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This Open Access site was originated September 2006 updated December 2008 Why is Menstrual Blood Sometimes Dark? What Causes Menstrual Blood Clots? Heavy or Irregular Menstrual Bleeding . . . for really helpful answers . . . and less worries scroll to bottom paragraphs of this page  Menstrual flow cleanses and renews the uterus for a new cycle. The body does not want to hold onto old tissue. |
Understanding Menstrual Fluid & Uterine Physiology
Each month during a woman's reproductive years the uterine lining (endometrium) prepares for a potential pregnancy. If fertilization is not established the uterus sheds and renews to prepare for another potential pregnancy. Below is an overview of uterine physiology as it relates to the shedding/regression of the endometrium. Much of this cellular and blood vessel activity takes place during the four days before the menstrual period. Although this information may seem complex it provides insight into the distinctions & symptoms experienced during certain stages (days) of the menstrual cycle. | | | | The uterine wall is made of three layers: perimetrium, the myometrium and the endometrium. The perimetrium is composed of a thin layer of loose connective tissue covered by mesothelium. The myometrium is a smooth muscle wall composed of three interwoven layers. The middle muscle layer contains large blood vessels and interlacing smooth muscle fibers. It is this middle layer of smooth muscle cells, that contract to flush out the menstrual flow. The outer and inner layers of the myometrium have smooth muscle fibers running parallel to the long axis of the uterus. The endometrium, the inner lining of the uterus receives a double blood supply and consists of two divisions: the functionalis and basalis. The functionalis is a temporary layer at the luminal surface. In response to fluctations in ovarian hormones the functionalis undergos cyclic thickening and shedding (mensturation). The functionalis is further subdivided into a zona compacta near the lumen and a deeper zona spongiosa. The basalis layer of the endometrium is thinner and is situated deeply, in direct contact with the myometrium. The basalis is permanent and provides the elements from which a new functionalis layer reguvenates. The phases of the endometrial cycle match the follicular and luteal phases of the ovarian cycle.
The uterus derives its blood supply from the left and right uterine arteries. These large blood vessels penetrate the myometrium to provide nutrients and oxygen to endometrial tissues and glands. Uterine arteries branch to form arcuate arteries in the middle of the myometrium. The arcuates then branch into straight arteries in the basalis and spiral arteries in the functionalis. There are approximately 100 - 150 elastic spiral arteries each with a diameter of 200 -300 microns. Spiral arteries retract into the basalis and constrict to limit blood loss during menstruation. These spiral arteries then extend like springs as the functionalis regenerates. Around days 25-26 of the menstrual cycle, constriction of the uterine arteries pinch off the large blood vessels passing through the myometrium to begin causing regression (break down) of the endometrium. In many women this blood vessel constriction may cause early menstrual cramps; three/four days prior to the actual period, without menstrual bleeding.
In the absence of pregnancy, and triggered by a sudden fall in the level of progesterone, the myometrium begins involuntary contractions to reduce the edematous (fluid filled) endometrium. Progesterone withdrawl results in increased coiling and constriction of the spiral arterioles. This results in decreased blood flow (tissue ischemia) to the endometrial layers: the spongiosa and compacta.
Prostaglandin F2a exerts its effects via the synthesis of endothelin 1 which inhibits steroidogenesis (hormone production) and stimulates the release of tumor necrosis factor alpha (TNFa), which induces cell apoptosis (programmed cell death). Endothelin-1 and thromboxin (TXA2) also mediate constriction of the spiral arteries. By day 28 of the menstrual cycle, or the first day of bleeding, low progesterone, high prostaglandin levels and a release of Ca2+ start spontaneous contractions of myometrial cells. Gap junctions initiate a signaling pathway inside myometrial cells causing synchronized smooth muscle contractions of the entire myometrium. Intense constriction further reduces blood and oxygen supply to the endometrium contributing to a healthy/necessary cell death (apoptosis) of the functionalis. Menstrual bleeding begins as the spiral arteries of the functionalis retract, constrict & rupture (secondary to ischemia & hypoxia), releasing some blood into the uterus. Arterial and venous blood, proteolytic enzymes, remnants of endometrial glands, stromal cells (connective tissue), leukocytes and red blood cells are all present in the menstrual fluid.
