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Chapter 19
The Blood
Copyright © John Wiley & Sons, Inc. All rights reserved.
The Blood
The cardiovascular system consists of
three components:
Blood
Heart
Blood vessels
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Functions of Blood Blood transports:
• oxygen & CO2 between lungs & tissues
• nutrients from the digestive tract
• metabolic wastes- from body to kidneys for elimination
• hormones from endocrine glands to target organs Blood regulates: • body temperature • pH using buffer systems
Blood protects• against blood loss by initiating hemostasis & coagulation• against infection – antibodies, complement proteins,
WBCs
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Physical Characteristics of Blood• It is viscous (thick) and more dense than water
• temperature slightly warmer than core body
temperature (T = 38o C)
• slightly alkaline pH (7.35-7.45)
• oxygenated blood bright red,
poorly oxygenated blood dark red
• makes up 8% of body mass
• Blood volume: 5–6 L for males, and 4–5 L for
females
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Constituents of Blood Blood is 5 liters of a specialized fluid connective
tissue composed of formed elements (45%)
suspended in a solution called plasma (55%)
If a sample of blood is centrifuged cellular portion
will precipitate out of solution and form a heavier
sediment below the straw colored liquid plasma
The normal RBC mass is almost
45% by volume – this is called the
hematocrit (Hct)
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Constituents of Blood
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Blood Plasma
Plasma is 92% water, with dissolved solutes: Plasma proteins – produced by the liver• albumin, globulins, fibrinogen
Nitrogenous wastes• urea, uric acid, creatinine
Nutrients –• glucose, fatty acids, amino acids
Electrolytes • sodium, potassium, calcium, chloride, bicarbonate
Respiratory gases • oxygen and carbon dioxide
Hormones Clotting factors If plasma is allowed to coagulate it is called serum -
serum is just plasma without the clotting factors-
used or blood testing
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Plasma Proteins Albumin contributes significantly to colloidal osmotic pressure
of blood It also plays an important role as a carrier molecule for
lipid soluble substances e.g. hormones
globulins, of which there are several types:
α-globulins and β- globulins are carrier proteins
δ-globulins are immunoglobulins (antibodies) made
by activated B lymphocytes called plasma cells
Fibrinogen- clotting factor –forms the blood clot
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Formed Elements The formed elements of blood include: Erythrocytes ( RBCs)- highest count Leukocytes( WBCs) Platelets Are continuously formed in the bone marrow
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Hematopoiesis
The process by which the formed elements of
blood develop is called hemopoiesis
(hematopoiesis).
blood cells are formed in red bone marrow
from pluripotent stem cells.
Red bone marrow:
In adults : bones of axial skeleton, pectoral &
pelvic girdles, heads of humerus & femur
In newborns- all bone marrow is red
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Hematopoiesis
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Hematopoiesis Blood cells are formed from pluripotent stem cells. The pluripotent stem cells (hemopoietic stem cells)
produce the myeloid stem cell and lymphoid stem cell myeloid stem cell gives rise to: RBCs, platelets,
monocytes, neutrophils, eosinophils, and basophils lymphoid stem cell gives rise to: T lymphocytes, B
lymphocytes, NK cells Regulation of hematopoiesis: Erythropoietin (EPO) regulates RBC formation Thrombopoietin regulates platelet formation Colony stimulating factors & interleukins stimulate WBC
formation
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Clinical connection
•Bone marrow examination by bone marrow aspiration or bone marrow biopsy
•For diagnosis of leukemias, anemias
•Site: usually iliac crest of hip bone, sternum
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Red Blood Cells
About 5 million RBCs/mm3 of blood Red blood cells are bi-concave discs-
increases the cell surface area- gives them a
high oxygen carrying capacity Mature RBCs don't have a nucleus or any
protein making machinery -die in about 120
days.
