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Seminar – 3
Presented by Dr. Nabeela Basha
CONTENTS
 Introduction
 History
 General features
 Erythropoiesis
 Hemoglobin
 ESR & PCV
 RBC Disorders
 Public Health Significance
 Conclusion
 References
 Previous year questions
INTRODUCTION
• RBC - red cells / red blood corpuscles / haematids / erythroid
cells / erythrocytes.
• Derived from Greek erythros for "red" and kytos for "hollow
vessel", with -cyte translated as "cell" in modern usage.
• Non-nucleated formed elements in the blood.
• It lacks cytoplasmic organelles such as nucleolus, mitochondria
& ribosomes.
• The red color of RBC is due to the presence of Hemoglobin
(90%).
HISTORICAL BACKGROUND
• JAN SWAMMERDAM-1658 - Dutch biologist and
microscopist. He called them ruddy globules
• ANTON VAN LEEUWENHOEK-1674- Discovered
Microscope and established its size.
• OTTO FUNKE 1851 - German physiologist was the first
scientist to successfully crystallize hemoglobin. "Blutfarbstoff"
• DR. MAX PERUTZ- 1959 - by use of X-ray crystallography
unravelled the structure of hemoglobin
• MENGHINI-1747- presence of iron in the blood, identified the
red corpuscles as the chief site of iron within the organism.
GENERAL FEATURES
• Dimensions
• Normal Count
• Composition
• Functions
• Fragility
• Variations
• Fate & Lifespan
DIMENSIONS
• Shape: Biconcave
• Size: 7.2um in diameter
• Thickness: 2um at the periphery and 1um at the center
• Volume: 87um3
Advantages of Biconcave Shape of RBCs:
• Greater surface area for exchange of gases.
• Flexibilty of RBC
• Minimal tension when the volume of cell alters.
How is the shape maintained?
 Spectrin
- a contractile protein
- maintains shape and flexibility of RBC
- Antigen on cell membrane – helps in blood group classification
NORMAL COUNT
• Adults males: 4.5 – 6 million cu mm of blood
• Adult females: 4 – 5.5 million cu mm of blood
• At birth: 6.7 million cu mm of blood
COMPOSITION
• 62.5% water
• 35% Hemoglobin
• 2.5% :
- Sugar – glucose
- Lipids – Cephalin, Cholesterol & Lecithin
- Protein – Glutathion : insoluble protein which acts as a
reducing agent and prevents damage of hemoglobin
- Enzymes – Carbonic anhydrase and catalase
- Ions – Na+, K+, Ca2+, PO4
3-
FUNCTIONS
• Respiratory
• Acid Base balance
• Maintain viscosity
• Pigment: various pigments are derived from hemoglobin after
disintegration of RBC.
FRAGILITY AND HEMOLYSIS
• Hemolysis- Breakdown of RBC and liberation of hemoglobin.
• Fragility- Susceptibility of RBC to hemolysis or tendency to
break easily.
• There are 2 types:
1. Osmotic fragility- due to exposure to hypotonic saline.
2. Mechanical fragility- due to mechanical trauma
VARIATIONS
Physiologic causes of increase count:
• Age
• Gender
• High altitude
• Exercise
• Temperature
• Meal
Decrease in count: High barometric pressure, Pregnancy, sleep
Pathological variations:
• Increase: Polycythemia
• Decrease: Anaemia
VARIATIONS IN SHAPE
• Crenation: Shrinkage as in hypertonic solutions.
• Spherocytosis: Globular form as in hypotonic conditions.
• Elliptocytosis: elliptical shape
• Sickle cell: Crescent shape
• Poikilocytosis: Flask, hammer or any other unusual shape.
VARIATIONS IN SIZE
• Physiological conditions: RBC in venous blood slightly larger
than those in arterial blood.
• Pathological conditions:
1. Microcytes – smaller cells
2. Macrocytes – larger cells
3. Anisocytes – cells of different sizes
LIFESPAN AND FATE OF RBC
• Lifespan – 120 days
• Site of destruction:
Reticuloendothelial system
ERYTHROPOIESIS
• The process of origin, development and maturation of
erythrocytes.
 Site of erythropoiesis:
• In fetal life: - Mesoblastic stage
- Hepatic stage
- Myeloid stage
• In newborns, children and adults
FIGURE 10.1: Stem cells. L = Lymphocyte, R = Red blood cell, N = Neutrophil, B = Basophil,
E = Eosinophil, M = Monocyte, P = Platelet.
• Factors necessary for erythropoiesis:
1. General factors:
-Erythropoietin
-Thyroxine
-Vitamins
2. Maturation factors:
-Vitamin B12 (Cyanocobalamin)
-Intrinsic factor of Castle
-Folic acid
HEMOGLOBIN
• Hb is the iron containing coloring pigment of RBC.
• 95% dry weight of RBC; 30 – 34% wet weight.
• Molecular weight of Hb is 68,000
• Normal value:
-At birth: 25g/dl
-From puberty: 14-16 g/dl
-Adult males: 15g/dl
-Adult females: 14.5g/dl
STRUCTURE OF HEMOGLOBIN
• Conjugated protein
• Protein part called Globin and iron containing pigment called
heme.
• Heme part is called porphyrin
and is formed by 4 pyrole rings
• Globin is made up of 4
polypeptide chains – 2 alpha and
2 beta chains.
Types of Hemoglobin:
• Normal: - Adult Hb
- Fetal Hb
• Abnormal derivatives:
-Carboxyhemoglobin
-Methemoglobin
-Sulfhemoglobin
ERYTHROCYTE SEDIMENTATION RATE
• Red cells have the property of Rouleaux (piling one on the other)
formation.
