SEMINARBLOOD

DEPARTMENT OF PUBLIC HEALTH DENTISTRY

Presented By:-Dr. Amrita RastogiM.D.S 1st Year

• INTRODUCTION

• PROPERTIES OF BLOOD

• FUNCTIONS OF BLOOD

• FORMATION OF BLOOD

• COMPOSTION OF BLOOD

Plasma

Red Blood Cells

White Blood Cells

Platelets

CONTENTS

• HEMOSTASIS

• BLOOD GROUPING

• BLOOD TRANSFUSION

• ROLE OF PUBLIC HEALTH DENTIST

• CONCLUSION

• REFERENCES

INTRODUCTION• Blood is a complex, living tissue that contains many cell types

and proteins. A transporter, regulator, and defender, blood courses through the body carrying out many important functions.

• Blood, fluid pumped by the heart that circulates throughout the body via the arteries, veins, and capillaries . An adult male of average size normally has about 6 quarts (5.6 litres) of blood. The blood carries oxygen and nutrients to the body tissues and removes carbon dioxide and other wastes. The colourless fluid of the blood, or plasma, carries the red and white blood cells, platelets, waste products, and various other cells and substances.

• Blood is the only tissue that flows throughout our body. This red liquid carries oxygen and nutrients to all parts of the body and waste products back to our lungs, kidneys and liver for disposal. It is also an essential part of our immune system, crucial to fluid and temperature balance, a hydraulic fluid for certain functions and a highway for hormonal messages.

• Blood is a wonderful tissue may be the easiest to transplant (transfuse).

PROPERTIES OF BLOOD Color

– Oxygen-rich blood is scarlet red bright crimson.(arterial blood)

– Oxygen-poor blood is purple red. (Venous blood)

– Red color comes from the several million red cells, present in it.

Volume− In a normal adult is 5 ltrs in women & 5.5 ltrs in men and

represents about 8% of total body weight.

Reaction and pH– Blood is slightly alkaline and its pH in normal conditions is

7.4.

Specific gravity

– total blood :1.052 to 1.061

– blood cells : 1.092 to 1.101

– plasma : 1.022 to 1.026

Viscosity− Blood is 5 times more viscous than water mainly due to red

blood cells and plasma proteins.

Temperature − 38 ◦c or 100.4 F

FUNCTIONS OF BLOOD•NUTRIENT FUNCTION.

•RESPIRATORY FUNCTION.

•EXCRETORY FUNCTION.

•TRANSPORT OF HORMONES AND

ENZYMES.

•REGULATION OF WATER BALANCE.

•REGULATION OF ACID BASE

BALANCE.

•REGULATIONOF BODY TEMPERATURE

STORAGE FUNCTION.

•DEFENCIVE FUNCTION.

1. NUTRIENT FUNCTION Nutritive substances like glucose, amino acids, lipids and

vitamins derived from digested food are absorbed from gastrointestinal tract and carried by blood to different parts of the body for growth and for production of energy.

2. RESPIRATORY FUNCTION Transport of respiratory gases is done by the blood. It carries

oxygen from alveoli of lungs to different tissues and carbon dioxide from tissues to alveoli.

3. EXCRETORY FUNCTION Waste products formed during various metabolic activitiesfrom

the tissues are removed by blood and carried to the excretory organs like kidney, skin, liver, etc.

4. TRANSPORT OF HORMONES AND ENZYMES The hormones and some of the enzymes are carried by blood

to different parts of the body from the source of secretion.

5. REGULATION OF WATER BALANCE Water content of the blood is freely interchangeable with interstitial

fluid. This helps in the regulation of water content of the body.

6. REGULATION OF ACID BASE BALANCE The plasma proteins and hemoglobin act as buffers and help in

regulation of acid base balance.

7. REGULATIONOF BODY TEMPERATURE Because of the high specific heat of blood, it is responsible for

maintaining the thermoregulatory mechanism in the body, i.e. the balance between heat loss and heat gain in the body.

8. STORAGE FUNCTION Water and some important substances like proteins, glucose,

sodium and potassium are constantly required by the tissues. Blood serves as a readymade source for these substances. And, these substances are taken from blood during the conditions like starvation, fluid loss, electrolyte

8.DEFENCIVE FUNCTION. Immunological functions, including circulation of white blood

cells, and detection of foreign material by antibodies.

FORMATION OF BLOOD• In foetus - bone marrow,liver & spleen

• In adults- bone marrow.

• In children, blood cells are actively produced in marrow

cavities of all the bones

• 75% of the cells - white blood cell producing myeloid series &

25% are maturing red cells

• Bone marrow contains pluripotent stem cells that differentiate

into progenitor cells that in turn differentiate into various

differentiated types of blood cells.

BONE MARROW

• The bone marrow is present in the bone cavities. • It can be considered as one of the largest organs in the body,

and also one of the most active. • In children, blood cells are produced in the marrow cavities of

all the bones. • Gradually, it gets replaced by fat (yellow marrow). • In the adult blood cells are produced in the bone marrow of

selected bones (e.g. backbone – vertebral column, ribs, bones of the skull, etc.)

HEMATOPOIESIS

Hematopoiesis is the process which includes origin, development and maturation of all the blood cells.

Hematopoiesis is the process which includes origin, development and maturation of all the blood cells.

• STEMCELLS• The stem cells are the primitive cells in the bone marrow,

which give rise to the blood cells. As the stem cells can give rise to different types of blood cells, these are called pluripotent hemopoietic stem cells (PHSC). In the earlier stages, the stem cells are not designed to form a particular type of blood cell. And it is also not possible to determine the blood cell to be developed from these stem cells.

So at this stage, the cells are called uncommitted pluripotent hemopoietic stem cells (Uncommitted PHSC). When the cells are designed to form a particular type of blood cell, the stem cells are called committed pluripotent hemopoietic stem cells (Committed PHSC). The committed stem cells are of two types namely:

1. Lymphoid stem cells (LSC) which give rise to lymphocytes.2. Colony forming blastocytes, which give rise to the blood cells

other than lymphocytes.

When grown in cultures, these cells form colonies hence the name colony forming blastocytes. There are different units of colony forming cells as follows:

a. Colony Forming Unit-Erythrocytes (CFU-E).The stem cells of this unit develop into erythrocytes.

b. Colony Forming Unit-Granulocytes/ Monocytes (CFU-GM). These cells give rise to granulocytes (neutrophils, basophils and eosinophils) or Monocytes.

c. Colony Forming Unit-Megakaryocytes (CFU-M).From these, platelets are developed.

BLOOD CELLS - TYPICAL COUNT

• Total Erythrocytes = 5,000,000,000 cells/ml blood

– RBC count = 5,000,000/mm3

• Total leukocytes = 7,000,000 cells/ml blood

– WBC count = 7,000/mm3

• Differential White Blood Cell Count

(% Distribution of Types of Leukocytes)Polymorphonuclear granulocytes Mononuclear agranulocytes

Neutrophils 60-70% Lymphocytes 25-33%

Eosinophils 1-4% Monocytes 2-6%

Basophils 0.25-0.5%

• Total Platelets = 250,000,000/ml blood

– Platelet count = 250,000/mm3

M

UNCOMMITTED PLEURIPOTENT HAEMOPOIETIC STEM CELL

COMMITTED PLEURIPOTENT HAEMOPOIETIC STEM CELL

LYMPHOID STEM CELLCOLONY FORMING BLASTOCYTE

C F U-E CF U-GMC F U-M

MEGAKARYOCYTE GRANULOCYTES

L R N B E P

ERYTHROPOIESIS

Erythropoiesis is the process by which the origin, develop-ment and maturation of erythrocytes occur.

