blood function, biochemistry, physiology
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Oct 19, 2024
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About This Presentation
Water soluble vitamins: Vitamins that dissolve in water. Because our body is a watery environment, these vitamins can move through our body pretty easily, and they can also be flushed out by the kidneys. Water-soluble vitamins include the B-complex vitamins and vitamin C.�There are eight B vitamin...
Slide Content
Blood Biochemistry BCH 577
Prof. Omar S. Al-Attas
Professor of Biochemistry
Biochemistry Department
King Saud University
Prof. Omar S. Al-Attas
Professor of Biochemistry
Biochemistry Department
King Saud University
Chapter 1
Introduction To Hematology
•Blood is the only tissue that flows throughout your body.
•This red liquid carries oxygen and nutrients to all parts of the body
and waste products back to your lungs, kidneys and liver for
disposal.
•It is also an essential part of your immune system, crucial to fluid
and temperature balance, a hydraulic fluid for certain functions and
a highway for hormonal messages.
•It represent about 8% of total body weight
•Average volume of 5 liters in women
•Average volume 5.6 liters in men
•99% of blood cells are erythrocytes
•Plasma accounts for the remaining of the blood volume.
•Consist of three types of cellular elements (Erythrocytes, Leukocytes
and Platelets)
•The cellular elements are suspended in plasma
•Blood is the only tissue that flows throughout your body.
•This red liquid carries oxygen and nutrients to all parts of the body
and waste products back to your lungs, kidneys and liver for
disposal.
•It is also an essential part of your immune system, crucial to fluid
and temperature balance, a hydraulic fluid for certain functions and
a highway for hormonal messages.
•It represent about 8% of total body weight
•Average volume of 5 liters in women
•Average volume 5.6 liters in men
•99% of blood cells are erythrocytes
•Plasma accounts for the remaining of the blood volume.
•Consist of three types of cellular elements (Erythrocytes, Leukocytes
and Platelets)
•The cellular elements are suspended in plasma
Hematopoiesis
•The cells normally found in the circulatory blood are of three main types:
•The erythrocytes ( RBC) are largely concerned with oxygen transport.
•The leukocytes (White blood cell) play various roles in defense against infections and
tissue injury.
•The thrombocytes (platelets) are immediately involved in maintaining the integrity of
blood vessels and in the prevention of blood clots
Hematopoiesis (poiesis= formation)
•Is the term used to describe the formation and development of blood cells.
•Cellular proliferation, differentiation and maturation take place in the hematopoietic
tissue, which consists primarily of the bone marrow. Only mature cells are released to the
peripheral blood.
•Hematopoietic begins in the nineteenth day after fertilization in the yolk sac of human
embryo. Then the fetal liver becomes the chief site of blood cell production( at about this
time the yolk sac discontinues its role in the hematopoiesis. Also at this time hematopoiesis
also begins to lesser degree in the spleen, kidney, thymus and lymph nodes.
•At about 4-5 months of gestation hematopoiesis commences in the bone marrow where it is
fully active by the seventh or eight month and at birth partially the whole bony skeleton
contain active marrows.
•During childhood and adolescence there is a marked recession of marrow activity in the
long bones so that in the adult activity is limited to the trunkcal skeleton and skull.
•The cells normally found in the circulatory blood are of three main types:
•The erythrocytes ( RBC) are largely concerned with oxygen transport.
•The leukocytes (White blood cell) play various roles in defense against infections and
tissue injury.
•The thrombocytes (platelets) are immediately involved in maintaining the integrity of
blood vessels and in the prevention of blood clots
Hematopoiesis (poiesis= formation)
•Is the term used to describe the formation and development of blood cells.
•Cellular proliferation, differentiation and maturation take place in the hematopoietic
tissue, which consists primarily of the bone marrow. Only mature cells are released to the
peripheral blood.
•Hematopoietic begins in the nineteenth day after fertilization in the yolk sac of human
embryo. Then the fetal liver becomes the chief site of blood cell production( at about this
time the yolk sac discontinues its role in the hematopoiesis. Also at this time hematopoiesis
also begins to lesser degree in the spleen, kidney, thymus and lymph nodes.
•At about 4-5 months of gestation hematopoiesis commences in the bone marrow where it is
fully active by the seventh or eight month and at birth partially the whole bony skeleton
contain active marrows.
•During childhood and adolescence there is a marked recession of marrow activity in the
long bones so that in the adult activity is limited to the trunkcal skeleton and skull.
Site of Hematopoiesis
Cont…
•In the yolk sac, most of
hematopoiesis activity at this
site is confined to
erythropoiesis (erythrocytes
formation). Cell production at
this site time is called Primitive
erythropoiesis because this
erythroblast and Hb are not
typical of that seen in later
developing erythroblasts
•Hematopoiesis in the bone
marrow is called medullary
hematopoiesis.
•In the yolk sac, most of
hematopoiesis activity at this
site is confined to
erythropoiesis (erythrocytes
formation). Cell production at
this site time is called Primitive
erythropoiesis because this
erythroblast and Hb are not
typical of that seen in later
developing erythroblasts
•Hematopoiesis in the bone
marrow is called medullary
hematopoiesis.
Hematopoietic Tissues
1.Spleen, is located in the upper left
quadrant of the diaphragm (muscle
near the stomach)
It is enclosed by capsule of connective
tissue which contains the largest
collection of lymphocytes and
mononuclear phagocytes in the body.
Splenic function:
•Immune defense
•Culling(The removal of aging or
abnormal red blood cells)
•Pitting (The ability of the spleen to
clear inclusions while maintaining
the integrity of the red cell)
1.Spleen, is located in the upper left
quadrant of the diaphragm (muscle
near the stomach)
It is enclosed by capsule of connective
tissue which contains the largest
collection of lymphocytes and
mononuclear phagocytes in the body.
Splenic function:
•Immune defense
•Culling(The removal of aging or
abnormal red blood cells)
•Pitting (The ability of the spleen to
clear inclusions while maintaining
the integrity of the red cell)
Culling
•The discriminatory filtering and destruction of senescent or damaged red
cells by the spleen
•ATP is important in cation pump of erythrocytes and because of entering the
spleen through the slow transit become concentrated in the hypoglycemic
due to low concentration of glucose and slow circulation in the splenic cords,
the supply of glucose in the damaged or senescent erythrocytes is rapidly
diminished.
•This decrease the availability of ATP and contributes to the demise of these
red cells. Slow passage through a macrophage-rich route before allows the
phagocytic cells to remove these old or damaged erythrocyte before or during
their squeeze through 3µm pores to cords and sinuses.
•Normal RBC withstand this adverse environment and eventually reenter the
circulation.
•The discriminatory filtering and destruction of senescent or damaged red
cells by the spleen
•ATP is important in cation pump of erythrocytes and because of entering the
spleen through the slow transit become concentrated in the hypoglycemic
due to low concentration of glucose and slow circulation in the splenic cords,
the supply of glucose in the damaged or senescent erythrocytes is rapidly
diminished.
•This decrease the availability of ATP and contributes to the demise of these
red cells. Slow passage through a macrophage-rich route before allows the
phagocytic cells to remove these old or damaged erythrocyte before or during
their squeeze through 3µm pores to cords and sinuses.
•Normal RBC withstand this adverse environment and eventually reenter the
circulation.
Cont…
Pitting
•The spleens ability to “pluck out” particles from intact
erythrocytes.
•The pinched off cell membrane can reseal itself, but the
cell cannot synthesize lipids and proteins for new
membrane because of its lack of cellular organelles.
Therefore extensive pitting causes reduced surface- area to
volume ratio resulting in the formation of spherocytes.
Pitting
•The spleens ability to “pluck out” particles from intact
erythrocytes.
•The pinched off cell membrane can reseal itself, but the
cell cannot synthesize lipids and proteins for new
membrane because of its lack of cellular organelles.
Therefore extensive pitting causes reduced surface- area to
volume ratio resulting in the formation of spherocytes.
For Example:
•Howell Jolly Bodies: Small, round or oval structure pinkish or bluish in
color, observed in erythrocytes in various anemias and leukemias and after
splenectomy, they also represent unphysiological red cell nuclear remnant.
•Pappenheimer Bodies: Basophilic containing iron granules observed in
various types of erythrocytes
•Heinz bodies: Resulting from oxidative injury to unprecipitation of Hb
(abnormal Hb) and also erythrocytes with enzyme deficiency. Blood cells
coated with Ab are also susceptible to pitting by macrophages. The
macrophage removes the antigen-antibody complex and the attached
membranes.
The presence of spherocytes on a blood film is evidence that the red blood cells
has undergone membrane assault in the spleen.
•Howell Jolly Bodies: Small, round or oval structure pinkish or bluish in
color, observed in erythrocytes in various anemias and leukemias and after
splenectomy, they also represent unphysiological red cell nuclear remnant.
•Pappenheimer Bodies: Basophilic containing iron granules observed in
various types of erythrocytes
•Heinz bodies: Resulting from oxidative injury to unprecipitation of Hb
(abnormal Hb) and also erythrocytes with enzyme deficiency. Blood cells
coated with Ab are also susceptible to pitting by macrophages. The
macrophage removes the antigen-antibody complex and the attached
membranes.
The presence of spherocytes on a blood film is evidence that the red blood cells
has undergone membrane assault in the spleen.
Inclusion Bodies
Pappenheimer bodies
Pappenheimer bodies
Cont…
Defense
•Spleen is rich supply of lymphocytes and phagocytic cells as well as its unique
circulation
•Reservoir for platelets
•Massive splenomegaly may result in pooling of 80-90% of the platelets
producing peripheral blood thrombocytopenia.
