Introduction
Amenorrhoea is a health condition that is characterised by the absence of menstruation. However, for a woman to be diagnosed with the condition, she must have missed at least three consecutive menstrual periods (Porth & Matfin, 2009). Dysmenorrhoea is a health condition that is exemplified by pain just before or during menstrual periods. In fact, the pain could be too severe for an individual to perform daily activities (Porth & Matfin, 2009).
This paper focuses on discussing the pathophysiology and possible causes of amenorrhoea. It also highlights the impacts of prior irregular cycles and dysmenorrhoea with regard to the pathophysiology of amenorrhoea. The paper makes reference to the 30-year-old female who presents with amenorrhoea for 6 months and previously encountered periods of dysmenorrhoea and irregular menstrual cycles.
The pathophysiology and causes of amenorrhoea
In the context of the patient in the case study, it would be critical to focus on the disruption of communication that occurs between gonads and FSH (Porth & Matfin, 2009). In unhealthy states, the pituitary gland and hypothalamus are characterised by disorders that interfere with normal secretion of FSH. As a result, low levels of the hormone are responsible for hypogonadotropic amenorrhoea. It is essential to note that the activities of FSH and oestrogen are interrelated. Generally, if a female secretes inadequate amounts of FSH, then her ovaries cannot secrete enough oestrogen that would be critical in stimulating the inner lining of the uterus.
Thus, amenorrhoea occurs. In fact, if there is inadequate stimulation of the inner lining of the uterus, then the lining is not shed off as required, resulting in anovulatory amenorrhoea, which could either be euestrogenic or hypoestrogenic (Huether & McCcance, 2012). Euestrogenic anovulatory amenorrhea could be caused by masculinising ovarian tumour, systemic illness and hypothalamic-pituitary dysfunction, among others (Huether & McCcance, 2012). On the other hand, hypoestrogenic anovulatory amenorrhoea could be caused by severe dysfunctions of the pituitary gland and hypothalamus, gonadal dysgenesis, radiotherapy and chemotherapy (Huether & McCcance, 2012; Porth & Matfin, 2009).
Endometrium could also be unable to respond to hormones that are essential in initiating menses, resulting in ovulatory amenorrhoea. This could have two causes. First, the uterus could be absent in an individual, which could be due to “utero-vaginal agenesis and XY-females (e.g. T.F.S)” (Porth & Matfin, 2009, p. 87). Second, some conditions could damage endometrium and make it unable to respond to hormones. An example of such conditions is Asherman’s syndrome.
Many scholars have identified four main causes of amenorrhoea (McPhee & Hammer, 2012). First, it is evident that females who engage in “excessive exercises or who lose a significant amount of weight have relatively high chances of suffering from ‘athletic’ amenorrhoea” (Porth & Matfin, 2009, p. 109). It is critical to note that when a woman does not have the energy that is required to mediate regular menses, then she does not menstruate. It is believed that the disruption of menstrual cycles, which is correlated with energy imbalance and weight loss, is mediated by a series of hormonal mechanisms (McPhee & Hammer, 2012).
Second, drugs have been shown to lead to the absence of menses. In particular, contraceptives have shown relatively high risks of causing amenorrhoea. Third, lactation could make a woman experience amenorrhoea for about 6 months after giving birth (Porth & Matfin, 2009). In fact, it is argued that lactational amenorrhoea is one of the best ways of preventing pregnancy after giving birth (up to about six months). Lastly, physical deformities have been shown to cause the condition. For example, a physical deformity might lead to altered development of ducts that prevent menstruation (McPhee & Hammer, 2012).
Impacts of the prior irregular cycles and dysmenorrhoea on the pathophysiology of amenorrhoea
Irregular menstrual cycles could have occurred in the woman due to altered hormonal pathways and stimulation thresholds. For example, decreased stimulation threshold of endometrium could require relatively high amounts of FSH for menstruation, which could not be available at regular intervals (Porth & Matfin, 2009). With time, it could have been observed that stimulation thresholds were too high to be met by normal FSH in the body.
Thus, the woman started to develop amenorrhoea. The woman could have developed dysmenorrhoea before she presented with amenorrhoea due to adenomyosis, which is a condition that is exemplified by pain. In fact, this is an important feature of the pathophysiology of amenorrhoea. Another reason that could have caused menstrual cramps in the 30-year-old woman is cervical stenosis (McPhee & Hammer, 2012). The condition is characterised by a relatively small opening of the cervix that could disrupt menstrual flow, “leading to a painful pressure in the uterus” (Sherwood, 2011, p. 75).
Conclusion
In conclusion, the pathophysiology of amenorrhoea is characterised by a series of hormonal pathways that are altered in disease states. Irregular cycles and dysmenorrhoea could be important features in the pathophysiology of amenorrhoea. It would be prudent to have a thorough understanding of the pathophysiology of the condition before initiating a clinical action.
References
Huether, S. E., & McCcance, K. L. (2012). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.
McPhee, S. J., & Hammer, G. D. (2012). Pathophysiology of disease. An introduction to clinical medicine. New York, NY: McGraw-Hill Medical.
Porth, C., & Matfin, G. (2009). Pathophysiology: Concepts of altered health states (8th ed.). Philadelphia, PA: Lippincott Williams & Wilkins.
Sherwood, L. (2011). Human physiology: from cells to systems. Boston, MA: Cengage Learning.