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PlasmaThe Non-cellular Components of Blood
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Various proteins belong to this group of globulins: α2-Macroglobulin. This is a protease inhibitor in plasma and is the major protein in the α2-globulin fraction (∼80%). It has inhibitory functions on plasma trypsin, chymotrypsin and plasmin. The primary function of α2-macroglobulin may be to inhibit proteases produced by infectious organisms.Prothrombin. Prothrombin is a clotting factor synthesized by the liver. About 60% of the extracellular pool of prothrombin is in the plasma and 40% in the extravascular space. It has a rapid turnover.Haptoglobin. This is a heterogeneous group of globulins that bind free Hb and transport it to the liver.Ceruloplasmin. Ceruloplasmin is a plasma protein that carries copper and is produced in the liver. It also functions as an oxidase enzyme and oxidizes ferrous to ferric ions before the binding of iron to transferrin. As an acute-phase protein, it may modulate inflammation by its free-radical scavenging properties.
Special Consideration of Drug Disposition
Published in Gary M. Matoren, The Clinical Research Process in the Pharmaceutical Industry, 2020
The clearance of all three drugs was lessened by the presence of liver disease. The greatest reduction in clearance was seen in those patients who exhibited raised bilirubin levels, prolonged prothrombin times, and low serum albumin concentrations. There was no significant degree of correlation with other tests of liver function, such as serum glutamic-oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT), or alkaline phosphatase.
Liver Function Tests in the Differential Diagnosis of Hepatotoxicity
Published in Robert G. Meeks, Steadman D. Harrison, Richard J. Bull, Hepatotoxicology, 2020
The liver synthesizes nearly all of the coagulation factors: prothrombin, fibrinogen, and factors V, VII, IX, and X (Suttie and Jackson, 1977). Clotting problems occur only when substantial impairment of the liver’s synthetic ability is compromised (Kaplowitz et al., 1982). Most factors are normally present in excess of the required quantities in the serum. Factor levels can be measured by direct assay or by tests assessing the interplay of many factors. The Quick, one-stage prothrombin time, is commonly used (Quick, 1966). This conversion of prothrombin to thrombin in the presence of calcium ions and thromboplastin (tissue extract) measures the extrinsic coagulation pathway. Since prothrombin time is increased when a variety of factors are lacking (factors I, II, V, VII, and X), it is particularly sensitive in detecting impaired hepatic synthetic abilities. The observance of prothrombin levels less than 50% of normal in humans suggest that a risk for bleeding may exist (Spector and Corn, 1967). Increases in prothrombin time in vitamin K deficiencies due to obstructive jaundice occur due to less binding of calcium ions to phospholipids. This is due to the presence of abnormal amounts of γ-carboxyglutamic acid residues which are necessary for calcium binding (Stenflo et al., 1974).
Comparison of bedside clotting tests for detecting venom-induced consumption coagulopathy following Sri Lankan viper envenoming
Published in Clinical Toxicology, 2022
Supun Wedasingha, Anjana Silva, Sisira Siribaddana, Kanishka Seneviratne, Geoffrey K. Isbister
Currently, antivenoms are the only specific treatment for VICC, and early administration of antivenom in envenomed patients is essential to prevent or neutralize VICC [4]. Unfortunately, in some settings antivenom reportedly causes severe reaction rates as high as 43% [5], so antivenom should only be given in patients with envenoming [6]. Therefore, establishing the diagnosis of ‘envenoming’ or VICC is a crucial step in managing all snakebites. Coagulation tests are key to diagnosing VICC in snakebite patients, and determine which patients should receive antivenom [7]. The prothrombin time (PT)/International normalized ratio (INR) is currently the best available diagnostic test in VICC [3], but such laboratory based clotting studies are expensive and not available in many resource poor countries. For this reason, simple bedside clotting tests are commonly used in places where most snakebites occur [7].
Central retinal artery occlusion and subsequent amaurosis fugax in the contralateral eye associated with the G20210A prothrombin gene (F2) variant: a case report
Published in Ophthalmic Genetics, 2022
María Camila Sierra-Cote, Juliana Muñoz-Ortiz, Juan Sebastián Botero-Meneses, Carolina Saldarriaga-Santos, Natalia Camacho, William Rojas-Carabali, Alejandra de-la-Torre
Regarding the genetic component, one of the most common variants in the prothrombin gene (F2) is the G20210A. Prothrombin is a glycoprotein and precursor form of Factor II (thrombin), and it is essential for the final phase of clotting (5). It is encoded by the F2 gene located in the short arm of chromosome 11 (11p11.2). Variants in this gene, including polymorphisms and variants, may lead to thrombophilic disorders in many patients (6,7). Although the G20210A is an established risk factor for venous thrombosis, and it is debatable that this variant is a risk factor for arterial thromboembolism, some cases have been linked to myocardial infarction and cerebral arterial disease (8). In the case of ocular vessel occlusions, studies are scarce (9–12). This study aims to report the fourth case described in the literature of CRAO associated with prothrombin G20210A pathogenic variant and the first case with bilateral ocular findings (9–11), emphasizing the usefulness of OCT-A in reaching the diagnosis and establishing the specific and timely therapeutic measures.
Nutritional deficiency presenting as acute pain, fatigue and bruising in a college health clinic
Published in Journal of American College Health, 2022
Adam Pallant, Tanya Sullivan, Andrew Kaluzny
Examination on follow-up 10 days after initial presentation is notable for a young man who now appears extremely fatigued with visible pallor. He is unable to stand fully upright due to pain in his joints, and demonstrates persistent mild flexion at both knees secondary to this pain (Figure 1). Vitals: temperature of 99.3, orthostasis with a supine pulse of 116 and a standing pulse of 140. Blood pressure remains stable and weight is unchanged. Physical exam is significant for markedly increased breadth and intensity of broad ecchymoses across the medial portion of bilateral thighs (Figure 2), and significant petechial hemorrhage on the lower extremities (Figure 3). Hemoglobin has dropped to 9.5 g/dl, and a mild lymphopenia is noted at 0.9 × 109/l with remainder of the differential normal. The platelet count remains normal at the 261 × 109/l. Total bilirubin has increased to 2.3 mg/dl (direct bilirubin of 0.4 mg/dl) with an elevated LDH of 240 IU/L. Prothrombin time is mildly elevated to 13.6 seconds (9.5-12.5) within normal INR of 1.2. ALT, AST, TIBC, and ferritin are normal.