•Condition associated with an enlargement of the spleen are also frequently
accompanied by leukopenia and anemia, the result of splenic pooling and
sequestration
•Removal of the spleen results in transient thrombocytosis, with the platelet
count returning to normal in about 10 days.
•Splenectomy does produce characteristic erythrocyte abnormalities that are
easily noted on blood smears by experienced technologist.
•After splenectomy, the red cells contain granular inclusion such as Howell-jolly
bodies, pappenheimer bodies. Target cells, cells with excess membrane to
volume ratio, have several mechanism of formation
•The splenectomized patients, these cells are probably formed as a result of
excess lipid on the membrane since the missing spleen would normally have
groomed the excess lipid from reticulocytes in their maturation process.
Defense
•Spleen is rich supply of lymphocytes and phagocytic cells as well as its unique
circulation
•Reservoir for platelets
•Massive splenomegaly may result in pooling of 80-90% of the platelets
producing peripheral blood thrombocytopenia.
•Condition associated with an enlargement of the spleen are also frequently
accompanied by leukopenia and anemia, the result of splenic pooling and
sequestration
•Removal of the spleen results in transient thrombocytosis, with the platelet
count returning to normal in about 10 days.
•Splenectomy does produce characteristic erythrocyte abnormalities that are
easily noted on blood smears by experienced technologist.
•After splenectomy, the red cells contain granular inclusion such as Howell-jolly
bodies, pappenheimer bodies. Target cells, cells with excess membrane to
volume ratio, have several mechanism of formation
•The splenectomized patients, these cells are probably formed as a result of
excess lipid on the membrane since the missing spleen would normally have
groomed the excess lipid from reticulocytes in their maturation process.
Hypersplenism
•Under certain conditions the spleen may become enlarged;
consequently exaggeration of its normal filtering and phagocytizing.
So anemia leukopenia, thrombocytopenia, then plasma volume
increases consequently cytopenias occurs.
A diagnosis of hypersplenism is made when four conditions are
met:
1.Anemia, leukopenia or thrombocytopenia in the blood.
2.2. Cellular or hyperplastic bone marrow ( increase in normal cells of
the tissue)corresponding to the peripheral blood cytopenias.
3.The occurrence of the splenomegaly
4.4. The correction of cytopenia as following splenectomy.
•Under certain conditions the spleen may become enlarged;
consequently exaggeration of its normal filtering and phagocytizing.
So anemia leukopenia, thrombocytopenia, then plasma volume
increases consequently cytopenias occurs.
A diagnosis of hypersplenism is made when four conditions are
met:
1.Anemia, leukopenia or thrombocytopenia in the blood.
2.2. Cellular or hyperplastic bone marrow ( increase in normal cells of
the tissue)corresponding to the peripheral blood cytopenias.
3.The occurrence of the splenomegaly
4.4. The correction of cytopenia as following splenectomy.
Hypersplenism
Primary
Occurs when no underlying
cause identified. The spleen
behaves normal but causes
disease.
The most common cause is
congestive splenomegaly
associated with liver cirrhosis
and portal hypertension.
Thrombosis of the splenic or
portal veins may contribute
Secondary
Caused by a disorder.
The causes: Inflammatory
and infectious diseases
increase the defense
function of the spleen.
Gaucher’s disease-
macrophages
accumulates large
quantities of
undigestable substance
causes splenomegaly
Primary
Occurs when no underlying
cause identified. The spleen
behaves normal but causes
disease.
The most common cause is
congestive splenomegaly
associated with liver cirrhosis
and portal hypertension.
Thrombosis of the splenic or
portal veins may contribute
Secondary
Caused by a disorder.
The causes: Inflammatory
and infectious diseases
increase the defense
function of the spleen.
Gaucher’s disease-
macrophages
accumulates large
quantities of
undigestable substance
causes splenomegaly
Lymphnodes
The lymphatic system is composed of lymph
node (bean-shaped)
2. Lymph Vessels:
•Node are composed of lymphocytes,
macrophages and reticular meshwork.
•The morphology: lymph nodes contain the
following: an inner area called medulla, outer
area called cortex.
•The medulla: surround the efferent lymphatics
and contains the B lymphocytes
•The cortex contains the T-lymphocytes
•The lymph nodes act as filter removing foreign
particles from the lymph by phagocytic cells.
Antigens pass through the nodes, they contact
and stimulate immune complex lymphocytes to
proliferate and differentiate into effector cells
The lymphatic system is composed of lymph
node (bean-shaped)
2. Lymph Vessels:
•Node are composed of lymphocytes,
macrophages and reticular meshwork.
•The morphology: lymph nodes contain the
following: an inner area called medulla, outer
area called cortex.
•The medulla: surround the efferent lymphatics
and contains the B lymphocytes
•The cortex contains the T-lymphocytes
•The lymph nodes act as filter removing foreign
particles from the lymph by phagocytic cells.
Antigens pass through the nodes, they contact
and stimulate immune complex lymphocytes to
proliferate and differentiate into effector cells
Thymus
3. Thymus
•The thymus is a well developed
organ at birth and continues to
increase in size until puberty, and
eventually would begin to atrophy
( hardening).
•It is bilobular organ packed with
small lymphocytes and a few
macrophages.
•Thymus is to serve for maturation of
T-lymphocytes. The thymic
hormone, thymosin, is important in
the maturation of virgin
lymphocytes into
immunocompetent T-cells.
3. Thymus
•The thymus is a well developed
organ at birth and continues to
increase in size until puberty, and
eventually would begin to atrophy
( hardening).
•It is bilobular organ packed with
small lymphocytes and a few
macrophages.
•Thymus is to serve for maturation of
T-lymphocytes. The thymic
hormone, thymosin, is important in
the maturation of virgin
lymphocytes into
immunocompetent T-cells.
Bone Marrow
4. Bone Marrow
•In adult the marrow normally
consist of islands of cellular active
marrow separated and supported by
fat (Yellow fat).
•Red marrow contains both
erythroid and myeloid precursors
with ration of (M:E) of 1.5:1 to 4:1
•For the first four years of life nearly
all marrow cavities are composed of
red hematopoietic marrow. After 4
years of age, the red marrow in
shafts of long bones is gradually
replaced by yellow fat tissues.
4. Bone Marrow
•In adult the marrow normally
consist of islands of cellular active
marrow separated and supported by
fat (Yellow fat).
•Red marrow contains both
erythroid and myeloid precursors
with ration of (M:E) of 1.5:1 to 4:1
•For the first four years of life nearly
all marrow cavities are composed of
red hematopoietic marrow. After 4
years of age, the red marrow in
shafts of long bones is gradually
replaced by yellow fat tissues.
The Assessment of Marrow
Activities
•In general if a patient has a normal peripheral blood count
and a bone marrow aspirate contains what appears to be
adequate number of cells, present in normal proportions it is
reasonable to assume normal activity
•Cellular or even hypercellular marrow may be associated
markedly defective output of cells to the peripheral
circulation:
e.g. megaloblast anemia is featured by excessive cellular
destruction in the marrow itself.
•Other cases a defective peripheral cell count may be
associated with hypercellular marrows, there being excessive
destruction of cells in the circulation or sequestration in an
enlarged spleen.
Activities
•In general if a patient has a normal peripheral blood count
and a bone marrow aspirate contains what appears to be
adequate number of cells, present in normal proportions it is
reasonable to assume normal activity
•Cellular or even hypercellular marrow may be associated
markedly defective output of cells to the peripheral
circulation:
e.g. megaloblast anemia is featured by excessive cellular
destruction in the marrow itself.
•Other cases a defective peripheral cell count may be
associated with hypercellular marrows, there being excessive
destruction of cells in the circulation or sequestration in an
enlarged spleen.
Chapter 2
Derivation of Blood Cells
•Replacement of effete peripheral hematopoietic cells is
the function of more primitive elements in the bone
marrow called stem cells.
Stem cells are characterize by:
Ability to differentiate into distinct cells lines with
specialize functions.
Ability to regenerate themselves in order to maintain the
stem cell compartment.
•Replacement of effete peripheral hematopoietic cells is
the function of more primitive elements in the bone
marrow called stem cells.
Stem cells are characterize by:
Ability to differentiate into distinct cells lines with
specialize functions.
Ability to regenerate themselves in order to maintain the
stem cell compartment.
Cont…
•Myeloblasts and erythroblasts (pronormoblasts) because of the high
mitotic index, were believed to responsible for maintaining normal
numbers of mature blood cells.
•But these two types of cells have limited ability to proliferate into the
billions of blood cells replaced daily.
•So two different theories on stem cells have been proposed to verify
the existence of stem cell different from myeloblasts and
erythroblasts.
1.Monophyletic theory: Pluripotential stem cell under unknown
hormonal factors may give rise to each of the principle blood cell
lines.
• These pluripotential cells have the capability to self-renewal,
proliferation and differentiation into all hematopoietic cells lines.
2.Polyphylitic theory. Each blood cell type come from a separate stem
cell. So each monopotential stem cell differentiates into only one type
of blood cell.
•Myeloblasts and erythroblasts (pronormoblasts) because of the high
mitotic index, were believed to responsible for maintaining normal
numbers of mature blood cells.
•But these two types of cells have limited ability to proliferate into the
billions of blood cells replaced daily.
•So two different theories on stem cells have been proposed to verify
the existence of stem cell different from myeloblasts and
erythroblasts.