Site of erythropoiesis in fetal life

During embryonic life, erythropoiesis occurs in three stages.

i) Mesoblastic stage: During the first two months of intrauterine life, the primitive red blood cells are produced from mesenchyme of yolk sac.

ii) Hepatic stage: From third month of intrauterine life, liver is the main organ that produces red blood cells. Some erythrocytes are also produced from spleen and lymphoid organs.

iii) Myeloid stage: During the last three months of intra uterine life, the red blood cells are produced from red bone marrow and liver.

In post natal life and In adults

1. Up to age of 5 to 6 years: The red blood cells are produced in red bone marrow of all bones.

2. From 6th year up to 20th year: The red blood cells are produced by red bone marrow of long bones and all the membranous (flat) bones.

3. After the age of 20 years: The red blood cells are produced from all membranous bones like vertebra, sternum, ribs, scapula, iliac bones and skull bones and from the ends of long bones. After 20 years of age, the shaft of the long bones becomes yellow bone marrow because of fat deposition and lose the erythropoietic function.

During disorders of bone, the RBC’s are produced in spleen.

Stages of Erythropoiesis

CELL DIAMETER NUCLEUS CYTOPLASM

15-20 μm Big & strongly Very scanty & basophilic basophilic No Hb.

11-16 μm Smaller Scanty & basophilic. No Hb.

10-12 μm Smaller & Hb starts to appear, Denser cytoplasm polychromatic.

8-10 μm Ink spot Plentiful, eosinophilic. nucleus increase in Hb.

8-10 μm Absent Some RNA still present.

7.5 μm Absent Hb++.

CELL DIAMETER NUCLEUS CYTOPLASM

15-20 μm Big & strongly Very scanty & basophilic basophilic No Hb.

11-16 μm Smaller Scanty & basophilic. No Hb.

10-12 μm Smaller & Hb starts to appear, Denser cytoplasm polychromatic.

8-10 μm Ink spot Plentiful, eosinophilic. nucleus increase in Hb.

8-10 μm Absent Some RNA still present.

7.5 μm Absent Hb++.

Factors Affecting Erythropoiesis• General factors

– Erythropoietin

– Thyroxine

– Hemopoietic growth factors

– Vitamins

• Maturation factors

– Vitamin B12

– Intrinsic Factor of Castle

– Folic Acid

• Factors necessary for Hb formation

– First class proteins & amino acids

– Iron

– Copper

– Co ,Ni

– vitamins

LEUKOPOIESISLeukopoiesis is the development and maturation of leukocytes.

STEM CELLSThe committed pluripotent stem cell gives rise to colony forming

unit and lymphoid stem cell. • COLONY FORMING UNIT• Different colony forming units are:1. Colony forming unit-Erythrocytes (CFU-E)2. Colony forming unit-Granulocytes and Monocytes (CFU-GM)3. Colony forming unit-Megakaryocytes (CFU-M)

• DEVELOPMENT OF GRANULOCYTES• Granulocytes are formed in bone marrow. The colony forming

unit-granulocyte-monocyte (CFU-GM) gives origin to myeloblast. From myeloblast, three types of cells are formed.

1. Neutrophil myelocyte2. Eosinophil myelocyte and3. Basophil myelocyte

• Neutrophil: Neutrophi myelocyte develops into neutrophils metamyelocyte that forms neutrophil.

• Basophil: Basophil myelocyte is converted into basophil metamyelocyte that is developed into basophil.

• Eosinophil: Eosinophil myelocyte is converted into eosinophils myelocyte and this forms eosinophil.

DEVELOPMENT OF AGRANULOCYTESFormation of MonocytesMonocytes are also developed from bone marrow; stem cell is

colony forming unit-granulocyte-monocyte [CFU-GM] that develops into myeloblast. The myeloblast is converted into monoblast, which develops into monocyte.

Formation of Lymphocytes The stem cells for lymphocytes are in the bone marrow. The

pluripotent stem cell gives origin to colony forming units (CFU) and lymphoid stem cells (LSC). The Lymph stem cells give origin to Lymphoblast, which develop lymphocytes. These lymphocytes are released from bone marrow into the circulation. Then, some of lymphocytes enter the thymus. In thymus, these lymphocytes are processed and come out of thymus as lymphocytes. The remaining cells enter liver and bone marrow and are processed as B lymphocytes.

THROMBOPOIESIS

DEVELOPMENT OF PLATELETS• Platelets are formed from bone marrow. The pluripotent stem

cell gives rise to the CFU-M. This develops into megakaryocyte. The cytoplasm of megakaryocyte form pseudopodium. A portion of pseudopodium is detached to form platelet, which enters the circulation

• Production of platelets is influenced by colony stimulating factors and thrombopoietin. Colony stimulating factors are secreted by monocytes and T lymphocytes. Thrombopoietin is a glycoprotein like erythropoietin. It is secreted by liver and kidneys.

• Factors regulating Thrombopoiesis

– Interleukins --IL3, IL6, IL11

– CSF’s

– Thrombopoietin—liver & kidney

– TGFβ

COMPOSTION OF BLOOD

• Blood contains the blood cells which are called formed elements and the liquid portion known as plasma.

• Blood is a specialized type of connective tissue in which living blood cells, (formed elements), are suspended in a non living fluid matrix called plasma.– Cellular Part (Formed Elements) – Non cellular part (Plasma)

• 55 % plasma– Plasma is the straw-colored liquid in which the blood cells

are suspended. • 45 % formed elements

– Red blood cells (Erythrocytes)– White blood cells (leukocytes)

– Platelets (thrombocytes)

PLASMA• Plasma is the relatively clear liquid water , sugar, fat, protein

and salt solution which carries the red cells, white cells, platelets, and some other chemicals.

• Normally, 55% of our blood's volume is made up of plasma. About 95% of it consists of water.

• As the heart pumps blood to cells throughout the body, plasma brings nourishment to them and removes the waste products of metabolism.

Organic Substances of Plasma

The following are the organic substances of the plasma.

1. Proteins: Proteins present in plasma, albumin, globulin & fibrinogen are specifically known as plasma proteins.

2. Carbohydrates: The carbohydrate is present in plasma mainly in the form of glucose.

3. Fats: The lipid substances present in plasma are the neutral fats, phospholipids and cholesterol.

4. Amino acids: Plasma contains both essential and non essential amino acids.

5. Non protein nitrogenous substances: The plasma also contains some non protein nitrogenous substances like ammonia, creatine, creatinine, xanthine, hypoxanthine, urea and uric acid.

