Chapter 21: Disorders of Oxygen Transport PDF
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This chapter discusses various disorders related to oxygen transport, specifically focusing on red blood cell issues and anemia. It explores different types of anemia, their causes, symptoms, and treatment options. The chapter includes details like diagnosis and clinical manifestations.
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CHAPTER 21: DISORDERS OF OXYGEN TRANSPORT Red blood cell disorders involve loss of oxygen in tissues and loss of mature erythrocytes Genetic variation ○ Prevents formation of mature erythrocytes or hemoglobin ○ Misshapen erythrocytes cause cells to clump together and can cause ischem...
CHAPTER 21: DISORDERS OF OXYGEN TRANSPORT Red blood cell disorders involve loss of oxygen in tissues and loss of mature erythrocytes Genetic variation ○ Prevents formation of mature erythrocytes or hemoglobin ○ Misshapen erythrocytes cause cells to clump together and can cause ischemia or hypoxia Excessive RBCs cause blood to thicken Anemia is a common clinical condition that involves a reduction in the # of erythrocytes and decline in ability of to carry oxygen Decreased production of erythrocytes, loss of erythrocyte (acute of chronic blood loss) Reduced survival time of erythrocytes Functional changes in structure of erythrocytes Also involved nutritional deficit → production of RBCs is decreased because lack of necessary components for synthesis of DNA = continued cell growth with lack of appropriate cell division Macrocytic anemia - vitamin B12 and folic acid Iron deficiency anemia and thalassemia - iron Aplastic anemia involves a reduction in stem cells Other causes include medication and radiation of anemia of chronic disease linical manifestation involve fatigue (most common), increased respiration and heart rate (to compensate), pallor, cyanosis C (usually not), headache and dizziness, muscle weakness Hypoxia effects on body Dilation of arterioles, capillaries, and venules to increase blood flow → increases heart rate and stroke volume, can lead to heart failure Rate and depth of breathing increases in an effort to increase oxygen availability and also an increase in the release of oxygen from hemoglobin iagnosis involves medical history, blood test, and identification of genetic cause D Lab test can be used to classify anemia and identify cause or risk of anemia 13.5 - 17.5 g/ dL for men 12.0 - 15.5 g/ dL for women Treatment involves blood transfusion (if caused by blood loss), replacement of iron and vitamin B12 as needed, education (nonheme iron absorption is enhanced by animal protein a rich source of vitamin c) MCV reflect the average erythrocyte size Hematocrit Microcytic vs macrocytic anemia MCH Hypochromic Normochromic Nutritional deficiency anemia Hemolytic anemias S everal nutrients are necessary for maturation and proliferation of RBCs Lack of iron and vitamin B12 affect cell maturation Hemolysis ( destruction) of RBCs Physical trauma and stress to RBC Disruption in hemoglobin formation Immune mediated response IRON DEFICIENCY Reduced dietary intake or malabsorption Chronic blood loss such as menstruation of GI bleeding Microcytic and hypochromic RBCs ajor causes are genetic - sickle cell disease and thalassemia M Signs and symptoms are similar to other forms of anime but it also include jaundice OBALAMIN DEFICIENCY C Vitamin B12, a water soluble vitamin necessary for cell metabolism and binds to intrinsic factor secreted by gastric parietal cells once consumed Pernicious anemia ○ Autoimmune mediated process that lead to loss of gastric parietal cells -> decrease secretion of intrinsic factor -> inability to properly absorb cobalamin Autoimmune response ○ Can contribute to weakening the intestinal wall Bowel disease ○ Can adversely affect the absorption of cobalamin F OLIC ACID DEFICIENCY Obtained primarily through the consumption of fruits and leafy green veggies important for the synthesis and repair of DNA, work alongside cobalamin More chronic, insidious(dangerous and gradually) presentation Medication that antagonize folate can contribute to development of anemia For cancers, antibiotics T reatment inclined determining severity, monitoring or hematocrit and hemoglobin levels, blood transfusion, consideration for sickle cell disease S ICKLE CELL DISEASE Cluster of autosomal recessive disorders Hemoglobin sickle or crescent in shape due to a genetic mutation Pathogenesis Hemoglobin cannot bind oxygen effectively RBC collapses into sickle shape when oxygen is released RBC clump together and can obstruct blood flow RBC lifespan is only 10-20 days (normal is 120 days) Chronic inflammation b/c inflammatory mediators are released in compensatory response to stimulate production of more RBCs Clinical manifestation include hypoxia and tissue ischemia Treatment includes: prevention, screening, supportive care (pain management), disease modifying strategies, curative procedures, genetic analysis and prenatal counseling T reatment may involve hydroxyurea for infants(stimulate production of hemoglobin), blood transfusion, stem cell transplantation T HALASSEMIA Group of autosomal recessive disease the affect production of hemoglobin caused by a defect in the production of one or more globin chains Increase incidence in individuals from mediterranean and asia linical manifestation include: defects at birth, growth retardation, C cognitive deficits, jaundice Anemia of chronic disease Aplastic anemia condition of inflammation A The process of inflammation is associated with the release of immune proteins that play a role in uptake and retention of iron In ACD, iron is taken up into macrophages, which divert it from being able to play a role in binding of oxygen ecrease in all cell population produced by the bone marrow: D erythrocytes, leukocytes, platelets (body stops producing enough new blood cells) aused include genetics, viral exposure, drugs or toxins, immune C mediated attack on the bone marrow Diagnosis - decrease in WBCs, RBCs, platelets, hemoglobin ormochromic and normocytic b/c maturation of N RBC has not been impacted, hyperproliferation Normocytic, normochromic Polycythemia vera is a bone marrow disorder Too many RBCs are produced → increase viscosity prevents blood from flowing efficiently, leading to end organ ischemia The increased thickness of the blood places the pt at an increased risk for the development of thrombi or blood clots Primary refers to an increase in the production of erythrocytes on the part of bone marrow while secondary results from genetic modification related to the production of erythropoietin, regulator of RBC production Clinical manifestation include: increase blood viscosity and volume, headache, dizziness, blurred vision, hypertension, thrombi Diagnosis include hematocrit over 70, increase erythrocytes and WBcs, decreased iron count Treatment includes anticoagulation, therapeutic erythropheresis (bloodletting), chemotherapeutic approaches