• Piled red cells are heavier than the individual ones.
• The rate at which the red cells fall is known as ESR.
• Normal values:
Wintrobe’s method: Males: 0 – 9mm/hr
Females: 0 – 20mm/hr
Westergren’s method: Males: 3 – 7mm/hr
Females: 5 – 9 mm/hr
Westergren’s method:
• Westergren’s tube is used which is 300 mm long & opened at
both the ends.
• It requires collecting 2 ml of venous blood into a tube
containing 0 .5 ml of sodium citrate. It should be stored no
longer than 2 hours at room temperature
or 6 hours at 4 °C. The blood is drawn into
the tube to the 200 mm mark. The tube is
placed in a rack in a strictly vertical position
for 1 hour at room temperature,
Wintrobe’s method:
• The Wintrobe method is performed similarly except that the
Wintrobe tube is smaller in diameter than the Westergren tube
and only 100 mm long.
• EDTA anticoagulated blood without extra diluent
is drawn into the tube, and the rate of fall of red
blood cells is measured in millimeters after 1 hour.
PACKED CELL VOLUME
• Hematocrit is the fractional volume of blood that the
erythrocytes occupy
• It is a reliable index of red cell population.
• Normal values : Males – 46%
Females – 42%
RBC INDICES
• MCV (MEAN CORPUSCULAR VOLUME)
– The average volume of single RBC
PCV per 100ml blood
MCV =  10um3
RBC count (million/cu mm)
Normal range : 78 – 94 um3
 RBC with normal volume are called Normocytes
 RBC with less then normal volume, Microcytes
 RBC with more than normal volume, Macrocytes
• MCH (mean corpuscular hemoglobin)
– The average content of Hb in average RBC.
Hb in gm%
MCH =  10pg
RBC count (million/cu mm)
• Normal range: 28 – 32pg
• MCHC (mean corpuscular hemoglobin concentration)
– Express the average concentration of hemoglobin per unit
volume of RBC.
– It defined as the ratio of the weight of hemoglobin to
volume of RBC.
Hb in gm%
MCHC =  100
PCV per 100ml blood
Normal range: 33 – 38 gm/100ml of cells
DISORDERS OF RBC
• Anemia
Morphologic classification
Etiologic classification
• Polycythemia
Polycythemia Vera
Relative polycythemia
Secondary polycythemia
ANEMIA
• Anemia is defined as Hb concentration in blood below the
lower limit of the normal range for the age and sex of the
individual.
• In adults, the lower extreme of normal Hb is taken as 13g/dl
for males and 11.5g/dl for females.
MORPHOLOGICAL CLASSIFICATION
• Depends upon the size and color of RBC.
• Size of RBC is determined by mean corpuscular volume
(MCV).
• Color is determined by mean corpuscular hemoglobin
concentration (MCHC).
• By this method, the anemia is classified into four types
Hyperchromic Hypochromic Macrocytic Microcytic
ETIOLOGICAL CLASSIFICATION
• On the basis of etiology, anemia is divided into five types:
1. Hemorrhagic anemia
2. Hemolytic anemia
3. Nutrition deficiency anemia
4. Aplastic anemia
5. Anemia of chronic diseases.
IRON DEFICIENCY ANEMIA
• Iron deficiency anemia is the most common type of anemia.
• It develops due to inadequate availability of iron for
hemoglobin synthesis.
• RBCs are microcytic and hypochromic.
• Causes of iron deficiency anemia:
i. Loss of blood
ii. Decreased intake of iron
iii. Poor absorption of iron from intestine
iv. Increased demand for iron in conditions like growth and
pregnancy.
• Features of iron deficiency anemia:
1. Brittle nails,
2. Spoon shaped nails (koilonychias),
3. Brittle hair,
4. Atrophy of papilla in tongue
5. Dysphagia (difficulty in swallowing).
Oral manifestations:
• Pallor of mucosa
• Atrophy of oral mucosa
• Tongue changes – redness, soreness or burning sensation.
Papillae of the anterior two thirds undergo atrophy.
• Angular cheilitis
• Ulcerations
• Slow healing
Diagnosis:
• Clinical – Koilonychia, angular cheilitis, depapillation of
tongue
• Lab diagnosis – Hb level as low as 4g/100ml. MCV, MCH &
MCHC all are reduced. RBC count slightly reduced or normal.
Management:
• Iron supplement: oral ferrous fumerate or ferrous sulphate
300mg three to four times a day for a period of 6 months
• Parenteral route : single dose of iron sorbitol 1.5mg/kg body
weight daily
Oral Health Considerations:
• For dental patients with extremely low Hb levels- physician
consultation
• When Hb is less than 8g/dl, GA should be avoided
• Narcotic use should be limited for those with sever anemia as
there is increased rick of ischemic heart disease.
PLUMMER VINSON SYNDROME
• Patterson Brown Kelly syndrome / Sideropenic dysphagia
• Characterized by iron deficiency anemia, dysphagia and
esophageal webs or strictures.
Clinical Features:
• Middle aged women- 4th to 7th decade of life
• Dysphagia, angular cheilitis, sore tongue.
• Patient complains of spasm in throat or food sticking in throat.
• Spoon shaped nails.
Management:
• Correction of anemia
• Dilation of esophagus – to correct dysphagia
SICKLE CELL ANEMIA
• First described by Herrick in 1910.
• Severe genetic disorder of hemoglobin synthesis.
• Autosomal dominant
• Abnormal hemoglobin, which under low oxygen tension,
results in sickling of the cell.
