BLOOD

JAI NARAIN VYAS UNIVERSITY, JODHPUR
ASSISTANT PROFESSOR:- ASHWIN SINGH
CHOUHAN
DEPARTMENT:- PHARMACOLOGY
E-mail:- anshukavya1993@gmail.com
BLOOD

BLOOD
One of the largest organs of the body. An average 70 kg
man has almost 5L blood (5.5 kg). blood is a connective
tissue. Like all connective tissues, it is made up of cellular
elements and an extracellular matrix.
The cellular elements referred to as the formed
elementsn include red blood cells (RBCs), white
blood cells (WBCs), and cell fragments
called platelets. The extracellular matrix, called plasma,
makes blood unique among connective tissues because it
is fluid. This fluid, which is mostly water, perpetually
suspends the formed elements and enables them to
circulate throughout the body within the cardiovascular
system.

Carrier of gases, nutrients, and waste products:-
Oxygen enters blood in the lungs and is transported to
cells. Carbon dioxide, produced by cells, is transported in
the blood to the lungs, from which it is expelled. Ingested
nutrients, ions, and water are carried by the blood from
the digestive tract to cells, and the waste products of the
cells are moved to the kidneys for elimination.
Clot formation:-Clotting proteins help stem blood loss
when a blood vessel is injured.
Transport of processed molecules:- Most substances
are produced in one part of the body and transported in
the blood to another part.
THE FUNCTIONS OF BLOOD

Protection against foreign substances:-Antibodies
help protect the body from pathogens.
Transport of regulatory molecules:- Various
hormones and enzymes that regulate body processes are
carried from one part of the body to another within the
blood.
Maintenance of body temperature:-Warm blood is
transported from the inside to the surface of the body,
where heat is released from the blood.
pH and osmosis regulation:- Albumin is also an
important blood buffer and contributes to the osmotic
pressure of blood, which acts to keep water in the blood
stream.

PHYSICAL PROPERTIES OF BLOOD
SPECIFIC GRAVITY
Whole blood: 1.055 - 1.065
Plasma: 1.024 - 1.028
Viscosity: 5-6 times that of water.
Mass: 6-8% of the body weight.
Blood volume: ~ 8% of body weight.
~ 86% ml/kg body weight.
5-6L in adults
[Infants have a larger blood volume in proportion to
body weight than adults].
Osmotic pressure: 7-8 atmosphere at body
temperature.

Blood is a sticky, opaque fluid with a characteristic
metallic taste.
Color. Depending on the amount of oxygen it is
carrying, the color of blood varies from scarlet (oxygen-
rich) to a dull red (oxygen-poor).
Weight. Blood is heavier than water and about five
times thicker, or more viscous, largely because of its
formed elements.
pH. Blood is slightly alkaline, with a pH
between 7.35 and 7.45.
Temperature. Its temperature (38 degrees Celsius,
or 100.4 degrees Fahrenheit) is always slightly higher
than body temperature.

JNVU PHARMACY, JODHPUR
Formed Elements
Red blood cells
(erythrocytes).
White blood cells
(leukocytes).
Platelets
(thrombocytes)
Fluid medium (plasma)
COMPOSITION OF BLOOD

SERUM
Whole blood Clot formation
Centrifuge
Clot +
Clear yellowish fluid (serum)
SERUM: The clear liquid that can be separated from
clotted blood. Serum differs from plasma, the liquid
portion of normal unclotted blood containing the red and
white cells and platelets. It is the clot that makes the
difference between serum and plasma.
The human serum is a circulating carrier of exogenous
and endogenous liquids in the blood. It allows substances
to stick to the molecules within the serum and be buried
within it. Human serum thus helps in the transportation
of fatty acids and thyroid hormones which act on most of
the cells found in the body

RED BLOOD CELLS/ ERYTHROCYTES
Normal concentration in blood 3.9-5.5 million/µL in
women and 4.1-6 million/µL in men.
Contain oxygen-carrying protein hemoglobin, which
accounts for their acidophilia.
Production = destruction with at least 2 million new
RBCs per second.
Biconcave disc – increases surface area.
7.5 µm in diameter.
2.6 µm thick at rim and 0.8 µm thick in center Strong,
flexible plasma membrane.
Glycolipids in plasma membrane responsible for ABO
and Rh blood groups.
Lack nucleus and other organelles
 No mitochondria.
 doesn’t use oxygen.