6. Internal secretions: The plasma contains many hormones.

7. Enzymes: The enzymes like amylase, carbonic anhydrase, alkaline phosphatase, acid phosphatase, lipase, esterase, protease and transaminase are present in plasma.

8. Antibodies: The plasma contains many antibodies, which are called immunoglobulins

Inorganic Substances of Plasma

ION SYMBOLCONC

(mmol/l)

Sodium Na+ 135-146

Potassium K+ 3.5-5.2

Calcium Ca++ 2.1-2.7

Chloride Cl- 98-108

HydrogenCarbonate

HCO3- 23-31

Phosphate PO4-- 0.7-1.4• GASES PRESENT IN PLASMA:

– O2 & CO2

Red Blood Cells

• Red cells, or erythrocytes , are relatively large microscopic cells without nuclei. • Red cells normally make up 40-50% of the total blood volume. • They transport oxygen from the lungs to all of the living tissues of the body and carry away carbon dioxide. • The red cells are produced continuously in our bone marrow from stem cells at a rate of about 2-3 million cells per second.

• Hemoglobin is the gas transporting protein molecule that makes up 95% of a red cell.

• Each red cell has about 270,000,000 iron-rich hemoglobin molecules.

– People who are anemic generally have a deficiency in red cells.

• The red color of blood is primarily due to oxygenated red cells.

Morphology

• Shape : circular, biconcave (dumb bell shaped)

• Size : 7.2 µm

• Thickness : 2.2 µm, 1 µm

• Volume : 90-95 µm3

• Surface area : 130 µm2

• Avg. count

– Male : 5-6 million/mm3

– Female : 4.5-5.5 million/mm3

– Infant : 6-7 million/mm3

Structure• Cell membrane consists of lipid and protein molecules.• Blood group antigens are present on the surface.• Spectrin is a contractile protein present on the cell membrane

which help to keep the biconcave shape.• Metabolic needs are met by glucose.• Normally, the red blood cells are disc shaped and biconcave

(dumb-bell shaped). The biconcave contour of red blood cells has the following mechanical advantages.

1. It helps in equal and rapid diffusion of oxygen other substances into the interior of the cell.

2. Large surface area is provided for absorption removal of different substances.

3. Minimal tension is offered on the membrane wh the volume of cell alters.

4. While passing through minute capillaries, these cells can squeeze through the capillaries very easily.

Properties Of Rbc’s1. ROULEAUX FORMATIONWhen blood is taken out of the blood vessel, the red blood cells

pile up one above another like the pile of coins. This property of the red blood cells is called rouleaux (pleural = rouleau) formation.

2. SPECIFICGRAVITYThe specific gravity of red blood cell is 1.092 to 1.101.

ROULEAUX FORMATION

ROULEAUX FORMATION

3. PACKED CELL VOLUME

When the blood is collected in a centrifuge tube along with proper anticoagulant and centrifuged for a period of 30 minutes at a speed of 3000 rpm (revolutions per minute),the red blood cells settle at the bottom of the tube leaving the clear plasma at the top. The red blood cells form 45% of the total blood. This is called the packed cell volume or hematocrit. The volume of plasma is 55%.

4. SUSPENSION STABILITY

During circulation, the red blood cells remain suspended uniformly in the blood. This property of the red blood cells is called the suspension stability.

FUNCTIONS• Transport of Hb

• Exchange of CO2 – carbonic anhydrase

• Acid base buffer – Hb

• Blood group antigens

Life Span and Fate of RBC’s

• Average life span of red blood cell is about 120 days. The senile blood cells are destroyed in reticuloendothelial system.

• When the cells become older (120 days), the cell membrane becomes more and more fragile. The diameter of the capillaries is less or equal to that of red blood cell. The younger red blood cells can pass through the capillaries easily. However, because of the fragile nature, the older cells are destroyed while trying to squeeze through the capillaries. The destruction occurs mostly in the capillaries of spleen because; the splenic capillaries have a thin lumen. So, the spleen is usually called Graveyard of red blood cells.

• The destroyed red blood cells are fragmented. From the fragmented parts, the hemoglobin is released. The iron and globin parts of the hemoglobin are separated with the production of bilirubin. Iron combines with the protein apo ferritin to form ferritin, which is stored in body. Globin also enters the protein depot the bilirubin is excreted by liver through bile.

• Daily 10% red blood cells, which are senile, get destroyed in normal young healthy adults. This causes release ofabout0.6 g% of hemoglobin into the plasma. From this 0.9 to 1.5mg% bilirubin is formed.

Variations In RBC Structure

• In Number

• In Size

• In Shape

• In Structure

PHYSIOLOGICAL VARIATIONS• Increase in count--Physiological Polycythemia

– Age

– Sex – High altitude– Muscular exercise– Emotional conditions– Increased environmental temperature

– After meals

• Decrease in count– High barometric pressure– After sleep– Pregnancy

PATHOLOGICAL VARIATIONS• Pathological Polycythemia

– Primary Polycythemia – Polycythemia Vera

– Secondary Polycythemia

• Anemia

Variations In RBC Size

• Microcytes– Iron deficiency anemia– Prolonged forced breathing– Increased osmotic pressure in blood

• Macrocytes

– Megaloblastic anemia– Muscular exercise– Decreased osmotic pressure in blood

• Anisocytes– Pernicious anemia

Variations In RBC Shape

1. Crenation: Shrinkage -- hypertonic solution

2. Spherocytosis: Globular -- hypotonic solution

3. Elliptocytosis: Elliptical -- certain anemias

4. Sickle cell: Crescentic -- sickle cell anemia

5. Poikilocytosis: flask, hammer, unusual shape--deformed cell

membrane

Variations In RBC Structure

1.Punctate Basophilism(In this condition, dots of basophilic

materials (porphyrin) appear in the red blood cells giving a

stripped appearance. This occurs in conditions like lead

poisoning.)

2. Ring(Ring or twisted strands of basophilic material appearing

at the periphery of the red blood cells. This is also called the

Goblet ring. This appears in the red blood cells in certain types

of anemia)

3. Howell-Jolly Bodies(In certain types of anemia, some nuclear

fragments are present in the ectoplasm of the red blood cells.

These nuclear fragments are called Howell-Jolly bodies.)

Hemoglobin• Hemoglobin is a conjugated protein. It consists of a protein

combined with an iron containing pigment. The protein part is globin and the iron containing pigment is heme.

IRON• It is present in ferrous (Fe++) form. It is in unstable or loose

form. Under certain conditions, the iron may be present in ferric (Fe+++) state, which is a stable form.

PORPHYRIN

• The pigment part is called porphyrin. This is formed by four pyrole rings (tetrapyrole) called, I, II, III and IV. The pyrole rings are attached to one another by methane (CH4) bridges. The iron is attached to N-of each pyrole ring and N-of globin molecule.

GLOBIN

• This contains four polypeptide chains. Among the four polypeptide chains, two are alpha chains and two are beta chains.

