Hemostasis is the process by which bleeding is stopped. It involves three main mechanisms: vascular spasm, platelet plug formation, and blood clotting. Vascular spasm causes constriction of damaged blood vessels. Platelets adhere to the site of injury and aggregate to form a platelet plug. The blood clotting process is a cascade of coagulation factors that results in the formation of a fibrin clot to seal the damaged vessel. Precise control mechanisms regulate hemostasis to prevent excessive clotting while still stopping bleeding.

1. Hemostasis:

2. Hemostasis:
• Sequence of responses that stops bleeding.
• When blood vessels are damaged or ruptured, the
hemostatic response must be quick, localized to the
region of damage, and carefully controlled in order to
be effective.
• 3 mechanisms reduce blood loss:
• 1. vascular spasm.
• 2. platelet plug formation.
• 3. blood clotting.
• When successful, hemostasis prevents h’gge (the loss
of a large amount of blood from the vessels).

4. • Hemostatic mechanisms can prevent h’gge from
smaller blood vessels, but extensive h’gge from larger
vessels usually requires medical intervention.
• Vascular spasm:
• When arteries or arterioles are damaged, the circularly
arranged smooth muscle in their walls contract
immediately, a reaction called ‘vascular spasm’.
• This reduces blood loss for several minutes to several
hours, during which time the other hemostatic
mechanisms go into operation.
• The spasm is probably caused by damage to the
smooth muscle, by substances released from activated
platelets, and by reflexes initiated by pain receptors.

5. • Platelet plug formation:
• Platelets store an impressive array of chemicals.
• Within many vesicles are clotting factors, ADP, ATP,
Ca2+, and serotonin.
• Also present are enzymes that produce TXA2; fibrin
stabilizing factor – helps to strengthen a blood clot;
lysosomes; some mitochondria; membrane systems
that take up and store calcium and provide channels
for release of the contents of granules; and glycogen.
• Also within platelets is ‘platelet-derived growth factor’
– hormone that can cause proliferation of vascular
endothelial cells, vascular smooth muscle fibers, and
fibroblasts to help repair damaged blood vessels.

6. • Platelet plug formation occurs as follows:
• 1. initially, platelets contact and stick to parts of a
damaged blood vessel, such as collagen fibers of the
connective tissue underlying the damaged endothelial
cells. This process is called ‘platelet adhesion’.
• 2. due to adhesion, the platelets become activated, and
their characteristics change dramatically. They extend
many projections that enable them to contact and
interact with one another, and they begin to liberate
that contents of their vesicles. This phase is called the
‘platelet release reaction’.
• Liberated ADP and TXA2 play a major role by
activating nearby platelets.

8. • Serotonin and TXA2 function as VCs, causing and
sustaining contraction of vascular smooth muscle,
which decreases blood flow through the injured vessel.
• 3. the release of ADP makes other platelets in the area
sticky, and the stickiness of the newly recruited and
activated platelets causes them to adhere to the
originally activated platelets. This gathering of
platelets is called ‘platelet aggregation’.
• Eventually, the accumulation and attachment of large
no.of platelets form a mass called a ‘platelet plug’.

9. • Platelet plug – very effective in preventing blood
loss in a small vessel. Initially the platelet plug is
loose, it becomes quit reinforced by fibrin
threads formed during clotting. Can stop blood
loss completely if the hole in a blood vessel is not
too large.

10. Blood clotting:
• Blood remains in its liquid form as long as it remains
within its vessels.
• When drawn from the body, it thickens and forms a
gel. Gel separates from the liquid.
• Straw colored liquid: ‘serum’.
• Serum = plasma – clotting proteins.
• Gel is called a ‘clot’.
• Consists of a network of insoluble protein fibers called
‘fibrin’ in which the formed elements of blood are
trapped.
• Process of gel formation: clotting or coagulation.

