Here is a compilation of term papers on ‘Human Blood’. Find paragraphs, long and short term papers on ‘Human Blood’ especially written for school and college students.
Term Paper on Human Blood
1. Term Paper on the Meaning and Functions of Blood:
ADVERTISEMENTS:
Blood is a fluid that circulates in the vascular system and forms most efficient transport system of the body. When circulation is impaired, it will impair the tissue functions.
i. Transport of Respiratory Gases ― Hemoglobin conveys oxygen from the lungs to tissues. The carbon dioxide from tissues are carried by hemoglobin to the lungs and exhaled.
ii. Excretory Functions ― Waste products like urea, uric acid and creatinine are carried by the blood and removed by the kidney.
iii. Transport of Food ― Blood carries the products of digestion like glucose, amino acids, fatty acids and glycerol from digestive tract to the tissues.
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iv. Transport of Hormones ― Various hormones are transported from the site of production to the target tissues.
v. Regulation of Body Temperature ― Human beings are homoeothermic. They maintain a constant body temperature. The high specific heat of water, major component of blood helps in the process. The evaporation of water from the skin helps in reducing the body temperature.
vi. Regulation of Blood pH ― Blood contains buffers that can prevent the alteration of pH.
vii. Role in Defense Mechanism ― Neutrophils and monocytes fight with the various bacteria and kill them. Blood transports antibodies, antitoxins, and lysins that are protective substances.
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viii. Maintenance of Osmotic Pressure ― The plasma proteins are responsible for maintaining the osmotic pressure of blood.
ix. Maintenance of Water Balance ― Blood maintains water content of tissues and plays a role in regulation of fluid in various compartments of the body.
2. Term Paper on the Properties of Blood:
Human blood is thick, viscous and opaque fluid. It is scarlet red in colour when taken from an artery and appears blue when seen through the skin.
ADVERTISEMENTS:
Laked Blood:
When erythrocytes are hemolysed, blood becomes transparent. This is called laked blood.
Blood pH:
Normal pH of blood is 7.4 (range is 7.35 to 7.45)
ADVERTISEMENTS:
Specific Gravity:
Specific gravity of whole blood:
In men – 1055-1060
In women – 1050-1055
ADVERTISEMENTS:
Specific gravity of plasma – 1025-1029
Specific gravity of red cells – 1085-1100
Copper sulphate is used to find out the specific gravity of blood.
Viscosity:
The viscosity of whole blood is 3 to 4 times that of water. It is due to the blood cells and plasma proteins.
Osmotic Pressure:
The colloid osmotic pressure of blood and plasma is about 25 mm Hg. Osmotic pressure is expressed in terms of osmolarity and is about 290 milliosmoles per liter.
3. Term Paper on the Composition of Blood:
Blood is a complex fluid consisting of 55% plasma and 45% formed elements.
Plasma:
Plasma is a clear yellowish fluid. It contains 91% water and 9% solids. Of the solids 7% are plasma proteins namely albumin, globulin, and fibrinogen. It also has non-protein nitrogenous substances like urea, uric acid, creatinine, xanthine and hypoxanthine.
Organic substances present are glucose, amino acids, fatty acids, phospholipids, cholesterol, hormones, enzymes, antibodies, etc.
Inorganic substances which form about 0.9% are sodium, potassium, calcium, magnesium, iron, copper, iodine and chloride.
Formed Elements:
Formed elements consist of RBC, WBC and platelets. The hematocrit can be determined by packed cell volume. Heparinized blood is taken in a hematocrit tube and rotated rapidly at 3000 revolutions per minute. The lower portion of packed red cell mass is called packed cell volume (or) PCV. Normal PCV is 45%. WBC and platelets appear as thin layer of buffy coat.
Normal PCV:
In men – 45-50%
In women – 40-45%
In newborn – 54%
When packed cell volume is less than the normal it means anemia. Along with PCV if hemoglobin is reduced it is a good clue for diagnosis of severity of anemia. PCV well above normal indicates polycythemia.