• Molecular weight of the polypeptide chains:• Alpha chains : 15,126• Beta chains : 15,866• Number of amino acids in the polypeptide chains:

• Alpha chains : 141• Beta chains : 146

• Structure of HaemIn a haem molecule, there are four pyrrole structures The four pyrroles are linked up with one another by methane(= CH - ) bridges, to form, what is known as porphyrin.There are various types of porphyrins. The particular type of porphyrin found in hemoglobin is called protopor­phyrin III and as it contains an iron in the central part of the molecule, it is called iron protoporphyrin. Haem is iron protoporphyrin.

Properties of Hb1. Oxygen affinity

2. Haem-haem interaction

Properties of Hb1. Oxygen affinity

2. Haem-haem interaction

DERIVATIVES OF HEMOGLOBINHemoglobin readily combines with gas or any other substances to

form some products, which are called the derivatives of hemoglobin. The following are the derivatives of hemoglobin.

1. OXYHEMOGLOBINThis is formed by the combination of hemoglobin with oxygen

by the physical process of oxygenation. Oxyhemoglobin is an unstable compound and the combination is reversible, i.e. the oxygen can be released from this compound. The iron remains in ferrous state in this compound.

2. REDUCED HEMOGLOBIN OR FERROHEMOGLOBINWhen O2 is released from oxyhemoglobin, it is called reduced

hemoglobin or ferrohemoglobin.

3. CARBHEMOGLOBINIt is the derivative of hemoglobin with carbon dioxide. Carbon

dioxide can be released easily from this. The affinity of hemoglobin for carbon dioxide is 20 times more than for oxygen.

4. CARBOXYHEMOGLOBINThe combination of hemoglobin with carbon monoxide produces

this. The affinity of hemoglobin for carbon monoxide is 200 times more than its affinity for oxygen.

5. SULFHEMOGLOBINIt is formed by the combination of hemoglobin with hydrogen

sulfide.

6. NITROUS OXIDE HEMOGLOBINIt is produced when hemoglobin combines with nitrous oxide.7. METHEMOGLOBIN OR FERRIHEMOGLOBINIt is formed when blood is treated with potassium ferricyanide. It

is a stable compound. The iron is in ferric form.

TYPES OF HEMOGLOBIN

1.Adult hemoglobin-HbA —globin contains 2 α

and 2 β chains

2.Fetal hemoglobin-HbF -- 2 α and 2 γ chains

instead of β chains.

Fetal HbAdult Hb

NORMAL VALUES• Average hemoglobin (Hb) -- 14 to 16 gm%. • At different ages:

– At birth : 25 gm%– After 3rd month : 20 gm%

– After1 year : 17 gm%

– Sex :

– In adult males : 15 gm%

– In adult females : 14.5 gm%

• SYNTHESIS OF HEMOGLOBIN

– Starts in proerythroblastic stage.

– Appears only in Intermediate normoblast stage

– Heme—Acetic acid & glycine -- mitochondria

– Globin -- ribosomes

• DESTRUCTION OF HEMOGLOBIN

– IRON: Stored in body as ferritin and hemosiderin and

reutilized for synthesis of new Hb.

– GLOBIN: Utilized for resynthesis of hemoglobin.

– PORPHYRIN: Converted into a green pigment - biliverdin.

ABNORMAL HEMOGLOBIN

• Due to gene mutation -- structural variation in polypeptide chains.

• In hemoglobinopathy, structural abnormality in polypeptide

chains.

– Hemoglobin S --sickle cell anemia. α chains normal & β

chains abnormal.

– Hemoglobin C --hemoglobin C disease. β chains abnormal.

– Hemoglobin E --hemoglobin E disease. β chains are abnormal.

• In thalassemia, polypeptide chains are decreased, absent or

abnormal.

– In α thalassemia, α chains are decreased, absent or abnormal

and

– In β thalassemia, β chains are decreased, absent or abnormal.

• Abnormalities of an individuals hemoglobin value can indicate defects in red blood cell balance.

• Both low and high values can indicate disease states

ERYTHROCYTE SEDIMENTATION RATE

• Also known as: Sed Rate; Sedimentation Rate; Westergren Sedimentation Rate.

• The erythrocyte sedimentation rate (ESR or sed rate) is a relatively simple, inexpensive, non-specific test that has been used to detect inflammation associated with conditions such as infections, cancers and autoimmune diseases.

• Determination– Westergren’s Method– Wintrobe’s Method

Variations of ESRPhysiological

• Age: Less in children & infants• Sex: F>M• Menstruation: Increased• Pregnancy: Increased

PathologicalIncreases- TB, Anemias, Malignant tumours, RA, RF, and

Liver diseases.Decreases – Allergic conditions, Sickle cell An, Peptone

shock, Polycythemia and Extreme Leukocytosis

FACTORS AFFECTING ESR

1. Specific gravity of RBC’s :

– ESR increased

2. Rouleaux formation -- Increases ESR.

– Albumin and globulin accelerate rouleaux formation.

3. Increased size of RBC’s -- ESR increased.

4. Viscosity of blood: ESR is reduced when viscosity more.

5. Number of RBC’s :

– number more -- ESR decreased.

– RBC count less -- ESR increased.

PACKED CELL VOLUME

• The hematocrit (Ht or HCT, British English spelling haematocrit), also known as packed cell volume (PCV) or erythrocyte volume fraction (EVF), is the volume percentage (%) of red blood cells in blood. It is normally 45% for men and 40% for women.

• The packed cell volume (PCV) can be determined by centrifuging heparinized blood in a capillary tube (also known as a microhematocrit tube) at 10,000 RPM for five minutes.This separates the blood into layers. The volume of packed red blood cells divided by the total volume of the blood sample gives the PCV. Since a tube is used, this can be calculated by measuring the lengths of the layers.

• With modern lab equipment, the hematocrit is calculated by an automated analyzer.

• SIGNIFICANCE OF DETERMINING PCV– Determination of anemia– Determination of polycythemia– Extent & recovery from dehydration.– Decision of blood transfusion

• VARIATIONS IN PCV– PCV increases in polycythemia and dehydration.– Decreases in anemia, pregnancy and cirrhosis of liver.

Blood Indices

• Different Blood Indices

– Mean Corpuscular Volume (MCV)

– Mean Corpuscular Hemoglobin (MCH)

– Mean Corpuscular Hemoglobin Concentration (MCHC)

– Color Index (CI)

MEAN CORPUSCULAR VOLUME (MCV)

Average volume of a single red blood cell

– Normal MCV = 90 cu µ (78to 90 cu µ).

– When increased-- macrocyte

• pernicious anemia

• megaloblastic anemia

– When decreased—microcyte

• microcytic anemia

MEAN CORPUSCULAR HEMOGLOBIN (MCH)

Quantity or amount of Hb present in one RBC

– Normal value of MCH is 30 pg (27 to32pg)

– Decreases or remains normal

• pernicious anemia

• megaloblastic anemia

– RBC’s are macrocytic & normochromic or hypochromic

– Decreases in hypochromic anemia.

– Normal MCH -- normochromic state.

MEAN CORPUSCULAR HEMOGLOBIN

CONCENTRATION (MCHC)

Conc of Hb in one RBC -- amount of Hb expressed in relation

to vol of one RBC.

– Most important absolute value in diagnosis of anemia.

