic visual field defect associated with mass lesions in the sella turcica?

A

bitemporal hemionopsia (lose both temporal fields)

20
Q

What’s clinically seen in patients with pituitary adenomas?

A

increased hormone secretion (type specific) or mass effect (includes: visual defects, increased ICP, hypopituitarism, hemorrhage associated with pituitary apoplexy, etc)

21
Q

What are 4 consequences of hyper-prolactinemia?

A

amenorrhea, galactorrhea, loss of libido, infertility (~hypo LH & FSH)

22
Q

What can potentially disrupt normal prolactin regulation?

A
  1. damage to dopaminergic neurons in hypothalamus
  2. damage to pituitary stalk
  3. DA inhibitory drugs that may lead to hyperprolactinemia
23
Q

What is associated with aromegaly?

A

due to increased GH following closure of growth plates

have increased facial structures, hands, feet, viscera, and soft tissues

24
Q

What is associated with gigantism?

A

due to increased GH before closure of growth plates

increased growth in long bones and overall body size, with disproportionately long arms and legs

25
Q

What’s the pathophysiology of Nelson Syndrome?

A

disease of hypothalamo-pituitary adrenal axis

development of pituitary adenoma due to lack of negative feedback by corticosteroids on a pre-existing ACTH microadenoma

may occur following dual removal of adrenals associated with Cushing’s Syndrome - technically it was Cushing’s disease

26
Q

What’s a null cell adenoma?

A

A hormone negative tumor - it does not function and has no specific hormonal predilection in a true example

Most of the ones today are silent gonadotrophic adenomas

27
Q

Why do patients with null cell adenomas typically present with mass effects?

A

since there are no hormonal symptoms, the tumors go undetected until large enough to cause mass effect

28
Q

What’s the relative frequency and typical functional status of pituitary carcinomas?

A

quite rare and normally nonfunctional

varies in differentiations (may cause hyperpituitary); evidence of metastasis is usu. diagnostic (as in parathyroid adenocarcinoma)

29
Q

What’s the functional reserve of anterior pituitary?

A

75% - bc of the large degree of redundancy, it can handle fairly major disruptions

30
Q

What are some causes of hypopituitarism?

A

ischemic necrosis, surgery, inflammation, tumor or other mass lesions, pituitary apoplexy, Rathke cleft cyst, empty sella syndrome, genetic defects (rare), defects in releasing hormone deficiency

31
Q

What’s Sheehan Syndrome?

A

associated with necrosis following delivery

pregnancy related physiological expansion is NOT associated with increase blood supply, so during delivery, obstetric hemorrhage leads to DECREASE blood volume and possibly shock

pituitary susceptible to infarct - MOST COMMON cuase of hypopituitarism

32
Q

What are 5 signs or symptoms of hypopituitarism.

A

Depends on the hormone that is reduced.

  1. GH - in children -> pituitary drawfism or just small stature
  2. GnRH -> LH & FSH - amenorrhea, infertility, decresed libido, impotence
  3. TSH & ACTH - lead to hypothyroid and hypoadrenal respectively
  4. PRL - lack of normal lactation
  5. MSH - lack of normal melanocyte stimulation -> hypopigmentation
33
Q

What are 2 products of posterior pituitary?

A

ADH/Vasopression (H2O balance and vasoconstriction)

Oxytocin (uterine contraction, milk ejection)

34
Q

Define diabetes insipidus.

A

polyuria due to ADH deficiency - kidney’s inability to reabsorb water (if lack of production [central] or lack of response [nephrogenic])

symptoms: dilute urine, hypernatremia, and increased osmolarity -> leads to polydipsia

35
Q

What are some causes of diabetes insipidus?

A

head trauma, inflammation, tumor, and surgery

36
Q

Define syndrome of inappropriate antidiuretic hormone (SIADH).

A

Excess secretion of ADH leads to excess volume retention & hyponatremia; leads to Cerebral Edema, increased Total Body Water, BUT normal BV & NO peripheral edema!

37
Q

What are the 4 most common causes of SIADH?

A
  1. Ectopic ADH by malignant neoplasm (esp small cell of lung)
  2. non-neoplastic lung disease
  3. local injury to hypothalamus or neurohypophysia
  4. per wiki: head injury, cancer, infection, drugs