12. • Series of chemical reactions that culminates in
formation of fibrin threads.
• If blood clots too easily, the result can be ‘thrombosis’
– clotting in an undamaged blood vessel.
• If the blood takes too long to clot, h’gge can occur.
• Clotting involves several substances known as ‘clotting
factors’.
• These factors include calcium ions, several inactive
enzymes that are synthesized by hepatocytes and
released into the bloodstream, and various molecules
associated with platelets or released by damaged
tissues.

13. Number Name Source Pathway of
activation:
I Fibrinogen Liver Common
II Prothrombin Liver Common
III Tissue factor
thromboplastin
Damaged tissue and
activated platelets.
Extrinsic
IV Calcium ion Diet, bones, and
platelets.
All
V Proacclererin, labile factor
or acclerator globulin
Liver and platelets Extrinsic and
intrinsic.
VII Serum prothrombin
conversion acclerator
liver extrinsic

14. Number Name Source Pathways of
activation:
VIII Antihemophilic factor A ,
antihemophilic globulin
Liver Intrinsic
IX Christmas factor or
antihemophiic factor B
Liver Intrinsic
X Stuart factor or
thrombokinase
Liver Extrinsic and intrinsic
XI Plasma thromboplastin
actecedent or antihemophilic
factor C
Liver Intrinsic
XII Hageman factor Liver Intrinsic
XIII Firbin stabilising factor Liver and
platelets
common

15. • Clotting is a complex cascade of enzymatic reactions in
which each clotting factor activates many molecules of
the next one in a fixed sequence.
• Finally, a large quantity of product (the insoluble
protein fibrin) is formed.
• Clotting can be divided into 3 stages:
• 1. 2 pathways, called the ‘extrinsic pathway’ and
‘intrinsic pathway’ lead to the formation of
prothrombinase.
• Once prothrombinase is formed, the steps involved in
the next 2 stages of clotting are the same for both the
pathways, and together these 2 stages are referred to
as the ‘common pathway’.

16. • 2. prothrombinase converts prothrombin into the
enzyme thrombin.
• 3. thrombin converts soluble fibrinogen into insoluble
fibers. Fibrin forms the threads of the clot.
• Extrinsic pathway:
• Fewer steps and occurs rapidly.
• Upon injury, tissue protein called ‘tissue factor’, also
known as ‘thromboplastin’, leaks into the blood from
cells to outside blood vessels.
• Initiates formation of prothrombinase.
• TF is a complex mixture of lipoproteins and
phospholipids released from the surfaces of damaged
cells.

18. • In the presence of Ca2+, TF begins a sequence of
reactions that ultimately activates clotting factor X.
• Once factor X is activated, it combines with factor V in
the presence of Ca2+ to form the active enzyme
prothrombinase, completing the extrinsic pathway.
• Intrinsic pathway:
• Complex; occurs slowly taking several minutes.
• Activators: are either in direct contact with blood or
contained within blood.
• Outside tissue damage isn’t needed.
• If endothelial cells become roughened or damaged,
blood can come in contact with collagen fibers in the
connective tissue around the endothelium of the blood
vessel.

19. • In addition, trauma to endothelial cells causes damage
to platelets, resulting in the release of phospholipids
by the platelets.
• Contact with collagen fibers activates clotting factor
XII, which begins a sequence of reactions that
eventually activates clotting factor X.
• Platelet phospholipids and Ca2+ can also participate
in the activation of factor X.
• Once factor X is activated, it combines with factor V to
form the active enzyme prothrombinase , completing
the intrinsic pathway.

21. • Common pathway:
• Formation of prothrombinase marks the beginnning
of the common pathway.
• In the second stage of blood clotting, prothrombinase
and Ca2+ catalyze the conversion of prothrombin to
thrombin.
• 3rd stage: thrombin, in the presence of Ca2+, converts
fibrinogen, which is soluble to loose fibrin threads,
which are insoluble.
• Thrombin also activates factor XIII, which strengthens
and stabilizes the fibrin threads into a sturdy clot.
• Plasma contains some factor XIII, which is also
released by platelets trapped in the clot.

