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112 Cards in this Set
- Front
- Back
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Why does hemoglobin need to stay in the red blood cells?
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otherwise, it would be removed from the body via the glomerulus or leak out of the capillary membranes
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RBC contain what enzyme to create carbonic acid?
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carbonic anhydrase
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RBCs are responsible for buffering blood by using which protein?
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hemoglobin
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Normal MCV (cubic μm)
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90-95 cubic μm
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Why is it important the RBC can change shape easily?
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so they can squeeze through small capillaries without damage
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Normal hematocrit % range
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40-45%
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Normal hemoglobin content of whole blood (g/100 mL)
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15 in men; 14 in women
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Maximum/normal hemoglobin content in RBC (g/100mL)
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34 g/100mL (34% volume)
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With less hemoglobin (perhaps due to poor synthesis), why do we see a lower MCV?
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RBC volume falls because less hemoglobin is available to fill the cell
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1 gram of pure hemoglobin binds how much oxygen (mL)?
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1.34 mL
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During early embryonic life, where are red blood cells first made?
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yolk sac
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During the 2nd trimester, where are red blood cells made?
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liver, and some are made in spleen/lymph nodes
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Where are red blood cells made after birth?
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bone marrow
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At age 30, are red blood cells made in tibia or femur bone marrow?
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no
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Bone marrow constantly forms RBC throughout life in which bones?
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Membranous: vertebrae, sternum, ribs, ilia
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A pluripotent hematopoetic stem cell can become what 2 stem cells?
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lymphoid stem cell or CFU-S (colony forming unit spleen)
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A committed stem cell to form erythrocytes is called ...
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CFU-E
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Growth of committed stem cells is controlled by what specific growth inducer?
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IL-3
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Fun Fact: Growth Inducers are different than Differentiation Inducers
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awesome story
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Proerythroblasts are formed from what committed stem cells?
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CFU-E
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Stages of RBC development. Start with Proerythroblast.
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Proerythroblast- basophilic erythroblast- polychromatophilic erythroblast- Orthochromatophilic erythroblast- reticulocyte- erythrocyte
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Why are basophilic erythroblasts basophilic?
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there is little hemoglobin in the RBC = less pink, rER making hemoglobin = blue
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In a forming erythrocyte, the nucleus becomes pyknotic when hemoglobin concentration becomes ...
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34%
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Diapedesis occurs during which phase of erythrocyte formation?
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reticulocytes
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Why will we not see any levels of polychromatophilic erythroblasts in the blood?
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They have not yet diapedesed from the bone marrow into the blood
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What is diapedesis?
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squeezing through pores of capillary membrane
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Why does the forming erythrocyte become less basophilic?
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more hemoglobin is being made (eosinophilic)
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Why should we make syre the RBC count is not too high?
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They can impede blood flow
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What is the primary regulator of RBC production?
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tissue oxygenation (leads to release of erythropoietin from kidneys)
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Why is there more erythropoiesis at high altitudes?
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less oxygen in the air = less oxygen to tissues = more RBC to ensure all tissues remain oxygenated
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Describe the pathway taken to release erythropoietin.
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Hypoxia- increased HIF1- HIF1 binds hypoxia response element of DNA- transcription of erythropoietin gene
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Which autonomic nervous system stimulates erythropoietin formation in the kidneys?
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sympathetics (epinephrine/norepinephrine)
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Where is erythropoietin made?
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90% kidneys, 10% liver
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Erythropoietin function
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stimulate formation of proerythroblasts which will lead to higher RBC counts; also makes differentiation process occur faster
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Vitamin B12 and folic acid are needed for what building block of DNA?
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thymidine triphosphate (TTP)
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Why does lack of Vitamin B12 or folic acid lead to anemia?
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erythrocytes are not able to fully mature. TTP is not able to be formed and DNA synthesis is impaired
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Macrocytic RBCs are formed by deficiency in what compound?
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B12 or folic acid
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Why are macrocytic RBCs bad?
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the membrane is flimsy and the half-life is shortened (1/2 normal) due to this fragility
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What does "maturation failure" in RBC refer to?
