SlideShare una empresa de Scribd logo
1 de 43
Descargar para leer sin conexión
Biochemistry of blood.
Respiratory function of
erythrocytes.
Pathobiochemistry of blood.
Red Blood Cells (erythrocytes)
The most numerous type in the blood.
•Features:
•The erythrocytes doesn’t contain nucleus, chromatine
•The erythrocytes doesn’t contain mytochondrias, thus АТP
producing due to the anaerobic glycolisis till to the lactate
(90%).
•The glycolisis has features. During it the 2,3 BPG will be
produced, not 1,3 BPG. This compound need for joining О2 to
hemoglobin: low concentration of 2,3 BPG will increase the
affinity hemoglobin (Нв) to О2.
• The PPP is the main path for producing of reductive
equivalents NADPН2 for taking part in glycolisis
Red blood cells are responsible for the
transport of oxygen and carbon dioxide.
 In adult humans the
hemoglobin (Hb) molecule
consists of four
polypeptides:
 two alpha (α) chains of
141 amino acids and
 two beta (β) chains of
146 amino acids
 Each of these is attached
the prosthetic group heme.
 There is one atom of iron at
the center of each heme.
 One molecule of oxygen
can bind to each heme.
 The reaction is reversible.
Transport of oxygen by hemoglobin
Hemoglobin has all the requirements of an ideal
respiratory pigment:
-It can transport large quantities of oxygen.
-It has great solubility.
-It can take up and release oxygen at appropriate partial
pressures.
-It is a powerful buffer.
Oxygenation and oxidation
• When hemoglobin carries oxygen, the Hb is
oxygenated. The iron atom in Hb is still in
the ferrous state.
• Oxidized hemoglobin is called Met-Hb; then
iron is in ferric state and the oxygen carrying
capacity is lost.
Oxygen Dissociation Curve
(ODC)• The ability of hemoglobin to load and unload
oxygen at physiological pO2 (partial pressure
of oxygen).
• At the oxygen tension in the pulmonary
alveoli, the Hb is 97% saturated with oxygen.
Normal blood with 15mg/dl of Hb can carry
20ml of O2/dl of blood.
• In the tissue capillaries, where the pO2 is only
40mm of Hg, the Hb is about 60% saturated.
So physiologically, 40% of oxygen is released.
Blood respiratory function & jaundice
 H+, CO2,
 BPG
Hb Equilibrium
b
b a
a
R
(high affinity)
O2
α β
β α
T
(low affinity)
Cooperativity
 Oxygen binding to one subunit of Hb,
increases the affinity of the other subunits
for additional oxygens. In other words, the
first one is the hardest, the rest are easy.
 Anaemia
 Anaemia is a shortage of RBCs and/or the
amount of haemoglobin in them.
Carbon Dioxide Transport
 Carbon dioxide (CO2) combines with water forming
carbonic acid, which dissociates into a hydrogen ion
(H+) and a bicarbonate ions:
 CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3−
 95% of the CO2 generated in the tissues is carried in
the red blood cells:
 It probably enters (and leaves) the cell by diffusing
through transmembrane channels in the plasma
membrane. (One of the proteins that forms the
channel is the D antigen that is the most important
factor in the Rh system of blood groups.)
 Once inside, about one-half of the CO2 is directly
bound to hemoglobin (at a site different from the one
that binds oxygen).
 The rest is converted — following the equation above —
by the enzyme carbonic anhydrase into
 bicarbonate ions that diffuse back out into the plasma
and
 hydrogen ions (H+) that bind to the protein portion of
the hemoglobin (thus having no effect on pH).
 Only about 5% of the CO2 generated in the tissues
dissolves directly in the plasma.
 When the red cells reach the lungs, these reactions are
reversed and CO2 is released to the air of the alveoli.
Blood respiratory function & jaundice
The ability of hemoglobin to release oxygen, is affected by pH, CO2
and by the differences in the oxygen-rich environment of the lungs and
the oxygen-poor environment of the tissues. The pH in the tissues is
considerably lower (more acidic) than in the lungs. Protons are
generated from the reaction between carbon dioxide and water to form
bicarbonate:
 CO2 + H20 -----------------> HCO3- + H+
This increased acidity serves a two fold purpose.
- First, protons are lower the affinity of hemoglobin for oxygen,
allowing easier release into the tissues. As all four oxygens
are released, hemoglobin binds to two protons. This helps to
maintain equilibrium towards the right side of the equation.
This is known as the Bohr effect, and is vital in the removal of
carbon dioxide as waste because CO2 is insoluble in the
bloodstream. The bicarbonate ion is much more soluble, and
can thereby be transported back to the lungs after being
bound to hemoglobin.
- If hemoglobin couldn’t absorb the excess protons, the
equilibrium would shift to the left, and carbon dioxide couldn’t
be removed
Bohr Effect (pH)
100 mm O2
20 mm O2
 In the lungs, this effect works in the reverse
direction. In the presence of the high oxygen
concentration in the lungs, lead to the proton
affinity decreasing. As protons are shed, the
reaction is driven to the left, and CO2 forms as
an insoluble gas to be expelled from the lungs.
The proton poor hemoglobin now has a greater
affinity for oxygen, and the cycle continues.
Blood respiratory function & jaundice
CO2 effect
20 mm CO2
80 mm CO2
Effect of BPG
BPGEffect
pO2 (mm Hg)
0 20 40 60 80 100 120 140 160
0
20
40
60
80
100
pO2 vs p50=8
pO2 vs p50=26
Hb alone
Hb + BPG
BPG is the main
player in Hb
cooperativity.
High altitude
increases BPG,
pushing curve
further to right
Myoglobin and Hemoglobin
 Mb is monomer, Hb is a tetramer (ex. a2b2).
 Hb subunits are structurally similar to Mb, with 8
a-helical regions, no b-strands and no interior
water.
 Both contain one heme prosthetic group per
chain.
 Both Mb and Hb contain proximal and distal
histidines.
 Affinity of Mb for oxygen is high, affinity of Hb for
oxygen is lower and more variable.
 The iron atom may either
be in the Fe2+ or Fe3+
state, but ferrihemoglobin
(methemoglobin) (Fe3+)
cannot bind oxygen. In
binding, oxygen
temporarily oxidizes Fe to
(Fe3+), so iron must exist
in the +2 oxidation state in
order to bind oxygen. The
body reactivates
hemoglobin found in the
inactive (Fe3+) state by
reducing the iron center.
Blood respiratory function & jaundice
Sickle cell hemoglobin (HbS)
β
α β
α
G lu
-
G lu
-
H b A 1
β
α β
α
G lu
-
H b S
( h e t e r o z y g o u s )
S i c k l e c e l l t r a i t
β
α β
α
H b S
( h o m o z y g o u s )
S i c k l e c e l l d i s e a s e
Polymerization of HbS
β
α β
α
β
α β
α
β
α β
α
β
α β
α
β
α β
α
β
α β
α β
α β
α
Association shown in
previous figure is
repeated over and over
to produce large, rod-like
aggregates that bind
oxygen poorly and distort
shape of erythrocytes.
 Sickle cell trait is usually asymptomatic, but
strenuous exercise at altitude could elicit
sickling and destruction of erythrocytes.
This lowers serum Hb and hematocrit, while
raising Hb breakdown products such as
bilirubin, which can accumulate to form
gallstones.
a-Thalassemias
 Rare, since a-gene is duplicated (four genes per diploid
chromosome set).
 Usually more severe than b-thalassemia because
 there is no substitute for b-gene in adults.
 Almost all b- thalassemias are deletions
 In α thalassemia intermedia (αo
α/αο
αo
) -
appearance of HbH (β4)
 In α thalassemia major (αo
αο
/αo
αo
), Hb Bart’s
(γ4) is predominant (usually lethal).
 BPG is ineffective in HbH & Hb Bart’s.
β Thalassemias
 More common, since β gene is present in only
one copy per chromosome.
 Less severe than α thalassemia, since δ chain
can effectively substitute in adults.
 The γ chain can also persist into adulthood
(HPFH).
 In βδ thalassemia major (βδ0
/βδ0
) excess α
chains do not form soluble homotetramers.
Blood respiratory function & jaundice
Blood respiratory function & jaundice
Blood respiratory function & jaundice
Blood respiratory function & jaundice
Plasma Bilirubin
• Normal plasma bilirubin level ranges from 0.2-0.8
mg/dl. The unconjugated bilirubin is about 0.2-0.6
mg/dl, while conjugated bilirubin is only 0- 0.2.
• If the level of plasma bilirubin exceeds 1 mg/dl, the
condition is called hyperbilirubinemia.
• Levels between 1 and 2 mg/dl are indicative of
latent jaundice.
• When the bilirubin level exceeds 2 mg/dl, it diffuses
into tissues producing yellowish discoloration of
skin and mucous membrane resulting in jaundice.
• Van den Bergh test is a test for detection of
bilirubin.
Hyperbilribunemias
• Depending on the nature of the
bilirubin elevated, the condition
may be grouped into conjugated or
unconjugated hyperbilirubinemia.
• Based on the cause it may also be
classified into congenital and
acquired.
1- Congenital
Hyperbilirubinemias
• They results from abnormal uptake, conjugation or excretion of
bilirubin due to inherited defects.
Crigler-Najjar syndrome:
 Here the defect is in conjugation.
 In type 1 (Congenital non-hemolytic jaundice), there is sever
deficiency of UDP glucuronyl transferase.
 The disease is often fatal and the children die before the age 2.
 Jaundice usually appears within the first 24 hours of life.
 Unconjugated bilirubin level increases to more than 20
mg/dl, and hence Kernicterus is resulted.
2- Acquired Hyperbilirubinemias
Physiological Jaundice:
It is also called as neonatal hyperbilirubinemia.
In all newborn infants after the second day of life, mild jaundice
appears.
This transient hyperbilirubinemia is due to an accelerated rate of
destruction of RBCs and also because of the immature hepatic system
of conjugation of bilirubin.
In such cases, bilirubin does not increase above
5mg/dl.
It disappears by the second week of life.
3- Hemolytic Jaundice
A) Hemolytic Disease of the Newborn:
This condition results from incompatibility between
maternal and fetal blood groups.
Rh+ve fetus may produce antibodies in Rh-ve mother,
leading to Rh incompatibility.
When blood level of bilirubin is more than 20mg/dl, the
capacity of albumin to bind bilirubin is exceeded.
In young children before the age of 1 year, the blood-
brain barrier is not fully matured, and therefore free
bilirubin enters the brain (Kernicterus).
It is deposited in brain, leading to mental retardation.
B) Hemolytic Diseases of Adults:
 This condition is seen in increased rate of
hemolysis.
 It usually occurs in adults.
 The characteristic features are increase in
unconjugated bilirubin in blood, absence of
bilirubinuria and excessive excretion of UBG in
urine and SBG in feces.
 Common causes are:
1.Congenital spherocytosis.
• Autoimmune hemolytic anemias.
• Toxins like carbon tetrachloride.
4- Hepatocellular Jaundice
• The most common cause is viral hepatitis,
caused by hepatitis viruses A, B, C, D, or G.
• Conjugation in liver is decreased and hence
free bilirubin is increased in circulation.
5- Obstructive
Jaundice• Conjugated bilirubin is increased in blood, and it is excreted in urine.
• UBG will be decreased in urine or even absent.
• Since no pigment are entering into the gut, the feces become clay colored.
• The common causes are:
1. Intrahepatic cholestasis. This may be due to cirrhosis or hepatoma.
2. Extrahepatic obstruction. This may be due to stones in the gallbladder or biliary
tract; carcinoma of head of pancreas.
Blood respiratory function & jaundice
Blood respiratory function & jaundice
Blood respiratory function & jaundice
Kidney in AB equilibrium

