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Endocrine > Pituitary Prolactin and GH > Flashcards

Pituitary Prolactin and GH Flashcards

1
Q

Describe the endocrine and non-endocrine roles of the hypothalamus.

A

non-endocrine functions: regulates temperature, control of autonomic nervous system and appetite by integrating input from higher centers of the brain, ANS and peripheral endocrine feedback

endocrine: serves as a coordinating center for endocrine system, produces hormones that are either stored in the pituitary or regulate activity of the pituitary

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2
Q

Describe the endocrine and non-endocrine roles of the hypothalamus.

A

non-endocrine functions: regulates temperature, control of autonomic nervous system and appetite by integrating input from higher centers of the brain, ANS and peripheral endocrine feedback

endocrine: serves as a coordinating center for endocrine system, produces hormones that are either stored in the pituitary or regulate activity of the pituitary

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3
Q

What is the role of the hypothalamus? (two differing roles)

A

non-endocrine functions

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4
Q

List the releasing hormones and inhibiting hormones released by the hypothalamus.

A

releasing hormones: CRH, GHRH, GnRH, TRH
inhibiting hormones: somatostatin (GH) and dopamine (prolactin)
posterior pituitary: vasopressin, oxytocin

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5
Q

List the releasing hormones and inhibiting hormones released by the hypothalamus.

A

releasing hormones: CRH, GHRH, GnRH, TRH
inhibiting hormones: somatostatin (GH) and dopamine (prolactin)
posterior pituitary: vasopressin, oxytocin

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6
Q

List the hormones that are released from the anterior pituitary hormones and their respective actions.

A 
FSH and LH -gonad function and hormone production
GH: bone and tissue growth
PRL: mammary glands
ACTH: adrenal cortex
TSH: production of thyroid hormones

(posterior pituitary: oxytocin for milk let down and SM in uterus, ADH for kidney tubules)

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7
Q

List the hormones that are released from the anterior pituitary hormones and their respective actions.

A 
FSH and LH -gonad function and hormone production
GH: bone and tissue growth
PRL: mammary glands
ACTH: adrenal cortex
TSH: production of thyroid hormones

(posterior pituitary: oxytocin for milk let down and SM in uterus, ADH for kidney tubules)

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8
Q

What are the 5 mechanisms of pituitary hormone excess?

A 
excess stimulation from hypothalamus
disruption of inhibition from hypothalamus
hyper secretion from pituitary
ectopic secretion of pituitary hormones
impaired clearance of pituitary hormones
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9
Q

What is the disease conditions associated with each of the anterior pituitary hormones in excess?

A

prolactin- hyperprolactinemia
GH- gigantism and acromegaly
TSH- TSH secreting tumors (hyperthyroidism?)
FSH/LH- gondotropin-secreting tumors (infertility?)

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10
Q

Lactotrophs and somatotrophs arise from which precursor cell?

A

lactotrophs and somatotrophs both aries from somatomammotroph (explains why some tumors invovling either cell type are known to secrete both hormones

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11
Q

What effect does prolactin have on gonadal function?

A

prolactin shuts off ovarian and testicular function producing hypogonadism

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12
Q

What effect does prolactin have on gonadal function?

A

prolactin shuts off ovarian and testicular function producing hypogonadism by inhibiting the pulsatile release of GnRH from the hypothalamus (inhibiting LH and FSH release)

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13
Q

Describe the secretion of prolactin. When and how is it typically released?

A

prolactin secretion is pulsatile, 4-14 pulses /24h

secretion also has a bimodal distribution, increasing 60-90 min after onset of sleep with peak levels around 4-7a and lowest around noon

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14
Q

What are the different ways in which prolactin release is inhibited?

A

*predominant signal from the hypothalamus is inhibitory mediated by DA release

any disruption of the pituitary stalk or blockade of DA receptors will increase prolactin release

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15
Q

What are the different ways in which prolactin release is stimulated?

A

release is stimulated by thyrotropin releasing hormone (hyperprolactinemia may be seen in hyperthyroidism when TRH levels are high)

estrogen also promotes prolactin release by reducing DA secretion

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16
Q

What are the different ways in which prolactin release is stimulated?

A

release is stimulated by thyrotropin releasing hormone (hyperprolactinemia may be seen in hyperthyroidism when TRH levels are high)

estrogen also promotes prolactin release by reducing DA secretion, reducing lactotroph sensitivity to DA and increasing lactotroph sensitivity to TRH

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17
Q

What are the different ways in which prolactin release is stimulated?