• In this, α-chains are normal and β-chains are abnormal.
Diagnosis:
• Newborn screening is an important starting point for simple
public health strategies such as parental education, penicillin
prophylaxis, immunization and utilization of prenatal testing.
• The HbS solubility test (Sickledex) can be performed in 5mins
for screening of adult hemoglobinopathies.
• Prenatal testing by DNA analysis of amniotic fluid at 14 to 16
weeks can be done to find out alterations and mutations in
genes.
Clinical Features:
 Periods of latency interrupted by periods of acute crisis.
Known sequelae include:
 Invasive infections
 Acute chest syndrome
 Strokes
 Severe anemia
 Chronic leg ulcers
 Hematuria
 Aseptic osteonecrosis
Oral Manifestations:
• Enamel hypomineralization
• Increased overjet and overbite
• Calcified canals
• Pallor of oral mucosa and delayed eruption of teeth.
• SCA is not associated with increased levels of gingivitis or
periodontitis.*
*Periodontal Disease in Sickle Cell Disease Subjects by John M. Crawford. Journal of
Periodontology. March 1988, Vol. 59, No. 3, Pages 164-169
Management:
• Regular monitoring of hematological state
• Blood transfusion – cerebrovascular symptoms in early
childhood , recurrent pulmonary thrombosis
• Mild to moderate anemia - Blood transfusion
• Risk of HIV and HEPATITIS infection – transfused patient
• Painful crisis – analgesics
• Incidence of hypoxia and dehydration should be avoided
Dental management
• Dental treatment - Directed towards palliative therapy during
crisis period
• Preventive dental care – antiseptic mouth rinses , topical fluoride
recommended
• Antibiotic prophylaxis – penicillin is the drug of choice
• Odontogenic and nonodontogenic infection should be
aggressively treated
• Periodontal status - closely monitored
THALASSEMIA
• Thalassemia is an inherited disorder, characterized by
abnormal hemoglobin.
• It is also known as Cooley’s anemia or Mediterranean
anemia.
• It is more common in Thailand and to some extent in
Mediterranean countries.
• Thalassemia is of two types:
1. α-thalassemia
2. β-thalassemia.
• In normal hemoglobin, number of α and β polypeptide chains is
equal.
• In thalassemia, the production of these chains become
imbalanced because of defective synthesis of globin genes.
• This causes the precipitation of the polypeptide chains in the
immature RBCs, leading to disturbance in erythropoiesis.
α-Thalassemia
• α -thalassemia occurs in fetal life or infancy.
• In this α-chains are less, absent or abnormal.
• In adults, β-chains are in excess and in children, γ-chains are
in excess.
• This leads to defective erythropoiesis and hemolysis.
• The infants may be stillborn or may die immediately after
birth.
β-Thalassemia
• More common type of thalassemia.
• In β-thalassemia, β-chains are less in number, absent or
abnormal with an excess of α-chains.
• Severity ranges from complete lack of symptoms to
transfusion dependence.
• Cooley’s anemia, or thalassemia major is the name for the
most severe form.
Oral Manifestations:
• Excessive overgrowth of maxilla
• Oral mucosa has a lemon yellow tint because of chronic
jaundice – hard palate and floor of the mouth.
• Chipmunk facies- Saddle nose, prominent malar bone, retracted
upper lip
• Poor healing
• Spacing between teeth
• Discoloration of dentin
General management
• Blood transfusion
• Iron chelating agents – desferroxamine
• Folic acid supplements
• Splenectomy – severe cases
Dental management
• Poor wound healing after any surgical procedure
• Surgery has been used successfully to treat the facial
deformities
• HIV and HEPATITIS infections are common in transfused
patients
• Prophylactic antibiotics in splenectomy cases
MEGALOBLASTIC (PERNICIOUS) ANEMIA &
VIT B12 (COBALAMIN) ANEMIA
• Occurs due to deficiency of Vit B12 or folic acid or both,
resulting in disordered cell proliferation.
Clinical Features & Oral Manifestations:
• Weakness, anemia, palpitations, diarrhoea
• Paresthesia of finger, toes & also dementia may be observed.
• Burning sensation of tongue, angular cheilitis
• Hunter’s glossitis: Atrophy of filiform and fungiform papillae
leading to smooth fiery red surface of tongue
Management:
• Blood tranfusion: when Hb level is less than 4g/dl of blood
• Folic acid supplements:
 initial dose - 5 mg orally daily
 maintenance dose - 5 mg orally once a week
• Vit B12 therapy:
 Initial dose – 1000 mcg , intramuscularly 4 to 6 wks
 Maintenance dose – 1000 mcg intramuscularly once every
week
APLASTIC ANEMIA
• A rare disorder characterized by peripheral blood pancytopenia
associated with bone marrow suppression.
• Occurs due to failure of haematopoietic precursor cells in bone
marrow to produce adequate number of all blood cell types.
Clinical Features:
• Commonly seen in young adults
• Erythrocyte deficiency: Headaches, pale skin, breathlessness
• Thrombocyte deficiency: Bruising & bleeding. Cerebral
haemorrhages
• Leukocyte deficiency: Bacterial and fungal infections are
common.
• Ankle edema, anginal pain, congestive cardiac failure
Management:
• Supportive therapy: Antibiotics & transfusion
• Bone marrow transplantation
• Stimulation of haemopoiesis and promote marrow recovery
 Androgenic steroids - oxymetholone
 Corticosteroids –Prednisolone or methyl prednisolone
 Antithymocyte or antilymphocyte globulin combined with
cyclosporine.
POLYCYTHEMIA
• Abnormal increase in the number of RBCs in the peripheral
blood, usually with increase in Hb level.