Más contenido relacionado

La actualidad más candente

Hb chemistry and disorders
Hb chemistry  and disorders Hb chemistry  and disorders
Hb chemistry and disorders ranjani n
 
Heme Biosynthesis and Its disorders (Porphyria)
Heme Biosynthesis and Its disorders (Porphyria)Heme Biosynthesis and Its disorders (Porphyria)
Heme Biosynthesis and Its disorders (Porphyria)Ashok Katta
 
Haemoglobin.
Haemoglobin.Haemoglobin.
Haemoglobin.EXCELRA
 
Hemoglobin metabolism
Hemoglobin metabolismHemoglobin metabolism
Hemoglobin metabolismAli Faris
 
Biochemistry of blood bds
Biochemistry of blood  bdsBiochemistry of blood  bds
Biochemistry of blood bdsUrooj Arif
 
Structure And Function Of Haemoglobin
Structure And Function Of  HaemoglobinStructure And Function Of  Haemoglobin
Structure And Function Of HaemoglobinPragmatic Learning
 
HEMOGLOBIN DERIVATIVES
HEMOGLOBIN DERIVATIVESHEMOGLOBIN DERIVATIVES
HEMOGLOBIN DERIVATIVESYESANNA
 
HEMOGLOBIN DERIVATIVES
HEMOGLOBIN DERIVATIVESHEMOGLOBIN DERIVATIVES
HEMOGLOBIN DERIVATIVESYESANNA
 
Hemoglobin and insulin
Hemoglobin and insulinHemoglobin and insulin
Hemoglobin and insulinDr-HAMDAN
 
Structure and function of haemoglobin
Structure and function of haemoglobinStructure and function of haemoglobin
Structure and function of haemoglobinKiruththikan Yogaraja
 
Normal & abnormal hemoglobin derivatives
Normal & abnormal hemoglobin derivativesNormal & abnormal hemoglobin derivatives
Normal & abnormal hemoglobin derivativesrohini sane
 
Hemoglobin Lecture for bs mlt
Hemoglobin Lecture for bs mltHemoglobin Lecture for bs mlt
Hemoglobin Lecture for bs mltHabibah Chaudhary
 
HEME CHEMISTRY
HEME CHEMISTRYHEME CHEMISTRY
HEME CHEMISTRYYESANNA
 
Composition of blood
Composition of bloodComposition of blood
Composition of bloodRaghu Veer
 

La actualidad más candente (20)

Hb chemistry and disorders
Hb chemistry  and disorders Hb chemistry  and disorders
Hb chemistry and disorders
 
Heme Biosynthesis and Its disorders (Porphyria)
Heme Biosynthesis and Its disorders (Porphyria)Heme Biosynthesis and Its disorders (Porphyria)
Heme Biosynthesis and Its disorders (Porphyria)
 
Haemoglobin.
Haemoglobin.Haemoglobin.
Haemoglobin.
 
