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Cardiovascular system
Published in Jagdish M. Gupta, John Beveridge, MCQs in Paediatrics, 2020
Jagdish M. Gupta, John Beveridge
8.22. In congenital heart disease, cyanosisis distinguished from that of respiratory origin by its failure to diminish on breathing 100% oxygen for 10 min.requires at least 5g/100ml of reduced Hb for recognition.causes polycythaemia.characteristically causes hyperventilation and respiratory alkalosis.requires urgent investigation.
Physiology Related to Special Environments
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
Polycythaemia occurs in a person exposed to altitude. There is a linear increase in polycythaemic response with increasing altitude up to 3700 m, and after that, the rise is more rapid. Erythropoietin production is increased because the decreased arterial Po2 is sensed by the macula densa of the kidneys. Plasma erythropoietin increases within the first 2 hours of exposure to altitude and reaches a maximum within a day. There is a lag between erythropoietin secretion and red cell production so that the red cell count rises after 3–5 days of exposure to altitude. The haemoglobin concentration rises and increases the oxygen-carrying capacity of blood. As the haematocrit increases, so does blood viscosity, and this tends to decrease blood flow and increase cardiac work. The oxyhaemoglobin dissociation curve is shifted to the right within 12 hours of altitude exposure by an increased concentration of erythrocyte 2,3-diphosphoglycerate that is induced by respiratory alkalosis.
Radioisotopes in Biology and Medicine
Published in Kedar N. Prasad, Handbook of RADIOBIOLOGY, 2020
Polycythemia vera is a disease of unknown etiology characterized by an increase in the circulating red cell mass, which is caused by overproduction of these elements by the bone marrow and certain extramedullary sites — such as the liver and spleen. There is often an associated increase in the white cells of the myeloid series and the platelets. At present, it is generally accepted that 32P is the most effective and most easily administered form of treatment for this disease, although some observers are concerned about a possible increase in the incidence of leukemia as a result of 32P therapy. 32P has been found to be useful in the treatment of chronic leukemia, but not in acute leukemia. Of course, the 32P therapy of the chronic leukemias must be accompanied by proper systematic care and judicious use of transfusions and other affective agents, such as localized X-ray therapy, nitrogen mustard, antifolic acid preparations, urathene, and 6-mercaptopurine. 198Au is used in carcinoma of the prostate. Gamma radiation from 60Co is widely used in the treatment of several types of malignant diseases.
Association between polycythemia and risk of ischemic stroke in males based on the national health insurance service-health screening cohort
Published in Expert Review of Hematology, 2023
Hyo-Sun You, Sang-Jun Shin, Joungyoun Kim, Hee-Taik Kang
Hematologic disorders are common causes of ischemic stroke but are frequently neglected [3]. Polycythemia is a hematological disorder that can cause ischemic stroke. Polycythemia refers to a state in which the hematocrit or hemoglobin concentration in peripheral blood is increased. Polycythemia, or erythrocytosis, is classified into spurious polycythemia and true polycythemia according to its etiology. Spurious polycythemia is induced by volume contraction, severe dehydration, and Gaisbock syndrome. True polycythemia is divided into primary and secondary polycythemia according to serum erythropoietin (EPO) levels. Polycythemia vera and primary familial and congenital polycythemia are the types of primary polycythemia with low serum EPO levels. Secondary polycythemia is caused by various diseases that cause hypoxia in cells, which induces EPO release. High altitude, respiratory diseases such as chronic obstructive pulmonary disease (COPD), cyanotic heart disease, elevated carboxyhemoglobin, hemoglobinopathies, and EPO-secreting tumors can also cause secondary polycythemia [4].
Polycythemia vera: aspects of its current diagnosis and initial treatment
Published in Expert Review of Hematology, 2023
Richard T Silver, Ghaith Abu-Zeinah
Although significant advances have been made in our understanding of the biology, pathogenesis, and treatment of polycythemia vera, important issues remain pertaining to its diagnosis and treatment. Although JAK2V617F has become a marker for PV, it does not distinguish it clinically from phenotypically similar patients with essential thrombocythemia or the cellular phase of myelofibrosis. Errors in diagnosis may result. This is abetted by the unavailability of radioactive chromium and iodine to determine red cell and plasma volume, respectively, in the United States and in parts of Europe. In these instances, the bone marrow findings, emphasized by the World Health Organization in 2016 and 2022 are important and are helpful in more than 90% of the cases [36]. Evidence suggests that marrow examination is performed infrequently at major hematologic centers, and far less often in community practice. This leads to significant errors in diagnosis and treatment, and ultimately in survival.
Frequency of JAK2V617F, MPL and CALR driver mutations and associated clinical characteristics in a Norwegian patient cohort with myeloproliferative neoplasms
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2023
Susanne Lilleskare, Marta Vorland, Anh Khoi Vo, Aasne K. Aarsand, Håkon Reikvam
We found that 81% of patients with polycythemia vera in our study had JAK2V617F (Figure 2). The consensus in international literature is that over 95% of polycythemia vera-patients have a mutation in JAK2, with JAK2 exon 12 accounting for approximately 3%, and the remaining share attributed to JAK2V617F [1]. JAK2 exon 12 analysis was not included in our study, however exon 12 variants would still likely account for only a few of the missing cases. In 2016, Almedal et al. published results from a study of JAK2V617F in a Norwegian cohort and found that 75% of patients with polycythemia vera had JAK2V617F. There is some overlap between the participants included in that study and in our recent study. A likely overdiagnosis of polycythemia vera was described, and it was assumed that not all would meet the current diagnostic criteria [15]. This causal explanation is also likely applicable to our population. Further analysis of the polycythemia vera cohort was therefore not performed. Yet the percentage is closer to international consensus, and this could indicate that diagnostic precision has improved in the later years.