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PHA 332 > sex hormones 1&2 > Flashcards

sex hormones 1&2 Flashcards

1
Q

what are sex hormones?

A

they are all steroid hormones

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2
Q

how are sex hormones synthesized?

A

by cholesterol

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3
Q

are male and female hormones present in both genders?

A

yes in all adults
the female body contains lower levels of testosterone and other androgen
the male body contains low levels of oestrogen

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4
Q

what are the male sex homrones?

A

androgens

testosterone the primary male sex hormone is an androgen

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5
Q

what produces testosterone?

A

mainly leydig cells of the testes and to a lesser extend the adrenal glands produce testosterone and other androgen

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6
Q

when do leydig cells become active?

A

after birth they become quiescent until activated by gonadropins during puberty
at puberty androgens cause the sex hormones to grow and cause secondary characteristics to develop

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7
Q

how does testosterone get secreted/produced?

A

hypothalamus secretes GnRH
GnRH goes via hypothalamo-pituitary portal vesseks
the anterior pituitary secretes FSH and LH
LH caueses leydig cells to produce testosterone
FSH causes sertoli cells to stimulate speromatogenesis
sertoli cells produce inhibin with produces a negative feedback only on FSH
tesosterone produces a negative feedback on LH and GnRH

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8
Q

What stimulates erythropoietin secretion by the kidneys?

A

testosterone

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9
Q

what are the dominant female sex hormones?

A

oestrogen and progesterone- produced by the ovaries

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10
Q

when is hormone production low in females?

A

during foetal development, infancy and childhood

at puberty it is high- sexual development

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11
Q

when are these female sex hormones at the highest?

A

these hormones are produced in higher level during pregnancy

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12
Q

how and why is andorgen produced in females?

A

androgen are produced in small amounts by the ovaries and adrenals and also have important functions in women

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13
Q

what are some of the other effects of oestrogen?

A

stimulates growth of ovary follices
stimulates growth of smooth musle and proliferation of epithelial linings of preproductive tract
stimulates external genitalia growth
stim breast growth
sexual development
stim fluid sex from lipid producing skin glands
stim bone growth and ultimate cessation of bone growth
vascular effects
has feedback on hypothalamus and anterior pituitary gland
stimulayes prolactin secretion but inhibits prolactin’s producing milk-inducing action on the breasts
protects against atherosclerosis by effects on plasma cholesterol, blood vessels and blood clotting

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14
Q

what are the other effects of progesterone?

A

converts oestrogen- ready for inplantation
induces thick, sticky cervical mucus
decreases contraction of fallopian tubes and myometrium
decreases proliferation of vaginal epithelial cells
stimulates breast growth, particularly glandurlar tissue
inhibits milk inducing effects of prolactin
has feedback effects on hypothalamus and anterior pituitary
increases body tem

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15
Q

how does the female reporoductive system work?

A

hypothalamus secretes GnRH -
anterior pit releases FSH AND LH
this stimulates ovaries to produce oestorgen and testosterone

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16
Q

what role does FSH have in the female reproductive cycle?

A

ovarian follicel matures and secretes oestrogen

uterine lining thickens

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17
Q

what role does LH have in the female reporductive system?

A

triggers ovulation
the follicular cells become corpus luteum which secretes progesterone
lining more vascular and glandular

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18
Q

what are the different types of contraception?

A 
coitus interrupts
rhythm method- absense at ovulation
mechanical barriers
chemical barriers
oral/injectible/insertable contraceptives
contraceptive implants
transdermal contraceptives
IUD
surgical method
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19
Q

what are some of the advantages of COC?

A

reliable and reversible
reduced dysmenorrhoea and menorrhagia
reduced indidenced of premenstrual tension
less symptomatic fibroids and functional ovarian cysts
less benign breast disease
reduced risk of ovarian and endometrial cancer
reduced risk of pelvic inflamatory disease

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20
Q

what is a monophasic COC?

A

fixed amount of an oestrogen and a progestogen in each active tablet

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21
Q

what is a bi/tri/quadraphasic COC?