Hemoglobin metabolism
Hemoglobin metabolismHemoglobin metabolism
Hemoglobin metabolism
 
HEMOGLOBIN SYNTHESIS
HEMOGLOBIN SYNTHESISHEMOGLOBIN SYNTHESIS
HEMOGLOBIN SYNTHESIS
 
Biochemistry of blood bds
Biochemistry of blood  bdsBiochemistry of blood  bds
Biochemistry of blood bds
 
Heamoglobin
HeamoglobinHeamoglobin
Heamoglobin
 
Structure And Function Of Haemoglobin
Structure And Function Of  HaemoglobinStructure And Function Of  Haemoglobin
Structure And Function Of Haemoglobin
 
HEMOGLOBIN DERIVATIVES
HEMOGLOBIN DERIVATIVESHEMOGLOBIN DERIVATIVES
HEMOGLOBIN DERIVATIVES
 
HEMOGLOBIN DERIVATIVES
HEMOGLOBIN DERIVATIVESHEMOGLOBIN DERIVATIVES
HEMOGLOBIN DERIVATIVES
 
Hemoglobin and insulin
Hemoglobin and insulinHemoglobin and insulin
Hemoglobin and insulin
 
Hemoglobin structure
Hemoglobin structure Hemoglobin structure
Hemoglobin structure
 
Structure and function of haemoglobin
Structure and function of haemoglobinStructure and function of haemoglobin
Structure and function of haemoglobin
 
Normal & abnormal hemoglobin derivatives
Normal & abnormal hemoglobin derivativesNormal & abnormal hemoglobin derivatives
Normal & abnormal hemoglobin derivatives
 
Hemoglobin
HemoglobinHemoglobin
Hemoglobin
 
Hemoglobin Lecture for bs mlt
Hemoglobin Lecture for bs mltHemoglobin Lecture for bs mlt
Hemoglobin Lecture for bs mlt
 
Hemoglobin Synthesis
Hemoglobin SynthesisHemoglobin Synthesis
Hemoglobin Synthesis
 
HEME CHEMISTRY
HEME CHEMISTRYHEME CHEMISTRY
HEME CHEMISTRY
 
Composition of blood
Composition of bloodComposition of blood
Composition of blood
 
HEMOGLOBIN
HEMOGLOBINHEMOGLOBIN
HEMOGLOBIN
 

Destacado

Cell biology journal abstract and summary
Cell biology journal abstract and summary Cell biology journal abstract and summary
Cell biology journal abstract and summary Shaina Mavreen Villaroza
 
Inflammation Part (2)
Inflammation Part  (2)Inflammation Part  (2)
Inflammation Part (2)hussamdr
 
Inflammation part 1 by
Inflammation  part 1 byInflammation  part 1 by
Inflammation part 1 byhussamdr
 
Guideline for blood transfusion in newborn (NNF)
Guideline for blood transfusion in newborn (NNF)Guideline for blood transfusion in newborn (NNF)
Guideline for blood transfusion in newborn (NNF)mandar haval
 
Approach to a child with jaundice
Approach to a child with jaundice Approach to a child with jaundice
Approach to a child with jaundice Bala Sankar
 
Blood functions and characteristics
Blood functions and characteristicsBlood functions and characteristics
Blood functions and characteristicsstewart_j
 
Bio 160 Parasitology - First prelim handouts Amoeba
Bio 160 Parasitology - First prelim handouts AmoebaBio 160 Parasitology - First prelim handouts Amoeba
Bio 160 Parasitology - First prelim handouts AmoebaShaina Mavreen Villaroza
 
Mitosis Cell division and general genetics
Mitosis Cell division and general geneticsMitosis Cell division and general genetics
Mitosis Cell division and general geneticsAli Safaa97
 
Effective phototherapy for neonatal jaundice
Effective phototherapy for neonatal jaundiceEffective phototherapy for neonatal jaundice
Effective phototherapy for neonatal jaundiceLaxmikant Deshmukh
 

Destacado (20)

Biochemistry of blood, heme biosynthesis and degradation
Biochemistry of blood, heme biosynthesis and degradationBiochemistry of blood, heme biosynthesis and degradation
Biochemistry of blood, heme biosynthesis and degradation
 
Storage Devices
Storage DevicesStorage Devices
Storage Devices
 
Cell biology journal abstract and summary
Cell biology journal abstract and summary Cell biology journal abstract and summary
Cell biology journal abstract and summary
 
Circulatory system handout
Circulatory system handoutCirculatory system handout
Circulatory system handout
 
What is stress
What is stressWhat is stress
What is stress
 
Inflammation Part (2)
Inflammation Part  (2)Inflammation Part  (2)
Inflammation Part (2)
 
Inflammation part 1 by
Inflammation  part 1 byInflammation  part 1 by
Inflammation part 1 by
 
Lecture notes 3
Lecture notes 3Lecture notes 3
Lecture notes 3
 
Guideline for blood transfusion in newborn (NNF)
Guideline for blood transfusion in newborn (NNF)Guideline for blood transfusion in newborn (NNF)
Guideline for blood transfusion in newborn (NNF)
 
Hyperbilirubinemia
HyperbilirubinemiaHyperbilirubinemia
Hyperbilirubinemia
 
Approach to a child with jaundice
Approach to a child with jaundice Approach to a child with jaundice
Approach to a child with jaundice
 
Rocks and minerals
Rocks and mineralsRocks and minerals
Rocks and minerals
 
Margins and apices
Margins and apicesMargins and apices
Margins and apices
 
NNJ
NNJNNJ
NNJ
 
Exchange transfusion
Exchange transfusionExchange transfusion
Exchange transfusion
 
Blood functions and characteristics
Blood functions and characteristicsBlood functions and characteristics
Blood functions and characteristics
 
Bio 160 Parasitology - First prelim handouts Amoeba
Bio 160 Parasitology - First prelim handouts AmoebaBio 160 Parasitology - First prelim handouts Amoeba
Bio 160 Parasitology - First prelim handouts Amoeba
 
Mitosis Cell division and general genetics
Mitosis Cell division and general geneticsMitosis Cell division and general genetics
Mitosis Cell division and general genetics
 
Effective phototherapy for neonatal jaundice
Effective phototherapy for neonatal jaundiceEffective phototherapy for neonatal jaundice
Effective phototherapy for neonatal jaundice
 
