Partial Thromboplastin Time
Blood Coagulation Disorders
International Normalized Ratio
Vitamin K Deficiency
Blood Coagulation Factors
Disseminated Intravascular Coagulation
Vitamin K 1
Liver Function Tests
Fibrin Fibrinogen Degradation Products
Lupus Coagulation Inhibitor
Liver Failure, Acute
Factor X Deficiency
Tosylarginine Methyl Ester
Factor XII Deficiency
Blood Component Transfusion
Blood Cell Count
Blood Specimen Collection
Drug-Induced Liver Injury
Indicators and Reagents
Hepatitis, Viral, Human
Activated Protein C Resistance
Values of three coagulation screening tests of precolostral calves. (1/733)Prothrombin times, partial thromboplastin times and platelet counts were performed to determine normal values and to screen for coagulation defects of precolostral calves. The precolostral calves were in two groups: one group of a few calves was tested two years before the second larger group. The results for both groups were similar. The tests were performed on postcolostral calves and on mature cows to compare their values with those of precolostral calves. The mean values of prothrombin times and partial thromboplastin times of precolostral calves in the first group were 18.8 seconds and 54.8 seconds respectively. The mean values of prothrombin times and partial thromboplastin times of precolostral calves in the second group were 18.8 seconds and 50.8 seconds respectively. The mean platelet count was 422,400/cmm for the first group and 482,800/cmm for the second group. (+info)
Factor VII as a marker of hepatocellular synthetic function in liver disease. (2/733)Factor VII levels have been measured in 100 patients with liver disease following parenteral vitamin K1 therapy. There was good agreement between specific factor VII measurements and the one-stage prothrombin time apart from six patients with compensated cirrhosis in whom the prothrombin time was prolonged despite the presence of normal factor VII levels. A mean activity of 58% was found in patients with cirrhosis. Cirrhotic patients with features of hepatic decompensation had a significantly lower mean level of activity (40%) than the "contrast" patients with surgical obstruction of the major bile ducts (93%). Patients with chronic active liver disease had moderate depression of factor VII levels and those with non-cirrhotic liver damage had mean activities similar to the contrast group. Factor VII levels could not be correlated with BSP retention but there was a correlation with serum albumin concentration. It is concluded that the prothrombin time using Quick test with a standardized thromboplastin showing good sensitivity to factor VII, eg, the Manchester reagent (BCT), provides a reliable index of coagulability in chronic liver disease, and specific factor VII assays are not indicated. (+info)
Medical liability risk avoidance: a case for adopting the International Normalized Ratio (INR) system. (3/733)Since bleeding is a common adverse effect associated with the oral anticoagulant warfarin, maximizing the therapeutic potential of this drug requires close laboratory monitoring. The International Normalized Ratio (INR) is a system that has been developed to improve and standardize the assessment of the intensity of oral anticoagulation therapy. Clinical information and medicolegal arguments supporting the adoption of this system are reviewed. The potential for improvement in patient outcomes and minimization of medical liability favors the adoption of the INR system. (+info)
Effect of liver disease and transplantation on urea synthesis in humans: relationship to acid-base status. (4/733)It has been suggested that hepatic urea synthesis, which consumes HCO-3, plays an important role in acid-base homeostasis. This study measured urea synthesis rate (Ra urea) directly to assess its role in determining the acid-base status in patients with end-stage cirrhosis and after orthotopic liver transplantation (OLT). Cirrhotic patients were studied before surgery (n = 7) and on the second postoperative day (n = 11), using a 5-h primed-constant infusion of [15N2]urea. Six healthy volunteers served as controls. Ra urea was 5.05 +/- 0.40 (SE) and 3.11 +/- 0.51 micromol. kg-1. min-1, respectively, in controls and patients with cirrhosis (P < 0. 05). Arterial base excess was 0.6 +/- 0.3 meq/l in controls and -1.1 +/- 1.3 meq/l in cirrhotic patients (not different). After OLT, Ra urea was 15.05 +/- 1.73 micromol. kg-1. min-1, which accompanied an arterial base excess of 7.0 +/- 0.3 meq/l (P < 0.001). We conclude that impaired Ra urea in cirrhotic patients does not produce metabolic alkalosis. Concurrent postoperative metabolic alkalosis and increased Ra urea indicate that the alkalosis is not caused by impaired Ra urea. It is consistent with, but does not prove, the concept that the graft liver responds to metabolic alkalosis by augmenting Ra urea, thus increasing HCO-3 consumption and moderating the severity of metabolic alkalosis produced elsewhere. (+info)
Adenovirus-mediated local expression of human tissue factor pathway inhibitor eliminates shear stress-induced recurrent thrombosis in the injured carotid artery of the rabbit. (5/733)The main cause of acute coronary syndrome may be recurrent thrombosis, which is initiated by the activation of the extrinsic coagulation pathway. Tissue factor (TF) pathway inhibitor (TFPI) efficiently inhibits an early step in this pathway by the formation of a complex with factor VIIa, TF, and factor Xa. We determined whether local TFPI gene transfer can inhibit thrombosis in an injured artery without inducing systemic side effects. Balloon-injured rabbit carotid arteries were infected with an adenoviral vector that expressed either human TFPI (AdCATFPI) or bacterial beta-galactosidase (AdCALacZ). Two to 6 days after gene transfer, thrombosis was induced by the production of constant stenosis of the artery, and blood flow was measured continuously with an electromagnetic flow probe. A cyclic flow variation, which is thought to reflect the recurrent formation and dislodgment of mural thrombi, was observed in all AdCALacZ-infected arteries as well as in saline-infused arteries. In contrast, no cyclic flow variation was detectable in AdCATFPI-transfected arteries, even in the presence of epinephrine (1 microg. kg-1. min-1 infusion). Prothrombin time, activated partial thromboplastin time, and the ex vivo platelet aggregation induced by either adenosine diphosphate or collagen were unaltered in AdCATFPI-infected rabbits. We found that in vivo TFPI gene transfer into an injured artery completely inhibits the recurrent thrombosis induced by shear stress even in the presence of catecholamine, without affecting systemic coagulation status. Adenovirus-mediated local expression of TFPI may have the potential for the treatment of human thrombosis. (+info)
