endocrine lecture1 Flashcards

1
Q

definition of a hormone?

A

effector molecule which is released into the blood and travels to its target

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2
Q

what are the 4 categories of hormones?

A
  1. tyrosine derivatives (norepi, dopamine)
  2. peptides (hypothalamic hormones)
  3. large proteins (insulin, GH)
  4. steroids (sex steroids, cortisol)
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3
Q

which types of hormones are secreted from vessicles?

A

water soluble ones (proteins and peptides)

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4
Q

what causes hormone vessicle release?

A

increase in intracellular Ca++

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5
Q

how are steroid molecules stored/secreted from the cell?

A

steroids are made only when required and released immediately

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6
Q

which hormones are carried mostly in the blood as free hormones?

A

water soluble ones (proteins and peptides)

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7
Q

what is the consequence of water soluble molecules being mostly “free hormone” in the blood?

A

short half life - because they are rapidly degraded by proteases in the blood

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8
Q

how are steroid hormones carried in the blood?

A

carrier molecules (globulins)

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9
Q

what percent of steroid hormone is in the bound form in the blood?

A

90-99%, (the body only “cares” about the free form)

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10
Q

does the body regulate hormone levels based on the “total” amount of hormone in the blood?

A

NO, only the “free” form of the hormone is regulated

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11
Q

What are the 2 general assays to measure hormone levels

A

check for function = bioassay

check hormone level directly = immunoassay

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12
Q

what are the advantages of bioassays?

A

good measure of actual hormone function, but its a very complicated experiement

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13
Q

what are the advantages of an immunoassay?

A

cheap, simple

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14
Q

What is ELISA?

A

enzyme linked immunosorbent assay
-have antibodies to a hormone in wells, then add hormone of interest, then add second antibody with an enzyme attached and measure enzyme activity. Tells you how much hormone was in your sample

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15
Q

describe the receptors that protein and peptide hormones interact with on target cells

A

3 types of cell membrane surface receptors

  • G protein receptors (hypothalalmic hormones)
  • Cytokine receptors (GH, prolactin)
  • EGF family receptors
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16
Q

what are the 3 g proteins?

A
Gs = stimulates Adenlyl cyclase
Gi = inhibits Adenlyl cyclase
Gq = activates PLC
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17
Q

what hormones tend to bind to g protein receptors?

A

hypothalamic hormones

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18
Q

what hormones tend to bind to Cytokine receptors?

A

GH, prolactin

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19
Q

what do cytokine receptors do when bound by ligand?

A

their cytosolic tyrosine kinase domain becomes active and phosphorylates “Signal transducers and activators of transcription” (JAK STAT) which go to the nucleus to affect transcription

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20
Q

What hormones bind to EGF family receptors?

A

insulin, IGF

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21
Q

What do EGF family receptors do when bound by ligand?

A

dimerizes, and activates its own tyrosine kinase domain to phosphorylate downstream stuff

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22
Q

which receptor type has ITS OWN tyrosine kinase domain?

A

EGF family

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23
Q

the most common way of regulating hormone levels is ________

A

feedback inhibition

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24
Q

describe the feedback inhibition of thyroid hormone levels

A

hypothalamus –> TRH –> pituitary –> TSH –> thyroid gland –> THYROID HORMONE –> feeds back to inhibit hypothalamus

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25
Q

in the most basic sense, what controls insulin/glucagon levels

A

high blood glucose = increased insulin

low blood glucose = increased glucagon

26
Q

Describe the idea of “spare receptors”

A

even when only a small percentage of receptors for a certain ligand are bound, you can get full signaling effect

27
Q

posterior and anterior pituitary developmental origins?

A
posterior = invagination of brain itself (neural crest)
anterior = epithelial origin from "rathke's pouch"
28
Q

which part of the pituitary can be directly controlled by the hypothalamus?

A

posterior pituitary

29
Q

how does the brain communicate with the anterior pituitary?

A

hypothalamus releases hormones into “hypophyseal portal system”, which leads to the anterior pituitary

30
Q

why is it important that the hypothalamus communicates with the anterior pituitary via the hypophyseal portal system rather then the general circulation?

A

hyposhyseal portal system is very small, and PREVENTS DILUTION of the very low concentration hormones released by the hypothalmus

31
Q

what are the hormones that the hypothalamus releases to control the anterior pituitary, and what do they cause the anterior pituitary to do?

A
TRH --> TSH, prolactin
GnRH --> LH, FSH
CRH --> POMC
GHRH --> GH
Somatostatin --> (-)GH, (-)TSH
PIH (dopamine) --> (-)prolactin
32
Q

which of the 6 hypothalamus hormones is NOT a peptide?

