Protein c and protein s
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Protein C and protein S are proteins that help regulate blood clot formation. They work together to inactivate factors V and VIII, slowing down clot formation. Deficiencies in protein C or protein S can lead to excessive clotting. There are inherited and acquired causes of low levels or abnormal function of these proteins. Inherited causes include insufficient production or abnormal function, while acquired causes include liver disease, vitamin K deficiency, and certain medical conditions or treatments.
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Paroxysmal nocturnal hematuria
Paroxysmal nocturnal hemoglobinuria (PNH) is a rare, acquired hematopoietic stem cell disorder characterized by hemolytic anemia. It arises due to a somatic mutation in the PIGA gene, causing deficiency of glycosylphosphatidylinositol-anchored proteins (GPI-APs) like CD55 and CD59 on the surface of blood cells. This renders the cells highly sensitive to complement-mediated lysis. Diagnosis involves flow cytometry to detect GPI-AP deficiency and tests like Ham and sucrose hemolysis to demonstrate complement sensitivity of the red blood cells. PNH is associated with hemoglobinuria, thrombosis, and bone marrow failure. It requires differentiation
Thrombophilia
Inherited thrombophilias such as deficiencies of protein C, protein S, and antithrombin III increase the risk of blood clots. Protein C, protein S, and antithrombin III are natural anticoagulants that help regulate the coagulation pathway. Deficiencies can be caused by genetic mutations and result in reduced levels or functions of these proteins. Clinical manifestations of deficiencies include venous thromboembolism, neonatal purpura fulminans, and arterial thrombosis. Diagnosis involves testing plasma levels of the deficient protein. Treatment involves long-term anticoagulation with warfarin or direct oral anticoagulants to prevent blood clots.
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Thrombophilia
Inherited thrombophilias such as deficiencies of protein C, protein S, and antithrombin III increase the risk of blood clots. Protein C, protein S, and antithrombin III are natural anticoagulants that help regulate the coagulation pathway. Deficiencies can be caused by genetic mutations and result in reduced levels or functions of these proteins. Clinical manifestations of deficiencies include venous thromboembolism, neonatal purpura fulminans, and arterial thrombosis. Diagnosis involves testing plasma levels of the deficient protein. Treatment involves long-term anticoagulation with warfarin or direct oral anticoagulants to prevent blood clots.
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- Ascitic fluid appearance can indicate underlying conditions, such as clear fluid indicating uncomplicated cirrhosis, milky fluid indicating malignancy or lymphoma, and bloody fluid indicating trauma or malignancy.
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1) Hemoglobinopathies are inherited disorders affecting hemoglobin structure or production, ranging from asymptomatic to fatal. The most common types are sickle cell disease and thalassemias.
2) Thalassemias are caused by deficient production of globin chains, leading to imbalanced globin synthesis and red blood cell damage. Beta thalassemias result from low beta chain production while alpha thalassemias involve alpha chains.
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G6PD Deficiency Anaemai
- Individuals with G6PD deficiency do not show symptoms until exposed to oxidative stress, such as certain foods or medicines.
- G6PD is responsible for producing NADPH, which generates glutathione to protect red blood cells from damage by free radicals. In G6PD deficiency, insufficient NADPH leads to hemolysis upon exposure to oxidative stress.
- Diagnosis involves testing for G6PD enzyme activity levels, which are reduced in deficiency. Exposure to oxidative triggers can cause a hemolytic crisis characterized by dark urine and jaundice.
Iron metabolism
Iron is an essential micronutrient, but both iron deficiency and excess can be harmful. Iron deficiency anemia affects 65-75% of people in India and can impact growth and development. The body tightly regulates iron levels through absorption in the duodenum, transport by transferrin, and storage in ferritin and hemosiderin. Hepcidin is the key regulator of iron absorption and release, inhibiting the iron exporter ferroportin. Disorders of iron metabolism include iron deficiency anemia, hemosiderosis, and hereditary hemochromatosis.
Bilirubin metabolism
- Old red blood cells are broken down, releasing bilirubin which is transported to the liver.
- In the liver, bilirubin is conjugated and excreted into bile ducts. It then passes to the intestines where bacteria convert it into urobilinogen.
- Jaundice occurs when there is excessive bilirubin production, impaired uptake or conjugation in the liver, or obstruction of bile flow, leading to accumulation of bilirubin in blood.
