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Pathophysiology > endocrine- pituitary > Flashcards

endocrine- pituitary Flashcards

1
Q

where is the anatomical location of the pituitary gland?

A

inferior to diencephalon. Rests in sella turcica, close proximity to optic nerves & chiasm
Connected to hypothalamus via infundibulum
(Neural & vascular)

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2
Q

what are the embryologic origins of the two pituitary lobes?

A

Posterior-neurohypophysis (ectoderm) - nervous nature

Anterior-adenohypophysis (mesoderm) - glandular in nature

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3
Q

what does the posterior pit. do?

A

Posterior secretes ADH(aka vasopressin) & oxytocin

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4
Q

what does the anterior pituitary do?

A

Anterior produces & secretes TSH, ACTH, FSH/LH (gonadotropins), GH, & prolactin

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5
Q

if the hypothalamus- pituitary axis is interrupted, how will hormone levels change?

A

ALL will decrease except prolactin which will increase

hormones that will increase: GH, TSH, ACTH, LH, FSH

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6
Q

why will prolactin increase if the hypothalamus-pituitary axis is interrupted?

A

the major control of prolactin is inhibitory in nature (dopamine) so if we stop this, we get an uncontrolled increase in prolactin

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7
Q

what are the hormones from the hypothalamus and what hormone in the anterior pituitary do they each produce?
(percentages of each given for extra info)

A 
20% somatotrophs (GH)
15% corticotrophs (ACTH)
15% gonadotrophs (FSH & LH)
15% lactotrophs (prolactin)
5% thyrotrophs (TSH)
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8
Q

how would we txt the most common pituitary tumor?

A

most common pit. tumor is a prolactin secreting tumor (dopamine inhibits this so we use dopamine to txt these tumors)

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9
Q

what are the three types of endocrine disorders?

A

primary, secondary and tertiary

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10
Q

what constitutes a primary endocrine disorder?

A

Primary disorders involve the gland responsible for producing the hormone in question
ex/ Total thyroidectomy produces primary hypothyroidism

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11
Q

what constitutes a secondary endocrine disorder?

A

Secondary disorders involve problems with the pituitary stimulation, target gland is normal
ex/Destruction of pituitary (source of TSH is gone) produces secondary hypothyroidism

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12
Q

what constitutes a tertiary endocrine disorder?

A

Tertiary disorders involve problems with the hypothalamus, pituitary & target glands are not stimulated
ex/ hypothalamus destroyed by tumor - tertiary hypothyroidism

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13
Q

hypo- and hyper-pituitarism is always referring to the anterior or posterior pituitary?

A

anterior

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14
Q

what is “simmond’s disease”?

A

type of hypopituitarism:

Loss of one or more of the hormones from the adenohypophysis (ant pit. hormones)

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15
Q

simmond’s dz:how much of the pituitary mass must be lost for clinical changes to occur?

A

Requires loss of 75% of the adenohypophysis (of pit mass) before clinical changes (b/c many in circulation)

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16
Q

what is “panhypopituitarism”?

A

Panhypopituitarism is loss of most or all of the hormones of the adenohypophysis.
** Underdiagnosed & deadly

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17
Q

loss of ant. pituitary hormones follow what kind of “predictable sequence”?

A

GH (“I don’t feel good”)
FSH/LH (“My sex drive is gone”)
TSH + ACTH (life-threatening)

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18
Q

4 kinds of pituitary destruction that can cause panhypopituitarism?

A

Adenoma- squeeze out normal pit cells.
Surgery- removal of pit.
Radiation
Trauma

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19
Q

postpartum pituitary necrosis that can cause panhypopituitarism?

A

**“Sheehan’s syndrome”

From hemorrhagic shock (low flow- ischemia) during complicated delivery

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20
Q

what is empty sella syndrome?

A

Arachnoid herniation into sella turcica

  • Slowly crushes gland
    explained: hypophysis has roof of dura w/ a hole that allows infundibulum thorough- but some people this is too big = herniation of arachnoid into pit.
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21
Q

3 ways one can get panhypopituitarism?

A
  1. pituitary destruction
  2. postpartum necrosis
  3. empty sella syndrome
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22
Q

panhypopituitarism: variable symptoms: loss of GH ?

A

accelerates body wasting (atherosclerosis)

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23
Q

panhypopituitarism: variable symptoms: loss of prolactin

A

prevents lactation after childbirth

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24
Q

panhypopituitarism: variable symptoms: loss of TSH

A

produces secondary hypothyroidism

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25
Q

panhypopituitarism: variable symptoms: loss of ACTH

A

secondary adrenal insufficiency (deadly) - need cortisol to live

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26
Q

how do you dx panhypopituitarism?

