Abnormal Uterine Bleeding (AUB)
Abnormal uterine bleeding refers to bleeding from the uterus that is abnormal in volume, timing, regularity, or duration and unrelated to pregnancy. Rather than representing a single diagnosis, AUB reflects failure of normal endometrial regulation and haemostasis. AUB bleeding patterns vary widely, which is why investigations may be normal despite significant symptoms, and why effective management depends on identifying the underlying mechanism rather than bleeding severity alone.
What You Need to Know
Abnormal uterine bleeding arises when the normal coordination between ovarian hormones, endometrial development, and local haemostatic control is disrupted. In a typical cycle, oestrogen-driven endometrial proliferation is followed by progesterone-mediated maturation, creating a lining that can shed in an organised manner and then repair efficiently. This balance maintains predictable timing, volume, and duration of bleeding. When hormonal signalling is poorly timed, insufficient, or prolonged, the endometrium becomes structurally unstable and prone to irregular breakdown.
Failure of regulation can occur through several overlapping mechanisms that affect how the endometrium grows, sheds, and repairs:
Anovulation or inadequate progesterone exposure leading to fragile, proliferative endometrium
Structural or inflammatory disruption of endometrial vasculature, impairing controlled shedding
Impaired local haemostasis, where normal vasoconstriction and clot formation are ineffective
The resulting bleeding pattern reflects the nature of the disruption rather than blood loss alone. Unopposed oestrogen may produce heavy or prolonged bleeding due to excessive but unstable tissue, while irregular hormonal exposure can cause unpredictable spotting or intermenstrual bleeding. Inflammatory or vascular changes may amplify bleeding despite normal hormone levels, and coagulation disturbances can prolong bleeding once it begins.
Abnormal uterine bleeding is therefore best understood as a disorder of endometrial regulation rather than a single diagnosis. The uterus responds appropriately to the signals it receives, even when those signals are abnormal or conflicting. Effective evaluation and management depend on identifying which regulatory processes have failed, whether hormonal coordination, endometrial integrity, vascular control, or systemic haemostasis, rather than focusing solely on the visible bleeding itself.
Beyond the Basics
Ovulatory dysfunction and unopposed oestrogen
Ovulatory dysfunction is one of the most common mechanisms underlying abnormal uterine bleeding, particularly during adolescence and the perimenopausal transition. When ovulation does not occur, the corpus luteum does not form and progesterone is not produced. Oestrogen exposure therefore remains unopposed, driving continuous endometrial proliferation without the cyclical differentiation that normally stabilises the lining.
Over time, the endometrium becomes thickened but structurally weak. Glandular growth outpaces stromal support, and vascular organisation becomes disordered. Bleeding occurs unpredictably when areas of fragile tissue outgrow their blood supply and break down, producing irregular, prolonged, or heavy bleeding rather than a coordinated menstrual flow.
Endometrial instability and local haemostasis
Normal menstrual bleeding is limited by local haemostatic mechanisms within the endometrium, including vasoconstriction of spiral arteries, platelet aggregation, and formation of fibrin clots. When these processes are impaired, blood loss increases even if hormonal cycling is otherwise intact.
Inflammation, altered prostaglandin activity, and impaired vasoconstriction interfere with effective vessel closure and repair after shedding begins. This explains why some individuals experience heavy menstrual bleeding despite regular ovulatory cycles, normal hormone levels, and unremarkable pelvic imaging.
Structural contributions to bleeding
Structural abnormalities such as polyps, fibroids, or adenomyosis alter uterine architecture and disrupt normal endometrial shedding. Irregular surfaces increase vascular exposure and interfere with uniform contraction and haemostatic control during menstruation. Bleeding severity, however, often reflects interaction between structural change and the surrounding hormonal environment rather than anatomy alone. Similar structural findings may produce very different bleeding patterns depending on ovulatory function, endometrial responsiveness, and local inflammatory activity.
Role of prostaglandins and vascular regulation
Prostaglandins play a central role in regulating uterine contractility and vascular tone. An excess of vasodilatory prostaglandins increases endometrial blood flow and reduces platelet aggregation, promoting heavier bleeding. Shifts in prostaglandin balance often occur alongside inflammatory changes and heightened uterine sensitivity. This overlap explains why heavy bleeding and dysmenorrhoea frequently coexist as parallel manifestations of endometrial dysregulation rather than separate conditions.
Systemic influences and coagulation
Systemic disorders can significantly influence menstrual bleeding patterns. Thyroid dysfunction alters hormone metabolism and feedback regulation, while inherited or acquired coagulation disorders impair clot formation and prolong bleeding once it begins. In these situations, abnormal uterine bleeding reflects failure of systemic haemostasis rather than primary uterine pathology. Bleeding that is disproportionate to pelvic findings should prompt consideration of systemic contributors rather than escalation of local treatment alone.
Chronic AUB and endometrial risk
When abnormal uterine bleeding persists, particularly in the setting of chronic anovulation, prolonged exposure to unopposed oestrogen increases the risk of endometrial hyperplasia. Ongoing proliferative stimulation promotes abnormal cellular growth and loss of normal regulatory control.
This progression explains why chronic AUB requires evaluation beyond symptom suppression. Even when bleeding patterns appear stable, underlying endometrial risk may continue to evolve, making identification and correction of the driving mechanisms essential rather than focusing solely on bleeding control.
Clinical Connections
Abnormal uterine bleeding may present as heavy menstrual bleeding, intermenstrual bleeding, prolonged or shortened cycles, or unpredictable spotting. Patterns often change over time rather than remaining consistent, reflecting shifts in ovulatory function, hormonal exposure, and local inflammatory activity. The amount of bleeding alone does not reliably indicate the severity or cause, as relatively modest bleeding may signal significant regulatory disruption, while heavy bleeding can arise from several different mechanisms.
Several features help link clinical presentation to underlying physiology:
Bleeding pattern reflects whether ovulation is occurring and whether progesterone exposure is adequate
Timing and regularity provide clues to hormonal coordination rather than endometrial volume alone
Disproportionate bleeding may indicate systemic or vascular contributors rather than uterine pathology
Assessment therefore extends beyond quantifying blood loss. Evaluation of ovulatory status, hormonal environment, structural factors within the uterus, and systemic disease such as thyroid dysfunction or coagulation disorders is essential to identify the dominant driver of bleeding. Management is guided by correcting the underlying mechanism, whether restoring hormonal balance, addressing structural distortion, or managing systemic contributors, rather than suppressing bleeding volume alone.
Concept Check
Why does anovulation lead to irregular or heavy uterine bleeding?
How does impaired endometrial haemostasis increase menstrual blood loss?
Why can AUB occur in individuals with normal imaging findings?
How do prostaglandins influence both bleeding and pain?
Why does chronic AUB increase the risk of endometrial pathology?