slide1 n.
Skip this Video
Download Presentation
Red Blood Cells (Erythrocytes)

Loading in 2 Seconds...

play fullscreen
1 / 63

Red Blood Cells (Erythrocytes) - PowerPoint PPT Presentation

  • Uploaded on

Red Blood Cells (Erythrocytes). Er ythrocytes (RBC). Structure Biconcave disc shape Includes Hemoglobin Lipid s , ATP, carbonic anhydrase Function O 2 and CO 2 transport. Er ythrocytes (RBC). Most abundant type of blood cells 4- 6 million /mm 3 anemi a ; number of RBC below normal

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
Download Presentation

PowerPoint Slideshow about 'Red Blood Cells (Erythrocytes)' - felix

Download Now An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
er ythrocytes rbc
Erythrocytes (RBC)
  • Structure
    • Biconcave disc shape
  • Includes
    • Hemoglobin
    • Lipids, ATP, carbonic anhydrase
  • Function
    • O2 and CO2 transport

Erythrocytes (RBC)

  • Most abundant type of blood cells
    • 4-6million/mm3
    • anemia; number of RBC below normal
    • polycythemia (erythrocytosis); number of RBC above normal range
  • No nucleus, mitochondria and ribosom
    • No protein synthesis
    • Energy is obtained through glycolisis, but there is no glycogen storage
  • Normal diameter 7-8 , volume 78-94 3
    • normocyte - microcyte - macrocyte

Energy use and source in RBC

  • Energy is used mainly for two functions:
    • Continuation of membrane shape - active transport
    • Homeostasis of intracellular oxidation-reduction
  • Only source of energy is glycolysis

RBC Membrane

  • The same as other biological membranes
    • Cannot synthesize its own cell membrane
  • Actin and spectrin provide strength
    • Contractility in the presence of Ca+2 ions
    • Changes in viscosity
  • Na+-K+ATPaseand Ca+2ATPase activity
  • Carbohydrates on the membrane are to do with blood types (antigens)

Hemoglobin (Hb)

  • Red color protein that carries oxygen
    • 1 g Hb binds 1,3 mlO2; 14,8 g Hb binds 20 ml O2
  • Normal range of hemoglobin: 14-16 g/dl
    • In adults, about 25-30 trillion RBC, and 900 g Hb
    • Hb constitutes 1/3 of erythrocyte weight
  • 4 globin molecules:carries CO2 (role of carbonic anhydrase)
  • 4 heme molecules:carries O2
    • Iron is required for oxygen transportation
hematopoiesis hemopoiesis
Hematopoiesis (Hemopoiesis)
  • Production of blood cells
  • Stem cells: All formed elements of blood stem from a colony of cells
    • Proerythroblast: forms erythrocytes
    • Myeloblast: forms neutrophils, eosinophils and basophils
    • Lenfoblast: forms lymphocytes
    • Monoblast: forms monocytes
    • Megakaryoblast: forms thrombocytes
what are stem cells
What are stem cells?
  • They are of many types: epidermal, intestinal, hematopoietic, etc.
  • The defining properties of a stem cell are:
    • It is not terminally differentiated.
    • It can divide without limit.
    • When it divides, the daughter cell has a “choice”:
      • Remain a stem cell, or
      • Terminally differentiate.
potentiality of stem cells1
Potentiality of Stem Cells

“Stem cells” have varying potentials:

  • Totipotent cells.Fertilized oocyte (zygote) & progeny of the first two cell divisions. Cells able to form the embryo and the trophoblast of the placenta.
  • Pluripotent cells. After about 4 days, the blastocyst forms; embryonic stem cells obtained from the inner cell mass, which becomes the embryo, are pluripotent, able to differentiate into almost all cells of the three germ layers – but not into an embryo.
  • Multipotential cells. Found in most tissues, these cells can produce a limited range of differentiated cell lineages appropriate to their location. (Hematopoietic stem cells from the bone marrow exemplify multipotential cells.)
  • Unipotential cells. Cells capable of generating only one cell type (epidermal stem cells, adult liver stem cells).
rbc formation erythropoiesis
RBC Formation (Erythropoiesis)
  • In the adult, all blood cell formation (including erythropoiesis) occurs in the red bone marrow
  • All blood cells develop from stem cells called hemocytoblasts

Red Blood Cells




Myeloid Stem Cell


Lymphoid Stem Cell


erythropoiesis production of rbc
Erythropoiesis (production of RBC)

Weeks 16-20

Week 2

Week 6


Week 8

Myeloid phase


Hepatic phase

Mesoblastic phase

Myeloid phase

Prenatal Life

Postnatal Life


Prenatal period-1

  • Mesoblastic phase
  • It starts in the vitellus sac at the second week
    • These are erythrocytes with nuclei
  • Embriyonic hemoglobins:
    • Hb Gower I, Gower II and Portland 1

Prenatal period-2

  • Hepatic phase
  • Liver takes part starting from the week 6
  • Spleen is involved starting from the week 8
  • Fetal hemoglobin:
    • HbF (2 and 2 )

