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Metabolic Endocrinology > Anterior Pituitary > Flashcards

Anterior Pituitary Flashcards

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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
What is notable about IGF-2 signalling?
receptor doesn't really do anything.. *but it can maybe bind to IGF-1 receptor but with 10% less affinity
26
the IGF-2 receptor can also bind ____
mannose-6-P
27
Pattern of GH release during sleep:
pulses: secretion every 1-2 hours
28
low blood ____ or the amino acid ____ will trigger increase in GH
glucose (hypoglycemia) | arginine
29
Glucose and fatty acids will increase ____ release from the hypothalamus
somatostatin (to stop GH)
30
The effects of IGF-1 are antagonized by ____
cortisol
31
What is a simple test for GH response? (2)
1. glucose spike: GH should decrease in response | 2. insulin injection (induced hypoglycemia): GH should rise
32
What hormones increase or decrease GH?
decrease: glucocorticoid increase: estrogen
33
Hypothyroid children have (increased/decreased) growth. Why?
decreased (stunted) | thyroxin (T4) promotes GH gene transcription
34
Why does estrogen increase GH?
sensitizes somatotrophs to produce GH
35
The 2 major growth spurts in life: | Which one relies on GH?
postnatal growth spurt | pubertal growth spurt (GH very important)
36
GH (increases/decreases) with age. What is this called?
decreases | somatopause
37
Is GH therapy beneficial for elderly?
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
38
Main function of PRL:
postpartum activation of lactation
39
Describe the hormones/development of the mammary gland:
estrogen, GH, cortisol -> growth of duct system estrogen, GH, cortisol, PRL -> alveolar growth (also involve insulin, thyroid hormone)
40
What 2 hormones are essential to initiate/maintain milk secretion?
PRL, cortisol
41
What happens to milk production if the pituitary is removed?
milk production immediately stops
42
What happens to milk production if the adrenals are removed?
gradual reduction in milk production
43
What hormones must decrease for milk production? What causes the decrease?
estrogen and progesterone (high levels suppress milk) | levels drop with loss of placenta
44
PRL stimulates the milk _____ from _____ cells into the ______. Oxytocin induces _____ in the _____, forcing the milk out through the ____.
production; alveolar epithelial cells; lumen contraction; alveoli; duct
45
What other functions (aside from milk) does PRL have?
regulate reproductive system immunomodulation act synergistically with other hormones
46
True/False: PRL receptors are found on most tissues
True (act together with other hormones)
47
How does high levels of PRL influence the reproductive system? (2)
too high -> hypogonadism Lactational amenorrhea (natural birth control)
48
How does PRL affect immune cells?
receptors on T cells, B cells, macrophages act as mitogen -> promote survival
49
The PRL receptor is similar to the ____ receptor. What type is it?
GH | recruited TK -> MAPK, STATs, IP3-K
50
what is the PRL releasing hormone?
Doesn't exist Only negative control (dopamine) (TRH and VIP can promote release through antagonizing dopamine)
51
ACTH stands for:
adrenocorticotrophin
52
What is the precursor for ACTH? What else does it yield?
pro-opiomelanocortin (POMC) Cleaved -> gamma-MSH, ACTH, Beta-lipotropin
53
Where does MSH come from?
alpha MSH: from amino-terminal fragment of POMC beta MSH: from cleaved ACTH gamma MSH: from cleaved beta -> gamma lipotropin
54
What gives rise to endorphins? (precursors)
POMC -> beta lipotropin -> beta endorphins
55
What effect does endorphins have?
morphine-like activity (high)
56
What role does MSH play?
darkening of skin
57
What role does ACTH play?
adrenal steroidogenesis
58
What is the purpose of MSH? Where does this occur?
produced by Keratinocyte (skin) -> stimulate melanocyte to make melanin keratinocyte uses melanin to protect from UV damage
59
Action of ACTH:
bind receptors in adrenals -> increased cholesterol mobilization/conversion to pregnenolone
60
What type of receptor is the ACTH receptor?
GPCR (Gsa) - cAMP
61
ACTH secretion is controlled by: ______ which is affected by factors such as (4)
CRH from hypothalamus stress (pain/fear/fever/hypoglycemia) dark/light cycle other hormones (vasopressin) feedback control from cortisol
62
At what time of day does ACTH peak? When is it lowest?
morning peak, lowest at midnight
63
What is TSH?
thyrotropin (thyroid stimulating hormone)
64
What is the structure of TSH?
2 protein chains (a and b), glycosylated
65
The TSH receptor is of what type?
GPCR-cAMP
66
What does TSH do?
stimulate metabolism of thyroid follicular cells (forming thyroid hormones)
67
What is the major control system for TSH release?
feedback control
68
What are the gonadotropins?
LH | FSH
69
compare the structure of the gonadotropins with TSH:
same a subunit, but different b subunits (overall same basic structure)
70
Actions of LH: (4)
female: steroidogenesis in ovarian follicle, induce ovulation , maintain steroidogenesis in CL male: stimulate testosterone production in Leydig cells (testes)
