5. RBC, Anemia, Polycythemia, Blood Typing and Hemostasis

Question 1 What are the two major components of blood?

Plasma and cellular elements.

Question 2 Approximately what percentage of plasma is water?

92%.

Question 3 Approximately what percentage of plasma is protein?

7%.

Question 4 Approximately what percentage of plasma consists of other molecules and ions?

1%.

Question 5 What are the cellular elements of blood?

RBCs, platelets, and WBCs.

Question 6 Which WBC types are listed in the lecture?

Lymphocytes, neutrophils, monocytes, eosinophils, and basophils.

Question 7 Where are primitive nucleated RBCs produced in early embryonic life?

The yolk sac.

Question 8 What is the main site of RBC production during the middle trimester?

The liver.

Question 9 Which other organs contribute to fetal RBC production during the middle trimester?

The spleen and lymph nodes.

Question 10 Where are RBCs produced during the last month of gestation and after birth?

Bone marrow.

Question 11 Until about what age does marrow in essentially all bones produce RBCs?

About 5 years.

Question 12 What happens to much of the marrow in long-bone shafts by about age 20?

It becomes fatty and largely stops producing RBCs.

Question 13 Which bones remain major RBC-producing sites in adults?

Vertebrae, sternum, ribs, and ilia.

Question 14 From what cell are all circulating blood cells ultimately derived?

The pluripotential hematopoietic stem cell.

Question 15 What is a committed stem cell?

A hematopoietic cell committed to a particular blood-cell lineage.

Question 16 What does CFU-E stand for?

Colony-forming unit–erythrocyte.

Question 17 What does CFU-GM form?

Granulocytes and monocytes.

Question 18 What cell gives rise to platelets?

Megakaryocytes.

Question 19 Which cytokine promotes growth of many committed stem-cell types?

Interleukin-3.

Question 20 What do growth inducers do?

Promote growth and reproduction of stem cells.

Question 21 What do differentiation inducers do?

Drive committed cells toward mature blood-cell forms.

Question 22 What external condition strongly increases RBC production?

Prolonged hypoxia.

Question 23 What regulates platelet production?

Thrombopoietin.

Question 24 Where is thrombopoietin produced mainly?

The liver, with some production in the kidneys.

Question 25 What do colony-stimulating factors regulate?

WBC production and development.

Question 26 What are cytokines?

Cell-released molecules that affect the growth or activity of other cells.

Question 27 What are the three major functions of erythrocytes emphasized in the lecture?

Transport O2, transport CO2, and act as acid-base buffers.

Question 28 What molecule inside RBCs transports oxygen?

Hemoglobin.

Question 29 Why is hemoglobin kept inside RBCs?

Free hemoglobin can leak through capillary and glomerular membranes.

Question 30 What RBC enzyme accelerates the reversible CO2-water reaction?

Carbonic anhydrase.

Question 31 In what major form is much CO2 transported after carbonic anhydrase activity?

Bicarbonate.

Question 32 Why do RBCs contribute greatly to blood buffering?

Hemoglobin is an effective acid-base buffer.

Question 33 What is the shape of a mature RBC?

Biconcave.

Question 34 Which organelles are absent from mature RBCs?

Nucleus, mitochondria, and endoplasmic reticulum.

Question 35 What is the first recognizable cell of the RBC series?

Proerythroblast.

Question 36 From which committed cell does the proerythroblast arise?

CFU-E.

Question 37 What happens to the nucleus during RBC maturation?

It condenses and is eventually absorbed or extruded.

Question 38 What is a reticulocyte?

An immature RBC containing small remnants of organelles.

Question 39 How do reticulocytes enter blood capillaries from marrow?

By diapedesis.

Question 40 How long does reticulocyte maturation usually take in blood?

About 1–2 days.

Question 41 What proportion of circulating RBCs is normally reticulocytes?

Slightly less than 1%.

Question 42 Where is erythropoietin produced?

The kidneys.

Question 43 What is the main stimulus for EPO release?

Hypoxia.

Question 44 What transcription factor rises with renal tissue hypoxia and promotes EPO transcription?

HIF-1.

Question 45 What does EPO stimulate?

Proerythroblast production and erythroid differentiation.

Question 46 How does high altitude affect erythropoiesis?

It increases EPO and RBC production.

Question 47 Which nutrients are especially important for normal RBC maturation?

Vitamin B12 and folic acid.

Question 48 What gastric factor is necessary for vitamin B12 absorption?

Intrinsic factor.

Question 49 What is the average lifespan of an RBC?

About 120 days.

Question 50 Which organ is especially important in removing old fragile RBCs?

The spleen.

Question 51 What plasma protein transports iron?

Transferrin.

Question 52 What protein stores iron?

Ferritin.

Question 53 What happens to iron from destroyed RBCs?

