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kris Endocrinology > 6 > Flashcards

6 Flashcards

1
Q

Which hormone is structurally similar to prolactin? What are the differences?

A

GH

peptide hormones, similar to GH
few differences- number of AAs- 198 a.a. (vs 191 in GH)

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2
Q

Apart from strucutre, how does GH differ from PRL?

A

the amount of prolactin you find in pituitary is much less, compared to GH
there’s more GH producing cells in the pituitary (50%)
only ~16% of prolactin producing cells-> less prolactin is produced by the pituitary compared to GH

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3
Q

how much PRL is secrted by pituitary?

A

0.1 mg

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4
Q

What hormones are essential for initiation and maintenance of milk secretion?

Milk produciton?

A

initiation and maintenance of milk secretion- PRL and cortisol

milk production- Decrease of estrogen and progesterone after parturition is permissive for milk production

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5
Q

What happens to milk after Hypophysectomy and adrenalectomy? WHat does it suggest?

A

Hypophysectomy leads to immediate cessation of milk production- thus PRL is absolutely essential for milk production

Adrenalectomy leads to a gradual reduction in milk production- thus cortisol is somewhat esential for milk production

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6
Q

What is the PRL locus? GH?

A

GH has multiple locus

Prolactin locus has one gene – PRL

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7
Q

What kind of hormone is PRL? is it stored?

A

peptide hormone

stored in granules in lactotrophs

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8
Q

What are the circulatory sizes of PRL?

A

After prodcution, PRL protein is processed-> Circulates in various sizes – monomeric, dimeric and polymeric

Monomeric, has 1 copy – most bioactive

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9
Q

What is PRL’sgene expression and release regulated by ?

A

Gene expression and release are regulated by

postivie regulation: PrRP, EGF, FGF, VIP, estrogen, TRH, thyroid hormone,

negative regulation: dopamine, endothelin, TGFb, somatostatin

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10
Q

Is PrRp the releasing factor of PRL? What is the structure of it>

A

we are not sure

it’s a peptide

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11
Q

What is major pathway of PRL release regulation?

A

negative pathways are most common, especially via negative regulation by dopmaine

dopamine has an inhibiting effect on prolactin releasing cells- these cells have a dopamine receptors
more dopamine = less prolactin

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12
Q

Does PRL have an effect on dopamin

A

They both have negative effects on each other

prolactin has negative feedback on dopamine release
prolactin receptors are expressed by dopaminergic neurones in the hypothalamus

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13
Q

What is the half-life of PRL

A

25-45 min-> short

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14
Q

What is the type of PRL release? When does it occur

A

episodic release- 4-14 pulses

lowest 10:00-12:00, highest at dark times of the day

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15
Q

PRL levels and age

A

Levels reduce with age

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16
Q

Where are PRL receptors expressed?

A

PRL receptors are expressed in breast tissue and in many other tissues including pituitary, liver, adrenal cortex, kidneys, prostate, ovary, testes, intestine, epidermis, pancreatic islets, lung, myocardium, brain, and lymphocytes

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17
Q

Prolactin signaling

A

PRL is a peptide-> uses a membrance receptor

Uses a tyrosine kinase with an adaptor in the form of JAK
dimerization of PRL receptro sometiemes requires PRL-> PRL dependent dimerization
in some, it doesn’t - indepenedent dimerization (dimerization occurs and only after PRL can interact wiht the receptor)

in any case, dimerization in essential with an adaptor-> needed to initiate kinase cascade

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18
Q

Desribe the mamary gland structure

A
  • Mammary gland has an epithelium layer which are milk-producing cells
    These alveolar epithelium cells act as exocrine gland
    Myoepithilum cells are contractile and surround the alveolar epithelium- needed to push out the milk produced by the alveolar epithelium
    Alveolar epithelium release- they produce milk and milk is released by exocytosis that damages the whole cell- half of the cells is taken out as milk is released- a lot of proliferation occurs there
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19
Q

what is the main target of prolactin?

A

mammary gland

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20
Q

is PRL necessary for the development of the mammary gland?

A

no

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21
Q

Which part of the breast tissue is under the control of PRL? WHat is their role?

A

alveolar epithelium- require PRL amongst other hormones such as estrogen and progestreone , as well as adrenal steroids

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22
Q

Hormonal regulation of production and secretion

A

milk synthesis and secretion regulation: PRL help epithelial cells to produce and secrete milk which then goest to alveolar cavity
oxytocin act on myoepithelial cells that are contractile and contract under the influence of oxytocin -> contraction of alveoli and ejection of milk
durign lactation both PRL and oxytocin are necessary- > coordinated function

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23
Q

Which hormones are required for Duct system development?

