Chapter 13: Alterations in Oxygen Transport

• Transport oxygen to tissues

• Remove carbon dioxide from the tissues

• Buffer blood pH (contain carbonic anhydrase)

Through hematopoiesis: two-stage process involving

• Mitotic division (proliferation)

• Maturation (differentiation)

Hormone from kidney that stimulates erythrocyte production

• 80-90% of RBCs get digested by macrophages in spleen and liver

• 10-20% inside blood vessels

• As RBCs age, enzyme activities decrease

• Amount of membrane lipids decrease

• Cell loses ability to deform and becomes fragile

• HbA levels increase

• Heme is reduced to bilirubin

• Globin and iron portions are conserved and reused

• Bilirubin is then degraded to the urobilinogen and excreted primarily in the feces and in the urine

Bilirubin

• Under production of RBC

• Over production of RBC (hemolysis)

• Blood loss

Stem cell disorder characterized by reduction of hematopoietic tissue, fatty marrow replacement

Caused by toxic, radiant, or immunologic injury to the bone marrow stem cells

• Pancytopenia (low RBC, WBC, and platelets)

• Low WBC is important for prognosis (low leukocytes = susceptibility

• Pernicious anemia

• Disruption in DNA synthesis of blast cells produces megaloblasts (macrocytic)

• Folate deficiencies are associated with neural tube defects

• Primarily from failure of the renal endocrine function, which causes impaired erythropoietin (EPO) production

• Secondarily from failure of renal excretory function

• Leads to hemolysis, bone marrow cell depression and blood loss

• Low RBC count

• Low hematocrit

• Low hemoglobin

• Some grossly deformed RBC

• General signs and symptoms of anemia usually manifest when hematocrit decreases to <20%

lack of intrinsic factor results in inability to absorb vitamin B12, which plays a role in RBC formation

• Low RBC, WBC, and platelet counts with increased MCV; megaloblastic dysplasia

• Macrocytic and hypersegmented neutrophils

• Most common

• Results in the unavailability of iron for hemoglobin synthesis

• Smaller and paler RBC

• Low red cell indices: MCV, MCH, MCHC

• Decreased serum ferritin

• Increased RBC destruction (hemolysis) resulting in decreased RBC survival rates

• Associated with mutant genes that suppress the rate of globin chain synthesis

• Classified by the polypeptide chain(s) with deficient synthesis)

• Most clinically severe from: thalassemia major (homozygous)

• Thalassemia minor (heterozygous) is less severe

• Hypochromic, microcytic RBCs

• Low MCV, MCH, and MCHC

• Erythroblastic hyperplasia (bone marrow)

• Genetically determined defect of hemoglobin synthesis resulting in hemoglobin instability and insolubility

• In Hemoglobin S, a single amino acid substitution causes the structural abnormality

• Sickled cells cause vascular occlusion

Sickled RBC present in blood smear

Excess RBC, which results in increased blood viscosity, leading to clinical symptoms, such as hypertension.

• Absolute increase in RBC mass, leukocytosis, thrombocytosis

• Increased uric acid because of excess proliferation

• Oxygen saturation is normal

• Hypertension

• Thrombosis

• Congested spleen and liver

Increased RBC production without increase in WBCs or platelets