Estrogen and progesterone withdrawl causes endometrial lysosomal instability, which results in prostaglandin synthase, collagenase and proteases. The endometrium releases prostaglandin F2 alpha which cause contractions of smooth muscle and contributes to the sloughing of the degrade endometrial tissue. Lysosomes are intracellular vacuoles containing hydrolytic enzymes. Lysosomal enzymes contribute to the digestion and removal of excess intracellular and extracellular material of endometrial tissue. Collagenase is an enzymatic debrider that cleans the wound of any dead tissue leaving the wound bed ready for healing. Proteases catalyze the disassembly of proteins. This enzymatic activity promotes a healthy cleansing of the endometrium.
During the first week of the follicular phase, day one through five of the menstrual cycle, the functionalis is completely shed. An average period corresponds to a loss of between 30ml to 50ml of whole blood (3-6 tablespoons). A few days after the onset of menstrual bleeding the functionalis begins to regenerate. Estrogen, from primordial follicles, stimulates the regeneration of the surface endometrial epithelium, while endometrial shedding (menstrual bleeding) is occurring. The estrogen secreted by the growing ovarian follicles, causes prolonged vasoconstriction enabling the formation of a clot over the denuded endometrial vessels. Additionally, the epithelial cells lining the glands of the basalis divide and cover the raw surface exposed during menstruation which also facilitates endometrial regeneration.
| | | | For an overview about Urinary Tract Infections click here | Key point: The healing of the endometrium, the completion of a menstrual cycle is dependent on the increasing estrogen levels produced from primordial follicles. | | | | | | | |
| |  Heavy or Irregular Menstrual Bleeding
The amount of menstrual fluid is determined by the size of the uterus and the hormonally induced endometrial thickness. During the follicular phase (about the first 2 weeks) of the menstrual cycle, estrogen gradually builds up the uterine lining (endometrium). Estrogen causes the proliferation (growth) of endometrial stroma cells (connective tissue), epithelial cells (tissue), glands, vascular cells and the number of gap junctions. Estrogen increases myometrial excitability and stimulates uterine contractility. Progesterone is the hormonal factor that promotes uterine relaxation. During the secretory phase (last 2 weeks) of the cycle, progesterone stops *proliferation of the endometrium. Progesterone opposes the excessive proliferation effects of estrogen. Heavy or irregular bleeding often occurs because estrogen dominance causes the functionalis layer of the endometrium to overgrow. To much endometrial tissue builds up and then breaks down in a disorderly way. Low levels of progesterone cannot counteract the excess estrogen. Symptoms of estrogen dominance and low progesterone include: irregular periods with excessive bleeding, depression, irritability, anxiety, bilateral pounding headache (especially premenstrually), menstrual and/or premenstrual hot flashes, feeling shaky, bloating/water retention, breast swelling & tenderness. *Progesterone decreases the biological activity of estradiol (estrogen) on the endometrium by decreasing the concentration of estradiol receptors, increasing the activity of 17 B-hydroxysteriod dehydrogenase type II, the enzyme responsible for the conversion of estradiol to estrone, and by increasing the activity of estrone sulfotransferase. The primary role of progesterone is to support implantation and sustain pregnancy. Progesterone supports pregnancy by inhibiting uterine contractions and by supressing the immune systems response to the developing embryo as a foreign body. Just before ovulation progesterone secretion is 2 - 3 mg per day. After ovulation progesterone secretion is 20 - 25 mg per day, one week post ovulation 30 mg per day and during the third trimester of pregnancy 300 - 400 mg per day.
Stress can contribute to endometrial tissue buildup because stress drains the body of hormone balancing and healing nutrients. Stress increases cortisol levels. Cortisol impairs progesterone activity, by blocking or competing for progesterone receptors. Low progesterone contributes to estrogen dominance. This unbalance of excess estrogen contributes to proliferation (growth) of the endometrium, and often results in heavy or irregular bleeding. | | |  Menstrual Cramps
Menstrual cramps often result when the endometrial and myometrial tissues; the uterine lining and muscle secrete excess series 2 prostaglandins. Prostaglandins are hormone type substances that can promote inflammation including pain, swelling and tenderness. Prostaglandin stimulates the activity of myometrial cells.
