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Metabolic Endocrinology > Hypothalamus-anterior pituitary > Flashcards

Hypothalamus-anterior pituitary Flashcards

1
Q

who discovered the pituitary was made up of 2 parts?

A

Rathke (19th century)

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2
Q

what are the 2 parts of the pituitary called?

A
  • anterior pituitary (adenohypophysis)

- posterior pituitary (neurohypophysis)

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3
Q

why is the pituitary considered the master gland?

A

it secrets a lot of hormones

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4
Q

who was the first to pioneer the surgical technique to remove part of tumor on the pituitary causing acromegaly through nose?

A

Harvey Cushing

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5
Q

what are the functions of the pituitary gland?

A
  • growth hormone
  • lactation (prolactin)
  • action on the Thyroid (thyrotropin or thyroid stimulating hormones TSH)
  • action on the adrenals (adrenocorticotropin or ACTH)
  • action on the gonads (gonadotropins: Luteinizing hormone LH and Follicle stimulating hormone FSH)
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6
Q

why do we refer to the hypothalamus-pituitary axis?

A

although the pituitary was considered as the master gland, it is controlled by the nervous system via the hypothalamus

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7
Q

what is the hypothalamus-pituitary axis

A

the link between the nervous and endocrine system

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8
Q

what structure separates the hypothalamus and pituitary

A

median eminence

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9
Q

what are the 2 difference ectodermal components making up the hypothalamo-hypophyseal tract?

A
  1. Rathke’s pouch

2. the infundibulum

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10
Q

what is Rathke’s pouch?

A

outgrowth of the buccal cavity, detaches and becomes the anterior pituitary

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11
Q

how does the infundibulum develop?

A

it develops from an outgrowth of neuroectoderm from the floor of the 3rd ventricle

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12
Q

what are the structures that the infundibulum gives rise to?

A

pituitary stalk, median eminence and posterior pituitary

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13
Q

the hypothalamus is organized into discrete nuclei. Which are the main ones?

A
  • paraventricular nuclei PVN (=PVH)
  • supraoptic nuclei SON
  • arcuate nucleus Arc
  • lateral nuclei
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14
Q

which hormones do PVN and SON produce?

A

oxytocin and vasopressin

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15
Q

3 characteristics of PVN and SON

A
  • large neurons (120-200nm diameter)
  • Herring bodies: hormone granules are visible and can be observes traveling down the axons
  • terminate in posterior pituitary
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16
Q

which nuclei are hypothalamic-hypophyseotropic?

A
  • periventricular nucleus PeVH
  • PVN (smaller neurons)
  • arcuate nucleus Arc
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17
Q

where are hypothalamic-hypophysiotropic nuclei located?

A

near the wall of the third ventricle

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18
Q

where do the nerves of small PVN, PeVN, Arc found in hypothalamus terminate?

A

in the external layer of the median eminence

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19
Q

where are magnicellular neurons located?

A

SON and PVH

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20
Q

can you see hormone containing vesicles in parvicellular hypophyseotropic neuron?

A

no unless they are at the axon terminal

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21
Q

which hypothalamic hormones are released by PeVN and small PVN?

A

TRH, CRH, Somatostatin

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22
Q

which hypothalamic hormones are released by Arc?

A

GHRH, GnRH, Dopamine

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23
Q

Mode of action of parvicellular hypophyseotropic neurons (hypothalamus to AP)

A
  • axon terminals of hypothalamic neurons release hypophyiotropic hormones in the area of the median eminence
  • hormones are taken up by capillary blood vessels
  • travel to the anterior pituitary via the portal vein
  • hormones enter the AP and trigger the reals of second wave of hormones
  • the pituitary hormones enter the blood stream via the venous capillaries
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24
Q

which organs do magnicellular neurons act on

A

uterus, kidney, mammary gland

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25
Q

which are the second wave hormones involved in the action of the hypothalamus on the Anterior pituitary?