A

release is stimulated by thyrotropin releasing hormone (hyperprolactinemia may be seen in hyperthyroidism when TRH levels are high)

estrogen also promotes prolactin release by reducing DA secretion, reducing lactotroph sensitivity to DA and increasing lactotroph sensitivity to TRH

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18
Q

What is a normal prolactin level?

A
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19
Q

What are physiologic cases of hyperprolactinemia?

A

++ pregnancy, lactation

nipple stimulation, REM sleep, stress, sexual intercourse, exercise

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20
Q

What are pharmacologic cases of hyperprolactinemia?

A

DA receptor blockers
antidepressants
estrogen (OC or replacement treatment)

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21
Q

What are pathologic cases of hyperprolactinemia?

A

prolactinomas, pituitary stalk distruption, primary hypothyroidism, renal failure, intercostal nerve stimulation or chest wall injury

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22
Q

Describe the most common cause of prolactemia.

A

prolactinoma, a benign tumor (adenoma) of lactroph cells that overproduce prolactin

a secondary cause in any lesion that compresses or damages the hypothalamus or pituitary stalk (interrupts delivery of DA) “stalk effect”

23
Q

What are the symptoms of prolactinemia? (both direct effects of prolactin and due to hypogonadism)

A

galactorrhea: mostly in PRE-menopausal women
women: irregular menses, amenorrhea, low libido, infertility due to inoculation, low bone density
men: erectile dysfunction, libido, less muscle mass, less body hair, gynecomastia, infertility due to decreased sperm count and low bone density

mass effect: headache, visual field defects (tunnel vision), cranial neuropathies, hypopituitarism

24
Q

Describe the most common cause of prolactemia.

A

prolactinoma, a benign tumor (adenoma) of lactroph cells that overproduce prolactin (accounts for 30% of pituitary tumors and can occur as part of MEN type 1)

a secondary cause in any lesion that compresses or damages the hypothalamus or pituitary stalk (interrupts delivery of DA) “stalk effect”

25
Q

What are the symptoms of prolactinemia? (both direct effects of prolactin and due to hypogonadism)

A

galactorrhea: mostly in PRE-menopausal women
women: irregular menses, amenorrhea, low libido, infertility due to inoculation, low bone density
men: erectile dysfunction, libido, less muscle mass, less body hair, gynecomastia, infertility due to decreased sperm count and low bone density

mass effect: headache, visual field defects (tunnel vision), cranial neuropathies, hypopituitarism

26
Q

How would a pituitary tumor appear on MRI?

A

hypodense region that often causes the pituitary to swing contralateral to the mass, tumors can also infiltrate laterally or up towards the hypothalamus/ optic chiasm

27
Q

What level of prolactin secretion would correlate with a microadenoma v. a macroadenoma?

A

micro adenoma 100-200 ng/mL
macro adenoma >200 ng/mL
(typically)

a prolactin level >200 is almost always indicative of a prolactinoma

28
Q

What are the first line and secondary treatments available for prolactinomas?

A

90% of prolactinomas (even giant ones) respond well to DA ANGONists including bromocriptine and carbergoline

20% cases may be cured after 2-5 years of tx.

surgery and radiation is reserved for only refractory cases

29
Q

What are the first line and secondary treatments available for prolactinomas?

A

90% of prolactinomas (even giant ones) respond well to DA ANGONists including bromocriptine and carbergoline

20% cases may be cured after 2-5 years of tx.

surgery and radiation is reserved for only refractory cases

30
Q

What are the potential side effects of dopamin agonists?

A

generally well tolerated treatment, suggest that patients take before bed due to the possibility of the following adverse effects:

nausea, vomiting, headache, nasal congestion, orthostasis

31
Q

How does growth hormone act on tissue and bone?

A

GH stimulates liver to produce insulin-like growth factor (IGF-1) and this is the way that most effects of GH are mediated

32
Q

How does growth hormone act on tissue and bone?

A

GH stimulates liver to produce insulin-like growth factor (IGF-1) and this is the way that most effects of GH are mediated

33
Q

What is the action of GH in children?

A

GH is an anabolic hormone (remember builds like anabolic steroids)

increases protein synthesis to be used as building blocks
increase lipolysis so lipids can be used as fuel
decreases carb utilization by causing an insulin resistant state

34
Q

Discuss the effects of GH and IGF-1 on cartilage, bone, visceral organs and skin.

A

increases bone length or width depending on closure of epiphyseal closure

organomegaly

increased hair growth, sweat gland hyperplasia, thickening of dermis

35
Q

Discuss the effects of GH and IGF-1 on cartilage, bone, visceral organs and skin.