A

estrogen, GH, adrenal steroids

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24
Q

Hormones required for alveolar growth

A

estrogen, progesterone, adrenal steroids, PRL

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25
Q

suckling effect on milk ejection and secretion

A

sucking stimulation is important
mechanic receptors bring these signals to the brain, and they are integrated in the hypothalamus which stimulate release PRL from anterior pituitary. oxytocin release from posterior pituitary is also stimulated
PEL form anterior pituitary acts to synthesis ans secrete milk
Oxytocin from posterior acts on myoepithelial cells around each alveolus-> lead to milk ejection

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26
Q

reproductive function and PRL

A

Involved in regulation of the reproductive systems

negative regulation in humans, in some species, the regulaiton is positive

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27
Q

Effects of high levels of PRL on the repdocutive system

A

hyperprolactinemic conditions associated with hypogonadism in males and females

high levels of PRL inhibits reproductive function, especially gonadotropins
high levels of PRL inhibit those
true for both males and females

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28
Q

PRL and amenorrhea

A

high levels of PRL associated with breast feeding associated with lactational amenorrhea

vcommon birth control method in many cultures

the longer the breast feeding - the longer is reproduction cessation

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29
Q

do gonadotrophs have PRL receptors?

A

yes

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30
Q

PRL and immunomodulation

A
  • PRLR on both B and T cells and macrophages
  • PRL acts as a mitogen (proliferation) and promotes survival, especially for resident macrophages
  • PRL receptors found in most tissues
  • exact role is no known, but it seems to act synergistically with many other hormones
  • deleted PRLR-> compromised function
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31
Q

What is Adrenocorticotrophin?

A

Adrenocorticotrophin (ACTH) is the anterior pituitary mediator of the hypothalamic–pituitary–adrenal axis that regulates responses to a variety of stressors, including hypoglycemia, psychological stressors such as fear, and physical stressors

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32
Q

What is ACTH derived from? How?

A
  • ACTH is derived by proteolytic cleavage of a large precursor molecule pro-opiomelanocortin (POMC)
  • POMC is cleaved by prohormone convertases PC1 and PC2
  • In ACTH producign cells, ACTH portion is kept, the rest is digested
33
Q

Molecular pathway of tanning

A
  • UV DNA damage – Local production of MSH by keratinocyte- this msh is not exogenous, it is localy produced by keratinocytes
  • Stimulate melanocyte to produce melanin
  • Melanin transported back to keratinocyte to reduce UV damage
  • significance of MSH/endorphin, which is thus not localy produced, but produced in the pituitary, production by human pituitary unclear
    *
34
Q

What is the target organ of ACTH?

A
35
Q

Use of MSH/endorphins produced by POMC neurons?

A

MSH/endorphins produced by POMC neurons and used as neurotransmitters in brain->reduction of pain sensation

36
Q

Mechanism of action of ACTH

A
  • Binds to receptors in the adrenal gland
  • Activate Gsα-protein-> stimulates AC-> cyclic AMP
  • Enhanced mobilization of cholesterol into mitochondria as adrenal cortex makes steroid hormones
  • Increased conversion of cholesterol to pregnenolone, which is the precursor for steroids
37
Q

Control of ACTH secretion

A
  • Circadian rhythm
  • Controlled by the hypothalamic hormone CRH, corticotropin releasing hormone from the hypothalamus
  • CRH induced by stress (pain, fear, fever, hypoglycemia)- these signals are analyzed by hypothalamus
  • Lowest around midnight, morning peak and then declines
  • CRH action is potentiated by other hormones (vasopressin) vSubject to feedback control by cortisol- negative feedback both on hypothalamus and pituitary
38
Q

Which hormones act in pain reduction

A

MSH/endorphins produced by POMC neurons in the hypothalamus ONLY- local produciton

39
Q

Feedback control of cortisol on the hypothalamus and pituitary

A
40
Q

Thyrotropin (TSH)- thyroid stimulating hormone strucurre

A
  • Secreted by the thyrotrophs
  • Two protein chains (⍺ and β) Glycosylated.
  • Unique β-chain; Common ⍺-chain with FSH/LH
41
Q

Thyrotropin (TSH)- receptor type

A
  • Receptor signaling via G-proteins (cAMP).
    *
42
Q

TRH and TSH control of release

A

Hypothalamus produced TRH which stimulates TSH release from pituitary
Short feedback loop: there seems to be a short feedback loop between the pituitary and the hypothalamus where TSH inhibits hypothalamic release of TRH