Antithrombotic efficacy of a novel murine antihuman factor IX antibody in rats. (6/733)A murine antihuman factor IX monoclonal antibody (BC2) has been generated and evaluated for its capacity to prolong the activated partial thromboplastin time (aPTT) in vitro and ex vivo and to prevent arterial thrombosis in a rat model in vivo. BC2 extended aPTT to a maximum of 60 to 80 seconds at 100 to 1000 nmol/L in vitro (rat and human plasma, respectively) and ex vivo (rat) after dosing of rats up to 6 mg/kg in vivo. BC2, administered as bolus (1 to 6 mg/kg) followed by infusion (0.3 to 2 mg x kg(-1) x h(-1)), dose-dependently prevented thrombosis of an injured rat carotid artery (FeCl(3)-patch model), increased time to artery occlusion, and reduced incidence of vessel occlusion. BC2 efficacy in preventing arterial thrombosis exceeded that of heparin (bolus 15 to 120 U/kg followed by infusion 0.5 to 4.0 U x kg(-1) x min(-1)), whereas the latter rendered the blood incoagulable (aPTT>1000 seconds). BC2 demonstrated complete antithrombotic efficacy also as a single bolus given either as prevessel or postvessel injury as evidenced by reduction of thrombus mass (from 4.18+/-0.49 to 1.80 +/-0.3 mg, P<0.001), increasing vessel patency time (from 14.9+/-0.9 minutes to 58.3+/-1.7 minutes, P<0.001) and decreasing incidence of vessel occlusion from 100% to 0% in vehicle- versus BC2-treated rats, respectively. BC2 (3 mg/kg, IV) administered in a single bolus resulted in 50% reduction in thrombus mass (P<0.01), extended vessel patency time (P<0.001), extended aPTT only 4-fold, and had no effect on blood loss via a tail surgical wound; heparin, at doses that reduced thrombus mass to a similar extent, extended aPTT beyond 1000 seconds (over 500-fold) and increased blood loss from 1.8+/-0.7 to 3.3 +/-0.6 mL (P<0.001). These data suggest that BC2 may provide enhanced therapeutic efficacy in humans at lesser interference with blood hemostasis than heparin. (+info)
An IgG antiprothrombin antibody enhances prothrombin binding to damaged endothelial cells and shortens plasma coagulation times. (7/733)OBJECTIVE: To test the hypothesis that some lupus anticoagulants are antiprothrombin antibodies, and that such antibodies enhance prothrombin binding to endothelial cells (EC) and thus promote clotting on the cell surface. METHODS: We generated a monoclonal antiprothrombin antibody (designated IS6) from a patient with primary antiphospholipid syndrome (APS). The antibody was analyzed for its binding properties, lupus anticoagulant activity, and pathophysiologic activity, using an EC-based plasma coagulation assay. RESULTS: IS6 is the first patient-derived monoclonal IgG antiprothrombin antibody. It bound to prothrombin with low affinity, reacted with 3 phospholipids (cardiolipin, phosphatidylethanolamine, and phosphatidylserine), and showed lupus anticoagulant activity. Moreover, IS6 enhanced the binding of prothrombin to damaged EC and shortened the EC-based plasma coagulation times. CONCLUSION: These findings suggest that IS6 may promote coagulation in areas of damaged EC in the host, and thus contribute to thrombosis in patients with APS. (+info)
Effect of maternal anticonvulsant treatment on neonatal blood coagulation. (8/733)AIMS: To investigate the impact of maternal anticonvulsant use on the ability of cord blood to coagulate. METHODS: Cord blood prothrombin times were measured, over 15 years in a consecutive series of 137 term babies born to women taking phenobarbitone, phenytoin, and/or carbamazepine while pregnant. The response to parenteral vitamin K was measured in 83 neonates. RESULTS: Only 14 of the 105 babies born to the mothers who had therapeutic anticonvulsant blood concentrations at birth had a prolonged prothrombin time (outside the 95% reference range). None had an overt bleeding tendency. The abnormality was corrected within 2 hours by 1 mg of parenteral vitamin K, but rapid intravenous prophylaxis produced complications in three infants. CONCLUSIONS: A policy of giving vitamin K throughout the last third of pregnancy to all women being treated with anticonvulsants, as recently recommended, is not justified by the available evidence. The belief that there is a distinct, early form of neonatal vitamin K deficiency that is different from, and more dangerous than, the classic form of the disease, is not supported by a review of the published evidence. (+info)
Types of Blood Coagulation Disorders:
1. Hemophilia A: A genetic disorder that affects the blood's ability to clot, leading to prolonged bleeding after injury or surgery.
2. Hemophilia B: Similar to hemophilia A, but caused by a deficiency of factor IX instead of factor VIII.
3. Von Willebrand Disease (VWD): A bleeding disorder caused by a deficiency of von Willebrand factor, which is needed for blood clotting.
4. Platelet Disorders: These include conditions such as low platelet count (thrombocytopenia) or abnormal platelet function, which can increase the risk of bleeding.
5. Coagulopathy: A general term for any disorder that affects the body's blood coagulation process.
Symptoms and Diagnosis:
Blood coagulation disorders can cause a range of symptoms, including easy bruising, frequent nosebleeds, and prolonged bleeding after injury or surgery. Diagnosis is typically made through a combination of physical examination, medical history, and laboratory tests such as blood clotting factor assays and platelet function tests.
Treatment and Management:
Treatment for blood coagulation disorders depends on the specific condition and its severity. Some common treatments include:
1. Infusions of clotting factor concentrates to replace missing or deficient factors.
2. Desmopressin, a medication that stimulates the release of von Willebrand factor and platelets.
3. Platelet transfusions to increase platelet count.
4. Anticoagulation therapy to prevent blood clots from forming.
5. Surgery to repair damaged blood vessels or joints.
Prevention and Prognosis:
Prevention of blood coagulation disorders is often challenging, but some steps can be taken to reduce the risk of developing these conditions. These include:
1. Avoiding trauma or injury that can cause bleeding.
2. Managing underlying medical conditions such as liver disease, vitamin deficiencies, and autoimmune disorders.
3. Avoiding medications that can interfere with blood clotting.
The prognosis for blood coagulation disorders varies depending on the specific condition and its severity. Some conditions, such as mild hemophilia A, may have a good prognosis with appropriate treatment, while others, such as severe hemophilia B, can have a poor prognosis without proper management.
Complications and Comorbidities:
Blood coagulation disorders can lead to a range of complications and comorbidities, including:
1. Joint damage and chronic pain due to repeated bleeding into joints.
2. Infection and sepsis from bacteria entering the body through bleeding sites.
3. Arthritis and other inflammatory conditions.
4. Nerve damage and neuropathy from bleeding into nerve tissue.
5. Increased risk of bleeding during surgery or trauma.
6. Emotional and social challenges due to the impact of the condition on daily life.
7. Financial burden of treatment and management costs.
8. Impaired quality of life, including reduced mobility and activity levels.
9. Increased risk of blood clots and thromboembolic events.
10. Psychological distress and anxiety related to the condition.
Blood coagulation disorders are a group of rare and complex conditions that can significantly impact quality of life, productivity, and longevity. These disorders can be caused by genetic or acquired factors and can lead to a range of complications and comorbidities. Diagnosis is often challenging, but prompt recognition and appropriate treatment can improve outcomes. Management strategies include replacing missing clotting factors, using blood products, and managing underlying conditions. While the prognosis varies depending on the specific condition and its severity, early diagnosis and effective management can improve quality of life and reduce the risk of complications.