22. • Thrombin has 2 positive feedback effects.
• 1st feedback loop, which involves factor V, it
accelerates the formation of prothrombinase.
• Prothrombinase, in turn, acclerates the production of
more thrombin, and so on.
• 2nd positive feedback loop: thrombin activates
platelets which reinforces their aggregation and the
release of platelet phopholipids.
• Clot retraction:
• Consolidation or tightening of the fibrin clot.
• Fibrin threads attached to the damaged surfaces of the
bv gradually contract as platelets pull on them.

23. • As the clot retracts, it pulls the edges of the damaged
bv closer together, decreasing the further damage.
• During retraction, some serum can escape b/n
threads, but the formed elements cannot.
• Normal retraction depends on an adequate no.of
platelets in the clot, which release factor XIII and
other factors, thereby strengthening and stabilizing
the clot.
• Permanent repair of the bv can then take place.
• In time, fibroblasts form connective tissue in the
ruptured area, and new endothelial cells repair the
vessel lining.

24. Role of vitamin K in clotting:
• Normal clotting depends on adequate level of vitamin
K in the body.
• Although vitamin K is not involved in actual clot
formation, it is required for the synthesis of 4 clotting
factors.
• Normally produced by bacteria that inhibit the large
intestine, vitamin K is a fat soluble vitamin that can be
absorbed through the lining of the intestine and into
the blood if absorption of lipids is normal.
• People suffering from disorders that slow absorption
of lipids often experience uncontrolled bleeding as a
consequence of vit. K deficiency.

25. Hemostatic control mechanisms:
• Many times a day little clots start to form, often at a
site of minor roughness or at a plaque.
• Clots have a tendency to enlarge due to positive
feedback cycles – impairment of blood flow through
undamaged vessels.
• Fibrinolytic system:
• Dissolves small, inappropriate clots.
• Also dissolves clots at a site of damage once the
damage is repaired.
• Dissolution of a clot is called ‘fibrinolysis’.

26. • When a clot is formed, an inactive plasma enzyme
‘plasminogen’ is incorporated into the clot.
• Both body tissues and blood contain substances that
can activate plasminogen to plasmin, an active plasma
enzyme.
• Activators: thrombin, activated factor XII, and tissue
plasminogen activator, which is synthesized in
endothelial cells of most tissues and liberated into the
blood.
• Once plasmin is formed, it can dissolve the clot by
digesting fibrin threads and inactivating subs. Such as
fibrinogen, prothrombin, and factors V and XII.

29. • Why doesn’t clot formation spreads into general
circulation??
• 1. fibrin absorbs thrombin into the clot.
• 2. dispersal of some of the clotting factors by the
blood, their concentrations aren’t high enough to
bring about widespread clotting.
• Other controls:
• Endothelial cells and WBC produce prostagladins
called ‘prostacyclin’ that opposes the actions of TXA2.
• Powerful inhibitor of platelet adhesion and release.
• Subs. That delay, suppress, or prevent blood clotting,
called ‘anticoagulants’, are present in blood.

30. • Include antithrombin – blocks action of several
factors, including XII, X and II.
• Heparin, an anticoagulant that is produced by mast
cells and basophils, combines with antithrombin and
increase effectiveness in blocking thrombin.
• Another anticoagulant, activated protein C, inactivates
the 2 major clotting factors not blocked by
antithrombin, and enhances activity of plasminogen
activators.
• Babies that lack the ability to produce APC due to a
genetic mutation usually die of blood clots in infancy.

31. • Anticoagulants:
• Patients who are at risk of forming blood clots amy
receive anticoagulants.
• E.g: heparin or warfarin.
• Heparin: administered during hemodialysis and open-
heart surgery.
• Warfarin: antagonist to vitamin K and thus blocks
synthesis of 4 clotting factors.
• Slower acting than heparin.
• To prevent clotting in donated blood, blood banks and
labs often add substances that remove Ca2+.
• E.g: EDTA – ethylene diamine tetraacetic acid, and
CPD – citrate phosphate dextrose.