A

ACTH, TSH, GH , LH, FSH, Prolactin

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26
Q

mode of action of magnicellular neurons involved in hypothalamus to posterior pituitary

A
  • posterior pituitary is composed of the axon endings of neurons whose cell bodies are in the hypothalamus
  • Hormones (oxytocin and vasopressin) are produced in the cell bodies, packaged into granules which migrate to the ends of the axons located in the posterior pituitary
  • stimulation of neurons in the hypothalamus triggers the release of the hormones from the axon tips located in the posterior pituitary
  • the hormones are taken up by capillaries ad enter the blood stream
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27
Q

how does the hypothalamus secrete these diverse hormones?

A

through the integration of external [light, temperature, odorants] and internal [blood pressure, osmolality, hormone and glucose levels] cues through circumventricular organs which are windows to the periphery of the hypothalamus, overcoming the blood brain barrier (impermeable to many macromolecules), through direct connection with hypothalamus nuclei.

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28
Q

which are circumventricular organs?

A
  • median eminence (ME)
  • organum vasculosum of the lamina terminals (OVLT)
  • subfornical organ (SFO)
  • subcommissural organ (SCO)
  • area postrema (AP)
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29
Q

characteristics of circumventricular organs

A
  • they have direct connection to hypothalamus nuclei
  • rich in blood supply with permeable blood vessels (unlike blood-brain barrier)
  • exposed to hormones, metabolites and toxins (i.e. OVLT neurons have estrogen receptors)
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30
Q

where do hypothalamic nuclei send outputs to?

A

regulatory sites: AP, PP, cerebral cortex, premotor and motor neurons in brainstem and spinal cord, and parasympathetic and sympathetic preganglionic neurons

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31
Q

role of pineal gland

A

secretes melatonin

integrate information from external cues and internal milieu

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32
Q

what is the role of the suprachiasmatic nucleus SCN

A
  • circadian pacemaker (“clock”) that controls many physiological functions including pineal
  • has melatonin receptors - light and melatonin can reset the clock
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33
Q

about melatonin

A
  • melatonin concentration follows circadian rhythm
    => pineal gland begins producing melatonin in the evening and melatonin levels peak in the middle of the night
  • synthesized from tryptophan
  • melatonin receptors are found (almost) everywhere in the human body
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34
Q

functions of pineal gland

A
  • core body temperature (entrain body’s biological rhythms to the dark-light cycle)
  • induction fo sleep
  • depression of reproductive activity, inhibition of ovulation and semen production in some animals (questionable role in humans)
  • seasonal fluctuation may affect the timing of breeding, migration and hibernation in mammals
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35
Q

melatonin is highest in which population?

A

young population (5-10 years) and decreases with age

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36
Q

what are 4 adverse side effects of melatonin?

A
  • daytime sleepiness and hypothermia
  • desensitization of melatonin receptors if doses too high
  • possible adverse events in those with seizures
  • possible interaction with those taking Coumadin/warfarin (anticoagulants)
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37
Q

name anterior hypothalamic hormones

A
  • dopamine
  • prolactin-releasing hormone PRH
  • thyrotropin-releasing hormone TRH
  • corticotropin-releasing hormone CRH
  • growth-hormone releasing hormone GHRH
  • gonadotropin-releasing hormone GnRH
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38
Q

characteristics of cells found in anterior pituitary gland

A

contain alot of endoplasmic reticulum for synthesis of protein/peptide hormones + many secretory granules

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39
Q

what are the 5 subgroups of cells found in the anterior pituitary

A
  • corticotroph (15-20%)
  • gonadotrophs (10-15%)
  • somatotroph (40-50%)
  • lactotroph (10-15%)
  • thyrotroph (3-5%)
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40
Q

product + target of corticotroph

A

ACTH -> adrenal cortex/gland

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41
Q

product + target of thyrotroph

A

TSH -> thyroid gland

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42
Q

product + target of gonadotrophs

A

LH and FSH -> gonads

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43
Q

product + target of somatotroph

A

GH -> all tissues

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44
Q

product + target of lactotroph

A

PRL -> mammary glands and gonads

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45
Q

what is the difference between GH/PRL and TSH?