There are several types of hypoprothrombinemias, including:
1. Classical hemophilia A: This is the most common type of hypoprothrombinemia and is caused by a deficiency of factor VIII, which is converted to prothrombin in the liver.
2. Non-classical hemophilia A: This type is less severe than classical hemophilia A and is also caused by a deficiency of factor VIII.
3. Prothrombin gene mutation: This is a rare type of hypoprothrombinemia caused by a mutation in the PROTHROMBIN gene, which is responsible for the production of prothrombin.
4. Acquired hypoprothrombinemia: This type can be caused by liver disease, vitamin K deficiency, or other conditions that affect the production or function of prothrombin.
The symptoms of hypoprothrombinemias can vary depending on the severity of the disorder and can include prolonged bleeding after injury or surgery, easy bruising, and frequent nosebleeds. Treatment for hypoprothrombinemias usually involves replacing the missing clotting factor or addressing any underlying conditions that may be contributing to the deficiency. In severe cases, liver transplantation may be necessary.
There are two main types of vitamin K deficiency:
1. Hypovitaminosis A (mild deficiency): This type of deficiency is characterized by low levels of vitamin K in the blood, but not low enough to cause bleeding or other serious symptoms. It can be caused by a diet that is low in vitamin K, or by conditions that interfere with vitamin K absorption, such as inflammatory bowel disease or liver disease.
2. Vitamin K deficiency bleeding (VKDB): This type of deficiency is characterized by bleeding that is caused by a lack of vitamin K. It can be caused by a diet that is very low in vitamin K, or by conditions that interfere with vitamin K absorption or clotting factor production.
Symptoms of vitamin K deficiency may include:
* Prolonged bleeding after injuries or surgery
* Bruising easily
* Bleeding gums
* Bloody stools
* Heavy menstrual periods
Causes of vitamin K deficiency may include:
* A diet that is low in vitamin K
* Conditions that interfere with vitamin K absorption, such as inflammatory bowel disease or liver disease
* Certain medications, such as anticoagulants (blood thinners)
* Malabsorption, such as in cases of celiac disease or Crohn's disease
* Vitamin K-dependent diseases, such as osteoporosis or cancer
Diagnosis of vitamin K deficiency is typically made based on a combination of symptoms, medical history, and laboratory tests. Treatment may involve supplementation with vitamin K, changes to the diet to increase vitamin K intake, and addressing any underlying conditions that may be contributing to the deficiency.
It is important to note that vitamin K deficiency can be difficult to diagnose, as symptoms can be subtle and may not always be immediately apparent. If you suspect you or someone you know may have a vitamin K deficiency, it is important to consult with a healthcare professional for proper evaluation and treatment.
In DIC, the body's normal blood coagulation mechanisms become overactive and begin to form clots throughout the circulatory system, including in small blood vessels and organs. This can cause a range of symptoms, including bleeding, fever, and organ failure.
DIC is often seen in sepsis, which is a severe infection that has spread throughout the body. It can also be caused by other conditions such as trauma, cancer, and autoimmune disorders.
Treatment of DIC typically involves addressing the underlying cause, such as treating an infection or injury, as well as supporting the body's natural clotting mechanisms and preventing further bleeding. In severe cases, hospitalization and intensive care may be necessary to monitor and treat the condition.
In summary, Disseminated Intravascular Coagulation (DIC) is a serious medical condition that can cause widespread clotting and damage to the body's organs and tissues. It is often seen in sepsis and other severe conditions, and treatment typically involves addressing the underlying cause and supporting the body's natural clotting mechanisms.
There are several types of thrombophilia, including:
1. Factor V Leiden: This is the most common inherited thrombophilia and is caused by a mutation in the Factor V gene.
2. Prothrombin G20210A: This is another inherited thrombophilia that is caused by a mutation in the Prothrombin gene.
3. Protein C and S deficiency: These are acquired deficiencies of protein C and S, which are important proteins that help to prevent blood clots.
4. Antiphospholipid syndrome: This is an autoimmune disorder that causes the body to produce antibodies against phospholipids, which can lead to blood clots.
5. Cancer-associated thrombophilia: This is a condition where cancer patients are at a higher risk of developing blood clots due to their cancer and its treatment.
6. Hormone-related thrombophilia: This is a condition where hormonal changes, such as those that occur during pregnancy or with the use of hormone replacement therapy, increase the risk of blood clots.
7. Inherited platelet disorders: These are rare conditions that affect the way platelets function and can increase the risk of blood clots.
8. Anti-cardiolipin antibodies: These are autoantibodies that can cause blood clots.
9. Lupus anticoagulant: This is an autoantibody that can cause blood clots.
10. Combined genetic and acquired risk factors: Some people may have a combination of inherited and acquired risk factors for thrombophilia.
Thrombophilia can be diagnosed through various tests, including:
1. Blood tests: These tests measure the levels of certain proteins in the blood that are associated with an increased risk of blood clots.
2. Genetic testing: This can help identify inherited risk factors for thrombophilia.
3. Imaging tests: These tests, such as ultrasound and venography, can help doctors visualize the blood vessels and look for signs of blood clots.
4. Thrombin generation assay: This test measures the body's ability to produce thrombin, a protein that helps form blood clots.
5. Platelet function tests: These tests assess how well platelets work and whether they are contributing to the development of blood clots.
Treatment for thrombophilia usually involves medications to prevent or dissolve blood clots, as well as measures to reduce the risk of developing new clots. These may include:
1. Anticoagulant drugs: These medications, such as warfarin and heparin, are used to prevent blood clots from forming.
2. Thrombolytic drugs: These medications are used to dissolve blood clots that have already formed.
3. Compression stockings: These stockings can help reduce swelling and improve blood flow in the affected limb.
4. Elevating the affected limb: This can help reduce swelling and improve blood flow.
5. Avoiding long periods of immobility: This can help reduce the risk of developing blood clots.
In some cases, surgery may be necessary to remove a blood clot or repair a damaged blood vessel. In addition, people with thrombophilia may need to make lifestyle changes, such as avoiding long periods of immobility and taking regular breaks to move around, to reduce their risk of developing blood clots.
Overall, the prognosis for thrombophilia is generally good if the condition is properly diagnosed and treated. However, if left untreated, thrombophilia can lead to serious complications, such as pulmonary embolism or stroke, which can be life-threatening. It is important for people with thrombophilia to work closely with their healthcare provider to manage the condition and reduce the risk of complications.