Crebs cycle 2013
Crebs cycle 2013Crebs cycle 2013
Crebs cycle 2013
 

Similar a Blood respiratory function & jaundice

The red blood_corpuscles_(r.b.c.s)
The red blood_corpuscles_(r.b.c.s)The red blood_corpuscles_(r.b.c.s)
The red blood_corpuscles_(r.b.c.s)zulujunior
 
haemoglobin derivatives and disorder
haemoglobin derivatives and disorder haemoglobin derivatives and disorder
haemoglobin derivatives and disorder ShahzebHUSSAIN5
 
HAEMOGLOBIN STRUCTURE & FUNCTION
HAEMOGLOBIN STRUCTURE & FUNCTIONHAEMOGLOBIN STRUCTURE & FUNCTION
HAEMOGLOBIN STRUCTURE & FUNCTIONAmudhaLakshmi1
 
Haemoglobin and Gas Transport.pptx
Haemoglobin and Gas Transport.pptxHaemoglobin and Gas Transport.pptx
Haemoglobin and Gas Transport.pptxEbot Walter Ojong
 
cape biology unit 2-_hb_dissociation_curve_and_blood
cape biology unit 2-_hb_dissociation_curve_and_bloodcape biology unit 2-_hb_dissociation_curve_and_blood
cape biology unit 2-_hb_dissociation_curve_and_bloodHilton Ritch
 
HAEMOGLOBIN & MYOGLOBIN STRUCTURE.pptx
HAEMOGLOBIN & MYOGLOBIN STRUCTURE.pptxHAEMOGLOBIN & MYOGLOBIN STRUCTURE.pptx
HAEMOGLOBIN & MYOGLOBIN STRUCTURE.pptxNiranjanShakya1
 
Gas transport(6).ppt
Gas transport(6).pptGas transport(6).ppt
Gas transport(6).pptAkhilaraj25
 
Transport of o2 and co2 between respiratory surface
Transport of o2 and co2 between respiratory surfaceTransport of o2 and co2 between respiratory surface
Transport of o2 and co2 between respiratory surfaceAbuzar Tabusam
 
slides conjugate proteins (1).pptx
slides conjugate proteins (1).pptxslides conjugate proteins (1).pptx
slides conjugate proteins (1).pptxAlhuurulayniyyah3714
 
HEMOGLOBIN - STRUCTURE IN RELATION TO FUNCTION
HEMOGLOBIN - STRUCTURE IN RELATION TO FUNCTIONHEMOGLOBIN - STRUCTURE IN RELATION TO FUNCTION
HEMOGLOBIN - STRUCTURE IN RELATION TO FUNCTIONMuunda Mudenda
 
Hemoglobin structure and metabolism by Dr. Anurag Yadav
Hemoglobin structure and metabolism by Dr. Anurag YadavHemoglobin structure and metabolism by Dr. Anurag Yadav
Hemoglobin structure and metabolism by Dr. Anurag YadavDr Anurag Yadav
 
Transport of oxygen and carbon dioxide
Transport of oxygen and carbon dioxideTransport of oxygen and carbon dioxide
Transport of oxygen and carbon dioxideOnikhilkumar Reddy
 
Estimation of Hemoglobin (hb) by Pandian M, Tutor, Dept of Physiology, DYPMCK...
Estimation of Hemoglobin (hb) by Pandian M, Tutor, Dept of Physiology, DYPMCK...Estimation of Hemoglobin (hb) by Pandian M, Tutor, Dept of Physiology, DYPMCK...
Estimation of Hemoglobin (hb) by Pandian M, Tutor, Dept of Physiology, DYPMCK...Pandian M
 
Hemoglobin and erythropoiesis bikal
Hemoglobin and erythropoiesis bikalHemoglobin and erythropoiesis bikal
Hemoglobin and erythropoiesis bikalBikal Lamichhane
 

Similar a Blood respiratory function & jaundice (20)

The red blood_corpuscles_(r.b.c.s)
The red blood_corpuscles_(r.b.c.s)The red blood_corpuscles_(r.b.c.s)
The red blood_corpuscles_(r.b.c.s)
 
haemoglobin derivatives and disorder
haemoglobin derivatives and disorder haemoglobin derivatives and disorder
haemoglobin derivatives and disorder
 
HAEMOGLOBIN STRUCTURE & FUNCTION
HAEMOGLOBIN STRUCTURE & FUNCTIONHAEMOGLOBIN STRUCTURE & FUNCTION
HAEMOGLOBIN STRUCTURE & FUNCTION
 
Haemoglobin
HaemoglobinHaemoglobin
Haemoglobin
 
Haemoglobin and Gas Transport.pptx
Haemoglobin and Gas Transport.pptxHaemoglobin and Gas Transport.pptx
Haemoglobin and Gas Transport.pptx
 
cape biology unit 2-_hb_dissociation_curve_and_blood
cape biology unit 2-_hb_dissociation_curve_and_bloodcape biology unit 2-_hb_dissociation_curve_and_blood
cape biology unit 2-_hb_dissociation_curve_and_blood
 
Hemoglobin.pptx
Hemoglobin.pptxHemoglobin.pptx
Hemoglobin.pptx
 
HAEMOGLOBIN & MYOGLOBIN STRUCTURE.pptx
HAEMOGLOBIN & MYOGLOBIN STRUCTURE.pptxHAEMOGLOBIN & MYOGLOBIN STRUCTURE.pptx
HAEMOGLOBIN & MYOGLOBIN STRUCTURE.pptx
 
hb.ppt
hb.ppthb.ppt
hb.ppt
 
Gas transport(6).ppt
Gas transport(6).pptGas transport(6).ppt
Gas transport(6).ppt
 
Transport of o2 and co2 between respiratory surface
Transport of o2 and co2 between respiratory surfaceTransport of o2 and co2 between respiratory surface
Transport of o2 and co2 between respiratory surface
 
Hemoglobin
HemoglobinHemoglobin
Hemoglobin
 
slides conjugate proteins (1).pptx
slides conjugate proteins (1).pptxslides conjugate proteins (1).pptx
slides conjugate proteins (1).pptx
 
HEMOGLOBIN - STRUCTURE IN RELATION TO FUNCTION
HEMOGLOBIN - STRUCTURE IN RELATION TO FUNCTIONHEMOGLOBIN - STRUCTURE IN RELATION TO FUNCTION
HEMOGLOBIN - STRUCTURE IN RELATION TO FUNCTION
 
Hemoglobin structure and metabolism by Dr. Anurag Yadav
Hemoglobin structure and metabolism by Dr. Anurag YadavHemoglobin structure and metabolism by Dr. Anurag Yadav
Hemoglobin structure and metabolism by Dr. Anurag Yadav
 
Transport of oxygen and carbon dioxide
Transport of oxygen and carbon dioxideTransport of oxygen and carbon dioxide
Transport of oxygen and carbon dioxide
 
Estimation of Hemoglobin (hb) by Pandian M, Tutor, Dept of Physiology, DYPMCK...
Estimation of Hemoglobin (hb) by Pandian M, Tutor, Dept of Physiology, DYPMCK...Estimation of Hemoglobin (hb) by Pandian M, Tutor, Dept of Physiology, DYPMCK...
Estimation of Hemoglobin (hb) by Pandian M, Tutor, Dept of Physiology, DYPMCK...
 
