BLOOD LOSS

Chapter 101. Hemolytic Anemias and Anemia Due to Acute Blood Loss (Part 12) Figure 101-6 Peripheral blood smear from a 5-year-old G6PD-deficient boy with acute favism. A very small minority of subjects with G6PD deficiency have CNSHA of variable severity. The patient is alw[r]

Chapter 101. Hemolytic Anemias and Anemia Due to Acute Blood Loss (Part 16) PNH has about the same frequency in men and women, and it is encountered in all populations throughout the world, but it is a rare disease: its prevalence is 1–5 per million (it may be somewhat less rare in So[r]

Chapter 101. Hemolytic Anemias and Anemia Due to Acute Blood Loss (Part 11) Table 101-5 Drugs that Carry Risk of Clinical Hemolysis in Persons with G6PD Deficiency Definite Risk Possible Risk Doubtful Risk Antimalarials Primaquine Chloroquine Quinine Dapsone/chlorproguanil Sulphona[r]

Chapter 101. Hemolytic Anemias and Anemia Due to Acute Blood Loss (Part 10) Epidemiology G6PD deficiency is widely distributed in tropical and subtropical parts of the world (Africa, Southern Europe, the Middle East, Southeast Asia, and Oceania) (Fig. 101-5) and wherever people from t[r]

Chapter 101. Hemolytic Anemias and Anemia Due to Acute Blood Loss (Part 9) Pyruvate Kinase Deficiency: Treatment Management of PK deficiency is mainly supportive. In view of the marked increase in red cell turnover, oral folic acid supplements should be given constantly. Blood[r]

Chapter 101. Hemolytic Anemias and Anemia Due to Acute Blood Loss (Part 8) Abnormalities of the Glycolytic Pathway (Fig. 101-1) Since red cells, in the course of their differentiation, have sacrificed not only their nucleus and their ribosomes but also their mitochondria, they rely ex[r]

Chapter 101. Hemolytic Anemias and Anemia Due to Acute Blood Loss (Part 7) Clinical Presentation and Diagnosis The spectrum of clinical severity of HS is broad. Severe cases may present in infancy with severe anemia, whereas mild cases may present in young adults or even later in life[r]

Chapter 101. Hemolytic Anemias and Anemia Due to Acute Blood Loss (Part 13) Pyrimidine 5'-Nucleotidase (P5N) Deficiency P5N is a key enzyme in the catabolism of nucleotides arising from the degradation of nucleic acids that takes place in the final stages of red cell maturation. How e[r]

Chapter 101. Hemolytic Anemias and Anemia Due to Acute Blood Loss (Part 6) Peripheral blood smear from patients with membrane-cytoskeleton abnormalities. A. Hereditary spherocytosis. B. Hereditary elliptocytosis, heterozygote. C. Elliptocytosis, with both alleles of the α-spec[r]

Chapter 101. Hemolytic Anemias and Anemia Due to Acute Blood Loss (Part 5) Hemolytic Anemias Due to Abnormalities of the Membrane-Cytoskeleton Complex The detailed architecture of the red cell membrane is complex, but its basic design is relatively simple (Fig. 101-2). The lipid bilay[r]

Chapter 101. Hemolytic Anemias and Anemia Due to Acute Blood Loss (Part 14) Autoimmune Hemolytic Anemia (AIHA) Except for countries where malaria is endemic, AIHA is the most common form of acquired hemolytic anemia. In fact, not quite appropriately, the two phrases are sometimes used[r]

Chapter 101. Hemolytic Anemias and Anemia Due to Acute Blood Loss (Part 3) Figure 101-1 RBC metabolism. The Embden-Meyerhof pathway (glycolysis) generates ATP for energy and membrane maintenance. The generation of NADPH maintains hemoglobin in a reduced state. The hexose monophosphat[r]

Chapter 101. Hemolytic Anemias and Anemia Due to Acute Blood Loss (Part 1) Harrison's Internal Medicine > Chapter 101. Hemolytic Anemias and Anemia Due to Acute Blood Loss Definitions A finite life span is a distinct characteristic of red cells. Hence, a logical,[r]

Chapter 101. Hemolytic Anemias and Anemia Due to Acute Blood Loss (Part 15) Severe acute AIHA can be a medical emergency. The immediate treatment almost invariably includes transfusion of red cells. This may pose a special problem because if the antibody involved is "unspecific," all[r]

Chapter 101. Hemolytic Anemias and Anemia Due to Acute Blood Loss (Part 2) Table 101-2 General Features of Hemolytic Disorders General examination Jaundice, pallor Other physical findings Spleen may be enlarged; bossing of skull in severe congenital cases Hemoglobin From normal to s[r]

(bilateral). In comparison, the mean drop in the post-op haemoglob in in Group-I was 1.49 gm/dl (unilateral) and1.94 gm/dl (bilateral), with a mean drainage of 826 ml (unilateral) and 1288 ml (bilateral) (p-value < 0.001).Interpretation: Tranexamic acid is effective in reducing post-operative[r]

(bilateral). In comparison, the mean drop in the post-op haemoglob in in Group-I was 1.49 gm/dl (unilateral) and1.94 gm/dl (bilateral), with a mean drainage of 826 ml (unilateral) and 1288 ml (bilateral) (p-value < 0.001).Interpretation: Tranexamic acid is effective in reducing post-operative[r]

Chapter 101. Hemolytic Anemias and Anemia Due to Acute Blood Loss (Part 17) Bone Marrow Failure—Relationship between PNH and AA It is not unusual that patients with firmly established PNH have a previous history of well-documented AA. On the other hand, sometimes a patient with PNH be[r]

indwelling Foley catheter and drainage will provide approximate and important information about maternal volume and intravas-cular status in real time. The operative or treating physician ’ s time is best confi ned to eliminating the focus of hemorrhage and relying on simple and adequate techniques f[r]

replenish plasma volume defi cits and replace fl uid and electrolyte losses from the interstitium [32,40,45 – 48] . Patients in shock from any cause should receive immediate volume replacement with crystalloid solution during the initial clinical evaluation. Aggressive administration of crystalloid ma[r]