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B12 or folic acid deficiency. the RBCs are not able to mature into full erythrocytes due to impeded DNA synthesis
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What is pernicious anemia?
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lack of intrinsic factor leads to a decreased absorption of B12 in the digestive tract. leads to macrocytic RBCs
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Why does atrophic gastric mucosa lead to anemia?
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intrinsic factor is needed to absorb B12 in the GI tract
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How does intrinsic factor lead to B12 absorption?
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1) binds B12; 2) binds receptor on ileum brush border; 3) pinocytosis of the complexed IF+B12
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Where is B12 stored after absorbed in the GI tract?
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liver
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Why does it take 3-4 years of B12 deficiency to see maturation failure anemia?
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only 1-3 micrograms of B12 are needed/day. liver can store 1000-3000 micrograms
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What is Cyanocobalamin?
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Vitamin B12
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What is Pteroylglutamic Acid?
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Folic Acid
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How does the disorder "sprue" lead to anemia?
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small intestine disease = difficult absorption of folic acid and B12
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Hemoglobin synthesis occurs during which stage of erythropoiesis?
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proerythroblast
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In the formation of Hb, where does Succinyl Co-a come from?
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Krebs cycle
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2 Succinyl Co-a + 2 glycine =
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pyrrole
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In Hb synthesis, 4 pyrrole can form what major structure?
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protoporphyrin IX
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Protoporphyrin IX combines with iron (Fe2+) to form ...
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heme
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Hemoglobin has 4 chains. What are they?
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2 alpha and 2 beta chains
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In Hb synthesis, heme joins the polypeptide to form ...
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alpha or beta chain
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Each hemoglobin molecule has how many irons?
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4
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Each hemoglobin molecule can carry how many oxygen atoms?
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8 (4 O2 molecules on 4 irons)
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What amino acid substitution is characteristic of sickle cell anemia?
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glutamic acid is replaced with valine in beta chains
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What form of oxygen is released into tissues, molecular oxygen (O2) or ionic (O-)?
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molecular, forms a looser bond with hemoglobin iron so it can be released into tissue easier
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What does oxygen bind to on hemoglobin?
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the coordination bonds of the iron, not the iron itself (wouldn't be able to release into tissue easily)
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What % of body iron is found in hemoglobin?
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65%
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What is transferrin?
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form of iron transport; apotransferrin + iron in the blood
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What is ferritin?
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form of iron storage; apoferritin + iron in the cytoplasm
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Why would we see an increase in iron stored as hemosiderin?
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if we had an iron excess that could not be accomodated by ferritin
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Why would we see a decrease in ferritin and an increase in transferrin?
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If the body was becoming anemic due to iron deficiency; iron is shifting from storage to transport to tissues
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Where in the erythroblast is heme synthesized?
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mitochondria
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How does transferrin get iron to the mitochondria of the erythroblast?
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it binds to erythroblasts membrane and is ingested
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Heme is synthesized in the erythroblast mitochondria. But mature RBC do not have mitochondria. Why?
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Mitochondria and other organelles are removed during the reticulocyte phase of development
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What type of anemia will we see in patients with low levels of transferrin?
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microcytic, hypochromic anemia. iron deficiency leads to microcytic, poor Hb synthesis leads to hypochromic
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Where is apotransferrin made?
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liver
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When total body iron levels are low, how will the body increase them?
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increasing rate of absorption in the intestines
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What is the human body's major source of iron?
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diet (minor source: hemoglobin recycling)
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RBC life span
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120 days
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In hemoglobin, we want iron to be in which form (ferrous or feric)?
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we want iron to be ferrous (2+). (feric is Fe3+)
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The removal of which organ would lead to high levels of old RBCs in circulation?
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spleen removes these normally
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Why do many old RBCs rupture in the spleen?
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spleen has very narrow passages and old/damaged RBCs can't stand the forces.
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What macrophages in the liver eat destroyed hemoglobin?
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Kuppfer cells
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Bilirubin is the degradative product of what part of hemoglobin?