• Types:
o Polycythemia Vera
o Relative Polycythemia
o Secondary Polycythemia
POLYCYTHEMIA VERA
• Polycythemia rubra vera / Osler’s disease / Erythremia /
Vaquez’s disease
• Uncontrolled proliferation of erythroid stem cells leading to
excess of erythroid cell mass in the body.
Clinical Features:
• Male predilection – Middle age
• Skin appears flushed, reddened
• Spleen is palpable
• Tip of the finger has cyanotic appearance.
• Erythromealgia: Burning sensation with erythema and warmth
in hand and feet.
• Dizziness and blackouts
Oral manifestations:
• Purplish red discoloration
of mucosa
• Swollen bleeding gingiva
• Petechiae
Management:
• Venesection: done at periodic intervals to remove 500-600ml
of blood. Also called Phlebotomy.
• Radioactive phosphorus: Excellent treatment modality when
the diagnosis is certain.
• Aspirin – given for thrombotic event
PUBLIC HEALTH SCENARIO
• Globally, anaemia affects 1.62 billion people, which corresponds
to 24.8% of the population.
• The highest prevalence is in preschool-age children (47.4%), and
the lowest prevalence is in men (12.7%).
• However, the population group with the greatest number of
individuals affected is pregnant women (41.8%).
• In women, anaemia may become the underlying cause of
maternal mortality and perinatal mortality.
• Nearly 50 per cent of women of reproductive age and 26 per cent
of men in the age group of 15-59 years are anemic.
• Nine out of ten anemia sufferers live in developing countries,
about 2 billion people suffer from anemia and an even larger
number of people present iron deficiency.
Anemia in India
• Infants, Pre-school Children, Adolescents and Women of
Childbearing age, particularly Pregnant Women, are at greatest risk
of developing Iron Deficiency Anaemia.
• The condition has a prevalence rate of 74 percent among pregnant
women in the region ranging from 13.4 percent in Thailand to 87
percent in India.
• According to the NFHS-(III), more than half of women in India
(55%) have anaemia, including 39 % with mild anemia, 15 % with
moderate anemia and 2 percent with severe anaemia.
• The survey further revealed that among the states, Assam is the
worst affected with 72% of married women being anaemic,
followed by Haryana (69.7%) and Jharkhand (68.4%).
*Anaemia ‘a silent killer’ among women in India: Present scenario Kawaljit Kaur . Euro J
Zool Res, 2014, 3 (1):32-36
Various health programmes:
• The National Nutritional Anemia Prophylaxis Programme
(NNAPP) was launched in 1972 during the 4th five year plan in
India with the aim to curb the prevalence of anemia.
• One of the largest nutritional supplement programmes, the
Integrated Child Development Services (ICDS) scheme was
initiated in 1975 in India to provide nutritious food to pregnant
women and children.
• Further, in 1991, the Government of India introduced policies to
control nutritional anemia through promotion of iron rich food
(green leafy vegetables: mustard leaves, bengal gram leaves,
clocasia leaves etc., shepu or sowa, cereals: wheats, ragi, jawar,,
pulses: sprouted pulses, and jaggery), provision of iron and folate
supplements to high risk groups (all pregnant and lactating
women, Intra-Uterine Device (IUD) users, and children between
1-5 years), and identification and treatment to severely anemic
people.
• National Rural Health Mission (NRHM), 2005, undertakes
programme once in a month in villages to educate mothers on
health and nutrition.
• In spite of the fact that the Health and Family Welfare
Department in India has policies to provide iron supplement to
pregnant women to prevent maternal anemia, evaluation from
large scale programmes shows that maternal anemia has not
declined significantly.
• Some plausible reasons are the side effects of the iron pills and
also improper utilization of health service and personal beliefs
(Fox, 1983; Galloway and Mcguire, 1994).
• Prevalence of Iron-Deficiency Anaemia in India: Results from a Large Nationwide
Survey by Ramesh Chellan. Lopamudra Paul. JOURNAL OF POPULATION AND
SOCIAL STUDIES Volume 19 Number 1 July 2010
CONCLUSION
• Red blood cells play an important role in our health by
carrying fresh oxygen throughout the body.
• Hemoglobin is the protein inside red blood cells that carries
oxygen.
• Most people don't think about their red blood cells unless they
have a disease that affects these cells. Problems with red blood
cells can be caused by illnesses or a lack of iron or vitamins in
the diet. Some diseases of the red blood cells are inherited.
• Anemia is the most common disorder of the blood with it
affecting about a quarter of people globally.
• Anemia goes undetected in many people, and symptoms can be
minor or vague.
• Appropriate dental care improves a patient’s quality of life by
preventing eating difficulties, oral diseases, and esthetic
concerns, and facilitates the management of the disease by the
hematologist.
• Preventive dental care is must for patients with blood cell
disorders of any kind in combinations with appropriate lab
investigations and diagnosis before planning of any treatment.
REFERENCES
• Essentials of medical physiology by Dr.Sembulingam.
• Medical physiology for dental students by Dr G K Pal
• Essential Pathology for dental students by Harsh Mohan 3rd
edn
• Text book of Oral Medicine Ghom 2nd edn
• Human physiology for B.D.S by Prof. A K Jain 3rd edn
• Burket’s Oral Medicine by Greenberg . Glick . Ship . 11th edn
PREVIOUS YEAR QUESTIONS
SHORT ESSAYS:
• RBC (10mks)
(MDS Degree examinations March 1994, 2000)
• RBC Morphology & Functions (10mks)
(MDS Degree examination April/May 07 & 2010)
• Iron deficiency anemia (10mks)
(MDS Degree examination Sept 2007)
RBC

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RBC

  • 1.
