Blood Lectures 2 2017
Blood Lectures 2 2017
Blood Lectures 2 2017
• Differentiation
• Maturation
• Release
• Functional RBC
• Senile RBC 8
Erythropoiesis
9
Formation of Hemoglobin
• Begins when the RBC is in the proerythroblast
stage and continues into the reticulocyte stage.
13
Regulation of Erythropoiesis
14
ABO Blood Group
Fig 13.5
13-16
Transfusion Reactions
• If blood types don't match, recipient’s
antibodies agglutinate donor’s RBCs
• Type O is “universal donor” because lacks A &
B antigens
– Recipient’s antibodies won’t agglutinate
donor’s Type O RBCs (which lack antigens)
• Type AB is “universal recipient” because
doesn’t make anti-A or anti-B antibodies
– Won’t agglutinate donor’s RBCs
13-17
Rhesus Blood Group
• Rh factor – Another antigen which may be present
(Rh +) or absent (Rh -) on RBCs.
• ε –Embryonic
• ζ- Embryonic
• Increasing
temperature, CO2 will
shift the curve to the
right
Types of Hb
Normal Abnormal
• Embryonic: • Haemoglobinopathies:
• Gower 1- ζ2ε 2 • HbS,
• Gower 2-α 2 ε 2 • HbC
• Hb Portland- ζ 2 γ 2 • Thallasaemias- α and β
• Fetal- Hb F - α 2 γ 2 • Hb Barts -γ 4
• Adult- Hb A- α 2β 2 • Hb H. β 4
• HbA 2 - α 2δ 2
• Glycosylated Hb Aic -
Sickle Cell Mutation
Chromosome 16
5' 3'
Chromosome 11 G A *
5' 3'
-O2 -O 2
+O 2 +O 2
• Repeated sickling and
unsickling damages RBC
membranes
• cells are less flexible and
block microcirculation and
hemolyse easily.
• Homozygotes SS have
severe hemolytic anaemia–
sickle cell anaemia
• Heterozygotes AS have
sickle cell trait. Dont
hemolyse
Clinical Relevance: Sickle cell disease
• flexibility
• fragility
• blood viscosity
• O2
• sickling
• “crisis”
• Painful ischemia
17.10b
– Lack of O2
Catabolism of Hemoglobin
• After 120 days old RBCs are removed from blood by
phagocytic cells in liver, spleen & bone marrow
• Globin is split from the heme.
• The globin is returned to the plasma protein and
amino acid pool.
• Heme iron is returned to the plasma iron pool and recycled
back into hemoglobin production
• Opening of the porphyrin ring yields biliverdin and
carbon monoxide.
• Biliverdin is converted to bilirubin
Catabolism of Hemoglobin
• Bilirubin(not water soluble) passes into the blood &
is bound to albumin (unconjugated bilirubin).
• Unconjugated bilirubin is conjugated with
glucuronic acid (conjugated bilirubin- water
soluble) by the liver & cleared from the blood.
• Bilirubin passes into bile and gets to intestine
where it is metabolised to urobilinogen.
• Urobilinogen is converted to stecobilin in feaces.
• A small fraction is excreted in kidney and becomes
oxidised to urobilin on exposure to air.
Clinical Relevance: Jaundice
• Jaundice is yellowish discoloration of skin and
mucous membrane due to excess bilirubin.
• Hemolytic: when there is increased destruction
of red blood cells.
• Occurs in neonates due to immature pathway for
glucuronidation causing physiological jaundice.
• Other causes: Infections , G6PD deficiency etc.
• Excess unconjugated bilirubin in circulation, can
cross blood brain barrier to cause brain damage.
Questions???
Summary
• RBCs are important cellular component of blood
containing Hb which is the O2 carrying pigment.