Reproductive Lifespan Flashcards
What are the primary and secondary sexual characteristics?
PRIMARY = internal & external genitalia, sex chromosomes
SECONDARY = pubic hair growth
- male = genital development, spermatogenesis
- female = breast development, menstruation
What are the different stages of female puberty?
8-13yrs
- THELARCHE = breast development (begins at ~9-13yrs and continues to ~12-18yrs)
- Prepubertal —> Breast bud —> Juvenile smooth contour —> Areola & papilla project —> Adult
- ~12 months between stages
- Tanner staging of breast develoment - ADRENARCHE = pubic hair growth along labia and up as a triangle (begins at ~9-14yrs and continues to ~12-16yrs)
- MENARCHE = onset of menstruation cycle (~11-15yrs)
- GROWTH SPURT = peak growth velocity at ~10-13yrs but completed earlier than males (shorter timespan)
- ended by fusion of epiphyses
What are the different stages of male puberty?
9-14yrs
- GONADARCHE = growth of external genitalia (onset of puberty —> 6yrs)
- Pre-adolescent —> Lengthening of penis —> Further growth in length/circumference —> Development of glans penis & darkening of scrotal skin —> Adult
note: increased testicle size due to FSH-induced increase in seminiferous tubules
2. ADRENARCHE = pubic hair growth from base of penis to medial thighs (shortly after gonadarche)
3. SPERMATOGENESIS
- GROWTH SPURT = peak growth velocity at ~12-17yrs, starts ~12 months after first signs of puberty, starts after females but lasts longer
- ends when epiphyses fuse
+ nocturnal emission/ejaculation
note: high intra-testicular levels of testosterone are needed for spermatogenesis
How is the timing of puberty controlled?
Prior to puberty:
- possibly due to increased sensitivity of the hypothalamus to negative feedback
- possibly the central mechanisms of the hypothalamus have not matured yet
note: hypothalamus does not produce GnRH and does not respond to stimuli which would normally increase GnRH in the post-pubertal adult
- oestrogen is unlikely to be the main cause of menarche, as the average age of menarche has reduced over time (1800s = 17yrs, 2010s = 13yrs)
How is the onset of puberty controlled?
Steady increase in GnRH secretion —> steady increase in FSH & LH
- menarche: increase in FSH —> follicular development —> beginning of menstrual cycle
- growth spurt: depends on GH & steroid hormones in both sexes, but testosterone is more potent than oestrogen (oestrogen closes epiphyses earlier in females)
- thelarche: stimulated by oestrogens
- adrenarche: stimulated by androgens in both sexes (source of androgens is from the adrenal gland in females)
- gonadarche (male): stimulated by testosterone
note: adrenal testosterone is different to testis-derived testosterone but stimulates the same processes
note: testosterone can be converted to oestrogen in some tissues (in significant amounts —> gynaecomastia)
Define precocious puberty, and give some examples of causes.
Development at an early age (before 8yrs) of the physical & physiological changes associated with puberty
- majority idiopathic
- neurological: early stimulation of central maturation e.g. pineal tumours (+++melatonin), meningitis (inflammation stimulates early rises in GnRH)
- true precocious puberty due to uncontrolled secretion of gonadotrophs/steroid hormone secretion e.g. hormone-secreting tumours, CNS lesions, post-encephalitis, neurofibromas, congenital adrenal hyperplasia, etc.
note: earlier fusion of epiphyses occurs —> reduced height as an adult
What defines the end of reproductive life in the male and female?
Male: no obvious event; spermatogenesis continues until ~60-70yrs
Female: menopuase/climacteric = when the ovaries cease to produce an ovum every 4wks, therefore menstruation ceases and the woman is no longer able to bear children
- PRE-MENOPAUSE (~40yrs)
- follicular phase shortens —> less oestrogen & inhibin secreted ———> reduced negative feedback —> increased LH & ++FSH (FSH affected by oestrogen & inhibin) —> reduced fertility —> ovulation can be early or absent - MENOPAUSE (~50yrs; variable)
- primordial follicles have been used up
- great decrease in oestrogen & inhibin —> increase in LH & +++FSH - POST-MENOPAUSE
Give some examples of effects of the menopause.
- “hot flushes” (~80%) = transient rises in skin temperature & flushing due to reduced oestrogen
- regression of endometrium & shrinkage of myometrium
- vaginal rugae lost
- involution of some breast tissue
- changes in skin (could be due to age) e.g. dryness, loss of collagen (wrinkles), thinning skin, hyperpigmentation
- changes in bladder (could be due to age) e.g. increase in freq., urgency, incontinence
- reduction in bone mass by ~2.5%/yr for several years due to loss of oestrogen —> osteoporosis
How can symptoms of the menopause be managed? What are the disadvantages of this treatment?