FUNCTION OF RBC
Transport of O2 from the lungs to the tissues & CO2 in
the opposite direction .
Hemoglobin
Carbonic anhydrase
Catalyses the reaction
H2O+ CO2 H2CO3
Maintenance of PH homeostasis ( globin, phosphate &
bicarbonate buffers) hemoglobin in the cells is an
excellent acid-base buffer.
Contribution to the blood viscosity.
Decrease blood oncotic p ( by keeping Hb protein
inside the cells).

HEMOGLOBIN
 Globin – 4 polypeptide chains.
 Heme in each of 4 chains.
 Iron ion can combine reversibly with one oxygen
molecule.
 Also transports 23% of total carbon dioxide.
 Combines with amino acids of globin.
 Hemoglobin combine reversibly with O2
(oxyhemoglobin) and CO2 (carbaminohemoglobin).
 Hemoglobin combine irreversibly with carbon monoxide
(carboxyhemoglobin) causes a reduced capacity to
transport O2.
 Nitric oxide (NO) binds to hemoglobin.
 Releases NO causing vasodilatation to improve blood
flow and oxygen delivery.

RBC LIFE CYCLE
Starts in red bone marrow with proerythroblast
Cell near the end of development ejects nucleus and
becomes a reticulocyte and released into blood stream
Contain residual ribosomal RNA, which is precipitated
and stained by some dyes (eg, brilliant cresyl blue)
Appear like few granules or net like structure in the
cytoplasm
Normally constitute about 1% of total circulating
erythrocytes
Increase number of reticulocyte may reflect increase
demand for O2
Develop into mature RBC within 1-2 days and loose its
mitochondria, ribosomes and many cytoplasmic enzymes

Live only about 120 days.
Cannot synthesize new components.
no nucleus.
Ruptured red blood cells removed from circulation and
destroyed by fixed phagocytic macrophages in spleen and
liver.
Breakdown products recycled.
Globin’s amino acids reused.
Iron reused.
Non-iron heme ends as yellow pigment urobilin in urine
or brown pigment stercobilin in feces.

WHITE BLOOD CELLS/ LEUKOCYTES
Have nuclei.
Do not contain hemoglobin.
Spherical shape in blood plasma.
6000-10000 leukocytes/µL .
Granular or agranular based on staining highlighting
large conspicuous granules.
Granulocytes (polymorphonuclear leukocytes) –
Neutrophils, eosinophils, basophils.
Agranulocytes (mononuclear leukocytes) – Lymphocytes
and monocytes.

TYPES OF WHITE BLOOD CELLS
BLOOD CELLS LIFESPAN IN BLOOD FUNCTION

FUNCTIONS OF WBCS
Usually live a few days.
Except for lymphocytes.
live for months or years.
Far less numerous than RBCs.
Leukocytosis is a normal protective response to
invaders, strenuous exercise, anesthesia and surgery.
Leukopenia is never beneficial.
General function to combat invaders by phagocytosis or
immune responses.

GRANULOCYTES
Have two types of granules – Specific granules.
Bind neutral, basic, or acidic components of dye
mixture.
Have specific functions – Azurophilic granules.
Stain purple and are lysosomes.
Have nuclei with two or more lobes.
Include neutrophils, eosinophils, basophils.
Nondividing terminal cells.

GRANULOCYTES FUNCTION
 NEUTROPHILS ( IN BACTERIAL INFECTION)
 EOSINOPHILS ( IN PARASITIC INFECTIONS OR ALLERGIES)
 BASOPHILS ( IN CHICKEN POX, SINUSITIS, DIABETES)

NEUTROPHILS
Constitute 60-70% of circulating leukocytes
12-14µm in diameter (in blood smear)
Nucleus consisting of 2-5 (usually 3) lobes connected
by fine threads of chromatin
Specific granules more abundant
Cytoplasm contain glycogen for energy production
Short lived cells with half life 6- 7 h in blood and 1-4
days in CT
 are active phagocytes

EOSINOPHILS
2-4% of leukocytes in blood.
Same size as neutrophils in blood.
Bilobed nucleus.
The main identifying characteristics is the presence of
many large and elongated refractile specific granules
(about 200/cell) that are stained by eosin.