  • 2. Seminar – 3 Presented by Dr. Nabeela Basha
  • 3. CONTENTS  Introduction  History  General features  Erythropoiesis  Hemoglobin  ESR & PCV  RBC Disorders  Public Health Significance  Conclusion  References  Previous year questions
  • 4. INTRODUCTION • RBC - red cells / red blood corpuscles / haematids / erythroid cells / erythrocytes. • Derived from Greek erythros for "red" and kytos for "hollow vessel", with -cyte translated as "cell" in modern usage. • Non-nucleated formed elements in the blood. • It lacks cytoplasmic organelles such as nucleolus, mitochondria & ribosomes. • The red color of RBC is due to the presence of Hemoglobin (90%).
  • 5. HISTORICAL BACKGROUND • JAN SWAMMERDAM-1658 - Dutch biologist and microscopist. He called them ruddy globules • ANTON VAN LEEUWENHOEK-1674- Discovered Microscope and established its size. • OTTO FUNKE 1851 - German physiologist was the first scientist to successfully crystallize hemoglobin. "Blutfarbstoff" • DR. MAX PERUTZ- 1959 - by use of X-ray crystallography unravelled the structure of hemoglobin • MENGHINI-1747- presence of iron in the blood, identified the red corpuscles as the chief site of iron within the organism.
  • 6. GENERAL FEATURES • Dimensions • Normal Count • Composition • Functions • Fragility • Variations • Fate & Lifespan
  • 7. DIMENSIONS • Shape: Biconcave • Size: 7.2um in diameter • Thickness: 2um at the periphery and 1um at the center • Volume: 87um3
  • 8. Advantages of Biconcave Shape of RBCs: • Greater surface area for exchange of gases. • Flexibilty of RBC • Minimal tension when the volume of cell alters. How is the shape maintained?  Spectrin - a contractile protein - maintains shape and flexibility of RBC - Antigen on cell membrane – helps in blood group classification
  • 9. NORMAL COUNT • Adults males: 4.5 – 6 million cu mm of blood • Adult females: 4 – 5.5 million cu mm of blood • At birth: 6.7 million cu mm of blood
  • 10. COMPOSITION • 62.5% water • 35% Hemoglobin • 2.5% : - Sugar – glucose - Lipids – Cephalin, Cholesterol & Lecithin - Protein – Glutathion : insoluble protein which acts as a reducing agent and prevents damage of hemoglobin - Enzymes – Carbonic anhydrase and catalase - Ions – Na+, K+, Ca2+, PO4 3-
  • 11. FUNCTIONS • Respiratory • Acid Base balance • Maintain viscosity • Pigment: various pigments are derived from hemoglobin after disintegration of RBC.
  • 12. FRAGILITY AND HEMOLYSIS • Hemolysis- Breakdown of RBC and liberation of hemoglobin. • Fragility- Susceptibility of RBC to hemolysis or tendency to break easily. • There are 2 types: 1. Osmotic fragility- due to exposure to hypotonic saline. 2. Mechanical fragility- due to mechanical trauma
  • 13. VARIATIONS Physiologic causes of increase count: • Age • Gender • High altitude • Exercise • Temperature • Meal Decrease in count: High barometric pressure, Pregnancy, sleep
  • 14. Pathological variations: • Increase: Polycythemia • Decrease: Anaemia
  • 15. VARIATIONS IN SHAPE • Crenation: Shrinkage as in hypertonic solutions. • Spherocytosis: Globular form as in hypotonic conditions. • Elliptocytosis: elliptical shape • Sickle cell: Crescent shape • Poikilocytosis: Flask, hammer or any other unusual shape.
  • 16. VARIATIONS IN SIZE • Physiological conditions: RBC in venous blood slightly larger than those in arterial blood. • Pathological conditions: 1. Microcytes – smaller cells 2. Macrocytes – larger cells 3. Anisocytes – cells of different sizes
  • 17. LIFESPAN AND FATE OF RBC • Lifespan – 120 days • Site of destruction: Reticuloendothelial system
  • 18. ERYTHROPOIESIS • The process of origin, development and maturation of erythrocytes.  Site of erythropoiesis: • In fetal life: - Mesoblastic stage - Hepatic stage - Myeloid stage • In newborns, children and adults
  • 19. FIGURE 10.1: Stem cells. L = Lymphocyte, R = Red blood cell, N = Neutrophil, B = Basophil, E = Eosinophil, M = Monocyte, P = Platelet.
  • 20.
  • 21. • Factors necessary for erythropoiesis: 1. General factors: -Erythropoietin -Thyroxine -Vitamins 2. Maturation factors: -Vitamin B12 (Cyanocobalamin) -Intrinsic factor of Castle -Folic acid
  • 22. HEMOGLOBIN • Hb is the iron containing coloring pigment of RBC. • 95% dry weight of RBC; 30 – 34% wet weight. • Molecular weight of Hb is 68,000 • Normal value: -At birth: 25g/dl -From puberty: 14-16 g/dl -Adult males: 15g/dl -Adult females: 14.5g/dl
  • 23. STRUCTURE OF HEMOGLOBIN • Conjugated protein • Protein part called Globin and iron containing pigment called heme. • Heme part is called porphyrin and is formed by 4 pyrole rings • Globin is made up of 4 polypeptide chains – 2 alpha and 2 beta chains.