– Normal value of MCHC is 30% (30 to 38%)

– Decreased in iron deficiency anemia -- RBC’s are

microcytic and hypochromic.

COLOUR INDEX (CI)

Ratio between % of Hb and % of RBC’s in blood.

Avg Hb content in 1 cell of a patient compared to avg Hb

content in 1 cell of a normal person.

– Normal colour index is 1.0 (0.8to 1.2).

– Useful in determining type of anemia.

– Raised in pernicious anemia and megaloblastic anemia.

– Reduced in iron deficiency anemia.

– Normal in normocytic normochromic anemia.

WHITE BLOOD CELLS

White Blood Cells: Battling Blood Cells

• Leukocyte is the colourless and nucleated formed element of blood. Leukocytes play very important role in defense mechanism of the body.

• Depending upon the presence or absence of granules in the cytoplasm, the leukocytes are classified into 2 types namely-

White cells, or leukocytes , exist in variable numbers and types but make up a very small part of blood's volume--normally only about 1% in healthy people. Leukocytes are not limited to blood. They occur elsewhere in the body as well, most notably in the spleen, liver, and lymph glands.

• NEUTROPHILS

• Size : 10- 14 µm diameter

• Nucleus : purple, multilobed

• Lobes :2,3 upto 5 or more. Young cell—less lobes. Arneth

Count

• Cytoplasm :blue , granular

• Granules : fine, amphophilic /neutrophilic, have lytic enzyme

1. Primary/azurophilic /lysosomal --phagocytosis

2. Secondary – inflammation

• Life span :2-5 days

• Functions : phagocytosis – 1st line of defense

• Neutrophilia:

– Physiological cause :

• exercise

• lactation

• pregnancy

– Pathological cause :

• acute pyogenic infection

• Neutropenia:

– Causes :

• typhoid and viral fever

• bone marrow depression

• EOSINOPHILS

• Size : 10- 14 µm diameter

• Nucleus : purple, bilobed

• Cytoplasm : acidophilic

• Granules : coarse, bright red, have lysozymes

– Major basic proteins (MBP) - histaminase

– Eosinophil peroxidase (EPO)– histamine secretion

– Cationic proteins -neurotoxin

• Life span : 7-12 days

• Functions :

– limit allergic intensity

• eg Bronchial asthma, hay fever

– mild phagocytosis

• Eosinophilia :

– Causes :

• allergic conditions

• parasitic infections

• Eosinopenia :

– Causes :

• injection Of corticosteroids

• BASOPHILS

• Size : 10-14 µm diameter

• Nucleus : bilobed, S shaped

• Cytoplasm : basophilic, granular

• Granules : coarse, purple/ blue, plenty, contain

– Heparin

– Histamine

– Hyaluronic acid

– Proteases & myeloperoxidases

• Life span : 12-15 days

• Functions :– librates histamine– librates heparin – mild phagocytosis

• Basophilia : – Causes :

• chicken pox • small pox• tuberculosis• influenza

• Basopenia– Causes :

• administration of glucocorticoids

• LYMPHOCYTES

• Can be classified in two ways

– Based on structure :

a) large : 10-14 µm

b) small : 7-10 µm– Based on maturation :

a) T Lymphocytes –80%

b) B Lymphocytes -15%

c) NK Cells-5%

• T cells – CD4 & CD8

• Life span : ½-1 day

• Function of T cells :

– secrete lymhokines

– induction of apoptosis in target cells

– create pores by perforin in target cells

• Function of B cells :

– produce plasma cells- immmunoglobins

• Nk cells/ large granular lymphocytes

– attack cancer cells and viruses

• Lymphocyte mediated immunity

• Cell mediated immunity

• Humoral immunity - Ag-Ab

• MONOCYTES

• Size : 10- 18 µm diameter (largest)

• Nucleus : pale , round/kidney shaped

• Cytoplasm : clear , pale blue , agranular

• Life span : 48-72 hrs in blood & 3 months in tissues.

• Reticuloendothelial system :

blood monocytes + tissue macrophages

• Functions :

– phagocytosis – 2nd line of defense

– secretions of chemical activators of inflammation

• IL-1,TNFβ, binding proteins like transferrin, lysozyme,

proteases, acid hydrlase

– lymphocyte mediated immunity – antigen presenting cells

– role in tissue repair

PROPERTIES OF WBC’s

1. Diapedesis

2. Ameboid Movement

– Neutrophils,

– Monocytes

– Lymphocytes

3. Chemo taxis

4. Phagocytosis

– Neutrophils

– Monocytes

VARIATIONS IN WBCs

Normal Count – 4000-11000/cmm of blood

Leucocytosis –↑ in WBC count above 11000/cmm of blood

Leucopenia – ↓ in WBC count below 4000/cmm of blood

PHYSIOLOGICAL VARIATIONS :-

1)Diurnal :- WBC count > in the evening than in the morning

2)Meals , Pregnancy, Fear, pain, anxiety & Exercise ↑ the count

3)Age :- Newborn :-20000/cmm of blood

Lymphocyte :- 40% to 60%

PATHOLOGICAL VARIATIONS :-

1)↑ in Neutrophils – Acute infection , haemorrhage , operations ,

tissue damage

2) ↑ in Eosinophils – Allergy,Parasitic infections

3) ↑ in Monocytes – Chronic infections

)↑ in lymphocyte – Whooping cough , Tuberculosis , leprosy

5) ↑ in Basophils – Lead poisoning

LEUKOPENIA

1) ↓ in Neutrophils – Viral infections

2) ↓ in Eosinophils – Cortisol therapy

3) Bone marrow depression causes in ↓ neutrophil , eosinophil , basophil , monocyte

LEUKEMIA• Group of disorders characterised by malignant

transformation of blood –forming cells• Proliferation of leukaemic cells –Primarily in the bone

marrow• Classification – 1)On the basis of cell types predominantly involved :- a) Myeloid b) Lymphoid 2) On the basis of natural history of disease :- a)Acute b)Chronic

• Account for 4% of all cancer deaths• Incidence higher in men than in women• Causes:- # Genetic factors # Environmental factors # Infection

PLATELETS

Platelets or thrombocytes are small colourless, non nucleated and moderately refractive bodies. These formed of blood are considered to be the fragments of plasm. Their diameter is 2.5 microns (2 to 4) and, the lume is 7.5 cubic microns (7 to 8 cubic microns). Normally, the platelets are spherical or rod shaped and become oval or disc shaped when inactivated. Some say the platelets are of dumb bell, comma, cigar or other unusual shape.

Platelets or thrombocytes are small colourless, non nucleated and moderately refractive bodies. These formed of blood are considered to be the fragments of plasm. Their diameter is 2.5 microns (2 to 4) and, the lume is 7.5 cubic microns (7 to 8 cubic microns). Normally, the platelets are spherical or rod shaped and become oval or disc shaped when inactivated. Some say the platelets are of dumb bell, comma, cigar or other unusual shape.