Hormone replacement therapy (oral/topical/gel) = combination of oestrogen +/- progesterone +/- progestin
Minimises symptoms of menopause, particularly osteoporosis
note: no longer advised for cardioprotection
Disadvantages:
- increased risk of breast/ovarian/uterine cancer due to constant proliferation of endometrial cells (hence oestrogen only preparations only given to women who have had a hysterectomy; progesterone inhibits this process)
- increased risk of stroke (therefore not recommended in previous stroke/DVT)
What is the average amount of blood lost per menstrual cycle? How can you assess whether menstrual blood loss is sufficient to cause adverse effects?
~ 30-45ml
NICE = heavy menstrual loss that interferes with a woman’s physical/social/emotional/quality of life
Menstrual loss greater than 80ml which will produce anaemia
Assess by pad and tampon counts & by measuring Hb/haemocrit levels
What is amenorrhoea? Give some examples of primary and secondary causes.
AMENORRHOEA = absence or stopping of menstrual periods
- PRIMARY: absence of menses by age 14yrs WITH absence of secondary sexual characteristics
- SECONDARY: established menstruation has ceased for 3 months in a woman with a history of regular cyclic bleeding and 9 months in a woman with a history of irregular bleeding
CAUSES: Most common causes of secondary amenorrhoea are pregnancy & menopause
Outflow tract obstruction:
- PRIMARY = uterine —> Müllerian agenesis (15% of cases)
= vaginal —> vaginal atresia, cryptomenorrhoea (severe cyclic abdominal pain in association with amenorrhoea), imperforate hymen
- SECONDARY = intrauterine adhesions e.g. Asherman’s syndrome - adhesions/fibrosis of endometrium e.g. due to dilatation & curretage of intrauterine cavity
Gonadal/end-organ disorders:
- PRIMARY = gonadal dysgenesis (most common cause is Turner’s syndrome), androgen insensitivity syndrome (testicular feminisation syndrome), receptor abnormalities for FSH/LH, specific forms of congenital adrenal hyperplasia
- SECONDARY = pregnancy (most common cause), anovulation, menopause (normal or premature), PCOS, drugs
Pituitary/hypothalamic/central regulatory disorders:
(inadequate FSH —> inadequate stimulation of ovaries
reduced oestrogen —> no endometrium stimulation)
- PRIMARY = Kallman syndrome - hypothalamic neurones responsible for GnRH secretion fail to migrate into the hypothalamus during embryonic development
- SECONDARY = hypo/hyperthyroidism, hypothalamic (exercise amenorrhoea, stress amenorrhoea, obesity, anorexia nervosa, bulimia), pituitary (haemochromatosis, hyperprolactinaemia, Sheehan syndrome - hypopituitarism due to ischaemic necrosis caused by blood loss & hypovolaemic shock during/after childbirth)
How should amenorrhoea be investigated and managed?
Investigations/history:
- menstrual history
- ?pregnancy
- ?contraception
- surgery
- medications
- stress
- diet
- chronic diseases
- weight change/BMI
- hair distribution
- thyroid function
- visual fields (pituitary disorders present as bilateral hemianopia)
- ?breast discharge
- ?abdominal masses/tenderness
- family history: age at menopause, thyroid dysfunction, diabetes, cancer
Management:
- rule out pregnancy
- levels of TSH, prolactin, FSH, LH (ovarian-axis)
- levels of testosterone (hirsutism)
- chronic disease: LFTs etc.
- CNS involvement: MRI
What is menorrhagia? Give some examples of causes.
Heavy vaginal bleeding not due to dysfunctional uterine bleeding (diagnosis of exclusion) = excessive (80ml+) & prolonged regularly (7days+)
Causes:
- most commonly due to distortion of the uterine cavity e.g. presence of fibroids (increases s.a. of endometrium) —> uterus unable to contract down on open venous sinuses in the zona basalis
- coagulation disorder
- endometrial carcinoma
- inflammation of endometrium e.g. intrauterine disease, PID
- pregnancy complications
How should menorrhagia be investigated and managed?
Investigations/history:
- FBCs for ?anaemia
- ?obesity
- ?androgen excess e.g. hirsutism, acne
- ?ecchymoses/purpura
- thyroid exam
- liver/spleen exam
- pelvic/uterine/cervical exam
Management:
- combined oral contraceptive pill
- progestrogens
- intra-uterine device
What is dysfunctional uterine bleeding? Give some examples of causes.
Abnormal bleeding with no obvious organic cause e.g. no pregnancy, pelvic disease, or systemic disease (therefore it is a diagnosis of exclusion)
Usually anovulatory
Changes in length of menstrual cycle due to disturbance to HPO axis: no progesterone withdrawal from an oestrogen-primed endometrium —> endometrium builds up and breaks down erratically
Causes:
- extremes in reproductive life
- PCOS