  • 24. Types of Hemoglobin: • Normal: - Adult Hb - Fetal Hb • Abnormal derivatives: -Carboxyhemoglobin -Methemoglobin -Sulfhemoglobin
  • 25. ERYTHROCYTE SEDIMENTATION RATE • Red cells have the property of Rouleaux (piling one on the other) formation. • Piled red cells are heavier than the individual ones. • The rate at which the red cells fall is known as ESR. • Normal values: Wintrobe’s method: Males: 0 – 9mm/hr Females: 0 – 20mm/hr Westergren’s method: Males: 3 – 7mm/hr Females: 5 – 9 mm/hr
  • 26.
  • 27. Westergren’s method: • Westergren’s tube is used which is 300 mm long & opened at both the ends. • It requires collecting 2 ml of venous blood into a tube containing 0 .5 ml of sodium citrate. It should be stored no longer than 2 hours at room temperature or 6 hours at 4 °C. The blood is drawn into the tube to the 200 mm mark. The tube is placed in a rack in a strictly vertical position for 1 hour at room temperature,
  • 28. Wintrobe’s method: • The Wintrobe method is performed similarly except that the Wintrobe tube is smaller in diameter than the Westergren tube and only 100 mm long. • EDTA anticoagulated blood without extra diluent is drawn into the tube, and the rate of fall of red blood cells is measured in millimeters after 1 hour.
  • 29. PACKED CELL VOLUME • Hematocrit is the fractional volume of blood that the erythrocytes occupy • It is a reliable index of red cell population. • Normal values : Males – 46% Females – 42%
  • 30. RBC INDICES • MCV (MEAN CORPUSCULAR VOLUME) – The average volume of single RBC PCV per 100ml blood MCV =  10um3 RBC count (million/cu mm) Normal range : 78 – 94 um3  RBC with normal volume are called Normocytes  RBC with less then normal volume, Microcytes  RBC with more than normal volume, Macrocytes
  • 31. • MCH (mean corpuscular hemoglobin) – The average content of Hb in average RBC. Hb in gm% MCH =  10pg RBC count (million/cu mm) • Normal range: 28 – 32pg
  • 32. • MCHC (mean corpuscular hemoglobin concentration) – Express the average concentration of hemoglobin per unit volume of RBC. – It defined as the ratio of the weight of hemoglobin to volume of RBC. Hb in gm% MCHC =  100 PCV per 100ml blood Normal range: 33 – 38 gm/100ml of cells
  • 33. DISORDERS OF RBC • Anemia Morphologic classification Etiologic classification • Polycythemia Polycythemia Vera Relative polycythemia Secondary polycythemia
  • 34. ANEMIA • Anemia is defined as Hb concentration in blood below the lower limit of the normal range for the age and sex of the individual. • In adults, the lower extreme of normal Hb is taken as 13g/dl for males and 11.5g/dl for females.
  • 35. MORPHOLOGICAL CLASSIFICATION • Depends upon the size and color of RBC. • Size of RBC is determined by mean corpuscular volume (MCV). • Color is determined by mean corpuscular hemoglobin concentration (MCHC). • By this method, the anemia is classified into four types
  • 37. ETIOLOGICAL CLASSIFICATION • On the basis of etiology, anemia is divided into five types: 1. Hemorrhagic anemia 2. Hemolytic anemia 3. Nutrition deficiency anemia 4. Aplastic anemia 5. Anemia of chronic diseases.
  • 38. IRON DEFICIENCY ANEMIA • Iron deficiency anemia is the most common type of anemia. • It develops due to inadequate availability of iron for hemoglobin synthesis. • RBCs are microcytic and hypochromic.
  • 39. • Causes of iron deficiency anemia: i. Loss of blood ii. Decreased intake of iron iii. Poor absorption of iron from intestine iv. Increased demand for iron in conditions like growth and pregnancy. • Features of iron deficiency anemia: 1. Brittle nails, 2. Spoon shaped nails (koilonychias), 3. Brittle hair, 4. Atrophy of papilla in tongue 5. Dysphagia (difficulty in swallowing).
  • 40. Oral manifestations: • Pallor of mucosa • Atrophy of oral mucosa • Tongue changes – redness, soreness or burning sensation. Papillae of the anterior two thirds undergo atrophy. • Angular cheilitis • Ulcerations • Slow healing
  • 41. Diagnosis: • Clinical – Koilonychia, angular cheilitis, depapillation of tongue • Lab diagnosis – Hb level as low as 4g/100ml. MCV, MCH & MCHC all are reduced. RBC count slightly reduced or normal. Management: • Iron supplement: oral ferrous fumerate or ferrous sulphate 300mg three to four times a day for a period of 6 months • Parenteral route : single dose of iron sorbitol 1.5mg/kg body weight daily
  • 42. Oral Health Considerations: • For dental patients with extremely low Hb levels- physician consultation • When Hb is less than 8g/dl, GA should be avoided • Narcotic use should be limited for those with sever anemia as there is increased rick of ischemic heart disease.
  • 43. PLUMMER VINSON SYNDROME • Patterson Brown Kelly syndrome / Sideropenic dysphagia • Characterized by iron deficiency anemia, dysphagia and esophageal webs or strictures. Clinical Features: • Middle aged women- 4th to 7th decade of life • Dysphagia, angular cheilitis, sore tongue. • Patient complains of spasm in throat or food sticking in throat. • Spoon shaped nails.
  • 44. Management: • Correction of anemia • Dilation of esophagus – to correct dysphagia
  • 45. SICKLE CELL ANEMIA • First described by Herrick in 1910. • Severe genetic disorder of hemoglobin synthesis. • Autosomal dominant • Abnormal hemoglobin, which under low oxygen tension, results in sickling of the cell. • In this, α-chains are normal and β-chains are abnormal.