32. Intravascular clotting:
• Despite anticoagulating and fibrinolytic systems,
blood clots sometimes form within the CVS.
• May be initiated by roughened endothelial surfaces of
a bv resulting in atherosclerosis, trauma or infection.
• Induce the adhesion of platelets.
• May also form when blood flows too slowly, allowing
clotting factors to accumulate locally in high enough
concentrations to initiate coagulation.
• Clotting in a unbroken vessel: thrombosis.
• Clot itself is called thrombus and it can dissolve
spontaneously.

33. • If it remains intact, the thrombus may become
dislodged and be swept away in the blood.
• A blood clot, air bubble, fat from broken bones, or a
piece of debris transported by the blood stream:
‘embolus’.
• An embolus that breaks away from an arterial wall
may lodge in a smaller-diameter artery downstream
and block blood flow to a vital organ.
• When an embolus lodges in the lungs – ‘pulmonary
embolism’.

34. • Aspirin:
• In pts. With heart and blood vessel disease, the events
of hemostasis may occur even without external injury
to a blood vessel.
• At low doses, aspirin inhibits vasoconstriction and
platelet aggregation by blocking synthesis of TXA2.
• Also reduces the chance of thrombus formation.
• Reduces risk of transient ischemic attacks, MO,
strokes, and blockage of peripheral arteries.
• Thrombolytic agents:
• Chemical substances that are injected into the body to
dissolve blood clots that have already formed to
restore circulation.

35. • Either directly or indirectly activate plasminogen.
• First agent approved for use: streptokinase –
produced by streptococcal bacteria.
• Genetically engineered version of human tissue
plasminogen activator (t-PA) is now used to treat
victims of heart attacks and brain attacks that are
caused by blood clots.

36. Blood groups and blood types:
• Surfaces of RBC contain a genetically determined
assortment of ‘antigens’ composed of glycoproteins
and glycolipids.
• Called ‘agglutinogens’ – occur in characteristic
combinations.
• Based on presence or absence of various antigens,
blood is categorized into different ‘blood groups’.
• 24 blood groups and more than 100 antigens on RBC
surface.
• 2 major blood groups – ABO and Rh
• Others – lewis, kell, kidd and duffy systems.

37. ABO blood group:
• Based on 2 glycolipid antigens called A and B.
• People whose RBCs display only antigen A have ‘type
A’ BLOOD.
• Those who have only antigen B are ‘type B’.
• Who have both – ‘type AB’.
• Neither – ‘type O’.
• Blood plasma usually contains ‘antibodies’ called
‘agglutinogens’ that react with A or B antigens if the
two are mixed.
• These are the ‘anti A antibody’, which reacts with
antigen A, and the ‘anti B antibody’, which reacts with
antigen B.

40. • We don’t have antibodies that react with the antigens
of our own RBCs.
• Instead we have antibodies for any antigens that our
RBCs lack.
• E.g: blood type B
• Antigens: type B.
• Anti A antibodies.
• Antibodies are large IgM type – they don’t cross
placenta.
• ABO incompatibility b/n mother and fetus rarely
occurs.

41. Transfusions:
• Transfusion : transfer of whole blood or blood
components into the bloodstream or directly into the
red bone marrow.
• Most often given to treat anemia, to increase blood
volume, or to improve immunity.
• Incompatible transfusion: antibodies in the recipient’s
plasma bind to the antibodies on the donated RBCs,
which causes agglutination or clumping of the RBCs.
• Agglutination: antigen-antibody response in which
RBCs become cross linked to one another.
• When these complexes form, they activate plasma
proteins of the complement family.

42. • Activated complement damages plasma membrane of
RBCs – leaky – hemolysis of the RBCs and the release
of Hb into the blood plasma.
• Liberated Hb may cause kidney damage by clogging
the filtration membranes.

