DJ COLLEGE OF DENTAL SCIENCES AND RESEARCH
SEMINAR TOPIC – BLOOD AND BLOOD DISORDERS
PRESENTED BY:-Dr Venisha Pandita1st Year Post GraduateDepartment of Public Health Dentistry
CONTENTS:
Introduction Characteristics Composition Plasma proteins Blood cells : RBC WBC Platelets Haemoglobin Haemopoiesis Haemostasis Functions of blood Blood groups
Disorders :
Diseases of red blood cells Anemia Polycythemia
Hemostasis and its disorders Thrombocytopenia Haemophilia Disseminated intravascular coagulation
Disorders of White Blood Cells Agranulocytosis Leukaemia Conclusion References
BLOOD:
William Harvey- father of physiology discovered blood circulated through the body in 1628. It is a fluid connective tissue which transports substance
from one part of the body to another. It provides nutrients and hormones to the tissues and
removes their waste products.
CHARACTERISTICS OF BLOOD Color: blood is red in color. Arterial blood is scarlet red and venous blood is
purple Volume: Average volume of blood in a normal adult is 5 l In females it is slightly less and it is about 4.5 l 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 five times more viscous than water.
COMPOSITION
1.PLASMA:
Straw colored, nonliving part of blood. Blood plasma is a mixture of proteins,
enzymes, nutrients, wastes, hormones and gases.
It contains :
91% Water
9% Solids : that comprises :
1% inorganic molecules: Na+,Ca2+,Cl-,
HCO3-,K+,Mg2+
o 8% organic molecules :7% plasma proteins
1% NPN (non –protein nitrogenous) ,
Substances,sugar,fats,enzymes and
hormones
The specific composition and function of its components are as follows:
1. PROTEIN : Normal value: 6.4 -8.3 gm% There are three major categories of plasma
proteins, and each individual type of proteins has its own specific properties and functions:
Albumin: 55% 3-5gm% helps substances dissolve in the plasma
by binding to them, hence playing an important role in plasma transport of substances such as drugs, hormones and fatty acids.
Globulin : 38 % 2-3 gm % alpha, beta and gamma globulins. eg: immunoglobulins, transport globulins immunoglobulins: antibiotics, attack foreign
proteins & pathogens transport globulins: bind small ions, hormones
Fibrinogen : functions in blood clotting accounts for roughly 7% of plasma proteins
OTHER FORMS
GLYCOPROTEIN LIPOPROTEIN : HDL, LDL, VLDL, Chylomicrons TRANSFERRIN : (mainly -globulin)-Iron binding
property HAPTOGLOBIN : 2 globulin - Regulates renal
threshold for hemoglobin
CERULOPLASMIN -(mainly 2 globulin) – binds with copper and helps in its storage and transport .
FETUIN –present in FOETUS, growth promoting protein
COAGULATION FACTORS -, -globulin ANGIOTENSIGEN -2 globulin HAEMAGGLUTININS -antibodies against red
cells Ag IMMUNOGLOBULIN (Ig) - globulin
2. Nutrients: These include glucose, amino acids, fats, cholesterol,
phospholipids, vitamins and minerals.
3. Gases: Some oxygen and carbon dioxide are transported by plasma.
4. Electrolytes: The most abundant of these are sodium ions
5. Amino acids6. Nitrogenous waste:o urea ,uric acid, creatine, creatnine
FUNCTIONS OF PLASMA PROTEINS:
1. Helps in coagulation of blood2. Helps to maintain colloidal osmotic pressure.3. Helps in maintaining viscosity of blood4. Provides stability to blood5. Helps in maintaining the acid-base balance in
the body6. Immune function7. Transport and reservoir function
BLOOD CELLS:
Red blood cellWhite blood cellPlatelet
RED BLOOD CELLS The most abundant blood cells are the red blood cells
(RBCs), which account for 99.9 percent of the formed elements.
