BLOOD

Part 2
 HEMOSTASIS
• Stoppage of bleeding
• Vitally important when blood vessels are
damaged
• Following an injury to a blood vessel, several
actions occur to help limit or prevent blood
loss
• Includes: blood vessel spasm, platelet plug
formation and blood coagulation
 Blood Vessel Spasm
• Smaller blood vessel cut or breaks smooth
muscles contract ( vasospasm)  blood loss
lessens immediately
• May last for a few minutes; but effect usually
continues for about 30 minutes
• Platelet plug is formed and blood is coagulating
• Platelets release serotonin which contracts
smooth muscles in the blood vessel walls
 Platelet Plug Formation
• Platelets adhere to any rough surface and to
collagen in connective tissue underlying the
endothelial lining of blood vessels
• Platelets also adhere to each other forming a
platelet plug
• Plug may control blood loss from a small break
• Larger breaks require a blood clot to halt
bleeding
 Blood Coagulation
• Clotting mechanism
• Coagulation – formation of a blood clot
• When larger vessels are damaged, the
constriction of the smooth muscles in the blood
vessel walls only slows down blood loss and the
clotting mechanism takes over
• Is complex and utilizes many biochemicals called
clotting factors ( some promote coagulation and
others inhibit it)
 Stages of the Clotting Mechanism
• First stage:
 Platelets aggregate or clump together at the
site of injury
 The damaged tissue release thromboplastin to
initiate a series of reactions
 These activities require the presence of Ca
ions and certain proteins and phospholipids
• Second stage:
 A plasma protein produced by the liver called
prothrombin is converted into thrombin in the
presence of Ca++ ions
 Thrombin , in turn, catalyzes a reaction that
cuts fibrinogen into pieces of fibrin
• Third stage:
 fibrinogen, another plasma protein, which is
soluble is then converted into insoluble fibrin
 Fibrin then forms long threads that act like a
fish net in the site of injury
 The fibrin then forms the clot
 As clot is formed, blood cells and platelets get
enmeshed/entrapped in the fibrin threads
forming a mass as a blood clot blocking the
break and prevent further blood loss
• In a few minutes or so, the clot will retract 
syneresis  tightening of the fibrin clot in
such a way that the ruptured area of the blood
vessel gets smaller and smaller to decrease
hemorrhage
• The clear yellowish fluid seen after clot if
formed is called serum
• As hemorrhage is stopped  blood vessel
tissues repair themselves by mitotic cell
division
• Once the tissue is repaired, fibrinolysis occurs
(dissolution of the blood clot)  caused by a
plasma protein that digests the fibrin threads
and other proteins associated with the
formation of the clot
• Fibroblasts invade blood clots that form in
ruptured vessels producing fibrous connective
tissue  help strengthen and seal vascular
breaks
• Many clots including those that form in tissues
as a result of blood leakage (hematomas)
disappear in time
• Occasionally, unwanted clotting may occur in
undamaged blood vessel
• Brought about by cholesterol-containing mass
called plaque  adheres to the smooth walls of
blood vessels  results in a rough surface ideal
for adhesion of platelets
• Too much cholesterol in the diet ( fatty food) 
form these plaques  may form as thrombus
• Thrombus may dissolve; clotting is such
unbroken vessel as thrombosis
• If it remains intact  can damage tissues
beneath it  cut off oxygen supplies  may
get dislodged and gets transported by the
bloodstream called an embolus  may
dislodge and gets transported and cuts off
circulation  embolism
• If brain is affected  cerebral thrombosis
• If heart is affected  coronary thrombosis
• If the tissues die  infarction (often fatal)
• A blood clot that travels and blocks a vessel
that supplies a vital organ such as the lungs 
pulmonary embolism
• Hemophilia – genetically inherited clotting
disorder (clotting factor VIII) inherited from the
mother and passed down to the male children
- most common form is Hemophilia A;
tendency to hemorrhage following minor