43. • Type A person received type B blood.
• Type A blood: type A antigen and anti-B antibody +.
• Type B blood: type B antigen and anti-A antibody +.
• 2 things can happen:
• 1. anti-B antibodies in the recipient's plasma can bind
to the B antigens on the donor’s RBC, causing
agglutination and hemolysis of the RBC.
• 2. anti-A antibodies in the donor’s plasma can bind to
the A antigens on the recipient’s RBC, a less serious
reaction coz the donor’s anti-A antibodies become so
diluted in the recipient’s plasma that they don’t cause
significant agglutination and hemolysis of recipient’s
RBCs.

44. Characterist
ic
Blood type
A B AB O
Agglutinogen
(antigen) on
RBC
A B Both A and B Neither A nor
B
Agglutinin
(antibody) in
plasma
Anti-B Anti-A Neither anti-A
nor anti-B.
Both anti-A
and anti-B.
Compatible
donor blood
types
A,O B,O A,B,AB,O O
Incompatible
blood groups
B,AB A, AB ------ A,B,AB.

45. • People with type AB – universal recipients because
theoritically they can receive blood from donors of all
4 types.
• They have no antibodies to attack antigens on donated
RBCs.
• Blood group O: universal donors coz theoretically they
can donate blood to all four groups.
• In practice, its dangerous and misleading.
• Blood contains antigens and antibodies other than
those associated with the ABO system that can cause
transfusion problems.
• Thus blood should be carefully cross matched or
screened before transfusion.

46. Rh blood group:
• Antigen was discovered in the blood of the rhesus
monkey.
• Alleles of 3 genes may code for the Rh antigen.
• People whose RBCs have Rh antigens are designated
as Rh+; those who lack Rh-.
• Normally, blood plasma doesn’t contain anti-Rh
antibodies.
• If an Rh- person receives an Rh+ blood transfusion,
the immune system starts to make anti-Rh antibodies
that will remain in the blood.
• If a second transfusion of Rh+ blood is given later, the
previously formed anti-Rh antibodies will cause
agglutination and hemolysis of the RBCs in donated
blood, and a severe reaction may occur.

47. Hemolytic disease of newborn:
• Most common problem with Rh compatibility.
• Arise during pregnancy.
• Normally, no direct contact occurs between maternal
and fetal blood while a woman is pregnant.
• If small amount of Rh+ blood leaks form the fetus
through the placenta into the blood stream of an Rh-
mother, the mother will start to make anti-Rh
antibodies.
• Greatest possibility of fetal blood leakage into the
maternal circulation occurs at delivery, the firstborn
baby usually is not affected.

48. • If the mother becomes pregnant again, her anti-Rh
antibodies can cross the placenta and enter the blood
stream of the fetus.
• If the fetus is Rh-, there is no problem coz Rh- blood
doesn’t have the Rh antigen.
• If the fetus is Rh+, agglutination and hemolysis
brought on by fetal-maternal incompatilibity may
occur.
• RX: an injection of anti-Rh antibodies called ‘anti-Rh
gamma globulin can be given to prevent HDN.
• All Rh- women should receive RhoGAM soon after
every delivery, miscarriage or abortion.

50. • These antibodies bind to and inactivate the fetal
Rh antigens before the mother’s immune system
can respond to the foreign antigens by
producing her own anti-Rh antibodies.

51. Typing and cross matching blood for
transfusion:
• ABO blood typing: single drops of blood are mixed
with different antisera, solutions that contain
antibodies.
• One drop of blood is mixed with anti-A serum, which
contains anti-A antibodies that will agglutinate RBCs
that possess A antigens.
• Another drop is mixed with anti-B serum, which
contains anti-B antibodies that will agglutinate RBC
that possess B antigens.
• If the RBC agglutinate only when mixed with anti-A
serum, the blood is ‘type A’.

