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Blood

The document details the history of blood circulation, emphasizing William Harvey's contributions and ancient Indian understandings of blood circulation as described in the Atharvaveda. It discusses the properties, functions, and composition of blood, including its cellular components and plasma proteins, as well as the process of erythropoiesis and hemoglobin synthesis. Additionally, it covers variations in red blood cell counts and the implications for health conditions such as anemia and polycythemia.

HISTORY William Harvey was the first known physician to describe completely and in detail the systemic circulation and properties of blood being pumped to the brain and body by the heart.
THE CONCEPT OF BLOOD CIRCULATION IN ANCIENT INDIA* *THE CONCEPT OF BLOOD CIRCULATION IN ANCIENT INDIA W.S.R TO THE HEART AS A PUMPING ORGAN P.N.Vinaya1, J.S.R.A. Prasad2 (International Ayurvedic Medical Journal) – The concept of blood circulation described in Atharvaveda is amazingly accurate. – Blood, its structure and functions, its importance as a carrier of nutrients and oxygen too find mention. – It is no surprise that the subject of blood circulation and its purpose i.e. carrying of Prana (oxygen technically) and rasa (nutrients) to the entire body in a cyclical manner with the heart acting as a pump to carry out this function were known to our ancient seers long before William Harvey discovered the circulation of blood in the 17th century.
INTRODUCTION Blood is a connective tissue in fluid form. BLOOD FLUID OF LIFE FLUID OF GROWTH FLUID OF HEALTH carries oxygen from lungs to all parts of the body and carbon dioxide from all parts of the body to the lungs. carries nutritive substances from the digestive system and hormones from endocrine gland to all the tissues. protects the body against the diseases and gets rid of the waste products and unwanted substances by transporting them to the excretory organs like kidneys.
PROPERTIES OF BLOOD: VOLUME-5 L. COLOUR-scarlet red because it contains more oxygen and venous blood is purple red because of more carbon dioxide. pH-slightly alkaline -7.4 SPECIFIC GRAVITY-1.052 to 1.061 VISCOSITY-five times more viscous than water
COMPOSITION OF BLOOD – Blood contains the blood cells which are called formed elements and the liquid portion known as plasma. BLOOD CELLS RBC GRANULOCYTES AGRANULOCYTES NEUTROPHILS WBC THROMBOCYTES BASOPHILS EOSINOPHILS LYMPHOCYTE MONOCYTE
Plasma is a straw-colored clear liquid part of blood. It contains 91% to 92% of water and 8% to 9% of solids.
SERUM – Serum is the clear straw-colored fluid that oozes from blood clot. – It is different from plasma only by the absence of fibrinogen, i.e. serum contains all the other constituents of plasma except fibrinogen. – Fibrinogen is absent in serum because it is converted into fibrin during blood clotting. Thus, Serum = Plasma – Fibrinogen
1. NUTRITIVE FUNCTION 2. RESPIRATORY FUNCTION 3. EXCRETORY FUNCTION 4.TRANSPORT OF HORMONES AND ENZYMES FUNCTIONS OF BLOOD
5. REGULATION OF WATER BALANCE 6. REGULATION OF ACID-BASE BALANCE 7. REGULATION OF BODYTEMPERATURE 8. STORAGE FUNCTION FUNCTIONS OF BLOOD 9. DEFENSIVE FUNCTION
1. Glucose, amino acids, lipids and vitamins are absorbed from GIT and carried by blood to different parts of the body for growth and production of energy. 2 Transport of respiratory gases is done by the blood 3 Waste products formed in the tissues during various metabolic activities are removed by blood and carried to the excretory organs like kidney, skin, liver, etc. for excretion. 4 Hormones which are secreted by ductless (endocrine) glands are released directly into the blood. The blood transports these hormones and enzymes to their target organs. 5. Water content of the blood is freely interchangeable with interstitial fluid. 6. Plasma proteins and hemoglobinact as buffers and help in the regulation of acid- base balance 7. 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 Blood serves as a readymade source for substances like proteins, glucose, sodium and potassium during the conditions like starvation, fluid loss, electrolyte loss, etc. 9. Blood plays an important role in the defense of the body. The white blood cells are responsible for this function. Neutrophils and monocytes engulf the bacteria by phagocytosis. Lymphocytes are involved in development of immunity. Eosinophils are responsible for detoxification, disintegration and removal of foreign Proteins
PLASMA PROTEINS – Plasma proteins are: 1. Serum albumin 2. Serum globulin 3. Fibrinogen. Normal values of the plasma proteins are: Total proteins : 7.3 g/dL (6.4 to 8.3 g/dL) Serum albumin : 4.7 g/dL Serum globulin : 2.3 g/dL Fibrinogen : 0.3 g/dL
PROPERTIES OF PLASMA PROTEINS 1. MOLECULAR WEIGHT – Albumin : 69,000 – Globulin : 1,56,000 – Fibrinogen : 4,00,000 2. ONCOTIC PRESSURE: 25 mm Hg 3. SPECIFIC GRAVITY: 1.026 4. BUFFER ACTION: The plasma proteins have 1/6 of total buffering action of the blood.
FUNCTIONS OF PLASMA PROTEINS 1. ROLE IN COAGULATION OF BLOOD 2. ROLE IN DEFENSE MECHANISM OF BODY 3. ROLE IN TRANSPORT MECHANISM 4. ROLE IN MAINTENANCE OF OSMOTIC PRESSURE IN BLOOD
5. ROLE IN REGULATION OF ACID-BASE BALANCE 6. ROLE IN VISCOSITY OF BLOOD 7. ROLE IN ERYTHROCYTE SEDIMENTATION RATE 8. ROLE IN SUSPENSION STABILITY OF RED BLOOD CELLS 9. ROLE IN PRODUCTION OF TREPHONE SUBSTANCES 10. ROLE AS RESERVE PROTEINS
VARIATIONS IN PLASMA PROTEIN LEVEL – Elevation of all fractions of plasma proteins is called hyperproteinemia and decrease in all fractions of plasma proteins is called hypoproteinemia.
RED BLOOD CELLS
RBCs -INTRODUCTION – Red blood cells are the non-nucleated formed elements in the blood. – Red color of the red blood cell is due to the presence of the coloring pigment called hemoglobin. – NORMAL RBC count ranges between 4 and 5.5 million/cu mm of blood.
>NORMAL SHAPE – Disk shaped and biconcave(dumbbell shaped). – Central portion is thinner and periphery is thicker. >NORMAL SIZE – Diameter : 7.2-7.5 μ – Surface area : 120 sq μ. >NORMAL STRUCTURE – Red blood cells are non-nucleated. – RBC has a special type of cytoskeleton, which is made up of actin and spectrin. – Both the proteins are anchored to transmembrane proteins by means of another protein called ankyrin.
PROPERTIES OF RED BLOOD CELLS 1. ROULEAUX FORMATION – When blood is taken out of the blood vessel, the RBCs pile up one above another like the pile of coins. – This property of the RBCs is called rouleaux (pleural = rouleau) formation. – It is accelerated by plasma proteins globulin and fibrinogen. 2. SPECIFIC GRAVITY : 1.092 to 1.101. 3. PACKED CELL VOLUME: Packed cell volume (PCV) is the proportion of blood occupied by RBCs expressed in percentage. It is also called hematocrit value. It is 45% of the blood and the plasma volume is 55%. 4. SUSPENSION STABILITY – During circulation, the RBCs remain suspended uniformly in the blood. This property of the RBCs is called the suspension stability.
LIFESPAN OF RED BLOOD CELLS – Average lifespan of RBC is about 120 days. – After the lifetime the senile (old) RBCs are destroyed in reticuloendothelial system.
FATE OF RED BLOOD CELLS
FUNCTIONS OF RED BLOOD CELLS 1. Transport of Oxygen from the Lungs to the Tissues 2. Transport of Carbon Dioxide from the Tissues to the Lungs 3. Buffering Action in Blood 4. In Blood Group Determination
VARIATIONS IN NUMBER OF RED BLOOD CELLS PHYSIOLOGICAL VARIATIONS: A. Increase in RBC Count – Increase in the RBC count is known as polycythemia 1. Age 2. Sex 3. High altitude 4. Muscular exercise 5. Emotional conditions 6. Increased environmental temperature 7. After meals B. Decrease in RBC count 1. High barometric pressures 2. During sleep 3. Pregnancy
VARIATIONS IN NUMBER OF RED BLOOD CELLS PATHOLOGICAL VARIATIONS: – Pathological Polycythemia Polycythemia is of two types: Primary polycythemia and Secondary polycythemia. 1.Primary Polycythemia – Polycythemia Vera – It is characterized by persistent increase in RBC count above 14 million/cu mm of blood. – This is always associated with increased white blood cell count above 24,000/cu mm of blood. – Polycythemia vera occurs in myeloproliferative disorders like malignancy of red bone marrow.