A

prolactin and growth hormones are exclusively produced by lactotrophs and somatotrophs respectively, where as there is no one cell that only produces TSH [co-expressed]

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46
Q

there is a ….. that can be noted with prolactin. what does it mean?

A

sexual dimorphism

aka females have more lactotrophs than age matched males

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47
Q

mechanism of action of hypothalamic hormones affecting the anterior pituitary

A
  • short half-life in circulation and fast action
  • hormones binds to receptors of target cells in the AP and trigger he release (exocytosis) of stored peptide hormones in granules
  • some feedback (mostly negative) control through modulation of receptor numbers
  • post-receptor intracellular signaling by G-protein
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48
Q

through which pathway do the releasing hormones from hypothalamus act?

A

GPCR pathway

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49
Q

tropic hormones (hormone produced by AP) use … and … which leads to an increase in …. and ….

A

Gs-alpha and Gq-alpha

which leads to an increase in calcium levels and exocytosis of hormone granules

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50
Q

inhibitory hormones (somatostatin and dopamine) act via ….

A

Gi-alpha

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51
Q

…. make up the largest portion of endocrine cells in anterior pituitary

A

somatotrophs that produce growth hormones

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52
Q

pituitary contains about ….. of GH

A

5-15mg of GH

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53
Q

where is the gene hGN-N expressed?

A

in somatotrophs in anterior pituitary

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54
Q

where are the hCS’s gene expressed [isoforms A, B, V and L]?

A

in chorionic somatotropins in placenta

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55
Q

what is the result of the transcription/alternative splicing/translation of the hGH-N gene?

A

2 proteins:

  • major 22 kDA form with 191 AA contributing to 90% of the GH pool
  • shorter isoform contributing to 10% of GH pool
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56
Q

growth hormone releasing hormone GHRH is a …. regulator of GH secretion

A

positive

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57
Q

somatostatin (SST) is a …. regulator of GH secretion

A

negative

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58
Q

GHRH and SST neurons both terminate in …..

A

median eminence

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59
Q

GHRH neuron stimulates … neuron which stimulates inhibitory neuron ….

A

NPY neuro stimulates inhibitory neuron SST

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60
Q

GH is a target hormone secreted by ….. which are under the influence of …. and ….

A

sometotrophs, GHRH and SST neurons

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61
Q

….. also has a negative feedback like … to GH secretion

A

IGF-1 and GH

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62
Q

stress (exercise, excitement, cold, surgery, hemorrhage) …. GH

A

increases

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63
Q

hyperglycaemia (oral glucose), free fatty acids …. GH

A

decrease

64
Q

hypoglycaemia (produced by insulin administration) and amino acids (arginine) …. GH

A

increase

65
Q

Leptin … GH

A

increases

66
Q

ghrelin …. GH

A

increases and decreases GH

67
Q

mechanism of how ghrelin decreases GH

A

Ghrelin positively regulates NPY which stimulates SST neuron which is a negative regulator of GH

68
Q

is there a difference in response in terms of GH levels between males and females?

A

yes -> sexual dimorphism
females respond more than males
-> GHRH treatment induces a greater secretion in GH than males

69
Q

somatostatin …. GH secretion but not ….

A

inhibits GH secretion but not synthesis

70
Q

why do we refer to bimodal increase when discussing GH secretion

A

GH levels vary throughout the life: levels fetus > child < adolescent > adult
=> bimodal increase

71
Q

how does GH circulate in the blood?

A

GH Binding Protein although Gh is a protein hormone - the extracellular domain of GHR
=> increase half life and bioavailability

72
Q

which cell types express GH receptor?

A

all cell types -> receptors are all over the body

73
Q

growth hormone signalling pathway

A

RTK signalling pathway with recruitment of tyrosine kinase JAKs

  • 1 GH hormone has to bind to 2 receptors
  • once hormone binds to receptor dimer, recruitment of tyrosine kinase in form of JAK protein
  • JAK proteins phosphorylate cytoplasmic domain of receptor:
    1. -> docking site of STAT protein, dimerization of STAT that is phosphorylated will go int nucleus and serve as transcription factor and regulate next level of hormone IGF-1
    2. MAPK pathway [cell proliferation genes]
    3. IRS/PI3K [glucose metabolism]
    4. CoAA [nuclear pro-proliferation genes]
    5. Ras/Raf - MEK - ERKs
74
Q

what does GH regulate?