A

varying amounts of the two hormones according to the stage of the cycle

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22
Q

what are the two types of oestrogen used in combined ?

A

ethinyl estadiol and mestranol

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23
Q

what is mestranol?

A

it is a prodrug that is converted in vivo to ethinyl estradiol

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24
Q

what is the usual oestrogen content of ethinylestradiol?

A

20-35ug

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25
Q

what are the different types of progestogen?

A

first- norethisterone- NET
second- levonorgestrel-lgn
3rd- desogestrel, gestodene, norgestimate
new/other: drospirenone, dienogest, nomegestrol acetate

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26
Q

how is a COC chosen?

A

chosen with the lowest oestrogen and progestogen content
well tolerated=good control
usually 21 days and 8 pill-free days- withdrawl bleed

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27
Q

how does the COC work?

A

oestrogen inhibits secretion of FSH via negative feedback on the anterior pituitary and thus suppresses development of the ovarian follicle
progestogen inhibits secretion of LH and thus prevents ovulation; it also makes the cervical mucus less suitable for the passage of sperm
they work in combination to alter the endometrium in such a way as to discourage implantation

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28
Q

how does the COC work on different parts of female reporductive system?

A

fallopian tuve- progestogen inhibits motility, oestrogen enhances motility causing abnormal reates of ovum transport
ovary- oestrogen inhibits ovulation by blocking gonadotrophin surge;progestogen much weaker but has same effect
endometrium- sustained levels of oestrogen or progestogen cause asynchromous development less receptive to implantation
cevical mucus- progestogen causes secretion of thick vuscoid mucus hostile to sperm

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29
Q

what are common s/e of COC?

A

weight gain
mild nausea, flushing,dizziness, depression or irritability
amenorrhoea of variable duration on cessation of taking the pill
dec breast milk prod

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30
Q

what are some C/I of COC?

A

vte
major surgery with prolonged immobilisation
ATE
TIA
history of migrane with aura
hiigh risk of thromboembolism
presence or history of severe hepatic disease as long as liver function values have not returned to normal
presence or history of liver tumours
known or suspected sex-steroid malignancies
undiagnosed vaginal bleeding
hypersensitivity to active substances or to any of the excipients

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31
Q

what is the causes of abdominal pain with COC?

A

gallstones, blood clot, pancreatitis

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32
Q

what does POP contain?

A

one active ingredient- progestogen- norethisterone or levonoregestrel

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33
Q

how should a POP be taken?

A

taken continuously- no break

offered as alt when oestrogens are c/i

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34
Q

what are some of the advantages of POPs?

A

alt to oestrogens
can be used at any age
useful in smokers and those 35 years and over
may help with premenstrual symptoms and painful periods
can be used in breastfeeding

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35
Q

when should you start a POP?

A

started on the first day of menses and taken at same time each day

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36
Q

what is the mechanism of action of POP?

A

mainly acts on cervical mucus which is made in hospitable to sperm
progestogen probably also hinders implantation through its effect on the endometrium of the fallopian tubes

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37
Q

what are the C/I for POPs?

A

active venous thromboembolic disorder
presence or history of sever hepatic disease as long as liver function values have not returned to normal
known/suspected sex-steroid malignancies
undiagnosed vaginal bleeding
hypersensitivity to the active substance or to any of the excipients
allergic to peanut or soya

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38
Q

what is levonelle 1500?

A

also called one step
it is a EHC
contains high dose progesterone-levonorgestrel
taken up to 72 hours after upsi
preferbly within 12 hours
prevents ovulation- not effective once implantation has begun

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39
Q

how does ulipristal acetate 30mg work?

A

high affinity to the progesterone receptir
m/a- delay of ovulation via suppression of the LH surge
it is able to postpone follicular rupture in some women
up to 120 hours after UPSI
another taken if vomiting occurs within 3 hours

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40
Q

what is menopause?

A

it is a biological stage in a woman’s life that occurs when she stops menstruating and reaches the end of her natural reproductive life
usually when a woman has not has a period for 12 consecutive months

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41
Q

what are the changes associated with menopause that occur in a womans body?