These cells give whole blood its deep red color. Red blood cells contain the red pigment hemoglobin . No nucleus Cell membrane : Lipids, Proteins, Spectrin,
Glycophorin No Mitochondria No Ribosome No Centriole In adult males,4.5–6.3 million per 1 cubic ml females,4.2–5.5 million per 1 cubic ml
HAEMOGLOBIN:
Normal values:At birth: 23gm/dlAt the end of 3 months: 10.5gm/dlAt the end of 1 year 12.5gm/dlAdults- males: 14-18gm/dl females: 12-15 gm/dl
STRUCTURE OF HAEMOGLOBIN :
Red oxygen carrying pigment in the RBCs, there are two parts.
Globin (96%) and Heme (4%). Each heme unit holds an iron ion in such a
way that the iron can interact with an oxygen molecule, forming oxyhemoglobin .
VARIETIES OF HEMOGLOBIN:
A haemoglobin molecule in which the iron has separated from the oxygen molecule is called deoxyhemoglobin .
The RBCs of an embryo or a foetus contain a different form of hemoglobin, known as fetal hemoglobin , which binds oxygen more readily than does the haemoglobin of adults.
Methaemoglobin - Hb with ferrous to form ferric
Carboxyhaemoglobin -CO bound at O2 binding site
Sulphaemoglobin n- Sulphur containing Hb usually
-Resulting from drug ingestion
FUNCTIONS OF HAEMOGLOBIN:
1. Facilitate transport of oxygen from lungs to tissues
2. Facilitate transport of CO2 from the tissues to the lungs
3. It acts as an excellent acid- base buffer, being a protein.
VARIATIONS Sex :males > females Diurnal variation: Lowest in morning; highest
in evening Altitude : Increased at higher altitude Exercise : Increased Excitement :Increased
VARIATIONS:
Poikilocytosis :variation in shape of RBC Anisocytosis:variation in size of RBC Phsiological: Diurnal variation – lowest during sleep maximum in
evening Muscular exercise: increases Altitude: increases Pathological: increases Hypoxia Shock dehydration Life span : 120 days Destruction: Mainly in spleen; liver; bone marrow
HAEMOPOEISISIn order to maintain the constant blood count it
is necessary that new cells should be formed to replace these that are destroyed. This phenomenon of cell production is called hemopoeisis.
Erythropoeisis -dev of RBCs Leucopoeisis -dev of WBCs Megakaryocytopoeisis -dev of platelets
HAEMOPOEISIS:
RBC LIFE SPAN & CIRCULATION
Erythropoiesis : development of RBCs During intrauterine life- 1. Mesoblastic stage: Intravascular erythropoeisis: Upto 3
months RBC are formed from mesoderm of yolk sac, hence erythropoeisis occurs within the vessel.
2. Hepatic stage: After 3 months, liver and spleen are the site
of blood formation. 3. Myeloid stage : from middle of foetal
life ,occur in bone marrow
In Children, erythropoiesis occurs in : all bones with red marrow mainly liver spleen. In adults : after 18-20 yrs end of long bones like humerus and femur,
because shaft is converted to yellow marrow Skull Vertebrae Ribs Sternum and pelvis.
