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Explain respect to AUB

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Here is a detailed explanation of everything in your notes on AUB (Abnormal Uterine Bleeding):

Abnormal Uterine Bleeding (AUB) - Causes Explained

AUB refers to any bleeding from the uterus that is abnormal in frequency, duration, or amount. The notes focus specifically on anovulatory causes - where the absence of ovulation disrupts the normal hormonal cycle, leading to unregulated estrogen stimulation of the endometrium without the stabilizing effect of progesterone.

1. Puberty

Most common cause of puberty menorrhagia: Anovulation > Coagulopathy

At puberty, the hypothalamic-pituitary-ovarian (HPO) axis is still immature. The hypothalamus has not yet established the mature pattern of GnRH pulsatility needed to trigger a proper LH surge. As a result:

Cycles are frequently anovulatory (no egg is released)
No corpus luteum forms, so no progesterone is produced
The endometrium is stimulated by estrogen alone and sheds irregularly, causing heavy, unpredictable bleeding

Coagulopathy (e.g., Von Willebrand disease) is the second most important cause to rule out - especially when a teenager presents with severe bleeding from her very first period.

2. Perimenopausal Females

As women approach menopause, the number of remaining oocytes (eggs) declines. Follicular development becomes irregular and erratic, leading to:

Fluctuating, unpredictable estrogen levels
Frequent anovulatory cycles
Irregular uterine shedding and abnormal bleeding

This is essentially the same mechanism as puberty - an immature HPO axis at one end of reproductive life, and a failing one at the other.

3. Obese Females

This is a key biochemical pathway:

Androgen → (via adipose tissue aromatase) → ↑ Estrogen → Continuous LH stimulation → No LH surge → Anovulation

Adipose (fat) tissue is rich in the enzyme aromatase, which converts androgens (like androstenedione) into estrogen (mainly estrone)
This creates a chronic, low-level, continuous estrogen state
A normal LH surge requires a sharp, rapid rise in estrogen - but continuous flat estrogen levels never produce this spike
Without the LH surge, ovulation does not occur
Without ovulation, no progesterone is produced, and the endometrium overgrows under estrogen stimulation alone, then sheds irregularly

This same chronic estrogen excess also explains why obese women are at higher risk of endometrial hyperplasia and carcinoma - Robbins Pathology notes: "A common cause of estrogen excess is obesity, as adipose tissue converts steroid precursors into estrogens." - Robbins & Kumar Basic Pathology, p. 609

4. PCOS (Polycystic Ovary Syndrome)

PCOS is listed as a separate cause but shares the same androgen-excess mechanism (see below). In PCOS:

There is chronic anovulation with irregular or absent periods
Elevated androgens and insulin resistance impair follicular maturation
Multiple immature follicles accumulate in the ovary, giving the classic "string of pearls" ultrasound appearance
The endometrium is exposed to unopposed estrogen, causing irregular bleeding or amenorrhoea

5. Androgen Excess

Folliculotoxic effect: No maturation of follicles → Anovulation

Excess androgens (from any source - adrenal, ovarian, exogenous) have a direct toxic effect on developing follicles:

They arrest follicular growth at an early, immature stage
The follicle never reaches the size or estrogen output needed to trigger an LH surge
Therefore, ovulation never occurs → anovulation → AUB (or amenorrhea if severe)

6. Hypothyroidism

Thyroid hormone deficiency causes AUB through several overlapping mechanisms:

Altered steroid hormone metabolism leads to elevated estrogen levels
Hyperprolactinemia can co-exist (TRH stimulates prolactin secretion, and in hypothyroidism, TRH is elevated)
Impaired clotting factor synthesis (factors VIII, IX, XI) can worsen bleeding
Overall HPO axis dysregulation leading to anovulation

7. Hyperprolactinemia

This is the most detailed pathway in your notes:

↑ Prolactin → negative feedback on GnRH → ↓LH, ↓FSH → [Anovulation / ↓ Progesterone → 2° amenorrhoea / Infertility]

Step by step:

High prolactin (from a prolactinoma, drugs like metoclopramide/antipsychotics, or physiologic lactation) suppresses GnRH pulsatility from the hypothalamus
Without GnRH pulses, the pituitary cannot secrete adequate LH and FSH
Without FSH, follicles don't mature. Without LH, no surge occurs and ovulation is absent (anovulation)
Without ovulation, there is no corpus luteum, so progesterone falls drastically
This leads to:
- Secondary amenorrhoea - no progesterone withdrawal means no proper menstruation
- Infertility - no egg released means no conception

Note in your book: Lactational amenorrhoea is the classic physiologic example of this mechanism - breastfeeding raises prolactin, which suppresses GnRH, which stops ovulation and menstruation. This is why breastfeeding offers temporary (though unreliable) contraception.

Summary Table

Cause	Core Mechanism	Result
Puberty	Immature HPO axis	Anovulation
Perimenopause	Failing HPO axis	Anovulation
Obesity	Peripheral androgen → estrogen conversion	No LH surge → Anovulation
PCOS	Androgen excess + insulin resistance	Anovulation
Androgen excess	Folliculotoxic effect	No follicle maturation → Anovulation
Hypothyroidism	Elevated TRH → ↑Prolactin + altered steroid metabolism	Anovulation
Hyperprolactinemia	↑Prolactin → ↓GnRH → ↓LH/FSH	Anovulation + amenorrhoea + infertility

Why Anovulation Causes Bleeding

The common thread through all these causes is anovulation. Here's why that leads to bleeding:

Normal cycle: Ovulation → corpus luteum → progesterone → stabilizes endometrium → organized shedding (normal period)
Anovulatory cycle: No ovulation → no corpus luteum → no progesterone → endometrium kept under unopposed estrogen → keeps proliferating → eventually outgrows its blood supply → breaks down irregularly → AUB

The bottom section of your notes introduces DUB (Dysfunctional Uterine Bleeding) - which is the older term used when AUB has no identifiable structural cause (no polyp, fibroid, or malignancy), only a hormonal/functional disturbance. The current FIGO classification uses the PALM-COEIN system to categorize AUB causes, where DUB largely falls under the "O" (Ovulatory dysfunction) and "E" (Endometrial) categories.

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