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Metabolic Endocrinology > Anterior Pituitary > Flashcards

Anterior Pituitary Flashcards

1
Q

What types of receptors are used by anterior pituitary hormones?

A

tyrosine kinase (STAT): GH, PRL

GPCR (cAMP): ACTH, LH, FSH, TSH

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2
Q

GH has ___ forms. What is the difference?

A

2

major form: 22kDa, shorter form 20kDA (less activity)

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3
Q

GH made from _____ is used to treat ____.

A

recombinant technology

pituitary dwarfism

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4
Q

What hypothalmic hormones control GH release?

A

GHIH/somatocrinin

GHRH/somatotropin

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5
Q

What is the effect of GH on the liver?

A

cause release of somatomedins (Insulin-like growth factors) -> cell division, protein synth, bone growth

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6
Q

What are metabolic effects of GH?

A

more fat breakdown

less glucose uptake by muscles (blood glucose rises)

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7
Q

GH has the opposite metabolic effects of _____

A

insulin

GH promotes growth/energy use, inhibit storage

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8
Q

What trigger the hypothalamus to stimulate Gh release?

A

deep sleep, exercise, stress, low blood glucose, high AA, low FA

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9
Q

What are the direct and indirect actions of GH?

A

Direct: mobilize energy and promote cell differentiation

Indirect: induce IGF-1 -> insulin-like effects + cell division

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10
Q

What does IGF stand for? What is another name for them, and what is their structure/function similar to?

A

insulin-like growth factors
somatomedins
similar to insulin

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11
Q

What are the IGF types?

A

IGF-1: GH dependent (made by liver/other tissues; act as endocrine, paracrine, or autocrine)

IGF-2: GH independent (fetal development)

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12
Q

True/false: IGF levels remain fairly constant

A

True (despite fluctuations in GH)

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13
Q

Does IGF have a carrier protein?

A

Yes, IGF binding protein

binds and modulates half life & activity

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14
Q

IGF-1 is most important during ______, but less important during _____, and is influenced by ____status

A

childhood growth
gestation/neonate
nutritional status

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15
Q

Describe the pattern of GH release in a growing child

A

pulsatile; pulses rise with age, maximum at puberty, then declines

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16
Q

What is the effect of GH and IGF-1 on bones in childhood?

A

promote growth at epiphyseal plates (chondrocyte proliferation)

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17
Q

What happens to bones at the end of puberty?

A

epiphyseal plates fuse (no more longitudinal growth)

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18
Q

___ stimulates chondroyte synthesis and increases their response to ____, stimulating _____

A

GH
IGF-1
cell division

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19
Q

____ produced by the ____ has negative feedback on GH

A

IGF-1

liver

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20
Q

The layer of bone cells (osteoblasts and osteoclasts) below the epiphyseal plate is known as the ____

A

diaphysis

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21
Q

The GH receptor is located in what tissues? What pathway is activated?

A

most tissues

Recruited TK -> STATs, MAPK, IP3-K

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22
Q

True/False: the GH ectodomain can break off into circulation

A

True (act as binding protein)

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23
Q

GHR is downregulated by ___ and ___

A

GH (bound -> endocytosed)

sex hormones

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24
Q

The IGF-1 receptor is of what type?

A

intrinsic TK

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25
Q

What is notable about IGF-2 signalling?

A

receptor doesn’t really do anything..

*but it can maybe bind to IGF-1 receptor but with 10% less affinity

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26
Q

the IGF-2 receptor can also bind ____

A

mannose-6-P

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27
Q

Pattern of GH release during sleep:

A

pulses: secretion every 1-2 hours

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28
Q

low blood ____ or the amino acid ____ will trigger increase in GH

A

glucose (hypoglycemia)

arginine

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29
Q

Glucose and fatty acids will increase ____ release from the hypothalamus

A

somatostatin (to stop GH)

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30
Q

The effects of IGF-1 are antagonized by ____

A

cortisol

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31
Q

What is a simple test for GH response? (2)

A
  1. glucose spike: GH should decrease in response

2. insulin injection (induced hypoglycemia): GH should rise

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32
Q

What hormones increase or decrease GH?

A

decrease: glucocorticoid
increase: estrogen

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33
Q

Hypothyroid children have (increased/decreased) growth. Why?

A

decreased (stunted)

thyroxin (T4) promotes GH gene transcription

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34
Q

Why does estrogen increase GH?

A

sensitizes somatotrophs to produce GH

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35
Q

The 2 major growth spurts in life:

Which one relies on GH?

A

postnatal growth spurt

pubertal growth spurt (GH very important)

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36
Q

GH (increases/decreases) with age. What is this called?

A

decreases

somatopause

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37
Q

Is GH therapy beneficial for elderly?

