3. Contents
• Introduction
• Classification
• Diagnosis and screening
• Clinically significant variants of anemia
• Drug therapy
• Management of dental patients with anemia
• Public Health Significance
• Conclusion
• References
• Previous year questions
4. Introduction
• Anemia is a general term for the most common blood disorder
in the world.
• Evidence of anemia goes back more than 4000 years.
• Anemia occurs when there are too few red blood cells in the
blood.
• Anemia is a symptom of a wide variety of mild to serious
diseases, disorders and conditions.
5. Introduction contd.
• Anemia is the blood disorder, characterized by the reduction
in:
1. Red blood cell (RBC) count
2. Hemoglobin content
3. Packed cell volume (PCV).
6. • Generally, reduction in RBC count, hemoglobin content and
PCV occurs because of:
1. Decreased production of RBC
2. Increased destruction of RBC
3. Excess loss of blood from the body.
• All these incidents are caused either by inherited disorders or
environmental influences such as nutritional problem,
infection and exposure to drugs or toxins.
7. CLASSIFICATION OF ANEMIA
• Anemia is classified by three methods:
1. Morphological Classification
2. Etiological Classification.
3.Quantitative Classification.
8. 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
10. ETIOLOGICAL CLASSIFICATION
• On the basis of etiology (study of cause or origin), anemia is
divided into five types:
1. Hemorrhagic anemia
2. Hemolytic anemia
3. Nutrition deficiency anemia
4. Aplastic anemia
5. Anemia of chronic diseases.
13. Red cell indices
• MCV (mean corpuscular volume)
▫ The average volume of RBC
PCV
= 10 (fl)
RBC count (m/µL)
e.g. PCV= 40%
RBC=5.0 (m /µL)
MCV= 40/5.0 10 = 80 fl
NR= 80-96 fl
14. • MCH (mean corpuscular hemoglobin)
▫ The average content of Hb in average RBC.
▫ It is directly proportional to the amount of Hb and RBC
size.
Hb
RBC count (m/µL)
10 (pg)MCH =
e.g. Hb = 14 g/dl
RBC = 4 (m/µL)
MCH= 14/4 10
= 35 pg
NR= 27-32 pg
15. • 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 (g/dl)
PCV (%)
100 (%)MCHC=
e.g. Hb = 14 g/dl
Hct = 45 %
MCHC 14/45 100 = 31%
NR= 32-36%
16. SIGNS AND SYMPTOMS OF ANEMIA
SKIN AND MUCOUS MEMBRANE:
• Colour of the skin and mucous membrane becomes pale.
• Paleness is more constant and prominent in buccal and
pharyngeal mucous membrane, conjunctivae, lips, ear lobes,
palm and nail bed.
• Skin looses the elasticity and becomes thin and dry.
• Thinning, loss and early grayness of hair occur. The nails
become brittle and easily breakable.
17. CARDIOVASCULAR SYSTEM
• There is an increase in heart rate (tachycardia) and cardiac
output.
• Heart is dilated and cardiac murmurs are produced.
• The velocity of blood flow is increased.
RESPIRATION
• There is an increase in rate and force of respiration.
• Sometimes, it leads to breathlessness and dyspnea (difficulty
in breathing).
• Oxygen hemoglobin dissociation curve is shifted to right.
18. DIGESTION
• Anorexia, nausea, vomiting, abdominal discomfort and
constipation are common.
• In pernicious anemia, there is atrophy of papillae in tongue.
• In aplastic anemia, necrotic lesions appear in mouth and
pharynx.
METABOLISM
• Basal metabolic rate increases in severe anemia.
KIDNEY
• Renal function is disturbed.
• Albuminuria is common.
19. REPRODUCTIVE SYSTEM
• In females, the menstrual cycle is disturbed.
• There may be menorrhagia, oligomenorrhea or amenorrhea.
NEUROMUSCULAR SYSTEM
• Common neuromuscular symptoms are increased sensitivity to
cold, headache, lack of concentration, restlessness, irritability,
drowsiness, dizziness or vertigo(especially while standing)
and fainting. Muscles become weak and the patient feels lack
of energy and fatigued quite often and quite easily.