A

IGF-1, cell proliferation genes, glucose metabolism, nuclear pro-proliferation

75
Q

…. protein inhibits phosphorylation and has a negative feedback on GHR signaling

A

suppressor of cytokine signaling SOCS

76
Q

…. knockout mouse -> gigantic

A

SOCS-2

77
Q

what is the direct action of GH effects

A

promotion of cell differentiation and growth

78
Q

what are the indirect actions of GH effects

A
  • acts on liver and induces expression of IGF-1 that promotes cell division
  • IGF-1 levees parallel growth rate in children
  • GH and IGF-1 promote growth of long bones at the epiphyseal plates (proliferation of chondrocytes)
  • > Epiphyses fuse at the end of puberty and longitudinal growth ceases
79
Q

…. produces 90% of IGF-1

A

liver

80
Q

how does IGF-1 circulate in blood

A

IGFBP 1 to 6

81
Q

how is bioavailability of IGF-1 increased?

A

by the action of proteases that specifically degrade IGFBP locally expressed as this will allow IGF-1 to be free for its signaling

82
Q

what are the metabolic effects fo GH?

A
  • in adults: optimizes body composition, physical function, and substrate metabolism
    -> interacts with insulin to regulate lipid, protein, and glucose metabolism
  • enhances lipolysis and FA oxidation into acetyl-coA (utilization of lipid for energy)
  • reduces urea synthesis and excretion -> protein sparing
  • increases AA uptake and protein synthesis
    0 inhibits insulin stimulates glucose uptake
83
Q

IGF-1 is …. dependent

A

GH

84
Q

IGF-1 produced by the liver is released in ….

A

blood stream

85
Q

IGF-1 produced by other tissues has a …… effect

A

paracrine/autocrine

86
Q

IGF-2 is GH …..

A

independent

87
Q

what is IGF-2 important for?

A

fetal development

88
Q

stricture of IGFs is similar to …

A

insulin

89
Q

what is the main difference between GH-receptor and IGF-1 receptor

A

GH-receptor acts via recruitment of tyrosine kinase JAK2 and activation off STATs, MAPK or IP3K where as IGF-1 receptor acts via intrinsic tyrosine kinase activity, MAPK, or IP3K

90
Q

which is the largets hormone

A

prolactin (198 AA vs 191 for GH)

91
Q

which is the most bioactive form of prolactin?

A

monomeric

92
Q

prolactin levels in males vs females

A

sexual dimorphism - females have more prolactin than males at any given time but levels reduce with age

93
Q

action of dopamine on prolactin

A

dopamine from Arc acts as the main inhibitor via dopamine D2 receptors on lactotrophs

94
Q

effect of prolactin on dopamine

A

prolactin stimulates dopamine response - positive regulation of negative regulator => overall: negative feedback loop

95
Q

which are the positive regulators of prolactin?

A

TRH, VIP (vasoactive intestinal peptide neurotransmitter) and oxytocin -> positive effect on lactotrophs

96
Q

estrogen …. dopamine neurons and …. lactotrophs

A

estrogen inhibits dopamine neurons and activates lactotrophs

97
Q

suckling stimulus …. oxytocin neurons and … dopamine neurons

A

suckling stimulates oxytocin neurons and inhibits dopamine neurons

98
Q

prolactin signaling (2)

A
  1. ligand-dependent dimerization
  2. ligand independent dimerization
    both tyrosine kinase receptors which requires a recruitment of tyrosine kinase as JAK - STAT
99
Q

main prolactin function

A
  • PRL is essential for initiation and maintenance of milk production - it stimulates milk production in alveolar epithelial cells
100
Q

which hormones are responsible for alveolar growth during mammary gland development?

A

prolactin, estrogen, progesterone, and adrenal steroids

101
Q

which hormones are responsible for the duct system development during mammary gland development

A

GH, estrogen and adrenal steroids

102
Q

PRL levels rise within ….. minutes of suckling and remain elevated for ….