1.Monophyletic theory: Pluripotential stem cell under unknown
hormonal factors may give rise to each of the principle blood cell
lines.
• These pluripotential cells have the capability to self-renewal,
proliferation and differentiation into all hematopoietic cells lines.
2.Polyphylitic theory. Each blood cell type come from a separate stem
cell. So each monopotential stem cell differentiates into only one type
of blood cell.
Cont…
•(Erythrocytic, myelocytic or megakaryocytic) It has been
suggested that nodules appearing at 7
th
days were
formed from more mature unipotent committed stem
cells
•In the day 14 the nodules showed mixed cell populations.
The cell that formed colony termed-Colony-forming unit
spleen (CFU-S)
•Suggesting the nodules at this time were derived from
more primitive multipotential stem cell.
•Stem cells number one per 1000 nucleated cells in the
marrows
•(Erythrocytic, myelocytic or megakaryocytic) It has been
suggested that nodules appearing at 7
th
days were
formed from more mature unipotent committed stem
cells
•In the day 14 the nodules showed mixed cell populations.
The cell that formed colony termed-Colony-forming unit
spleen (CFU-S)
•Suggesting the nodules at this time were derived from
more primitive multipotential stem cell.
•Stem cells number one per 1000 nucleated cells in the
marrows
Erythropoiesis
0The earliest recognizable erythroid cells in the bone marrow is the
pronormoblast which is a long cell measuring 15-20 µm in diameter. With dark
blue cytoplasmin, a central rounded nucleus with nucleoli and slightly clumped
chromatin. The deep color of the more immature cells due to the presence of
large amount of RNS which is associated with active protein synthesis.
0They also contain Hb (which stain pink) in the cytoplasm; the cytoplasm stain
pale blue as it does its RNS and protein synthetic apparatus while the nuclear
chromatin becomes more condensed.
0Any remaining nuclear material is removed by a process of pitting during
passage through the splenic sinus walls.
0The successive cytoplasmic charge from blue to pink earning them name
basophilic, polychromatic and orthochromatic
0After extruding the nucleus from the normoblast the new stage of cells is called
reticulocytes which still contain some ribosomal RNA and still able to synthesis
Hb. This cell spends 1-2 days in the bone marrow and also circulates in the
peripheral blood for 1-2 days before maturing mainly in the spleen when RNS is
completely lost and completely pink-staining mature erythrocytes (red cell).
0The earliest recognizable erythroid cells in the bone marrow is the
pronormoblast which is a long cell measuring 15-20 µm in diameter. With dark
blue cytoplasmin, a central rounded nucleus with nucleoli and slightly clumped
chromatin. The deep color of the more immature cells due to the presence of
large amount of RNS which is associated with active protein synthesis.
0They also contain Hb (which stain pink) in the cytoplasm; the cytoplasm stain
pale blue as it does its RNS and protein synthetic apparatus while the nuclear
chromatin becomes more condensed.
0Any remaining nuclear material is removed by a process of pitting during
passage through the splenic sinus walls.
0The successive cytoplasmic charge from blue to pink earning them name
basophilic, polychromatic and orthochromatic
0After extruding the nucleus from the normoblast the new stage of cells is called
reticulocytes which still contain some ribosomal RNA and still able to synthesis
Hb. This cell spends 1-2 days in the bone marrow and also circulates in the
peripheral blood for 1-2 days before maturing mainly in the spleen when RNS is
completely lost and completely pink-staining mature erythrocytes (red cell).
Kinetics of Erythropoiesis
•In man, time required for erythropoiesis to proceed from the undifferentiated stem cell
to reticulocyte is about 7 days and the final maturation of these cells in the peripheral
blood and spleen takes about 24 hours
•This means that some 210 thousand million erythrocytes must be produced by the
marrow each day about 9 thousand million per hour. This requires the synthesis of 6.5g
Hb and involves the turnover of about 22mg of iron.
To maintain regular erythropoiesis
1.Erythropoietin- the principle site of erythropoietin production in the kidney.
Erythropoiesis is regulated by hormone erythropoietin which:
• Acts primarily on more mature committed erythroid cells of erythroid colony-forming
units.
•Increasing Hb synthesis in red cells precursors.
•Decreasing maturation time of red cell precursors.
•Releasing marrow reticulocytes into peripheral blood at an earlier stage than normal.
•In man, time required for erythropoiesis to proceed from the undifferentiated stem cell
to reticulocyte is about 7 days and the final maturation of these cells in the peripheral
blood and spleen takes about 24 hours
•This means that some 210 thousand million erythrocytes must be produced by the
marrow each day about 9 thousand million per hour. This requires the synthesis of 6.5g
Hb and involves the turnover of about 22mg of iron.
To maintain regular erythropoiesis
1.Erythropoietin- the principle site of erythropoietin production in the kidney.
Erythropoiesis is regulated by hormone erythropoietin which:
• Acts primarily on more mature committed erythroid cells of erythroid colony-forming
units.
•Increasing Hb synthesis in red cells precursors.
•Decreasing maturation time of red cell precursors.
•Releasing marrow reticulocytes into peripheral blood at an earlier stage than normal.
Cont…
2.For normal erythropoiesis to be established there must be adequate
supply of stem cells in a satisfactory environment containing all the
essential materials for their normal growth and differentiation.
The materials include beside those require by all cells certain specific
factors:
•Vit B12, folate, Vit C, Vit E, Vit B6, pyroxidine, thiamine, riboflavin.
•Metal: Iron, manganese, cobalt
•Amino acids
•Hormone: erythropoeitin, thyroxine and androgens
2.For normal erythropoiesis to be established there must be adequate
supply of stem cells in a satisfactory environment containing all the
essential materials for their normal growth and differentiation.
The materials include beside those require by all cells certain specific
factors:
•Vit B12, folate, Vit C, Vit E, Vit B6, pyroxidine, thiamine, riboflavin.
•Metal: Iron, manganese, cobalt
•Amino acids
•Hormone: erythropoeitin, thyroxine and androgens
Erythrocytes
The mature erythrocytes of the
peripheral blood of a man are:
Non-nucleated and contain organelles
Contain enzyme of both anearobic glycolytic
pathway of Embden-Myerhoff and aerobic
pentose P pathway
•It stains pink to orange because of the
large amount intracellular acidophilic
protein called Hb.
•The 7 μm RBC must be flexible corpuscle
to squeeze through the tiny 3 μm
fenestrations of the capillaries of the
spleen.
The mature erythrocytes of the
peripheral blood of a man are:
Non-nucleated and contain organelles
Contain enzyme of both anearobic glycolytic
pathway of Embden-Myerhoff and aerobic
pentose P pathway
•It stains pink to orange because of the
large amount intracellular acidophilic
protein called Hb.
•The 7 μm RBC must be flexible corpuscle
to squeeze through the tiny 3 μm
fenestrations of the capillaries of the
spleen.
Erythrocytes Membrane
•The cells flexibility is a property of both the erythrocyte
membrane and the fluidity of the cell’s content which is main
hemoglobin.
It is a biphospholipid protein composed of the following:
49 % protein (composed of contractile protein, enzyme,
surface antigens)
43% lipid (95% of lipid is equal amounts of unspecified
cholesterol and phospholipids. The remaining are glycolipids.
The polar lipids on the external and internal surfaces and non
polar at the center of the membrane.
8% CHO ( occurs on the external surface)
•The cells flexibility is a property of both the erythrocyte
membrane and the fluidity of the cell’s content which is main
hemoglobin.
It is a biphospholipid protein composed of the following:
49 % protein (composed of contractile protein, enzyme,
surface antigens)
43% lipid (95% of lipid is equal amounts of unspecified
cholesterol and phospholipids. The remaining are glycolipids.
The polar lipids on the external and internal surfaces and non
polar at the center of the membrane.
8% CHO ( occurs on the external surface)
Cont…
Cholesterol responsible for the passive cation permeability if the membrane. It
appears that membrane cholesterol exist in free equilibrium with plasma cholesterol.
Increase cholesterol in plasma (such as occur in lecithin-cholesterol acyltransferase
LCAT deficiency) results in accumulation of cholesterol on membrane.
These cholesterol laden erythrocytes appears distorted with formation of target cells
and spicules (tiny spike-like structure)
Increase in cholesterol: Phospholipids increases the microviscosity and the degree of
order of the membrane.
The phospholipids are:
Phosphatidylethanolamine (Cephalin)
Phosphatidylcholin (Lecithin)
Sphengomyelin
Phosphatidylserine
Cholesterol responsible for the passive cation permeability if the membrane. It
appears that membrane cholesterol exist in free equilibrium with plasma cholesterol.
Increase cholesterol in plasma (such as occur in lecithin-cholesterol acyltransferase
LCAT deficiency) results in accumulation of cholesterol on membrane.
These cholesterol laden erythrocytes appears distorted with formation of target cells
and spicules (tiny spike-like structure)
Increase in cholesterol: Phospholipids increases the microviscosity and the degree of
order of the membrane.
The phospholipids are:
Phosphatidylethanolamine (Cephalin)
Phosphatidylcholin (Lecithin)
Sphengomyelin
Phosphatidylserine
Cont…
•Glycolipids is in the form of glycosphingolipids (cerebrosides and gangliosides) are responsible for some
antigenic properties of the membrane in particular those coresponding to the A,B, H and lewis blood
groups.
•Glycoprotien have similar antigenic properties.
Proteins in the membrane
Two types (both synthesized during cell development)
Integral protein consist of two types: Glycophorin A and band 3.
