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Patient > Endocrinology in pharmacy > Flashcards

Endocrinology in pharmacy Flashcards

1
Q

_____ ______ sheds in period

A

mucosal lining

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2
Q

does the lumen of the muscle (uterus) wall change thickness throughout the period?

A

yes in the course of regrowing

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3
Q

______ ______ triggers regrowth of uterine lining

A

oestrogen increasing

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4
Q

increase in LH causes decrease in ______ and an increase in ______

A

oestrogen

progesterone

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5
Q

what is menarche

A

onset of ovulation/ puberty

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6
Q

what does monarch activate?

A

oocytes

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7
Q

roughly _____ cycles in a lifetime

A

468

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8
Q

3 phases of the period? and time frames

A

menses 1-5
follicular 5-14
luteal 14-28

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9
Q

3 stages of ovulation?

A

follicle– rupture– corpus luteum

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10
Q

when does ovulation occur in the cycle?

A

day 14

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11
Q

gonadotrophin are _______ hormones

A

polypeptide hormones

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12
Q

what do the gonadotrophin regulate

A

steroid production

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13
Q

progesterone starts to _____ before ovulation

A

rise

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14
Q

when does progesterone peak?

A

about a week after ovulation

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15
Q

what are the gonadotrophin

A

LH and FSH

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16
Q

What do female steroids all contain?

A

4 carbon rings

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17
Q

why is oestrogen unique?

A

has an aromatic ring

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18
Q

sex steroid synthesis pathway?

A

acetate—- cholesterol —– pregnenolone—— progesterone OR 17a-hydroxypregnenolone

17a-hydroxypregnenolone —–DHEA —– androstenedione—— testosterone

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19
Q

what are androstenedione and testosterone

A

androgens

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20
Q

what do androgens give rise to?

A

oestrogen compounds

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21
Q

how do androgens give rise to oestrogen compounds?

A

aromatise enzyme is involved- needed for the aromatic ring

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22
Q

what does hormone action require?

A

receptors on target tissues

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23
Q

how do steroids travel in the blood?

A

binding proteins

very unsoluble

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24
Q

where are the major steroid receptors?

A

intracellular in the nucleus

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25
Q

what does binding to steroid receptors in the nucleus lead to?

A

production of mRNA which usually leads to translation of a protein

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26
Q

receptors for all the major classes of steroid hormones (e.g.???) belong to a ______ ______

A

e.g. androgens, oestrogen, progestins

superfamily

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27
Q

structures of the major steroid super family receptors?

A

2 binding sites

one for the steroid and there for DNA

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28
Q

What happens when the steroidal ligand binds to the receptor?

A

conformational change produces a complex that acts on DNA

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29
Q

what does this complex then do to the DNA after the steroidal ligand has bound?

A

alters the repertoire of genes being expressed by those cells

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30
Q

the way the steroids can change gene expression makes them _______ _______

A

transcription factors

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31
Q

can gonadotrophins (LH and FSH) get into cells?

A

no

need receptors at the cell surface

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32
Q

oestrogen dominates the ______ phase of the cycle

A

follicular

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33
Q

progesterone dominates the _______ phase of the cycle

A

luteal

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34
Q

how is the production of gonadotrophin regulated?

A

HPO axis

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35
Q

what is the HPO axis?

A

hypothalamic pituitary access
connected by short blood vessels
hypothalamus signals to the pituitary (gonadotrophin releasing hormone) which controls gonadotrophin release

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36
Q

Gonadotrophins control ______ ______ production

A

sex steroid

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37
Q

TF: Gonadotrophins control follicle maturation/ ovulation?

A

true

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38
Q

is GnRH release in the HPO axis continuous or pulsatile?

A

PULSATILE

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39
Q

TF: the pulsatile release of GnRH at the anterior pituitary depend on pulse frequency not amplitude.

A

TRUE- depends on pulse frequency not amplitude

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40
Q

GnRH acts at what type of receptor?

A

GPCR

41
Q

GnRH is regulated by?

A

sex steroids

42
Q

what does GnRH stimulate the release of?

A

LH and FSH

43
Q

FSH is stimulated by _____ GnRH pulse frequencies

A

SLOW

44
Q

LH is stimulated by _____ GnRH pulse frequencies

A

FAST

45
Q

How many AA’s in GnRH?

A

10

46
Q

antagonists or agonists of GnRH can be used to?

A

shut down the ovary in advance of a controlled cycle of ovulatory stimulation- good in IVF

47
Q

Buserelin mechanism of action?

A

GnRH receptor agonist
stimulates FSH and LH production at long term constant levels
this causes GnRHR down regulation and loss of FSH and LH production.