  • 46. Diagnosis: • Newborn screening is an important starting point for simple public health strategies such as parental education, penicillin prophylaxis, immunization and utilization of prenatal testing. • The HbS solubility test (Sickledex) can be performed in 5mins for screening of adult hemoglobinopathies. • Prenatal testing by DNA analysis of amniotic fluid at 14 to 16 weeks can be done to find out alterations and mutations in genes.
  • 47. Clinical Features:  Periods of latency interrupted by periods of acute crisis. Known sequelae include:  Invasive infections  Acute chest syndrome  Strokes  Severe anemia  Chronic leg ulcers  Hematuria  Aseptic osteonecrosis
  • 48. Oral Manifestations: • Enamel hypomineralization • Increased overjet and overbite • Calcified canals • Pallor of oral mucosa and delayed eruption of teeth. • SCA is not associated with increased levels of gingivitis or periodontitis.* *Periodontal Disease in Sickle Cell Disease Subjects by John M. Crawford. Journal of Periodontology. March 1988, Vol. 59, No. 3, Pages 164-169
  • 49. Management: • Regular monitoring of hematological state • Blood transfusion – cerebrovascular symptoms in early childhood , recurrent pulmonary thrombosis • Mild to moderate anemia - Blood transfusion • Risk of HIV and HEPATITIS infection – transfused patient • Painful crisis – analgesics • Incidence of hypoxia and dehydration should be avoided
  • 50. Dental management • Dental treatment - Directed towards palliative therapy during crisis period • Preventive dental care – antiseptic mouth rinses , topical fluoride recommended • Antibiotic prophylaxis – penicillin is the drug of choice • Odontogenic and nonodontogenic infection should be aggressively treated • Periodontal status - closely monitored
  • 51. THALASSEMIA • Thalassemia is an inherited disorder, characterized by abnormal hemoglobin. • It is also known as Cooley’s anemia or Mediterranean anemia. • It is more common in Thailand and to some extent in Mediterranean countries. • Thalassemia is of two types: 1. α-thalassemia 2. β-thalassemia.
  • 52. • In normal hemoglobin, number of α and β polypeptide chains is equal. • In thalassemia, the production of these chains become imbalanced because of defective synthesis of globin genes. • This causes the precipitation of the polypeptide chains in the immature RBCs, leading to disturbance in erythropoiesis.
  • 53. α-Thalassemia • α -thalassemia occurs in fetal life or infancy. • In this α-chains are less, absent or abnormal. • In adults, β-chains are in excess and in children, γ-chains are in excess. • This leads to defective erythropoiesis and hemolysis. • The infants may be stillborn or may die immediately after birth.
  • 54. β-Thalassemia • More common type of thalassemia. • In β-thalassemia, β-chains are less in number, absent or abnormal with an excess of α-chains. • Severity ranges from complete lack of symptoms to transfusion dependence. • Cooley’s anemia, or thalassemia major is the name for the most severe form.
  • 55. Oral Manifestations: • Excessive overgrowth of maxilla • Oral mucosa has a lemon yellow tint because of chronic jaundice – hard palate and floor of the mouth. • Chipmunk facies- Saddle nose, prominent malar bone, retracted upper lip • Poor healing • Spacing between teeth • Discoloration of dentin
  • 56. General management • Blood transfusion • Iron chelating agents – desferroxamine • Folic acid supplements • Splenectomy – severe cases
  • 57. Dental management • Poor wound healing after any surgical procedure • Surgery has been used successfully to treat the facial deformities • HIV and HEPATITIS infections are common in transfused patients • Prophylactic antibiotics in splenectomy cases
  • 58. MEGALOBLASTIC (PERNICIOUS) ANEMIA & VIT B12 (COBALAMIN) ANEMIA • Occurs due to deficiency of Vit B12 or folic acid or both, resulting in disordered cell proliferation. Clinical Features & Oral Manifestations: • Weakness, anemia, palpitations, diarrhoea • Paresthesia of finger, toes & also dementia may be observed. • Burning sensation of tongue, angular cheilitis • Hunter’s glossitis: Atrophy of filiform and fungiform papillae leading to smooth fiery red surface of tongue
  • 59.
  • 60. Management: • Blood tranfusion: when Hb level is less than 4g/dl of blood • Folic acid supplements:  initial dose - 5 mg orally daily  maintenance dose - 5 mg orally once a week • Vit B12 therapy:  Initial dose – 1000 mcg , intramuscularly 4 to 6 wks  Maintenance dose – 1000 mcg intramuscularly once every week
  • 61. APLASTIC ANEMIA • A rare disorder characterized by peripheral blood pancytopenia associated with bone marrow suppression. • Occurs due to failure of haematopoietic precursor cells in bone marrow to produce adequate number of all blood cell types.
  • 62. Clinical Features: • Commonly seen in young adults • Erythrocyte deficiency: Headaches, pale skin, breathlessness • Thrombocyte deficiency: Bruising & bleeding. Cerebral haemorrhages • Leukocyte deficiency: Bacterial and fungal infections are common. • Ankle edema, anginal pain, congestive cardiac failure
  • 63. Management: • Supportive therapy: Antibiotics & transfusion • Bone marrow transplantation • Stimulation of haemopoiesis and promote marrow recovery  Androgenic steroids - oxymetholone  Corticosteroids –Prednisolone or methyl prednisolone  Antithymocyte or antilymphocyte globulin combined with cyclosporine.