A

the ovaries stop maturing eggs and stop secreting oestrogen and progesterone

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42
Q

what is perimenopause?

A

woman has irregular cycles of ovulation leadung up to menopause and continuing until 12 months after her final period- i.e. the transition period

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43
Q

what are the symptoms that occur in menopause?

A 
hot flushes
vaginal dryness
atrophy of breasts
depression
loss of libido
loss of self esteem
weight gain
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44
Q

what is vasomotor and urogenital?

A

vasomotor- hot flushes, night sweats, formicatin

urogenital- dry vagina, atrophic baginitis, dyspareunia, local microtrauma, incontinence

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45
Q

what changes occur in elacticity of the skin and support tissues in menopause?

A

loss of elasticity of skin and support tissues- worsening prolapse, loss of breast tissue, wrinkling

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46
Q

what effect does menopause have on the bones?

A

may cause osteopenia/ osteoporosis

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47
Q

what causes hot flushes?

A

oestrogen withdrawl affects the central- adrenergic system. this causes release of catecholamines and prostaglandins that produce hot flushes
LH is released coincoided to hot flushes

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48
Q

what are some hot flush triggers?

A 
cigarette smoking
alcohol
caffine
stress
heat
hot spicy foods
exercise
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49
Q

what happens to fsh at the menopause?

A

at the menopause ovaries no longer respond to FSH

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50
Q

what advice would you give for menopause lifestyle planning?

A 
diet
exercise
stop smoking
interpersonal relationshops
stress relief and relacation
holistic approach
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51
Q

when is hormone replacement therapy given?

A

normally given to women who have intact uterus either alone or in combination with progesterone

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52
Q

what ways is HRT given?

A

oestrogen used in HRT can be given orally, vaginally as a pessary and cream- oestriol, by transdermal patches- oestradiol, or subcutaneous implant-oestradiol

53
Q

does HRT provide contraceptive cover?

A

no- potentially fertile for 2 yr if she is below the age of 50 years and 1 year if she is over the age of 50

54
Q

what does HRT increase the risk of?

A

increases the risk of endometrial, breast and ovarian cancer

breast cancer

55
Q

what does oestrogen stimulation cause?what should a woma with a uterus thus be given?

A

causes proliferation of the endometrium increasing the risk of malignancy.
woman with uterus should also be given progesterone mostly 14 days of the cycle only

56
Q

what will all women who have not had a hysterectomy be advised to take?

A

combied HRT- oestrogen and progestogen

57
Q

what should women who have had an endometrial ablation be advised to take?

A

progestogen in cause any part of the endometrium is left

58
Q

does one bleed in HRT cycle? what influences it?

A

the way progestogen is taken along with oestrogen determines whether or not HRT will lead to bleeding
by adding progetogen for 10-14 days a month; a bleed occurs in the days following this course similar to that of a natrual cycle

59
Q

what is the continuous combined HRT?

A

HRT that give continuous progestogen with the oestrogen have been developed to avoid bleeding altogether.
thought to reduce risk of endometrial cancer
this can be used in postmenopausal

60
Q

how does the timing of progestogen affect bleeding?

A

10-14 days in a month- monthly bleed
14 days every 13 weeks- bleed every 3 months
continuous- no bleed

61
Q

what is there an increased risk of for patients taking HRT?

A

CV disease
stroke and venous thromboembolism
c/i in breast cancer- clonidine used

62
Q

what is tibolone?

A

prodrug with weak oestrigenic, progestrogenic and androgenic activity
pre-dominantly oestrogen effects

63
Q

what does tibolone do?

A

in breast tissue, it inhibits the enzyme responsible for activation of its metabolites
in the endometrium it activates progestrogen and androgen receptors without the stimulation of endometrium and bleeding
post menopausal bone loss is prevented and reduces post menopausal symptoms

64
Q

when is tibolone not given?

A

to women who are within 12 months of their last period

65
Q

what is ralocifene?

A

it is a selective oestrogen receptor modulator-SERM
it binds to both types of oestrogen receptors ERa and ERb
oestrogenic activity on the bones and lipids but anti-oestrogenic on breast and uterine receptors
inc bone mineral density but no effect on post menopausal symptoms

66
Q

what are the s/e of raloxifene?