A

Overall no.
It can decrease fat, increase lean muscle, bone density, cog. function

BUT: side effects - edema, joint pain, breast dev., metabolic imbalance, cancer risk

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38
Q

Main function of PRL:

A

postpartum activation of lactation

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39
Q

Describe the hormones/development of the mammary gland:

A

estrogen, GH, cortisol -> growth of duct system
estrogen, GH, cortisol, PRL -> alveolar growth

(also involve insulin, thyroid hormone)

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40
Q

What 2 hormones are essential to initiate/maintain milk secretion?

A

PRL, cortisol

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41
Q

What happens to milk production if the pituitary is removed?

A

milk production immediately stops

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42
Q

What happens to milk production if the adrenals are removed?

A

gradual reduction in milk production

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43
Q

What hormones must decrease for milk production? What causes the decrease?

A

estrogen and progesterone (high levels suppress milk)

levels drop with loss of placenta

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44
Q

PRL stimulates the milk _____ from _____ cells into the ______.

Oxytocin induces _____ in the _____, forcing the milk out through the ____.

A

production; alveolar epithelial cells; lumen

contraction; alveoli; duct

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45
Q

What other functions (aside from milk) does PRL have?

A

regulate reproductive system
immunomodulation
act synergistically with other hormones

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46
Q

True/False: PRL receptors are found on most tissues

A

True (act together with other hormones)

47
Q

How does high levels of PRL influence the reproductive system? (2)

A

too high -> hypogonadism

Lactational amenorrhea (natural birth control)

48
Q

How does PRL affect immune cells?

A

receptors on T cells, B cells, macrophages

act as mitogen -> promote survival

49
Q

The PRL receptor is similar to the ____ receptor. What type is it?

A

GH

recruited TK -> MAPK, STATs, IP3-K

50
Q

what is the PRL releasing hormone?

A

Doesn’t exist
Only negative control (dopamine)

(TRH and VIP can promote release through antagonizing dopamine)

51
Q

ACTH stands for:

A

adrenocorticotrophin

52
Q

What is the precursor for ACTH? What else does it yield?

A

pro-opiomelanocortin (POMC)

Cleaved -> gamma-MSH, ACTH, Beta-lipotropin

53
Q

Where does MSH come from?

A

alpha MSH: from amino-terminal fragment of POMC

beta MSH: from cleaved ACTH

gamma MSH: from cleaved beta -> gamma lipotropin

54
Q

What gives rise to endorphins? (precursors)

A

POMC -> beta lipotropin -> beta endorphins

55
Q

What effect does endorphins have?

A

morphine-like activity (high)

56
Q

What role does MSH play?

A

darkening of skin

57
Q

What role does ACTH play?

A

adrenal steroidogenesis

58
Q

What is the purpose of MSH? Where does this occur?

A

produced by Keratinocyte (skin) -> stimulate melanocyte to make melanin

keratinocyte uses melanin to protect from UV damage

59
Q

Action of ACTH:

A

bind receptors in adrenals -> increased cholesterol mobilization/conversion to pregnenolone

60
Q

What type of receptor is the ACTH receptor?

A

GPCR (Gsa) - cAMP

61
Q

ACTH secretion is controlled by: ______ which is affected by factors such as (4)

A

CRH from hypothalamus

stress (pain/fear/fever/hypoglycemia)
dark/light cycle
other hormones (vasopressin)
feedback control from cortisol

62
Q

At what time of day does ACTH peak? When is it lowest?

A

morning peak, lowest at midnight

63
Q

What is TSH?

A

thyrotropin (thyroid stimulating hormone)

64
Q

What is the structure of TSH?

A

2 protein chains (a and b), glycosylated

65
Q

The TSH receptor is of what type?

A

GPCR-cAMP

66
Q

What does TSH do?

A

stimulate metabolism of thyroid follicular cells (forming thyroid hormones)

67
Q

What is the major control system for TSH release?

A

feedback control

68
Q

What are the gonadotropins?

A

LH

FSH

69
Q

compare the structure of the gonadotropins with TSH:

A

same a subunit, but different b subunits (overall same basic structure)

70
Q

Actions of LH: (4)

A

female: steroidogenesis in ovarian follicle, induce ovulation , maintain steroidogenesis in CL
male: stimulate testosterone production in Leydig cells (testes)

71
Q

Actions of FSH: (5)

A

female: stimulate dev. of ovarian follicle, estradiol production
male: spermaogenesis, producing sex-hormone binding globulin
both: inhibin secretion (neg feedback)

72
Q

____ is stimulated by FSH, which has negative feedback effects

A

inhibin

73
Q

What is the pattern of gonadotropin release?

A

pulsatile (every 60 min in response to GnRH)

74
Q

Where is inhibin produced?

A 
Sertoli cells (testes)
Ovary
75
Q

How can LH stimulate the sertoli cells indirectly?

A

stimulate testosterone production from leydig cells -> testosterone stimulates sertoli cells

76
Q

Most anterior pituitary disorders are due to:

A

benign tumors (adenomas)

77
Q

What is an adenoma?

A

benign tumor, arises from adenohypophyseal cells, slow growing

microadenomas <10mm
macroadenomas >10mm

78
Q

What is a non-functioning adenoma? In what age group is this more common?