A

PIH (dopamine)

33
Q

All of the hormones that the hypothalamus releases to control the anterior pituitary act via ___________ receptors

A

g protein

34
Q

what are the specialized cell types in the anterior pituitary that hypothalamus hormones act upon?

A
TRH --> thyrotropes
GnRH / GHRH --> gonadotropes
CRH --> corticotrophs
somatostatin--> somatotrophs
PIH (dopamine) --> lactotrophs
35
Q

which of the hormones released by the anterior pituitary are “end hormones” which dont act upon other endocrine organs but instead just cause their desired effect directly on the target organs

A

GH

prolactin

36
Q

prolactin is what kind of hormone? what releases it?

A

protein, released from lactotrophs in the anterior pituitary

37
Q

does prolactin (as a protein hormone) have a long or short half life?

A

short (30 min)

38
Q

what kind of receptor does prolactin bind to?

A

Cytokine receptor, TWO molecules of prolactin must bind in a stepwise manner, activates JAK STAT pathway

39
Q

what does prolactin do? (ie physiological effect)

A

mammary gland function (3 things):

  • mammogenesis = grows the mammary glands
  • lactogenesis = prepares cells for milk production
  • galactopoesis = final release of milk
40
Q

what modulates prolactin’s actions during pregnancy?

A

estrogen and progesterone effect prolactin in the following ways:
(+) mammogenesis
(-) lactogenesis, galactopoesis

(estrogen and progesterone are high while pregnant, drop after giving birth)

41
Q

main control of prolactin function comes from what hormone ?

A

PIH (prolactin inhibiting hormone)(dopamine)

-so the major control of prolactin is INHIBITORY

42
Q

if you remove the hypothalamus what would happen to all your anterior pituitary hormone levels?

A

all would decrease, except prolactin which would go up since it is now dis-inhibited (no more PIH (dopamine))

43
Q

what would happen if you have HYPER-prolactin?

A

galactorhea (uncontrolled milk production)

  • *amenhorea (absence of menstrual cycle)
  • *loss of libido

(**amenhorrea and loss of libido are due to feedback inhibition of GnRH at the hypothalamus)

44
Q

what could cause HYPER-prolactin?

A

tumor

anti-psychotic medications (block dopamine release)

45
Q

what could cause HYPO-prolactin?

A

-panhypopituitaryism (Shehan’s syndrome)

46
Q

what would happen if you have HYPO-prolactin?

A

-lack of milk production

47
Q

what kind of hormone is GH? what produces it?

A

protein hormone, released from somatotrophs in the anterior pituitary

48
Q

GH is highly ________

A

conserved across many species

49
Q

what kind of receptor for GH bind to? what happens when it binds?

A

Cytokine receptors, activates JAK STAT pathway

50
Q

what are the physiological effects of GH?

A

metabolic effects: increases blood glucose

growth effects: increases amino acid uptake of muscles, lipolysis in fat (creates FFA’s)

51
Q

how does GH increase blood glucose?

A
  • antagonizes insulin action

- stimulates gluconeogenesis in liver

52
Q

what hormone is also known as “diabetogenic hormone”?

A

GH, because prolonged high levels of GH can chronically elevate blood glucose causing diabetes

53
Q

GH actually has NO direct effect on growth. So, what does then?

A

IGF (which is regulated by GH)

-all growth requires IGF

54
Q

how does GH affect IGF production?

A

GH must be present ALONG WITH INSULIN, only then is IGF produced

55
Q

GH production in the somatotrophs is controlled by a balance between ______ and ______

A
  • GHRH (increases GH production)

- somatostatin (decreases GH production)

56
Q

besides GHRH and somatostatin, what else has an effect on GH levels?

A
  • GH’s own feedback inhibition on GH production
  • increased amino acids will stimulate GH production
  • hypoglycemia will stimulate GH production
57
Q

what happens to GH levels during starvation? why?

A

-GH goes up due to hypoglycemia, supplying the body with glucose. However its growth effects are blocked becasue there is low insulin–>no IGF production, and IGF is needed for growth.

58
Q

what happens with HYPER-GH?

A
  • gigantism (before puberty, severe long bone growth)

- acromegaly (after puberty, not as severe)

59
Q

what are the health effects of gigantism? acromegaly?

A
gigantism = super tall, hyperglycemia, enlarged heart, delayed puberty so growth continues
acromegaly = hand/jaw/feet growth, hyperglycemia, heart disease
60
Q

what happens with HYPO-GH?

A

-Dwarfism

61
Q

what can cause HYPO-GH?

A
  • defective GH receptors (Laron’s dwarfism)

- IGF receptor defect (African pygmys)