A

1-3min and ate elevated for 10-20min

103
Q

PRL effect on milk production is …. from neural regulation of milk ejection

A

distinct

104
Q

which hormone enables milk ejection

A

instantaneous release of OXYTOCIN in response to suckling

105
Q

which muscle does oxytocin stimulate?

A

oxytocin stimulates alveolar smooth muscles

106
Q

normally, PRL activates …. neurons but not during lactation

A

dopamine

107
Q

oxytocin is a hormone from the … pituitary

A

posterior

108
Q

which hormone is an example of an end product that can cause a negative feedback loop and switch to a positive feedback loop?

A

prolactin: negative Feedback loop when stimulates dopamine release from Arc neurons but positive feedback loop during lactation

109
Q

what are other prolactin functions

A
  • involved in regulation of reproductive system
  • > if you have high levels of prolactin -> negative feedback on ovarian function causing hypogonadism
  • immunomodulation: PRL receptors on B and T lymphocytes and macrophages
  • > PRL acts a mitogen and promotes survival
110
Q

how is ACTH synthesized

A

ACTH is derived by proteolytic cleavage of a large precursor molecule POMC

111
Q

what are the related peptides to ACTH

A

beta-endorphin, melanocyte stimulating hormones (MSH)

112
Q

function of B-endorphin

A

morphin-like analgesic activity via m-opioid receptor MOR

113
Q

function of MSH

A

protection against UV damage via melanocortin receptor MCR1

114
Q

function of ACTH

A

adrenal steroidogenesis via MCR2

115
Q

what is the molecular pathway of tanning?

A
  • UV DNA damage causes local production of MSH by keratinocytes
  • MSH stimulates melanocyte to produce melanin
  • melanin transported back to keratinocyte to reduce UV damage and protect the DNA
116
Q

mechanism of action of ACTH

A

binds to MCR2 in the adrenal Cortex where MRAP is needed
this activates Gs-alpha protein and cAMP-PKA pathway
enhanced mobilization of cholesterol -> increased conversion of cholesterol to prognenolone
cortisol production which has a negative feedback control on the hypothalamus and pituitary

117
Q

what protein catalyzes the movement of cholesterol found in lipid storage to mitochondria

A

StAR

118
Q

which hypothalamic hormone controls ACTH secretion

A

CRH corticotropin releasing hormone
(stress info collected by hypothalamus which positively acts on CRH neurones producing CRH going to ME to AP where CRH stimulates ACTH production)

119
Q

CRH action is potentiated by other hormones such as …

A

vasopressin

120
Q

cortisol is a …. regulator of ACTH production

A

negative

121
Q

what do TSH/FSH and LH have in common

A

they both have 2 protein chains coded by 2 different genes of which the alpha chain is identical. therefore, they are differentiated by their unique beta chains

122
Q

what are the actions of TSH - thyroid stimulating hormone

A
  • regulator of thyroid gland - receptor signaling via G-proteins (cAMP)
  • major factor controlling the formation of thyroid hormones
  • stimulates metabolism off thyroid follicular cells
123
Q

… and … neurons stimulate TRH neurons

A

CRH and POMC

124
Q

… neurons inhibit TRH nurons

A

NPY

125
Q

…. sensory inputs stimulate TRH neurons

A

temperature sensory inputs

126
Q

TRH stimulates … release

A

TSH

127
Q

TSH-stimulated T3 and T4 have … feedback on thyrotrophs and TRH neurons

A

negative

128
Q

what is the action of FSH in females

A

development of ovarian follicles and estradiol secretion

129
Q

FSH and LH are regulated by …

A

GnRH - gonadotropin releasing hormones

130
Q

what is the action of FSH in males

A

spermatogenesis and estradiol secretin

131
Q

what is the action of FSH in both males and females

A

stimulates secretion of inhibin - negative feedback on FSH

132
Q

actions of LH in females

A

steroidogenesis in follicles, induction of ovulation, maintenant of steroidogenesis by corpus luteum

133
Q

actions of LH in males

A

stimulation of testosterone production in Leydig cells

134
Q

for females, steroid production in follicles requires ….