specific purpose – to carry O2
to the tissues of the body-
also carry 23 % CO2
• Their shape also allows them to
deform and fit in small capillary beds
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Each RBC contains 280 million molecules of Hb
Hemoglobin (Hb) is a protein molecule
adapted to carry O2 (and CO2 as well) A Hgb molecule consists of globin protein
(2 alpha and 2 beta polypeptide chains), each embedding an iron-containing heme group
Oxygen binds to the heme group ( one Hb binds 4 oxygen molecules)CO2 binds to globin proteins
RBCs and Hemoglobin
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RBCs RBCs and CO2:
Red blood cells contain the enzyme carbonic
anhydrase
Carbon dioxide diffuses fron tissues into RBCs
It combines with water to form carbonic acid-
H2CO3 which quickly dissociates into hydrogen
ions and bicarbonate ions
70 % of CO2 is transported in blood as
bicarbonate ions which is an important blood
buffer
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RBCs Life Cycle Erythropoiesis is the part of hematopoiesis
that deals with the production of RBCs.
Control is by negative feedback
Erythropoiesis increases when states of
hypoxia (O2 deficiency)- stimulates the kidneys
to release the hormone erythropoietin (EPO)
•EPO circulates to the red
marrow and speeds up the
maturation and release of
immature red cells
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Some stimulus disrupts
homeostasis by
Oxygen delivery to kid-neys (and other
tissues)
Receptors
Kidney cellsdetect lowoxygen level
Control center
Proerythroblasts inred bone marrowmature more quicklyinto reticulocytes
EffectorsLarger numberof RBCs incirculation
Increased oxygendelivery to tissues
Return to homeostasiswhen oxygen deliveryto kidneys increases tonormal
Increased erythropoietinsecreted into blood
Input
Increased erythropoietinsecreted into blood
Output
Decreasing
Negative feedback
regulation of Erythropoiesis
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RBCs Life Cycle As cells mature in the
bone marrow, they
become smaller
• the nucleus is lost
•Most organelles lost
•the amount of Hb
increases
At reticulocyte
stage RBCs are sent
out into the blood
stream
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ReticulocytesReticulocytes:
At this stage the RBCs are sent out into the
blood stream
Normally 1-2% of the RBCs in the peripheral
circulation are reticulocytesThe rate of erythropoiesis is measured by the
number of immature RBCs (called reticulocytes or
“retics”) in the peripheral circulation
•A low retic count (<.5%) indicates a low rate of
erythropoiesis while an elevated rate (>2%)
indicates a high rate of erythropoiesis
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RBC Life Cycle RBCs live only about 120 days- are destroyed
mainly in spleen
To maintain normal numbers, new cells must enter
the circulation at 2 million/s to balance high rate of
RBC destruction
• Ruptured RBCs are destroyed by macrophages in
the spleen and liver Heme and globin are separated Globin is metabolized into amino acids- released
into the circulation Iron of the heme is salvaged for re-use Heme is degraded to bilirubin
Copyright © John Wiley & Sons, Inc. All rights reserved.
Red blood celldeath andphagocytosis
Key:
in blood
in bile
Macrophage inspleen, liver, orred bone marrow
1
Globin
Red blood celldeath andphagocytosis
Key:
in blood
in bile
Macrophage inspleen, liver, orred bone marrow
Heme2
1
Aminoacids
Reused forprotein synthesisGlobin
Red blood celldeath andphagocytosis
Key:
in blood
in bile
Macrophage inspleen, liver, orred bone marrow
Heme
3
2
1
Aminoacids
Reused forprotein synthesisGlobin
Red blood celldeath andphagocytosis
Transferrin
Fe3+
Key:
in blood
in bile
Macrophage inspleen, liver, orred bone marrow
Heme
4
3
2
1
Aminoacids
Reused forprotein synthesisGlobin
Red blood celldeath andphagocytosis
Transferrin
Fe3+
Liver
Key:
in blood
in bile
Macrophage inspleen, liver, orred bone marrow
FerritinHeme
54
3
2
1
Aminoacids
Reused forprotein synthesisGlobin
Red blood celldeath andphagocytosis
Transferrin
Fe3+
Fe3+ Transferrin
Liver
Key:
in blood
in bile
Macrophage inspleen, liver, orred bone marrow
FerritinHeme