71
Actions of FSH: (5)
female: stimulate dev. of ovarian follicle, estradiol production male: spermaogenesis, producing sex-hormone binding globulin both: inhibin secretion (neg feedback)
72
____ is stimulated by FSH, which has negative feedback effects
inhibin
73
What is the pattern of gonadotropin release?
pulsatile (every 60 min in response to GnRH)
74
Where is inhibin produced?
``` Sertoli cells (testes) Ovary ```
75
How can LH stimulate the sertoli cells indirectly?
stimulate testosterone production from leydig cells -> testosterone stimulates sertoli cells
76
Most anterior pituitary disorders are due to:
benign tumors (adenomas)
77
What is an adenoma?
benign tumor, arises from adenohypophyseal cells, slow growing microadenomas <10mm macroadenomas >10mm
78
What is a non-functioning adenoma? In what age group is this more common?
does not cause excessive hormone production, usually cause function loss due to pressure/increasing size more common in older people
79
What is the least common pituitary adenoma type
TSH cell adenoma (1%)
80
What is the most common cell-specific adenoma types?
PRL cell adenoma (30%) GH cell adenoma (15%) ACTH cell adenoma (10%) Gonadotroph adenoma (10%)
81
What are the possible impacts of tumours on pituitary function? (4)
``` hypofunction hyperfunction mass effect (pushes on gland) impinges on optic chiasm -> visual field defects (diplopia, ptosis, altered facial sensation) ```
82
A swelling pituitary tumor can push on the ___ ____, causing visual field defects such as ___, ___, or _____
optic chiasm diplopia (double vision) ptosis (droopy eyelids) altered facial sensation
83
hypopituitarism can be caused by: (4)
adenomas, surgery, radiation, trauma
84
What is the sequence of function loss of the pituitary, due to mass effect (swelling)
GH Gn ACTH TSH
85
GH deficiency leads to (3):
decreased muscle strength/exercise tolerance lower libido more body fat
86
Gn deficiency lead to: (5)
``` oligo/amenorrhea lower libido infertility hot flashes impotence ```
87
ACTH deficiency leads to: (4)
malaise fatigue anorexia hypoglycemia
88
TSH deficiency leads to: (5) The symptoms are clinically similar to ______
``` malaise leg cramps fatigue dry skin cold intolerance ``` similar to primary hypothyroidism
89
Why might tumours arise in the pituitary? (2)
``` de novo (mutation) lack of feedback control ```
90
what causes Cushing's disease?
defect in negative feedback control of CRH and ACTH by cortisol body keeps releasing CRH to stimulate ACTH-producing cells -> forms tumour
91
tumours affecting the _____ and ____ hormones are rare
gonadotropins (FSH, LH) | TSH
92
What is the most common cure for hyperpituitarism?
surgery through nose -> remove part of gland
93
excess of PRL is known as _____, and causes: (6).
prolactinoma ``` oligo/amenorrhea galactorrhea infertility decreased libido headache visual field defects ```
94
Effect of GH excess: (2)
gigantism/acromegaly | elevated IGFs
95
What is the treatment (2) for GH excess?
long-acting somatostatin analogues surgical removal (best option)
96
symptoms of acromegaly:
``` high GH visual field defects large nose/jaw, separated teeth abnormal glucose tolerance test (glucosuria) sweat gland hypertrophy sexual dysfunction ```
97
What would be the results of a glucose tolerance test in a patient with acromegaly
no decrease in GH (remains high constantly)
98
What is the treatment for dwarfism?
GH therapy (hypertropin) -> allows growth to catch up to normal range
99
What is Cushing's disease?
excess ACTH -> excess cortisol production
100
Symptoms of cushing's disease:
``` upper body obesity buffalo hump red round face high BP, blood sugar acne cognitive difficulties ```
101
What does excess TSH cause? (symptoms) What is it clinically similar to?
``` heat intolerance weight loss weakness tremor sinus tachycardia heart failure ``` similar to hyperthyroidism
102
How is diagnosis done for pituitary disorders? (2)
MRI | specific tests to see if hypo or hyperfunctional
103
How is GH deficiency diagnosed? (3)
insulin tolerance test GH-RH arginine test IGF-1 levels
104
How is gonadotropin deficiency diagnosed? (3)
sexual history menstrual history FSH/LH/estradiol/PRL/testosterone levels
105
How is ACTH deficiency diagnosed? (3)
Morning cortisol levels cosyntropin test insulin tolerance test
106
How is TSH deficiency diagnosed? (2)
T4 levels | TSH levels
107
the insulin tolerance test is used for diagnosing what pituitary hormone deficiencies?
GH | ACTH
108
How is PRL excess diagnosed?
PRL level drug history clinical setting
109
How is acromegaly diagnosed?
IGF-1 level, oral glucose tolerance test
110
How is Cushing's disease diagnosed?
24 hr urine cortisol | overnight dexamethasone suppresion test
111
How is TSH excess diagnosed? (2)
free T4, T3 levels | TSH levels
112
What is the usual treatment for prolactinoma?
dopamine agonist therapy to suppress | bromocriptine -> bind/activate dopamine receptors
113
Somatostatin analogues are used to treat : _____ (2)
acromegaly | TSH producing adenomas

Metabolic Endocrinology (6 decks)

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