– 2.Secondary Polycythemia – This is secondary to some of the pathological conditions (diseases) such as: 1. Respiratory disorders like emphysema. 2. Congenital heart disease. 3. Chronic carbon monoxide poisoning. 4. Poisoning by chemicals like phosphorus and arsenic. 5. Repeated mild hemorrhages. – Anemia – Abnormal decrease in RBC count is called anemia.
VARIATIONS IN SIZE OF RED BLOOD CELLS – Under physiological conditions, the size of RBCs in venous blood is slightly larger than those in arterial blood. – In pathological conditions, the variations in size of RBCs are: • Iron-deficiency anemia • Prolonged forced breathing • Increased osmotic pressure in blood MICROCYTES • Megaloblastic anemia • Decreased osmotic pressure in blood MARCOCYTES • Pernicious anemia ANISOCYTES
VARIATIONS IN SHAPE OF RED BLOOD CELLS 1. Crenation: Shrinkage as in hypertonic conditions. 2. Spherocytosis: Globular form as in hypotonic conditions. 3. Elliptocytosis: Elliptical shape as in certain types of anemia. 4. Sickle cell: Crescentic shape as in sickle cell anemia. 5. Poikilocytosis: Unusual shapes due to deformed cell membrane(flask,hammer shape,etc)
Erythropoiesis – DEFINITION – Erythropoiesis is the process of the origin, development and maturation of erythrocytes. STAGE IN LIFE SITE OF ERYTHROPOIESIS EMBRYO 1-3 MONTHS YOLK SAC FOETUS 3-6 MONTHS LIVER AND SPLEEN AFTER BIRTH BONE MARROW OF ALL BONES(long & flat bones) AFTER 20 YEARS BONE MARROW OF SMALL AND FLAT BONES
CHANGES DURING ERYTHROPOIESIS – 1. Reduction in size of the cell (from the diameter of 25 to 7.2 μ) – 2. Disappearance of nucleoli and nucleus. – 3. Appearance of hemoglobin – 4. Change in the staining properties of the cytoplasm
STAGES OF ERYTHROPOIESIS – 1. Proerythroblast – 2. Early normoblast – 3. Intermediate normoblast – 4. Late normoblast – 5. Reticulocyte – 6. Matured erythrocyte
– Stage of erythropoiesis – Proerythroblast- Synthesis of haemoglobin starts – Early normoblast -Nucleoli disappear – Intermediate normoblast - Hemoglobin starts appearing – Late normoblast -Nucleus disappears – Reticulocyte -Reticulum is formed.Cell enters capillary from site of production – Matured RBC- Reticulum disappears Cell attains biconcavity
REGULATION OF ERYTHROPOIESIS MECHANISM HYPOXIA KIDNEYS REF PLASMA PROTEINS ERYTHRO POIETIN BONE MARROW RBC COUNT INCREASES
FACTORS NECESSARY FOR ERYTHROPOIESIS: General factors •Erythropoietin •Thyroxine •Hemopoietic growth factors • Vitamins. Maturation factors •Vitamin B12 •Intrinsic factor •Folic acid Factors necessary for hemoglobin formation •Proteins and amino acids •Iron •Copper •Cobalt and nickel •Vitamins
MATURATION FACTORS 1.Vitamin B12 (Cyanocobalamin) – Source – Vitamin B12 is called extrinsic factor since it is obtained mostly from diet. Its absorption from intestine requires the presence of intrinsic factor of Castle. – Vitamin B12 is stored mostly in liver and in small quantity in muscle. – When necessary, it is transported to the bone marrow to promote maturation of RBCs. It is also produced in the large intestine by the intestinal flora. – Action – Vitamin B12 is essential for synthesis of DNA in RBCs. – Its deficiency leads to failure in maturation of the cell and reduction in the cell division. Also, the cells are larger with fragile and weak cell membrane resulting in macrocytic anemia. – Deficiency of vitamin B12 causes pernicious anemia. So, vitamin B12 is called antipernicious factor.
2. Intrinsic Factor of Castle – Intrinsic factor of castle is produced in gastric mucosa by the parietal cells of the gastric glands. – It is essential for the absorption of vitamin B12 from intestine. – In the absence of intrinsic factor, vitamin B12 is not absorbed from intestine. – This leads to pernicious anemia. – Deficiency of intrinsic factor occurs in: Severe gastritis Ulcer Gastrectomy
3. Folic Acid – Folic acid is also essential for maturation. – It is required for the synthesis of DNA. – In the absence of folic acid, the synthesis of DNA decreases causing failure of maturation. – This leads to anemia in which the cells are larger and appear in megaloblastic (proerythroblastic) stage.
Hemoglobin
– Hemoglobin (Hb) is the iron containing coloring matter of red blood cell (RBC). – Molecular weight of hemoglobin is 68,000 NORMAL HEMOGLOBIN CONTENT – Average hemoglobin (Hb) content in blood is 14 to 16 g/dL. – At the time of birth, hemoglobin content is very high because of increased number of RBCs – In adult males : 15 g/dL – In adult females : 14.5 g/dL
FUNCTIONS OF HEMOGLOBIN – TRANSPORT OF RESPIRATORY GASES – 1. Transport of Oxygen from the lungs to tissues – 2. Transport of Carbon Dioxide from tissues to lungs – BUFFER ACTION – Hemoglobin acts as a buffer and plays an important role in acidbase balance
STRUCTURE OF 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. – GLOBIN – Globin contains four polypeptide chains. Among the four polypeptide chains, two are β-chains and two are α-chains – IRON – Normally, it is present in ferrous (Fe2+) form. – It is in unstable or loose form. In some abnormal conditions,the iron is converted into ferric (Fe3+) state, which is a stable form. – PORPHYRIN - pigment part of heme. Molecular weight Amino acids α-chain 15,126 141 β-chain 15,866 146
TYPES OF NORMAL HEMOGLOBIN – 1. Adult hemoglobin – HbA – 2. Fetal hemoglobin – HbF – Structural Difference – Functional Difference – Functionally, fetal hemoglobin has more affinity for oxygen than that of adult hemoglobin. two α- chains two β- chains HbA two α chains two γ- chains HbF
ABNORMAL HEMOGLOBIN 1. Hemoglobinopathies – Hemoglobinopathy is a genetic disorder caused by abnormal polypeptide chains of hemoglobin. – i. Hemoglobin S – ii. Hemoglobin C – iii. Hemoglobin E – iv. Hemoglobin M 2. Hemoglobin in thalassemia and related disorders – In α-thalassemia, – the α-chains are decreased, absent or abnormal – In β-thalassemia, – the β-chains are decreased, absent or abnormal
ABNORMAL HEMOGLOBIN DERIVATIVES – Abnormal hemoglobin derivatives are formed by carbon monoxide (CO) poisoning or due to some drugs like nitrites, nitrates and sulphanamides. – Abnormal hemoglobin derivatives are: – 1. Carboxyhemoglobin – 2. Methemoglobin – 3. Sulfhemoglobin.
SYNTHESIS OF HEMOGLOBIN – Synthesis of hemoglobin actually starts in proerythroblastic stage. – However, hemoglobin appears in the intermediate normoblastic stage only. – Production of hemoglobin is continued until the stage of reticulocyte. – Heme portion of hemoglobin is synthesized in mitochondria. – And the protein part, globin is synthesized in ribosomes.
ALA synthase ALA dehydratase Uroporphobilinogen synthase Uroporphyrinogen decarboxylase Coproporphyrinogen oxidase Ferrochelatase.
DESTRUCTION OF HEMOGLOBIN – After the lifespan of 120 days, the RBC is destroyed in the reticuloendothelial system, particularly in spleen and the hemoglobin is released into plasma. – Soon, the hemoglobin is degraded in the reticuloendothelial cells and split into globin and heme.