1. Decrease in PCV:
i. Physiological:
a. Pregnancy
b. Excess water intake
ii. Pathological:
a. Anemia
b. Hyperaldosteronism
2. Increase in PCV:
i. Physiological:
a. High altitude
b. Newborn
c. Excess sweating
ii. Pathological:
a. Congenital heart disease
b. Emphysema
c. Polycythemia
d. Hemoconcentration, e.g. vomiting.
Plasma Proteins:
Composition:
Plasma contains proteins namely:
i. Serum albumin 3.5-5 gm%
ii. Serum globulin 2.0-3.5 gm%
iii. Fibrinogen 0.2-0.3 gm%
Plasma protein fractions are separated into serum albumin, serum globulin, alpha 1, alpha 2, beta, and gamma globulins by the technique of electrophoresis. In serum electrophoresis, fibrinogen is not seen, as serum does not contain fibrinogen. Other globulins are protease inhibitors alpha 1 antitrypsin, alpha 2 macroglobulin, several transport proteins, coagulation factors, anti-thrombin hormone binding proteins, lipoproteins and complement components.
Methods to detect tiny amounts of proteins are:
i. Radioimmunoassay
ii. Enzyme linked immunosorbent assay (ELISA).
Functions of Plasma Proteins:
1. Colloid Osmotic Pressure ― Plasma colloid osmotic pressure is due to albumin.
Hence albumin has a role in:
i. Fluid exchange between blood and tissue fluids
ii. Regulation of blood volume
iii. Water balance
2. Viscosity ― Plasma proteins give viscosity to blood and this contributes to the peripheral resistance a factor in the maintenance of blood pressure.
3. Acid-Base Balance ― Proteins act as buffer and hence regulate the acid base balance.
4. Clotting of Blood ― Fibrinogen, prothrombin, and factor V, VIII, etc. are essential for clotting of blood.
5. Immune Substances ― The gamma globulins react with antigens present on microorganisms. These gamma globulins give passive immunity.
6. Protein Store ― When a person is fasting, plasma proteins serve as a reservoir on which the body can depend on for some time.
7. Rouleaux Formation ― Fibrinogen and globulin fraction help in rouleaux formation thus helping in erythrocyte sedimentation rate.
Formation of Plasma Proteins:
Albumin, globulin, fibrinogen and prothrombin are formed in liver. The antibodies (gamma globulin) are formed by plasma cells and B lymphocytes. Proteins of food help in the formation of plasma proteins.
Albumin globulin ratio (A: G ratio) is 3:2. This albumin globulin ratio is reversed in cirrhosis, kidney diseases like nephritis; nephrosis, etc.
i. Decrease in Albumin ― Reduced intake, liver diseases, and when albumin escapes into tissue spaces
ii. Increase in Globulin ― Liver disease, multiple myeloma, acute nephritis, leukaemia’s, and tuberculosis
iii. Increase in Fibrinogen ― Pregnancy, menstruation, tissue injuries of various type, acute infectious diseases, and malaria
iv. Decrease in Fibrinogen ― Hepatectomy and liver diseases. All fractions of plasma proteins are reduced in haemorrhage.
4. Term Paper on Blood Volume:
Average healthy male has 5 liters of blood. Normal blood volume is 60-80 ml/kg body weight. Blood volume is less in children. It increases gradually to adult value by 18 years.
Methods of Measurement of Blood Volume:
Blood volume can be estimated using a non-toxic dye.
Characteristics of an Ideal Dye:
i. Dye must not diffuse too rapidly out of the blood stream.
ii. Must colour the plasma but it must not be absorbed by the cells of blood.
iii. Dye must not cause hemolysis.
iv. Dye must mix evenly throughout plasma.
Evans blue or T-1824 satisfies all these criteria.
Method of Estimation of Blood Volume:
Blood sample is collected before the dye is injected intravenously. Dye is injected intravenously and blood samples are collected at 10, 20, 30, 40, 50 minutes interval after the injection. Concentration of dye in the plasma is measured by a photoelectric colorimeter and from the value, plasma volume can be calculated. The hematocrit value of the blood sample before injecting the dye gives relative volumes of plasma and corpuscles. From this the total volume of blood can be calculated.