A

hot flushes and leg cramps

67
Q

what are the benefits of using raloxifene?

A

reduction in the risk of oestrogen positibe breast cncer in post menopaisal women
risk of vertebral fractures is reduced by around 40%

68
Q

who is raloxifene recommended for?

A

women who have a vertebral fragility fracture and cannot take a bisphosphonate or those who have had a fragility fracture after at least 1 year of treatment with bisphosphonate

69
Q

what does raloxifene increase the risk of?

A

increases risk of venous thromboembolism- especiallly during first 4 months of treatment

70
Q

how can one tell if they are post menopausal?

A

80% are post menopausal by the age of 50
if periods stopped at an earlyage
if blood tests have showed raised levels of FSH

71
Q

When would you treat women for their sympyoms locally? what would you give?

A

people who wish to not use or cannot take systemic HRT

oestrogen can be given locally to the vagina in the form of a low dose cream, pessary, tablet or ring

72
Q

why is progestogen not needed in local symptom treatment?

A

since local doses of oestrogen do not affect the endometrium

73
Q

what are the side effects with HRT?

A

short term- breast tenderness, leg cramps, nausea, irritability and depression
irregular bleeding/ spotting in first 4-6 months- combined

74
Q

what are the treatment options for people not on HRT?

A

vasomotor symptoms- paroxetine, fluoxetine, citalopram, venladaxine or clonidine
vaginal dryness- vaginal lubricant or moisterriser
psycholohical symptoms- self help groups, counselling antidepressants, psychotherapy

75
Q

how do you diagnosed menopause?

A

usually 45+ done by stmptoms

can measure FSH- can be misleading

76
Q

what does an inc conc of FSH suggest?

A

ovarian failre- but does not indicate an inability to conceive

77
Q

what drugs are used to modift pregnant uterus and cervix?

A

oxytocin is administered as a slow IV infusion to induce or augment labour/ IM OR IV for prevention and treatment of uterne atont and postpartum haemhorrhage
vasopressin- prolonged admin- pulmonary oedema, fluid overload and water intoxication

78
Q

what are the prostaglandins that affect the female reproductive system?

A

misoprostol, gemeprost, dinoprostone and carboprost

79
Q

what are prostaglandins used to stimulate?

A

contractions of the myometrium to induce medical termination of pregnancy after pre-treatment midepristone OR prime the cervix prior to surgical termination of pregnancy
cervical priming of induction of labour
treatment of postpartum haemorrhage

80
Q

what are tocolytics?

A

they stop uterine contractions, postpone delivery of the infant and allow adequate time to administer corticosteroids to promote lung maturation in the baby

81
Q

give some exaamples of tocolytics?

A

atosiban, b adrenoreceptor agonist, CCB and cox inhibitor

oxytocin antagonist atosiban blocks affects of oxytocin on myometrium0 IV

82
Q

how does b2 adrenoreceptor work as a tocolytic?

A

salbutamol and terbutaline sulfate- eg
bind to b2 receptors on myometrial cell membrane which activates adnylaye cyclase leads to increase levels of cAMP and decreases intracellular calcium leading to relaxation of the uterus

83
Q

how does a CCB work as a tocolytic?

A

nifedipine- decreases contractile activity of the uterus by inhibiting entry of calcium into cells through slow calcium channels in the cell membrane

84
Q

how does COX inhibitor work as a tocolytic?

A

reduces prostaglandin production and consequently decreases uterine contractions

85
Q

what are some ovulation induction agents? how do they work?

A

clomiphenen and tamoxiden- oestroegn receptor antagonists

prevent negative feedback of oestrogen causing sec of FSH and LH

86
Q

how is clomiphene - ovulation inducing agent taken?

A

used sub-ferbially and is taken once a day for 5 days starting within 5 days of menstruation

87
Q

how does tamoxifen , an ovulation induction agent used?