DESTRUCTION OF HEMOGLOBIN.. – Globin is utilized for the resynthesis of hemoglobin. – Heme is degraded into iron and porphyrin. – Iron is stored in the body as ferritin and hemosiderin, which are reutilized for the synthesis of new hemoglobin. – Porphyrin is converted into a green pigment called biliverdin. – In human being, most of the biliverdin is converted into a yellow pigment called bilirubin. – Bilirubin and biliverdin are together called the bile pigments.
Erythrocyte Sedimentation Rate – Erythrocyte sedimentation rate (ESR) is the rate at which the erythrocytes settle down. – DETERMINATION OF ESR 1. Westergren method 2. Wintrobe method
NORMAL VALUES OF ESR By Westergren Method In males : 3 to 7 mm in 1 hour In females : 5 to 9 mm in 1 hour Infants : 0 to 2 mm in 1 hour By Wintrobe Method In males : 0 to 9 mm in 1 hour In females : 0 to 15 mm in 1 hour Infants : 0 to 5 mm in 1 hour
SIGNIFICANCE OF DETERMINING ESR: – Determination of ESR is especially helpful in assessing the progress of patients treated for certain chronic inflammatory disorders such as: – 1. Pulmonary tuberculosis – 2. Rheumatoid arthritis – 3. Polymyalgia rheumatica (inflammatory disease characterized by pain in shoulder and hip) – 4. Temporal arteritis (inflammation of arteries of head) – It helps in diagnosis as well as prognosis.
VARIATIONS OF ESR – PHYSIOLOGICAL VARIATION Age: ESR is less in children and infants because of more number of RBCs Sex: It is more in females than in males because of less number of RBCs. Menstruation: The ESR increases during menstruation because of loss of blood and RBCs Pregnancy: From 3rd month to parturition, ESR increases up to 35 mm in 1 hour because of hemodilution.
PATHOLOGICAL VARIATION ESR increases • 1.Tuberculosis • 2. All types of anemia • 3. Malignant tumors • 4. Rheumatoid arthritis • 5. Rheumatic fever • 6. Liver diseases. ESR decreases • 1.Allergic conditions • 2. Sickle cell anemia • 3. Peptone shock • 4. Polycythemia • 5. Severe leukocytosis
Packed Cell Volume and Blood Indices – Packed cell volume (PCV) is the proportion of blood occupied by RBCs, expressed in percentage. – METHOD OF DETERMINATION.. – SIGNIFICANCE OF DETERMINING PCV.. NORMAL VALUES OF PCV: – In males = 40% to 45% – In females = 38% to 42%
VARIATIONS IN PCV INCREASE IN PCV • 1.Polycythemia • 2. Dehydration • 3. Dengue shock syndrome DECREASE IN PCV • 1. Anemia • 2. Cirrhosis of liver • 3. Pregnancy • 4. Hemorrhage due to ectopic pregnancy
DIFFERENT BLOOD INDICES 1. Mean corpuscular volume (MCV)--- 78 to 90 cu μ 2. Mean corpuscular hemoglobin (MCH)---27 to 32 pg 3. Mean corpuscular hemoglobin concentration (MCHC)---30% to 38% 4. Color Index (CI)---0.8 to1.2 IMPORTANCE OF BLOOD INDICES Blood indices help in diagnosis of the type of anemia
ANEMIA – INTRODUCTION.. – CLASSIFICATION OF ANEMIA 1. Morphological classification 2. Etiological classification.
Morphological classification of anemia
Etiological classification of anemia
SIGNS AND SYMPTOMS OF ANEMIA SKIN AND MUCOUS MEMBRANE CARDIOVASCULAR SYSTEM RESPIRATION DIGESTION METABOLISM KIDNEY REPRODUCTIVE SYSTEM NEUROMUSCULAR SYSTEM
Oral and periodontal manifestations in anemic patients – Pernicious anemia results in tongue changes in 75% of patients. – The tongue appears red, smooth, and shiny because of atrophy of the papillae. – There is also marked pallor of the gingiva. – Iron deficiency anemia induces similar tongue and gingival changes. – A syndrome consisting of glossitis and ulceration of the oral mucosa and oropharynx, inducing dysphagia ( Plummer-Vinson syndrome) has been described in patients with iron deficiency anemia. – Sickle cell anemia is a hereditary form of chronic hemolytic anemia that occurs almost exclusively in blacks. – Oral changes include: generalized osteoporosis of the jaws, with a peculiar stepladder alignment of the trabeculae of the interdental septa, along with pallor and yellowish discoloration of the oral mucosa.
Periodontal manifestations in anemic patients – Periodontal infections may precipitate sickle cell crisis. – Aplastic anemia result from a failure of the bone marrow to produce erythrocytes. – The etiology is usually the effect of toxic drugs on the marrow or displacement of RBCs by leukemic cells. – Oral changes include pale discoloration of the oral mucosa and increased susceptibility to infection because of the concomitant neutropenia.
CLASSIFICATION OF WBCs 1. Granulocytes – Depending upon the staining property of granules, the granulocytes are classified into three types: i. Neutrophils with granules taking both acidic and basic stains ii. Eosinophils with granules taking acidic stain iii. Basophils with granules taking basic stain 2. Agranulocytes Agranulocytes have plain cytoplasm without granules. Monocytes Lymphocytes
NORMAL WHITE BLOOD CELL COUNT – 1. Total WBC count (TC): 4,000 to 11,000/cu mm of blood. – 2. Differential WBC count (DC):
PROPERTIES OF WHITE BLOOD CELLS 1. Diapedesis Diapedesis is the process by which the leukocytes squeeze through the narrow blood vessels. 2. Ameboid Movement Neutrophils, monocytes and lymphocytes show amebic movement, characterized by protrusion of the cytoplasm and change in the shape. 3. Chemotaxis Chemotaxis is the attraction of WBCs towards the injured tissues by the chemical substances released at the site of injury. 4. Phagocytosis Neutrophils and monocytes engulf the foreign bodies by means of phagocytosis.
FUNCTIONS OF WHITE BLOOD CELLS- NEUTROPHILS Substances Present in Granules and Cytoplasm of Neutrophils – Granules of neutrophils contain enzymes like proteases,myeloperoxidases, elastases and metalloproteinases. – These enzymes destroy the microorganisms. – Membrane of neutrophils contains an enzyme called NADPH oxidase. – It is activated by the toxic metabolites released from infected tissues. The activated NADPH oxidase is responsible for bactericidal action of neutrophils. – Neutrophils also secrete platelet-activating factor (PAF), which is a cytokine. – It accelerates the aggregation of platelets during injury to the blood vessel, resulting in prevention of excess loss of blood.
Mechanism of Action of Neutrophils Neutrophils are released in large number at the site of infection from the blood. At the same time, new neutrophils are produced from the progenitor cells. All the neutrophils move by diapedesis towards the site of infection due to chemotaxis. Chemotaxis occurs due to the attraction by some chemical substances called chemoattractants, which are released from the infected area. After reaching the area,the neutrophils surround the area and get adhered to the infected tissues. Chemoattractants increase the adhesive nature of neutrophils so that all the neutrophils become sticky and get attached firmly to the infected area. Each neutrophil can hold about 15 to 20 microorganisms at a time. Now, the neutrophils start destroying the invaders. First, these cells engulf the bacteria and then destroy them by means of phagocytosis
EOSINOPHILS – Eosinophils are responsible for detoxification, disintegration and removal of foreign proteins. – Mechanism of Action of Eosinophils – The lethal substances present in the granules of eosinophils and released at the time of exposure to parasites or foreign proteins are: 1. Eosinophil peroxidase: This enzyme is capable of destroying helminths (parasitic worms), bacteria and tumor cells. 2. Major basic protein (MBP): It is very active against helminths. It destroys the parasitic worms by causing distension (ballooning) and detachment of the tegumental sheath (skin-like covering) of these organisms. 3. Eosinophil cationic protein (ECP): This substance is the major destroyer of helminths and it is about 10 times more toxic than MBP. It destroys the parasites by means of complete disintegration. It is also a neurotoxin. 4. Eosinophil-derived neurotoxin: It destroys the nerve fibers particularly, the myelinated nerve fibers. 5. Cytokines: Cytokines such as interleukin-4 and interleukin-5 accelerate inflammatory responses by activating eosinophils. These cytokines also kill the invading organisms
BASOPHILS – Basophils play an important role in healing processes. – Basophils also play an important role in allergy or acute hypersensitivity reactions. – This is because of the presence of receptors for IgE in basophil membrane. Mechanism of Action of Basophils – Functions of basophils are executed by the release of some important substances from their granules such as: – 1. Heparin: Heparin is essential to prevent the intravascular blood clotting. – 2. Histamine, slow-reacting substances of anaphylaxis, bradykinin and serotonin: Theses substances produce the acute hypersensitivity reactions by causing vascular and tissue responses. – 3. Proteases and myeloperoxidase: These enzymes destroy the microorganisms – 4. Cytokine: Cytokine such as interleukin-4 accelerates inflammatory responses and kill the invading organisms.
