Menstrual Disorders Flashcards
HPO Axis
Hypothalamus secretes GnRH in a pulsatile fashion to stimulate LH and FSH secretion by Pituitary gland
o High levels of Oestrogen in Late-Follicular phase acts as a Positive feedback
mechanism to produce a Periovulatory LH surge from Pituitary
o Low levels of Progesterone have a Positive Feedback effect on Pituitary LH and FSH;
High levels, as seen in Luteal phase, Inhibit LH and FSH production
Follicular Phase
FSH levels rise in first few days of Menstrual Cycle when Oestrogen, Progesterone
and Inhibin Levels are low; This stimulates a small cohort of Antral Follicles to grow
o Follicles comprise Theca and Granulosa cells; LH stimulates Androgen production in
Theca cells, which is Aromatised into Oestrogens by Granulosa cells under the
influence of FSH
o As Follicles grow and Oestrogen secretion increases, Negative Feedback on the
Pituitary decreases FSH production – Allowing for selection of Dominant Follicle
▪ Follicle with most efficiency Aromatase activity and Highest Concentration of
FSH-induced LH receptors most likely to survive when FSH levels drop
What is inhibin
Secreted by Granulosa cells, which downregulates FSH and enhances
Androgen synthesis; Activin has the opposite action
LH Surge
end of Follicular phase, Dominant Follicle has grown to about 20mm Diameter; FSH induces LH receptors to compensate for lower FSH levels
o Production of Oestrogen increases until they reach necessary threshold to cause
Positive Feedback onto Hypothalamus and Pituitary, causing the LH surge
Progesterone produced by Dominant Follicle in response to rising LH – Adding further
to positive LH feedback and small, Periovulatory rise in FSH
o LH surge stimulates Resumption of Meiosis in Oocyte prior to Ovulation
Ovulation
Occurs after Breakdown of Follicle wall under the influence of LH, FSH,
Progesterone-controlled Proteolytic enzymes (e.g. Plasminogen Activators and
Prostaglandins); Inflammatory response leads to Extrusion by stimulating Smooth Muscle
Luteal Phase
Remaining Granulosa and Theca Cells then form Corpus Luteum
o Extensive Vascularisation (aided by local VEFG production) to supply Granulosa cells
for continued Steroidogenesis
o Progesterone stabilises the Endometrium in preparation for pregnancy; Progesterone
also suppresses FSH and LH secretion to inhibit further Follicular growth
o In the Absence of β-HCG produced by Implanting Embryo, Corpus Luteum undergoes luteolysis; Less sensitive to LH, produces far less Progesterone and regresses
eventually
Withdrawal of Progesterone leads to Endometrial Shedding =Menstruation
Proliferation Phase of Endometrium
Glandular and Stromal Growth occurs –
Change from Columnar cells to Pseudostratified Epithelium; Endometrial
Thickness rises rapidly, from 0.5mm at Menstruation, to 3.5 – 5mm at end of
Proliferative Phase
Secretory Phase of Endometrium
o Following Progesterone Surge, Oestrogen-
induced Proliferation is Inhibited
o Decidualisation (Formation of Specialised
Glandular Endometrium)
▪ Increased Tortuosity of Endometrial Glands, Spiral Artery growth, Fluid
secretion into Glandular Cells and Uterine Lumen
What causes menstruation
Loss of Tissue Fluid, Vasoconstriction of Spiral Arterioles and Distal Ischaemia leading to
Tissue Breakdown; Menstruation is the shedding of Endometrium in response to Progesterone withdrawal; Bleeding stops as the Endometrium regenerates (around day 5 – 6)
Normal Menstrual Cycle
Cycles vary but usually 21-32 days with basically regular pattern
Variation occurs during Follicular phase
Bleeding can be for 1-7 days
Pain occurs due to vasospasm and ischaemia
Primary Amenorrhoea
Absence of menstruation by age 16 in presence of secondary sexual characteristics
or age 14 in their absence
Secondary Amenorrhoea
Absence of menstruation for 6 months
Investigating Amenorrhoea
Pregnancy test FSH/LH (Raised in POF, Low in hypothalamic causes) Testosterone and SHBG (PCOS) Prolactin TFTs USS Pelvis Karyotyping if suspected Turners
Causes of Amenorrhoea
Hypothalamic: Stress, Anorexia, Excessive Exercise, SOL, Intervention, Kallman’s
Ovarian Dysgenesis
Physiological: Pregnancy, lactation, menopause, iatrogenic-contraceptives, HRT, GnRH analogues
Pituitary: Tumours, Surgery, Sheehan’s
Ovarian: PCOS, POF
Genital Outflow Obstruction: Imperforate septum, Asherman’s, stenosis
Hyperprolactinaemia, Cushing’s, Severe hypo/hyperthyroid, CAH, AID, Oestrogen or androgen-secreting tumours
Oligomenorrhoea
Cycles lasting longer than 32 days
Transient: Self limiting, typically related to stress or emotional factors
PCOS most common cause
Other causes: Low BMI, obesity, ovarian resistance