Glycophorin A serves as receptors for certain viruses and lectins.
Band 3 (the name is from its migration with erythrocyte proteins on SDS polyacrylamide gel
electrophoresis. It is responsible for an ion transport across the membrane.
Peripheral proteins lack CHO moieties and are to the cytoplasmic side of the lipid bilipid layer
These proteins include:
•Enzyme glycealdehyde-3-p dehydrogenase.
•Skeletal proteins e.g. spectrin actin viscoelastic properties and contribute to cell shape deformability
and membrane stability.
•Calcium is a membrane component. 80% of intracellular calcium is found in membrane.
It is maintained at an extremely low intracellular concentration by the activity of an ATP pump.
The accumulation of calcium cation induces irreversible cross-linking and alteration of cytoskeletal
proteins.
•Glycolipids is in the form of glycosphingolipids (cerebrosides and gangliosides) are responsible for some
antigenic properties of the membrane in particular those coresponding to the A,B, H and lewis blood
groups.
•Glycoprotien have similar antigenic properties.
Proteins in the membrane
Two types (both synthesized during cell development)
Integral protein consist of two types: Glycophorin A and band 3.
Glycophorin A serves as receptors for certain viruses and lectins.
Band 3 (the name is from its migration with erythrocyte proteins on SDS polyacrylamide gel
electrophoresis. It is responsible for an ion transport across the membrane.
Peripheral proteins lack CHO moieties and are to the cytoplasmic side of the lipid bilipid layer
These proteins include:
•Enzyme glycealdehyde-3-p dehydrogenase.
•Skeletal proteins e.g. spectrin actin viscoelastic properties and contribute to cell shape deformability
and membrane stability.
•Calcium is a membrane component. 80% of intracellular calcium is found in membrane.
It is maintained at an extremely low intracellular concentration by the activity of an ATP pump.
The accumulation of calcium cation induces irreversible cross-linking and alteration of cytoskeletal
proteins.
Erythrocyte Metabolism
•Although the binding, transport and release of oxygen and carbon dioxide
is a passive process not requiring energy, a variety of energy-dependent
metabolic processes occur that are essential to cell viability.
•The metabolism of the red cell is limited because of the absence of a
nucleus, mitochondria and other subcellular organelles.
•The most important metabolic pathway in the mature erythrocytes require
glucose as substrate.
•Although the binding, transport and release of oxygen and carbon dioxide
is a passive process not requiring energy, a variety of energy-dependent
metabolic processes occur that are essential to cell viability.
•The metabolism of the red cell is limited because of the absence of a
nucleus, mitochondria and other subcellular organelles.
•The most important metabolic pathway in the mature erythrocytes require
glucose as substrate.
Metabolic Pathways
These pathways include:
a.Embden-Meyerhof pathway
b.Hexose-monophosphate (HMP) shunt
c.Methemoglobin reductase pathway
d.Rapoport-leubering pathway
These pathways contribute:
The first pathway for providing energy for maintaining high intracelllur
K
+
, low intracellular Na
+
and very low Ca
2+
(cation pump)
The second pathway provides reducing power to protect Hb in reducing
state.
The third pathway regulates oxygen affinity of Hb
Maintains Hb in reduced state
These pathways include:
a.Embden-Meyerhof pathway
b.Hexose-monophosphate (HMP) shunt
c.Methemoglobin reductase pathway
d.Rapoport-leubering pathway
These pathways contribute:
The first pathway for providing energy for maintaining high intracelllur
K
+
, low intracellular Na
+
and very low Ca
2+
(cation pump)
The second pathway provides reducing power to protect Hb in reducing
state.
The third pathway regulates oxygen affinity of Hb
Maintains Hb in reduced state
Embden-Meyerhof Pathway
•90-95% of the red cell’s glucose consumption is utilized by this pathway. Normal red
cells have glycogen deposits. They depend entirely on environmental glucose for
glycolysis.
•Glucose enters the cell by the facilitated diffusion an energy-free process.
ATP’s
•Are necessary to maintain red cell shape and flexibility.
•Membrane integrity through regulation of intracellular cation concentration:
•Na
+
& Ca
2+
are more concentrated in the plasma.
•K
+
is more concentrated within the cell.
Erythrocyte osmotic equilibrium is maintained by:
•The selective permeability of the membrane
•By the cation pumps located in the cell membrane
•90-95% of the red cell’s glucose consumption is utilized by this pathway. Normal red
cells have glycogen deposits. They depend entirely on environmental glucose for
glycolysis.
•Glucose enters the cell by the facilitated diffusion an energy-free process.
ATP’s
•Are necessary to maintain red cell shape and flexibility.
•Membrane integrity through regulation of intracellular cation concentration:
•Na
+
& Ca
2+
are more concentrated in the plasma.
•K
+
is more concentrated within the cell.
Erythrocyte osmotic equilibrium is maintained by:
•The selective permeability of the membrane
•By the cation pumps located in the cell membrane
Cont…
•The Na
+ &
K
+
pump ADP + Pi
In the expulsion of 3 Na
+
and the uptake of 2K
+
.
Ca
2+
is maintained in low concentration by the action of a similar but
separate cation pump that utilized ATP for fuel.
•Excess leakage of Ca
2+
into the cell or failure of the pump causes rigid
shrunken cells with protrusions (echinocytes)
•An increase in calcium is associated with excess K
+
leakage from cell.
•Magnesium is another major intracellular cation. It reacts with ATP to
form the substrate complex, Mg-ATP for Ca
2+
- MgCT- ATPase (calcium
cation pump).
•Upon the exhaustion of glucose, the fuel for the cation pumps is no
longer available. Cells cannot maintain normal intracellular cation
concentrations and this leads to cell death
hydrolysis
One ATP
•The Na
+ &
K
+
pump ADP + Pi
In the expulsion of 3 Na
+
and the uptake of 2K
+
.
Ca
2+
is maintained in low concentration by the action of a similar but
separate cation pump that utilized ATP for fuel.
•Excess leakage of Ca
2+
into the cell or failure of the pump causes rigid
shrunken cells with protrusions (echinocytes)
•An increase in calcium is associated with excess K
+
leakage from cell.
•Magnesium is another major intracellular cation. It reacts with ATP to
form the substrate complex, Mg-ATP for Ca
2+
- MgCT- ATPase (calcium
cation pump).
•Upon the exhaustion of glucose, the fuel for the cation pumps is no
longer available. Cells cannot maintain normal intracellular cation
concentrations and this leads to cell death
hydrolysis
One ATP
Hexose Monophosphate Shunt (HMP shunt)
•5% of cellular glucose enters the oxidative HMP shunt, an ancillary aerobic energy
system.
•In the pathway glucose-6- P is converted to 6-phosphogluconate and so to ribulose-5- P.
• NADPH is generated and is linked with GSH which maintains sulfhydryl (-SH) groups
intact in the cell including those in Hb and RBC membrane.
•Reduced glutathione (GSH) protects the cell from permanent oxidant injury (H
2
O
2
).
•Oxidants, within the cell will oxidize Hb-SH groups, unless they are reduced by
glutathione.
•This reduction oxidizes glutathione (GSSG), which in turn is reduced by adequate levels
of NADPH. The red cell normally maintains a large ratio of NADPH to NADP
+.
•Failure to maintain reducing power through levels of GSH or NADPH leads to oxidation
of Hb - SH groups, followed by denaturation and precipitation of Hb in the form of Heinz
bodies.
•Heinz bodies with a portion of the membrane are then plucked out by the macrophages
of the spleen.
•Reduced GSH is also responsible for maintaining reduced-SH groups at the membrane
level. Decrease of GSH lead to injury of membrane sulfhydryl groups resulting in leak of
cell membrane.
•5% of cellular glucose enters the oxidative HMP shunt, an ancillary aerobic energy
system.
•In the pathway glucose-6- P is converted to 6-phosphogluconate and so to ribulose-5- P.
• NADPH is generated and is linked with GSH which maintains sulfhydryl (-SH) groups
intact in the cell including those in Hb and RBC membrane.
•Reduced glutathione (GSH) protects the cell from permanent oxidant injury (H
2
O
2
).
•Oxidants, within the cell will oxidize Hb-SH groups, unless they are reduced by
glutathione.
•This reduction oxidizes glutathione (GSSG), which in turn is reduced by adequate levels
of NADPH. The red cell normally maintains a large ratio of NADPH to NADP
+.
•Failure to maintain reducing power through levels of GSH or NADPH leads to oxidation
of Hb - SH groups, followed by denaturation and precipitation of Hb in the form of Heinz
bodies.
•Heinz bodies with a portion of the membrane are then plucked out by the macrophages
of the spleen.
•Reduced GSH is also responsible for maintaining reduced-SH groups at the membrane
level. Decrease of GSH lead to injury of membrane sulfhydryl groups resulting in leak of
cell membrane.
Methemoglobin Reductase Pathway
•The methemoglobin reductase pathway, an offshoot of the
Embden-Meyerhof pathway, is essential to maintain heme iron
in the reduced state, Fe++
•Hemoglobin with iron in the ferric state Fe
++
is known as
methoglobin. This form of Hb cannot combine with O
2
•Methemoglobin reductase together with NADPH produced by
the Embden-Meyerhof pathway protect the heme iron from
oxidation.
•The absence of this system, the 2% of heme methemoglobin
formed daily will eventually raise to 20-40% surely limiting
the oxygen-carrying capacity of the blood.