Hemoglobin and erythropoiesis bikal
Hemoglobin and erythropoiesis bikalHemoglobin and erythropoiesis bikal
Hemoglobin and erythropoiesis bikal
 
Haemoglobin
HaemoglobinHaemoglobin
Haemoglobin
 
Haemoglobin
HaemoglobinHaemoglobin
Haemoglobin
 

Más de Ivano-Frankivsk National Medical University (IFNMU)

Más de Ivano-Frankivsk National Medical University (IFNMU) (15)

Heme synthesis and degradation
Heme synthesis and degradationHeme synthesis and degradation
Heme synthesis and degradation
 
Nucleic acids and proteins synthesis
Nucleic acids and proteins synthesisNucleic acids and proteins synthesis
Nucleic acids and proteins synthesis
 
Nucleic acids and nucleotides methabolism
Nucleic acids and nucleotides methabolismNucleic acids and nucleotides methabolism
Nucleic acids and nucleotides methabolism
 
Specific and general pathway etc(new)2013
Specific and general pathway etc(new)2013Specific and general pathway etc(new)2013
Specific and general pathway etc(new)2013
 
!!!Glycolysis, neoglucogenesis, the anaerobic degradation of glucose
!!!Glycolysis, neoglucogenesis, the anaerobic degradation of glucose!!!Glycolysis, neoglucogenesis, the anaerobic degradation of glucose
!!!Glycolysis, neoglucogenesis, the anaerobic degradation of glucose
 
Hormones 2
Hormones 2Hormones 2
Hormones 2
 
Cell membrane transduction 1
Cell membrane transduction 1Cell membrane transduction 1
Cell membrane transduction 1
 
Water solublevitamins
Water solublevitaminsWater solublevitamins
Water solublevitamins
 
Enzymes. classification. isoenzymes
Enzymes. classification. isoenzymesEnzymes. classification. isoenzymes
Enzymes. classification. isoenzymes
 
Biochemistry of liver&muscles
Biochemistry of liver&musclesBiochemistry of liver&muscles
Biochemistry of liver&muscles
 
Water minerals metabolism & kidney function
Water minerals metabolism & kidney functionWater minerals metabolism & kidney function
Water minerals metabolism & kidney function
 
Metabolism of lipids 1 1
Metabolism of lipids 1 1Metabolism of lipids 1 1
Metabolism of lipids 1 1
 
Metabolism of lipids 1 2
Metabolism of lipids 1 2Metabolism of lipids 1 2
Metabolism of lipids 1 2
 
Individual path of aminoacids
Individual path of aminoacidsIndividual path of aminoacids
Individual path of aminoacids
 
Amino acids metabolism new
Amino acids metabolism newAmino acids metabolism new
Amino acids metabolism new
 

Último

DLL Catch Up Friday March 22.docx CATCH UP FRIDAYS
DLL Catch Up Friday March 22.docx CATCH UP FRIDAYSDLL Catch Up Friday March 22.docx CATCH UP FRIDAYS
DLL Catch Up Friday March 22.docx CATCH UP FRIDAYSTeacherNicaPrintable
 
Arti Languages Pre Seed Send Ahead Pitchdeck 2024.pdf
Arti Languages Pre Seed Send Ahead Pitchdeck 2024.pdfArti Languages Pre Seed Send Ahead Pitchdeck 2024.pdf
Arti Languages Pre Seed Send Ahead Pitchdeck 2024.pdfwill854175
 
BÀI TẬP BỔ TRỢ TIẾNG ANH 11 THEO ĐƠN VỊ BÀI HỌC - CẢ NĂM - CÓ FILE NGHE (GLOB...
BÀI TẬP BỔ TRỢ TIẾNG ANH 11 THEO ĐƠN VỊ BÀI HỌC - CẢ NĂM - CÓ FILE NGHE (GLOB...BÀI TẬP BỔ TRỢ TIẾNG ANH 11 THEO ĐƠN VỊ BÀI HỌC - CẢ NĂM - CÓ FILE NGHE (GLOB...
BÀI TẬP BỔ TRỢ TIẾNG ANH 11 THEO ĐƠN VỊ BÀI HỌC - CẢ NĂM - CÓ FILE NGHE (GLOB...Nguyen Thanh Tu Collection
 
Metabolism of lipoproteins & its disorders(Chylomicron & VLDL & LDL).pptx
Metabolism of  lipoproteins & its disorders(Chylomicron & VLDL & LDL).pptxMetabolism of  lipoproteins & its disorders(Chylomicron & VLDL & LDL).pptx
Metabolism of lipoproteins & its disorders(Chylomicron & VLDL & LDL).pptxDr. Santhosh Kumar. N
 
Plant Tissue culture., Plasticity, Totipotency, pptx
Plant Tissue culture., Plasticity, Totipotency, pptxPlant Tissue culture., Plasticity, Totipotency, pptx
Plant Tissue culture., Plasticity, Totipotency, pptxHimansu10
 
LEAD6001 - Introduction to Advanced Stud
LEAD6001 - Introduction to Advanced StudLEAD6001 - Introduction to Advanced Stud
LEAD6001 - Introduction to Advanced StudDr. Bruce A. Johnson
 
HỌC TỐT TIẾNG ANH 11 THEO CHƯƠNG TRÌNH GLOBAL SUCCESS ĐÁP ÁN CHI TIẾT - HK2 (...
HỌC TỐT TIẾNG ANH 11 THEO CHƯƠNG TRÌNH GLOBAL SUCCESS ĐÁP ÁN CHI TIẾT - HK2 (...HỌC TỐT TIẾNG ANH 11 THEO CHƯƠNG TRÌNH GLOBAL SUCCESS ĐÁP ÁN CHI TIẾT - HK2 (...
HỌC TỐT TIẾNG ANH 11 THEO CHƯƠNG TRÌNH GLOBAL SUCCESS ĐÁP ÁN CHI TIẾT - HK2 (...Nguyen Thanh Tu Collection
 
The First National K12 TUG March 6 2024.pdf
The First National K12 TUG March 6 2024.pdfThe First National K12 TUG March 6 2024.pdf
The First National K12 TUG March 6 2024.pdfdogden2
 
POST ENCEPHALITIS case study Jitendra bhargav
POST ENCEPHALITIS case study  Jitendra bhargavPOST ENCEPHALITIS case study  Jitendra bhargav
POST ENCEPHALITIS case study Jitendra bhargavJitendra Bhargav
 
2024 March 11, Telehealth Billing- Current Telehealth CPT Codes & Telehealth ...
2024 March 11, Telehealth Billing- Current Telehealth CPT Codes & Telehealth ...2024 March 11, Telehealth Billing- Current Telehealth CPT Codes & Telehealth ...
2024 March 11, Telehealth Billing- Current Telehealth CPT Codes & Telehealth ...Marlene Maheu
 