654
3
2
1
Aminoacids
Reused forprotein synthesisGlobin
Red blood celldeath andphagocytosis
Transferrin
Fe3+
Fe3+ Transferrin
Liver
+Globin
+Vitamin B12
+Erythopoietin
Key:
in blood
in bile
Macrophage inspleen, liver, orred bone marrow
FerritinHeme Fe3+
7
654
3
2
1
Aminoacids
Reused forprotein synthesisGlobin
Circulation for about120 days
Red blood celldeath andphagocytosis
Transferrin
Fe3+
Fe3+ Transferrin
Liver
+Globin
+Vitamin B12
+Erythopoietin
Key:
in blood
in bile
Erythropoiesis inred bone marrow
Macrophage inspleen, liver, orred bone marrow
FerritinHeme Fe3+
8
7
654
3
2
1
Aminoacids
Reused forprotein synthesisGlobin
Circulation for about120 days
Red blood celldeath andphagocytosis
Transferrin
Fe3+
Fe3+ Transferrin
Liver
+Globin
+Vitamin B12
+Erythopoietin
Key:
in blood
in bile
Erythropoiesis inred bone marrow
Macrophage inspleen, liver, orred bone marrow
FerritinHeme
Biliverdin Bilirubin
Fe3+
9
8
7
654
3
2
1
Aminoacids
Reused forprotein synthesisGlobin
Circulation for about120 days
Bilirubin
Red blood celldeath andphagocytosis
Transferrin
Fe3+
Fe3+ Transferrin
Liver
+Globin
+Vitamin B12
+Erythopoietin
Key:
in blood
in bile
Erythropoiesis inred bone marrow
Macrophage inspleen, liver, orred bone marrow
FerritinHeme
Biliverdin Bilirubin
Fe3+
10
9
8
7
654
3
2
1
Aminoacids
Reused forprotein synthesisGlobin
Stercobilin
Bilirubin
Urobilinogen
Feces
Smallintestine
Circulation for about120 days
Bacteria
Bilirubin
Red blood celldeath andphagocytosis
Transferrin
Fe3+
Fe3+ Transferrin
Liver
+Globin
+Vitamin B12
+Erythopoietin
Key:
in blood
in bile
Erythropoiesis inred bone marrow
Macrophage inspleen, liver, orred bone marrow
FerritinHeme
Biliverdin Bilirubin
Fe3+
12
1110
9
8
7
654
3
2
1
Aminoacids
Reused forprotein synthesisGlobin
Urine
Stercobilin
Bilirubin
Urobilinogen
Feces
Smallintestine
Circulation for about120 days
Bacteria
Bilirubin
Red blood celldeath andphagocytosis
Transferrin
Fe3+
Fe3+ Transferrin
Liver
+Globin
+Vitamin B12
+Erythopoietin
Key:
in blood
in bile
Erythropoiesis inred bone marrow
Kidney
Macrophage inspleen, liver, orred bone marrow
Ferritin
Urobilin
Heme
Biliverdin Bilirubin
Fe3+
13 12
1110
9
8
7
654
3
2
1
Aminoacids
Reused forprotein synthesisGlobin
Urine
Stercobilin
Bilirubin
Urobilinogen
Feces
Largeintestine
Smallintestine
Circulation for about120 days
Bacteria
Bilirubin
Red blood celldeath andphagocytosis
Transferrin
Fe3+
Fe3+ Transferrin
Liver
+Globin
+Vitamin B12
+Erythopoietin
Key:
in blood
in bile
Erythropoiesis inred bone marrow
Kidney
Macrophage inspleen, liver, orred bone marrow
Ferritin
Urobilin
Heme
Biliverdin Bilirubin
Fe3+
14
13 12
1110
9
8
7
654
3
2
1
RBC Life Cycle
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Clinical connections Anemia is a condition of insufficient RBC’s or
hemoglobin (quality or quantity)
It is most often the result of low iron intake,
hemolysis, blood loss, or lack of production
in the bone marrow
Polycythemia is a condition of excess
number of RBCs
It occurs in response to hypoxia, shots of
EPO (illegal “doping”), COPD
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Anemias
Iron deficiency anemia is the most common
anemia in the U.S., and affects primarily
menstruating women
• Chronic blood loss is a cause
Hemorrhagic anemia is the result of
precipitous blood loss, and results in an equal
decrease in Hct, Hb content, and RBC count
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Anemias Sickle-cell disease (SCD), also called sickle-
cell anemia, is an autosomal recessive
disorder. A genetic defect in the primary DNA
sequence leads to production of a faulty Hb β
chain, and RBCs that take on a rigid, sickle-
shape
• Sickling decreases the cells' flexibility and
results in a variety of complications; life
expectancy is shortened
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White Blood Cells WBCs number- between 5000-10,000 cells/mm3
There are 5 different types of WBCs
(WBCs) or leukocytes have nuclei and other
organelles
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Leukocytes Leukocytes are divided into two groups
depending on whether they contain
conspicuous cytoplasmic granules (when
stained)
• Granulocytes include the neutrophils,