STAGES OF ERYTHROPOIESIS
Stem cell
Haemocytoblast ProerythroblastEarly
normoblastintermediatenormoblast
LateNormoblast
Reticulocyte Erythrocyte
Committed cell
Developmental pathway
REGULATION OF ERYTHROPOIESIS
for erythropoiesis to proceed normally myeloid tissues must receive adequate supplies of amino acids, Fe, & vitamins required for protein synthesis
essential coenzymes: B6, B12, folic acid – necessary for DNA replication (mitosis)
vitamin B12: obtained from dairy products & meat; its absorption requires presence of intrinsic factor produced in stomach
LEUKOCYTES (WBCS)
Leukocytes found in blood in the following proportions:
Granulocytes–WBC with granules in their cytoplasm
60% Neutrophils 1-4% Eosinophils <1% Basophils Agranulocytes–lack visible
cytoplasmic granules 20 - 40% Lymphocytes 2 - 8% Monocytes
TLC:At birth is 20000/ ulIn adults is 4000-11000/ ul Leucopenia : decreases less than 4000/
cummCauses: starvation Typhoid fever Viral/ protozoal infection
Leucocytosis : increases above 11,000/ cumm
Causes: newborn Evening Exercise Stress Pregnancy Menstruation Any pyogenic / pyrogenic infections
1. NEUTROPHILS Size: 10-12 diam Nucleus: Multilobed (2-6)-PMNL Cytoplasm: Granular, Neutrophilic Granules: pin point granules neutrophilic in nature Contains proteins and lipids These granules are regarded as lysosomes as
they can lyse any type of substances using varieties of enzymes like nucleases,glycosidases
Functions: Phagocytosis : whenever the body gets
invaded by bacteria, neutrophils are the first to seek out to ingest and kill bacteria. (First line defense)
2. EOSINOPHIL Size : 10-12 diam Nucleus : Bilobed spectacle appearance Cytoplasm : Acidophilic, granular Granules: coarse, acidic High peroxidase content Lysosomal enzymes
Functions
Mild phagocytic
Anti-allergic effect: collect at the site of the
tissues where allergic reactions occur by
degrading the effects of mediators
(histamine,bradykinin)
Inhibits Mast cells degranulation
Kills parasites
Eosinophilia: increase in eosinophilsCauses: Allergic reactions ( bronchial asthma) Skin diseases Eosinopenia: decrease After injection of corticosteroids
3. BASOPHIL Size : 10-12 m Nucleus : Bilobed Cytoplasm : Basophilic Granules: Coarse,basic Plenty in no., overcrowd the nucleus Contain- Histamine, Heparin Eosinophil chemotactic factor (ECF-A):
chemical mediator of immediate hypersensitivity reactions.
Functions:
Liberates Histamine and ECF-A: which leads to
allergic manifestations
Liberates Heparin : which acts as Anticoagulant and
keeps the blood in fluid state
Mild phagocytosis Basophilia: increaseChickenpoxTuberculosisInfluenzaBasopenia : decreaseAfter administration of gluco-corticoids
4. MONOCYTE
Largest WBC Size :12-18 diam Nucleus : Kidney shaped eccentric in
position Cytoplasm : Clear Enzymes- proteolytic,
hydrolytic
Functions Active Phagocytosis : second line defence Enter the tissues to become tissue macrophage Kill tumor cells after sensitization by
Lymphocytes.Monocytosis:TuberculosisSome leukaemiaMonocytopenia:Hypoplastic bone marrow
5. LYMPHOCYTES
2 types: Large Lymphocyte : 10-14 diam,
precursor of small lymphocyte Small Lymphocyte : 7-10 diam
Nucleus : Single, round, oral or indented central,
occupies whole of the cell Nuclear chromatin is coarse and
lumpy Cytoplasm: Only narrow ring around nucleus
Functions produce antibodies and hence responsible for
Immunity Immunity: Resistance exhibited by the host towards
the injury caused by bacteria or foreign proteins. Humoral Immunity: Antibodies which are -
globulins produced by B-Lymphocytes Cell-mediated Immunity: Due to T-Lymphocytes
Lymphocytosis: In children : 60 % more than neutrophils (relative
Lymphocytosis)Lymphopenia: AIDSHypoplastic bone marrow
LIFE SPAN AND FATE OF WBC
Neutrophils : 2-4 days
Eosinophils : 8-12 days (Last through
GIC or Resp.
tract)
Monocyte : 1 day in circulation
B-Lymphocytes : Few days or weeks
T-Lymphocytes : 2-4 years
PLATELETS (THROMBOCYTES)
Structure :General smallest blood cells, colorless disc shaped (in activated from) to sphere
shaped (activated) granulated bodies. Size : 2-5 m in diameter, average volume
5.8 m3 Leishman staining : faint blue cytoplasm with
distinct reddish purple granules. Nucleus is not present.