Auchitya Theory by Kshemendra Indian Poetics
Auchitya Theory by Kshemendra Indian PoeticsAuchitya Theory by Kshemendra Indian Poetics
Auchitya Theory by Kshemendra Indian PoeticsDhatriParmar
 
PHARMACOGNOSY CHAPTER NO 5 CARMINATIVES AND G.pdf
PHARMACOGNOSY CHAPTER NO 5 CARMINATIVES AND G.pdfPHARMACOGNOSY CHAPTER NO 5 CARMINATIVES AND G.pdf
PHARMACOGNOSY CHAPTER NO 5 CARMINATIVES AND G.pdfSumit Tiwari
 
BBA 205 BE UNIT 2 economic systems prof dr kanchan.pptx
BBA 205 BE UNIT 2 economic systems prof dr kanchan.pptxBBA 205 BE UNIT 2 economic systems prof dr kanchan.pptx
BBA 205 BE UNIT 2 economic systems prof dr kanchan.pptxProf. Kanchan Kumari
 
3.12.24 The Social Construction of Gender.pptx
3.12.24 The Social Construction of Gender.pptx3.12.24 The Social Construction of Gender.pptx
3.12.24 The Social Construction of Gender.pptxmary850239
 
UNIT I Design Thinking and Explore.pptx
UNIT I  Design Thinking and Explore.pptxUNIT I  Design Thinking and Explore.pptx
UNIT I Design Thinking and Explore.pptxGOWSIKRAJA PALANISAMY
 
Material Remains as Source of Ancient Indian History & Culture.ppt
Material Remains as Source of Ancient Indian History & Culture.pptMaterial Remains as Source of Ancient Indian History & Culture.ppt
Material Remains as Source of Ancient Indian History & Culture.pptBanaras Hindu University
 
The basics of sentences session 8pptx.pptx
The basics of sentences session 8pptx.pptxThe basics of sentences session 8pptx.pptx
The basics of sentences session 8pptx.pptxheathfieldcps1
 
25 CHUYÊN ĐỀ ÔN THI TỐT NGHIỆP THPT 2023 – BÀI TẬP PHÁT TRIỂN TỪ ĐỀ MINH HỌA...
25 CHUYÊN ĐỀ ÔN THI TỐT NGHIỆP THPT 2023 – BÀI TẬP PHÁT TRIỂN TỪ ĐỀ MINH HỌA...25 CHUYÊN ĐỀ ÔN THI TỐT NGHIỆP THPT 2023 – BÀI TẬP PHÁT TRIỂN TỪ ĐỀ MINH HỌA...
25 CHUYÊN ĐỀ ÔN THI TỐT NGHIỆP THPT 2023 – BÀI TẬP PHÁT TRIỂN TỪ ĐỀ MINH HỌA...Nguyen Thanh Tu Collection
 
LEAD6001 - Introduction to Advanced Stud
LEAD6001 - Introduction to Advanced StudLEAD6001 - Introduction to Advanced Stud
LEAD6001 - Introduction to Advanced StudDr. Bruce A. Johnson
 

Último (20)

t-test Parametric test Biostatics and Research Methodology
t-test Parametric test Biostatics and Research Methodologyt-test Parametric test Biostatics and Research Methodology
t-test Parametric test Biostatics and Research Methodology
 
DLL Catch Up Friday March 22.docx CATCH UP FRIDAYS
DLL Catch Up Friday March 22.docx CATCH UP FRIDAYSDLL Catch Up Friday March 22.docx CATCH UP FRIDAYS
DLL Catch Up Friday March 22.docx CATCH UP FRIDAYS
 
Arti Languages Pre Seed Send Ahead Pitchdeck 2024.pdf
Arti Languages Pre Seed Send Ahead Pitchdeck 2024.pdfArti Languages Pre Seed Send Ahead Pitchdeck 2024.pdf
Arti Languages Pre Seed Send Ahead Pitchdeck 2024.pdf
 
BÀI TẬP BỔ TRỢ TIẾNG ANH 11 THEO ĐƠN VỊ BÀI HỌC - CẢ NĂM - CÓ FILE NGHE (GLOB...
BÀI TẬP BỔ TRỢ TIẾNG ANH 11 THEO ĐƠN VỊ BÀI HỌC - CẢ NĂM - CÓ FILE NGHE (GLOB...BÀI TẬP BỔ TRỢ TIẾNG ANH 11 THEO ĐƠN VỊ BÀI HỌC - CẢ NĂM - CÓ FILE NGHE (GLOB...
BÀI TẬP BỔ TRỢ TIẾNG ANH 11 THEO ĐƠN VỊ BÀI HỌC - CẢ NĂM - CÓ FILE NGHE (GLOB...
 
Metabolism of lipoproteins & its disorders(Chylomicron & VLDL & LDL).pptx
Metabolism of  lipoproteins & its disorders(Chylomicron & VLDL & LDL).pptxMetabolism of  lipoproteins & its disorders(Chylomicron & VLDL & LDL).pptx
Metabolism of lipoproteins & its disorders(Chylomicron & VLDL & LDL).pptx
 
Plant Tissue culture., Plasticity, Totipotency, pptx
Plant Tissue culture., Plasticity, Totipotency, pptxPlant Tissue culture., Plasticity, Totipotency, pptx
Plant Tissue culture., Plasticity, Totipotency, pptx
 
LEAD6001 - Introduction to Advanced Stud
LEAD6001 - Introduction to Advanced StudLEAD6001 - Introduction to Advanced Stud
LEAD6001 - Introduction to Advanced Stud
 
HỌC TỐT TIẾNG ANH 11 THEO CHƯƠNG TRÌNH GLOBAL SUCCESS ĐÁP ÁN CHI TIẾT - HK2 (...
HỌC TỐT TIẾNG ANH 11 THEO CHƯƠNG TRÌNH GLOBAL SUCCESS ĐÁP ÁN CHI TIẾT - HK2 (...HỌC TỐT TIẾNG ANH 11 THEO CHƯƠNG TRÌNH GLOBAL SUCCESS ĐÁP ÁN CHI TIẾT - HK2 (...
HỌC TỐT TIẾNG ANH 11 THEO CHƯƠNG TRÌNH GLOBAL SUCCESS ĐÁP ÁN CHI TIẾT - HK2 (...
 
The First National K12 TUG March 6 2024.pdf
The First National K12 TUG March 6 2024.pdfThe First National K12 TUG March 6 2024.pdf
The First National K12 TUG March 6 2024.pdf
 
POST ENCEPHALITIS case study Jitendra bhargav
POST ENCEPHALITIS case study  Jitendra bhargavPOST ENCEPHALITIS case study  Jitendra bhargav
POST ENCEPHALITIS case study Jitendra bhargav
 
2024 March 11, Telehealth Billing- Current Telehealth CPT Codes & Telehealth ...
2024 March 11, Telehealth Billing- Current Telehealth CPT Codes & Telehealth ...2024 March 11, Telehealth Billing- Current Telehealth CPT Codes & Telehealth ...
2024 March 11, Telehealth Billing- Current Telehealth CPT Codes & Telehealth ...
 