There are several types of hemorrhagic disorders, including:
1. Hemophilia: A genetic disorder that affects the blood's ability to clot and stop bleeding. People with hemophilia may experience spontaneous bleeding or bleeding after injury or surgery.
2. von Willebrand disease: A mild bleeding disorder caused by a deficiency of a protein called von Willebrand factor, which is important for blood clotting.
3. Platelet disorders: Disorders that affect the platelets, such as thrombocytopenia (low platelet count) or thrombocytosis (high platelet count).
4. Bleeding and clotting disorders caused by medications or drugs.
5. Hemorrhagic stroke: A type of stroke that is caused by bleeding in the brain.
6. Gastrointestinal bleeding: Bleeding in the digestive tract, which can be caused by a variety of factors such as ulcers, inflammation, or tumors.
7. Pulmonary hemorrhage: Bleeding in the lungs, which can be caused by a variety of factors such as pneumonia, injury, or tumors.
8. Retinal hemorrhage: Bleeding in the blood vessels of the retina, which can be caused by high blood pressure, diabetes, or other eye disorders.
Symptoms of hemorrhagic disorders can vary depending on the specific condition and the location of the bleeding. Common symptoms include bruising, petechiae (small red spots on the skin), nosebleeds, gum bleeding, and heavy menstrual periods. Treatment for hemorrhagic disorders depends on the underlying cause and may include medications, blood transfusions, or surgery.
Example sentence: The patient had a hemorrhage after the car accident and needed immediate medical attention.
There are several types of thrombosis, including:
1. Deep vein thrombosis (DVT): A clot forms in the deep veins of the legs, which can cause swelling, pain, and skin discoloration.
2. Pulmonary embolism (PE): A clot breaks loose from another location in the body and travels to the lungs, where it can cause shortness of breath, chest pain, and coughing up blood.
3. Cerebral thrombosis: A clot forms in the brain, which can cause stroke or mini-stroke symptoms such as weakness, numbness, or difficulty speaking.
4. Coronary thrombosis: A clot forms in the coronary arteries, which supply blood to the heart muscle, leading to a heart attack.
5. Renal thrombosis: A clot forms in the kidneys, which can cause kidney damage or failure.
The symptoms of thrombosis can vary depending on the location and size of the clot. Some common symptoms include:
1. Swelling or redness in the affected limb
2. Pain or tenderness in the affected area
3. Warmth or discoloration of the skin
4. Shortness of breath or chest pain if the clot has traveled to the lungs
5. Weakness, numbness, or difficulty speaking if the clot has formed in the brain
6. Rapid heart rate or irregular heartbeat
7. Feeling of anxiety or panic
Treatment for thrombosis usually involves medications to dissolve the clot and prevent new ones from forming. In some cases, surgery may be necessary to remove the clot or repair the damaged blood vessel. Prevention measures include maintaining a healthy weight, exercising regularly, avoiding long periods of immobility, and managing chronic conditions such as high blood pressure and diabetes.
Thromboembolism can be caused by a variety of factors, such as injury, surgery, cancer, and certain medical conditions like atrial fibrillation. It can also be inherited or acquired through genetic mutations.
The symptoms of thromboembolism depend on the location of the clot and the severity of the blockage. They may include:
* Swelling or redness in the affected limb
* Pain or tenderness in the affected area
* Weakness or numbness in the affected limb
* Shortness of breath or chest pain if the clot has traveled to the lungs (pulmonary embolism)
* Dizziness, lightheadedness, or fainting
Thromboembolism can be diagnosed through a variety of tests, such as ultrasound, computed tomography (CT), magnetic resonance imaging (MRI), and blood tests. Treatment typically involves anticoagulant medications to prevent the clot from growing and to prevent new clots from forming. In some cases, thrombolysis or clot-busting drugs may be used to dissolve the clot. Filters can also be placed in the vena cava to prevent clots from traveling to the lungs.
Prevention of thromboembolism includes:
* Moving around regularly to improve blood flow
* Avoiding long periods of immobility, such as during long-distance travel
* Elevating the affected limb to reduce swelling
* Compression stockings to improve blood flow
* Avoiding smoking and managing weight
* Taking anticoagulant medications if recommended by a healthcare provider.
There are many different types of liver diseases, including:
1. Alcoholic liver disease (ALD): A condition caused by excessive alcohol consumption that can lead to inflammation, scarring, and cirrhosis.
2. Viral hepatitis: Hepatitis A, B, and C are viral infections that can cause inflammation and damage to the liver.
3. Non-alcoholic fatty liver disease (NAFLD): A condition where there is an accumulation of fat in the liver, which can lead to inflammation and scarring.
4. Cirrhosis: A condition where the liver becomes scarred and cannot function properly.
5. Hemochromatosis: A genetic disorder that causes the body to absorb too much iron, which can damage the liver and other organs.
6. Wilson's disease: A rare genetic disorder that causes copper to accumulate in the liver and brain, leading to damage and scarring.
7. Liver cancer (hepatocellular carcinoma): Cancer that develops in the liver, often as a result of cirrhosis or viral hepatitis.
Symptoms of liver disease can include fatigue, loss of appetite, nausea, abdominal pain, dark urine, pale stools, and swelling in the legs. Treatment options for liver disease depend on the underlying cause and may include lifestyle changes, medication, or surgery. In severe cases, a liver transplant may be necessary.
Prevention of liver disease includes maintaining a healthy diet and lifestyle, avoiding excessive alcohol consumption, getting vaccinated against hepatitis A and B, and managing underlying medical conditions such as obesity and diabetes. Early detection and treatment of liver disease can help to prevent long-term damage and improve outcomes for patients.
1. Viral hepatitis (hepatitis A, B, or C)
2. Overdose of medications or supplements
3. Toxic substances (e.g., alcohol, drugs, or chemicals)
4. Sepsis or other infections that spread to the liver
5. Certain autoimmune disorders (e.g., hemochromatosis, Wilson's disease)
6. Cancer that has metastasized to the liver
7. Blood vessel blockage or clotting in the liver
8. Lack of blood flow to the liver
1. Jaundice (yellowing of skin and eyes)
2. Nausea and vomiting
3. Abdominal swelling and discomfort
4. Fatigue, weakness, and loss of appetite
5. Confusion or altered mental state
6. Seizures or coma
7. Pale or clay-colored stools
8. Dark urine
1. Physical examination and medical history
2. Laboratory tests (e.g., liver function tests, blood tests, imaging studies)
3. Biopsy of the liver tissue (to rule out other liver diseases)
1. Supportive care (fluids, nutrition, and medication to manage symptoms)
2. Addressing underlying causes (e.g., stopping alcohol or drug use, treating infections)
3. Transjugular intrahepatic portosystemic shunt (TIPS), a procedure that creates a new pathway for blood to flow through the liver
4. Liver transplantation (in severe cases where other treatments have failed)
The prognosis for acute liver failure depends on the underlying cause of the condition and the severity of the liver damage. In general, the earlier the diagnosis and treatment, the better the outcome. However, acute liver failure can be a life-threatening condition, and the mortality rate is high, especially in cases where there is severe liver damage or no available donor liver for transplantation.