eosinophils, and basophils
• Agranulocytes are the monocytes and
lymphocytes
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Neutrophils The most numerous WBC in normal blood (60-
70% )is the neutrophil, or
polymorphonucleocyte (PMN)
• PMNs are granulocytes lilac granules and nuclei
have 2-5 lobes
• They are phagocytes - their principal role is to
fight bacterial infectionsPMN phagocytizing
a microbe
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Eosinophils Eosinophils are characterized by their large
red granules and bilobed nuclei
They are (2-4% of circulating WBCs), but their
numbers increase slightly with allergic
reactions & parasitic infections
they have also been associated with
the development of allergies
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Basophils Basophils are the granulocytes that contain
large, dark blue, histamine containing granules
Normally, they are the lowest number of
circulating WBCs (only 0-1%),
May have a role to play in the
inflammatory responses
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Monocytes While monocytes are not granulocytes, they
come from the same immediate precursor cell
as the 3 granulocytes (the myeloid stem
cell)
3-8% of the circulating WBCs
• Along with neutrophils, monocytes are the
other major group of phagocytic cells.
• they are more numerous in
the peripheral, tissues where they
act as “fixed” phagocytes
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Lymphocytes Approximately 20-30% of circulating WBCs
are lymphocytes
increase in number in acute viral
infections
Most lymphocytes continually move between
lymphoid tissues, lymph, and blood, spending
only a few hours in blood
Lymphocytes are the cornerstone of the
specific immune response There are two types of lymphocytes: T cells
and B cells•T cells control immune responses •B cells give rise to plasma cells, which produce antibodies
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Functions of Leukocytes To get rid of pathogens the WBCs have to leave the
blood stream and collect at sites of infection or injury
WBCs leave the bllod vessels by the process called
emigration :
Rolling along the endothelium & then sticking- by
complementary adhesion molecules on endothelium
(selectins) and on leucocytes (integrins )
Squeeze out between endothelial cells -diapedesis
Chemicals released by microbes and inflamed
tissues attract phagocytes, a phenomenon called
chemotaxis
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Functions of Leukocytes Neutrophils are the first to emigrate in bacterial
infections
Reach by chemotaxis & engulf pathogen by phagocytosis
Release strong oxidants & defensins to destroy engulfed
bacteria
Neutrophils are followed by monocytes- which get
transformed into phagocytic tissue macrophages
Lymphocytes take part in immune responses
B cells- antobody mediated humoral immunity
T cells – immune regulation & destruction of viral infected
and cancer cells
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Interstitial fluid
Neutrophil
Endothelial cell
Rolling
Sticking
Squeezing betweenendothelial cells
Key:Selectins onendothelial cells
Integrins onneutrophil
Blood flowBlood flow
Emigrationof neutrophils
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From Wikimedia Commons
Diapedesis
Chemotaxis & phagocytosis
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WBC Indices For diagnostic purposes, physicians measure the total leucocyte count
• A leukocytosis is any WBC count > 10,000/mm3, and usually indicate an
infectious process or inflammation
• A leukopenia is any WBC count < 5,000/mm3, and usually indicates a severe
disease (AIDS, bone marrow failure, severe malnutrition, or chemotherapy)
• Differential leucocyte count : percentages of each of the 5 types of WBCs
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WBC Indices
Shifts in the normal percentages of circulating
WBCs will often point towards a bacterial infection
(elevated neutrophils) or a viral infection (elevated
lymphocytes)
• In this peripheral blood smear
a patient with lymphocytic
leukemia has a WBC >150,000
and 90% of the WBCs are
cancerous lymphocytes! Lymphocytic leukemia.