A few days prior to or upon menstruation, prostaglandin release helps start the contractions that are necessary to shed the functionalis layer of the endometrium. Excess prostaglandin can create mild to extreme discomfort such as spasm/cramps in the uterine muscle (myometrium), back ache, sweating, chills, nausea, constipation or diarrhea and feeling faint. Women with menstrual cramps have prostaglandin blood levels that are significantly higher than women who do not experience cramps. Many women can lessen the intensity of menstrual cramps by taking a daily ibuprofen (over the counter) each day pre-menstrually. . . and during the onset/start of their period. Ibuprofen blocks the production of the prostaglandin hormone that causes menstrual cramps. Keep in mind if experiencing severe menstrual cramps, and your prostaglandin levels are very high, over the counter ibuprofen probably will not be potent enough to relieve the severe cramping. A prescription ibuprofen would bring better relief. | | |  Why is Menstrual Blood Sometimes Dark? Menstrual fluid tends to be brightest red when your flow is heaviest. As the menstrual flow slows down, it takes longer to exit the vagina, as a result, the blood component loses its oxygenated red hue and becomes darker red, then brown and at times practically black. Arterial and venous blood, proteolytic enzymes, remnants of endometrial glands, stromal cells (connective tissue), leukocytes and red blood cells are present in menstrual fluid. Many women have dark brown (slow menstrual blood) before their period and some have the darker light flow as the period tappers off. The color of menstrual blood can vary month to month. A darker fluid most often reflects a slow exit from the body. | | |  Understanding Menstrual Blood Clots
Clots are the natural result of the body functioning well. They are a natural way of controlling bleeding. When menstrual bleeding is heavy, clotting tends to occur. Experiencing menstrual clots can be upsetting. If the clots are large they can be painful and cause cramping as they pass through the cervix.
The following is a brief explanation as to why menstrual clots (often large clots) are formed. All blood contains a clotting factor. To enable menstrual blood to flow freely from the uterus and leave the body without clotting, the uterus produces an anti-clotting agent: plasmin. However, when menstrual loss is heavy, the anti-clotting agent may not be adequate for the menstrual period and the blood is likely to form clots. Additionally, if menstrual blood accumulates faster than the body’s ability to transfer it out of the uterus, clots can result.
More technically . . . fibrin is a protein that creates a blood clot by forming a network of trapped red blood cells and platelets. plasmin is an enzyme that digests or breaks down fibrin. In general, menstrual blood clots form when there is an slight imbalance between fibrin (builds) and plasmin (breakdown). | |
Dysfunctional uterine bleeding (DUB) is a diagnosis of exclusion that requires some form of endometrial sampling for a diagnosis.
Fibrinolysis is the mechanism by which fibrin or a blood clot is broken down. Research studies have shown that fibrinolysis is normal in the human endometrium and that fibrinolytic activity is measurable in menstrual fluid. Plasminogen activator is an enzyme which activates plasminogen. This converts plasminogen to plasmin which breaks down fibrin. Plasminogen activator is normally present in the human endometrium.
Studies have demonstrated that fibrinolysis and endometrial plasminogen activator are further increased in the menstrual fluid of women with dysfunctional uterine bleeding than in women with more stable periods. Source:
International Women's Health Update: Menorrhagia Heavy Periods
Professor David L Healy, Faculty of Medicine, Nursing and Health Sciences
Monash University, Victoria 3800
Australia
http://www.med.monash.edu.au/ob-gyn/research/menorr.html | “Ownership and Rights. Vascular Events (a nonprofit organization), Inc., shall own all and exclusive right, title, and interest in the work throughout the world, including copyrights, domain names, trademarks, and all other intellectual property rights in the work. The work shall be deemed to be a work-for-hire under the Copyright Act of 1976, Title 17 U.S.Code, and Vascular Events Inc., shall be deemed to be the author.” | | | | Information is provided for educational purposes to help individuals form an understanding of biological processes as they effect health. This information is not intended for medical diagnosis or treatment. | | | |
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