The condition can be caused by a variety of factors, including excessive alcohol consumption, viral hepatitis, non-alcoholic fatty liver disease, and certain medications. It can also be a complication of other diseases such as hemochromatosis and Wilson's disease.
The symptoms of liver cirrhosis can vary depending on the severity of the disease, but may include fatigue, loss of appetite, nausea, abdominal swelling, and pain in the upper right side of the abdomen. As the disease progresses, it can lead to complications such as esophageal varices, ascites, and liver failure, which can be life-threatening.
There is no cure for liver cirrhosis, but treatment options are available to manage the symptoms and slow the progression of the disease. These may include medications to control swelling and pain, dietary changes, and in severe cases, liver transplantation. In some cases, a liver transplant may be necessary if the disease has caused significant damage and there is no other option to save the patient's life.
In conclusion, liver cirrhosis is a serious and potentially life-threatening condition that can cause significant damage to the liver and lead to complications such as liver failure. It is important for individuals to be aware of the risk factors and symptoms of the disease in order to seek medical attention if they suspect they may have liver cirrhosis. With proper treatment and management, it is possible to slow the progression of the disease and improve the patient's quality of life.
Factor X deficiency can be inherited or acquired, and it can have mild to severe effects on the body. People with factor X deficiency may experience prolonged bleeding after an injury or surgery, easy bruising, and frequent nosebleeds. In severe cases, factor X deficiency can lead to spontaneous bleeding, especially in the joints and internal organs.
There are two types of factor X deficiency:
1. Classic factor X deficiency: This is the most common type of factor X deficiency and is caused by a mutation in the gene that codes for factor X. It is usually inherited in an autosomal recessive pattern, which means that the child must inherit two copies of the mutated gene, one from each parent, to develop the condition.
2. Acquired factor X deficiency: This type of factor X deficiency can occur due to certain medical conditions, such as liver disease, vitamin K deficiency, or exposure to certain medications. It can also occur in people who have a high risk of bleeding, such as those with hemophilia.
Treatment for factor X deficiency typically involves replacing the missing clotting factor through infusions of factor X concentrate. In some cases, medications that help the body produce more factor X may also be used. People with factor X deficiency may need to receive regular infusions to maintain adequate levels of factor X in their blood.
Overall, factor X deficiency is a rare but potentially serious condition that can affect the body's ability to form blood clots and stop bleeding. With proper diagnosis and treatment, however, most people with factor X deficiency can lead normal lives.
Symptoms of venous thrombosis may include pain, swelling, warmth, and redness in the affected limb. In some cases, the clot can break loose and travel to the lungs, causing a potentially life-threatening condition called Pulmonary Embolism (PE).
Treatment for venous thrombosis typically involves anticoagulant medications to prevent the clot from growing and to prevent new clots from forming. In some cases, a filter may be placed in the vena cava, the large vein that carries blood from the lower body to the heart, to prevent clots from traveling to the lungs.
Prevention of venous thrombosis includes encouraging movement and exercise, avoiding long periods of immobility, and wearing compression stockings or sleeves to compress the veins and improve blood flow.
There are several causes of liver failure, including:
1. Alcohol-related liver disease: Prolonged and excessive alcohol consumption can damage liver cells, leading to inflammation, scarring, and eventually liver failure.
2. Viral hepatitis: Hepatitis A, B, and C are viral infections that can cause inflammation and damage to the liver, leading to liver failure.
3. Non-alcoholic fatty liver disease (NAFLD): A condition where there is an accumulation of fat in the liver, leading to inflammation and scarring.
4. Drug-induced liver injury: Certain medications can cause liver damage and failure, especially when taken in high doses or for extended periods.
5. Genetic disorders: Certain inherited conditions, such as hemochromatosis and Wilson's disease, can cause liver damage and failure.
6. Acute liver failure: This is a sudden and severe loss of liver function, often caused by medication overdose or other toxins.
7. Chronic liver failure: A gradual decline in liver function over time, often caused by cirrhosis or NAFLD.
Symptoms of liver failure can include:
1. Jaundice (yellowing of the skin and eyes)
3. Loss of appetite
4. Nausea and vomiting
5. Abdominal pain
6. Confusion and altered mental state
7. Easy bruising and bleeding
Diagnosis of liver failure is typically made through a combination of physical examination, medical history, and laboratory tests, such as blood tests to check for liver enzymes and bilirubin levels. Imaging tests, such as ultrasound and CT scans, may also be used to evaluate the liver.
Treatment of liver failure depends on the underlying cause and severity of the condition. In some cases, a liver transplant may be necessary. Other treatments may include medications to manage symptoms, such as nausea and pain, and supportive care to maintain nutrition and hydration. In severe cases, hospitalization may be required to monitor and treat complications.
Prevention of liver failure is important, and this can be achieved by:
1. Avoiding alcohol or drinking in moderation
2. Maintaining a healthy weight and diet
3. Managing underlying medical conditions, such as diabetes and high blood pressure
4. Avoiding exposure to toxins, such as certain medications and environmental chemicals
5. Getting vaccinated against hepatitis A and B
6. Practicing safe sex to prevent the spread of hepatitis B and C.
Factor XII deficiency can be acquired or inherited. Acquired factor XII deficiency can occur due to autoantibodies, liver disease, or vitamin K deficiency. Inherited factor XII deficiency is caused by mutations in the F12 gene, which is responsible for producing factor XII.
People with factor XII deficiency may experience recurring bleeding episodes, especially after injury or surgery. The bleeding can be severe and may occur spontaneously without any apparent cause. Other symptoms include easy bruising, petechiae (small red or purple spots on the skin), and nosebleeds.
Factor XII deficiency is diagnosed through blood tests that measure the levels of factor XII in the blood. A low level of factor XII indicates a deficiency. Other tests, such as a platelet aggregation test or a bleeding time test, may also be performed to assess the severity of the condition.
Treatment for factor XII deficiency typically involves replacing the missing factor XII with infusions of the protein. This can be done on an as-needed basis or regularly, depending on the severity of the condition. Desmopressin, a hormone that stimulates the release of von Willebrand factor and platelets, may also be used to treat mild cases of factor XII deficiency. In severe cases, surgery may be necessary to repair damaged blood vessels or organs.
The prognosis for factor XII deficiency is generally good if the condition is properly treated. With regular infusions of factor XII and proper management, most people with the condition can lead normal lives and avoid complications. However, untreated factor XII deficiency can lead to serious complications, such as bleeding or organ damage, which can be life-threatening.