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Platelets Platelets (thrombocytes) are about 150,000-
400,000 cells/mm3 , they have a short life span (5
to 9 days)
Their granules contain chemicals
(serotonin, Ca2+, ADP) that,
once released, promote
blood clotting
Also release PDGF-
promotes growth & healing
of damaged vessels
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Megakaryocytes (immediate precursors of
platelets) are huge cells that splinter into
2000 to 3000 fragments while still in the
red bone marrow
• Each disc shaped fragment is a platelet
• Platelets leave the red bone marrow
and enter the circulation
Platelets
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Hemostasis
Hemostasis is a sequence of responses that
stops bleeding when blood vessels are
damaged or ruptured
• Three mechanisms reduce blood loss
1. Vascular spasm
2. Formation of a platelet plug
3. Blood clotting (coagulation)
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Hemostasis1. Vascular spasm occurs as damaged blood
vessels constrict- (by neural & chemical stimuli)
2. Platelets adhere to damaged
endothelium to form a
platelet plug
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1
Red blood cell
Platelet
Collagen fibersand damagedendothelium
Platelet adhesion11
2
Red blood cell
Platelet
Collagen fibersand damagedendothelium
Liberated ADP,serotonin, andthromboxane A2
Platelet adhesion1
Platelet release reaction2
1
2
3
Red blood cell
Platelet
Collagen fibersand damagedendothelium
Liberated ADP,serotonin, andthromboxane A2
Platelet plug
Platelet adhesion1
Platelet release reaction2
Platelet aggregation3
2.Platelet Plug Formation
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Hemostasis3. Clotting (coagulation) is possible because of the
presence of several clotting proteins normally
dissolved in the blood in inactive state
Coagulation occurs in a cascade whereby one
activated clotting protein triggers the next step in
the process, which triggers the next
• There are 2 pathways to
activate the clotting cascade:
extrinsic & intrinsic
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Tissue trauma
Tissuefactor(TF)
Blood trauma
Damagedendothelial cellsexpose collagenfibers
(a) Extrinsic pathway (b) Intrinsic pathway
Activated XII
Ca2+
Damagedplatelets
Ca2+
Plateletphospholipids
Activated X
Activatedplatelets
Activated X
PROTHROMBINASECa2+
VCa2+
V
1
Tissue trauma
Tissuefactor(TF)
Blood trauma
Damagedendothelial cellsexpose collagenfibers
(a) Extrinsic pathway (b) Intrinsic pathway
Activated XII
Ca2+
Damagedplatelets
Ca2+
Plateletphospholipids
Activated X
Activatedplatelets
Activated X
PROTHROMBINASECa2+
VCa2+
Prothrombin(II)
Ca2+
THROMBIN
(c) Common pathway
V
1
2
+
+
Tissue trauma
Tissuefactor(TF)
Blood trauma
Damagedendothelial cellsexpose collagenfibers
(a) Extrinsic pathway (b) Intrinsic pathway
Activated XII
Ca2+
Damagedplatelets
Ca2+
Plateletphospholipids
Activated X
Activatedplatelets
Activated X
PROTHROMBINASECa2+
VCa2+
Prothrombin(II)
Ca2+
THROMBIN
Ca2+
Loose fibrinthreads
STRENGTHENEDFIBRIN THREADS
Activated XIIIFibrinogen(I)
XIII
(c) Common pathway
V
1
2
3
+
+
Blood clotting cascade
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Hemostasis The extrinsic pathway has few
steps, occurs within seconds,
once the protein “tissue factor”
(TF) or tissue thromboplastin
leaks into the blood from cells
The intrinsic pathway is more
complex, & slower in response
blood contact with collagen under
endothelial cells- activates
factor XII
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Both the extrinsic and intrinsic clotting
pathways converge at a common
point (pathway) where factor X
becomes activated (Xa), combines with
factor V to form:
• Prothrombin
activator(prothombokinase)
• Prothrombin is converted into
thrombin
• Thrombin converts soluble fibrinogen
into insoluble fibrin threads,
Hemostasis
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Ca2+ plays an important role throughout the
clotting system
Clot retraction is the consolidation of the fibrin
clot.