A

can be used as a sub-fertility agent and also as an adjuuvant in oestrogen dependant tumours such as breast cancer
taken once a day on day 2,3,4,5 of cycle

88
Q

how is metformin used as an ovulation induction agent?

A

is used in obese insulin resistant women for polycystic ovary syndrome

89
Q

how does danazol- an ovulatio suppression agent work?

A

inhibits pituitary gonadotriphin release thereby reducing ovarian function and producing atrophy of endometrium
blocks oestrogen and progesterone receptors

90
Q

when should danazol be avoided?

A

during pregnancy

91
Q

what is the clinical use for danazol?

A

endometriosis, menorrhagia and pain benign fibrocystic breast cancer

92
Q

what are the s/e of danazol?

A

acne, hisutism and voice change

93
Q

what treatment would you give for benign prostatic hyperplasic in men?

A

alpha blockers- tamsulosin and 5a reductase inhibitors- finasteride and duasteride

94
Q

what treatment would you give for an overactive bladder ?

A

m3 receptor antagonists- solifenacin; b3 receptor agonists- mirabegron

95
Q

what treatment would you give for postate cancer?

A

anti-androgens( cyproterone acetate) and GnRh analogues- goserelin and buserelin

96
Q

what treatment would you give for erectile dysfunction?

A

PDE5 inhibitors- sildenaful, tadalafil and varenafil and alprodastil

97
Q

what is benign prostatic hyperplasia?

A

enlargement of the prostate gland that leads to several symptoms in the male reproductive system such as poor stream, hesitancy and nocturia

98
Q

how is benign prostatic hyperplasia treated?

A

treated by a1 adrenoreceptor blockers and 5a reductase inhibitors

99
Q

how do a1 adrenorecptor blockers work? give example?

A

alfuzosin, prazosin, tamsulosin
-relax smooth muscle and improve urinary flow
caution in patients with hpt
s/e- tachycardia, palpitations, dizziness and retrograde ejaculation

100
Q

how does 5areductase inhibitors work- give examples?

A 
dutasteride and finasteride
the enzyme 5a reductase converts testosterone into active metabolite dihydrotestosterone which activates the androgen recptor
2 isoforms- type one and 2
duasteride blocks bloth 1 and 2
finasteride only blocks 1
101
Q

how much can 5 alpha recutase inhibitors shrink the prostate?

A

about 20%

can also give combination of duasterude and tamsulosin if severly enlarged prostate

102
Q

how does the anticholinergic agents work to treat an overactive bladder? give examples

A

oxybutinin, solifenacin and tolterodine
block the muscarinic acetylcholine receptor and are used in the treatment of overactive bladder
m2 is predominant in the detrusor muscle
m3 seems to be involved in micturition

103
Q

what s/e occur with anticholinergic agents?

A

dry mouth, blurred vision, constipation and drousiness
solifenacin can aslo prolong the QT interval
c/i - renal failure, closed angle glaucoma and hepatic dysfucntion

104
Q

how does mirabegegron work?

A

it is a b3 adrenoceptor agonist
recommended for people who rest are inneffective/ c/i or not tolerated
causes relacation of the bladder smooth muscle
stim of the b3 adrenoceptors in the bladder increases mean void volume per micturition and decreases freq on non-voiding contractions

105
Q

what are the s/e of mirabegron?

A

arrhythmias, constipation, diarrhoea, dizziness, headache, inc risk of infection, nausa

106
Q

how are antiandrogens used to treat prostate cancer?

A

steroidal- cyproterone acetate or non-steroidal- flutamide and bicalutamide
competitively bind to androgen receptor and suppress the androgen mediated gene expression
cyproterone also acts on androgen rec in pituitary suppressing LH dependent production of androgens

107
Q

what are the s/e of anti androgens?

A

breast tenderness, gynacomastia, erectile dysfunction adn depression
non-steroidal- GI upset and hepatic dysfunction

108
Q

what is Erectile dysfunction?

A

also called impotence- defined as the inability to maintain and achieve an erection for satisfactory intercourse

109
Q

what are some disorders that may cause ED?