injuries; frequent nosebleeds, hematomas is
muscles, bloody urine; may also bleed inside
body (knees, ankles, elbows)
• Von Willebrand disease – inherited clotting
disorder; tendency to bleed and bruise easily
• Can cause spontaneous bleeding
 Blood Groups and Transfusions
• Human blood is of different types and only
certain combinations of these blood types are
compatible
• Procedures were developed for typing blood
to ensure that donor and recipient blood
transfusions are compatible
 Antigens and Antibodies
• If blood groups are mismatched  agglutination
occurs  clumping of red blood cells 
transfusion reaction  reaction between
protein antibodies (formerly called agglutinins)
in the blood plasma and RBC surface molecules
called antigens (formerly called agglutinogens)
• Transfusion reactions include: headache,
difficulty in breathing, face appear flushed,
accompanying pain in the neck, chest and lower
back
• The RBCs will be destroyed (phagocytized by
macrophages)
• Their hemoglobin converted to bilirubin which
accumulates causing jaundice
• The kidneys may fail (free Hgb)
• Only a few of the many antigens on RBC
membranes can produce serious transfusion
reactions  includes the antigen of the ABO
group and those of the Rh group
• Avoiding mixture of certain kinds of antigens
and antibodies prevents adverse reactions
 ABO Blood Group
• Based on the presence or absence of two
major protein antigens on RBC membranes 
antigen A and antigen B
• A person has on their RBC surfaces one of the
4 antigen combinations  only A, only B, both
A and B, or neither A nor B  inherited
• A person with only antigen A has type A blood
• A person with only antigen B has type B blood
• If with both antigen A and antigen B, type AB
• If with neither antigen A nor B, type O blood
• Thus, all humans have one of four possible
ABO blood types – A, B, AB, or O
• Certain antibodies that affect the ABO blood
group are synthesized in the plasma about 2-8
months after birth  antibodies are formed
during infancy against the ABO antigens not
present in our own RBCs
• Type A blood  antibody anti-B in their plasma
• Type B blood  antibody anti-A in their plasma
• Type AB  no antibody
• Type O  have both antibody anti-A and anti-B
• An antibody of one type will react with an
antigen of the same type and cause
agglutination
• Therefore :
- type A (anti-B) blood must not receive blood
of type B or AB
- type B (anti-A) blood must not receive blood
of type A or AB
- type O (anti- A and anti-B) must not receive
type A, B or AB blood; but can donate to type
A, B and AB  universal donor
- type AB (no anti-A and anti-B) can receive
blood of any type  universal recipient
 Rh Blood Group
• Named after the rhesus monkey in which it
was first studied
• Humans  includes several Rh antigens; most
important is antigen D
• If any of the antigen D and other Rh antigens
are present on the RBC membranes  Rh +
• If the RBCs lack Rh antigens  blood is Rh –
• Like antigens A and B, presence (or absence) of Rh
antigens is inherited trait
• But antibodies for Rh (anti-Rh) do not appear
spontaneously  form only in Rh negative
persons in response to a special stimulation
• If Rh – person receives Rh+ blood  Rh antigens
will stimulate the recipient’s antibody cells to
produce anti-Rh antibodies
• Initial transfusion no serious consequences; but
recipient is sensitized (become sensitive) to Rh+
blood if 2nd transfusion occur  some months
later donated blood will agglutinate
• If mother is Rh – and father is Rh +  child is Rh +
• Cells of fetus enter mother’s bloodstream 
develop antibodies to fight Rh+ blood cells
• First pregnancy, no serious consequences
• On 2nd pregnancy, the mother’s antibodies (anti-
Rh called hemolysins) will croos the placental
membrane  destroy the fetal RBCs  fetus
develops a condition as erythroblastosis fetalis
(hemolytic disease of the newborn ( anemic, brain
damage, kidney and heart failure and possible
death)
• Mother can be given immunoglobulin
(RhoGAM)
• Blood transfusion, IV, monitor breathing
• Exchange transfusion