•The methemoglobin reductase pathway, an offshoot of the
Embden-Meyerhof pathway, is essential to maintain heme iron
in the reduced state, Fe++
•Hemoglobin with iron in the ferric state Fe
++
is known as
methoglobin. This form of Hb cannot combine with O
2
•Methemoglobin reductase together with NADPH produced by
the Embden-Meyerhof pathway protect the heme iron from
oxidation.
•The absence of this system, the 2% of heme methemoglobin
formed daily will eventually raise to 20-40% surely limiting
the oxygen-carrying capacity of the blood.
Rapoport-Luebering Pathway
•The Rapoport-Luebering Pathway is a shunt of Embden-
Meyerhof pathway.
•DPG is present in the erythrocytes in a conclusion of 1,ol DPG/
1 mol Hb, and it binds exclusively to deoxyHb.
•As more DPG binds to deoxy Hb, glycolysis is stimulated to
produce more DPG and ATP.
•Increase in DPG concentration facilitate the release of O
2 to the
tissues by causing a decrease in Hb affinity for oxygen. Thus,
the red cell has built-in mechanism for regulation of O
2
delivery to the tissues
•The Rapoport-Luebering Pathway is a shunt of Embden-
Meyerhof pathway.
•DPG is present in the erythrocytes in a conclusion of 1,ol DPG/
1 mol Hb, and it binds exclusively to deoxyHb.
•As more DPG binds to deoxy Hb, glycolysis is stimulated to
produce more DPG and ATP.
•Increase in DPG concentration facilitate the release of O
2 to the
tissues by causing a decrease in Hb affinity for oxygen. Thus,
the red cell has built-in mechanism for regulation of O
2
delivery to the tissues
Hexose monophophate shunt
pathway
pathway
Chapter 3
Lifespan and Faith of RBC
0Normally, the average life span of
red blood cells is 120 days. This
cells live in blood circulation.
0In in typical adult produces 200
billion RBC per day.
0At the end of their lifespan, they
become senescent, and are
removed from circulation.
0In many chronic diseases, the
lifespan of the erythrocytes is
markedly reduced (e.g. patients
requiring haemodialysis).
0The destruction of RBC is about 2-
3 million per second on average.
Causes of reduction in the life
span of RBC.
1.Defects in RBC (curpuscular
defects)
e.g. Hereditary spherocytosis
Sickle cell anemia,
Thalassemias
2.Deficiency of red
cell enzyme such as: G6PD,
Pyruvate kinase def.,
Autoimmune disorder,
Hypersplenism
0Normally, the average life span of
red blood cells is 120 days. This
cells live in blood circulation.
0In in typical adult produces 200
billion RBC per day.
0At the end of their lifespan, they
become senescent, and are
removed from circulation.
0In many chronic diseases, the
lifespan of the erythrocytes is
markedly reduced (e.g. patients
requiring haemodialysis).
0The destruction of RBC is about 2-
3 million per second on average.
Causes of reduction in the life
span of RBC.
1.Defects in RBC (curpuscular
defects)
e.g. Hereditary spherocytosis
Sickle cell anemia,
Thalassemias
2.Deficiency of red
cell enzyme such as: G6PD,
Pyruvate kinase def.,
Autoimmune disorder,
Hypersplenism
Cont…
The fate of the RBC
0After 120 days , the RBC becomes more
fragile due to decrease NADPH activity.
0Younger RBC RBCs can easily pass
through the capillaries which have the
diameter smaller than the mature RBC’c
0With a fragile membrane, the mature
RBC are destroyed while trying to
squeeze through capillaries.
0The destruction most occurs in the
capillaries of the spleen. This is why
spleen is called the “grave yard of the
RBC”.
0The hemoglobin is released and taken up
the macropharges
Pathway of RBC destruction
The fate of the RBC
0After 120 days , the RBC becomes more
fragile due to decrease NADPH activity.
0Younger RBC RBCs can easily pass
through the capillaries which have the
diameter smaller than the mature RBC’c
0With a fragile membrane, the mature
RBC are destroyed while trying to
squeeze through capillaries.
0The destruction most occurs in the
capillaries of the spleen. This is why
spleen is called the “grave yard of the
RBC”.
0The hemoglobin is released and taken up
the macropharges
Pathway of RBC destruction
Cont…
Bilirubin
0Is the yellow breakdown product of normal heme catabolism.
0Bilirubin is excreted in bile and urine, and elevated levels may
indicate certain diseases.
0It is a toxic waste product in the body
0It is extracted and biotransformed mainly in the liver and excreted
in bile and liver.
0Elevation in serum and urine bilirubin is associated with juandice
0Is the yellow breakdown product of normal heme catabolism.
0Bilirubin is excreted in bile and urine, and elevated levels may
indicate certain diseases.
0It is a toxic waste product in the body
0It is extracted and biotransformed mainly in the liver and excreted
in bile and liver.
0Elevation in serum and urine bilirubin is associated with juandice
Bilirubin Excretion
Bilirubin diglucuronide
Intrahepatic
urobilinogen cycle
Stercobilinogen
Bacterial enzymes
Bilirubin
Bacterial enzyme2 glucuronate
Bacterial enzyme
Urobilinogen
8H
liver
Urobilin
kidneys
urine
Stercobilin feces
kidneys
intestines
Bilirubin diglucuronide
Intrahepatic
urobilinogen cycle
Stercobilinogen
Bacterial enzymes
Bilirubin
Bacterial enzyme2 glucuronate
Bacterial enzyme
Urobilinogen
8H
liver
Urobilin
kidneys
urine
Stercobilin feces
kidneys
intestines
Cont…
•The globin is recycled into amino acids, which
in turn are recycled or catabolized as required.
•Heme is oxidized with the heme porphyrin
ring being oped by the endoplasmic reticulum
enzyme, heme oxigenase.
•The oxidation occurs on the specific carbon
producing equimolar amount of the biliverdin,
iron, and carbon monoxide (CO). This is the
only reaction in the body that is known to
produce CO.
•Most of the CO is excreted through the lungs,
with the result that the CO content of expired
air is a direct measure of the activity of heme
oxygenase in an individual.
•The globin is recycled into amino acids, which
in turn are recycled or catabolized as required.
•Heme is oxidized with the heme porphyrin
ring being oped by the endoplasmic reticulum
enzyme, heme oxigenase.
•The oxidation occurs on the specific carbon
producing equimolar amount of the biliverdin,
iron, and carbon monoxide (CO). This is the
only reaction in the body that is known to
produce CO.
•Most of the CO is excreted through the lungs,
with the result that the CO content of expired
air is a direct measure of the activity of heme
oxygenase in an individual.
Cont…
0In the first reaction, a
bridging methylene group
is cleaved by heme
oxygenase to form linear
Bilivirdin from cyclic
heme molecule.
0Fe 2+ is release from the
ring in this process
0In the first reaction, a
bridging methylene group
is cleaved by heme
oxygenase to form linear
Bilivirdin from cyclic
heme molecule.
0Fe 2+ is release from the
ring in this process
Cont….
•In the next reaction, a second
bridging methylene (between rings
III and IV is reduced by the
biliverdin reductase producing
bilirubin
•In the next reaction, a second
bridging methylene (between rings
III and IV is reduced by the
biliverdin reductase producing
bilirubin
In Blood
0The bilirubin synthesized in
spleen, liver and bone marrow
is unconjugated bilirubin
0It is hydrophobic in nature so it
is transported to the liver as
complex with the plasma
protein, albumin
Unconjugated bilirubin(Free
Bilirubin)
0Lipid soluble
01gm albumin binds 8.5 mg of
bilirubin
0Fatty acids and drugs can
displace bilirubin
0Indirect positive reaction in
van den Berg test
0The bilirubin synthesized in
spleen, liver and bone marrow
is unconjugated bilirubin
0It is hydrophobic in nature so it
is transported to the liver as
complex with the plasma
protein, albumin
Unconjugated bilirubin(Free
Bilirubin)
0Lipid soluble
01gm albumin binds 8.5 mg of
bilirubin
0Fatty acids and drugs can
displace bilirubin
0Indirect positive reaction in
van den Berg test
Cont…
Bilirubin is conjugated in a
two step process to form
bilirubin mono and di-
glucuronide
Bilirubin is conjugated in a
two step process to form
bilirubin mono and di-
glucuronide
0Conjugated (Direct) bilirubin is
released into the bile by the liver
and stored in the gallbladder, or
transferred directly to the small
intestines.
0Bilirubin is further broken down by
bacteria in the intestines, and those
breakdown products contribute to
the color of the feces.
0A small percentage of these
breakdown compounds are taken in
again by the body, and eventually
appear in the urine
0Unconjugated (indirect)
Erythrocytes generated in
the bone marrow are disposed of
in the spleen when they get old or
damaged.
0This releases hemoglobin, which is
broken down to heme as the
globin parts are turned into amino
acids.
0The heme is then turned into
unconjugated bilirubin in the
reticuloendothelial cells of the
spleen.
0This unconjugated bilirubin is not
soluble in water, due to
intramolecular hydrogen bonding.
It is then bound to albumin and
sent to the liver.
released into the bile by the liver
and stored in the gallbladder, or
transferred directly to the small
intestines.
0Bilirubin is further broken down by
bacteria in the intestines, and those
breakdown products contribute to
the color of the feces.
0A small percentage of these
breakdown compounds are taken in
again by the body, and eventually
appear in the urine
0Unconjugated (indirect)
Erythrocytes generated in
the bone marrow are disposed of
in the spleen when they get old or
damaged.