BASOPHILS
Less than 1% of leukocytes in blood.
12-15 µm in diameter.
Nucleus is divided into irregular lobes, but the overlying
specific granules usually obscure the division.
The specific granules 0.5 µm in diameter.
Basophils may supplement the function of mast cells in
immediate hypersensitivity reactions by migrating into CT
There is some similarity between granules of basophils
and mast cells; both are metachromatic and contain
heparin and histamine.

AGRANULOCYTES
Don’t have specific granules.
Contain azurophilic granules that bind azure dyes.
The nucleus is round or indented.
Include lymphocytes and monocytes.
LYMPHOCYTES
Nucleus files most of the cell.
Play an important role in the immune response.
MONOCYTES
Largest of the white blood cells.
Function as macrophages.
Important in fighting chronic infection.
AGRANULOCYTES FUNCTION

LYMPHOCYTES
A family of spherical cells with similar morphological
characteristics.
Small lymphocytes with 6-8 µm in diameter.
Has spherical nucleus.
Its chromatin is condensed and appears as coarse
clumps.
Cytoplasm is scanty and appear as thin rim around the
nucleus.
Small number of medium-sized and large lymphocytes
with diameter up to 18 µm.
Vary in life span; some live few days and others survive
in the circulating blood for many years.
The only type of leukocytes that return from tissue back
into the blood.

Lymphocytes are the major soldiers of the immune
system.
B cells.
destroying bacteria and inactivating their toxins.
T cells.
attack viruses, fungi, transplanted cells, cancer cells
and some bacteria.
Natural Killer (NK) cells.
attack a wide variety of infectious microbes and certain
tumor cells.

MONOCYTES
Bone marrow-derived agranulocytes.
12-20 µm in diameter.
Nucleus is oval, horseshoe or kidney shaped and is
generally eccentrically placed.
The chromatin is less condensed than that of
lymphocytes, and so nucleus stain lighter.
Cytoplasm is basophilic and may contain very fine
azurophilic granules, which gives cytoplasm a bluish-gray
color.
It is not terminal cell.
When inters CT, monocytes differentiate into
macrophages.

PLATELETS/ THROMBOCYTES
200000-400000/µL.
Fragments of megakaryocyte.
Myeloid stem cells develop eventually into a
megakaryocyte.
Splinters into 2000-3000 fragments.
Each fragment enclosed in a piece of plasma
membrane.
Disc-shaped with many vesicles but no nucleus.
Help stop blood loss by forming platelet plug.
Granules contain blood clot promoting chemicals.
Short life span.
5-9 days
In stained blood smears, platelets often appear in
clumps

FUNCTIONS OF PLATELETS
Secrete vasoconstrictors which constrict blood vessels,
causing vascular spasms in broken blood vessels.
Form temporary platelet plugs to stop bleeding.
Secrete procoagulants (clotting factors) to promote
blood clotting.
Dissolve blood clots when they are no longer needed.
Play a role in hemostasis platelet plug formation. This is
important for closing minute vascular holes formed during
everyday life.
Adhesion:- platelets adhere to the exposed collagen on
the injured endothelium & to von willebrand factor.
Activation:- they undergo a stape change & become
activated & release the contents of the granules.
Aggregation:- the released ADP, PAF & Thromboxane
act to produce even more aggregation of platelets leading
to formation of platelet plug.

Blood plasma is a 'yellowish liquid' component
of blood that holds the blood cells in whole
blood in suspension. It is the liquid part of the blood that
carries cells and proteins throughout the body. It makes up
about 55% of the body's total blood volume. It is
the intravascular fluid part of extracellular fluid (all body
fluid outside cells).
It is mostly water (up to 95% by volume), and contains
important dissolved proteins (6–8%)(e.g., serum
albumins, globulins, and fibrinogen), glucose, clotting
factors, electrolytes (Na+, Ca2+, Mg2+, HCO3
−, Cl−,
etc.), hormones, carbon dioxide (plasma being the main
medium for excretory product transportation), and oxygen.
It plays a vital role in an intravascular osmotic effect that
keeps electrolyte concentration balanced and protects the
body from infection and other blood disorders
PLASMA

