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Physiology of Pregnancy
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
Plasminogen concentration is markedly raised, but this is offset by plasminogen activator inhibitors produced by the placenta. Antithrombin III levels decrease. There is an increase in fibrinolysis and fibrin formation in late pregnancy.
Disorders in tHemostasis System and Changes in the Rheological Properties of the Blood in Ischemic Heart Disease and Diabetes Mellitus Patients
Published in E.I. Sokolov, Obesity and Diabetes Mellitus, 2020
Antithrombin III ensures the anticoagulant function of the blood. In healthy persons, the reaction of the vessels to an ischemic test is attended by a considerable growth in the activity of AT III. This was also confirmed by our studies. In healthy persons, the activity of AT III after a cuff test increased from 37.6 to 49.0 s; the opposite reaction occurs in IHD patients — the activity of AT III dropped from 27.3 to 22.1 s. A similar reaction was noted for the fibrinolytic activity of the blood: in healthy persons it grows from 20.3 to 32.1%, while in IHD patients it drops from 11.2 to 8.4%.
Inflammation
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Hemorrhagic syndromes are connected with inherited defects of coagulation factors (Table 2). In these disorders the defect is mainly due to the synthesis of an abnormal protein rather than the lack of production.376 Deficiences of Factors VII, VIII, and IX are the most frequently occurring disease conditions. Both defects are related to extrinsic and intrinsic pathways of coagulation 89,157 Factor VIII and Factor IX deficiencies are X chromosomelinked disorders, and they are mainly found in males. The management of Factor VIII inhibitors in nonhemophilic patients seems to be essential.157 Hereditary antithrombin III deficiency is connected with venous thrombosis.309 In certain conditions, such as colon adenocarcinoma, the production of acquired factors has been observed.81
Point-of-care ultrasound for diagnosis of pneumothorax in a pregnant COVID-19 patient in the emergency department
Published in Journal of Obstetrics and Gynaecology, 2022
Muge Gulen, Salim Satar, Nurdan Unlu, Cemre Ipek Esen, Mehmet Bozkurt, Sarper Sevdimbas, Selen Acehan
Except for the most common pneumothorax aetiologies, the connective tissue dysplasias (Rheumatoid arthritis, Ankylosing spondylitis, Polymyositis and dermatomyositis, Scleroderma, Marfan’s syndrome, Ehlers–Danlos syndrome, Pleuroparenchymal fibroelastosis and SLE) can also causes pneumothorax. SLE causes secondary pulmonary fibrosis, resulting in pneumothorax (Sahn and Heffner 2000). Because of the presence of pneumothorax with thrombophilia in our patient, tests were performed for antiphospholipid syndrome secondary to SLE. The patient’s Lupus Anticoagulant, Anticardiolipin Antibody and Anti β 2-glycoprotein I antibodies, anti-nuclear antibodies (ANA) and anti-double stranded DNA (anti-dsDNA) tests were also negative (Knight and Kanthi 2022). Since the patient had a history of recurrent abortion and deep vein thrombosis, tests were also performed for conditions that could cause thrombophilia (Grandone and Piazza 2021). Belonging to the most common causes of thrombophilia, Antithrombin III deficiency, Protein C deficiency, Protein S deficiency, Factor V Leiden mutation and Prothrombin G20210A mutation tests were negative.
Acute myocardial infraction and pulmonary embolism in a same patient with COVID -19: a rare association
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Preet Randhawa, Parminder P. Singh, Nirmal Guragai, Parminder Kaur, Balraj Singh, Jasjit S. Walia
To our best of knowledge, there is only one reported case of COVID-19 with simultaneous acute myocardial infarction (MI) and acute pulmonary embolism (PE) [1]. However, in that case the patient had significant comorbidities that could predispose to MI or PE. In contrast, our case highlights the unusual presentation of acute COVID-19 illness triggering simultaneous acute MI and PE in a young patient without comorbidities. Other potentials hypercoagulable conditions and thrombophilia were excluded since factor V Leiden, prothrombin gene mutation, lupus anticoagulant, phosphatidylserine, beta 2 glycoprotein 1, cardiolipin antibodies were unremarkable. Antithrombin III and protein C and S were also within normal limits. It is exceedingly rare to see two of such fatal illness co-existing together, in a patient without any known predisposing risk factor except COVID−19.
Acute portal vein thrombosis in noncirrhotic patients – different prognoses based on presence of inflammatory markers: a long-term multicenter retrospective analysis
Published in Scandinavian Journal of Gastroenterology, 2019
Radan Keil, Jana Koželuhová, Jiří Dolina, Aleš Hep, Radek Kroupa, Vladimír Kojecký, Tomáš Krejčí, Jan Havlín, Ivana Hadačová, Jitka Segethová, Petra Koptová, Zdena Zádorová, Jan Matouš, Barbora Frýbová, Petr Chmátal, Martin Wasserbauer, Jan Šťovíček, Melvin Bae, Tolga Guven, Mahmood Zaeem, Štěpán Hlava
The most commonly detected prothrombotic hematologic factor was a higher level of coagulation factor VIII. Values over 150% were considered pathological [3]. Elevation was found in 49 patients (62.8%). Significantly reduced antithrombin III was found in 27 patients (34.6%), and reduced levels of protein C and S were found in 39 (50.0%) and 36 patients (46.2%), respectively. A significantly elevated blood pellet count was found in 17 (21.8%) patients, four of them had essential thrombocytosis with JAK2 mutation positivity. Positivity for JAK2 was completely present in 10 patients (12.8%). Three patients (3.8%) had diagnosed primary myelofibrosis, 4 (5.1%) patients had essential thrombocytosis, and 3 (3.8%) patients had polycythemia vera. Polycythemia vera was diagnosed 4 years after thrombosis in one patient. Twelve patients (15.4%) had APC resistance or a factor V Leiden mutation. Three (9.4%) females (27, 35, and 54 years old) used hormonal contraception or hormonal substitution therapy. The youngest one was JAK2+ and had elevated factor VIII while the other two had no other risk factors. Antiphospholipid syndrome was excluded in all investigated patients. One patient was positive for anti-beta 2GPI antibodies.