Fibrin threads contract as platelets pull on them
As the clot retracts, it pulls the edges of
the damaged vessel closer together,
decreasing the risk of further
damage – new endothelial cells can
then repair the vessel lining
Hemostasis
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Fibrinolysis
Because blood clotting involves positive
feedback cycles, a clot has a tendency to
enlarge, this is checked by:
• The fibrinolytic system - dissolves clots
• Vessel endothelial cells release tissue
plasminogen activator ( tPA) that can
activate plasminogen an inactive plasma
enzyme to become plasmin, (the enzyme
that actively dissolves clots)
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Intravascular Clotting Inappropriate clotting in an unbroken blood vessel is
called thrombosis; the clot itself, called a thrombus
• Such clots may be initiated by:
• endothelial injury resulting from atherosclerosis,
trauma, or infection
• Stasis of blood- allowing clotting factors to
accumulate locally and initiate the coagulation
cascade
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Intravascular Clotting A thrombus may become dislodged and be
swept away in the blood
blood clot transported
by the bloodstream is
called an embolusemboli can obstruct a
blood vessel and cause ischemia to
the tissue beds e.g. pulmonary embolism,
stroke
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Blood Groups
Red cells have antigens or agglutinogens
on their surface These antigens are:• Unique to the individual • Recognized as foreign if transfused into
another individual Presence or absence of these antigens is used
to classify blood groups Major blood group antigens are A and B
antigens & Rh antigen The major blood groups are ABO & Rh blood
groups
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In transfusion medicine the presence or absence of the
A and B red cell antigens forms the basis of the ABO
blood group system
Blood Groups
Another major red cell antigen is the Rh
antigen, which 85% of the population have,
and comprises the other important blood
grouping
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Blood Groups For reason that are not totally clear, serum
contains anti-ABO antibodies of a type opposite to the ABO antigen on the red cell surface• For instance, those with A antigens on their
red cells have anti-B antibodies in their serum
Copyright © John Wiley & Sons, Inc. All rights reserved.
Blood Groups
By knowing the status of the A antigen, B antigen, and
Rh antigen, most of the major blood incompatibility
issues can be avoided
• Type AB individuals are “universal recipients”
because they has neither anti-A nor anti-B antibodies
in their serum that would destroy transfused RBCs
• Type O individuals are “universal donors” because
their RBCs have no antigens on the cell surface that
can potentially react with the recipients serum
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Rh Incompatibility
Individuals whose RBCs have the Rh antigen are
said to be Rh+ while those who lack the Rh
antigen are Rh-
Unlike ABO blood groups, anti-Rh antibodies are
not spontaneously formed in Rh– individuals
If an Rh– individual is exposed to Rh+ blood, anti-
Rh antibodies form( e.g. receiving Rh+
transfusion)
A second exposure to Rh+ blood will result in a
transfusion reaction
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Hemolytic Disease of the Newborn
Rh– mother carries a Rh+ fetus At the time of birth she gets
exposed to Rh+ blood- anti RH antibodies are formed
In a subsequent pregnancy, these Rh+ antibodies cross the placenta and attack the RBCs of a Rh+ baby
Results in hemolyis of babys RBCs- baby is born with severe anemia
Prevention- RhoGAM given to Rh– mother ( during pregnancy & at birth)
RhoGAM destroys any Rh+ cells before the mother’s immune system can produce
anti-Rh antibody
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Blood Typing & Cross Matching Blood typing for ABO status is done
using single drops of blood mixed with
different antisera:
Anti-A serum contains anti-A antibodies
Anti-B serum contains anti-B antibodies
Agglutination with an antisera
indicates the presence of that antigen
on the RBC
Rh typing: a drop of blood mixed with
antiserum containing anti- Rh
antibodies
Cross matching: RBCs of donors blood
of same type mixed with recipients
serum- checked for agglutination
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Transfusion Reactions
Mismatched transfusions cause transfusion reactions
Donor’s cells are attacked by the recipient’s plasma
antibodies causing agglutination & hemolysis :
• Clumped cells block small blood vessels & hemolyse
• Ruptured RBCs release free hemoglobin into the
bloodstream
• Free hemoglobin can block kidneys tubules and
cause acute renal failure
• Person can go into shock
•
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