  • 64. POLYCYTHEMIA • Abnormal increase in the number of RBCs in the peripheral blood, usually with increase in Hb level. • Types: o Polycythemia Vera o Relative Polycythemia o Secondary Polycythemia
  • 65. POLYCYTHEMIA VERA • Polycythemia rubra vera / Osler’s disease / Erythremia / Vaquez’s disease • Uncontrolled proliferation of erythroid stem cells leading to excess of erythroid cell mass in the body. Clinical Features: • Male predilection – Middle age • Skin appears flushed, reddened • Spleen is palpable
  • 66. • Tip of the finger has cyanotic appearance. • Erythromealgia: Burning sensation with erythema and warmth in hand and feet. • Dizziness and blackouts Oral manifestations: • Purplish red discoloration of mucosa • Swollen bleeding gingiva • Petechiae
  • 67. Management: • Venesection: done at periodic intervals to remove 500-600ml of blood. Also called Phlebotomy. • Radioactive phosphorus: Excellent treatment modality when the diagnosis is certain. • Aspirin – given for thrombotic event
  • 68. PUBLIC HEALTH SCENARIO • Globally, anaemia affects 1.62 billion people, which corresponds to 24.8% of the population. • The highest prevalence is in preschool-age children (47.4%), and the lowest prevalence is in men (12.7%). • However, the population group with the greatest number of individuals affected is pregnant women (41.8%). • In women, anaemia may become the underlying cause of maternal mortality and perinatal mortality.
  • 69. • Nearly 50 per cent of women of reproductive age and 26 per cent of men in the age group of 15-59 years are anemic. • Nine out of ten anemia sufferers live in developing countries, about 2 billion people suffer from anemia and an even larger number of people present iron deficiency.
  • 70. Anemia in India • Infants, Pre-school Children, Adolescents and Women of Childbearing age, particularly Pregnant Women, are at greatest risk of developing Iron Deficiency Anaemia. • The condition has a prevalence rate of 74 percent among pregnant women in the region ranging from 13.4 percent in Thailand to 87 percent in India. • According to the NFHS-(III), more than half of women in India (55%) have anaemia, including 39 % with mild anemia, 15 % with moderate anemia and 2 percent with severe anaemia.
  • 71. • The survey further revealed that among the states, Assam is the worst affected with 72% of married women being anaemic, followed by Haryana (69.7%) and Jharkhand (68.4%). *Anaemia ‘a silent killer’ among women in India: Present scenario Kawaljit Kaur . Euro J Zool Res, 2014, 3 (1):32-36
  • 72. Various health programmes: • The National Nutritional Anemia Prophylaxis Programme (NNAPP) was launched in 1972 during the 4th five year plan in India with the aim to curb the prevalence of anemia. • One of the largest nutritional supplement programmes, the Integrated Child Development Services (ICDS) scheme was initiated in 1975 in India to provide nutritious food to pregnant women and children.
  • 73. • Further, in 1991, the Government of India introduced policies to control nutritional anemia through promotion of iron rich food (green leafy vegetables: mustard leaves, bengal gram leaves, clocasia leaves etc., shepu or sowa, cereals: wheats, ragi, jawar,, pulses: sprouted pulses, and jaggery), provision of iron and folate supplements to high risk groups (all pregnant and lactating women, Intra-Uterine Device (IUD) users, and children between 1-5 years), and identification and treatment to severely anemic people.
  • 74. • National Rural Health Mission (NRHM), 2005, undertakes programme once in a month in villages to educate mothers on health and nutrition. • In spite of the fact that the Health and Family Welfare Department in India has policies to provide iron supplement to pregnant women to prevent maternal anemia, evaluation from large scale programmes shows that maternal anemia has not declined significantly.
  • 75. • Some plausible reasons are the side effects of the iron pills and also improper utilization of health service and personal beliefs (Fox, 1983; Galloway and Mcguire, 1994). • Prevalence of Iron-Deficiency Anaemia in India: Results from a Large Nationwide Survey by Ramesh Chellan. Lopamudra Paul. JOURNAL OF POPULATION AND SOCIAL STUDIES Volume 19 Number 1 July 2010
  • 76. CONCLUSION • Red blood cells play an important role in our health by carrying fresh oxygen throughout the body. • Hemoglobin is the protein inside red blood cells that carries oxygen. • Most people don't think about their red blood cells unless they have a disease that affects these cells. Problems with red blood cells can be caused by illnesses or a lack of iron or vitamins in the diet. Some diseases of the red blood cells are inherited.
  • 77. • Anemia is the most common disorder of the blood with it affecting about a quarter of people globally. • Anemia goes undetected in many people, and symptoms can be minor or vague. • Appropriate dental care improves a patient’s quality of life by preventing eating difficulties, oral diseases, and esthetic concerns, and facilitates the management of the disease by the hematologist.
  • 78. • Preventive dental care is must for patients with blood cell disorders of any kind in combinations with appropriate lab investigations and diagnosis before planning of any treatment.
  • 79. REFERENCES • Essentials of medical physiology by Dr.Sembulingam. • Medical physiology for dental students by Dr G K Pal • Essential Pathology for dental students by Harsh Mohan 3rd edn • Text book of Oral Medicine Ghom 2nd edn • Human physiology for B.D.S by Prof. A K Jain 3rd edn • Burket’s Oral Medicine by Greenberg . Glick . Ship . 11th edn
  • 80. PREVIOUS YEAR QUESTIONS SHORT ESSAYS: • RBC (10mks) (MDS Degree examinations March 1994, 2000) • RBC Morphology & Functions (10mks) (MDS Degree examination April/May 07 & 2010) • Iron deficiency anemia (10mks) (MDS Degree examination Sept 2007)