- Neonatal jaundice is common and usually temporary, due to the immature liver's reduced ability to clear bilirubin from the blood. Some genetic conditions can also cause jaundice
Acute phase reactants
It is an increase in the concentration of serum proteins (APR) accompanies inflammation and tissue injury. Focus on the acute phase phenomenon, termed the acute phase response, first occurred with the discovery of C-reactive protein (CRP) in the serum of patients during the acute phase of pneumococcal pneumonia. During the acute phase response, usual levels of various proteins maintained by homeostatic mechanisms can change substantially. These changes are thought to contribute to host defense and other adaptive capabilities.
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2) The basic mechanisms of thrombocytopenia include decreased platelet production, ineffective production, increased destruction, increased consumption, and sequestration.
3) Diagnosing thrombocytopenia involves ruling out pseudothrombocytopenia, examining the blood counts, bone marrow, and performing additional lab tests to determine the underlying cause and guide treatment.
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Platelet function testing assesses platelet adhesion, activation, granule release and aggregation in response to agonists using light transmission platelet aggregometry (LTA) as the gold standard test. Abnormal LTA results can indicate defects in platelet adhesion receptors, activation and secretion, aggregation receptors, or the thromboxane pathway. The pattern of abnormal aggregation in response to different agonists helps localize the platelet function defect.
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ASCITIC FLUID ANALYSIS
- Ascitic fluid appearance can indicate underlying conditions, such as clear fluid indicating uncomplicated cirrhosis, milky fluid indicating malignancy or lymphoma, and bloody fluid indicating trauma or malignancy.
- Diagnosis of ascites involves physical examination and ultrasound, as 1,500mL of fluid is needed for flank dullness. Cell count with differential is most helpful test, with >250 polymorphonuclear cells indicating spontaneous bacterial peritonitis.
- Causes of ascites include portal hypertension from cirrhosis, hypoalbuminemia, peritoneal disease like cancer, and other rare conditions. Serum-ascites albumin gradient helps determine if ascites is caused by portal hypertension.
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The hemoglobin E thalassemias
Hemoglobin E beta-thalassemia is caused by coinheritance of the hemoglobin E structural variant and a beta-thalassemia mutation. It has wide clinical heterogeneity, ranging from asymptomatic to life-threatening. Factors influencing severity include the specific beta-thalassemia mutation, coinheritance of alpha-thalassemia, levels of fetal hemoglobin, amounts of abnormal hemoglobin E mRNA splicing, and environmental exposures like malaria. Treatment depends on symptoms and severity, with regular blood transfusions for more severe cases and options like hydroxyurea or bone marrow transplantation in some situations.
sideroblastic anemia
This document discusses sideroblastic anemia, which is caused by an abnormal accumulation of iron in the mitochondria of red blood cell precursors called ring sideroblasts. There are several types of sideroblastic anemia, including hereditary forms caused by genetic mutations and acquired forms caused by drugs, toxins, or diseases. The condition is characterized by ring sideroblasts seen on bone marrow biopsy along with ineffective red blood cell production and iron overload. Treatment depends on the underlying cause but may include blood transfusions, vitamin supplements, iron chelation therapy, or bone marrow transplant in severe cases.
DISSEMINATED INTRAVASCULAR COAGULATION
DIC is one condition that always trouble patients and doctor, though its a nightmare for any clinician , its also a potent question in both UG and PG exams. I hope this will help you in answering those questions well.
Hemoglobinopathies
1) Hemoglobinopathies are inherited disorders affecting hemoglobin structure or production, ranging from asymptomatic to fatal. The most common types are sickle cell disease and thalassemias.
2) Thalassemias are caused by deficient production of globin chains, leading to imbalanced globin synthesis and red blood cell damage. Beta thalassemias result from low beta chain production while alpha thalassemias involve alpha chains.
3) Clinical features vary by specific disorder from mild anemia to transfusion-dependent anemia and organ damage. Management involves treatment of complications, transfusions, chelation therapy, and in severe cases, stem cell transplant.
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challenges in interpreting abnormal hemoglobin study- the key is to correlate with patient age, ethnicity,RBC indices & morphology findings. Two tier approach for correct characterization of abnormal hemoglobins of HPLC &/or capillary electrophoresis.
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This document summarizes platelet function testing. It discusses how platelets are formed from megakaryocytes in the bone marrow and circulate in the bloodstream. The major platelet function tests are platelet aggregometry, flow cytometry, and point-of-care tests like the impact cone and plate analyzer and thromboelastography. These tests are used to diagnose platelet disorders and monitor antiplatelet therapy. The document also briefly discusses platelet-derived microparticles and microRNAs, which can provide information about platelet activation and signaling.
