week 1 Flashcards
Define the menstrual transition and menopause in physiological terms
menopause- means the last period.
avg age 51.
perimenopause- can last 10 years. hormonal fluctuation and decline.
menopause- 12 months after last period.
postmenopause- time after menopause has occurred.
FSH stims ovaries to produce eggs, and oestrogen/ progesterone. as ageing occurs ovaries are less sensitive to FSH.
Consider which symptoms can be ascribed to the menopause, and relate symptoms to what is known about the physiology
85% of people have symptoms.
75% have vasomotor symptoms. usually last 5-7 years.
hot flushes, night sweats, disrupted sleep, palpitations, aches and pains, forgetfulness, mood changes. vulvovaginal / urinary
drop in serotonin level leads to mood changes.
women less likely to present with exertional chest pain, more at rest. CVD affects smaller vessels in women.
oestrogen helps prevent CHD in women, increased HDL and dec LDL. helps release NO to vasodilate.
oestrogen promotes osteoblastic activity. fall results in perosis
Outline the clinical management of menopausal symptoms
lifestyle- classic: exercise, diet, calcium and vit D. wt management.
hormonal- oestrogen and progesterone if they have a uterus. start low dose and titrate up.
non hormonal- see picture.
Describe the potential health benefits and harms of postmenopausal hormone therapy
studies have shown in young women no inc risk of breast Ca.
oestrogen only- no increasing risk, combined have a little risk.
always use progesterone in women with a uterus.
first hormone to decrease in menopause
AMH (anti-malarial hormone)
but we measure for FSH which increases towards menopause.
discuss genitourinary syndrome of menopause.
List and use the common terminology relating to transgender and gender non-conforming individuals
Describe common conservative and medical support options available to transgender people through the NHS
conservative- mental health support. SALT to help create a voice more appropriate to the patients chosen gender.
Outline the UK law surrounding gender identity and the place of cooperative care between NHS and private healthcare services for transgender people
provide care they are entitled to. share results if same investigation is needed.
cervical screening etc.
same sex wards- ask patients preferance.
describe common surgical support options available to transgender people through the NHS.
Understand the different ways in which gender and / or sex can be defined
genotypic sex (XX)–> gonadal sex (testes/ovaries) –> phenotypic sex (look like) –> legal sex assigned at birth –> gender identity.
Describe the process of sexual differentiation and the chromosomal and endocrine factors that control it
Y chromasone contains sex determining region Y (SRY) codes a protein transcription factor (transcribes itself and other things) - says make a testes.
if absence then cascades occur to create ovaries.
gonads instigate further development.
genital ridge create gonads, - posterior wall of lower T/L area.
mullarian duct - upper vagina and tubes (muller light )
wolffian- epididymiss vas defferens and prostate. (start with both)
these ridges are invaded by 3 layers of cells.
sertoli cells secrete AMH and SRY. mullerian duct wil grow into uterine tubes unless inhibited by AMH. wolffian duct will break down and go unless stimmed by tesosterone.
Relate the process of sexual differentiation to clinical disorders
Which hormones signal which way
need test to stim wolf growth
need AMH to promote muller degen
discuss testosterone in external differentiation,
male
genital tubercle –> glans penis
urethral folds–> shaft of the penis
female
genital tubercle –> clitoris
fold–> labia/ urethra - look up.
sex differentiation summary
outline androgen insensitivity syndrome
think they may be female
present with primary amenorrhoea- lack of body hair
male levels of androgens, don’t respond to them
can be partial or full, varying degrees of penile or clitoral development (small penis, large clitoris)
outline 5 alpha reductase deficiency
testosterone made, but not Dihydrotestostrone.
? inter related marrage.
testes form, amh acts, test acts.
internal structures form.
external does not.
appear mainly female, reach puberty - test spikes- may start masculinising genitalia.
describe turners syndrome.
X O
ovaries
mullarian ducts. no wolfian
female genitalia.
congenital adrenal hyperplasia
in addition discuss carbons in each adrenal hormones.
congenital adrenal hyperplasia- make lots of steroid hormones
exposure of female to steroid hormones.
disorder of 21hydrooxylase (which makes aldosterone, glucocorticoids, cortisol)
continued stim on adrenals from the HPA- excess conversion of cholesterol to androgens (testosterone as no aromatase in fetus)
androgen have 19carbon atoms
progesterones have 21 carbons.
estrogens have 18 carbons.
Describe the hormonal control and principle of feedback in coordinating the hypothalamus -pituitary-gonadal axis
kisspeptin is big, gets cleaved to various lengths (10 most common) sec in the brain to activate kis receptors. may start off gonadotrophin releasing hormone. (releases FSH and LH)
Detail the key hormones of the HPG axis and the mechanisms controlling their synthesis and secretion
FSH and LH - anterior lobes.
Understand the importance of pulsatile GnRH secretion and how this has been pharmacologically exploited
needs to be pulsatile- otherise the response is ceased- as the receptors are all being recycled. - turns on LH and FSH.
fast pulse - favours LH
slow pulses - FSH
Describe the two endocrine processes of puberty
transition from non reproductive state to reproductive state.