Direct feedback loop: thyroid hormones inhibit TSH release by pituitary

Indirect feedback loop: thyroid hormones inhibit hypothalmic release fo TRH

43
Q

Gonadotropins: LH and FSH structure

A

Secreted by the gonadotrophs

Same basic structure as TSH- share the same alpha-chain, but different beta-chains which are expressed by specific genes

44
Q

Action of FSH

A

Act via G-coupled receptors

Females: Development of ovarian follicles and estradiol secretion

Males: Spermatogenesis, production of sex-hormone binding globulin, which is necessary for transport of testosterone

Both sexes: Secretion of inhibin (negative feedback on FSH)

45
Q

Actions of LH in both sexes

A
  • Females: Steroidogenesis in follicles, induction of ovulation (main function), maintenance of steroidogenesis by the corpus luteum (corpus luteum is a major source of progesterone )
  • Males: Stimulation of testosterone production in the Leydig cells
46
Q

Leydig cells, FHS and LH connection

A

make testosterone and express LH receptor
FSH is necessary as it allow testosterone to be transported

47
Q

Describe LH and FSH secretion

A
  • LH and FSH secretion is pulsatile:
  • vabout every 60 min in response to GnRH pulses
  • each pulse of GnRH is followed by a pulse of LH
  • FSH seems to be more independent
48
Q

The hypothalamo-pituitary-gonadal axis in males

A
  • GnRh from hypothalamus stimulates anterior pituitary to release LH and FSH which act on testes
  • in testes, LH receptors are expressed on leydig cells, which produce testosterone
  • FSH receptors are expressed on sertoli cells . Sertoli cells support sperm differentiation
  • together, testosterone and sertoli cells produce binding protein that brings both gonadotropins, regulation male response to testosterone
    *
49
Q

Describe inhibin in males + it’s negative fedback

vs

testosterone

A

inhibin- peptide hormone; produced by sertoli cells

has -ve feedback on pituitary to inhibit ONLY FSH production (no effect on LH)

testosterone has effect on BOTH hypothalamus and pituitary to regulate BOTH gonadotropins

BOTH inhibin and testosterone act through negative regulation

50
Q

The hypothalamo-pituitary-gonadal axis in females

A

GnRH form hypothalamus acts on pituitary-> FSH and LH production
FSH stimulates follicular cells-> estrogen production
LH stimulates luteal cells-> secretes progesterone and estrogen.
These 2 steroids mainly have negative effect at pituitary and hypothalamic levels

51
Q

Inhibin impact in LH and FSH

A
  • Inhibin is produced in the ovary; Has negative impact on FSH, but no effect on LH
  • main action of inhibin is at pituitary level
52
Q

Hypothalamic-Pituitary target organ axes summary

A

for each anterior pituitary hormone there’s a target organ
a hormone produced by that organ has manly negative feedback

53
Q

What are Disorders of the anterior pituitary most commonly caused by? Are they easy to diagnose

A

Most commonly due to benign tumors of the pituitary (adenomas)-> arise from adenomaphysis

have very slow growth rate-> hard to diagnose

54
Q

Types of adenomas in terms of size

A

Microadenomas < 10mm

Macroadenomas > 10mm

55
Q

2 types of pituitary adenomas

A
  • Functional tumors more common at younger age-> hyperpituitary
  • Non-functional tumors are more typical in older patients-> hypopituitary
    • as these cells are already poorly functioning in old people
    • tumor occurs-> further reduction of function
56
Q

Stages of development of adenomas

A

Normal-> hyperplasia-> adenoma

hyperplasia result in non-uniform strucutre-> adenoma

57
Q

Prevalence of pituitary adenomas

A
  • Prolactin cell adenoma - most common (30%)
  • Nonfunctioning adenoma 2nd most common (25%)
  • unclassified (2%)
  • Also - GH cell adenoma, ACTH, Gonadotroph, TSH
58
Q

Pituitary adenomas – signs and symptoms

A
  • Usually due to hypofunction, hyperfunction, or mass effect
  • as pituitary are close to optic chiasma-> eyes are usually affected first
  • Lateral extension to cavernous sinuses – diplopia (double vision), ptosis (drooping eyelids), altered facial sensation
59
Q

Hypopituitarism- 4 types- name

A

GH, Gonadotropin, ACTH and TSH deficiencies

60
Q

Describe Hypopituitarism- GH deficiency

A

decreased muscle strength and exercise tolerance, diminished libido, increased body fat

61
Q

Describe Hypopituitarism- Gonadotropin deficiency

A

oligo/amenorrhea, diminished libido, infertility, hot flashes, impotence (clinically like primary hypothyroidism)