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G6PD Deficiency Anaemai
- Individuals with G6PD deficiency do not show symptoms until exposed to oxidative stress, such as certain foods or medicines.
- G6PD is responsible for producing NADPH, which generates glutathione to protect red blood cells from damage by free radicals. In G6PD deficiency, insufficient NADPH leads to hemolysis upon exposure to oxidative stress.
- Diagnosis involves testing for G6PD enzyme activity levels, which are reduced in deficiency. Exposure to oxidative triggers can cause a hemolytic crisis characterized by dark urine and jaundice.
Iron metabolism
Iron is an essential micronutrient, but both iron deficiency and excess can be harmful. Iron deficiency anemia affects 65-75% of people in India and can impact growth and development. The body tightly regulates iron levels through absorption in the duodenum, transport by transferrin, and storage in ferritin and hemosiderin. Hepcidin is the key regulator of iron absorption and release, inhibiting the iron exporter ferroportin. Disorders of iron metabolism include iron deficiency anemia, hemosiderosis, and hereditary hemochromatosis.
Bilirubin metabolism
- Old red blood cells are broken down, releasing bilirubin which is transported to the liver.
- In the liver, bilirubin is conjugated and excreted into bile ducts. It then passes to the intestines where bacteria convert it into urobilinogen.
- Jaundice occurs when there is excessive bilirubin production, impaired uptake or conjugation in the liver, or obstruction of bile flow, leading to accumulation of bilirubin in blood.
- Neonatal jaundice is common and usually temporary, due to the immature liver's reduced ability to clear bilirubin from the blood. Some genetic conditions can also cause jaundice
Acute phase reactants
It is an increase in the concentration of serum proteins (APR) accompanies inflammation and tissue injury. Focus on the acute phase phenomenon, termed the acute phase response, first occurred with the discovery of C-reactive protein (CRP) in the serum of patients during the acute phase of pneumococcal pneumonia. During the acute phase response, usual levels of various proteins maintained by homeostatic mechanisms can change substantially. These changes are thought to contribute to host defense and other adaptive capabilities.
Albumin and albumin & globin ratio
albumin role , synthesis, function, factor affect, increase in , decrease in use of a\g ratio how calculate a\g ratio. why need,
Platelet Aggregation
A patient has a history of recurrent gum bleeding since childhood. While platelet counts and coagulation tests are normal, an inherited platelet disorder is suspected. The doctor's diagnostic approach would include a detailed bleeding history, physical exam looking for bruises/petechiae, and first-line screening tests like a bleeding time and platelet function analyzer. Further specific tests may include light transmission aggregometry to assess platelet aggregation in response to various agonists and help identify potential defects in adhesion, activation, secretion or aggregation. Interpreting the different waveforms is important to determine abnormalities consistent with disorders like Glanzmann's thrombasthenia or storage pool disease.
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This document provides an overview of pancytopenia, including its definition, etiology, clinical presentation, diagnostic workup, and treatment approach. Pancytopenia is defined as a low hemoglobin, white blood cell count, and platelet count. It can be caused by primary bone marrow diseases or secondary to other conditions that impair bone marrow function. The diagnostic workup involves blood tests, peripheral smear examination, bone marrow aspiration and biopsy for cytogenetics and immunophenotyping to identify the underlying cause. Specific tests help diagnose conditions like Fanconi anemia, lymphoproloferative disorders, and paroxysmal nocturnal hemoglobinuria. Treatment is directed at managing the specific disease identified as the cause
Approach to thrombocytopenia.pptx
The document provides information on evaluating and diagnosing thrombocytopenia, including:
1) Normal platelet counts range from 150,000-450,000/microL and are slightly higher in females and younger people. Thrombocytopenia is defined as a platelet count below 150,000/microL.
2) The basic mechanisms of thrombocytopenia include decreased platelet production, ineffective production, increased destruction, increased consumption, and sequestration.
3) Diagnosing thrombocytopenia involves ruling out pseudothrombocytopenia, examining the blood counts, bone marrow, and performing additional lab tests to determine the underlying cause and guide treatment.
Platelet Function Tests
Platelet function testing assesses platelet adhesion, activation, granule release and aggregation in response to agonists using light transmission platelet aggregometry (LTA) as the gold standard test. Abnormal LTA results can indicate defects in platelet adhesion receptors, activation and secretion, aggregation receptors, or the thromboxane pathway. The pattern of abnormal aggregation in response to different agonists helps localize the platelet function defect.