21. Anemia as a laboratory diagnosis
Men Women
Hemoglobin (g/dL) 14-17.4 12.3-15.3
Hematocrit (%) 42-50% 36-44%
RBC Count (106/mm3) 4.5-5.9 4.1-5.1
Reticulocytes 1.6 ± 0.5% 1.4 ± 0.5%
WBC (cells/mm3) ~4,000-11,000
MCV (fL) 80-96
MCH (pg/RBC) 30.4 ± 2.8
MCHC (g/dL of RBC) 34.4 ± 1.1
22. Symptoms of Anemia
Hemoglobin/HematocritNormal or High
Check other
Causes of symptoms
e.g. Cardiac Pulmonary Low
RBC indices
MCV < 80
MCHC < 32
Serum iron and Total
Iron binding capacity of
Ferritin
Low Iron
IDA, chronic
diseases, Renal
diseases
Normal
Hb
electrophoresis
for Thalassemia.
High Iron
BM exam
For
Sideroblastic
anemia
MCV=80-96
History of acute blood loss
Auto immune Hemolytic anemia
Anemia of chronic Diseases
Anemia of infection
MCV > 98
B12 and folate
levels
Low B12
PA, GI
problems
Severe
malnutrition.
Low folate
Folate
malnutrition
GI problems
Liver disease
High or Normal
Myeloblastic disease
Liver Disease
24. 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.
25. • 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).
26. Pernicious anemia or Addison’s anemia
• Pernicious anemia is the anemia due to deficiency of vitamin B12. It is
also called Addison’s anemia.
• It is due to atrophy of the gastric mucosa because of autoimmune
destruction of parietal cells.
• The gastric atrophy results in decreased production of intrinsic factor and
poor absorption of vitamin B12, which is the maturation factor for RBC.
• RBCs are larger and immature with almost normal or slightly low
hemoglobin level.
• Synthesis of hemoglobin is almost normal in this type of anemia. So, cells
are macrocytic and normochromic/ hypochromic.
27. • Pernicious anemia is common in old age and it is more common in
females than in males.
• It is associated with other autoimmune diseases like disorders of
thyroid gland, Addison’s disease, etc.
• Characteristic features of this type of anemia are lemon yellow
color of skin (due to anemic paleness and mild jaundice) and red
sore tongue.
• Neurological disorders such as paresthesia (abnormal sensations
like numbness, tingling, burning, etc.), progressive weakness and
ataxia (muscular incoordination) are also observed in extreme
conditions.
28. Megaloblastic anemia
• Megaloblastic anemia is due to the deficiency of another
maturation factor called folic acid. Here, the RBCs are not
matured.
• The DNA synthesis is also defective, so the nucleus remains
immature.
• The RBCs are megaloblastic and hypochromic.
• Features of pernicious anemia appear in megaloblastic anemia
also.
• However, neurological disorders may not develop.
30. Sickle cell anemia
• Sickle cell anemia is an inherited blood
disorder, characterized by sickle shaped
red blood cells.
• It is also called hemoglobin SS disease or
sickle cell disease.
• It is common in people of African origin.
• Sickle cell anemia is due to the abnormal
hemoglobin called hemoglobin S (sickle
cell hemoglobin).
• In this, α-chains are normal and β-chains
are abnormal.
31. • The molecules of hemoglobin S polymerize into long chains and
precipitate inside the cells.
• Because of this, the RBCs attain sickle (crescent) shape and become more
fragile leading to hemolysis
• Sickle cell anemia occurs when a person inherits two abnormal genes (one
from each parent).
• In children, hemolyzed sickle cells aggregate and block the blood vessels,
leading to infarction (stoppage of blood supply). The infarction is common
in small bones.
• The infarcted small bones in hand and foot results in varying length in the
digits. This condition is known as hand and foot syndrome. Jaundice
also occurs in these children.
32. 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.
33. Thalassemia contd.
• 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.