62
Q

Describe Hypopituitarism- ACTH deficiency

A

malaise, fatigue, anorexia, hypoglycemia

63
Q

Describe Hypopituitarism- TSH deficiency

A

malaise, leg cramps, fatigue, dry skin, cold intolerance

low thyrid hormone levels

64
Q

Name hormones of anterior pituitary

A

Adrenocorticotrophic hormone (ACTH)
Thyroid-stimulating hormone (TSH)
Luteinising hormone (LH)
Follicle-stimulating hormone (FSH)
Prolactin (PRL)
Growth hormone (GH)
Melanocyte-stimulating hormone (MSH)

65
Q

Why may tumors arise>

A

Tumors may arise de novo (cells either become more active or increase in number) or because of the lack of feed-back control

66
Q

Give an example of over-secretion of hormones of the anterior pituitary due to the absence of negative feedback

A

Cushing disease → primary defect in negative feedback control of CRH and ACTH secretion by cortisol → ACTH-producing cells are continuously stimulated by CRH → tumor formation

67
Q

What are the most common tumors that result in the over-production of hormones? rare?

A

Tumors secreting PRL, GH or ACTH are most common.

Tumors affecting the release of thyroid stimulating hormone (TSH) and the gonadotropins release (LH and FSH) are rare.

68
Q

What is the most common cure for tumors that result in Over-secretion of hormones of the anterior pituitary

A

Most common cure is surgery through the nose

69
Q

Describe Prolactinoma

A
  • excess of PRL-> negative effect on reproduction
  • oligo/amenorrhea (less cycles, incomplete or absence ), galactorrhea (production of milk/secretion at the wrong time), infertility, *decreased libido, *headaches, *visual field defects
  • often the presentation in men and post- menopausal women
70
Q

Effects of GH over-secreting tumors

best way of treating?

A
  • Gigantism (high levels of GH during the growth phase e.g. in adolescents ) and acromegaly (GH levels increased in adults after they stopped growing-> large bones, jaws)
  • GH produced at a high level without pulsatility.
  • IGFs elevated as a consequence (positive effect on most tissues in terms of growth)
  • Treated with long-acting somatostatin analogues
  • Best is surgical removal
71
Q

Effect of GH therapy

A

Administration of GH allows growth to catch up, but there are a lot of side-effects

72
Q

Diagnosis of adenomas

A
  • Usually delayed due to non-specific nature of many symptoms
  • MRI is imaging is the best way to confirm
  • Tests can reveal whether adenoma is hypo- or
  • hyperfunctional
  • Visual field defects (first symptom) often require resection of pituitary gland
73
Q

Diagnosis of deficiency for gh, gonadotropins, ACTH, TSH

A

hormone levels can be measures
either the hormone itself, or associated hormones

  • GH: insulin tolerance test, GHRH/arginine test, IGF-1 levels
  • Gonadotropins: sexual history, menstrual history, FSH/LH/estradiol/prolactin/testosterone levels (directly on indirectly- e.g. by measuring LH or FSH or target hormones such es estradiol)
  • ACTH: AM cortisol, cosyntropin test (ACTH), insulin tolerance test
  • TSH: T4 and TSH levels
74
Q

Describe cosyntropin test

A

The ACTH stimulation test measures how well the adrenal glands respond to adrenocorticotropic hormone (ACTH).

An increase in cortisol after stimulation by ACTH is normal.

No increase in cortisol-> problems

75
Q

Diagnosis of excess- prolactinoma, acromegaly, TSH

A

directly from blood or MRI

  • Prolactinoma: prolactin level, drug history, clinical setting (e.g. pregnancy, breast stimulation, stress, hypoglycemia)
    • PRL < 200ng/ml w/ large adenoma suggests stalk compression as etiology
  • Acromegaly: IGF-1 level, oral glucose tolerance test
  • TSH overproduction: free T4, T3, TSH levels
76
Q

Treatment of overpdouction of hormones

A
  • Typically requires surgical resection of adenoma
  • Exception: prolactinoma in which 1st line treatment is dopamine agonist therapy- as prolactin’s regulation is primarily through negative regulation by dopamine
  • Treatment with bromocriptine: Binds and activates dopamine receptors → inhibition of PRL secretion
  • Somatostatin analogs (inhibit GH secretion) are used for acromegaly
  • Deficiency states require replacement of the indicated hormone
77
Q

Estogen and progesterone

Impacts on LH, FSH and GnRH

A

estrogen inhibits both GnRH and FSH release

progesterone inhibits both LH and GnRH release.

78
Q

Name POMC derived hormones

A
  • b- lipotropin
  • ACTH
  • MSH
  • PRL
  • Endorphin
79
Q

testtosterone and inhibin interaction

A

testosterone promotes inhibin production

kris Endocrinology (17 decks)

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