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porphyrin portion
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What is anemia?
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low hemoglobin in the blood (either due to low RBCs or low hemoglobin in RBCs)
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After major blood loss, how long does it take for RBC concentration to return normal?
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3-6 weeks (plasma returns to normal in 1-3 days)
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A patient with chronic blood loss will have what type of RBCs?
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microcytic, hypochromic anemia
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What is bone marrow aplasia?
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dysfunctional bone marrow
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After undergoing chemotherapy, a patient has anemia. What type of anemia is most likely?
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aplastic anemia (bone marrow may be damaged from chemo)
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Why does B12 deficiency lead to large RBCs?
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poor DNA synthesis = slow maturation. during this long maturation process, the cells continue growing despite the lack of maturation
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What is hemolytic anemia?
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anemia caused by weak RBCs
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Why do many old RBCs rupture in the spleen?
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spleen has very narrow passages and old/damaged RBCs can't stand the forces.
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What macrophages in the liver eat destroyed hemoglobin?
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Kuppfer cells
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Bilirubin is the degradative product of what part of hemoglobin?
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porphyrin portion
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What is anemia?
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low hemoglobin in the blood (either due to low RBCs or low hemoglobin in RBCs)
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After major blood loss, how long does it take for RBC concentration to return normal?
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3-6 weeks (plasma returns to normal in 1-3 days)
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A patient with chronic blood loss will have what type of RBCs?
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microcytic, hypochromic anemia
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What is bone marrow aplasia?
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dysfunctional bone marrow
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After undergoing chemotherapy, a patient has anemia. What type of anemia is most likely?
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aplastic anemia (bone marrow may be damaged from chemo)
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Why does B12 deficiency lead to large RBCs?
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poor DNA synthesis = slow maturation. during this long maturation process, the cells continue growing despite the lack of maturation
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What is hemolytic anemia?
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anemia caused by weak RBCs
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Why does hereditary spherocytosis lead to anemia?
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spherical RBCs cannot withstand compression as well as biconcave discs; easily damaged
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What is hereditary spherocytosis?
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very small spherical RBCs rather than biconcave discs; more easily damaged
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What type of hemoglobin is found in sickle cell anemia RBCs?
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HbS
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In sickle cell anemia, the mutation is found on what chain of Hb?
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beta chain
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"Sickling" of RBCs is induced by what condition?
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low oxygen concentrations
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What is "sickle cell crisis"?
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low oxygen (to begin with) causes sickling of RBCs. now the RBCs are even more damaged and rupture and even less oxygen is able to be used by tissues. can lead to death
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What is erythroblastosis fetalis?
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Rh+ RBCs in a fetus are attacked by Rh- mother's immune system. baby is born with anemia
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In sever anemia, blood become (more or less) viscous?
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less viscous. RBCs determine viscosity
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Why does cardiac output increase with anemia?
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anemia = less viscous blood = less resistance in vessels = more venous return = high cardiac output. hypoxia dilates systemic blood vessels also decreasing resistance
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Why is it good that anemia increases cardiac output?
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it is now able to compensate. even though each RBC has less oxygen, more RBCs get to tissues faster
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Why do patients with anemia have cardiac failure during exercise?
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the baseline anemic cardiac output is already maximum to compensate for anemia. it can't increase more to keep up with tissue demand during exercise
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What is secondary polycythemia?
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RBC formation induced by hypoxia in breathed air
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Physiologic polycythemia is seen in patients who have adapted to what condition?
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low atmospheric oxygen
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What is polycythemia vera?
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high RBC, Hct due to genetic defect in hemocytoblastic cells
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Why does the vascular system become engorged in polycythemia vera?
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total blood volume also increases in this disease
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Would blood be (more or less) viscous in polycythemia vera?
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more viscous due to overproduction of RBCs
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Why does polycythemia vera result is a normal cardiac output?
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Blood viscosity increases (lower venous return/cardiac output), but blood volume increases (higher cardiac output). these offset each other
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What color skin is usually seen in patients with polycythemia vera?
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blue tint. slower moving deoxygenated blood accumulates
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