• The precipitation also occurs in mature red cells, resulting in
hemolysis.
34. 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.
35. 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.
• The α-chains precipitate causing defective
erythropoiesis and hemolysis.
36. Aplastic Anemia
• Aplastic anemia is due to the disorder of red bone marrow.
• Red bone marrow is reduced and replaced by fatty tissues.
• Bone marrow disorder occurs in the following conditions:
I. Repeated exposure to Xray or gamma ray radiation.
II. Presence of bacterial toxins, quinine, gold salts, benzene, radium, etc.
III. Tuberculosis.
IV. Viral infections like hepatitis and HIV infections.
• In aplastic anemia, the RBCs are normocytic and normochromic.
42. Iron therapy
• Iron is absorbed best from the duodenum and proximal jejunum
• Enteric coated or sustained release capsules may be
counterproductive
• Iron salts should not be given with food because the phosphates,
phytates, and tannates in food bind the iron and impair its absorption
• Iron is best absorbed as the ferrous (Fe2+) salt
• Acidic environment favors ferrous over ferric state
• Ascorbic acid can enhance iron absorption
• antacids impair absorption
43. Iron therapy
• The recommended daily dose for the treatment of iron
deficiency in adults is in the range of 150 to 200 mg/day of
elemental iron eg 200mg (=65mg elemental iron) ferrous
sulphate tds.
• No evidence that one iron preparation is more effective than
another
• Reticulocytosis begins in approx 7 days and a rise in Hb of
approximately 2 g/dL over three weeks
44. Iron therapy contd
• The iron preparation used should be based on cost and effectiveness
with minimal side effects. The cheapest preparation is iron sulfate
• Upper gastrointestinal tract discomfort is directly related to the
amount of elemental iron ingested
• Titrate the dose down to the level at which the gastrointestinal
symptoms become acceptable
45. Side effects
• 10 to 20 percent of patients complain of nausea,
epigastric distress and/or vomiting after taking oral iron
preparations
• Constipation
• Black stools (can confuse with melaena)
• Try smaller dose of elemental iron
• switch from a tablet to a liquid preparation
46. Duration of treatment
• Some physicians stop when the hemoglobin level becomes
normal, so that further blood loss will cause anemia and alert
the patient and physician to the return of the problem which
caused the iron deficiency in the first place
• Others believe that it is wise to treat for about six months after
the hemoglobin normalizes, in order to completely replenish
iron stores
47. Failure to respond to oral iron
• Incorrect diagnosis (eg, thalassemia)
• Presence of a coexisting disease interfering with response
(eg, anemia of chronic disease, renal failure)
• Patient is not taking the medication
• Medication is not being absorbed (eg, enteric coated tablets,
concomitant use of antacids, malabsorption)
• Iron (blood) loss or need is in excess of the amount ingested (eg,
severe continuous GI bleeding, dialysis patient)
48. Parenteral Iron Therapy
• Parenteral iron, given IM or IV, is used in the rare patient who
is unable to tolerate even modest doses of oral iron, or in
patients whose level of continued gastrointestinal bleeding
exceeds the ability of the gastrointestinal tract to absorb iron
(eg, hereditary hemorrhagic telangiectasia)
49. Intramuscular iron
• Mobilization of iron from intramuscular sites is slow and
occasionally incomplete
• As a result, the rise in the hemoglobin concentration is only
slightly faster then that which occurs with oral iron
• s/e- pain, muscle necrosis, and phlebitis
• Anaphylactic reactions occur in about 1% of patients
50. Iron overload
• Venesection eg haemochromatosis
• Iron chelators
• Complex with trivalent ions (ferric ions) to form ferrioxamine,
which is excreted by the kidneys
• Desferrioxamine iv or s/c infusion
• Deferiprone po s/e blood dyscrasias
51. B12 & Folate deficiency
• Macrocytosis, with or without anemia
• Examination of the peripheral blood smear, looking
specifically for oval macrocytic red cells and hypersegmented
neutrophils
• Pancytopenia (anemia, thrombocytopenia, neutropenia) of
uncertain cause
• Unexplained neurologic signs and symptoms, especially
dementia.