Mast Cell – Mast cell is a large tissue cell resembling the basophil. – Origin – Mast cells are developed in the bone marrow – Functions – Mast cell plays an important role in producing the hypersensitivity reactions like allergy and anaphylaxis. – Two types of substances are secreted by mast cell: – 1. Preformed mediators: These substances are already formed and stored in secretory granules. These substances are histamine, heparin, serotonin, hydrolytic enzymes, proteoglycans and chondroitin sulfates. – 2. Newly generated mediators: These substances are absent in the mast cell during resting conditions and are produced only during activation. These substances are arachidonic acid derivatives such as leukotriene C (LTC), prostaglandin and cytokines.
MONOCYTES – Monocytes are the largest cells among the leukocytes. – Monocytes secrete: – 1. Interleukin-1 (IL-1). – 2. Colony stimulating factor (M-CSF). – 3. Platelet-activating factor (PAF). – Monocytes are the precursors of the tissue macrophages. – Matured monocytes stay in the blood only for few hours. Afterwards, these cells enter the tissues from the blood and become tissue macrophages. – Examples of tissue macrophages are Kupffer cells in liver, alveolar macrophages in lungs and macrophages in spleen.
LYMPHOCYTES – Lymphocytes play an important role in immunity. – T lymphocytes and B lymphocytes. – T lymphocytes are responsible for the development of cellular immunity – B lymphocytes are responsible for the development of humoral immunity.
FUNCTIONS OF WBCs
LEUKEMIA – Abnormal increase in non functional immature leukocytes due to carcinogenic reason.
LEUKEMIA.. – CAUSES: – CLINICAL SIGNS AND SYMPTOMS: – TREATMENT: Genetic Environmental factors Infection by RNA viruses Bone marrow transplant Periodic blood transfusion Use of anticancer drugs
Periodontium in leukemic patients – Oral and periodontal manifestations of leukemia consist of leukemic infiltration, bleeding, oral ulcerations, and infections. – Leukemic cells can infiltrate the gingiva and less frequently the alveolar bone. – Gingival infiltration often results in leukemic gingival enlargement. – Clinically,the gingiva appears initially bluish red and cyanotic, with a rounding and tenseness of the gingival margin; – then it increases in size, most often in the interdental papilla and partially covering the crowns of the teeth.
Periodontium in leukemic patients.. – Bleeding-Bleeding gingiva can be an early sign of leukemia. It is caused by the thrombocytopenia resulting from replacement of the bone marrow cells by leukemic cells. – This bleeding tendency can also manifest in the skin and throughout the oral mucosa, where petechiae are often found, with or without leukemic infiltrates. – A more diffuse submucosal bleeding manifests as ecchymosis.
Periodontium in leukemic patients.. – Oral Ulceration and Infection – Discrete, puched-out ulcers penetrating deeply into the submucosa and covered by a firmly attached white slough can be found on the oral mucosa. – Acute gingivitis and lesions resembling necrotizing ulcerative gingivitis are more frequent and severe in terminal cases of acute leukemia. – Gingiva is a peculiar bluish red, is spongelike and friable, and bleeds persistently on the slightest provocation. – Eliminating or reducing local factors (e.g.bacterial plaque) can minimize severe oral changes in leukemia.
PLATELETS
Platelets – INTRODUCTION.. – NORMAL COUNT-2,00,000 and 4,00,000/cu mm of blood. – Size of Platelets – Diameter : 2.5 μ (2 to 4 μ) – Volume : 7.5 cu μ (7 to 8 cu μ). – SHAPE.. – STRUCTURE AND COMPOSITION – Platelet is constituted by: – 1. Cell membrane or surface membrane – 2. Microtubules – 3. Cytoplasm.
– Cytoplasm of platelets contains the cellular organelles,Golgi apparatus, endoplasmic reticulum, mitochondria,microtubule, microvessels, filaments and granules. – Cytoplasm also contains some chemical substances such as proteins, enzymes, hormonal substances, etc.
PLATELET GRANULES Alpha granules • 1. Clotting factors – fibrinogen, V and XIII • 2. Platelet-derived growth factor • 3. Vascular endothelial growth factor (VEGF) • 4. Basic fibroblast growth factor (FGF) • 5. Endostatin • 6. Thrombospondin. Dense granules • 1. Nucleotides • 2. Serotonin • 3. Phospholipid • 4. Calcium • 5. Lysosomes.
PHYSIOLOGICAL VARIATIONS 1. Age: Platelets are less in infants (1,50,000 to 2,00,000/cu mm) and reaches normal level at 3rd month after birth. 2. Sex: There is no difference in the platelet count between males and females. In females, it is reduced during menstruation. 3. High altitude: Platelet count increases. 4. After meals: After taking food, the platelet count increases
PROPERTIES OF PLATELETS – Platelets have three important properties (three ‘A’s): 1. Adhesiveness 2. Aggregation 3. Agglutination
1. ROLE IN BLOOD CLOTTING 2.ROLE IN CLOT RETRACTION 3.ROLE IN PREVENTION OF BLOOD LOSS (HEMOSTASIS) 4.ROLE IN REPAIR OF RUPTURED BLOODVESSEL FUNCTIONS OF PLATELETS 5. ROLE IN DEFENSE MECHANISM
LIFESPAN AND FATE OF PLATELETS – Average lifespan of platelets is 10 days. It varies between 8 and 11 days. – Platelets are destroyed by tissue macrophage system in spleen. – So, splenomegaly (enlargement of spleen) decreases platelet count and splenectomy (removal of spleen) increases platelet count.
APPLIED PHYSIOLOGY – PLATELET DISORDERS – Platelet disorders occur because of pathological variation in platelet count and dysfunction of platelets. – Platelet disorders are: – 1. Thrombocytopenia – 2. Thrombocytosis – 3. Thrombocythemia – 4. Glanzmann’s thrombasthenia
Oral and periodontal manifestations in patients with THROMBOCYTOPENIA – Purpura refers to the purplish appearance of the skin or mucous membranes where bleeding has occurred as a result of decreased platelets. – Etiologic factors: – aplasia of the marrow; – displacement of the megakaryocytes in the marrow, as in leukemia; – replacement of the marrow by tumor; – destruction of the marrow by irradiation or radium or by drugs, such as benzene, aminopyrine, and arsenical agents.
Oral and periodontal manifestations in patients with THROMBOCYTOPENIA – Thrombocytopenic purpura is characterized by: – There is spontaneous bleeding into the skin or from mucous membranes. – Petechiae and hemorrhagic vesicles occur in the oral cavity, particularly in the palate, tonsillar pillars, and the buccal mucosa. – The gingivae are swollen, soft, and friable. – Gingival changes represent an abnormal response to local irritation; the severity of the gingival condition is dramatically alleviated by removal of the local factors. low platelet count prolonged clot retraction and bleeding time normal or slightly prolonged clotting time
CONCLUSION BLOOD
REFERENCES – Guyton and Hall Textbook of Medical Physiology,10th edition – Essentials of Medical Physiology, K. Sembulingam, Prema Sembulingam,6th edition – Carranza’s Clinical Periodontology,11th edition
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Blood

  • 2.
    HISTORY William Harvey wasthe first known physician to describe completely and in detail the systemic circulation and properties of blood being pumped to the brain and body by the heart.
  • 3.