52. • If the RBC agglutinate only when mixed with anti-B
serum, the blood is ‘type B’.
• The blood is type AB if both drops agglutinate, if
neither drop agglutinates, the blood is type O.
• Determining Rh factor:
• A drop of blood is mixed with antiserum containing
antibodies that will agglutinate RBCs displaying Rh
antigens.
• If the blood agglutinates, it is Rh+, no agglutination
indicates Rh-.
•

55. • Cross matching:
• The possible donor RBCs are mixed with the
recipient’s serum.
• If agglutination doesn’t occur, the recipient doesn’t
have antibodies that will attack the donor RBCs.
• Alternatively, the recipient’s serum can be screened
against a test panel of RBCs having antigens known to
cause blood transfusion reactions to detect any
antibodies that may be present.

56. Anemia:
• Condition in which O2 carrying capacity of blood is
decreased.
• Characterized by reduced no.of RBCs or a decreased
amount of Hb in the blood.
• Person feels fatigued and is intolerant of clod, both of
which are related to lack of O2 needed for ATP and
heat production.
• Skin appears pale, due to the low content of red-
colored hemoglobin circulating in skin blood vessels.

57. • 1. iron deficiency anemia:
• Inadequate absorption of iron, excessive loss of iron,
increased iron requirement, or insufficient intake of
iron.
• Most common type of anemia.
• Women have a greater risk for iron-deficiency due to
menstrual blood losses and increased demands of the
growing fetus during pregnancy.
• GI loses (malignancy, ulceration) – also contributes to
this type.

59. • 2. megaloblastic anemia:
• Inadequate intake of vitamin B12 or folic acid.
• Red bone marrow produces large, abnormal red blood
cells.
• 3. pernicious anemia:
• Insufficient hemopoiesis – due to inability of stomach
to produce intrinsic factor, needed for absorption of
vit. B12 in small intestine.

60. • 4. hemolytic anemia:
• RBC plasma membranes rupture prematurely.
• Released hemoglobin pours into the plasma and may
damage the filtering units in the kidneys.
• Condition may result form inherited defects such as
abnormal red blood cell enzymes, or from outside
agents such as parasites, toxins or antibodies from
incompatible transfused blood.

61. • 5. h’ggic anemia:
• Excessive loss of RBCs though blooding resulting from
large wounds, stomach ulcers, or esp. heavy
menstruation.
• 6. thalassemia:
• Group of hereditary hemolytic anemias.
• RBCs are small (microcytic), pale (hypochromic), and
short lived.
• 7. aplastic anemia:
• Destruction of red bone marrow.
• Caused by toxins, gamma radiation and certain
medications that inhibit enzymes needed for
hemopoiesis.

62. Sickle cell disease:
• RBCs of a person with SCD contain Hb-S, an
abnormal kind of hemoglobin.
• When Hb-S gives up O2 to the interstitial fluid, it
forms long, stiff, rodlike structures that bend the
erythrocyte into a sickle shape.
• Sickled cells rupture easily.
• Even though erythropoiesis is stimulated by the loss of
the cells, it cannot keep pace with hemolysis.
• People with SCD always have some degree of anemia
and mild jaundice and may experience joint or bone
pain, breathelessness, rapid HR, abdominal pain,
fever, and fatigue as a result of tissue damage.

64. • Any activity that reduces the amount of O2 in the
blood, such as vigorous exercise, may produce a ‘sickle
cell crisis’ (worsening of the anemia, pain abd, and
pain in long bones of the limbs, fever, and shortness of
breathe).
• SCD is inherited.
• People with 2 sickle cell genes have severe anemia;
those with only one defective gene have minor
problems.
• Persons wit SCD are resistance to malaria??
• The gene responsible for the tendency of the RBCs to
sickle also alters the permeability of the plasma
membranes of sickled cells, causing potassium ions to
leak out.

66. • Low levels of potassium kill the malaria parasites that
may infect sickled cells.
• A person with one normal gene and one sickle cell
gene has higher-than-average resistance to malaria.
• Rx: administration of analgesics to relieve pain, fluid
therapy to maintain hydration, O2 to reduce the
possibility of O2 debt, antibiotics to counter
infections, and blood transfusions.
• Hydroxyurea: promotes transcription of the normal
Hb-F gene, elevated the level of HbF, and reduces the
chance of sickling.
• But not safe for long term use coz of toxic effects on
bone marrow.