A

vasculogenic- CV disease/ hpt/ diabetes smoking
neurogenic- MS/ parkinsons/ tumours / stroke
anatomical- peyronies disease/ hypospasdias
hormonal- hypogonadism/ cushings disease/ hypothyroidism/ hyperthyroidism
drugs- diuretics/ anti-hpt/ antidepressants/ cytotoxics/ alcohol
psychosocial- relationship prob/ mental health

110
Q

what is the inital assessment for ED?

A

sexual history- desc of problem/ duration/ symptoms
current medical/ psychiatric and surgcial history
current relationshop status, history of previous sexual partners and relationships
sexual orientation and gender identity
alcohol, smoking and ilicit drug misuse

111
Q

what does the physical examination of ED include?

A

body weight, waist, circumference, HR, blood pressure
exam of henitalia- may reveal hypogonadism or malformation - peyronieses/ enlarged prostate
serum liid and fasting glucose levels and serum free tesosterone

112
Q

who are the ED referals to a specalist?

A

urology- young men, mostly with tramua to genitalia, pelvis or spin, or abnormalities , no response to max dose of at least two pde5 inhibitors
to endocrinology- hypogonadism syspected
cardiolgy- if cv disease
if mental health services- if psychogenic cause is suspected

113
Q

what is the treatment of ED?

A

identify cause and treat any curable cause
lifestle change and risk factor modification
patient counselling to patient and partner

114
Q

what would be the identifiable causes of ED?

A 
hormonal
post traumatic
drug induced
partners sexual prob
radial prostectomy
115
Q

what is hypogonadism and testosterone replacement therapy?

A

determine cause before treatment with testosterone

116
Q

how does hypogonadism and testosterone therapy work?

A

a 6 month trial of testosterone replacement therapy may beusefyl in men who have serum testosterone level of less than 12nmol/l

117
Q

what are the various forms of testosterone available?

A

long acting testosterone injection- every 3 months

transdermal testosterone gel- applied daily

118
Q

what role does nitric ocide have in ED?

A

l-arginine combined with eNOS and nNOS cause a sexual stimulation and lead to the production of nitric oxide
this activates theguanylate cyclase - with gmp to produce cGMP
this gives cGK
and this does not give an errection

119
Q

what are the PDE 5 inhibitors responsible for? how do they work?

A

inhibit phosphodiesterase 5 which is responsible for the breakdown of cGMP
cGMP relaxes the smooth muscle and increases blood flow to the corpus cavernosum

120
Q

do pde5 inhibitors cause a chemical errection?

A

no- sexual stimulation is still needed to cause the initial release of nitric oxide which stimulates the synthesis of cGMP

121
Q

what is the half life, time taken and side effects of dildeafil?

A

half lifr- 4 hr
time taken- 30min-4 hr
s/e- headache, flushing, bluish vision, dyspepsia

122
Q

what is the half life of tadalafil, time taken and s/e?

A

half life- 17.5hr
12 hour onset
headache, dyspepsia, backpain, myalgia

123
Q

what is the half life, time taken and s/e of vardenafil?

A

half life- 4 hours
time taken- 1 hour
s/e- headache, flushing, flu synome, rhinitis

124
Q

when should dosages for pde-5 inhibitors be lowered?

A

in patients who take potent P450 CYP3A4 inhibitors

125
Q

when is PDE-5 inhibitors c/i?

A

in patients who use nitrates- cautious in patients who take alpha blockers for HPT or benign prostatic hyperplasia

126
Q

what are the ADR from vacuum erection device?

A

bruising, local pain and failure of ejaculation

127
Q

what is first and second line/ 3rd treatment for ed?

A

first- vacuum pump
second- intravenous injection therapy- intrauethral alprostadil
or topical alprostadil
3rd- penile prosthesis

128
Q

how does alprostadil work?

A

stable for of prostaglandin E1
powerful vasodilator
effective for psuchogenic and neuropathic ED
inc the inflow and recudes venous outflow by contracting the corporal smooth muscle that occuldes the draining venules

129
Q

who is penile prosthesis offered to?

A

patients who are
unwilling to consider medical therapy or external device
failing to respond
unable to continue

PHA 332 (42 decks)

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