It is recycled via transferrin or stored as ferritin.

Question 54 What happens to the porphyrin portion of hemoglobin?

It is converted to bilirubin and excreted through bile.

Question 55 How is total body iron regulated mainly?

By changing intestinal iron absorption.

Question 56 What happens to iron absorption when iron stores are depleted?

It increases.

Question 57 What happens to iron absorption when iron stores are saturated?

It decreases.

Question 58 What is anemia?

A deficiency of hemoglobin due to too few RBCs or too little hemoglobin in them.

Question 59 What four broad anemia types are emphasized?

Blood-loss, aplastic, megaloblastic, and hemolytic anemia.

Question 60 What happens to plasma volume 1–3 days after rapid hemorrhage?

It is largely replaced, leaving a low RBC concentration.

Question 61 How long may RBC concentration take to recover after a single hemorrhage?

About 3–6 weeks.

Question 62 Why can chronic blood loss cause microcytic hypochromic anemia?

Iron cannot be absorbed rapidly enough to replace hemoglobin loss.

Question 63 What does microcytic mean?

RBCs are smaller than normal.

Question 64 What does hypochromic mean?

RBCs contain less hemoglobin than normal.

Question 65 What is aplastic anemia?

Anemia due to failure of functioning bone marrow.

Question 66 What treatments are mentioned for severe aplastic anemia?

Blood transfusion and bone marrow transplantation.

Question 67 What is the basic problem in megaloblastic anemia?

Slow erythroblast reproduction and maturation.

Question 68 Which deficiencies can lead to megaloblastic anemia?

Vitamin B12, folate, or intrinsic factor deficiency.

Question 69 Why can pernicious anemia cause megaloblastic anemia?

Loss of intrinsic factor impairs vitamin B12 absorption.

Question 70 Why can total gastrectomy cause megaloblastic anemia?

It removes the gastric source of intrinsic factor.

Question 71 What is hemolytic anemia?

Anemia caused by RBC destruction faster than RBC formation.

Question 72 What RBC shape occurs in hereditary spherocytosis?

Small spherical RBCs.

Question 73 Why are spherocytes fragile?

They tolerate compression poorly in narrow vascular spaces.

Question 74 What abnormal hemoglobin is present in sickle cell anemia?

Hemoglobin S.

Question 75 What triggers HbS polymerization?

Deoxygenation or low oxygen tension.

Question 76 What happens to RBC shape when HbS polymerizes?

The cells become sickle-shaped.

Question 77 What vicious cycle occurs in sickle crisis?

Hypoxia causes sickling, sickling worsens flow and hemolysis, which causes more hypoxia and sickling.

Question 78 How can erythroblastosis fetalis produce anemia?

Maternal anti-Rh antibodies destroy fetal Rh-positive RBCs.

Question 79 What happens to blood viscosity in severe anemia?

It decreases.

Question 80 What happens to peripheral vascular resistance in severe anemia?

It decreases.

Question 81 Why does tissue hypoxia in anemia further increase blood flow?

It causes peripheral vasodilation.

Question 82 What happens to cardiac output in severe anemia?

It increases markedly.

Question 83 Why can severe anemia cause cardiac failure during exercise?

The heart may already be near maximal output and cannot meet increased oxygen demand.

Question 84 What is polycythemia?

An increase in circulating RBCs.

Question 85 What is secondary polycythemia?

Increased RBC production caused by tissue hypoxia.

Question 86 Give two causes of secondary polycythemia from the lecture.

High altitude and impaired oxygen delivery such as cardiac failure.

Question 87 What is physiological polycythemia?

A normal hypoxic adaptation, such as in high-altitude residents.

Question 88 What RBC count is typical of secondary polycythemia in the lecture?

About 6–7 million/mm³.

Question 89 What is polycythemia vera?

Pathologic overproduction of blood cells due to abnormal hematopoietic cells.

Question 90 What RBC count may occur in polycythemia vera?

About 7–8 million/mm³.

Question 91 What hematocrit may occur in polycythemia vera?

About 60–70%.

Question 92 Which cells besides RBCs may increase in polycythemia vera?

WBCs and platelets.

Question 93 What happens to blood viscosity in polycythemia vera?

It increases markedly.

Question 94 How does high viscosity affect peripheral blood flow?

It makes flow sluggish.

Question 95 What skin appearance is typical of polycythemia vera?

A ruddy complexion with a bluish or cyanotic tint.

Question 96 Which two blood-group systems are most important for transfusion reactions?

ABO and Rh.

Question 97 What antigen is on type A RBCs?

A antigen.

Question 98 What antigen is on type B RBCs?

B antigen.

Question 99 What antigens are on type AB RBCs?

A and B antigens.

Question 100 What ABO antigens are on type O RBCs?

Neither A nor B.