PLASMA PROTEINS
Albumins are the most common plasma proteins and
they are responsible for maintaining the osmotic pressure
of blood. Without albumins, the consistency of blood
would be closer to that of water. The increased viscosity
of blood prevents fluid from entering the bloodstream
from outside the capillaries.
The second most common type of protein in the blood
plasma are globulins. Important globulins include
immunoglobins which are important for the immune
system and transport hormones and other compounds
around the body.
Fibrinogen proteins make up most of the remaining
proteins in the blood. Fibrinogens are responsible for
clotting blood to help prevent blood loss

FUNCTION OF PLASMA
Fluid Exchange.
Maintenance Of Ph Buffering.
Transport Of Substances.
Hemostasis Clotting
Immunity.
Reserve Of Body Proteins.

PHYSIOLOGY OF BLOOD CLOTTING
1.INJURY TO WALL OF BLOOD VESSEL:- Injury (cut)
to a blood vessel is followed by a series of reactions
that result in the formation of a blood clot, which seals
the injured opening & prevents the loss of blood .
2.VASOCONSTRICTION:- Adhesion of blood platelets
to the exposed collagen fibers (in the wall of the
injured vessel) cause the release of serotonin from
platelets, which induces strong vasoconstriction and
decrease blood flow.

3.PLATELET PLUG FORMATION:- contact of the
platelets with collagen in the injured wall releases
thromboxane A2, which induces aggregation of more
platelets in the plug area and stimulates the formation of
platelet pseudopods . These enable the platelet
aggregates to bind together , forming a temporary plug
to stop blood loss. (platelets adhere to rough surfaces
and to each other, forming a plug).

4. CLOT FORMATION : To strengthen the plug.
Fibrinogen, a blood protein is converted to fibrin; fibrin
forms a net over the platelets. Red cells in the center and
exterior of the plug adhere to this net. The combination
of platelets and red cells entangled within a thight fibrin
net forms a blood clot, a stronger and more permanent
plug to stop blood loss.

BLOOD COAGULATION
Regulated by extrinsic (from injured tissue) and intrinsic
( from blood) mechanisms .
In extrinsic mechanism , damaged blood vessels in
the injured area release "tissue thromboplastin " , which
after a series of chemical reaction , produces "prothrombin
activator ".
In intrinsic mechanism , blood being exposed to
collagen fibers or other foreign substances after blood
vessels are opened , will release the "Hageman factor",
which will also produce the "pro thrombin activator".
"Prothrombin activator " converts prothrombin
(produced by liver) into thrombin , which in turn converts
fibrinogen into fibrins . These steps require calcium and
"clotting factors" (proteins that facilitate blood
coagulation).
To dissolve the clot, the enzyme plasmin lyses (breaks
up) the fibrin net ; plasmin is formed from an inactive
precursor , plasminogen .

FACTOR NAME SOURCE FUNCTION
i Fibrinogen liver Adhesive protein which aids in fibrin clot formation
ii Prothrombin liver
Presence in the activated form & the main enzyme of
coagulation
iii Tissue Thromboplastin
Secrete by the
damaged cells &
platelets
Lipoprotein initiator of the extrinsic of pathway
iv Calcium Bone & gut Metal cation which is important in coagulation mechanisms
v labile factor or Proaccelerin Liver & platelets
Cofactor of the activation of prothrombin to thrombin
( prothrombinase complex)
vi Accelerin - Perform Both pathway function extrinsic & intrinsic
Vii
Stable factor or Proaccelerin
precursor
liver
With the tissue factor, initiates extrinsic pathway
( factor ix & x)
Viii Antihemophilic factor
Platelets &
endothelium
Cofactor of the initiates activation of factor x
( which it the tenase complex)
ix
Christmas factor or Plasma
Thromboplastin
liver
Activator form is enzyme for intrinsic activates of factor x
( which it the tenase complex with factor viii)
x stuart-prower factor liver
Activates form is the enzyme for final the common pathway
activation of prothrobin ( form prothrombin complex with
factor ix)
xi
Plasma Thromboplastin-antecedent
(AHC)
liver Activates of intrinsic of activator of factor ix
xii Hageman factor liver
Initiase activated partial thromboplastin time (Aptt) based
intrinsic pathway activates factor xi, vii & prekallikrein
xiii Fibrin stabilizing factor liver Transmidease which cross link fibrin clot
CLOTTING FACTORS NAME, SOURCE & FUNCTION