Platelets: Sticky Situations

Platelets

• Size : 2-4 µm diameter (Smallest)

• Count : 1.5- 4 lakh/µl

• Shape : spherical, oval/ rounded granulated

• Structure : non-nucleated mass of protoplasm

disc like -- inactive

spherical--active

• Life span : 8 -12 days

• Destruction : Spleen

PROPERTIES OF PLATELETS1. ADHESIVENESS

When platelets come in contact with any wet surface, rough surface, these are activated and stick to the surface. The factors, which cause adhesiveness, are collagen, thrombin, ADP, Thromboxane A2, calcium ions and von Willebrand factor.

2. AGGREGATION (GROUPING OF PLATELETS)

The activated platelets group together and become sticky. The stickiness is due to ADP and thromboxane A2.

3. AGGLUTINATION

Agglutination is the clumping together of platelets. The agglutination of platelets occurs due to the actions of platelet agglutinins.

1. ROLE IN BLOOD CLOTTINGThe platelets are responsible for the formation of intrinsic

prothrombin activator. This substance is responsible for the onset of blood clotting.

Functions

2. ROLE IN CLOT RETRACTION

In the blood clot, the blood cells including platelets are entrapped in between the fibrin threads. The cytoplasm of platelets contains the contractile proteins namely actin, myosin and thrombosthenin. The contractile proteins are responsible for clot retraction.

3. ROLE IN PREVENTION OF BLOOD LOSS (HEMOSTASIS)

Platelets accelerate the processes of hemostasis by three ways:

a. Platelets secrete 5 HT, which causes the constriction of blood vessels.

b, Due to the adhesive property, the platelets can seal the damage in blood vessels like capillaries.

c, By formation of temporary plug also platelets seal the damage in blood vessels.

4. ROLE IN REPAIR OF RUPTURED BLOOD VESSEL

The platelet derived growth factor (PDGF) formed in cytoplasm of platelets is useful for the repair of the endothelium and other structures of the ruptured blood vessels.

5. ROLE IN DEFENSE MECHANISM

By the property of agglutination, platelets encircle the foreign bodies and kill them by the process of phagocytosis.

PHYSIOLOGICAL• Age: Platelets are less in infants (1,50,000 to 2,00,000/ cu

mm) and reaches normal level at 3rd month after birth.• Sex: There is no difference in the platelet count I between

males and females. In females, it is reduced I during menstruation.

• High altitude: Platelet count is increased in high I altitude.• After meals: After taking food, the platelet count is increased.

VARIATIONS

• PATHOLOGICAL VARIATIONS

• Thrombocytosis :

– Causes :

• After trauma • Splenectomy• Stress• Hemorrhage • Bone fractures

• Rheumatic fever and

• Thrombocytopenia :

– Causes :

• Acute infections • Acute leukemia

• Aplastic and pernicious anemia

• Splenomegaly • Scarlet fever • Typhoid and • Tuberculosis

• Thrombocythemia -

• Occurs in

Carcinoma

Chronic leukemia and

Hodgkin's disease.

HEMOSTASIS• The term hemostasis means

prevention of blood loss. Whenever a vessel is servered or ruptured, hemostasis is achived by :-

Eventual growth of fibrous tissue into blood clot

1.VASOCONSTRICTION:

• Immediately after injury, there is constriction of blood vessel and this decreases loss of blood from the damaged vessel. Usually, arterioles and small arteries constrict. The vasoconstriction is purely a local phenomenon. When the blood vessels are cut, the endothelium is damaged and the collagen is exposed. The platelets adhere to this collagen, and get activated. The activated platelets secrete serotonin and other vasoconstrictor substances. These substances cause constriction of the blood vessels. The adherence of platelets to the collagen is accelerated by von Willebrand factor.

• This factor acts as a bridge between a specific glycoprotein present on the surface of platelet and collagen fibrils. The platelet aggregation is also accelerated by another factor called platelet activating factor (PAF) secreted by neutrophils, monocytes and platelets.

2. FORMATION OF PLATELET PLUG• When platelets adhere to the collagens of ruptured blood

vessel, these platelets secrete ADP and thromboxane A2. These two substances attract more and more platelets and activate them. So, more platelets aggregate and form a temporary loose plug, which closes the vessel am prevents the blood loss.

3. COAGULATION OF BLOOD• During this process, the fibrinogen is converted into fibrin.

The fibrin threads get attached to the loose platelet plug, which blocks the ruptured part of blood vessels and prevents blood loss completely.

• When blood is shed out or collected in a container, it looses its fluidity and becomes a jelly like mass after few minutes. This process is called coagulation or clotting of blood. The clot is a mesh of thin fibrils entangling the blood cells. These fibrils consist of fibrin which is formed from fibrinogen.

CLOTTING FACTORSFACTORS NAME

I Fibrinogen

II Prothrombin

III Thromboplastin

IV Calcium

V Proaccelerin, labile factor

VII Stable factor, proconvertin

VIII Antihaemophilic factor (AHF),

IX Christmas factor

X Stuart – Power factor

XI antihaemophilic factor C

XII Hageman factor

XIII Fibrin stabilizing factor

OTHER FACTORS

HMN-K Pre kallikrein,

Pre-K feltcher factor

Ka Kallikrein

PL Platelet phospholipids

STAGES OF CLOTTING

• Formation of prothrombin activator

– Extrinsic pathway-- initiated by tissue thromboplastin.

– Intrinsic pathway-- initiated by factor XII

• Conversion of prothrombin into thrombin

• Conversion of fibrinogen into fibrin• During the process of blood clotting, the clotting factors,

which are in inactive forms, are converted into active forms. And their enzymatic actions produce the successive reactions one after another in a cascading manner.

Thus, the various reactions involved in blood clotting are explained by enzyme cascade theory

Coagulation Cascade

CLOT FORMATION

Role of Thrombin

BLOOD CLOT• The fibrin threads run in all directions. The red blood cells,

white blood cells and the platelets get entrapped within the meshwork of fibrin. The entire mass of fibrin meshwork and the blood cells entrapped within this is called blood clot. The external blood clot is also called scab.

• This blood clot adheres to the opening of damaged blood vessel and prevents blood loss.

• Red blood cell and white blood cells are not necessary for clotting process. However, when clot is formed, these cells are trapped in it. The trapped red blood cells are responsible for the red color of the clot.

CLOT RETRACTION• After the formation, the blood clot starts contracting. After

about 30 to 45 minutes, a straw coloured fluid called serum oozes out of the clot. The process involving contraction of blood clot and oozing of serum is called clot retraction. The contractile proteins namely, actin, myosin and thrombosthenin present in cytoplasm of platelets are responsible for clot retraction.

Lysis Of Blood Clot• The lysis of blood clot inside the blood vessel is called

fibrinolysis. This occurs by a substance known as plasmin or fibrinolysin.

Significance of Lysis of Clot• In certain organs, particularly the heart, the blood may

obstruct the minute blood vessel leading to cardial infarction. The lysis of blood clot allows reopening of affected blood vessels and prevents the development of infarction. The fibrinolytic enzymes like streptokinase used for the lysis of blood clot during the treated early stages of myocardial infarction.

Why circulating blood does not clot?