    THE CONCEPT OFBLOOD CIRCULATION IN ANCIENT INDIA* *THE CONCEPT OF BLOOD CIRCULATION IN ANCIENT INDIA W.S.R TO THE HEART AS A PUMPING ORGAN P.N.Vinaya1, J.S.R.A. Prasad2 (International Ayurvedic Medical Journal) – The concept of blood circulation described in Atharvaveda is amazingly accurate. – Blood, its structure and functions, its importance as a carrier of nutrients and oxygen too find mention. – It is no surprise that the subject of blood circulation and its purpose i.e. carrying of Prana (oxygen technically) and rasa (nutrients) to the entire body in a cyclical manner with the heart acting as a pump to carry out this function were known to our ancient seers long before William Harvey discovered the circulation of blood in the 17th century.
  • 4.
    INTRODUCTION Blood is aconnective tissue in fluid form. BLOOD FLUID OF LIFE FLUID OF GROWTH FLUID OF HEALTH carries oxygen from lungs to all parts of the body and carbon dioxide from all parts of the body to the lungs. carries nutritive substances from the digestive system and hormones from endocrine gland to all the tissues. protects the body against the diseases and gets rid of the waste products and unwanted substances by transporting them to the excretory organs like kidneys.
  • 5.
    PROPERTIES OF BLOOD: VOLUME-5L. COLOUR-scarlet red because it contains more oxygen and venous blood is purple red because of more carbon dioxide. pH-slightly alkaline -7.4 SPECIFIC GRAVITY-1.052 to 1.061 VISCOSITY-five times more viscous than water
  • 6.
    COMPOSITION OF BLOOD –Blood contains the blood cells which are called formed elements and the liquid portion known as plasma. BLOOD CELLS RBC GRANULOCYTES AGRANULOCYTES NEUTROPHILS WBC THROMBOCYTES BASOPHILS EOSINOPHILS LYMPHOCYTE MONOCYTE
  • 7.
    Plasma is astraw-colored clear liquid part of blood. It contains 91% to 92% of water and 8% to 9% of solids.
  • 8.
    SERUM – Serum isthe clear straw-colored fluid that oozes from blood clot. – It is different from plasma only by the absence of fibrinogen, i.e. serum contains all the other constituents of plasma except fibrinogen. – Fibrinogen is absent in serum because it is converted into fibrin during blood clotting. Thus, Serum = Plasma – Fibrinogen
  • 9.
    1. NUTRITIVE FUNCTION 2.RESPIRATORY FUNCTION 3. EXCRETORY FUNCTION 4.TRANSPORT OF HORMONES AND ENZYMES FUNCTIONS OF BLOOD
  • 10.
    5. REGULATION OFWATER BALANCE 6. REGULATION OF ACID-BASE BALANCE 7. REGULATION OF BODYTEMPERATURE 8. STORAGE FUNCTION FUNCTIONS OF BLOOD 9. DEFENSIVE FUNCTION
  • 11.
    1. Glucose, aminoacids, lipids and vitamins are absorbed from GIT and carried by blood to different parts of the body for growth and production of energy. 2 Transport of respiratory gases is done by the blood 3 Waste products formed in the tissues during various metabolic activities are removed by blood and carried to the excretory organs like kidney, skin, liver, etc. for excretion. 4 Hormones which are secreted by ductless (endocrine) glands are released directly into the blood. The blood transports these hormones and enzymes to their target organs. 5. Water content of the blood is freely interchangeable with interstitial fluid. 6. Plasma proteins and hemoglobinact as buffers and help in the regulation of acid- base balance 7. 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 Blood serves as a readymade source for substances like proteins, glucose, sodium and potassium during the conditions like starvation, fluid loss, electrolyte loss, etc. 9. Blood plays an important role in the defense of the body. The white blood cells are responsible for this function. Neutrophils and monocytes engulf the bacteria by phagocytosis. Lymphocytes are involved in development of immunity. Eosinophils are responsible for detoxification, disintegration and removal of foreign Proteins
  • 12.
    PLASMA PROTEINS – Plasmaproteins are: 1. Serum albumin 2. Serum globulin 3. Fibrinogen. Normal values of the plasma proteins are: Total proteins : 7.3 g/dL (6.4 to 8.3 g/dL) Serum albumin : 4.7 g/dL Serum globulin : 2.3 g/dL Fibrinogen : 0.3 g/dL
  • 13.
    PROPERTIES OF PLASMA PROTEINS 1.MOLECULAR WEIGHT – Albumin : 69,000 – Globulin : 1,56,000 – Fibrinogen : 4,00,000 2. ONCOTIC PRESSURE: 25 mm Hg 3. SPECIFIC GRAVITY: 1.026 4. BUFFER ACTION: The plasma proteins have 1/6 of total buffering action of the blood.
  • 14.
    FUNCTIONS OF PLASMA PROTEINS 1.ROLE IN COAGULATION OF BLOOD 2. ROLE IN DEFENSE MECHANISM OF BODY 3. ROLE IN TRANSPORT MECHANISM 4. ROLE IN MAINTENANCE OF OSMOTIC PRESSURE IN BLOOD
  • 15.
    5. ROLE INREGULATION OF ACID-BASE BALANCE 6. ROLE IN VISCOSITY OF BLOOD 7. ROLE IN ERYTHROCYTE SEDIMENTATION RATE 8. ROLE IN SUSPENSION STABILITY OF RED BLOOD CELLS 9. ROLE IN PRODUCTION OF TREPHONE SUBSTANCES 10. ROLE AS RESERVE PROTEINS
  • 16.
    VARIATIONS IN PLASMA PROTEINLEVEL – Elevation of all fractions of plasma proteins is called hyperproteinemia and decrease in all fractions of plasma proteins is called hypoproteinemia.
  • 17.
  • 19.
    RBCs -INTRODUCTION – Red bloodcells are the non-nucleated formed elements in the blood. – Red color of the red blood cell is due to the presence of the coloring pigment called hemoglobin. – NORMAL RBC count ranges between 4 and 5.5 million/cu mm of blood.
  • 20.
    >NORMAL SHAPE – Diskshaped and biconcave(dumbbell shaped). – Central portion is thinner and periphery is thicker. >NORMAL SIZE – Diameter : 7.2-7.5 μ – Surface area : 120 sq μ. >NORMAL STRUCTURE – Red blood cells are non-nucleated. – RBC has a special type of cytoskeleton, which is made up of actin and spectrin. – Both the proteins are anchored to transmembrane proteins by means of another protein called ankyrin.
  • 21.
    PROPERTIES OF REDBLOOD CELLS 1. ROULEAUX FORMATION – When blood is taken out of the blood vessel, the RBCs pile up one above another like the pile of coins. – This property of the RBCs is called rouleaux (pleural = rouleau) formation. – It is accelerated by plasma proteins globulin and fibrinogen. 2. SPECIFIC GRAVITY : 1.092 to 1.101. 3. PACKED CELL VOLUME: Packed cell volume (PCV) is the proportion of blood occupied by RBCs expressed in percentage. It is also called hematocrit value. It is 45% of the blood and the plasma volume is 55%. 4. SUSPENSION STABILITY – During circulation, the RBCs remain suspended uniformly in the blood. This property of the RBCs is called the suspension stability.
  • 22.
    LIFESPAN OF REDBLOOD CELLS – Average lifespan of RBC is about 120 days. – After the lifetime the senile (old) RBCs are destroyed in reticuloendothelial system.
  • 23.
    FATE OF REDBLOOD CELLS
  • 24.
    FUNCTIONS OF RED BLOODCELLS 1. Transport of Oxygen from the Lungs to the Tissues 2. Transport of Carbon Dioxide from the Tissues to the Lungs 3. Buffering Action in Blood 4. In Blood Group Determination
  • 25.
    VARIATIONS IN NUMBEROF RED BLOOD CELLS PHYSIOLOGICAL VARIATIONS: A. Increase in RBC Count – Increase in the RBC count is known as polycythemia 1. Age 2. Sex 3. High altitude 4. Muscular exercise 5. Emotional conditions 6. Increased environmental temperature 7. After meals B. Decrease in RBC count 1. High barometric pressures 2. During sleep 3. Pregnancy
  • 26.