Auchitya Theory by Kshemendra Indian Poetics
Auchitya Theory by Kshemendra Indian PoeticsAuchitya Theory by Kshemendra Indian Poetics
Auchitya Theory by Kshemendra Indian Poetics
 
PHARMACOGNOSY CHAPTER NO 5 CARMINATIVES AND G.pdf
PHARMACOGNOSY CHAPTER NO 5 CARMINATIVES AND G.pdfPHARMACOGNOSY CHAPTER NO 5 CARMINATIVES AND G.pdf
PHARMACOGNOSY CHAPTER NO 5 CARMINATIVES AND G.pdf
 
BBA 205 BE UNIT 2 economic systems prof dr kanchan.pptx
BBA 205 BE UNIT 2 economic systems prof dr kanchan.pptxBBA 205 BE UNIT 2 economic systems prof dr kanchan.pptx
BBA 205 BE UNIT 2 economic systems prof dr kanchan.pptx
 
3.12.24 The Social Construction of Gender.pptx
3.12.24 The Social Construction of Gender.pptx3.12.24 The Social Construction of Gender.pptx
3.12.24 The Social Construction of Gender.pptx
 
UNIT I Design Thinking and Explore.pptx
UNIT I  Design Thinking and Explore.pptxUNIT I  Design Thinking and Explore.pptx
UNIT I Design Thinking and Explore.pptx
 
Material Remains as Source of Ancient Indian History & Culture.ppt
Material Remains as Source of Ancient Indian History & Culture.pptMaterial Remains as Source of Ancient Indian History & Culture.ppt
Material Remains as Source of Ancient Indian History & Culture.ppt
 
The basics of sentences session 8pptx.pptx
The basics of sentences session 8pptx.pptxThe basics of sentences session 8pptx.pptx
The basics of sentences session 8pptx.pptx
 
25 CHUYÊN ĐỀ ÔN THI TỐT NGHIỆP THPT 2023 – BÀI TẬP PHÁT TRIỂN TỪ ĐỀ MINH HỌA...
25 CHUYÊN ĐỀ ÔN THI TỐT NGHIỆP THPT 2023 – BÀI TẬP PHÁT TRIỂN TỪ ĐỀ MINH HỌA...25 CHUYÊN ĐỀ ÔN THI TỐT NGHIỆP THPT 2023 – BÀI TẬP PHÁT TRIỂN TỪ ĐỀ MINH HỌA...
25 CHUYÊN ĐỀ ÔN THI TỐT NGHIỆP THPT 2023 – BÀI TẬP PHÁT TRIỂN TỪ ĐỀ MINH HỌA...
 
LEAD6001 - Introduction to Advanced Stud
LEAD6001 - Introduction to Advanced StudLEAD6001 - Introduction to Advanced Stud
LEAD6001 - Introduction to Advanced Stud
 