The amount of dye injected = 10 mg
Concentration in plasma = 0.4 mg/100 ml plasma
Plasma volume = Amount of dye injected/Concentration of the dye in 100 ml × 100
= 10 × 100/0.4 = 2500 ml
Total blood volume is calculated from this by knowing the hematocrit value of the blood. If hematocrit is 45% Total blood volume = Plasma volume/100-hematocrit × 100
= 2500/(100–45)
= 2500 × 100/55
= 4545 ml
The other methods used to measure the blood volume are:
1. Radiotracer Method ― Radioiodine tagged albumin is injected intravenously and sufficient time is allowed for mixing. Radioactivity is determined by an appropriate counter.
2. Red Cell Marking Method ― RBCs are labeled with radioactive iron, radioactive chromium or radioactive phosphorus.
Conditions Causing Reduction in Blood Volume:
i. Hemorrhage ― Loss of whole blood causes reduction in total blood volume.
ii. Burns ― Plasma is exuded from burned surface causing reduction in blood volume.
iii. Dehydration ― Loss of water due to diarrhea and vomiting causes decrease blood volume.
iv. Anemia ― Decrease in blood cells causes decrease in blood volume.
iv. Posture ― Erect posture for 30 minutes cause a reduction in blood volume as fluids leak from vessels of lower limbs into extra-capillary tissues.
Regulation of Blood Volume:
Exchange of Fluid between Blood and Tissue Fluids:
When blood volume is increased, capillary hydrostatic pressure is increased and plasma colloid osmotic pressure is decreased. This causes movement of fluid from the blood vessel into tissue space.
When blood volume is decreased, capillary hydrostatic pressure is decreased and osmotic pressure is increased, drawing fluid from tissue space into vascular space.
Hormones Regulating Blood Volume:
i. Angiotensin II
ii. Aldosterone
iii. Vasopressin
Thirst:
When water content of body is low, thirst is felt due to stimulation of thirst center in hypothalamus. When the person drinks water, blood volume and water content are restored.
Erythrocyte Sedimentation Rate:
The rate at which the red cells settle is called erythrocyte sedimentation rate (ESR). ESR is measured by depth in millimeter at the end of one hour. Erythrocyte sediment is due to the formation of rouleaux (red cells piling up like coins).
Uses of ESR:
ESR gives additional information in diagnosing a disease. It also helps in determining the prognosis of a disease.
Methods:
ESR is determined by:
i. Westergren’s method
ii. Wintrobe’s method
Normal Values:
Men – 1 to 10 mm/hr
Women – 4 to 15 mm/hr
Increase in ESR:
Menstruation, pregnancy, acute bacterial septicemia, tuberculosis, rheumatic fever, pelvic inflammatory disease, malignant tumors, anemia and trauma.
Decrease in ESR:
Allergy, sickle cell anemia and acholouric jaundice.
Factors that Determine ESR:
i. Concentration of fibrinogen (increase in fibrinogen increases ESR).
ii. Concentration of gamma globulin (increase in gamma globulin increases ESR).
iii. Serum albumin (decrease in albumin increases ESR).
Other Factors Influencing ESR:
i. Viscosity of plasma
ii. Specific gravity
iii. Size of RBC
C-Reactive Protein:
C-Reactive protein is a better alternative to ESR. Normal value is less than 1 mg/100 ml of blood. It is synthesized in liver. Its rise occurs within 6 hours and follows the course of the disease.
Increase in CRP:
i. Inflammation
ii. Tissue trauma
5. Term Paper on Hemoglobin:
i. Hb is an oxygen binding protein
ii. Molecular weight of ‘Hb’ ― 68,000
iii. It carries respiratory gases.
Normal Values:
i. Birth – up to 23 gm/dl
ii. Adult female – 12-14 gm/dl
iii. Adult male – 15-17 gm/dl
Functions of Hemoglobin:
i. Transport of Oxygen from Lungs into Tissue:
O2 is loosely and reversibly bound to ‘Hb’.
ii. Transport of Carbon Dioxide from Tissues to Lungs:
Carboxyhemoglobin is formed rapidly than oxyhemoglobin.
iii. Hemoglobin plays an important role as blood buffer. It is 6 times more potent than plasma proteins.
iv. Structure of Hemoglobin (Fig. 4.7c):
v. Hemoglobin is a spherical molecule with molecular weight of 64,500.
vi. Hemoglobin molecule has 2 Parts:
a. Heme
b. Globin
a. Heme:
i. Heme is made up of iron and protoporphyrin
ii. Iron is in ferrous form
iii. Fe++ is attached to N– atom of each.