Understand the endocrinology control of adrenarche, pubarche and gonarche
noone knows what causes adrenarche- causes hair growth. adrenal androgen secretion.
pulsatile increase starts gonadarche- may be linked to kisspeptin.
Understand the Tanner stages of puberty and physical changes occurring during these 5 stages
Understand the concept of consonance
Differentiate between central and peripheral cause of precocious puberty
central- gonadotrophin-dependant precocious puberty
excess GnRH (idiopathic or 2’)
excess gonadotrophin- pituitary tumor.
central is generally right order
peripheral is wrong order - e.g mutating LH receptor leads to early androgens, no fsh increase.
Recognise major causes of delayed puberty
eating disorders (? need 17-18% body fat to start, 22% to maintain menstrual cycle)
Describe the formation of the follicle from primordial germ cells in utero, with an understanding of how mitosis and meiosis are involved in this
If enter ovary they will become Oocytes. (primary oocytes,)
initially divide by mitosis, then they enter meiosis - will remain in 1st stage meiosis until ovulation of that egg.
mitotic divisions are critical and provide eggs for life.
Describe the process of growth of follicles from the resting primordial follicle to ovulation of a mature oocyte and the time span of this process
oocyte becomes surrounded by protective layers and cells
fetal ovary surrounding cells condense and differentiate into granulosa cells
granular cells secrete an acellular layer called basal lamina- whole structure is called the follicle.
Name the cellular composition of the follicle and the function of each layer
follicle needs oocyte
and granulosa cells
and a secreted acellular layer (basal lamina)
Detail the production of steroids and the compartmentalisation of steroid enzymes in the follicle
vascularisation in the theca allows feedback/forward from pituitary and ovary.
aromatase only present in granulosa cells.
Theca produce progesterone. also pass intermediate mollecules to granulosa to finish into androgens
granulosa estrogen and for 3/4 of cycle progesterone also.
List the events in the follicle and oocyte leading up to ovulation and fertilisation, including the mechanism of chromosome number reduction
spindle pulling causes issues most often in chromasonal division (triesomy etc)
discuss cytoplasmic division in folliculogenesis and oogenesis
only get one mature egg from this division, in sperm you would get 4 sperms.
discuss folliculogenesis
defined as growth and dev of follicles.
most follicles are not growing. after puberty a cohort start growing everyday.
as follicles start to grow granulosa cells multiply and the oocyte secretes another protective acellular zone (zona pelucida- facilitates transfer of nutrients and prevents polyspermy)
FSH drives most folliculogenesis but early stages independent of it.( need FSH to start antral growth)
once growth stared a 2nd layer of cels diff around the basal lamina (the theca) which is vascularised.
breifly summarise folliculogenesis
follicle that is ovulated this month, started growing about 3 months ago!
List the aims of the menstrual cycle
Describe the phases of the menstrual cycle and its endocrinological control
GnRH is pulsatile. if constant LH switched off.
2 phases separated by ovulation. begins on day one- bleeding. 14 day follicular phase.
ovulation
luteal phase.
Describe the processes of follicle selection, ovulation and formation of the corpus luteum
raised FSH presents a window of oppotunity to recruit antral follicles that are at right stage of growth.
one follicule becomes the dominant follicle.
survives FSH fall by acquiring LH receptors on granulosa cells. (other cells do not) also has increased FSH receptor amounts
follicle cells Luetonise- form coppus luteum due to LH surge.
discuss hypothalamic/ pituitary/ ovarian axis in the luteal and follicular phase
luteal phase is progesterone negative feedback dominated.
intra cycle rise and fall of FSH is very important to select a single follicle. E2 leads to a fall in FSH
discuss secretions of the CL and its lifespan
Describe the functional anatomy of the uterine tubes, uterus, cervix and vagina. detail the layers
myometrium - not replaced- estrodiol is main signal. 3 layered of smooth muscle- all diff directions I- circular, M- circle of 8. O - longitudinal.
endometrium - replaceable
Describe the cyclical changes in female reproductive organs co-ordinated by the menstrual cycle
endometrial proliferative phase- follows menses. stromal cell division, max cell div 12-14 days. when greater than 4 mm progresterone receptors are induced.
endometrial secretory phase- (luteal phase) 2-3 days after ovulation, gradual rise in progesterone causes dec in cell division.
glands inc tortousity + distend. glycoproteins and lipids secreted (helps make it receptive for embryo)
vessels become increasingly convoluted to increase surface area.
corpus luteum regresses (can be saved by LH or mimic during pregnancy - hCG) falling steroid leads to menses.
Briefly describe invasive and non-invasive methods of testing tubal patency
lap + Dye- inject dye into uterus. look from outside to see if anything leaks out.
hystero salpingo-contrast sonography. - use ultrasound to monitor dye progress- less invasive.
overview of how the lining is broken down in menses.
discuss changes in cells lining the uterine tubes
discuss changes in mucosa
estrogen causes it to become permissive and allow sperm through
progesterone causes less of it and makes it thicker. glycoproteins form a mesh like structure- barrier to sperm + microorganisms.
one mechanism of oral contraceptives.