1. Continuous movement of blood

2. Smooth endothelium lining

3. Circulatory anticoagulants

4. Fibrinolytic mechanism

5. All the clotting factors are in inactive form

• Role of Ca-First two steps in the intrinsic pathway, calcium ions are required for the

promotion of all reactions in blood coagulation.

Therefore in the absence of calcium ions, clotting will not occur.

Thus, coagulation in vitro can be prevented in vitro (eg. for storage in the blood bank) by removal of the calcium ions.

The use of oxalates and citrates as in vitro anticoagulants is based on this principle.

• Role of vit K-

• Vitamin K is a complex naphthoquinone derivative.

• It is obtained from food as well as synthesized by bacterial flora in the gut.

• In the liver, synthesis of the following factors is dependent upon vitamin K:– Coagulant like prothrombin– Factor VII, IX, X, and– Circulatory anticoagulant protein.

• Deficiency of vitamin K causes prolonged prothrombin time and blood clotting time

• Role of liver-Liver plays following significant role in the coagulation

mechanism:• Synthesis of procoagulants – factor V, VII, IX, X, prothrombin

and fibrinogen.• Removal of activated procoagulants from the blood• Synthesis of anticoagulants like heparin, antithrombin C and

protein C.

Liver failure can cause:

• Bleeding disorders due to hypercoagulability of the blood• Uncontrolled excessive clotting inside blood vessels where

clotting is not only unwanted but also dangerous.

ANTI-COAGULANTS• Invivo:

– Heparin-

– Coumarin derivatives- Dicoumoral and Warfarin inhibit action of vit k

– Genetically engineered steptokinase for treating intravascular clots

• Invitro:– Heparin-

– EDTA – remove calcium from blood .

– Oxalate compounds- calcium oxalate

– Citrates – Na, NH3,K citrate

– ACD, CPD

TESTS FOR CLOTTINGThree tests are available to test the process of coagulation of

blood.• BLEEDING TIME

This is the time interval from oozing of blood after a cut or injury till arrest of bleeding. The normal duration of bleeding time is 3 to 6 minutes. It is prolonged in purpura.

• Screening for – platelet disorders and Willebrand’ s disease• DUKES method• Ivy method

• CLOTTING TIME

The time interval from oozing of blood after a cut or injury till the formation of clot is called clotting time. The normal duration of the clotting time is 3 to 8 minutes. And it is prolonged in hemophilia.

• Wright s capillary tube method: 1-3 min• Lee & White method: 5-11 min

• PROTHROMBIN TIME

Blood is collected and oxalated so that, the calcium is precipitated and prothrombin is not converted into thrombin. Thus, the blood clotting is prevented. Then a large quantity of tissue thromboplastin with calcium is added to this blood. Calcium nullifies the effect of oxalate.

And, the tissue thromboplastin activates prothrombin and blood clotting occurs. During this procedure, the time taken by blood to clot after adding tissue thromboplastin is called prothrombin time. Prothrombin time indicates the total quantity of prothrombin present in the blood.

The normal duration of prothrombin time is about 12 seconds. The prothrombin time is prolonged in deficiency of prothrombin and other factors like factors I, V, VII and X. However, it is normal in hemophilia.

BLEEDING DISORDERS• Hemophilia

– Def of factor VIII

– Secondary hemostatic mechanism faulty

– CT increased but BT, PT normal, Platelet aggregatation normal

• Purpura

– Primary hemostatic mechanism faulty

– Prolonged BT but normal CT, PT, APTT

– Spontaneous bleeding from capillaries-- small tiny hemorrhagic spots in body -- purpuric spots – PURPURA

• von Willebrand disease

– excessive bleeding even with a mild injury.

– reduction in platelet adhesion and 2O deficiency of factor VIII -- excessive bleeding

THROMBOSIS Coagulation of blood inside the blood vessels is called

thrombosis or intravascular blood clotting. Normally, blood does not clot in the blood vessel because of the following reasons.

1. All the clotting factors are in inactive form.

2. Smooth endothelial lining of the blood vessels does not allow the formation of clot.

3. Continuous movement of blood does not allow clot formation.

4. The natural anticoagulants like heparin present in the blood prevent blood clotting.

CAUSES OF THROMBOSIS

1. Injury to Blood Vessels: During infection or mechanical obstruction, the endothelial lining of the blood vessel is damaged and this initiates the thrombosis.

2. Roughened Endothelial Lining: In infection, damage or arteriosclerosis, the endothelium becomes rough and this initiates clotting.

3. Sluggishness of Blood Flow: Decreased rate of blood flow causes aggregation of platelets and formation of thrombus. Slowness of blood flow occurs in reduced cardiac action, hypotension, low metabolic rate, prolonged confinement to bed and immobility of limbs.

4. Agglutination of Red Blood Cells: Agglutination of red blood cells can occur by the foreign antigens or toxic substances. The blood clotting occurs inside the blood vessel during the agglutination of the red blood cells.

5. Toxic Thrombosis: Thrombosis is common due to action of chemical poisons like arsenic compounds, mercury, poisonous mushrooms and snake venom.

6. Congenital Absence of Protein C: Protein C is a circulating anticoagulant, which inactivates factors V and VIII. The thrombosis occurs in the absence of this protein. Congenital absence of protein C can cause thrombosis and death in infancy.

COMPLICATIONS OF THROMBOSIS

• Thrombus

• Embolism and Embolus

– lungs (pulmonary embolism)

– brain (cerebral embolism) or

– heart (coronary embolism).

• Infarction and Infarct

BLOOD GROUPING

• Around 30 different common antigens and hundreds of rare ones

• 21 different systems. Common ones are:

• ABO System

• Rh system

• Lewis system

• MNS system

• P system

• Kell system

• Duffie system

• Lutheran system

• ABO system & Rh system

– Karl Landsteiner – 1900 & 1940

Landsteiner -1901

• Landsteiner laws:– If a particular antigen is present in the RBC , corresponding

antibody must be absent in the plasma– If the particular antigen is absent in the RBC, the

corresponding antibody must be present in the plasma.

Genetics of Blood TypesGenetics of Blood Types

Our blood type is established before we are BORN, by specific GENES inherited from our parents.

We inherit one gene from our MOTHER and one from our FATHER.

These genes determine our blood type by causing proteins called AGGLUTINOGENS to exist on the surface of all of our red blood cells.

Our blood type is established before we are BORN, by specific GENES inherited from our parents.

We inherit one gene from our MOTHER and one from our FATHER.

These genes determine our blood type by causing proteins called AGGLUTINOGENS to exist on the surface of all of our red blood cells.

ABO blood grouping system

• Blood group A If you belong to the blood group A, you have A antigens on the surface of your RBCs and B antibodies in your blood plasma.

• Blood group B If you belong to the blood group B, you have B antigens on the surface of your RBCs and A antibodies in your blood plasma.

Blood group OIf you belong to the blood group O (null), you have neither A or B antigens on the surface of your RBCs but you have both A and B antibodies in your blood plasma.

Rh Blood Group

Rh FACTOR• Rh factor is an antigen present in red blood cell. The antigen

was discovered by Landsteiner and Wiener. Since it was first discovered in rhesus monkey, it was named as Rh factor. There are many Rh antigens but only the D is more antigenic.