Protoporphyrin:
The 4 pyrrole rings are linked together by methane bridges to form protoporphyrin.
b. Globin:
i. There are 4 polypeptide chains in each Hb molecule.
ii. Normal adults have HbA
iii. HbA has 2 alpha-chains – each with 141 amino acid 2 beta-chain: each with 146 amino acids. So, HbA is 2, 2.
Synthesis of Hemoglobin:
Synthesis of Hemoglobin Occurs in 4 steps:
i. 2 succinyl CoA + 2 glycine → pyrrole
ii. 4 pyrrole → protoporphyrin IX
iii. Protoporphyrin IX + Fe → heme
iv. Heme + globin → hemoglobin
a. Succinyl CoA formed in Kreb’s cycle combines with glycine to form pyrrole molecule.
b. 4 pyrrole molecules join to form protoporphyrin IX.
c. Protoporphyrin IX combines with iron to form heme.
d. Each heme combines with globin synthesized by ribosomes to form hemoglobin.
Each Hb Molecule has:
i. 4 Hb chain
ii. Each Hb chain has 1 Fe atom
iii. Each Fe atom loosely binds with 1 molecule of oxygen (8 oxygen atoms)
1 gm of Hb combines with 1.34 ml of oxygen.
In men:
15.5 gm Hb + 1.34 ml O2 = 21 ml of oxygen.
In women:
14 gm Hb + 1.34 ml of O2 = 18.5 ml.
Physiological Varities of Hb:
Hb embryo – Gower 1, Gower 2, hemoglobin Portland
Hb F (fetal) – α2ү2
Hb A (adult) α2β2
HbA2 – α2δ2
Adult Hemoglobin:
In adults― 98% of hemoglobin is α2β2.
2% of adult Hb is α2δ2
Fetal Hemoglobin:
i. HbF is present in fetal RBC.
ii. By the end of 1st year of child’s life, fetal hemoglobin almost disappears and adult Hb appears.
Destruction of Hb:
i. RBCs are destroyed by reticuloendothelial system, particularly the spleen.
ii. Hb is released into plasma.
iii. Hb is degraded by RES to form ―
a. Iron
b. Globin
c. Porphyrin
Iron is stored in the body as ferritin and hemosiderin.
Porphyrin gets converted into green pigment called biliverdin which in turn gets converted into bilirubin.
Globin is used in the resynthesis of Hb.
Applied Physiology:
a. Defect in Globin Synthesis:
i. Sickle cell anemia
ii. Thalassemia
b. Defect in Synthesis Of Heme:
i. Porphyrias
ii. Increased activity of amino levulinic acid leads to increased synthesis of porphyrins.
iii. Porphyrias may be inherited or acquired.
iv. Symptoms include photosensitivity and psychosis.
Hemoglobin Complexes:
i. Oxyhemoglobin: (HbO2):
Oxygen combines with hemoglobin to form oxyhemoglobin and the combination is loose and reversible.
ii. Glycosylated Hemoglobin:
a. Glucose gets attached to chain of HbA to form glycated hemoglobin (GHb).
b. GHb must not exceed 6%
c. GHb above 6% indicates poor control of blood sugar in diabetes mellitus.
iii. Methemoglobin:
It is combination of NO with Hb. Normally, small amount of methemoglobin is present. Methemoglobinemia occurs in smokers, drugs, e.g. dapsone (antileprosy drugs).
a. Sulphemoglobin
b. Glycosylated hemoglobin
iv. Reduced hemoglobin
v. Carboxyhemoglobin
vi. Carbaminohemoglobin
Iron Metabolism:
Requirement of Iron:
Iron in needed to form:
Hemoglobin, myoglobin, cytochromes, cytochrome oxidases, peroxidase and catalase.