Prenatal period-3

  • myeloid phase
  • Starts between the weeks 16 and 20 in the bone marrow
    • All bones
    • Hemopoiesis
  • HbA (2 and 2 ): mature hemoglobin

Postnatal Period

  • Only in the bone marrow(myeloid)
    • All bones contribute up to the age of 5
    • Later, erythropoiesis regresses from the distal to the proxymale
    • vertebra, sternum, costa, cranium and femur
    • Red bone marrow turns into yellow marrow (reversible)
      • Lipid infiltration


  • BFU-E and CFU-E cells
    • Response to different levels of EPO
  • proerythroblast
  • basophil erythroblast
  • Polychromatophil erythroblast
  • Orthochromatophil erythroblast
  • Reticulocyte
  • Erythrocytes

Regulation of Erythropoiesis

  • Primary stimulus is hypoxia
  • Tissue oxygenation
    • Blood flow
    • Blood hemoglobin levels
    • Oxygen saturation of hemoglobin
    • Affinity of hemoglobin to oxygen

Erythropoietin (EPO)

  • Fetus and newborn
    • 85% Liver
      • hepatocyte, Kupffer cells, endothelial cells
    • 15% kidney
      • Endothelial cells, glomerulus, JGH, proxymal tubule
  • Adult
    • 85% kidney
    • 15% liver and other tissues
      • glomus caroticum, macrophages
e rythropoiesis
  • Erythropoietin: a hormone that stimulates erythropoiesis
    • It stimulates both differentiation and maturation

Maturation of red blood cells – Vit B12 and Folic acid

  • Both vitamins are necessary for DNA synthesis
  • Deficiency of either of these vitamins causes maturation failure in the process of erythropoiesis
  • Pernicious anemia – Megaloblastic anemia
  • Vit B12 absorption and storage
  • Intrinsic factor: released from parietal cells in the stomach
  • Complex of Vit B12 + intrinsic factor cannot be digested by the enzymes in the stomach
  • Lack of intrinsic factor causes serious absorption abnormalities of Vit B12

Hemoglobin (Hb)

  • Normal range of hemoglobin: 14-16 g/dl
    • Men: 16 g/dl = 21 ml O2 /dl blood
    • Women: 14 g/dl = 19 ml O2 /dl blood
formation of hemoglobin
Formation of Hemoglobin
  • 2 succinyl-CoA + 2 glycine = pyrrole
  • 4 pyrrole protoporphyrin IX
  • protoporphyrin IX + Fe++ Heme
  • Heme + globin hemoglobin chain (alpha or beta)
  • 2 alpha + 2 beta chains Hemoglobin A
hemoglobi n
  • Hemoglobin synthesis begins in the proerythroblasts and continues until reticulocytes
  • It consists of iron containing heme and globin
  • Hemoglobin A contains 2a ve 2b chain
  • There are different types of these chains (a, b, d ve g)
  • Hb molecule binds to oxygen loosely and reversibly
hemoglobin a
Hemoglobin A
  • 4 globin molecules:carries CO2 (role of carbonic anhydrase)
  • 4 hem molecules:carries O2
    • Iron is required for oxygen transportation
lifecycle of an rbc
Lifecycle of an RBC
  • RBCs are subjected to incredible mechanical stress.
    • Why are they unable to synthesize replacements for damaged parts?
  • After ≈120d, the RBC cell membrane ruptures, or the damage is detected by phagocytic cells and the RBC is engulfed.
  • If the RBC hemolyzes, its contained Hb will be excreted by the kidneys

A macrophage phagocytizing multiple RBCs

life span and destruction of rbcs
Life span and destruction of RBCs
  • Because of lack of nuclei, they cannot divide and grow
  • They have a life span of 120 days
  • Old erythrocytes are destructed in the spleen, liver and bone marrow
  • Hemoglobin is broken down to heme and globin
  • Iron part of heme is stored for re-use
  • Porphyrin part of hemoglobin is converted to bilirubin and secreted into bile

Iron – Fe+2,+3

  • 50 in men and 35 mg/kg in women (total 4-5 gr)
    • 60-65% in hemoglobin
    • 4% myoglobin
    • 1% bound to plasma transferrin
    • The rest is in ferritin or hemosiderin
  • Amount of iron bound to transferrin 110-130 g
  • Daily need of iron lost through urine, feces and bleeding should be compensated

Transferrin - siderofilin

  • It is a 1-globulin
  • It has two sides to bind iron (ferri)
    • One side leaves iron to the liver and the other to bone marrow for hemoglobin synthesis
  • Saturation of transferrin with iron (normally 35%)

Absorption of iron

  • Iron is absorbed in ferro (+2) form
    • Absorption in all parts of the small intestine
  • It binds to apoferritin in the intestinal cells and stored as ferritin
  • Iron in ferritin is in the form of ferri (+3)
    • Liver is the largest storage site
    • Homeostasis is maintaned through the intestinal depot

