Introduction
From a clinical viewpoint, amenorrhea can be defined as a health condition that is exemplified by the absence of menstruation. Nevertheless, a patient can only be diagnosed with amenorrhea if she misses more than two menstrual periods in a consecutive manner (Gould, 2002). Clinically, there is a difference between amenorrhea and dysmenorrhea, since intense levels of pain typify the latter, just before or during regular menstrual periods (Gould, 2002). This paper highlights the pathophysiology and causes of amenorrhea as well as the pathophysiology that is associated with patients who present with a prior history of dysmenorrhea and irregular menstrual cycles.
The pathophysiology and causes of amenorrhea
A person’s gonads and FSH are critical in ensuring that menstrual periods occur in a programmed manner. If an individual is healthy, then the pituitary gland and hypothalamus communicate in a way that is not disrupted. On the other hand, unhealthy persons are typified by abnormal levels of FSH, which are required for normal menstrual cycles (Gordon, 2010; Gould, 2002). In the context of gonadotrophic amenorrhea, FSH levels are relatively low. It is worth to note that the activities of FSH and estrogen are related. For example, if one does not produce adequate FSH, then it would imply that she would also not secrete enough estrogen that is essential for initiating the breaking down of the inner walls of the uterus, resulting in an anovulatory amenorrhea. An anovulatory amenorrhea can be initiated by two biological events (Gordon, 2010). First, it can be caused by ovarian cancer and poor communication between the pituitary gland and hypothalamus, among others. Second, it can be caused by malfunctions of the pituitary gland, radiotherapy, and chemotherapy. The discussion above outlines the major aspects of the pathophysiology of amenorrhea (Gordon, 2010; Sherwood, 2011).
Research has identified four common causes of amenorrhea. First, some medicines have relatively high risks of causing the condition. For example, many women have reported that some contraceptives could lead to the absence of menses. Second, breastfeeding has been shown to result in cessation of menses, which could persist for about six months after child delivery. Third, during human development, some body parts, such as ducts, might not develop normally, leading to disruption of processes that culminate in menses. Lastly, it has been demonstrated that some females who engage in intensive physical exercises could experience amenorrhea for the reason that they do not have the energy that is required for mediating hormonal events.
The pathophysiology of prior irregular cycles
If a patient presents with amenorrhea and her medical history indicates that she has had irregular menstrual cycles, then a clinician can conclude that the patient’s hormonal pathways and stimulation levels could have been negatively impacted (Gould, 2002; Sherwood, 2011). In most cases, the amount of FSH that is required for normal menses increases remarkably, leading to the absence of menstrual periods because the new amount of FSH cannot be supplied. Adenomyosis is the condition that associates amenorrhea with dysmenorrhea (Gould, 2002). Essentially, the condition is typified by intense pain before menses. In many cases, adenomyosis is utilized as a critical component of the pathophysiology of amenorrhea. Irregular menses in the past could also be caused by cervical stenosis that is typified by a relatively small opening of the cervix, implying that the flow of menses is constrained.
Conclusion
As demonstrated in this paper, the pathophysiology of amenorrhea is strongly correlated with hormonal events. The pathophysiology could be characterized by painful and irregular menstrual cycles.
References
Gordon, C. M. (2010). Functional hypothalamic amenorrhea. New England Journal of Medicine, 363(4), 365-371.
Gould, B. E. (2002). Pathophysiology for the health professions (pp. 526-528). Philadelphia, PA.
Sherwood, L. (2011). Human physiology: from cells to systems. Boston, MA: Cengage Learning.