There are no specific lifestyle changes that can cure factor XII deficiency, but certain lifestyle modifications may help manage the condition. These include avoiding activities that could trigger bleeding, taking regular breaks to rest and elevate the affected limb, and avoiding alcohol and other drugs that can exacerbate the condition.
There are no alternative treatments for factor XII deficiency, as infusions of the protein are the only effective way to manage the condition. However, some complementary therapies, such as acupuncture or herbal supplements, may help reduce symptoms and improve quality of life.
Factor XII deficiency cannot be prevented, as it is an inherited condition. However, early diagnosis and proper management can help prevent complications and ensure a good prognosis. Pregnant women with a history of factor XII deficiency should receive regular prenatal care to monitor the health of their baby.
Living With Factor XII Deficiency:
Living with factor XII deficiency can be challenging, as it can impact daily life and increase the risk of bleeding. However, with proper management and support, people with this condition can lead fulfilling lives. It is essential to work closely with a healthcare provider to develop a personalized treatment plan and make necessary lifestyle adjustments.
The prognosis for factor XII deficiency is generally good if the condition is properly managed. With regular infusions of the protein, most people with this condition can lead normal lives and avoid serious complications. However, in some cases, the condition may progress to more severe bleeding episodes or other complications, which can be life-threatening.
In conclusion, factor XII deficiency is a rare genetic disorder that can cause excessive bleeding due to a lack of a critical blood clotting protein. While there is no cure for the condition, infusions of the protein can help manage symptoms and prevent complications. Early diagnosis and proper management are essential to ensure a good prognosis and improve quality of life for those affected by this condition.
This condition is most commonly seen in people with advanced liver disease, such as cirrhosis or liver cancer. It can also be caused by other conditions that affect the liver, such as hepatitis or portal hypertension.
Symptoms of hepatic encephalopathy can include confusion, disorientation, slurred speech, memory loss, and difficulty with coordination and balance. In severe cases, it can lead to coma or even death.
Diagnosis of hepatic encephalopathy is typically made through a combination of physical examination, medical history, and diagnostic tests such as blood tests and imaging studies. Treatment options include medications to reduce the production of ammonia in the gut, antibiotics to treat any underlying infections, and transjugular intrahepatic portosystemic shunt (TIPS) to improve liver function. In severe cases, a liver transplant may be necessary.
Overall, hepatic encephalopathy is a serious condition that can have significant impact on quality of life and survival in people with advanced liver disease. Early detection and prompt treatment are essential to prevent complications and improve outcomes.
Symptoms of hemophilia A can include spontaneous bleeding, easy bruising, and prolonged bleeding after injury or surgery. Treatment typically involves replacing the missing factor VIII with infusions of clotting factor concentrate, which helps to restore the blood's ability to clot and stop bleeding. Regular infusions are often needed to prevent bleeding episodes, and patients with severe hemophilia A may require lifelong treatment.
Complications of hemophilia A can include joint damage, muscle weakness, and chronic pain. In severe cases, the condition can also increase the risk of bleeding in the brain or other internal organs, which can be life-threatening. However, with proper treatment and management, most patients with hemophilia A can lead active and relatively normal lives.
It is important to note that there is no cure for hemophilia A, but advances in medical technology and treatment have significantly improved the quality of life for many patients with the condition.
1. Injury to blood vessels during surgery
2. Poor suturing or stapling techniques
3. Bleeding disorders or use of anticoagulant medications
4. Infection or hematoma (a collection of blood outside the blood vessels)
5. Delayed recovery of blood clotting function
Postoperative hemorrhage can range from mild to severe and life-threatening. Mild bleeding may present as oozing or trickling of blood from the surgical site, while severe bleeding can lead to hypovolemic shock, organ failure, and even death.
To diagnose postoperative hemorrhage, a physical examination and medical history are usually sufficient. Imaging studies such as ultrasound, computed tomography (CT) or magnetic resonance imaging (MRI) may be ordered to evaluate the extent of bleeding and identify any underlying causes.
Treatment of postoperative hemorrhage depends on the severity and location of the bleeding. Mild bleeding may be managed with dressings, compression bandages, and elevation of the affected limb. Severe bleeding may require interventions such as:
1. Surgical exploration to locate and control the source of bleeding
2. Transfusion of blood products or fresh frozen plasma to restore clotting function
3. Use of vasopressors to raise blood pressure and perfuse vital organs
4. Hemostatic agents such as clotting factors, fibrin sealants, or hemostatic powder to promote clot formation
5. In some cases, surgical intervention may be required to repair damaged blood vessels or organs.
Prevention of postoperative hemorrhage is crucial in reducing the risk of complications and improving patient outcomes. Preventive measures include:
1. Proper preoperative evaluation and preparation, including assessment of bleeding risk factors
2. Use of appropriate anesthesia and surgical techniques to minimize tissue trauma
3. Conservative use of hemostatic agents and blood products during surgery
4. Closure of all bleeding sites before completion of the procedure
5. Monitoring of vital signs, including pulse rate and blood pressure, during and after surgery
6. Preoperative and postoperative management of underlying conditions such as hypertension, diabetes, and coagulopathies.
Early recognition and prompt intervention are critical in effectively managing postoperative hemorrhage. In cases of severe bleeding, timely and appropriate interventions can reduce the risk of complications and improve patient outcomes.
The definition of DILI has been revised several times over the years, but the most recent definition was published in 2013 by the International Consortium for DILI Research (ICDCR). According to this definition, DILI is defined as:
"A clinically significant alteration in liver function that is caused by a medication or other exogenous substance, and is not related to underlying liver disease. The alteration may be biochemical, morphological, or both, and may be acute or chronic."
The ICDCR definition includes several key features of DILI, including:
1. Clinically significant alteration in liver function: This means that the liver damage must be severe enough to cause symptoms or signs of liver dysfunction, such as jaundice, nausea, vomiting, or abdominal pain.
2. Caused by a medication or other exogenous substance: DILI is triggered by exposure to certain drugs or substances that are not related to underlying liver disease.
3. Not related to underlying liver disease: This means that the liver damage must not be caused by an underlying condition such as hepatitis B or C, alcoholic liver disease, or other genetic or metabolic disorders.
4. May be acute or chronic: DILI can occur as a sudden and severe injury (acute DILI) or as a slower and more insidious process (chronic DILI).
The ICDCR definition provides a standardized way of defining and diagnosing DILI, which is important for clinicians and researchers to better understand the cause of liver damage in patients who are taking medications. It also helps to identify the drugs or substances that are most likely to cause liver injury and to develop strategies for preventing or treating DILI.
In general, surgical blood loss is considered excessive if it exceeds 10-20% of the patient's total blood volume. This can be determined by measuring the patient's hemoglobin levels before and after the procedure. A significant decrease in hemoglobin levels post-procedure may indicate excessive blood loss.