Iron Overload Disease

  • hemosiderin
  • hemochromatosis
    • Bronze diabetes
    • Cirrhosis
    • Cancer
    • Gonadal atrophy

Iron Deficiency

  • Hepatic diseases
  • Deficiency of reducing substances in the digestive tract
    • Ca+2, ascorbic acid, lactic acid, pyruvate, glucose and sorbitol
    • Excessive Ca+2
  • Oxalate, phytate, phosphate
  • Important symptom: geophagy

Other factors

  • Time of iron supplementation
  • Injections in cases of absorption problems
  • Overload of iron facilitates production of microorganisms
    • transferrin and lactoferrin are anti-microbial


  • Decrease in RBC count and/or amount of Hb
  • Reduced capacity of blood to carry O2
    • Tachycardia, tachypnea
    • Tiredness, feeling cold
  • General causes
    • Blood loss
    • Reduced erythropoiesis
    • Increased destruction of RBC
    • Inadequate of production of EPO

Classification of Anemias

  • Hemorrhagic anemias; blood loss
  • Hemolytic anemias; hemolysis
  • Vitamin deficiency anemias (megaloblastic anemia)
  • Iron deficiency anemia
  • EPO deficiency caused anemia
  • Aplastic anemia (Fanconi anemia)

Hemolytic Anemias

  • Intracorpuscular causes
    • hereditary spherocytosis
    • sickle cell anemia; HbS
    • thalassemia (Mediterranian anemia, cooley anemia)
    • glucose-6-phosphate dehydrogenase deficiency
    • Pyruvate kinase deficiency
    • Paroxysmal nocturnal hemoglobinuria
  • Extracorpuscular causes
    • Blood transfusion – autoantibodies
sickle cell anemia
Sickle Cell Anemia
  • Seen in black population
  • A mutation in the βchain of globin results in HbS
  • This hemoglobin precipitates as long crystals in RBC when it exposes to O2
  • As a result, RBC become sickle shaped and may cause blockage in small blood vessels
sickle cell anemia sca
Sickle cell anemia (SCA)
  • In SCA, aa valine takes the place of glutamic acid at the Hemoglobin beta polypeptide chain
Thalassaemia (Mediterranean Anemia)
  • It is usually seen in populations in Mediterranean countries
  • One of the genes coding globin is faulty or missing
glucose 6 phosphate dehydrogenase
Glucose 6-Phosphate Dehydrogenase
  • Regenerates NADPH, allowing regeneration of glutathione
  • Protects against oxidative stress
  • Lack of G6PD leads to hemolysis during oxidative stress
    • Infection
    • Medications
    • Fava beans (that contain high level of oxidants)
  • Oxidative stress leads to Heinz body formation,extravascular hemolysis
glucose 6 phosphate dehydrogenase g6pd anemia
Glucose -6-Phosphate Dehydrogenase (G6PD) Anemia

Hereditary defect in RBC metabolism

  • Direct oxidation of hemoglobin damages RBC
  • occurs when person exposed to stressors: aspirin, sulfonamides, Vitamin K derivatives

Manifestations: pallor, jaundice, hemoglobinuria, elevated reticulocyte count

Diagnostics: quantitative assay of G6PD

er yth roblastosis f e talis
Erythroblastosis Fetalis
  • It is a hemolytic type of anemia
  • Rh- mother, Rh+ father
  • First baby will be Rh+
  • Mixture of baby’s blood with that of mothers during labor
  • Sensitization develops in the mother against Rh+ and antibodies are formed against to Rh antigen
  • First baby is healthy
  • During the second pregnancy, the antibodies formed against Rh are transported to the baby through placenta and attack fetus’ RBC
  • This condition is known as erythroblastosis fetalis (hemolytic disease of new born)
  • Baby is anemic and hypoxic.
  • Exchange transfusion of compatible blood to the baby
  • If not treated, it may cause brain damage and death

Vitamin Deficiency Caused Anemia

  • folic acid
  • vitamin B12
  • vitamin B6
  • vitamin C
  • vitamin E

Iron Deficiency Anemia

  • How does iron deficiency affect O2 transport?
  • It could develop secondary to hemorrahegia
  • Iron deficiency may also present as a result of low iron intake or absorption problems in the GI tract


  • Total number of erythrocytes is more than the normal range
  • Polycythemia vera (erythremia):
    • Cancer of red bone marrow
    • RBC count 7-8 million/mm3
    • Hematocrit value 60-70 %
  • Secondary polycythemia: long term hypoxia
    • Cardiac failure
    • Pulmonary diseases
    • High altitude (physiological)
    • Sportive activity (physiological)


  • Causes an increase in blood pressure
  • Less blood supply to the tissues
  • Decreased blood flow as a result of increased viscosity
  • Color of the skin with polycythemia vera looks bluish (cyanotic) – subpapillary plexus
  • For treatment, blood whould be diluted with an isotonic solution (serum physiologic)

► Some athletes try to induce physiological polycythemia?

Why and How?