• The persons having D antigen are called Rh positive and those without D antigen are called Rh negative. Among Asian population, 85% of people are Rh positive and 15% are Rh negative.

Percentage of People Belonging to Different Blood Groups

Population A B AB O

Europeans 42 9 3 46

Asians 25 25 5 45

Asians

25%

25%5%

45% A

B

AB

O

Europeans

42%

9%3%

46% A

B

AB

O

Asian population – 85% Rh +ve and 15% Rh -ve Asian population – 85% Rh +ve and 15% Rh -ve

• According to above blood grouping systems, you can belong to either of following 8 blood groups:

Erythroblastosis Fetalis

• Importance of blood grouping

– For blood transfusion

– In criminal practice or in forensic medicine

– In study of anthrophology

– Predominance of certain diseases

– In the study of disputed paternity.

BLOOD TRANSFUSIONBlood transfusion is defined as the process of

receiving blood products into one’s circulation

intravenously. this is usually done as a life saving

maneuver to replace blood cells or blood products

lost through severe bleeding, during surgery when

severe blood loss occurs or to increase the blood

count in an anaemic patient.

Transfusions usually involve the use of two sources ofBlood – one’s own (autologous transfusion) orSomeone else’s (allogenic transfusion).Blood transfusions involves the use of whole blood ,Red blood cells, white blood cells, plasma, clottingFactors and platelets.

Who can give you blood?

People with TYPE O blood are called Universal Donors, because they can give blood to any blood type.

People with TYPE AB blood are called Universal Recipients, because they can receive any blood type.

Rh + Can receive + or -

Rh - Can only receive -

Universal Donor

Universal Recipient

• When conducting a blood transfusion, it is important to carefully match the donor and recipient blood types. If the donor blood cells have surface molecules that are different from those of the recipient, antibodies in the recipient's blood recognize the donor blood as foreign. This triggers an immune response resulting in blood clotting.

• If the donor blood cells have surface molecules that are the same as those of the recipient, the recipient's body will not see them as foreign and will not mount an immune response.

Indications for transfusion of whole blood or its derivatives

• WHOLE BLOOD TRANSFUSION

Loss of whole blood due to--

– Accidental injuries

– During and after major surgery

PACKED CELL TRANSFUSION :

Patients with severe anaemia - Hb conc < 4 gms%

Patients suffering from agranulocytosis.

• LEUKOCYTE TRANSFUSION :

• Patients with decreased immunity (increased susceptibility for

infections) or

• Patients suffering from agranulocytosis.

• PLATELET TRANSFUSION

– Disorders due to Thrombocytopenia.

• TRANSFUSION OF COAGULATION FACTORS

– Factors VIII or AHG -- hemophilic patient

– Factor IX -- patient suffering from Christmas disease.

– Factors obtained in concentrated form from fresh plasma

(human) by way of cryoprecipitation.

Precautions while Blood transfusion

Precautions while Blood transfusion

BEFOREBEFORE DURING DURING AFTERAFTER

No

communicable

diseases

No

communicable

diseases

Matching ABO &Rh compatibility

Matching ABO &Rh compatibility

Volume overloadVolume overload Observation for delayed effects

Observation for delayed effects

Metabolic side effectsMetabolic side effects

Complications of Blood Transfusion

• Can be of different types:

– Transfusion reactions

– Transmission of diseases

– Reaction caused by massive transfusion

– Complication of IV fluid administration

• Transfusion reactions:– Incompatibility

– Allergic reactions

– Sensitization to leukocytes & platelets

• Transmission of diseases:– Serum hepatitis

– AIDS

– Bacterial infections

• Reaction due to massive transfusion :

– Acid-base imbalance

– Hyperkalemia

– Hypothermia

• Complication of general IV fluid

administration:

– Thrombo embolism

– Air embolism

ROLE OF PUBLIC HEALTH DENTIST Dental professionals can play an important role in early

detection and referral of patients with hypertension and prehypertensives. During their practice, dentists come across significant number of patients with undetected high BP or uncontrolled hypertension and also known hypertensives. These patients are at high risk for various complications as well as for acute medical problems when receiving dental treatment.

Dental practitioners as other healthcare workers confront a identified risk of occupational exposure to blood-borne pathogens like the Human Immunodeficiency Virus (HIV), the hepatitis B virus (HBV), and the hepatitis C virus (HCV).

LIST OF BLOOD DONATION AGENCIES IN INDIA

• Blood Cross Society

• Indian Red Cross Society

• friends2support

• ISBTI- Indian Society of Blood Transfusion & Immunohaematology

• Sankalap Indian Foundation

• Sujla Blood doner

CONCLUSION

• The function of the circulation is to service the needs of the tissues to transport nutrients to the tissues, to transport waste products away, to conduct harmones from one part of the body to another and the ability to provide immunity to the body.

• In general to maintain an appropriate environment in all the tissue fluids for optimal survival and function of the cells.

• Disorders of the blood can influence dental treatment . The dentist should be able to detect abnormalities by history, clinical examination, and screening laboratory tests .

• Patients with disorders of the blood may be susceptible to abnormal bleeding, delayed wound healing, infection, or mucosal ulceration.

• Only those who have had bloodborne pathogen training should clean up a blood spill, because they understand the hazards and how to keep them selves safe while properly handling the clean-up process.

• Wear appropriate protective equipment. At a minimum you must wear gloves and eye protection during spill clean-up to protect yourself from exposure.

• Use disposable towels to soak up most of the blood and properly dispose of immediately after use.

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• Review of medical physiology – William Ganong

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• Essentials of medical physiology, : Sembulingam 4th ed jaypee publications

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• Review of medical physiology , William F Ganong ; 22nd edition

• Understanding medical physiology , RL Bijlani ; 2nd edition jaypee publications.

• Jelkmann . Erythropoetin ; structure ,control of production , and function . Physiol rev 2002 ; 72; 449 – 489.

• Johnston RB . Monocytes and macrophages , N engl –j med 1998 ; 318 :747-52.

• Rao G H R . Physiology of blood platelet activation .Indian space J Physiol pharmacol 1998; 37 : 263-275

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• Alberts, Bruce (2012). "Table 22-1 Blood Cells". Molecular Biology of the Cell. NCBI Bookshelf. Retrieved 1 November 2012.

• Elert, Glenn and his students (2012). "Volume of Blood in a Human". The Physics Factbook. Archived from the original on 2012-11-01. Retrieved 2012-11-01

• Shmukler, Michael (2004). "Density of Blood". The Physics Factbook. Retrieved 4 October 2006.

• "Medical Encyclopedia: RBC count". Medline Plus. Retrieved 18 November 2007.

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• The who handbook on the clinical use of blood – who blood transfusion safety , geneva , 2007.

• Bailey & love’s short practice of surgery – 25

edition –2008.

• Davidson’s principle & practice of medicine – 21edition –2010.

• Essential paediatrics – o.p. ghai – 6Th edition.

• Online text from the british medical journal –

www.bmj.co.uk/bloodtransfusionsafety31781/o3.