A

FSH and LH

135
Q

ovulation requires

A

mainly LH

136
Q

LH and FSH secretion is ….

A

pulsatile

137
Q

what is the feedback regulation of estradiol and progesterone on hypothalamus and pituitary?

A

both positive and negative feedback

138
Q

ACTH deficiency symptoms + diagnosis

A

malaise, fatigue, anorexia, hypoglycemia
diagnosis: AM cortisol (usually high), Cosyntropin test (injection of exogenous ACTH and see cortisol response), insulin tolerance test

139
Q

TSH deficiency symptoms + diagnosis

A

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

diagnosis” T4 and TSH levels

140
Q

Gonadotropin deficiency symptoms + diagnosis

A

oligo/amenorrhea, diminished libido, infertility, hot flashes, impotence
diagnosis: sexual history, menstrual history, FSH/LH/estradiol/prolactin/testosterone levels (low during deficiency)

141
Q

GH deficiency symptoms + diagnosis

A

decreased muscle strength and exercise tolerance, diminished libido, increased body fat
diagnosis: insulin tolerance test, GHRH/ariginine test, IGF-1 levels (best test: low levels show GH deficiency)

142
Q

PRL deficiency symptoms

A

infertility in both male and female, azoospermia in men

143
Q

what causes over-secretion fo hormones of the AP

A

most commonly due to benign tutors of pituitary (adenomas)

- they may arise de novo or because of lack of feedback control

144
Q

what are the most common tumors of AP

A

tumors secreting PRL, GH, ACTH

145
Q

pituitary tumors (adenomas) arise from … cells

A

adenohypophyseal cells (AP cells)

146
Q

… tumors are more common at younger age

… tumors are more typical in older patients

A

functional (tutor resulting from very high production of cell types that they’re made of) - younger
non-functional - older

147
Q

symptoms of prolactinoma + diagnosis

A

tumor over-secreting PRL - oligo/amenorrhea, galactorrhea (milk discharge), infertility
decreased libido, headaches, visual field defects often in men and post-monopausal women
diagnosis: PRL level with clinical history (e.g. pregnancy, breast stimulation, stress, hypoglycemia)

148
Q

symptoms of GH-secreting tumors + diagnosis

A

gigantism and acromegaly
elevated IGFs
diagnosis: IGF-1 levels, oral glucose tolerance test

149
Q

what is the mass effect for functional and non-functional tumors

A

due to large size of pituitary, impingement on optic chasm - visual field defect - diplopia (double vision), ptosis (drooping eyelids), altered facial sensation

150
Q

symptoms of acromegaly

A
  • visual field defects
  • prominent supraorbital ridge
  • teeth are separated/lacking
  • abnormal glucose tolerance test
  • glycosuria/polyuria
  • spade-shaped hands and feed
  • arthrosis
  • hypertrophy of sweat and sebaceous glands
  • galactorrhea
151
Q

how do you diagnose pituitary adenomas

A
  • usually delayed due to non-specific nature of symptoms but you can use MRI imaging and there are additional tests that can reveal whether the adenoma is hypo or hyper-functional
    + tests for visual field defects
152
Q

what is the aim of doing an insulin tolerance test for the diagnosis of GH and ACTH deficiency

A

injection of exogenous insulin in patient causes stress as it induces hypoglycemia. this will cause stress on the brain which allow to evaluate the response of GH and ACTH

153
Q

what does PRL<200ng/ml with large adenoma suggest?

A

stalk compression as etiology - reduced release of prolactin

154
Q

diagnosis of TSH overproduction

A

free T4, T3, TSH levels

155
Q

treatment of prolactinoma

A

dopamine agonist therapy with bromocriptine - binds and activates dopamine receptors which inhibits PRL secretion

156
Q

treatment for acromegaly

A

somatostatin analogs such as octreotide which reduces GH

157
Q

what are the treatments for deficiencies

A

replacement of the indicated hormone

Metabolic Endocrinology (10 decks)

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