Total Body Iron:
Total iron content of our body is 6 g.
Distribution of Iron:
i. Hemoglobin – 65%
ii. Myoglobin – 4%
iii. Various forms of Fe compound – 1%
iv. Combination with transferrin – 1%
v. Stored in liver – 15 to 30%
Absorption of Iron from Intestinal Tract:
i. Iron is absorbed from duodenum (2nd part)
ii. Iron can be absorbed only as ferrous form – Fe+++
iii. Liver forms a betaglobulin called “apotransferrin”.
iv. Iron combines with apotransferrin to form transferrin.
By the process of pinocytosis, transferrin containing ‘Fe’ is absorbed into epithelial cells.
v. From the enterocytes, it is released into blood capillaries to form plasma transferrin.
Transport of Iron:
Transferrin is the transport form of iron. Iron is bound loosely to transferrin and released in any tissue as per need.
Storage Form of Iron:
Iron is stored in the liver and bone marrow as:
i. Ferritin
ii. Hemosiderin
Regulation of Total Body Iron:
Body is saturated with iron → Decreased iron absorption from intestines
Iron stores are depleted → Iron absorption increased ↑ by 5 times
Daily Loss of Iron:
Human beings excrete 0.6 milligrams of iron each day into feces.
Menstrual loss of iron = 1.3 mg/day.
When blood loss is more peripheral smear shows — microcytic hypochromic picture:
i. Hb content is less
ii. MCV: < 75 u3 (unit)
iii. MCH: < 25 picograms
iv. Total Fe binding capacity (TIBC) is increased.
6. Term Paper on Blood Platelets:
Platelets also called as thrombocytes, are minute discs.
Size – 2-4 µm
Shape – Discoid, oval, or round in shape.
Platelet Membrane:
i. Platelet membrane is made up of glycoprotein and phospholipids.
ii. Glycoprotein: Repels vascular endothelium
iii. Phospholipids: That activates various stages.
iv. Platelet membrane has receptors for collagen, fibrinogen, ADP, von Willebrand factor (vWF).
Cytoplasm of Platelets:
Cytoplasm of platelets contains:
i. Actin, myosin, thrombosthenin that are contractile proteins.
ii. Endoplasmic reticulum and Golgi apparatus that synthesize various enzymes.
iii. Mitochondria ― Synthesize ATP and ADP
iv. Prostaglandin ― A local hormone synthesized by enzymes.
v. Fibrin stabilizing factor
vi. Growth factor
vii. Granules ― Cytoplasm contains granules like
a. Alpha granules ― Contain von Willebrand factor, fibrinogen and platelet derived growth factor.
b. Dense granules ― Contain ATP, ADP, 5HT, non-protein substances.
c. Lysosomes
Microtubules:
It is responsible for the shape of platelets.
Nucleus:
Platelets have no nucleus, DNA, RNA and hence cannot reproduce.
Canaliculi:
1. Open canaliculi
2. Closed canaliculi.
Development of platelets (thrombopoiesis) → Pluripotent hematopoietic stem cells → Committed stem cells → Promegakaroblast → Megakaryoblast → Megakaryocyte → Platelets (1000-1500 platelets)
Lifespan:
Lifespan of platelets is 8-14 days. After completing their lifespan they are destroyed in spleen.
Factors controlling thrombopoiesis:
i. Colony Stimulating Factor:
Interleukin 1, 2, 6, 11
ii. Thrombopoietin:
Produced by liver and kidney.
Count and Variations:
Normal Count:
i. 1.5 lakhs to 3 lakhs
ii. 75% of platelets are in circulating pool.
iii. 25% of platelets are seen in spleen (reservoir of platelets).
Thrombocytosis:
i. After trauma and surgery
ii. Splenectomy
iii. Stress.
Thrombocytopenia:
i. Bone marrow depression
ii. Hypersplenism
iii. Viral infection.
Functions of Platelets:
Hemostasis:
Various steps that bring about hemostasis are:
i. Platelet adhesion
ii. Platelet activation
iii. Platelet aggregation.