Under Electron Microscope: Platelet membrane: Features Identical structure with cells membranes
thickness: 60 nm Main lipids in lipo-protein layer of cell
membrane: Phospholipids. Cholesterol, and glycolipids
Contains various receptors meant for combining with specific substances like:
Collagen Fibrinogen Von-Willebrand’s factor: important role in
platelet adhesion
Cytoplasm : contains Golgi apparatus Endoplasmic reticulum Few mitochondria Microvesicles and microtubules: Contractile protein –actin and myocin :
helps in clot retraction. Glycogen Lysosomes
Granules - 2 types. Dense granules- contains Non-proteins substances like phospholipid,
triglycerides. Cholesterol etc. Serotonin - Vasoconstrictor agent ADP- helps platelet aggregation ATP- stores energy Other adenine nucleotides -Granules- contains secreted proteins including Clotting factors Platelet derived growth factor (PDGF)-
stimulates wound healing, helps in repair of damaged vessel wall
Count
Normal count: 1.5 to 4 lacs /cumm
(average 2.59 lac/cumm)
Life span : 8-12 days
Destruction : Mainly in spleen
VARIATIONS:
Thrombocytosis :increase in platelet count after administration of epinephrine After trauma Splenectomy Stress Thrombocytopenia :decrease in platelet
count Bone marrow depression Hypersplenism
FUNCTIONS OF PLATELET
1. Hemostasis:Spontaneous arrest of bleeding by physiological process. Platelet adhesion Platelet activation Platelet aggregation : Hemostatic plug that prevents blood loss
2 . Blood coagulation- release of clotting factors,
Prostaglandins, Phospholipids
3. Clot Retraction- 40% of original volume and release of Thrombosthetin
4. Phagocytic functions – helps in phagocytosis
of carbon particles,viruses.
MECHANISM OF HAEMOSTASIS Injury to vessel wall initiates series of events A. Constriction of injured blood vessel. B. Formation of a 'temporary haemostatic
plug' of platelets. C. Conversion of temporary haemostatic
plug into the 'definitive haemostatic clot'. Formation of clot Seals off the damaged blood vessel prevents further loss of blood
PHYSIOLOGY OF CLOTTING MECHANISM
The clotting mechanism responsible for the formation of fibrin involves a 'complex series' or 'cascade' of reactions. Here 'inactive' enzymes are activated, and the activated enzymes in turn activate other inactive enzymes.
ANTICOAGULANTS
Types Natural Anticoagulants Synthetic Anticoagulants 1. Heparin A powerful anticoagulant first isolated from
liver (hence its name) present in many other organs e.g. lungs. It facilitates the action of antithrombin III,
thereby inhibiting the active forms of clotting factors IX, X, XI and XII.
Origin: Heparin is secreted by -(i) granules of circulating basophils(ii) granules of "mast cells". These cells are
found in large numbers in tissues that are rich in connective tissue;
Destruction: by an enzyme "Heparinase" in the liver.
2. Anti-Thrombin or Heparin co-factor II: It inhibits thrombin.
3. Protein C: It inactivates factors V and VIII.
Synthetic Anticoagulants 1. Vitamin K Antagonists: effective orally These include coumarin derivatives e.g.
dicoumarol. and warfarin.2. Malayan (Malaysian) Pit Viper3. Arvin (Ancord)
FUNCTIONS OF BLOOD
Transport of Respiratory gases: - Blood and particularly red cells are responsible
for transport of O2 from lungs to the tissues. This is done due to the presence of hemoglobin,
which combines with O2 to form oxy-Hb; Co2 from tissue is taken up by the blood and released in the lungs.
Transport of Nutrition: - The substances such as glucose, fatty acids,
amino acids, vitamins, electrolytes and trace metals are absorbed from the intensive transported to all parts of the body for utilization and storage via blood.
Excretory: Blood transports urea, uric acid, creatinine to kidney, lungs, skin, and gastro-intestinal tract for excretion.
Regulation of Body Temperature: Blood forms internal environment of the cell
i.e. MILLIEU INTERIUER in terms of volume, composition, concentration, pH and temperature which is regulated to normal physiological limits with respect to miner changes in the body.