48
Q

once Buserelin is used to stop FSH and LH production, what can you do to make a synthetic cycle?

A

add exogenous steroids

49
Q

puberty in girls is believed to be controlled by _______.

A

leptin

50
Q

what neurone does leptin act through?

A

kisspeptin

51
Q

what does the kisspeptin neurone stimulate when leptin acts on it?

A

the anterior pituitary to produce gonadotophins

52
Q

being ______ _____ can stimulate earlier puberty.

A

over weight

more leptin

53
Q

early puberty is associated with higher risks of….. in women or men?

A

CVD
type 2 diabetes
in both women and men

54
Q

why can early puberty be associated with higher risks of CVD and T2D?

A

longer time exposed to cyclical oesterogen

55
Q

TF: increasing age of menarche is associated with lower risks of osteoporosis

A

FALSE- increasing risk

56
Q

TF: increasing age of menarche is associated with lower risks of breast cancer?

A

TRUE

57
Q

if steroid production kicks in earlier you get a ______ bone density

A

higher

58
Q

___ causes ovulation

A

LH

59
Q

we start out with about ______ follicles

A

a million

60
Q

how many follicles are recruited each month?

A

20

61
Q

what happens to these 20 follicles?

A

19 die away and you’re left with a dominant follicle

62
Q

where does this dominant follicle go?

A

moves to the ovarian surface and ovulates

63
Q

when does early menopause occur?

A

when follicular stores are depleted quicker

64
Q

what is the name of the cells that grow in the follicle?

A

granulosa cells

65
Q

what do granulose cells contain?

A

full chromosomal complement- pink cells. these cells continue to grow and surround the follicle

66
Q

what stimulates the development of follicle from the primary to tertiary state

A

FSH

67
Q

what causes ovulation?

A

LH

68
Q

What happens to the corpus luteum and steroid production if there’s no pregnancy?

A

CL: regressed

steroid production declines

69
Q

meiosis one (n equation)?

A

2n–> n

70
Q

meiosis II (n equation)?

A

n–>n

71
Q

where does meiosis take place?

A

in the ovaries

72
Q

when is the only time oestrogen has positive feedback? what does this result in?

A

when close to ovulation, this results in a spike in LH

73
Q

progesterone only exerts _____ feedback

A

negative

74
Q

post ovulation both FSH and LH _____

A

decline

75
Q

when does the spike in LH occur? why?

A

about 36 hours before ovulation.

as it causes ovulation

76
Q

in females, positive feedback by steroid to the hypothalamus is followed by…..

A

negative feedback

77
Q

in males androgens feed back ______ . there’s no ______ feedback

A

negatively

no positive feedback

78
Q

combined oestrogen and progesterone inhibit _____. so can be used for?

A

GnRH

contraceptives

79
Q

effect of high prolonged oestrogen?

A

inhibits GnRH

can cause endometrial cancer

80
Q

______ is the target tissue of sex steroids.

A

endometrial tissue

81
Q

oestrogen stimulates the growth of the _____

A

endometrium

82
Q

why does oestrogen cause DNA synthesis?

A

incorporation of thymidine increases

83
Q

how does an anti-oestrogen (faslodex) work?

A

binds the oestrogen receptor and blocks its ability to activate target genes- doesn’t create complex which can activate gene expression

84
Q

TF: oestrogen compounds are those which look like oestrogen. explain.

A

FALSE- they’re classified as those which bind to a receptor and does something down stream

85
Q

TF: tamoxifen is a oestrogen antagonist.

A

FALSE- its a partial agonist and partial antagonist

86
Q

positive effects of oestrogen on the brain?

A

delay memory loss, sexual and reproductive development

improve cognitive function

87
Q

positive effects of oestrogen on the bones?

A

preserves bone density

88
Q

define menopause?

A

permanent cessation of ovarian activity usually said to have occurred after 12 consecutive months of amenorrhoea

89
Q

define perimenopause?

A

period before menopause and 1st year after it

90
Q

define climacteric?

A

transition from reproductive life to non reproductive state

91
Q

net effect of a later menopause is a _______ life span

A

increased

92
Q

how are menopause flushes treated?

A

low dose oestrogen

93
Q

effect of menopause in the genital tract tissues?

A

genitalia and bladder- more UTIs

94
Q

what dose of oestrogen is required to stimulate receptors in the vagina and lower urethra?

A

10mg daily

95
Q

wound healing is ______ after menopause.

A

slower

96
Q

TF: oestrogen is a potent anti-inflammatory agent.

A

TRUE

97
Q

bone density _____ with declining oestrogen

A

decreases

98
Q

_____ is an option in osteoporosis

A

HRT

Patient (19 decks)

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