A

does not cause excessive hormone production, usually cause function loss due to pressure/increasing size

more common in older people

79
Q

What is the least common pituitary adenoma type

A

TSH cell adenoma (1%)

80
Q

What is the most common cell-specific adenoma types?

A

PRL cell adenoma (30%)
GH cell adenoma (15%)
ACTH cell adenoma (10%)
Gonadotroph adenoma (10%)

81
Q

What are the possible impacts of tumours on pituitary function? (4)

A 
hypofunction
hyperfunction
mass effect (pushes on gland)
impinges on optic chiasm -> visual field defects (diplopia, ptosis, altered facial sensation)
82
Q

A swelling pituitary tumor can push on the ___ ____, causing visual field defects such as ___, ___, or _____

A

optic chiasm
diplopia (double vision)
ptosis (droopy eyelids)
altered facial sensation

83
Q

hypopituitarism can be caused by: (4)

A

adenomas, surgery, radiation, trauma

84
Q

What is the sequence of function loss of the pituitary, due to mass effect (swelling)

A

GH
Gn
ACTH
TSH

85
Q

GH deficiency leads to (3):

A

decreased muscle strength/exercise tolerance

lower libido

more body fat

86
Q

Gn deficiency lead to: (5)

A 
oligo/amenorrhea
lower libido
infertility
hot flashes
impotence
87
Q

ACTH deficiency leads to: (4)

A

malaise
fatigue
anorexia
hypoglycemia

88
Q

TSH deficiency leads to: (5)

The symptoms are clinically similar to ______

A 
malaise
leg cramps
fatigue
dry skin
cold intolerance

similar to primary hypothyroidism

89
Q

Why might tumours arise in the pituitary? (2)

A 
de novo (mutation)
lack of feedback control
90
Q

what causes Cushing’s disease?

A

defect in negative feedback control of CRH and ACTH by cortisol
body keeps releasing CRH to stimulate ACTH-producing cells -> forms tumour

91
Q

tumours affecting the _____ and ____ hormones are rare

A

gonadotropins (FSH, LH)

TSH

92
Q

What is the most common cure for hyperpituitarism?

A

surgery through nose -> remove part of gland

93
Q

excess of PRL is known as _____, and causes: (6).

A

prolactinoma

oligo/amenorrhea
galactorrhea
infertility
decreased libido
headache
visual field defects
94
Q

Effect of GH excess: (2)

A

gigantism/acromegaly

elevated IGFs

95
Q

What is the treatment (2) for GH excess?

A

long-acting somatostatin analogues

surgical removal (best option)

96
Q

symptoms of acromegaly:

A 
high GH
visual field defects
large nose/jaw, separated teeth
abnormal glucose tolerance test (glucosuria)
sweat gland hypertrophy
sexual dysfunction
97
Q

What would be the results of a glucose tolerance test in a patient with acromegaly

A

no decrease in GH (remains high constantly)

98
Q

What is the treatment for dwarfism?

A

GH therapy (hypertropin) -> allows growth to catch up to normal range

99
Q

What is Cushing’s disease?

A

excess ACTH -> excess cortisol production

100
Q

Symptoms of cushing’s disease:

A 
upper body obesity
buffalo hump
red round face
high BP, blood sugar
acne
cognitive difficulties
101
Q

What does excess TSH cause? (symptoms)

What is it clinically similar to?

A 
heat intolerance
weight loss
weakness
tremor
sinus tachycardia
heart failure

similar to hyperthyroidism

102
Q

How is diagnosis done for pituitary disorders? (2)

A

MRI

specific tests to see if hypo or hyperfunctional

103
Q

How is GH deficiency diagnosed? (3)

A

insulin tolerance test
GH-RH arginine test
IGF-1 levels

104
Q

How is gonadotropin deficiency diagnosed? (3)

A

sexual history
menstrual history
FSH/LH/estradiol/PRL/testosterone levels

105
Q

How is ACTH deficiency diagnosed? (3)

A

Morning cortisol levels
cosyntropin test
insulin tolerance test

106
Q

How is TSH deficiency diagnosed? (2)

A

T4 levels

TSH levels

107
Q

the insulin tolerance test is used for diagnosing what pituitary hormone deficiencies?

A

GH

ACTH

108
Q

How is PRL excess diagnosed?

A

PRL level
drug history
clinical setting

109
Q

How is acromegaly diagnosed?

A

IGF-1 level, oral glucose tolerance test

110
Q

How is Cushing’s disease diagnosed?

A

24 hr urine cortisol

overnight dexamethasone suppresion test

111
Q

How is TSH excess diagnosed? (2)

A

free T4, T3 levels

TSH levels

112
Q

What is the usual treatment for prolactinoma?

A

dopamine agonist therapy to suppress

bromocriptine -> bind/activate dopamine receptors

113
Q

Somatostatin analogues are used to treat : _____ (2)

A

acromegaly

TSH producing adenomas

Metabolic Endocrinology (6 decks)

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