There are several factors that can contribute to surgical blood loss, including:
1. Injury to blood vessels or organs during the surgical procedure
2. Poor surgical technique
3. Use of scalpels or other sharp instruments that can cause bleeding
4. Failure to control bleeding with proper hemostatic techniques
5. Pre-existing medical conditions that increase the risk of bleeding, such as hemophilia or von Willebrand disease.
Excessive surgical blood loss can lead to a number of complications, including:
1. Anemia and low blood counts
2. Hypovolemic shock (a life-threatening condition caused by excessive fluid and blood loss)
3. Infection or sepsis
4. Poor wound healing
5. Reoperation or surgical intervention to control bleeding.
To prevent or minimize surgical blood loss, surgeons may use a variety of techniques, such as:
1. Applying topical hemostatic agents to the surgical site before starting the procedure
2. Using energy-based devices (such as lasers or ultrasonic devices) to seal blood vessels and control bleeding
3. Employing advanced surgical techniques that minimize tissue trauma and reduce the risk of bleeding
4. Monitoring the patient's hemoglobin levels throughout the procedure and taking appropriate action if bleeding becomes excessive.
Note: This definition may have some variations in different contexts and medical fields.
APC resistance can be caused by genetic or acquired factors and can lead to a range of clinical presentations, including:
1. Hereditary bleeding disorders: Familial APC resistance is caused by mutations in the APC gene and can result in severe bleeding, especially during childhood.
2. Acquired APC resistance: This can occur due to certain medical conditions, such as liver disease, sepsis, or cancer, which can impair APC function.
3. Drug-induced APC resistance: Certain medications, like anticoagulants, can reduce APC activity and lead to APC resistance.
Diagnosis of APC resistance typically involves testing for APC activity in the blood, as well as genetic analysis to identify mutations in the APC gene. Treatment options for APC resistance depend on the underlying cause and may include:
1. Fresh frozen plasma (FFP): FFP can be used to replace missing or deficient APC in the blood.
2. Recombinant APC: This is a synthetic version of APC that can be used to replace missing or deficient APC.
3. Anticoagulants: These medications can help prevent blood clots and reduce the risk of thrombotic events.
4. Platelet inhibitors: These medications can help prevent platelet aggregation, which can contribute to bleeding.
Overall, APC resistance is a rare but important condition that can affect blood coagulation and increase the risk of bleeding or thrombotic events. Prompt diagnosis and appropriate treatment are essential to manage the condition effectively and prevent complications.
Vitamin K deficiency bleeding
Rabbit hemorrhagic disease
Liver function tests
Armand J. Quick
Deep vein thrombosis
Factor X deficiency
The International Committee for Standardization of Hematology
Sex differences in human physiology
Pericardial heart valves
Lower gastrointestinal bleeding
CU-2010 and CU-2020
Eastern brown snake
Acute liver failure
List of MeSH codes (G09)
Polycystic liver disease
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- The prothrombin time (PT) represents the most commonly used coagulation test in clinical laboratories. (nih.gov)
- PT or prothrombin time is derived from the prothrombin ratio along with the international normalized ratio to measure the extrinsic coagulation pathway. (differencebetween.net)
- On the other hand, PTT, or the partial thromboplastin time, is the measurement of the intrinsic coagulation pathway and the common coagulation pathway. (differencebetween.net)
- Complication includes coagulation impairment however Shortened activated partial thromboplastin time (aPTT) values may reflect hypercoaguable state, which is associated with increased thrombotic risk and adverse cardiovascular events. (who.int)
- By measuring the amount of time the body takes to form a blood clot in a test tube, the aPTT test can determine the amount and the function of certain coagulation factors. (anylabtestnow.com)
- Most of the time, results are also given as what is called INR (international normalized ratio). (medlineplus.gov)
- The INR or international normalized ratio provides an estimated time that a normal blood plasma sample will take to form the clot. (flebo.in)
- Advancements in the treatment of warfarin-associated intracranial hemorrhage (ICH) include the use of four-factor prothrombin complex concentrate (4F-PCC), which has demonstrated more rapid reversal of the international normalized ratio (INR) when compared with fresh frozen plasma. (medscape.com)
- Prolonged prothrombin time (PT) and international normalized ratio (INR) (24 to 72 hours after exposure) persisting for weeks to months, as determined by hospital laboratory tests. (cdc.gov)
- A related blood test is partial thromboplastin time (PTT) , which measures the function of a different part of the clotting system. (medlineplus.gov)
- Two of the most effective measurements relating to anti-coagulants are prothrombin time and partial thromboplastin time. (differencebetween.net)
- Prothrombin time (PT) and activated partial thromboplastin time (aPTT) may be prolonged in patients with DIC. (medscape.com)
- Along with a PT/INR test, a partial thromboplastin time (PTT) test is regularly done. (newsparq.com)
- Effect of diabetes mellitus type ii on activated partial thromboplastin time and prothrombin time. (who.int)
- The Activated Partial Thromboplastin Time (aPTT) measures the body's Ability To Form Blood Clots appropriately. (anylabtestnow.com)
- Abnormal assays for factors II and VII in patients with unexplained bleeding and a normal PT, partial thromboplastin time, or INR, as determined by hospital or commercial laboratory tests. (cdc.gov)
- This study investigated the in vivo effect of alum on platelet aggregation and bleeding time in rabbits. (who.int)
- contradiction in the mechanism of action of alum, we evaluated the in vivo effect of Alum (aluminium potassium sulfate) is a alum in terms of collagen-induced platelet food additive and traditional remedy used to aggregation and bleeding time. (who.int)
- If more than 24 hours have elapsed since ingestion, decontamination measures are not effective and the patient should be monitored closely using prothrombin time (PT) and plasma thromboplastin time (PTT). (inchem.org)
- ABSTRACT Traditionally known as a haemostatic agent, alum shows a paradoxical effect of increased prothrombin and partial thromboplastin times. (who.int)
- 2. PT stands for prothrombin time and is used to ascertain whether the dosage of Warfarin needs to be adjusted or not. (differencebetween.net)
- The prothrombin time test also monitors the effects of the medicine warfarin. (flebo.in)
- If you're on a blood-thinning medication like warfarin, heparin, enoxaparin, etc. this test is suggested regularly to watch the doses or to ascertain if the therapy is functioning.The Prothrombin Time test can also be performed to gauge your disease. (orangehealth.in)
- The Prothrombin Time (PT) test is used to measure:The plasma's ability to clot to detect a bleeding disorder or clotting disorder and to watch the consequences of the anticoagulant medication, warfarin.In the event of any bleeding, the body responds by forming a grume to stop the blood loss as quickly as possible.The effectiveness of the warfarin treatment. (orangehealth.in)