This mechanism is called Homeostasis. (W. E. Cannen).
Defensive Action: Blood acts as a great defensive mechanisms through WBC s , lymphocytes
Transport of Other Substances: Blood acts as a vehicle through hormones, vitamins, and other essential chemicals are transported to the various tissues.
Coagulation Property: It is a mechanism by which various factors present in the blood form a cell and thus prevent blood less
Plasma Proteins: The plasma proteins of blood have various functions which will be discussed subsequently
BLOOD GROUPS The chief blood groups are : Classical ‘ABO’ blood group Rhesus (Rh) blood group M and N blood group
1.CLASSICAL ‘ABO’ BLOOD GROUP
Blood Type
Antigens on Red Blood Cell
Can Donate Blood To
Antibodies in Serum
Can Receive Blood From
A A A,AB Anti-A A,O
B B B.AB Anti-B B,O
AB A and B AB None AB,O
O None A,B,AB and O
Anti-A and Anti-B
O
RELATIONSHIPS BETWEEN BLOOD TYPES AND ANTIBODIES
Blood typing is a laboratory test done to discover a person's blood type. If the person needs a blood transfusion, cross-matching is done following blood typing to locate donor blood that the person's body will accept. (Illustration by Electronic Illustrators Group.)
2.RHESUS (RH) BLOOD GROUP
Landsteiner and Weiner (1940) Present in > 85% of individuals Rh + Ve No corresponding Agglutinin in plasma Rh antigen is called D and its antibody is
called Anti-D also known as warm antibodies.
Rh incompatibility
3. M N SYSTEM
Significance in the determination of paternity in medico legal cases.
M and N factors depend on two minor genes. Each person carries of the two of the genes
of the M and N group. i.e. M + M = M N +N = N M+ N =MNo These are antigenic to rabbits
USES OF BLOOD GROUPING TESTS
Blood transfusion In pregnancy (Rh Incompatibility) Investigating cases of paternity dispute In forensic medicine Medico legal value
BLOOD DISORDERS
DISEASES OF RED BLOOD CELLS (ERYTHROCYTES):-
Anaemia Iron Deficiency Anaemia Anaemia Of Chronic Disease Sideroblastic Anaemia
megaloblastic anaemia haemolytic anaemia sickle cell anaemia thalassemia aplastic anaemia Polycythemia
ANAEMIA
At birth, haemoglobin is 20g/dl and at 3 months lower limit of normal is taken as 9.5g/dl. A haemoglobin level of 12g/dl or less is usually regarded as anaemia in adult males and less than 11g/dl is taken as anaemia in females.
SYMPTOMS
Pallor or lack of color fatigue, dizziness, headaches decreased exercise tolerance rapid heartbeat, and shortness of breath haemic murmurs Untreated anemia may progress to death
from heart failure
ETIOLOGICAL CLASSIFICATION OF ANEMIA Blood loss:
Acute Post hemorrhagic Chronic blood loss
Deficiency of Hemopoetic factors:- Iron deficiency Folate and vitamin b12deficiency Protein deficiency.
Bone marrow aplasia:- Aplastic anemia Pure red cell aplasia
Anemia due to systemic infections:- Due to chronic infection Due to chronic renal disease Due to chronic liver disease Endocrinal diseases
Anemia due to bone marrow infiltration:- Leukemia’s Lymphomas Myelofibrosis Multiple myeloma Congenital sideroblastic anemia
Anemia due to increased red cell destruction:- Intra-corpuscular defect Extra-corpuscular defect
Morphological classification of anemia:- Microcytic hypochromic Normocytic normochromic Macrocytic normochromic
TYPES OF ANAEMIA Macrocytic anemia: Megaloblastic anemia
and non-megaloblastic macrocyctic anemia. Primary cause of this sort of anemia is collapse of DNA synthesis with kept RNA synthesis that occurs due to the division of the divisional cells.
Microcytic anemia: Sort of anemia occurs due to hemoglobin synthesis shortage or collapse.