0This releases hemoglobin, which is
broken down to heme as the
globin parts are turned into amino
acids.
0The heme is then turned into
unconjugated bilirubin in the
reticuloendothelial cells of the
spleen.
0This unconjugated bilirubin is not
soluble in water, due to
intramolecular hydrogen bonding.
It is then bound to albumin and
sent to the liver.
Jaundice
Treatment for Neonatal Jaundice
Bilirubin Lab values
Bilirubin form Normal value
Total (elderly, adult, child)
(newborn)
Critical value (a(newborn)
0.1 to 1.0 mg/dL
1.0 to 12.0 mg/dL
>12 mg/dL
>15 mg/dL
Pre-hepatic, unconjugated, indirect 0.0 to 0.8 mg/dL
Post-hepatic, conjugated, direct 0.0 to 0.25 mg/dL
Fecal urobilinogen 40 to 280 mg/day
Urine 0.0 to 0.02 mg/dL
Conjugated bilirubin - water soluble -
direct reaction with dyes
Unconjugated bilirubin - water insoluble - alcohol
is needed for dye (indirect) reaction
Observe the color changes associated with heme degradation by
watching the progress of a bruise (dark red to green to yellow).
Bilirubin form Normal value
Total (elderly, adult, child)
(newborn)
Critical value (a(newborn)
0.1 to 1.0 mg/dL
1.0 to 12.0 mg/dL
>12 mg/dL
>15 mg/dL
Pre-hepatic, unconjugated, indirect 0.0 to 0.8 mg/dL
Post-hepatic, conjugated, direct 0.0 to 0.25 mg/dL
Fecal urobilinogen 40 to 280 mg/day
Urine 0.0 to 0.02 mg/dL
Conjugated bilirubin - water soluble -
direct reaction with dyes
Unconjugated bilirubin - water insoluble - alcohol
is needed for dye (indirect) reaction
Observe the color changes associated with heme degradation by
watching the progress of a bruise (dark red to green to yellow).
Chapter 4
Anemia
Diagnosis of Anemia:
•History- Information solicited by
the physician which should
include:
Dietary habits
Medications taken
Possible exposure to chemical or
toxins
The most complaint is tiredness.
Muscle weakness and fatigue
when there is not enough oxygen
available to burn fuel for
production of energy. When no
oxygen to the brain, headache
vertigo and syncope may occur.
Physical Examination :
General Signs
•Organomegaly of the spleen and liver
may develop since they are
important in hematopoietic system
production and destruction.
•Heart abnormalities may occur as a
result of increased cardiac workload
associated with the physiologic
adaptations to anemia.
Specific Signs
Jaundice in hemolytic anemias
Diagnosis of Anemia:
•History- Information solicited by
the physician which should
include:
Dietary habits
Medications taken
Possible exposure to chemical or
toxins
The most complaint is tiredness.
Muscle weakness and fatigue
when there is not enough oxygen
available to burn fuel for
production of energy. When no
oxygen to the brain, headache
vertigo and syncope may occur.
Physical Examination :
General Signs
•Organomegaly of the spleen and liver
may develop since they are
important in hematopoietic system
production and destruction.
•Heart abnormalities may occur as a
result of increased cardiac workload
associated with the physiologic
adaptations to anemia.
Specific Signs
Jaundice in hemolytic anemias
Red Cell Indices
MCH, MCV, MCHC , RDW- These indices are used for
classifying anemias.
MCH- Mean Cell Hemoglobin
-is derived from the Hb devided by RBC
Hb (g/dl) x 10 ÷ RBC (10¹²/l)
MCV-Mean Cell Volume
-is calculated by deviding the PCV by RBC
PCV (l/l) x 1000 ÷ RBC (10¹²/l)
MCHC-Mean Cell Hemoglobin Concentration
-is derived from the Hb, MCV, and RBC
Hb (g/dl) ÷ PCV (l/l)
RDW- red Cell distribution Width
is derived from pulse height analysis can be expressed either as standard
deviation or as the coefficient variable (CV) (%)
MCH, MCV, MCHC , RDW- These indices are used for
classifying anemias.
MCH- Mean Cell Hemoglobin
-is derived from the Hb devided by RBC
Hb (g/dl) x 10 ÷ RBC (10¹²/l)
MCV-Mean Cell Volume
-is calculated by deviding the PCV by RBC
PCV (l/l) x 1000 ÷ RBC (10¹²/l)
MCHC-Mean Cell Hemoglobin Concentration
-is derived from the Hb, MCV, and RBC
Hb (g/dl) ÷ PCV (l/l)
RDW- red Cell distribution Width
is derived from pulse height analysis can be expressed either as standard
deviation or as the coefficient variable (CV) (%)
Classification of anemia
Morphologic
0Normocytic: MCV= 80-100fL
0Macrocytic: MCV > 100 fL
0Microcytic : MCV < 80 fL
Pathogenic (underlying mechanism)
0Blood loss (bleeding)
0Decreased RBC production
0Increased RBC destruction/pooling
Morphologic
0Normocytic: MCV= 80-100fL
0Macrocytic: MCV > 100 fL
0Microcytic : MCV < 80 fL
Pathogenic (underlying mechanism)
0Blood loss (bleeding)
0Decreased RBC production
0Increased RBC destruction/pooling
Other causes: Inadequate production of mature red
cells
1.Deficiency of essential substances like iron, folic
acid, vit B12, protein and other elements like copper,
cobalt, etc.
2.Deficiency of erythroblast.. i.e.Aplastic anemia, Pure
red cell aplasia
3.Infiltration of the bone marrow i.e. leukemia,
lymphoma, carcinoma, myelofibrosis
4.Endocrine abnormalities i.e. myxedema, addisons
disease, pituitary insuficiency
5.Chronic renal disease
6.Chronic inflammatory disease
7.Cirrhosis of liver
cells
1.Deficiency of essential substances like iron, folic
acid, vit B12, protein and other elements like copper,
cobalt, etc.
2.Deficiency of erythroblast.. i.e.Aplastic anemia, Pure
red cell aplasia
3.Infiltration of the bone marrow i.e. leukemia,
lymphoma, carcinoma, myelofibrosis
4.Endocrine abnormalities i.e. myxedema, addisons
disease, pituitary insuficiency
5.Chronic renal disease
6.Chronic inflammatory disease
7.Cirrhosis of liver
The etiologic possibilities are
Iron deficiency
Thalassemia
Sideroblastic anemia
Anemias of chronic disease.
Severe microcytic anemia (MCV
<70 fL) is
caused mainly by iron deficiency
or thalassemia.
Chronic inflammatory disease—
(1)infection (2)collagen vascular
disease (3)inflammatory bowel
disease
Recent blood loss
Malignancy/Marrow infiltration
Chronic renal failure
Transient erythroblastopenia of
chidhood
Marrow aplasia/hypoplasia
HIV infection
Hemophagocytic syndrome
Hypochromic Microcytic Anemia Normochromic Normocytic Anemia
Iron deficiency
Thalassemia
Sideroblastic anemia
Anemias of chronic disease.
Severe microcytic anemia (MCV
<70 fL) is
caused mainly by iron deficiency
or thalassemia.
Chronic inflammatory disease—
(1)infection (2)collagen vascular
disease (3)inflammatory bowel
disease
Recent blood loss
Malignancy/Marrow infiltration
Chronic renal failure
Transient erythroblastopenia of
chidhood
Marrow aplasia/hypoplasia
HIV infection
Hemophagocytic syndrome
Hypochromic Microcytic Anemia Normochromic Normocytic Anemia
Macrocytic Anemia Normocytic Anemias
Megaloblastic anemias
• Vit.B12 def. - (1) pernicious anemia (2)
malabsorption
• Folate def. - (1) malnutrition (2) malabsorption
(3) chronic hemolysis (4)drugs - phenytoin,
sulfa
Hemolysis
Myelodysplastic syndrome
Marrow failure - Aplastic anemia
Chronic liver disease
Hypothyroidism
Macrocytic anemia may be the result of
megaloblastic (folate or vitamin B12 deficiency)
or nonmegaloblastic causes. Folate deficiency
can in turn be due to either reduced intake or
diminished absorption. Severe macrocytic
anemia (MCV >125 fL) is almost always
megaloblastic.
These may be classified as follows:
underproduction of erythrocytes due to
(1) the anemia of chronic disease
(2) marrow failure
(3) renal failure (decreased erythropoietin)
loss or destruction of erythrocytes due to
(1) hemolysis
(2) acute blood loss
The reticulocyte count is useful in drawing
this distinction, being elevated in (b) and
reduced in (a).
The causes of normocytic anemias include
aplastic anemia, bone-marrow replacement,
pure red-cell aplasia, anemias of chronic
disease, hemolytic anemia, and recent blood
loss. A number of anemias have a genetic
etiology. Examples of such inherited
disorders include hereditary spherocytosis,
sickle-cell (SC) anemia, and thalassemia
Megaloblastic anemias
• Vit.B12 def. - (1) pernicious anemia (2)
malabsorption
• Folate def. - (1) malnutrition (2) malabsorption
(3) chronic hemolysis (4)drugs - phenytoin,
sulfa
Hemolysis
Myelodysplastic syndrome
Marrow failure - Aplastic anemia
Chronic liver disease
Hypothyroidism
Macrocytic anemia may be the result of
megaloblastic (folate or vitamin B12 deficiency)
or nonmegaloblastic causes. Folate deficiency
can in turn be due to either reduced intake or
diminished absorption. Severe macrocytic
anemia (MCV >125 fL) is almost always
megaloblastic.
