OG23.1-3,OG24.1,OG25.1 | Puberty and Menstrual Disorders — Practice Quiz

Correct. Thelarche (breast budding, Tanner B2) is typically the first sign of puberty in girls, occurring around age 8–13. It is driven by rising oestradiol from the developing follicles. The growth spurt in girls occurs early (Tanner B2–B3), unlike boys where it occurs later. Menarche follows approximately 2–2.5 years after thelarche.

Normal pubertal sequence in girls: thelarche (B2) first → pubarche → growth spurt → menarche. Growth spurt occurs early in girls (Tanner B2–B3), about 6–12 months before menarche.

The correct answer is B — thelarche. The normal sequence is: thelarche → pubarche → peak height velocity (growth spurt) → menarche. Menarche is the last major event, not the first.

Correct. Tanner staging for breast (B) and pubic hair (PH) each uses 5 stages (1–5). B1 = prepubertal; B2 = breast bud; B3 = breast mound enlarges; B4 = areola forms secondary mound; B5 = adult contour. Similarly, pubic hair PH1–PH5.

Tanner staging: breast B1–B5 and pubic hair PH1–PH5. B2 = onset of thelarche; B5 = adult. Both axes are assessed independently.

Both breast and pubic hair Tanner staging use 5 stages (1–5). B1 is prepubertal, B5 is adult.

Correct. Constitutional delay of growth and puberty (CDGP) is the most common cause of delayed puberty in girls, accounting for the majority of cases. It is benign, often familial, and resolves spontaneously. Turner syndrome and Kallmann syndrome are important pathological causes but far less common overall.

Most common cause of delayed puberty in girls = Constitutional Delay of Growth and Puberty (CDGP). Features: positive family history, bone age delayed, FSH/LH low-normal, will self-resolve. Requires expectant management.

CDGP is the most common cause of delayed puberty. Turner syndrome and Kallmann syndrome are important to diagnose but are less frequent causes overall.

Correct. Elevated (hypergonadotrophic hypogonadism) FSH and LH with absent puberty localise the failure to the gonads — the pituitary is working hard but the gonads do not respond. Turner syndrome (45,X0 or mosaic) is the most common cause of hypergonadotrophic hypogonadism in girls. Management includes oestrogen replacement and, importantly, cardiac MRI (not just echo) to screen for aortic arch anomalies.

FSH/LH interpretation in delayed puberty: HIGH = gonadal failure (Turner syndrome, gonadal dysgenesis); LOW = central/hypothalamic failure (CDGP, Kallmann, functional). Localises the level of axis failure.

Elevated FSH/LH = hypergonadotrophic hypogonadism = gonadal failure. CDGP and Kallmann syndrome have low or normal FSH/LH (hypogonadotrophic). Turner syndrome is the classic cause of gonadal failure in girls.

Correct. Precocious puberty in girls is defined as development of secondary sexual characteristics (breast development, pubic hair) before age 8 years. (For boys the cut-off is age 9 years.) The majority (80–90%) of central precocious puberty in girls is idiopathic, but brain MRI is still mandatory in every case.

Precocious puberty: girls <8 years, boys <9 years. 80–90% of central PP in girls is idiopathic. Brain MRI is mandatory for all central PP to exclude hypothalamic hamartoma/glioma/craniopharyngioma.

The cut-off for precocious puberty in girls is before age 8 years. In boys it is before age 9 years. Age 9 is for boys.

Correct. In central (GnRH-dependent) precocious puberty, the HPO axis is prematurely activated. GnRH stimulation produces an adult-pattern pubertal LH response — LH rises to >5 IU/L (pubertal response) and the LH:FSH ratio is >1, confirming central activation. A flat response suggests peripheral PP (sex steroids are produced independently, suppressing the axis).

GnRH stimulation test: central PP → pubertal LH response (LH >5 IU/L, LH:FSH >1). Peripheral PP → flat response (HPO axis suppressed by autonomous sex steroids). Distinguishes the two mechanistically.

Central PP = HPO axis activated = GnRH stimulation → exaggerated pubertal LH response. Peripheral PP = autonomous sex steroid production → flat (suppressed) response to GnRH stimulation.

Correct. PALM = Polyp, Adenomyosis, Leiomyoma, Malignancy/hyperplasia — all STRUCTURAL causes detectable on imaging or histology. COEIN = Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not yet classified — NON-STRUCTURAL causes. Adenomyosis falls under 'A' in the structural PALM group.

FIGO PALM-COEIN: PALM = structural (Polyp, Adenomyosis, Leiomyoma, Malignancy/hyperplasia); COEIN = non-structural (Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not classified). This replaced 'DUB' as a diagnostic category.

PALM = structural: Polyp, Adenomyosis, Leiomyoma, Malignancy/hyperplasia. COEIN = non-structural. Coagulopathy, Ovulatory dysfunction, and Not-yet-classified are all non-structural (COEIN).

Correct. The LNG-IUS (Mirena) reduces menstrual blood loss by 80–90% — superior to all oral medical treatments including tranexamic acid, combined oral contraceptives, and progestogens. It is the first-line medical option for women who do not desire immediate pregnancy and who have no contraindication to its use (e.g. structural abnormality, infection).

LNG-IUS (Mirena) = most effective medical treatment for heavy menstrual bleeding; 80–90% reduction in blood loss. Tranexamic acid and combined OCP are useful but less effective. Choose LNG-IUS as first-line when structural cause excluded and no immediate pregnancy desired.

The LNG-IUS reduces blood loss by 80–90%, making it the most effective single medical treatment for heavy menstrual bleeding — superior to oral agents.

Correct. Primary amenorrhoea is defined as: (1) no menarche by age 15 in a girl WITH normal secondary sexual characteristics (SSC), OR (2) no menarche by age 13 in a girl WITH NO secondary sexual characteristics. The rationale: if SSC are absent by 13, the HPO axis has not activated at all — a more urgent workup threshold. If SSC are present but menarche is delayed, waiting until 15 is reasonable.

Primary amenorrhoea: no menarche by age 13 (without SSC) OR by age 15 (with SSC). Secondary amenorrhoea: ≥3 months absence with previously regular cycles, or ≥6 months with irregular cycles. Always check for pregnancy first.

The dual definition: no menarche by 13 (without SSC) OR no menarche by 15 (with SSC present). The thresholds differ depending on whether secondary sexual characteristics have developed.

Correct. Markedly elevated prolactin (>100 ng/mL) with galactorrhoea and headaches (bitemporal headache from mass effect) localises the cause to a pituitary adenoma (prolactinoma) until proven otherwise. MRI pituitary is the investigation of choice to identify and characterise the tumour. Thyroid function is relevant if prolactin is mildly elevated (hypothyroidism stimulates TRH → prolactin), but is not the primary investigation here.

Prolactin >100 ng/mL + galactorrhoea + headaches → MRI pituitary (prolactinoma). Mild elevation (<50 ng/mL) → check TFTs first (hypothyroidism). Karyotype is for gonadal dysgenesis (primary amenorrhoea + elevated FSH/LH).

Significantly elevated prolactin + galactorrhoea + headaches = pituitary adenoma (prolactinoma) until proven otherwise. MRI pituitary is the investigation to confirm and characterise the lesion.