Blood Coagulation:
ADP from platelets causes platelet activation and “Temporary hemostatic plug” formation.
Clot Retraction:
Thrombosthenin causes clot retraction in a blood clot.
Phagocytic Function:
Platelets can phagocytize:
i. Carbon particles
ii. Viruses
iii. Immune complexes.
Storage and Transport:
Platelets can store:
i. Histamine
ii. 5-hydroxytryptamine.
Mechanism of Platelet Plug Formation:
Platelets form part of primary hemostasis. Hemostasis means prevention of blood loss.
It is of two types:
1. Primary hemostasis
2. Secondary hemostasis.
1. Events of Primary Hemostasis:
i. Vasoconstriction
ii. Platelet plug formation.
2. Events of Secondary Hemostasis:
i. Formation of blood clot
ii. Growth of fibrous tissue into blood clot.
Vasoconstriction:
Vasoconstriction is achieved after a blood vessel has been cut by:
i. Local myogenic spasm
ii. Local autacoids from injured blood vessels and platelets
iii. Nervous reflexes initiated by pain nerve impulses from traumatized blood vessels
iv. Thromboxane A2 released from injured platelets are responsible for vasoconstriction of smaller vessels.
Formation of Platelet Plug:
1. Adhesion of platelets to the site of injury.
2. Change in the shape of platelets and formation of pseudopods.
3. Release of chemical substances.
4. Attract more platelets leading to aggregation of platelets.
I. Platelet Adhesion:
When platelets come in contact with damaged vessels exposing collagen, the platelets adhere to the vessel. Platelets need a rough surface to adhere.
Factors responsible for adhesion are:
i. Adenosine diphosphate
ii. Thromboxane A2
iii. Calcium ions
iv. Von Willebrand factor
v. Collagen
II. Change in Shape of Platelets:
On adhering to the collagen, platelets begin to swell and assume irregular forms with numerous pseudo- pods protruding from their surface.
Release of Chemical Substances:
The contractile proteins namely actin, myosin, thrombosthenin within the platelets contract forcefully and release granules. These granules make the platelets to become sticky to each other and to collagen and von Willebrand factor that is from plasma.
Aggregation of Platelets:
ADP and thromboxane act on nearby platelets to activate them and more number of platelets are recruited to form platelet plug.
First, a loose plug is formed. Then, subsequently fibrin threads are formed on the platelet plug thus converting the loose plug into an unyielding plug.
Importance of Platelet Plug:
Platelet plugging is important for closing minute ruptures in very small blood vessels that occur multiple times a day. If the platelet count is less, thousands of small hemorrhages occur under the skin.
Blood Clot:
The clot is composed of a meshwork of fibrin threads running in all directions with blood cells, platelets and plasma.
Clot Retraction:
After the clot is formed, within minutes, it begins to contract and usually express most fluid within 20-60 minutes. The fluid expressed is called serum. This serum cannot clot as it does not have fibrinogen and other clotting factors.
Platelet is essential for clot retraction. Failure of clot retraction is an indication of low platelet count. The contractile proteins namely actin, myosin, and thrombosthenin in platelets cause strong clot retraction.
As clot retraction proceeds, the injured blood vessel is pulled together and hemopoiesis is achieved.
Dissolution of Clot:
Fibroblasts invade the clot and complete organization of the clot into fibrous tissue occurs in 1 to 2 weeks.
7. Term Paper on Blood Group:
Blood transfusion in earlier days led to the death of recipients. In 1901, Landsteiner demonstrated that human beings could be classified into four groups depending on antigens presents on red cell surface.
ABO system:
Two agglutinogens were found on surface of red cell. If agglutinogen A is present on red cell surface, it is blood group A. It is further divided into A1 and A2.
If B agglutinogen is present on the surface of red cell, it is blood group B.
If A and B agglutinogen are present on the red cell surface, it is blood group AB. It is further divided into A1B and A2B.
If no agglutinogen is present on the red cell surface, it is O blood group.