    VARIATIONS IN NUMBEROF RED BLOOD CELLS PATHOLOGICAL VARIATIONS: – Pathological Polycythemia Polycythemia is of two types: Primary polycythemia and Secondary polycythemia. 1.Primary Polycythemia – Polycythemia Vera – It is characterized by persistent increase in RBC count above 14 million/cu mm of blood. – This is always associated with increased white blood cell count above 24,000/cu mm of blood. – Polycythemia vera occurs in myeloproliferative disorders like malignancy of red bone marrow.
  • 27.
    – 2.Secondary Polycythemia –This is secondary to some of the pathological conditions (diseases) such as: 1. Respiratory disorders like emphysema. 2. Congenital heart disease. 3. Chronic carbon monoxide poisoning. 4. Poisoning by chemicals like phosphorus and arsenic. 5. Repeated mild hemorrhages. – Anemia – Abnormal decrease in RBC count is called anemia.
  • 28.
    VARIATIONS IN SIZEOF RED BLOOD CELLS – Under physiological conditions, the size of RBCs in venous blood is slightly larger than those in arterial blood. – In pathological conditions, the variations in size of RBCs are: • Iron-deficiency anemia • Prolonged forced breathing • Increased osmotic pressure in blood MICROCYTES • Megaloblastic anemia • Decreased osmotic pressure in blood MARCOCYTES • Pernicious anemia ANISOCYTES
  • 29.
    VARIATIONS IN SHAPEOF RED BLOOD CELLS 1. Crenation: Shrinkage as in hypertonic conditions. 2. Spherocytosis: Globular form as in hypotonic conditions. 3. Elliptocytosis: Elliptical shape as in certain types of anemia. 4. Sickle cell: Crescentic shape as in sickle cell anemia. 5. Poikilocytosis: Unusual shapes due to deformed cell membrane(flask,hammer shape,etc)
  • 30.
    Erythropoiesis – DEFINITION – Erythropoiesisis the process of the origin, development and maturation of erythrocytes. STAGE IN LIFE SITE OF ERYTHROPOIESIS EMBRYO 1-3 MONTHS YOLK SAC FOETUS 3-6 MONTHS LIVER AND SPLEEN AFTER BIRTH BONE MARROW OF ALL BONES(long & flat bones) AFTER 20 YEARS BONE MARROW OF SMALL AND FLAT BONES
  • 31.
    CHANGES DURING ERYTHROPOIESIS – 1.Reduction in size of the cell (from the diameter of 25 to 7.2 μ) – 2. Disappearance of nucleoli and nucleus. – 3. Appearance of hemoglobin – 4. Change in the staining properties of the cytoplasm
  • 32.
    STAGES OF ERYTHROPOIESIS – 1.Proerythroblast – 2. Early normoblast – 3. Intermediate normoblast – 4. Late normoblast – 5. Reticulocyte – 6. Matured erythrocyte
  • 33.
    – Stage oferythropoiesis – Proerythroblast- Synthesis of haemoglobin starts – Early normoblast -Nucleoli disappear – Intermediate normoblast - Hemoglobin starts appearing – Late normoblast -Nucleus disappears – Reticulocyte -Reticulum is formed.Cell enters capillary from site of production – Matured RBC- Reticulum disappears Cell attains biconcavity
  • 34.
  • 35.
    FACTORS NECESSARY FOR ERYTHROPOIESIS: Generalfactors •Erythropoietin •Thyroxine •Hemopoietic growth factors • Vitamins. Maturation factors •Vitamin B12 •Intrinsic factor •Folic acid Factors necessary for hemoglobin formation •Proteins and amino acids •Iron •Copper •Cobalt and nickel •Vitamins
  • 36.
    MATURATION FACTORS 1.Vitamin B12(Cyanocobalamin) – Source – Vitamin B12 is called extrinsic factor since it is obtained mostly from diet. Its absorption from intestine requires the presence of intrinsic factor of Castle. – Vitamin B12 is stored mostly in liver and in small quantity in muscle. – When necessary, it is transported to the bone marrow to promote maturation of RBCs. It is also produced in the large intestine by the intestinal flora. – Action – Vitamin B12 is essential for synthesis of DNA in RBCs. – Its deficiency leads to failure in maturation of the cell and reduction in the cell division. Also, the cells are larger with fragile and weak cell membrane resulting in macrocytic anemia. – Deficiency of vitamin B12 causes pernicious anemia. So, vitamin B12 is called antipernicious factor.
  • 37.
    2. Intrinsic Factorof Castle – Intrinsic factor of castle is produced in gastric mucosa by the parietal cells of the gastric glands. – It is essential for the absorption of vitamin B12 from intestine. – In the absence of intrinsic factor, vitamin B12 is not absorbed from intestine. – This leads to pernicious anemia. – Deficiency of intrinsic factor occurs in: Severe gastritis Ulcer Gastrectomy
  • 38.
    3. Folic Acid –Folic acid is also essential for maturation. – It is required for the synthesis of DNA. – In the absence of folic acid, the synthesis of DNA decreases causing failure of maturation. – This leads to anemia in which the cells are larger and appear in megaloblastic (proerythroblastic) stage.
  • 39.
  • 40.
    – Hemoglobin (Hb)is the iron containing coloring matter of red blood cell (RBC). – Molecular weight of hemoglobin is 68,000 NORMAL HEMOGLOBIN CONTENT – Average hemoglobin (Hb) content in blood is 14 to 16 g/dL. – At the time of birth, hemoglobin content is very high because of increased number of RBCs – In adult males : 15 g/dL – In adult females : 14.5 g/dL
  • 41.
    FUNCTIONS OF HEMOGLOBIN – TRANSPORTOF RESPIRATORY GASES – 1. Transport of Oxygen from the lungs to tissues – 2. Transport of Carbon Dioxide from tissues to lungs – BUFFER ACTION – Hemoglobin acts as a buffer and plays an important role in acidbase balance
  • 42.
    STRUCTURE OF 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. – GLOBIN – Globin contains four polypeptide chains. Among the four polypeptide chains, two are β-chains and two are α-chains – IRON – Normally, it is present in ferrous (Fe2+) form. – It is in unstable or loose form. In some abnormal conditions,the iron is converted into ferric (Fe3+) state, which is a stable form. – PORPHYRIN - pigment part of heme. Molecular weight Amino acids α-chain 15,126 141 β-chain 15,866 146
  • 43.
    TYPES OF NORMALHEMOGLOBIN – 1. Adult hemoglobin – HbA – 2. Fetal hemoglobin – HbF – Structural Difference – Functional Difference – Functionally, fetal hemoglobin has more affinity for oxygen than that of adult hemoglobin. two α- chains two β- chains HbA two α chains two γ- chains HbF
  • 44.
    ABNORMAL HEMOGLOBIN 1. Hemoglobinopathies – Hemoglobinopathyis a genetic disorder caused by abnormal polypeptide chains of hemoglobin. – i. Hemoglobin S – ii. Hemoglobin C – iii. Hemoglobin E – iv. Hemoglobin M 2. Hemoglobin in thalassemia and related disorders – In α-thalassemia, – the α-chains are decreased, absent or abnormal – In β-thalassemia, – the β-chains are decreased, absent or abnormal
  • 45.
    ABNORMAL HEMOGLOBIN DERIVATIVES – Abnormalhemoglobin derivatives are formed by carbon monoxide (CO) poisoning or due to some drugs like nitrites, nitrates and sulphanamides. – Abnormal hemoglobin derivatives are: – 1. Carboxyhemoglobin – 2. Methemoglobin – 3. Sulfhemoglobin.
  • 46.
    SYNTHESIS OF HEMOGLOBIN – Synthesisof hemoglobin actually starts in proerythroblastic stage. – However, hemoglobin appears in the intermediate normoblastic stage only. – Production of hemoglobin is continued until the stage of reticulocyte. – Heme portion of hemoglobin is synthesized in mitochondria. – And the protein part, globin is synthesized in ribosomes.
  • 47.
  • 48.
    DESTRUCTION OF HEMOGLOBIN – Afterthe lifespan of 120 days, the RBC is destroyed in the reticuloendothelial system, particularly in spleen and the hemoglobin is released into plasma. – Soon, the hemoglobin is degraded in the reticuloendothelial cells and split into globin and heme.
  • 49.