These may be classified as follows:
underproduction of erythrocytes due to
(1) the anemia of chronic disease
(2) marrow failure
(3) renal failure (decreased erythropoietin)
loss or destruction of erythrocytes due to
(1) hemolysis
(2) acute blood loss
The reticulocyte count is useful in drawing
this distinction, being elevated in (b) and
reduced in (a).
The causes of normocytic anemias include
aplastic anemia, bone-marrow replacement,
pure red-cell aplasia, anemias of chronic
disease, hemolytic anemia, and recent blood
loss. A number of anemias have a genetic
etiology. Examples of such inherited
disorders include hereditary spherocytosis,
sickle-cell (SC) anemia, and thalassemia
Iron Deficiency Anemia
0It is a condition when supply of iron in the body to bone marrow
falls short of that required for the production of red blood cells. It is
the commonest cause of anemia throughout the world.
0The incidence of anemia in the general population is about 1.5%.
0Iron deficiency related to inadequate replacement of lost iron is the
most frequent cause of asymptomatic anemia and has a variety of
causes.
0Iron deficiency is common among women of childbearing age; 10%
to 20% of menstruating women have abnormally low
concentrations of hemoglobin (usually <12 g per 100 mL).
0Between 20% and 60% of pregnant women have hemoglobin levels
<11 g per 100 mL. Anemia was found in 6% of white women and
17% of black women during the first trimester and in 25% of white
women and 46% of black women during the third trimester.
0It is a condition when supply of iron in the body to bone marrow
falls short of that required for the production of red blood cells. It is
the commonest cause of anemia throughout the world.
0The incidence of anemia in the general population is about 1.5%.
0Iron deficiency related to inadequate replacement of lost iron is the
most frequent cause of asymptomatic anemia and has a variety of
causes.
0Iron deficiency is common among women of childbearing age; 10%
to 20% of menstruating women have abnormally low
concentrations of hemoglobin (usually <12 g per 100 mL).
0Between 20% and 60% of pregnant women have hemoglobin levels
<11 g per 100 mL. Anemia was found in 6% of white women and
17% of black women during the first trimester and in 25% of white
women and 46% of black women during the third trimester.
Iron
Function as electron transporter; Vital
for life
Must be in ferrous (Fe
++
) state of
activity.
0In anaerobic condition, easy to
maintain ferrous state
0Iron readily donates electrons to
oxygen, superoxide radicals, H2O2
OH Radicals
0Ferric (Fe
+++
) ions cannot transport
electrons or O2.
0Organisms able to limit exposure to
iron had major survival advantage
Function as electron transporter; Vital
for life
Must be in ferrous (Fe
++
) state of
activity.
0In anaerobic condition, easy to
maintain ferrous state
0Iron readily donates electrons to
oxygen, superoxide radicals, H2O2
OH Radicals
0Ferric (Fe
+++
) ions cannot transport
electrons or O2.
0Organisms able to limit exposure to
iron had major survival advantage
Cont…
Iron absorption
0Duodenum
0Proximal jejunum
(influenced by rate of
erythropoiesis)
Factor Affecting Iron Absorption
0Form of iron
0Acids
0Amount of iron
0Rate erythropoiesis
Iron absorption
0Duodenum
0Proximal jejunum
(influenced by rate of
erythropoiesis)
Factor Affecting Iron Absorption
0Form of iron
0Acids
0Amount of iron
0Rate erythropoiesis
Sickle-cell anemia is a molecular disease
of Hb
Comparison of normal and sickle-shaped Comparison of normal and sickle-shaped
erythrocytes erythrocytes
of Hb
Comparison of normal and sickle-shaped Comparison of normal and sickle-shaped
erythrocytes erythrocytes
Normal and sickle-cell hemoglobin
Mutation of Sickle Cell Gene
Characterization of HbS
HbS has between 2 & 4 more net + charges per
molecule than net HbA
A S
pI of Oxy Hb 6.87 7.09 =0.22
pI of deoxy Hb 6.88 6.91 =0.23
Non-polar residue on the outside of HbS (due to Val)
causing low solubility
Sticky patch on the outside of its β chains & are present on
both deoxy HbS & oxy HbS but not on HbA
HbS has between 2 & 4 more net + charges per
molecule than net HbA
A S
pI of Oxy Hb 6.87 7.09 =0.22
pI of deoxy Hb 6.88 6.91 =0.23
Non-polar residue on the outside of HbS (due to Val)
causing low solubility
Sticky patch on the outside of its β chains & are present on
both deoxy HbS & oxy HbS but not on HbA
Biochemical basis for sickling
0The substitution of nonpolar
Valine for a charge glutamate
forms a protrusion on the beta-
globin that fits in to a
complementary site on the
alpha-chain of another
hemoglobin molecule in the cell
0At low oxygen tension, HbS
polymerizes inside the RBC then
subsequently assembling in to a
net work of fibrous polymers
that stiffen and distort the cell,
producing rigid misshapen
erythrocytes-sickle shaped
erythrocytes.
0The substitution of nonpolar
Valine for a charge glutamate
forms a protrusion on the beta-
globin that fits in to a
complementary site on the
alpha-chain of another
hemoglobin molecule in the cell
0At low oxygen tension, HbS
polymerizes inside the RBC then
subsequently assembling in to a
net work of fibrous polymers
that stiffen and distort the cell,
producing rigid misshapen
erythrocytes-sickle shaped
erythrocytes.
Signs and Symptoms of Sickle cell
Episodes of pain
Pain develops when sickle-shaped red
blood cells block blood flow through tiny
blood vessels to your chest, abdomen and
joints. Pain can also occur in your bones.
Frequent infections
Sickle cells can damage your spleen, an
organ that fights infection. This may make
you more vulnerable to infections.
Vision problems
Tiny blood vessels that supply your eyes
may become plugged with sickle cells. This
can damage the retina — the portion of the
eye that processes visual images.
Episodes of pain
Pain develops when sickle-shaped red
blood cells block blood flow through tiny
blood vessels to your chest, abdomen and
joints. Pain can also occur in your bones.
Frequent infections
Sickle cells can damage your spleen, an
organ that fights infection. This may make
you more vulnerable to infections.
Vision problems
Tiny blood vessels that supply your eyes
may become plugged with sickle cells. This
can damage the retina — the portion of the
eye that processes visual images.
Prevention of Sickle Cell Disease
0Screen for Hb S at birth.
This method of finding
allows institution of early
treatment and control
0Prenatal diagnosis. Prenatal
testing is sensitive and rapid
and must be accompanied
with genetic testing and
psychological counseling
0Screen for Hb S at birth.
This method of finding
allows institution of early
treatment and control
0Prenatal diagnosis. Prenatal
testing is sensitive and rapid
and must be accompanied
with genetic testing and
psychological counseling
Thalasemia
0Diverse group of disorders which manifest as anemia of varying degrees.
0Result of defective production of globin portion of hemoglobin molecule.
0Distribution is worldwide.
0May be either homozygous defect or heterozygous defect.
0Defect results from abnormal rate of synthesis in one of the globin
chains.
0Globin chains structurally normal (is how differentiated from
hemoglobinopathy), but have imbalance in production of two different
types of chains.
0Results in overall decrease in amount of hemoglobin produced and may
induce hemolysis.
0Two major types of thalassemia:
Alpha (α) - Caused by defect in rate of synthesis of alpha chains.
Beta (β) - Caused by defect in rate of synthesis in beta chains.
0May contribute protection against malaria.
0Diverse group of disorders which manifest as anemia of varying degrees.
0Result of defective production of globin portion of hemoglobin molecule.
0Distribution is worldwide.
0May be either homozygous defect or heterozygous defect.
0Defect results from abnormal rate of synthesis in one of the globin
chains.
0Globin chains structurally normal (is how differentiated from
hemoglobinopathy), but have imbalance in production of two different
types of chains.
0Results in overall decrease in amount of hemoglobin produced and may
induce hemolysis.
0Two major types of thalassemia:
Alpha (α) - Caused by defect in rate of synthesis of alpha chains.
Beta (β) - Caused by defect in rate of synthesis in beta chains.
0May contribute protection against malaria.
Cont…
0Also called Alpha Thalassemia
Minor.
0Caused by two missing alpha
genes. May be homozygous (-a/-
a) or heterozygous (--/aa).
0Exhibits mild microcytic,
hypochromic anemia.
0MCV between 70-75 fL.
0May be confused with iron
deficiency anemia.
0Although some Bart's hemoglobin
(γ
4) present at birth, no Bart's
hemoglobin present in adults.
0Also called Alpha Thalassemia
Minor.
0Caused by two missing alpha
genes. May be homozygous (-a/-
a) or heterozygous (--/aa).
0Exhibits mild microcytic,
hypochromic anemia.
0MCV between 70-75 fL.
0May be confused with iron
deficiency anemia.
0Although some Bart's hemoglobin
(γ
4) present at birth, no Bart's
hemoglobin present in adults.
Alpha thalassemia
0Has wide range clinical expressions.
0Is difficult to classify alpha thalassemias due to wide variety of
possible genetic combinations.
0Absence of alpha chains will result in increase of gamma chains
during fetal life and excess beta chains later in life; Causes
molecules like Bart's Hemoglobin (γ
4
) or Hemoglobin H (β
4
),
which are stable molecules but physiologically useless.
0Predominant cause of alpha thalassemias is large
number of gene deletions in the alpha-globin gene.