67. Hemophilia:
• Inherited deficiency of clotting in which bleeding may
occur spontaneously or after only minor trauma.
• Usually affects males.
• Different types of hemophilia are due to deficiencies of
different blood clotting factors and exhibit varying
degrees of severity, ranging from mild to severe
bleeding tendencies.
• Characterized by spontaneous or traumatic
subcutaneous and intramuscular hemorrhaging,
nosebleeds, blood in the urine, and h’gges in joints –
pain and tissue damage.

68. • Rx: transfusions of fresh blood plasma or conc.
Of the deficient clotting factor to relieve the
tendency to blood.
• Drug desmopressin (DDAVP) – boosts levels of
clotting factors.

69. Leukemia:
• Group of red bone marrow cancers in which abnormal
WBC multiply uncontrollably.
• Accumulation of the cancerous WBC in red bone
marrow interferes with the production of RBC, WBC,
and platelets.
• O2 carrying capacity of the blood is reduced, and
individual is more susceptible to infection, and blood
clotting is abnormal.
• Cancerous WBC spread to the lymphnodes, liver and
spleen, causing them to enlarge.
• Produce the usual symptoms of anemia. In addition,
weight loss, fever, night sweats, excessive bleed and
recurrent infections also occur.

70. • In general, leukemias are classified as acute and
chronic.
• Adults may have either type, but children usually have
the acute type.
• Risk factors: radiation exposure, or chemotherapy for
other cancers, genetics, environmental factors, and
microbes such as human T cell leukemia-lymphona
virus (HTLV-1) and EBV.
• Rx: chemotherapy, radiation, stem cell
transplantation, interferon, antibodies, and blood
transfusion.

72. • Acute normovolemic hemodilution:
• Removal of blood immediately before surgery and its
replacement with a cell free solution to maintain
sufficient blood volume for adequate circulation.
• At the end of surgery, once bleeding has been
controlled, the collected blood is returned to the body.
• Autologous preoperative transfusion:
• Donating one’s own blood.
• Can be done upto 6weeks before elective surgery. Also
called predonation.
• This procedure eliminates the risk of incompatibility
and blood borne diseases.

73. • blood bank:
• Cyanosis:
• Gamma globulin:
• Solution of immunoglobulins form blood consisting of
antibodies that react with specific pathogens, such as
viruses.
• Prepared by injecting the specific virus into animals,
removing blood from the animals after antibodies
have accumulated, isolating antibodies and injecting
them into a human to provide short term immunity.
• H’gge:
• Loss of blood.
• Either b either internal or external.

74. • Hemochromatosis:
• Disorder of iron metabolism.
• Excessive absorption of ingested iron and excess
deposits of iron in tissues that result in bronze
discoloration of the skin, cirrhosis, diabetes mellitus,
and bone and joint abnormalities.
• Phlebotomist:
• Technician who specializes in withdrawing blood.
• Septicemia:
• Toxins or disease causing bacteria in the blood.
• Also called ‘blood poisoning’.
• Thrombocytopenia:
• Very low platelet count that results in a tendency to
bleed from capillaries

75. • Jaundice:
• Abnormal yellowish discoloration of sclera of eyes,
skin and mucous membranes due to excess bilirubin
in the blood.
• 1. prehepatic jaundice: excess production of bilirubin.
• 2. hepatic jaundice: abnormal bilirubin processing by
the liver caused by congenital liver disease, cirrhosis,
hepatitis.
• 3. extrahepatic jaundice: blockage of bile drainage by
gall stones or cancer of the bowel or pancreas.

76. • Venesection:
• Opening of a vein for withdrawl of blood.
• Phlebotomy: synonym for venesection.
• In clinical practice it refers to therapeutic bloodletting,
such as the removal of some blood to lower its
viscosity in a patient with polycythemia.
• Whole blood:
• Blood containing all formed elements, plasma and
plasma solutes in natural concentrations.