    DESTRUCTION OF HEMOGLOBIN.. – Globinis utilized for the resynthesis of hemoglobin. – Heme is degraded into iron and porphyrin. – Iron is stored in the body as ferritin and hemosiderin, which are reutilized for the synthesis of new hemoglobin. – Porphyrin is converted into a green pigment called biliverdin. – In human being, most of the biliverdin is converted into a yellow pigment called bilirubin. – Bilirubin and biliverdin are together called the bile pigments.
  • 50.
    Erythrocyte Sedimentation Rate – Erythrocytesedimentation rate (ESR) is the rate at which the erythrocytes settle down. – DETERMINATION OF ESR 1. Westergren method 2. Wintrobe method
  • 51.
    NORMAL VALUES OFESR By Westergren Method In males : 3 to 7 mm in 1 hour In females : 5 to 9 mm in 1 hour Infants : 0 to 2 mm in 1 hour By Wintrobe Method In males : 0 to 9 mm in 1 hour In females : 0 to 15 mm in 1 hour Infants : 0 to 5 mm in 1 hour
  • 52.
    SIGNIFICANCE OF DETERMINING ESR: –Determination of ESR is especially helpful in assessing the progress of patients treated for certain chronic inflammatory disorders such as: – 1. Pulmonary tuberculosis – 2. Rheumatoid arthritis – 3. Polymyalgia rheumatica (inflammatory disease characterized by pain in shoulder and hip) – 4. Temporal arteritis (inflammation of arteries of head) – It helps in diagnosis as well as prognosis.
  • 53.
    VARIATIONS OF ESR –PHYSIOLOGICAL VARIATION Age: ESR is less in children and infants because of more number of RBCs Sex: It is more in females than in males because of less number of RBCs. Menstruation: The ESR increases during menstruation because of loss of blood and RBCs Pregnancy: From 3rd month to parturition, ESR increases up to 35 mm in 1 hour because of hemodilution.
  • 54.
    PATHOLOGICAL VARIATION ESR increases • 1.Tuberculosis •2. All types of anemia • 3. Malignant tumors • 4. Rheumatoid arthritis • 5. Rheumatic fever • 6. Liver diseases. ESR decreases • 1.Allergic conditions • 2. Sickle cell anemia • 3. Peptone shock • 4. Polycythemia • 5. Severe leukocytosis
  • 55.
    Packed Cell Volume andBlood Indices – Packed cell volume (PCV) is the proportion of blood occupied by RBCs, expressed in percentage. – METHOD OF DETERMINATION.. – SIGNIFICANCE OF DETERMINING PCV.. NORMAL VALUES OF PCV: – In males = 40% to 45% – In females = 38% to 42%
  • 56.
    VARIATIONS IN PCV INCREASEIN PCV • 1.Polycythemia • 2. Dehydration • 3. Dengue shock syndrome DECREASE IN PCV • 1. Anemia • 2. Cirrhosis of liver • 3. Pregnancy • 4. Hemorrhage due to ectopic pregnancy
  • 57.
    DIFFERENT BLOOD INDICES 1.Mean corpuscular volume (MCV)--- 78 to 90 cu μ 2. Mean corpuscular hemoglobin (MCH)---27 to 32 pg 3. Mean corpuscular hemoglobin concentration (MCHC)---30% to 38% 4. Color Index (CI)---0.8 to1.2 IMPORTANCE OF BLOOD INDICES Blood indices help in diagnosis of the type of anemia
  • 58.
    ANEMIA – INTRODUCTION.. – CLASSIFICATIONOF ANEMIA 1. Morphological classification 2. Etiological classification.
  • 59.
  • 60.
  • 62.
    SIGNS AND SYMPTOMSOF ANEMIA SKIN AND MUCOUS MEMBRANE CARDIOVASCULAR SYSTEM RESPIRATION DIGESTION METABOLISM KIDNEY REPRODUCTIVE SYSTEM NEUROMUSCULAR SYSTEM
  • 63.
    Oral and periodontal manifestationsin anemic patients – Pernicious anemia results in tongue changes in 75% of patients. – The tongue appears red, smooth, and shiny because of atrophy of the papillae. – There is also marked pallor of the gingiva. – Iron deficiency anemia induces similar tongue and gingival changes. – A syndrome consisting of glossitis and ulceration of the oral mucosa and oropharynx, inducing dysphagia ( Plummer-Vinson syndrome) has been described in patients with iron deficiency anemia. – Sickle cell anemia is a hereditary form of chronic hemolytic anemia that occurs almost exclusively in blacks. – Oral changes include: generalized osteoporosis of the jaws, with a peculiar stepladder alignment of the trabeculae of the interdental septa, along with pallor and yellowish discoloration of the oral mucosa.
  • 64.
    Periodontal manifestations in anemicpatients – Periodontal infections may precipitate sickle cell crisis. – Aplastic anemia result from a failure of the bone marrow to produce erythrocytes. – The etiology is usually the effect of toxic drugs on the marrow or displacement of RBCs by leukemic cells. – Oral changes include pale discoloration of the oral mucosa and increased susceptibility to infection because of the concomitant neutropenia.
  • 66.
    CLASSIFICATION OF WBCs 1.Granulocytes – Depending upon the staining property of granules, the granulocytes are classified into three types: i. Neutrophils with granules taking both acidic and basic stains ii. Eosinophils with granules taking acidic stain iii. Basophils with granules taking basic stain 2. Agranulocytes Agranulocytes have plain cytoplasm without granules. Monocytes Lymphocytes
  • 67.
    NORMAL WHITE BLOOD CELLCOUNT – 1. Total WBC count (TC): 4,000 to 11,000/cu mm of blood. – 2. Differential WBC count (DC):
  • 68.
    PROPERTIES OF WHITE BLOODCELLS 1. Diapedesis Diapedesis is the process by which the leukocytes squeeze through the narrow blood vessels. 2. Ameboid Movement Neutrophils, monocytes and lymphocytes show amebic movement, characterized by protrusion of the cytoplasm and change in the shape. 3. Chemotaxis Chemotaxis is the attraction of WBCs towards the injured tissues by the chemical substances released at the site of injury. 4. Phagocytosis Neutrophils and monocytes engulf the foreign bodies by means of phagocytosis.
  • 70.
    FUNCTIONS OF WHITEBLOOD CELLS- NEUTROPHILS Substances Present in Granules and Cytoplasm of Neutrophils – Granules of neutrophils contain enzymes like proteases,myeloperoxidases, elastases and metalloproteinases. – These enzymes destroy the microorganisms. – Membrane of neutrophils contains an enzyme called NADPH oxidase. – It is activated by the toxic metabolites released from infected tissues. The activated NADPH oxidase is responsible for bactericidal action of neutrophils. – Neutrophils also secrete platelet-activating factor (PAF), which is a cytokine. – It accelerates the aggregation of platelets during injury to the blood vessel, resulting in prevention of excess loss of blood.
  • 71.
    Mechanism of Actionof Neutrophils Neutrophils are released in large number at the site of infection from the blood. At the same time, new neutrophils are produced from the progenitor cells. All the neutrophils move by diapedesis towards the site of infection due to chemotaxis. Chemotaxis occurs due to the attraction by some chemical substances called chemoattractants, which are released from the infected area. After reaching the area,the neutrophils surround the area and get adhered to the infected tissues. Chemoattractants increase the adhesive nature of neutrophils so that all the neutrophils become sticky and get attached firmly to the infected area. Each neutrophil can hold about 15 to 20 microorganisms at a time. Now, the neutrophils start destroying the invaders. First, these cells engulf the bacteria and then destroy them by means of phagocytosis
  • 72.
    EOSINOPHILS – Eosinophils areresponsible for detoxification, disintegration and removal of foreign proteins. – Mechanism of Action of Eosinophils – The lethal substances present in the granules of eosinophils and released at the time of exposure to parasites or foreign proteins are: 1. Eosinophil peroxidase: This enzyme is capable of destroying helminths (parasitic worms), bacteria and tumor cells. 2. Major basic protein (MBP): It is very active against helminths. It destroys the parasitic worms by causing distension (ballooning) and detachment of the tegumental sheath (skin-like covering) of these organisms. 3. Eosinophil cationic protein (ECP): This substance is the major destroyer of helminths and it is about 10 times more toxic than MBP. It destroys the parasites by means of complete disintegration. It is also a neurotoxin. 4. Eosinophil-derived neurotoxin: It destroys the nerve fibers particularly, the myelinated nerve fibers. 5. Cytokines: Cytokines such as interleukin-4 and interleukin-5 accelerate inflammatory responses by activating eosinophils. These cytokines also kill the invading organisms
  • 73.