Normcytic anemia: Occurs when Hb levels decreases overall. Size of RBC is often normal.
Heinz Body anemia: Considered a cell abnormality that usually occurs in cells under anemia.
Iron-deficiency anaemia – hypochromic microcytic anemia characterized by low serum iron, increased serum iron-binding capacity, decreased serum ferritin, and decreased marrow iron stores.
Megaloblastic (pernicious) anaemia – predominant number of megaloblastic erythroblasts, and relatively few normoblasts, among the hyperplastic erythroid cells in the bone marrow
Hemolytic anaemia – increased rate of erythrocyte destruction.
Sickle cell anemia – autosomal recessive anemia characterized by crescent- or sickle-shaped erythrocytes and accelerated hemolysis, due to substitution of a single amino acid - chromosome 11
Aplastic anemia – greatly decreased formation of erythrocytes and hemoglobin, usually associated with pronounced granulocytopenia and thrombocytopenia
Chronic anemia Anemia of folate deficiency
Cooley's anemia (beta thalassemia) – syndrome of severe anemia resulting from the homozygous state of one of the thalassemia genes or one of the hemoglobin Lepore genes with onset, in infancy or childhood, of pallor, icterus, weakness, splenomegaly, cardiac enlargement, thinning of inner and outer tables of skull, microcytic hypochromic anemia with poikilocytosis, anisocytosis, stippled cells, target cells, and nucleated erythrocytes
CAUSES Accurate blood loss Anemia of chronic disease Bone marrow failure and Plastic anemia.
TREATMENT A successful treatment of anemia depends
on successful diagnosis of the cause that brings about the disease.
There are several causes of anemia including blood loss, cancer, a nutritional deficiency, chronic illness, bone marrow infiltration, lower response to erythropoietin and inflammation.
These causes can be determined with laboratory test results and physical examination.
Specific treatment for anemia will be determined by the physician based on:
Age, overall health, and medical history Extent of the disease Tolerance for specific medications,
procedures, or therapies Expectations for the course of the disease Opinion or preference of the patient
Treatment of the causative disease Vitamin and mineral supplements Change in diet Medication Blood transfusion Bone marrow transplant Surgery (to remove the spleen, if related to
hemolytic anemia) Antibiotics (if an infection is the causative
agent)
HEMOPHILIA Persons with hemophilia lack the ability to
stop bleeding because of the low levels, or complete absence, of specific proteins, called "factors," in their blood that are necessary for clotting.
Inherited bleeding or coagulation, disorder. Proper clotting of blood helps prevent
excessive bleeding. Types of hemophilias –
hemophilia A - lack of factor VIII hemophilia B - lack of factor IX
CAUSES Hemophilia types A and B are inherited
diseases passed on from a gene located on the X chromosome.
Females carrier of hemophilia has the hemophilia gene on one of her X chromosomes, and there is a 50 percent chance that she may pass the defective gene to her male offspring.
Males who inherit the defective gene will develop hemophilia.
Males with hemophilia do not pass the gene to their sons; however, they do pass the gene to their daughters.
Females who inherit the defective gene will become carriers who may, in turn, have a 50 percent chance of passing it on to their children. Although females who inherit the gene generally have no active problems related to hemophilia, some may have other problems associated with bleeding, such as excessive menstrual bleeding, frequent or severe nosebleeds, or bleeding after dental procedures or surgery.
In about 1/3rd of hemophilia cases, there is no family history of the disease. These cases are due to a new or spontaneous development of the defective gene in the female
SYMPTOMS:
Excessive, uncontrollable bleeding Bleeding may occur even if there is no injury. Often occurs in the joints and in the head. Bruising - Occur from small accidents, which
can result in a large hematoma. Bleeds easily - Tendency to bleed. Bleeding into a joint - Hemarthrosis can
cause pain, immobility, and eventually deformity if not medically managed properly
Bleeding into the muscles - Bleeding into the muscles can cause swelling, pain, and redness.