A
  1. stimulate the gland, a lack of hormone response = positive Dx
    - example: CRH, ACTH, or TRH stimulation
  2. brain MRI
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27
Q

testing for panhypotituitarism by giving them synthetic ACTH, why would there be no response?

A
  • no response = positive Dx

- if they haven’t had ACTH in a really long time , adrenal cortex atrophies, so will have NO response to ACTH

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28
Q

txt for panhypopituitarism?

A

hormone replacement and surgical resection of adenoma

29
Q

hyperpituitarism: what is it and what are the 3 usual causes?

A

Too much of one (or two) of the hormones from the adenohypophysis
Usual cause(s)
1. Autonomous overproduction-pituitary adenoma
2. Excess/under production of hypothalamic RH/RIH
3. Loss of feedback inhibition from destruction/removal of other glands

30
Q

pituitary adenoma: what are the sizes for microadenoma vs macroadenoma?

A

Microadenomas < 1 cm

Macroadenomas ≥ 1 cm

31
Q

presentation of pituitary adenoma (2)

A
  1. Hormone excess (functional) or deficit from destruction of remaining gland
  2. Visual problems-monocular blindness or bitemporal hemianopsia (can’t see peripheral vision in either eye) -smashes optic chiasm - crushed crossing optic fibers
32
Q

Incidental “enlarged sella turcica” on skull films- what would this indicate?

A

pituitary adenoma

33
Q

how do you test for hyperpituitarism ? (2)

A
  1. May require a “suppression” test-lack of suppression may indicate autonomous production (tumor)
  2. head CT/MRI
34
Q

what are the two major ways we induce hormone suppression to test hyperpituitarism?

A
  1. Low-dose dexamethasone suppression
  2. High-dose dexamethasone suppression (usually will suppress a pituitary ACTH-oma)
  • dexamethasone- a potent glucocorticoid.
  • low dose:isnt enough to suppress the ACTH-oma, its used as a screen.
  • high dose: suppression- reduce ACTH levels, used if you suspect the disease
35
Q

what does a prolactinoma cause (men vs women) ?

A

Prolactin-producing pituitary adenoma (anterior lobe)…
Men-impotence, loss of libido, obesity
Women-amenorrhea, galactorrhea, infertility, obesity

36
Q

what may cause hyperprolactinemia other than a prolactinoma?

A

dopamine antagonists

-if you inhibit dopamine - take away the inhibitory effect- stimulatory effect (TRH) stays = hyperprolactinemia

37
Q

2 txt options for prolactinoma

A

Bromocriptine (dopamine agonist)

Surgery or gamma knife

38
Q

GH aka somatotropin: what does it do? (2)

A
  1. Promotes linear growth & protein synthesis

2. Causes insulin resistance & increase in insulin levels

39
Q

actions of growth hormones (somtatotropins) are regulated by what?

A

mediated by liver-derived somatomedins (insulin-like growth factors, IGF)
- can stimulate hypothalamus or inhibit ant. pitutary to control GH levels

40
Q

where does growth hormone come from?

A

hypothalamus secretes:
GHRH –> stimulates ant. pituitary release of GH
(*also negative feedback to hypothal)
somatostatin (SRIF) –> inhibits ant. pituitary release of GH

41
Q

where does prolactin come from?

A

hypothalamus secretes:
TRH –> stimulates ant. pituitary release of prolactin
dopamine –> inhibits ant. pituitary release of prolactin

42
Q

what is gigantism? (signs)

A

excess GH before puberty (before epiphyseal closure)

- Height > 7 ft (200 cm)

43
Q

what is acromegaly? (signs- kinda weeds)

A

excess GH after epiphyseal closure

  • Huge hands, tongue, brow, & jaw (prognathism)
  • Oily skin
  • Secondary diabetes
  • Osteoporosis
  • Increased coronary risk
  • Early mortality
44
Q

what usually causes gigantism or acromegaly?

A

pituitary macroadenoma

45
Q

Dx of gigantism/acromegaly? (2 ways)

A
  1. Spot IGF-1 (normal levels essentially rule out)

2. GH suppression test

46
Q

2 ways to txt gigantism/acromegaly?