Agglutinogen (Antigen):
Agglutinogens are inherited as Mendelian dominant. Agglutinogen A and B first appear in the sixth week of fetal life. They are complex oligosaccharides. Red cell surface has ‘H’ antigen which is the precursor of A and B antigen. In blood group O, this ‘H’ antigen persist.
Marathi speaking people around Mumbai were reported to have RBC that had ―
No H antigen
No A antigen
No B antigen
This blood group is called as “Bombay blood group” and symbolized as Oh. Since the RBC have neither H, nor A or B antigen, on their red cell surface, their serum contains all three agglutinins (antibody A, B, AB). So, if they need blood transfusion, only Bombay blood group must be given.
Secretors:
Agglutinogens of ABO group are present not only on the RBC surface but also on salivary glands, pancreas, kidney, liver, lungs and testis. They are water soluble and present in gastric juice, saliva and other body fluids of 80% people. They are called as secretors.
Non-Secretors:
The agglutinogens of non-secretors are confined to the red cells.
Agglutinin (Antibody):
Antibody A and antibody B present in the serum are IgM type and hence do not cross the placenta.
Concentration of agglutinin is negligible at birth. It increases gradually and reaches a peak at 10 years. This is caused by entry of antigen A and B via food and bacteria.
Landsteiners Law:
If an antigen is present on the surface of RBC, the corresponding antibody will be absent in plasma.
If an antibody is present in the plasma, the corresponding antigen will be absent on the surface of RBC.
Determination of Blood Group:
To determine the blood group of an individual, a suspension of red cells is made in isotonic saline. A drop of red cell in saline is taken on a slide and a drop of antisera A, antisera B is placed over the blood (contains antibody).
If agglutination occurs with antisera A, then the blood group is A.
If agglutination occurs with antisera B, then the blood group is B.
If agglutination occurs with antisera A and antisera B then the blood group is AB.
If agglutination does not occur with antisera A or B then the blood group is O.
Inheritance of ABO Blood Groups:
ABO genes are located in the ninth pair of human chromosomes. A child’s blood group is determined by two genes received from the parents.
If the child is O → the father cannot be AB
If the child is AB → the father cannot be O
If the child is A and mother is B or O → the father cannot be B or O
If the child is B and mother is A or O → the father cannot be A or O
Rh Typing:
There are several varieties of Rh antigens, e.g. C, D, E. D is the most common antigen present and is highly immunogenic. It is the presence or absence of D agglutinogen that determines whether a person is Rh positive or negative. If D agglutinogen is present, a person is Rh (D) positive. If D agglutinogen is absent, a person is Rh (D) negative. There is no naturally occurring antibody for Rh (D) antigen.
Two conditions where Rh antibodies are formed are:
a. When Rh negative person receives Rh positive blood.
b. Erythroblastosis Fetalis:
Erythroblastosis fetalis is a disease of fetus and newborn due to development of Rh incompatibility between mother and fetus. If Rh -ve mother, carries Rh +ve fetus, (father Rh +ve), during severance of cord, Rh -ve fetal red cell enter into maternal circulation. First baby is not affected. Mother starts producing Rh antibodies against fetal red cells. During the second pregnancy, the preformed antibodies in the mother cross the placenta and enter into fetus causing hemolysis of fetal RBC.
As a result of hemolysis the newborn develops:
a. Anemia due to hemolysis
b. Erythroblasts in peripheral blood as the body tries to replace hemolyzed RBC
c. Jaundice within 24 hours of birth
d. Kernicterus ― Elevated serum bilirubin crosses the blood brain barrier and fix to the basal ganglia leading to the disturbance in motor activities
e. Hydrops fetalis ― Grossly edematous fetus.
Investigations:
a. Blood grouping
b. Rh typing
c. Serum bilirubin
d. Peripheral blood smear
e. Reticulocyte count
f. Direct Coombs’ test is positive in erythroblastosis fetalis.
Prevention and Treatment:
Anti-D agglutinin is given as single dose to mother within 72 hours of delivery. This destroys the Rh +ve RBC of fetus in maternal circulation before they form antibodies.
Treatment of Baby:
a. Phototherapy
b. Double exchange transfusion.
Minor Blood Groups:
In 1927, Landsteiner with Levine found blood groups M, N and MN.