COAGULATION CASCADE
INTRINSIC PATHWAY EXTRINSIC PATHWAY
COMMON PATHWAY

FACTORS THAT INHIBIT BLOOD CLOT
FORMATION
Smooth lining of blood vessel – prevents activation of
intrinsic blood clotting mechanism .
Prostacyclin- inhibits adherence of platelets to blood
vessel wall .
Fibrin threads- absorbs thrombin .
Antithrombin in plasma- interferes with the action of
thrombin.
Heparin from mast cells and basophils- interferes with
the formation of prothrombin activator .
Aspirin- inhibits prostaglandin production resulting in a
defective platelet release reaction .

BLOOD GROUPING
blood grouping is critical in blood transfusion , so that
agglutination (clumping of erythrocytes) caused by
binding of antigens to antibodies can be prevented
blood is grouped based on the presence of surface
proteins on erythrocytes called antigens , that are
genetically inherited .

ANTIGEN ANTIBODY
ROLE Substance that can
induce an immune
response
Proteins that
recognize and bind to
antigens
MOLECULE TYPE Usually proteins, may
also be
polysaccharides, lipids
or nucleic acids
Proteins
ORIGIN Within the body or
externally
Within the body
SPECIFIC BINDING
SITE
Epitope Paratope
IMAGE

Antigens are molecules capable of stimulating an
immune response. Each antigen has distinct surface
features, or epitopes, resulting in specific responses.
Antibodies (immunoglobins) are Y-shaped proteins
produced by B cells of the immune system in response to
exposure to antigens. Each antibody contains a paratope
which recognizes a specific epitope on an antigen, acting
like a lock and key binding mechanism. This binding
helps to eliminate antigens from the body, either by
direct neutralization or by ‘tagging’ for other arms of the
immune system.

THE ROLE OF ANTIGENS & ANTIBODIES IN
VACCINATIONS
Vaccines contain antigens which stimulate the B
lymphocytes of the immune system to respond by
producing plasma cells which secrete disease specific
antibodies (Primary response). Some of the B cells
become memory B cells, which will recognise future
exposure to the disease. This results in a faster and more
intense production of antibodies, which effectively work
to eliminate the disease by binding to the antigens
(Secondary response).

ABO BLOOD GROUPING SYSTEM
The ABO blood types were discovered by karl
landsteiner in 1901 he received the nobel prize in
physiology or medicine in 1930 for this discovery. ABO
blood types are also present in other primates such
as apes and old world monkeys.
- based on the presence of antigen A or antigen B on
the surface of RBC .
- 4 possible blood types in this system :
type A (carries antigen A ; 27-41% of population) ,
type B (carries antigen B; 10-20%),
type AB(carries both antigens A and B ; 4-7%) , and
type O (carries neither antigens ;45-50%).

Your blood group depends on which antigens occur on the
surface of your red blood cells. Your genetic make-up,
which you inherit from your parents, determines which
antigens are present on your red blood cells. Your blood
group is said to be:
A+ (A positive) if you have A and rhesus antigens.
A− (A negative) if you have A antigens but don't have
rhesus antigens.
B+ (B positive) if you have B and rhesus antigens.
B− (B negative) if you have B antigens but don't have
rhesus antigens.
AB+ (AB positive) if you have A, B and rhesus antigens.
AB− (AB negative) if you have A and B antigens but don't
have rhesus antigens.
O+ (O positive) if you have neither A nor B antigens but
you have rhesus antigens.
O− (O negative) if you don't have A, B or rhesus
antigens.
BLOOD GROUP NAMES

If you have a blood transfusion, it is vital that the blood
you receive is well matched (compatible) with your own.
For example, if you receive blood from a person who is A
positive and you are B positive then the anti-A antibodies
in your plasma will attack the red blood cells
(erythrocytes) of the donated blood. This causes the red
cells of the donated blood to clump together. This can
cause a serious or even fatal reaction in your body.
Therefore, before a blood transfusion is done, a donor
bag of blood is selected with the same ABO and rhesus
blood group as yourself. Then, to make sure there is no
incompatibility, a small sample of your blood is mixed with
a small sample of the donor blood. After a short time the
mixed blood is looked at under a microscope to see if there
has been any clumping of blood. If there is no clumping,
then it is safe to transfuse the blood.
BLOOD TRANSFUSIONS AND CROSS
MATCHING