A
  1. Surgical removal

2. Somatostatin analogue (octreotide)-reduces tumor size

47
Q

GH suppression test for acromegaly explained (Weeds)

A 
Growth hormone (hGH) suppression by a glucose load is the classic screening test for acromegaly
Failure to suppress hGH is diagnostic of acromegaly when coupled with elevated IGF1 and clinical signs of excess growth hormone.
48
Q

cushing’s syndrome vs cushing’s disease

A

Cushing’s syndrome (Cushingism)-excess glucocorticoids (cortisol)
Cushing’s disease (Cushingism) caused by overproduction of ACTH by pituitary adenoma

49
Q

what can cause cushing’s disease

A

ACTH-oma (Microadenomas)

50
Q

dx of cushing’s disease

A

microadenoma: Not suppressed by low-dose dexammethasone

Usually can be suppressed by high-dose dexamethasone

51
Q

txt of cushing’s disease?

A

surgical removal

52
Q

posterior pituitary disorders: what can cause suppression of each of the two hormones secreted here?

A
  1. Lithium therapy & alcohol use: suppress ADH secretion

2. No known syndromes: oxytocin excess/deficiency

53
Q

what hormone regulates plasma osmolarity?

A

ADH

54
Q

what prompts the secretion of ADH from the post. pituitary?

A

increased osmolarity or decreased plasma volume

55
Q

decreased plasma volume causes what changes that effect ADH/vasopressin?

A

Acts on renal collecting ducts to increase water reabsorption

  • water retention into blood = concentrated urine
  • Higher concentrations ADH/vasopressin = produce vasoconstriction (hence “vasopressin”)
56
Q

how is hypothalamus prompted to secrete ADH or increase thirst?

A

it has osmoreceptors that read plasma osmolarity (normal 270-280)
- if they sense 300+ osmolarity- secrete ADH to decrease it.

57
Q

what is diabetes insipidus? two types?

A

Deficiency of ADH or normal ADH with decreased response

  1. Neurogenic (central) - lack of response from neuro system
  2. Nephrogenic - lack of response from kidney
58
Q

what causes diabetes insipidus?

A

head trauma or brain surgery

59
Q

what are the signs of diabetes insipidus?

A

Polyuria, polydipsia

-3-20 L/day, dilute

60
Q

what is the test for diabetes inspidus? (what do you do?what do results mean? how do you distinguish between central and nephrogenic?)

A

“water deprivation test”

  1. Measure plasma/urine osmolarity, restrict water overnight, re-measure (trying to raise osmolality - can also do by giving them hypertonic saline)
  2. Dx: Failure of urine osmolarity to increase
  3. Adding ADH assays before & during distinguishes between central & nephrogenic
61
Q

neurogenic (central) diabetes inspidus: txt

A

usually incomplete lack of hormone (not complete lack of ADH) so..

  • can Auto-regulate based on thirst
  • Synthetic ADH (dDAVP, Desmopressin) for chronic or severe cases
62
Q

txt for nephrogenic DI

A
  • if you can’t remove the cause–> TZD diuretics

- drinking more water prevents hyperosmotic

63
Q

what causes SIADH? (persistent vs transient)

A

persistent: ectopic ADH production (rarely a pituitary problem)
* *Oat cell lung carcinoma (most common ectopic ADH)

transient: may be caused by head injury or brain surgery

64
Q

what is syndrome of inappropriate ADH? (SIADH)?

A

Continual ADH production regardless of plasma osmolarity

  • Persistent water reabsorption, plasma hypotonicity (hyponatremia - low Na+ conc., dilute blood)
  • concentrated urine
  • Hyponatremia leads to seizures & death
65
Q

5 Dx criteria for SIADH?

A
  1. Hypotonic hyponatremia
  2. Natriuresis (urine sodium > 20 mEq/L)
  3. Urine osmolarity > plasma osmolarity
  4. Absence of volume depletion & edema
  5. Normal renal, adrenal, & thyroid function
66
Q

best txt for SIADH?

A

water restriction-make the “inappropriate ADH” appropriate

67
Q

3 other txt options for SIADH?

A
  1. Normal saline + furosemide to promote free water clearance
  2. Lithium & demeclocycline poison collecting duct ADH receptors
  3. Newer ADH-receptor antagonists (conivaptan, tolvaptan)
68
Q

what can be used to txt SEVERE cases of SIADH? what precautions to take with this?

A

Hypertonic saline (3%)
Too much, too fast can cause central pontine myelinolysis (neuronal issues —> death)
- 0.5 mEq/L/hr

69
Q

Most non-thyroid endocrine diseases will require ________ or ________ for diagnosis

A

“stimulation” or “suppression” test

Pathophysiology (28 decks)

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