Bleeding from injury or bleeding in the brain - Bleeding from injury or spontaneously in the brain, is the most common cause of death in children with hemophilia and the most serious bleeding complication.
Other sources of bleeding - Blood found in the urine or stool may also be a symptom of hemophilia.
The symptoms of hemophilia may resemble other blood disorders or medical problems.
DIAGNOSIS & EFFECTS
Complete medical history and physical examination
Clotting factor levels Complete blood count (CBC) Assessment of bleeding times DNA testing. Most common cause of disability from
hemophilia is chronic joint disease or arthropathy, which is caused by uncontrolled bleeding into the joints.
Hemorrhage – severe internal or external discharge of blood, is a continuing problem.
TREATMENT
Blood transfusions
Prophylactic (preventive) treatment with infused clotting factors
IMMUNE THROMBOCYTOPENIC PURPURA
(THROMBOCYTOPENIA) Blood disorder characterized by an abnormal
decrease in the number of blood platelets, which results in internal bleeding.
Acute thrombocytopenic purpura – Most common in young children, the symptoms may follow a virus infection and disappears within a year - usually disorder does not recur.
Chronic thrombocytopenic purpura – Onset of the disorder can happen at any age, and symptoms can last six months or longer. Adults have this form more often than children, and females have it 3 times more often than males.
CAUSES
Medications - including over-the-counter Infection Pregnancy Immune disorders However, about half of all cases are classified
as idiopathic.
SYMPTOMS Internal bleeding, which may cause: ecchymosis - bruising , petechiae - tiny red dots on skin or mucous
membranes Occasionally, bleeding from the nose, gums,
digestive tract, urinary tract Rarely, bleeding within the brain Symptoms may resemble other blood
disorders or medical problems.
DIAGNOSIS
Complete medical history and physical examination
Additional blood and urine tests Other evaluation procedures Careful review of patient's medications Bone marrow examination
TREATMENT Treatment of the causative disease Discontinuation of causative drugs Treatment with corticosteroids Treatment with medications Lifestyle changes, such as: use of protective
gear , avoidance of certain activity causing injuries.
HODGKIN'S DISEASE Type of lymphoma, a cancer in the lymphatic
system. Rare disease usually occurs most often in
people between the ages of 15 and 34, and in people over age 55.
Hodgkin's disease causes the cells in the lymphatic system to abnormally reproduce, eventually making the body less able to fight infection.
Hodgkin's disease cells can also spread to other organs.
LYMPHADENOMA – HODGKIN'S DISEASE (PSEUDO-LEUKEMIA OF GERMAN AUTHORS)
SIGNS AND SYMPTOMS
Painless swelling of lymph nodes in neck, underarm, and groin
Fever Night sweats Fatigue Weight loss Itching of the skin It may resemble other blood disorders or
medical problems, such as influenza or other infections.
DIAGNOSIS
Additional blood tests X-rays of the chest, bones, liver, and spleen Biopsy of the lymph node
TREATMENT
Radiation therapy Chemotherapy
LEUKAEMIA
Cancer of the blood cells, usually the white blood cells.
Leukemic cells look different than normal cells and do not function properly.
LYMPHOCYTIC OR MYELOGENOUS LEUKEMIA
Cancer can occur in either the lymphoid or myeloid white blood cells.
When the cancer develops in the lymphocytes (lymphoid cells), it is called lymphocytic leukemia.
Cancer develops in the granulocytes or monocytes (myeloid cells) – myelogenous leukemia.
ACUTE OR CHRONIC LEUKEMIA
Acute leukemia - The new or immature cells, called blasts, remain very immature and cannot perform their functions. The blasts increase in number rapidly, and the disease progresses quickly.
Chronic leukemia - There are some blast cells present, but they are more mature and are able to perform some of their functions. The cells grow more slowly, and the number increases less quickly, so the disease progresses gradually.