Basically, a sample of your blood is mixed with different
samples of plasma known to contain different antibodies.
For example, if plasma which contains anti-A antibodies
makes the red cells in your blood (erythrocytes) clump
together, you have A antigens on your blood cells. Or, if
plasma which contains rhesus antibodies makes the red
cells in your blood clump together, you have rhesus
antigens on your blood cells. By doing a series of such
tests it is possible to determine what antigens are on
your red blood cells and therefore determine your blood
group.
Routine blood grouping checks for your ABO and rhesus
status. Other red cell antigens are tested for in certain
other situations.
BLOOD GROUP TEST

BLOOD GROUP & TRANSFUSION
Antigens are synthesized during fetal development .
about 2-8 months after birth , the immune system will
spontaneously develop specialized proteins called
antibodies to be "compatible" with these antigens : type
A develops anti-B antibodies , type B developed anti-A
antibodies , type AB will have no antibodies and type O
develops both anti-A and antiB antibodies .
Type O, the universal donor , can be donated to any
other blood groups since it has no antigens and will cause
only minimal agglutination . by the same token , type AB
, the universal recipient , can receive blood from any
other blood groups since it has no antibodies to bind to
the donor's antigens and will also cause minimal
agglutination .

A blood group test is always done on pregnant women. If
the mother is rhesus negative and the unborn baby is
rhesus positive (inherited from a rhesus positive father)
then the mother's immune system may produce anti-
rhesus antibodies. These may attack and destroy the
baby's blood cells. This is rarely a problem in a first
pregnancy. However, without treatment, this can become
a serious problem in subsequent pregnancies, as the
mother's immune system will be 'sensitised' after the first
pregnancy.
BLOOD GROUPS AND PREGNANCY

THE RHESUS SYSTEM
RH BLOOD GROUPING
"Rh" is named after the rhesus monkey , whom we did
the scientific research on this blood grouping .
In addition to antigens A and B , erythrocytes might
also carry another surface protein called Rh factor .
10 Rh factors have been found in human blood , the
most important one for transfusion purposes is antigen D
people who carry Rh factors are Rh+ (85-100% of
population), while people who don't have Rh factors are
Rh- .

The red blood cell membrane antigen important here is
the Rhesus (Rh) antigen, or Rhesus factor. About 85% of
people have this antigen; they are Rhesus positive (Rh+)
and do not therefore make anti-Rhesus antibodies. The
remaining 15% have no Rhesus antigen (they are Rhesus
negative, or Rh−). Rh− individuals are capable of making
anti-Rhesus antibodies, but are stimulated to do so only
in certain circumstances, e.g. in pregnancy, or as the
result of an incompatible blood transfusion.

RH positive
man
Rh negative
woman with Rh
positive fetus
RH positive fetus
antigen can enter
the mother’s blood
during delivery
Mother will
produce
antiRh
antibodies
In the next Rh
positive pregnancy
mother’s antiRh
antibodies will attack
fetal red blood cells

Hemorrhage (bleeding): Blood leaking out of blood
vessels may be obvious, as from a wound penetrating the
skin. Internal bleeding (such as into the intestines, or
after a car accident) may not be immediately apparent.
Hematoma: A collection of blood inside the body tissues.
Internal bleeding often causes a hematoma.
Leukemia:A form of blood cancer, in which white blood
cells multiply abnormally and circulate through the blood.
The abnormal white blood cells make getting sick from
infections easier than normal.
Multiple myeloma: A form of blood cancer of plasma
cells similar to leukemia. Anemia, kidney failure and high
blood calcium levels are common in multiple myeloma.