Other minor blood groups are Lutheran, Levis, Kidd, Duffy, etc.
MN blood group was used in disputed paternity. Now, DNA techniques are used in disputed paternity.
If child is M father cannot be N
If child is N father cannot be M
Gene for MN group is located in chromosome 4.
Uses of Blood Grouping:
a. Before blood transfusion
b. In paternal disputes
c. Medicolegal case
d. Knowing susceptibility of disease.
Blood Transfusion:
Blood transfusion is a life saving measure and must be given only when it is absolutely essential.
Indications:
i. Blood Loss:
For example: Accidents, during surgery
ii. Severe Anemia:
In severe anemia, it is better to administer packed red blood cells to prevent volume overload.
ii. Exchange Transfusion:
Acute poisoning, e.g. carbon monoxide poisoning.
Criteria to Select a Donor:
i. Age: 18 to 60 years
ii. Hemoglobin >11 gm/dl
iii. PCV: Must be normal
iv. Exclude HIV, hepatitis, malaria and syphilis.
v. Non-pregnant and non-lactating mother.
Precautions before Blood Transfusion:
i. Must be an absolute indication ― Must be life-saving.
ii. Cross-matching must be done.
iii. Major cross-matching ― Donor’s RBC is mixed with recipient’s plasma.
iv. Minor cross-matching ― Recipient’s RBC is mixed with donor’s plasma.
v. For doubtful clumping, keep a drop of the sample on a cover slip and examine under a microscope.
vi. Blood bag must be checked:
a. Transfusion must be given at the rate of 100-200 ml/hour
b. Proper aseptic precautions must be taken.
Temperature for Storage:
Blood is stored at 4 degree until it is required.
1 Unit of blood ― 1 unit of blood is 450 ml of whole blood, 63 ml of anticoagulant and preservative made up of citrate, phosphate, dextrose, and adenine. Dextrose maintains the Na K pump.
Stored Blood:
Blood can be stored at 4°C for 21 days.
At the end of this period 70 to 80% of RBC is viable but not WBC or platelets:
i. K+ content of red cell is reduced
ii. Na+ content of red cell is increased
iii. K+ content of plasma is increased.
Effects of Mismatched Blood Transfusion:
i. Death can occur due to anaphylaxis
ii. Hemolysis of agglutinated red cells → hemolytic jaundice
iii. Hemoglobinuria
iv. Hemoglobin precipitates in renal tubules, blocking the tubules leading to acute renal failure.
v. Circulatory overload → Congestive cardiac failure
vi. Agglutinated RBCs block the small blood vessels leading to shooting pain in lumbar region and precordium.
Minor Transfusion Reactions:
a. Fever, chills and rigor occurs due to pyrogens.
b. Allergic reactions like anaphylaxis, urticaria can occur.
Autologous Blood Transfusion:
Blood can be withdrawn from a person and can be transfused into the same person during elective surgery. If iron rich diet is given, 1000-1500 ml of blood can be withdrawn over a three-week period.
Advantages:
a. Transmission of AIDS and other blood borne infections can be avoided.
b. Incompatibility is NIL.
Blood Substitutes:
Various blood substitutes are used where volume replacement is needed more urgently.
Plasma or Serum:
i. Plasma can be stored for many months
ii. Plasma is used in the treatment of burns and shock
iii. There is no need for cross-matching.
Colloid:
Dextran is a colloid which gives proper osmotic equilibrium without causing untoward reactions.
Crystalloid:
i. Crystalloids do not remain in blood vessels.
ii. They are used in cases of fluid loss with hemo-concentration (dehydration).
iii. Intravenous mannitol solution is useful in relieving cerebral edema.
Blood Products:
i. Fresh Frozen Plasma:
It can be obtained by freezing plasma to 30°C. FFP is used in clotting factor deficiency.
ii. Plasma Protein Fraction:
PPF is used in hypo-albuminemia.
iii. RBC Concentrates:
It is used in severe anemia.
Platelet Concentrate:
Used in reduced platelet count with bleeding. Matching must be done for ABO and Rh groups as the concentrates are likely to contain some RBC.