Histopathology
In case an ovarian cyst is surgically removed, a more definite diagnosis can be made by histopathology:

Treatment
Cysts associated with hypothyroidism or other endocrine problems are managed by treating the underlying condition. About 95% of ovarian cysts are benign, not cancerous. Functional cysts and hemorrhagic ovarian cysts usually resolve spontaneously. However, the bigger an ovarian cyst is, the less likely it is to disappear on its own. Treatment may be required if cysts persist over several months, grow, or cause increasing pain. Cysts that persist beyond two or three menstrual cycles, or occur in post-menopausal women, may indicate more serious disease and should be investigated through ultrasonography and laparoscopy, especially in cases where family members have had ovarian cancer. Such cysts may require surgical biopsy. Additionally, a blood test may be taken before surgery to check for elevated CA-125, a tumour marker, which is often found in increased levels in ovarian cancer, although it can also be elevated by other conditions resulting in a large number of false positives. Pain
Pain associated with ovarian cysts may be treated in several ways:

Pain relievers such as acetaminophen, nonsteroidal anti-inflammatory drugs, or opioids. While hormonal birth control prevents the development of new cysts in those who frequently get them, it is not useful for the treatment of current cysts. Surgery
Although most cases of ovarian cysts involve monitoring, some cases require surgery. This may involve removing the cyst, or one or both ovaries. Technique is typically laparoscopic, unless the cyst is particularly large, or if pre-operative imaging suggests malignancy or complex anatomy.
Morawitz believed that his enzyme came from cells such as platelets yet, in keeping with the state of knowledge about enzymes at that time, he had no clear idea about the chemical nature of his thrombokinase or its mechanism of action. Those uncertainties led to decades during which the terms thrombokinase and thromboplastin were both used to describe the activator of prothrombin and led to controversy about its chemical nature and origin.In 1947, J Haskell Milstone isolated a proenzyme from bovine plasma which, when activated, converted prothrombin to thrombin. Following Morawitz’s designation, he called it prothrombokinase  and by 1951 had purified the active enzyme, thrombokinase. Over the next several years he showed  that thrombokinase was a proteolytic enzyme that, by itself, could activate prothrombin. Its activity was greatly enhanced by addition of calcium, other serum factors, and tissue extracts, which represented the thromboplastins that promoted the conversion of prothrombin to thrombin by their interaction with thrombokinase. In 1964 Milstone summarized his work and that of others: “There are many chemical reactions which are so slow that they would not be of physiological use if they were not accelerated by enzymes. We are now confronted with a reaction, catalyzed by an enzyme, which is still too slow unless aided by accessory factors.”

Interactions
Factor X has been shown to interact with Tissue factor pathway inhibitor. References
External links
The MEROPS online database for peptidases and their inhibitors: S01.216
med/3495 at eMedicine
Factor X deficiency


== Further reading ==