- Prothrombin Time (PT): 8.7-11.5 seconds.International normalised ratio (INR): 0.8-1.2INR during warfarin treatment: 2.0 to 3.0. (orangehealth.in)
- The purpose of this study was to evaluate the impact of a pharmacist-driven protocol on time to 4F-PCC administration in warfarin-associated ICH. (medscape.com)
- Implementation of a pharmacist-driven protocol for 4F-PCC in the ED at our institution significantly reduced time to administration in patients presenting with warfarin-associated ICH. (medscape.com)
- Until recently, warfarin-associated ICH in the United States was typically treated with fresh frozen plasma (FFP) and intravenous (IV) vitamin K. [ 2 ] However, a four-factor prothrombin complex concentrate (4F-PCC) was approved by the U.S. Food and Drug Administration (FDA) in 2013 and has since become widely available for reversal of vitamin K antagonists, such as warfarin. (medscape.com)
- Prothrombin time (PT) is a blood test that measures the time it takes for the liquid portion (plasma) of your blood to clot. (medlineplus.gov)
- This test also measures the time it takes for blood to clot. (cdc.gov)
- The duration required for a blood clot to form is measured with a prothrombin time (PT) test . (newsparq.com)
- Since the Prothrombin time (PT) evaluates the ability of blood to clot properly, it can be used to help diagnose bleeding. (healthonelabs.com)
- The prothrombin time or pt inr test in Noida is conducted to check the time that prothrombin takes in order to form a clot. (flebo.in)
- The test measures the time that prothrombin takes to form a clot. (flebo.in)
- This is done by collecting the plasma from the blood and subjecting it to some tissue factor and then recording the time taken for the clot to form. (flebo.in)
- The time taken for the clot to form is between 10 to 13 seconds. (flebo.in)
- In a PT test, chemicals are added to your blood sample, and the lab measures the time in seconds that it takes to clot. (rochester.edu)
- The INR is a ratio, so it's just a number, not a number tied to time or another value. (rochester.edu)
- A clinically compatible case in which a high index of suspicion (credible threat or patient history regarding location and time) exists for a long-acting anticoagulant exposure, or an epidemiologic link exists between this case and a laboratory-confirmed case. (cdc.gov)
- Why should I book a Prothrombin Time (PT) test with Orange Health Labs in Delhi? (orangehealth.in)
- This is the normal time, in seconds. (flebo.in)
- In terms of INR, 1.1 or below is considered normal, and the prothrombin functioning is healthy. (flebo.in)
- What are the normal ranges for the Prothrombin Time(PT) test? (orangehealth.in)
- The four infants had laboratory-confirmed coagulopathy, defined as elevation of prothrombin time (PT) greater than or equal to four times the laboratory limit of normal, correctable by vitamin K administration, and symptomatic bleeding. (cdc.gov)
- The results of this test will show a longer clotting time among some people with VWD. (cdc.gov)
- This is because the levels of clotting factors in the blood vary over time as a result of changes the body might be reacting to―such as stress, pregnancy, and infections―that can affect the test results. (cdc.gov)
- The INR is found using the results of the prothrombin time (PT) test. (rochester.edu)
- PURPOSE: Results of an investigation of the pharmacodynamic effect of rivaroxaban anticoagulation, as measured by prothrombin time (PT), on bleeding risk and other outcomes in hospitalized patients are reported. (wustl.edu)
- In a survey of United Kingdom (UK) stroke physicians, specific delays identified included time to hematology approval for 4F-PCC use, time to receive INR results, time to 4F-PCC delivery to the emergency department (ED), and time to infusion start. (medscape.com)
- Although mortality rates after CVT have declined over time, this condition can result in devastating neurologic outcomes. (lww.com)
- Typically, PTT and PT are conducted at the same time in order to trace the source of the disease if clotting factors are lacking or if clotting factors are being used up faster than they should be. (differencebetween.net)
- Often these tests need to be repeated several times before an accurate diagnosis can be made. (cdc.gov)
- Association between prothrombin time and bleeding in hospitalized patients receiving rivaroxaban. (wustl.edu)
- Ces résultats semblent indiquer que l'utilisation de l'alun en tant qu'antiplaquettaire oral pourrait faire l'objet d'études complémentaires, en tenant compte des effets secondaires éventuels notamment chez les patients dont la fonction rénale est altérée. (who.int)
- The relative risk for developing late VKDB has been estimated at 81 times greater among infants who do not receive intramuscular vitamin K than in infants who do receive it ( 4 ). (cdc.gov)
- In all cases, parental knowledge about the risk for development of late VKDB was either incomplete or absent at the time of declining prophylaxis, with most parents learning about the possibility of late VKDB only after their infants developed the condition. (cdc.gov)
- The mean value of prothrombin time (PT) among T2DM individuals was (14.04 ±2.96) seconds and the mean value of PT among healthy individuals was (13.5 ± 1.54) seconds. (who.int)
- A second UK hospital observed a large delay in 4F-PCC administration with a median time of approximately five hours from initial presentation and almost two hours after vitamin K administration. (medscape.com)
- Treatment is based on the administration of vitamin K1 (phytomenadione) as indicated by the prothrombin time. (inchem.org)
- L'agrégation plaquettaire induite par le collagène dans des échantillons de plasma riche en plaquettes de 14 lapins sains a été mesurée par turbidimétrie en utilisant un agrégomètre, avant et une heure après une injection intra- veineuse d'alun. (who.int)
- Sample physicians were screened at the time of the survey to assure that they met the above-mentioned criteria, 794 physicians did not meet all of the criteria and were, therefore, ruled out of scope (ineligible) for the study. (cdc.gov)
- The rationale behind the number of clotting factors checked by PT is the fact that prothrombin is factor II of the clotting factors and thus serves as the one for checking the other four clotting factors. (differencebetween.net)
- Prothrombin or factor II is essential for clotting. (flebo.in)
- It is this factor that determines how soon or how delayed the clotting time is. (flebo.in)
- At the same time a group of 20 randomly selected healthy adults to participate in the study as control group. (who.int)
- Both high and low production of prothrombin is harmful to the body. (flebo.in)
- The prothrombin time test requires blood samples for the checking procedure. (flebo.in)
- They live in a high-rise apartment building where the patient has been a handyman and part-time building manager for the past year. (cdc.gov)
- The Prothrombin Time (PT) test is prescribed by your doctor after a complete assessment of your symptoms and conditions. (orangehealth.in)
- OSHA STEL (short-term exposure limit) = 10 ppm (over a 15-minute time period). (cdc.gov)
- If you log out, you will be required to enter your username and password the next time you visit. (medscape.com)
- This means that every time you visit this website you will need to enable or disable cookies again. (anylabtestnow.com)