0Are four clinical syndromes present in alpha
thalassemia:
0Silent Carrier State
0Alpha Thalassemia Trait (Alpha Thalassemia Minor)
0Hemoglobin H Disease
0Bart's Hydrops Fetalis Syndrome
0Has wide range clinical expressions.
0Is difficult to classify alpha thalassemias due to wide variety of
possible genetic combinations.
0Absence of alpha chains will result in increase of gamma chains
during fetal life and excess beta chains later in life; Causes
molecules like Bart's Hemoglobin (γ
4
) or Hemoglobin H (β
4
),
which are stable molecules but physiologically useless.
0Predominant cause of alpha thalassemias is large
number of gene deletions in the alpha-globin gene.
0Are four clinical syndromes present in alpha
thalassemia:
0Silent Carrier State
0Alpha Thalassemia Trait (Alpha Thalassemia Minor)
0Hemoglobin H Disease
0Bart's Hydrops Fetalis Syndrome
Alpha thalassemia
Alpha thalasemia
Cont…
ALPHA THALASSEMIA
Deletion of one alpha gene, leaving three
functional alpha genes.
Alpha/Beta chain ratio nearly normal.
No hematologic abnormalities present.
No reliable way to diagnose silent
carriers by hematologic methods; Must
be done by genetic mapping.
May see borderline low MCV (78-80fL).
Silent Carrier state
Deletion of one alpha gene, leaving three
functional alpha genes.
Alpha/Beta chain ratio nearly normal.
No hematologic abnormalities present.
No reliable way to diagnose silent
carriers by hematologic methods; Must
be done by genetic mapping.
May see borderline low MCV (78-80fL).
Silent Carrier state
Beta thalassemia
Beta thalassemia
Chapter 5
Collecting and Handling of
Blood
Blood
THE VASCULAR SYSTEM
ARTERIES
•Have thick walls to withstand the pressure
of ventricular contraction, that creates a
pulse
•Normal systemic arterial blood is bright
red.
VEINS
•have thinner walls because blood in
them is under less pressure
•Collapse more easily
•Dark bluish red (oxygen poor)
Capillary
• only one cell
•Can easily be punctured to provide
blood specimen
ARTERIES
•Have thick walls to withstand the pressure
of ventricular contraction, that creates a
pulse
•Normal systemic arterial blood is bright
red.
VEINS
•have thinner walls because blood in
them is under less pressure
•Collapse more easily
•Dark bluish red (oxygen poor)
Capillary
• only one cell
•Can easily be punctured to provide
blood specimen
VASCULAR ANATOMY (phlebotomy related)
2 basic patterns of the veins
2 basic patterns of the veins
VASCULAR ANATOMY (phlebotomy related)
VASCULAR ANATOMY (phlebotomy related)
OTHER VEINS:
•Veins on the back of the hand
or at the ankle may be used,
although these are less
desirable and should be avoided
in diabetics and other
individuals with poor
circulation.
•Leg, ankle and foot veins are
sometimes used but not without
permission of the patient’s
physician due to potential
medical complications
OTHER VEINS:
•Veins on the back of the hand
or at the ankle may be used,
although these are less
desirable and should be avoided
in diabetics and other
individuals with poor
circulation.
•Leg, ankle and foot veins are
sometimes used but not without
permission of the patient’s
physician due to potential
medical complications
SOURCE AND COMPOSITION OF BLOOD SPECIMENS
ARTERIAL BLOOD
Primarily reserved for blood gas evaluation and certain emergency situations
VENOUS BLOOD
•affected by metabolic activity of the tissue it drains and varies by collection site
chloride, glucose, pH, CO2, lactic acid and ammonia levels differ may from
arterial blood
CAPILLARY BLOOD
•Contains arterial and venous blood plus tissue fluid
•Calcium, potassium and total protein are normally lower
ARTERIAL BLOOD
Primarily reserved for blood gas evaluation and certain emergency situations
VENOUS BLOOD
•affected by metabolic activity of the tissue it drains and varies by collection site
chloride, glucose, pH, CO2, lactic acid and ammonia levels differ may from
arterial blood
CAPILLARY BLOOD
•Contains arterial and venous blood plus tissue fluid
•Calcium, potassium and total protein are normally lower
TYPES OF BLOOD SPECIMENS
SERUM- Serum is that part of blood which
is similar in composition with plasma but
exclude clotting factors of blood.
PLASMA- Plasma is considered as the
medium of blood in which RBCs (Red Blood
Cells), WBC (White Blood Cells) and other
components of blood are suspended
WHOLE BLOOD
SERUM- Serum is that part of blood which
is similar in composition with plasma but
exclude clotting factors of blood.
PLASMA- Plasma is considered as the
medium of blood in which RBCs (Red Blood
Cells), WBC (White Blood Cells) and other
components of blood are suspended
WHOLE BLOOD
VENIPUNCTURE EQUIPMENT
Venipuncture can be
performed by 3 basic
methods
Evacuated tube system
(ETS) – most preferred because
blood is collected directly from the
vein in the tube, minimizing the risk
of specimen contamination and
exposure to the blood
Needle and syringe – used on
small, fragile and damaged veins
Winged infusion set
(butterfly) – can be used with
the ETS and syringe
•Used to draw blood from infants
and children, hand veins and other
difficult to draw situations
Venipuncture can be
performed by 3 basic
methods
Evacuated tube system
(ETS) – most preferred because
blood is collected directly from the
vein in the tube, minimizing the risk
of specimen contamination and
exposure to the blood
Needle and syringe – used on
small, fragile and damaged veins
Winged infusion set
(butterfly) – can be used with
the ETS and syringe
•Used to draw blood from infants
and children, hand veins and other
difficult to draw situations
VENIPUNCTURE EQUIPMENT
1. Tourniquet
•Applied to a patient’s arm during venipuncture
•Distends the veins, making them larger and easier to find, stretches the
wall so they are thinner and easier to find
•Must not be left on longer than 1 minute because specimen quality
may be affected
2. Needles
3. Evacuated Tube System (Vacutainer)
1. Tourniquet
•Applied to a patient’s arm during venipuncture
•Distends the veins, making them larger and easier to find, stretches the
wall so they are thinner and easier to find
•Must not be left on longer than 1 minute because specimen quality
may be affected
2. Needles
3. Evacuated Tube System (Vacutainer)
•The bevel is the slanted opening at the end of
the needle.
•bevel of the needle must face upward when
the needle is inserted into the vein.
VENIPUNCTURE EQUIPMENT
the needle.
•bevel of the needle must face upward when
the needle is inserted into the vein.
VENIPUNCTURE EQUIPMENT
VENIPUNCTURE EQUIPMENT
Tube Additives
A.Anticoagulants
•Prevent blood from clotting and include EDTA, citrates, heparin and oxalates
B. Antiglycolitic agents
•Prevent glycolysis which can decrease glucose concentration by upto 10 mg/dl
per hour
•Sodium fluoride : most common antiglycolitic agent
Preserves glucose for upto 3 days, and inhibits bacterial growth
C. Clot activators
•Are coagulation factors like thrombin
•Glass particles (silica)
•Inert clays ex. Diatomite (celite)
Enhance clotting by providing more surface for platelet activation
Tube Additives
A.Anticoagulants
•Prevent blood from clotting and include EDTA, citrates, heparin and oxalates
B. Antiglycolitic agents
•Prevent glycolysis which can decrease glucose concentration by upto 10 mg/dl
per hour
•Sodium fluoride : most common antiglycolitic agent
Preserves glucose for upto 3 days, and inhibits bacterial growth
C. Clot activators
•Are coagulation factors like thrombin
•Glass particles (silica)
•Inert clays ex. Diatomite (celite)
Enhance clotting by providing more surface for platelet activation
ORDER OF DRAW AND ADDITIVE CARRY OVER
COMMON TESTS AFFECTED BY ADDITIVE CONTAMINATION
Citrate – ALP, Ca,Phosporus
EDTA - ALP, Ca, CK,PTT,K,PT,Serum Iron, Na
Heparin – Activated CT, ACP, Ca, PT, PTT Na, Li
Oxalates- ACP, ALP, Amylase,Ca, LDH, PT, PTT, K, Red cell
Silica (clot activator) – PTT, PT
Sodium fluoride – Na, BUN
COMMON TESTS AFFECTED BY ADDITIVE CONTAMINATION
Citrate – ALP, Ca,Phosporus
EDTA - ALP, Ca, CK,PTT,K,PT,Serum Iron, Na
Heparin – Activated CT, ACP, Ca, PT, PTT Na, Li
Oxalates- ACP, ALP, Amylase,Ca, LDH, PT, PTT, K, Red cell
Silica (clot activator) – PTT, PT
Sodium fluoride – Na, BUN
PROCEDURAL ERROS RISKS
1.Hematoma formation
- rapid swelling near the venipuncture site due to blood leaking into the
tissues
Situations that can trigger hematoma formation?
1.Hematoma formation
- rapid swelling near the venipuncture site due to blood leaking into the
tissues
Situations that can trigger hematoma formation?
Capillary Specimen Collection
Collection sites
1.Fingers – adults and children over the age of 2
2.Heels - infants
Collection sites
1.Fingers – adults and children over the age of 2
2.Heels - infants
Neonatal Bilirubin Collection – must be protected from
light
•Neonatal Screening
screens for phenylketonuria,
a disorder which could be
managed by dietary
adjustment if diagnosed
early.
light
•Neonatal Screening
screens for phenylketonuria,
a disorder which could be
managed by dietary
adjustment if diagnosed
early.
End
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