LEUKEMIA IS CLASSIFIED INTO ONE OF THE FOUR MAIN TYPES OF LEUKEMIAS
Acute myelogenous leukemia (AML) Chronic myelogenous leukemia (CML) Acute lymphocytic leukemia (ALL) Chronic lymphocytic leukemia (CL
SIGNS AND SYMPTOMS More frequent infections and fevers Anaemia and its symptoms: pale skin, fatigue,
weakness, bleeding, bruising, fever, chills, loss of appetite, loss of weight, swollen or tender lymph nodes, liver, or spleen, petechiae (tiny red spots under the skin), swollen or bleeding gums, sweating, bone or joint pain.
Acute leukaemia: headaches, vomiting, confusion, loss of muscle control, seizures, swollen testicles, sores in the eyes or on the skin.
Chronic leukemia may affect the skin, central nervous system, digestive tract, kidneys, and testicles.
DIAGNOSIS Physician examination for swelling in the:
liver, spleen, lymph nodes under the arms, in the groin, and in the neck
Blood tests and laboratory tests Blood tests to examine the blast (immature)
blood cells Bone marrow aspiration and biopsy Lymph node biopsy Spinal tap Imaging procedures, such as x-ray,
ultrasound, and computed tomography (CT)
TREATMENT
Chemotherapy Radiation therapy Bone marrow stem cell transplantation Biological therapy Platelet transfusion Red blood cell transfusion Medications to prevent or treat damage to
other systems of the body caused by leukemia treatment
NON-HODGKIN'S LYMPHOMA
Type of lymphoma, which is a cancer in the lymphatic system.
Non-Hodgkin's disease causes the cells in the lymphatic system to abnormally reproduce eventually causing tumors to grow and can also spread to other organs.
Etiology is idiopathic
SYMPTOMS Painless swelling of lymph nodes in neck,
underarm, and groin Fever Night sweats Fatigue Weight loss Itching of the skin Recurring infections
DIAGNOSIS Blood tests X-rays of the chest, bones, liver, and spleen Biopsy of the lymph nodes, bone marrow,
and other sites Lymphangiograms - lymphatic system x-rays CT scan Ultrasonography scan
TREATMENT
Radiation therapy Chemotherapy
THROMBOCYTHEMIA
It is a myeloproliferative blood disorder. It is characterized by the production of too
many platelets in the bone marrow. Too many platelets make normal clotting of
blood difficult Etiology is idiopathic
SYMPTOMS
Increased blood clots in arteries and veins Bleeding Bruising easily Bleeding from the nose, gums,
gastrointestinal tract Bloody stools Hemorrhaging after injury or surgery Weakness Enlarged lymph nodes
DIAGNOSIS Complete medical history and physical
examination Blood counts and elevated platelet levels Bone-marrow biopsy
TREATMENT Chemotherapy Plateletpheresis - a procedure to remove
extra platelets from the blood
BONE MARROW TRANSPLANTATION [BMT]
BMT is a special therapy for patients with cancer or other diseases which affect the bone marrow.
A bone marrow transplant involves taking cells that are normally found in the bone marrow (stem cells), filtering those cells, and giving them back either to the patient or to another person.
The goal of BMT is to transfuse healthy bone marrow cells into a person after their own unhealthy bone marrow has been eliminated
NORMAL ANATOMY
INDICATION
PROCEDURE
A BONE MARROW TRANSPLANT CAN BE USED TO
Replace diseased, non-functioning bone marrow with healthy functioning bone marrow
Replace the bone marrow and restore its normal function after high doses of chemotherapy or radiation are given to treat a malignancy – process called "rescue".
Replace bone marrow with genetically healthy functioning bone marrow to prevent further damage from a genetic disease process
CONCLUSION :
Human body is an intricate system of various tissues and organs
Blood and lymphatic system forms an integral part of life’s sustainance.
As a public health dentist ,it is essential to have a proper understanding of blood and its components and blood related diseases so as to be well prepared for their diagnosis and appropriate treatment
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Prema Sembulingam , 4th edition, page no. 53-87
Textbook of Pathology: Harsh MohanMalik A Neelima. Textbook of oral and
maxillofacial surgery.2nd ed:jaypee;new delhi:2010;p.205-225