Blood respiratory function & jaundice

  • 1. Biochemistry of blood. Respiratory function of erythrocytes. Pathobiochemistry of blood.
  • 2. Red Blood Cells (erythrocytes) The most numerous type in the blood. •Features: •The erythrocytes doesn’t contain nucleus, chromatine •The erythrocytes doesn’t contain mytochondrias, thus АТP producing due to the anaerobic glycolisis till to the lactate (90%). •The glycolisis has features. During it the 2,3 BPG will be produced, not 1,3 BPG. This compound need for joining О2 to hemoglobin: low concentration of 2,3 BPG will increase the affinity hemoglobin (Нв) to О2. • The PPP is the main path for producing of reductive equivalents NADPН2 for taking part in glycolisis
  • 3. Red blood cells are responsible for the transport of oxygen and carbon dioxide.  In adult humans the hemoglobin (Hb) molecule consists of four polypeptides:  two alpha (α) chains of 141 amino acids and  two beta (β) chains of 146 amino acids  Each of these is attached the prosthetic group heme.  There is one atom of iron at the center of each heme.  One molecule of oxygen can bind to each heme.  The reaction is reversible.
  • 4. Transport of oxygen by hemoglobin Hemoglobin has all the requirements of an ideal respiratory pigment: -It can transport large quantities of oxygen. -It has great solubility. -It can take up and release oxygen at appropriate partial pressures. -It is a powerful buffer.
  • 5. Oxygenation and oxidation • When hemoglobin carries oxygen, the Hb is oxygenated. The iron atom in Hb is still in the ferrous state. • Oxidized hemoglobin is called Met-Hb; then iron is in ferric state and the oxygen carrying capacity is lost.
  • 6. Oxygen Dissociation Curve (ODC)• The ability of hemoglobin to load and unload oxygen at physiological pO2 (partial pressure of oxygen). • At the oxygen tension in the pulmonary alveoli, the Hb is 97% saturated with oxygen. Normal blood with 15mg/dl of Hb can carry 20ml of O2/dl of blood. • In the tissue capillaries, where the pO2 is only 40mm of Hg, the Hb is about 60% saturated. So physiologically, 40% of oxygen is released.
  • 8.  H+, CO2,  BPG Hb Equilibrium b b a a R (high affinity) O2 α β β α T (low affinity)
  • 9. Cooperativity  Oxygen binding to one subunit of Hb, increases the affinity of the other subunits for additional oxygens. In other words, the first one is the hardest, the rest are easy.  Anaemia  Anaemia is a shortage of RBCs and/or the amount of haemoglobin in them.
  • 11.  Carbon dioxide (CO2) combines with water forming carbonic acid, which dissociates into a hydrogen ion (H+) and a bicarbonate ions:  CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3−  95% of the CO2 generated in the tissues is carried in the red blood cells:  It probably enters (and leaves) the cell by diffusing through transmembrane channels in the plasma membrane. (One of the proteins that forms the channel is the D antigen that is the most important factor in the Rh system of blood groups.)  Once inside, about one-half of the CO2 is directly bound to hemoglobin (at a site different from the one that binds oxygen).
  • 12.  The rest is converted — following the equation above — by the enzyme carbonic anhydrase into  bicarbonate ions that diffuse back out into the plasma and  hydrogen ions (H+) that bind to the protein portion of the hemoglobin (thus having no effect on pH).  Only about 5% of the CO2 generated in the tissues dissolves directly in the plasma.  When the red cells reach the lungs, these reactions are reversed and CO2 is released to the air of the alveoli.
  • 14. The ability of hemoglobin to release oxygen, is affected by pH, CO2 and by the differences in the oxygen-rich environment of the lungs and the oxygen-poor environment of the tissues. The pH in the tissues is considerably lower (more acidic) than in the lungs. Protons are generated from the reaction between carbon dioxide and water to form bicarbonate:  CO2 + H20 -----------------> HCO3- + H+ This increased acidity serves a two fold purpose. - First, protons are lower the affinity of hemoglobin for oxygen, allowing easier release into the tissues. As all four oxygens are released, hemoglobin binds to two protons. This helps to maintain equilibrium towards the right side of the equation. This is known as the Bohr effect, and is vital in the removal of carbon dioxide as waste because CO2 is insoluble in the bloodstream. The bicarbonate ion is much more soluble, and can thereby be transported back to the lungs after being bound to hemoglobin. - If hemoglobin couldn’t absorb the excess protons, the equilibrium would shift to the left, and carbon dioxide couldn’t be removed
  • 15. Bohr Effect (pH) 100 mm O2 20 mm O2
  • 16.  In the lungs, this effect works in the reverse direction. In the presence of the high oxygen concentration in the lungs, lead to the proton affinity decreasing. As protons are shed, the reaction is driven to the left, and CO2 forms as an insoluble gas to be expelled from the lungs. The proton poor hemoglobin now has a greater affinity for oxygen, and the cycle continues.
  • 18. CO2 effect 20 mm CO2 80 mm CO2
  • 19. Effect of BPG BPGEffect pO2 (mm Hg) 0 20 40 60 80 100 120 140 160 0 20 40 60 80 100 pO2 vs p50=8 pO2 vs p50=26 Hb alone Hb + BPG BPG is the main player in Hb cooperativity. High altitude increases BPG, pushing curve further to right
  • 20. Myoglobin and Hemoglobin  Mb is monomer, Hb is a tetramer (ex. a2b2).  Hb subunits are structurally similar to Mb, with 8 a-helical regions, no b-strands and no interior water.  Both contain one heme prosthetic group per chain.  Both Mb and Hb contain proximal and distal histidines.  Affinity of Mb for oxygen is high, affinity of Hb for oxygen is lower and more variable.
  • 21.  The iron atom may either be in the Fe2+ or Fe3+ state, but ferrihemoglobin (methemoglobin) (Fe3+) cannot bind oxygen. In binding, oxygen temporarily oxidizes Fe to (Fe3+), so iron must exist in the +2 oxidation state in order to bind oxygen. The body reactivates hemoglobin found in the inactive (Fe3+) state by reducing the iron center.
  • 23. Sickle cell hemoglobin (HbS) β α β α G lu - G lu - H b A 1 β α β α G lu - H b S ( h e t e r o z y g o u s ) S i c k l e c e l l t r a i t β α β α H b S ( h o m o z y g o u s ) S i c k l e c e l l d i s e a s e
  • 24. Polymerization of HbS β α β α β α β α β α β α β α β α β α β α β α β α β α β α Association shown in previous figure is repeated over and over to produce large, rod-like aggregates that bind oxygen poorly and distort shape of erythrocytes.
  • 25.  Sickle cell trait is usually asymptomatic, but strenuous exercise at altitude could elicit sickling and destruction of erythrocytes. This lowers serum Hb and hematocrit, while raising Hb breakdown products such as bilirubin, which can accumulate to form gallstones.
  • 26. a-Thalassemias  Rare, since a-gene is duplicated (four genes per diploid chromosome set).  Usually more severe than b-thalassemia because  there is no substitute for b-gene in adults.  Almost all b- thalassemias are deletions  In α thalassemia intermedia (αo α/αο αo ) - appearance of HbH (β4)  In α thalassemia major (αo αο /αo αo ), Hb Bart’s (γ4) is predominant (usually lethal).  BPG is ineffective in HbH & Hb Bart’s.
  • 27. β Thalassemias  More common, since β gene is present in only one copy per chromosome.  Less severe than α thalassemia, since δ chain can effectively substitute in adults.  The γ chain can also persist into adulthood (HPFH).  In βδ thalassemia major (βδ0 /βδ0 ) excess α chains do not form soluble homotetramers.
  • 32. Plasma Bilirubin • Normal plasma bilirubin level ranges from 0.2-0.8 mg/dl. The unconjugated bilirubin is about 0.2-0.6 mg/dl, while conjugated bilirubin is only 0- 0.2. • If the level of plasma bilirubin exceeds 1 mg/dl, the condition is called hyperbilirubinemia. • Levels between 1 and 2 mg/dl are indicative of latent jaundice. • When the bilirubin level exceeds 2 mg/dl, it diffuses into tissues producing yellowish discoloration of skin and mucous membrane resulting in jaundice. • Van den Bergh test is a test for detection of bilirubin.
  • 33. Hyperbilribunemias • Depending on the nature of the bilirubin elevated, the condition may be grouped into conjugated or unconjugated hyperbilirubinemia. • Based on the cause it may also be classified into congenital and acquired.
  • 34. 1- Congenital Hyperbilirubinemias • They results from abnormal uptake, conjugation or excretion of bilirubin due to inherited defects. Crigler-Najjar syndrome:  Here the defect is in conjugation.  In type 1 (Congenital non-hemolytic jaundice), there is sever deficiency of UDP glucuronyl transferase.  The disease is often fatal and the children die before the age 2.  Jaundice usually appears within the first 24 hours of life.  Unconjugated bilirubin level increases to more than 20 mg/dl, and hence Kernicterus is resulted.
  • 35. 2- Acquired Hyperbilirubinemias Physiological Jaundice: It is also called as neonatal hyperbilirubinemia. In all newborn infants after the second day of life, mild jaundice appears. This transient hyperbilirubinemia is due to an accelerated rate of destruction of RBCs and also because of the immature hepatic system of conjugation of bilirubin. In such cases, bilirubin does not increase above 5mg/dl. It disappears by the second week of life.
  • 36. 3- Hemolytic Jaundice A) Hemolytic Disease of the Newborn: This condition results from incompatibility between maternal and fetal blood groups. Rh+ve fetus may produce antibodies in Rh-ve mother, leading to Rh incompatibility. When blood level of bilirubin is more than 20mg/dl, the capacity of albumin to bind bilirubin is exceeded. In young children before the age of 1 year, the blood- brain barrier is not fully matured, and therefore free bilirubin enters the brain (Kernicterus). It is deposited in brain, leading to mental retardation.
  • 37. B) Hemolytic Diseases of Adults:  This condition is seen in increased rate of hemolysis.  It usually occurs in adults.  The characteristic features are increase in unconjugated bilirubin in blood, absence of bilirubinuria and excessive excretion of UBG in urine and SBG in feces.  Common causes are: 1.Congenital spherocytosis. • Autoimmune hemolytic anemias. • Toxins like carbon tetrachloride.
  • 38. 4- Hepatocellular Jaundice • The most common cause is viral hepatitis, caused by hepatitis viruses A, B, C, D, or G. • Conjugation in liver is decreased and hence free bilirubin is increased in circulation.
  • 39. 5- Obstructive Jaundice• Conjugated bilirubin is increased in blood, and it is excreted in urine. • UBG will be decreased in urine or even absent. • Since no pigment are entering into the gut, the feces become clay colored. • The common causes are: 1. Intrahepatic cholestasis. This may be due to cirrhosis or hepatoma. 2. Extrahepatic obstruction. This may be due to stones in the gallbladder or biliary tract; carcinoma of head of pancreas.
  • 43. Kidney in AB equilibrium