HbA1c : glycosylated hemoglobin
Glycosylated hemoglobin (HbA1c) represents the average plasma glucose over the previous 2-3 months and is measured to monitor long-term glycemic control in patients with diabetes. The document discusses the relationship between HbA1c levels and diabetes complications, factors that affect HbA1c, and recommendations for using HbA1c to diagnose diabetes. International expert committees now recommend using HbA1c ≥6.5% to diagnose diabetes due to standardization of assays and its correlation with complications.
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Anemia
Blood is made up of many parts, including red blood cells, white blood cells, platelets (PLATE-lets), and plasma (the fluid portion of blood).
Red blood cells are disc-shaped and look like doughnuts without holes in the center. They carry oxygen and remove carbon dioxide (a waste product) from your body. These cells are made in the bone marrow—a sponge-like tissue inside the bones.
White blood cells and platelets (PLATE-lets) also are made in the bone marrow. White blood cells help fight infection. Platelets stick together to seal small cuts or breaks on the blood vessel walls and stop bleeding. With some types of anemia, you may have low numbers of all three types of blood cells.
Coagulation Disorders
1. Coagulation disorders are caused by deficiencies in clotting factors that lead to defects in normal clot formation. They can be hereditary or acquired.
2. Hereditary disorders include hemophilia A and B which are sex-linked deficiencies in factors VIII and IX respectively, and von Willebrand disease which is an autosomal disorder involving a defect in von Willebrand factor.
3. Acquired disorders involve deficiencies in multiple clotting factors and can result from vitamin K deficiency, liver disease, fibrinolytic defects, or disseminated intravascular coagulation (DIC). DIC occurs as a complication of other systemic illnesses.
Diagnostic proteins
This document discusses several diagnostic proteins and enzymes that can be used as biomarkers for various medical conditions:
- Alpha-feto protein is measured in pregnant women to screen for fetal abnormalities. It can also indicate liver cancer or tumors.
- Bence-Jones proteins in the urine can indicate multiple myeloma or other blood cancers affecting the bones.
- C-reactive protein is a marker for inflammation and can help detect conditions causing inflammation like infections, autoimmune disorders, or osteomyelitis.
- Albumin in urine, measured via a 24-hour urine test, can help identify kidney damage from things like diabetes, high blood pressure, or cirrhosis.
- Various enzymes are biomarkers for specific diseases
Blood coagulation disorders and laboratory diagnosis
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Coagulation disorders are disruptions in the body's ability to control blood clotting. Coagulation disorders can result in either a hemorrhage (too little clotting that causes an increased risk of bleeding) or thrombosis (too much clotting that causes blood clots to obstruct blood flow).
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Protein c and protein s
- 1. PROTEIN C AND PROTEIN S SURAMYA BABU
- 2. Protein C and protein S are two proteins in the blood that help regulate blood clot formation Often these two test are performed together as part of investigation of a possible excessive clotting disorder. The test measure the amount of each protein ( antigen tests) and evaluate whether they are performing their proper functions
- 3. Protein S act as principle cofactor to protein C They work together to help regulate and control blood clot formation by inactivating coagulation factors (factor V and factor VIII) that required to generate and form blood clots. This has a net effect on slowing down clot formation . therefor, if there is not enough protein C or protein S or they are not functioning normally, clot formation can go unchecked , possibly leading to excessive clotting . These conditions can range from mild to severe,
- 4. There are two types of inherited protein C deficiencies TYPE I : due to insufficient quantity TYPE II : due to abnormal function (it is less common than type I)
- 5. Protein S exists in two forms in blood free and bound to another protein, but only the free protein S is available to be a cofactor for protein C. 3 types of inherited protein S deficiencies: TYPE I : due t insufficient quantity TYPE II : due to abnormal function TYPE III : due to decreased free protein S levels , though total protein S levels are normal
- 6. Normal activity and level of protein C and protein S usually indicate adequate clotting regulation Low protein C or protein S level or activity indicates blood clotting is not sufficiently regulated and there is an increased risk of developing a clot that blocks the flow of blood in the veins
- 7. Acquired deficiencies Both proteins are produced in liver and depend on Vitamin K. Therefore, low levels may be due to ; Liver disease Vitamin K deficiency Warfarin anticoagulant therapy (a vitamin K antagonist ) DIC Infections Inflammmation Kidney disease Chemotherapy HIV Pregnancy
- 8. Inherited deficiencies Decreased production of protein C or protein S Abnormal protein C or S that cannot function normally Abnormal protein S that is cleared more rapidly by the body ( type 3 deficiency)