THALASSEMIA
The thalassemias are a group of inherited blood disorders
in which the genes that produce hemoglobin, the protein
in red blood cells that carries oxygen from the lungs to all
parts of the body, are broken. As a result, the red blood
cells do not contain enough hemoglobin,
causing anemia that can range from mild to life
threatening. Thalassemia can come in different forms
depending on the genetic mutations causing it. The
transfusion-dependent form, also called thalassemia
major or Cooley’s Anemia, requires lifelong follow-up care
and regular blood transfusions. Some other forms are
more readily managed and may require little or no
treatment.

THROMBOSIS (BLOOD CLOTS) IN CHILDREN
A thrombosis is a blood clot that develops within veins or
sometimes arteries in the body. Thrombosis may be
serious or inconvenient and often occurs as a
complication of a procedure, medication, or other
disease. Left untreated, a thrombosis can cause long-
term problems, such as chronic swelling, pain, or even
permanent damage to internal organs.
Thrombophilia refers to anything that increases one’s
tendency to develop blood clots. Thrombosis in children is
uncommon and is most often seen in children with
complex medical problems or procedures. Thrombophilia
can be considered the opposite of hemophilia, a disorder
that prevents blood from clotting.

Autoimmune hemolytic anemia (AIHA) is a rare red blood
cell disorder that occurs when antibodies directed against
a person’s own red blood cells cause them to burst,
leading to insufficient concentration in the blood. When
this happens, the lifetime of red blood cells decrease from
100 to 120 days to just a few days in serious cases.
Intracellular components of red blood cells are then
released into the circulating blood and tissue, causing
characteristic symptoms.
The causes of autoimmune hemolytic anemia are poorly
understood. It may be a primary disorder or secondary to
an underlying illness, such as Epstein-Barr
Virus, lymphoma, lupus, immunodeficiency
disorders, rheumatoid arthritis or ulcerative colitis. AIHA
may also be a component of Evans Syndrome, an
autoimmune disease that affects more than one blood cell
line.
AUTOIMMUNE HEMOLYTIC ANEMIA

Lymphoma: A form of blood cancer, in which white blood
cells multiply abnormally inside lymph nodes and other
tissues. The enlarging tissues, and disruption of blood's
functions, can eventually cause organ failure.
Anemia: An abnormally low number of red blood cells in
the blood. Fatigue and breathlessness can result,
although anemia often causes no noticeable symptoms.
Hemolytic anemia: Anemia caused by rapid bursting of
large numbers of red blood cells (hemolysis). An immune
system malfunction is one cause.
Hemochromatosis: A disorder causing excessive levels
of iron in the blood. The iron deposits in the liver,
pancreas and other organs, causing liver problems and
diabetes.

Sickle cell disease: A genetic condition in which red
blood cells periodically lose their proper shape (appearing
like sickles, rather than discs). The deformed blood cells
deposit in tissues, causing pain and organ damage.
Bacteremia: Bacterial infection of the blood. Blood
infections are serious, and often require hospitalization
and continuous antibiotic infusion into the veins.
Malaria: Infection of red blood cells by Plasmodium, a
parasite transmitted by mosquitos. Malaria causes
episodic fevers, chills, and potentially organ damage.
coronary arteries, which supply blood to the heart.
Thrombocytopenia: Abnormally low numbers of
platelets in the blood. Severe thrombocytopenia may lead
to bleeding.

Leukopenia: Abnormally low numbers of white blood
cells in the blood. Leukopenia can result in difficulty
fighting infections.
Disseminated intravascular coagulation (DIC): An
uncontrolled process of simultaneous bleeding and
clotting in very small blood vessels. DIC usually results
from severe infections or cancer.
Hemophilia: An inherited (genetic) deficiency of certain
blood clotting proteins.
Frequent or uncontrolled bleeding can result from
hemophilia.
Hypercoaguable state: Numerous conditions can result
in the blood being prone to clotting. A heart attack,
stroke, or blood clots in the legs or lungs can result.

Polycythemia: Abnormally high numbers of red blood
cells in the blood. Polycythemia can result from low blood
oxygen levels, or may occur as a cancer-like condition.
Deep venous thrombosis (DVT): A blood clot in a deep
vein, usually in the leg.
DVTs are dangerous because they may become dislodged
and travel to the lungs, causing a pulmonary embolism
(PE).
Myocardial infarction (MI): Commonly called a heart
attack, a myocardial infarction occurs when a sudden
blood clot develops in one of the

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