Prothrombin is a glycoprotein that occurs in blood plasma and functions as a precursor to the enzyme, thrombin, which acts to convert fibrinogen into fibrin, therefore, fortifying clots. This clotting process is known as coagulation.The mechanism specific to prothrombin (factor II) includes the proteolytically cleaving, breakdown of proteins into smaller polypeptides or amino acids, of this coagulation factor in order to form thrombin at the beginning of the cascade, leading to stemming of blood loss. A mutation in factor II would essentially lead to hypoprothrombinemia. The mutation is presented on chromosome 11.Areas where the disease has been shown to present itself at include the liver, since the glycoprotein is stored in this area. Acquired cases are results from an isolated factor II deficiency. Specific cases include:

Vitamin K deficiency: In the liver, vitamin K plays an important role in the synthesis of coagulation factor II. Bodys capacity in the storage of vitamin K is typically very low. Vitamin K-dependent coagulation factors have a very short half-life, sometimes leading to a deficiency when a depletion of vitamin K occurs. The liver synthesizes inactive precursor proteins in the absence of vitamin K (liver disease). Vitamin K deficiency leads to impaired clotting of the blood and in some cases, causes internal bleeding without an associated injury. Disseminated intravascular coagulation (DIC): Involving abnormal, excessive generation of thrombin and fibrin within the blood. Relative to hypoprothrombinemia, due to increased platelet aggregation and coagulation factor consumption involved in the process.
Calcific tendinitis is a common condition where calcium deposits form in a tendon, sometimes causing pain at the affected site. Deposits can occur in several places in the body, but are by far most common in the rotator cuff of the shoulder. Around 80% of those with deposits experience symptoms, typically chronic pain during certain shoulder movements, or sharp acute pain that worsens at night. Calcific tendinitis is typically diagnosed by physical exam and X-ray imaging. The disease often resolves completely on its own, but is typically treated with non-steroidal anti-inflammatory drugs to relieve pain, rest and physical therapy to promote healing, and in some cases various procedures to breakdown and/or remove the calcium deposits. Adults aged 30–50 are most commonly affected by calcific tendinitis. It is twice as common in women as men, and is not associated with exercise. Calcifications in the rotator cuff were first described by Ernest Codman in 1934. The name, "calcifying tendinitis" was coined by Henry Plenk in 1952. Signs and symptoms
Up to 20% of those with calcific tendinitis have no symptoms. For those with symptoms, the symptoms vary based on the phase of the disease. In the initial "formative phase" when the calcium deposits are being formed, people rarely experience any symptoms. Those that do have symptoms tend to have intermittent shoulder pain, particularly during forward should flexion (i.e. lifting the arm in front of the body). In the "resorptive phase" when the calcium deposit is breaking down, many experience severe acute pain that worsens at night.