A

increases bone length or width depending on closure of epiphyseal closure

organomegaly

increased hair growth, sweat gland hyperplasia, thickening of dermis

36
Q

Describe how and when growth hormone is secreted.

A

secretion is pulsatile, 4-11 pulses/hr, esp. at night

**extremely low or undetectable levels between pulses due to short half life (important for diagnostic tests)

37
Q

Describe how and when growth hormone is secreted.

A

secretion is pulsatile, 4-11 pulses/hr, esp. at night

**extremely low or undetectable levels between pulses due to short half life (important for diagnostic tests)

38
Q

What should be measured to gauge GH activity?

A

IGF-1 levels are relatively stable, having a longer half-life and random sampling is a good way to access GH status

39
Q

What are the potential side effects of dopamine agonists?

A

generally well tolerated treatment, suggest that patients take before bed due to the possibility of the following adverse effects:

nausea, vomiting, headache, nasal congestion, orthostasis

40
Q

What should be measured to gauge GH activity?

A

IGF-1 levels are relatively stable, having a longer half-life and random sampling is a good way to access GH status

41
Q

What hormones encourage GH secretion and which inhibit?

A

GHRH increases secretion, somatostatin decreases secretion

IGF-1 also feeds back to decrease GHRH and GH secretion

42
Q

Contrast physiologic, pharmacological and pathologic reasons for increased GH.

A

.

43
Q

Contrast physiologic and pharmacological reasons for increased GH.

A

physiological (stress, exercise, REM sleep, fasting)

pharmacologic: anything that decreases blood glucose (insulin induced hypoglycemia, NE, clonidine, estrogen)

44
Q

What pathological conditions cause increased GH secretion?

A

pituitary adenomas** or ectopic GHRH secreting tumors (primary excess secretion)
anorexia nervosa, cachexia (low blood sugar)
hepatic/renal failure (clearance)

**most common

45
Q

How does a GH-secreting pituitary adenoma change the rate at which GH is secreted?

A

GH remains episodic but frequency, duration and amplitude of GH pulses are random and increased

nocturnal rise in GH and GH response to hypoglycemia is lost

46
Q

Why is acromegaly difficult to diagnose?

A

signs and symptoms have insidious onset, official diagnosis is often delayed by at least 5-10 years (by the time disease is physically apparent)

47
Q

Why is acromegaly difficult to diagnose?

A

signs and symptoms have insidious onset, official diagnosis is often delayed by at least 5-10 years (by the time disease is physically apparent)

48
Q

What are the signs and symptoms of acromegaly?

A 
acral enlargement
frontal bossing
thickening of nasolabial folds
large lips and elongated chin
widening of digits causing spade-like appearance
soft tissue overgrowth
hyperhidrosis- sweat/oily skin
fatigue
arthralgia
weight gain
parathesias/carpal tunnel
hypertrichosifs
acanthuses nigricans (sign of insulin resistance)
headaches
kidney stones (excess Ca++)
cardiomegaly
49
Q

What are the signs and symptoms of acromegaly?

A 
acral enlargement
frontal bossing
thickening of nasolabial folds
large lips and elongated chin
widening of digits causing spade-like appearance
soft tissue overgrowth
hyperhidrosis- sweat/oily skin
fatigue
arthralgia
weight gain
parathesias/carpal tunnel
hypertrichosifs
acanthuses nigricans (sign of insulin resistance)
headaches
kidney stones (excess Ca++)
cardiomegaly
50
Q

Acromegaly can lead to what other (mostly metabolic) pathologies?

A 
impaired glucose tolerance/diabetes
hypertriglyceridemia
hypercalciuria
cardiac disease/ heart failure
sleep apnea (hypertrophy of throat muscles)
cooling polyps/colon cancer
51
Q

What are the best tests for excess GH?

A

elevated IGF-1 is the best SCREENing test

gold standard diagnostic test is a glucose tolerance test with measurement of GH (normally glucose surprises GH to

52
Q

What are the best tests for excess GH?

A

elevated IGF-1 is the best SCREENing test

gold standard diagnostic test is a glucose tolerance test with measurement of GH (normally glucose surprises GH to

53
Q

What is the initial and second line treatments of GH excess due to pituitary adenoma?

A

** transsphenoidal surgery

pharmacologic treatment is an option for patients with persistent GH excess after TSS

radiation is only for patients that are refractory to surgical and medical therapies

54
Q

What are some of the second line pharmacologic treatments available for excess GH?

A 
somatostatin analogs (octreotide and lanreotide)
dopamine agonists for co-secretors (bromocriptine and cabergoline
GH-receptor antagonist: pegvisomant, drop in IGF-1

Endocrine (28 decks)

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