    BASOPHILS – Basophils playan important role in healing processes. – Basophils also play an important role in allergy or acute hypersensitivity reactions. – This is because of the presence of receptors for IgE in basophil membrane. Mechanism of Action of Basophils – Functions of basophils are executed by the release of some important substances from their granules such as: – 1. Heparin: Heparin is essential to prevent the intravascular blood clotting. – 2. Histamine, slow-reacting substances of anaphylaxis, bradykinin and serotonin: Theses substances produce the acute hypersensitivity reactions by causing vascular and tissue responses. – 3. Proteases and myeloperoxidase: These enzymes destroy the microorganisms – 4. Cytokine: Cytokine such as interleukin-4 accelerates inflammatory responses and kill the invading organisms.
  • 74.
    Mast Cell – Mastcell is a large tissue cell resembling the basophil. – Origin – Mast cells are developed in the bone marrow – Functions – Mast cell plays an important role in producing the hypersensitivity reactions like allergy and anaphylaxis. – Two types of substances are secreted by mast cell: – 1. Preformed mediators: These substances are already formed and stored in secretory granules. These substances are histamine, heparin, serotonin, hydrolytic enzymes, proteoglycans and chondroitin sulfates. – 2. Newly generated mediators: These substances are absent in the mast cell during resting conditions and are produced only during activation. These substances are arachidonic acid derivatives such as leukotriene C (LTC), prostaglandin and cytokines.
  • 75.
    MONOCYTES – Monocytes arethe largest cells among the leukocytes. – Monocytes secrete: – 1. Interleukin-1 (IL-1). – 2. Colony stimulating factor (M-CSF). – 3. Platelet-activating factor (PAF). – Monocytes are the precursors of the tissue macrophages. – Matured monocytes stay in the blood only for few hours. Afterwards, these cells enter the tissues from the blood and become tissue macrophages. – Examples of tissue macrophages are Kupffer cells in liver, alveolar macrophages in lungs and macrophages in spleen.
  • 76.
    LYMPHOCYTES – Lymphocytes playan important role in immunity. – T lymphocytes and B lymphocytes. – T lymphocytes are responsible for the development of cellular immunity – B lymphocytes are responsible for the development of humoral immunity.
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  • 79.
    LEUKEMIA – Abnormal increasein non functional immature leukocytes due to carcinogenic reason.
  • 80.
    LEUKEMIA.. – CAUSES: – CLINICALSIGNS AND SYMPTOMS: – TREATMENT: Genetic Environmental factors Infection by RNA viruses Bone marrow transplant Periodic blood transfusion Use of anticancer drugs
  • 81.
    Periodontium in leukemicpatients – Oral and periodontal manifestations of leukemia consist of leukemic infiltration, bleeding, oral ulcerations, and infections. – Leukemic cells can infiltrate the gingiva and less frequently the alveolar bone. – Gingival infiltration often results in leukemic gingival enlargement. – Clinically,the gingiva appears initially bluish red and cyanotic, with a rounding and tenseness of the gingival margin; – then it increases in size, most often in the interdental papilla and partially covering the crowns of the teeth.
  • 82.
    Periodontium in leukemicpatients.. – Bleeding-Bleeding gingiva can be an early sign of leukemia. It is caused by the thrombocytopenia resulting from replacement of the bone marrow cells by leukemic cells. – This bleeding tendency can also manifest in the skin and throughout the oral mucosa, where petechiae are often found, with or without leukemic infiltrates. – A more diffuse submucosal bleeding manifests as ecchymosis.
  • 83.
    Periodontium in leukemicpatients.. – Oral Ulceration and Infection – Discrete, puched-out ulcers penetrating deeply into the submucosa and covered by a firmly attached white slough can be found on the oral mucosa. – Acute gingivitis and lesions resembling necrotizing ulcerative gingivitis are more frequent and severe in terminal cases of acute leukemia. – Gingiva is a peculiar bluish red, is spongelike and friable, and bleeds persistently on the slightest provocation. – Eliminating or reducing local factors (e.g.bacterial plaque) can minimize severe oral changes in leukemia.
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  • 85.
    Platelets – INTRODUCTION.. – NORMALCOUNT-2,00,000 and 4,00,000/cu mm of blood. – Size of Platelets – Diameter : 2.5 μ (2 to 4 μ) – Volume : 7.5 cu μ (7 to 8 cu μ). – SHAPE.. – STRUCTURE AND COMPOSITION – Platelet is constituted by: – 1. Cell membrane or surface membrane – 2. Microtubules – 3. Cytoplasm.
  • 86.
    – Cytoplasm ofplatelets contains the cellular organelles,Golgi apparatus, endoplasmic reticulum, mitochondria,microtubule, microvessels, filaments and granules. – Cytoplasm also contains some chemical substances such as proteins, enzymes, hormonal substances, etc.
  • 87.
    PLATELET GRANULES Alpha granules •1. Clotting factors – fibrinogen, V and XIII • 2. Platelet-derived growth factor • 3. Vascular endothelial growth factor (VEGF) • 4. Basic fibroblast growth factor (FGF) • 5. Endostatin • 6. Thrombospondin. Dense granules • 1. Nucleotides • 2. Serotonin • 3. Phospholipid • 4. Calcium • 5. Lysosomes.
  • 88.
    PHYSIOLOGICAL VARIATIONS 1. Age: Plateletsare less in infants (1,50,000 to 2,00,000/cu mm) and reaches normal level at 3rd month after birth. 2. Sex: There is no difference in the platelet count between males and females. In females, it is reduced during menstruation. 3. High altitude: Platelet count increases. 4. After meals: After taking food, the platelet count increases
  • 89.
    PROPERTIES OF PLATELETS –Platelets have three important properties (three ‘A’s): 1. Adhesiveness 2. Aggregation 3. Agglutination
  • 90.
    1. ROLE INBLOOD CLOTTING 2.ROLE IN CLOT RETRACTION 3.ROLE IN PREVENTION OF BLOOD LOSS (HEMOSTASIS) 4.ROLE IN REPAIR OF RUPTURED BLOODVESSEL FUNCTIONS OF PLATELETS 5. ROLE IN DEFENSE MECHANISM
  • 91.
    LIFESPAN AND FATEOF PLATELETS – Average lifespan of platelets is 10 days. It varies between 8 and 11 days. – Platelets are destroyed by tissue macrophage system in spleen. – So, splenomegaly (enlargement of spleen) decreases platelet count and splenectomy (removal of spleen) increases platelet count.
  • 92.
    APPLIED PHYSIOLOGY – PLATELETDISORDERS – Platelet disorders occur because of pathological variation in platelet count and dysfunction of platelets. – Platelet disorders are: – 1. Thrombocytopenia – 2. Thrombocytosis – 3. Thrombocythemia – 4. Glanzmann’s thrombasthenia
  • 93.
    Oral and periodontalmanifestations in patients with THROMBOCYTOPENIA – Purpura refers to the purplish appearance of the skin or mucous membranes where bleeding has occurred as a result of decreased platelets. – Etiologic factors: – aplasia of the marrow; – displacement of the megakaryocytes in the marrow, as in leukemia; – replacement of the marrow by tumor; – destruction of the marrow by irradiation or radium or by drugs, such as benzene, aminopyrine, and arsenical agents.
  • 94.
    Oral and periodontalmanifestations in patients with THROMBOCYTOPENIA – Thrombocytopenic purpura is characterized by: – There is spontaneous bleeding into the skin or from mucous membranes. – Petechiae and hemorrhagic vesicles occur in the oral cavity, particularly in the palate, tonsillar pillars, and the buccal mucosa. – The gingivae are swollen, soft, and friable. – Gingival changes represent an abnormal response to local irritation; the severity of the gingival condition is dramatically alleviated by removal of the local factors. low platelet count prolonged clot retraction and bleeding time normal or slightly prolonged clotting time
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  • 96.
    REFERENCES – Guyton andHall Textbook of Medical Physiology,10th edition – Essentials of Medical Physiology, K. Sembulingam, Prema Sembulingam,6th edition – Carranza’s Clinical Periodontology,11th edition
  • 97.