• Special populations, such as the elderly, alcoholics, and
patients with malnutrition.
54. Treatment
• Hydroxocobalamin dose of 1000 µg (1 mg) IM every day for
one week, followed by 1 mg every week for four weeks and
then, if the underlying disorder persists, as in PA, 1 mg every 3
months for life
• s/e allergic reactions; hypokalaemia
• high dose oral cobalamin is an alternative but requires much
greater patient compliance.
56. Folate deficiency
• Folic acid (1 to 5 mg/day PO) for one to four months, or until
complete hematologic recovery occurs. A dose of 1 mg/day is
usually sufficient, even if malabsorption is present.
• These doses are in excess of those recommended for disease
prevention (eg, recommended daily allowance in normal
adults, alcoholics, the elderly, prevention of neural tube
defects) 200-500mcg/day
57. • Folic acid can partially reverse some of the hematologic
abnormalities of Vitamin B12 deficiency, although the
neurologic manifestations will progress.
• Thus, it is important to rule out Vitamin B12 deficiency before
treating a patient with megaloblastic anemia with folic acid
58. Blood transfusion
• In patients who are severely anemic at presentation, the decision
to transfuse can be a difficult one, particularly in elderly patients
at risk for congestive heart failure due to volume overload
• If the anemia is extreme and the patient is critically ill, one unit
can be given initially at a slow rate, in combination with a
diuretic, if fluid status is a concern
• In extreme circumstances, isovolemic exchange can be
performed
59. Oral health considerations
• Anemia may be accompanied by common oral symptoms and
signs which can present early in the development of the
condition, giving particular importance to the observations by
dental professionals in contributing to early diagnosis
• It commonly include one or more of
i. pallor of the oral mucosa
ii. glossitis
iii. glossodynia
iv. taste disturbance
60. Aplastic anemia
• It may increase susceptibility to
i. oral infection, which may require
1. antibiotic prophylaxis
2. antibiotic mouthwash
ii. spontaneous or uncontrolled gingival bleeding, which may
require
1. antifibrinolytic medications to reduce bleeding risk
2. avoidance of intramuscular injections and nerve-block
anesthesia
61. • Pernicious anemia
It may be signalled by the common oral symptoms and signs
plus
i. angular cheilitis
ii. mucositis
iii. thrush
iv. recurrent oral ulcer
• Sickle cell anemia
• (CDHO Advisory) which requires a specialized regimen of
oral healthcare.
62. Sickle cell anemia
• The main contraindication for dental treatment with the SCA
patient is routine care during a crisis. Following are a few
guidelines that may be helpful:
1. Schedule dental appointments during the morning with
minimum treatment for a brief visit (Primley et al. 1982)
2. Prescribe CNS depressants judiciously (Primley et al. 1982)
3. Use acetaminophen for treatment of pain because salicylates
may induce acidosis (Smith et al. 1987)
4. Avoid elective surgery, such as the removal of asymptomatic
impacted teeth (Rouse and Hays 1979)
5. Incorporate home fluoride therapy and routine dental recall
visits into the preventive dental treatment regimen (Rouse and
Hays 1979).
63. Sickle cell anemia
• The dentist should monitor preventive dental care at routine follow-
up visits.
• A three-month recall may be necessary in some cases.
• The dentist must be sure that SCA patients are receiving the latest
preventive dental measures (e.g., sealants, fluorides, antimicrobial
rinses, etc.)
• Finally, team approach including the physician, dentist, and patient
is vital to the successful dental management of the patient with
sickle cell anemia.
64.
65.
66. Public health Scenario
• A moderate degree of iron-deficiency anemia affected
approximately 610 million people worldwide or 8.8% of
the population.
• It is slightly more common in female (9.9%) than males
(7.8%).
• Mild iron deficiency anemia affects another 375 million.
67. 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.
• However, adult males may also be at risk, especially where there
is inadequate food intake or frequent parasitic infestation.
68. Based on Hemoglobin%
• Iron Deficiency anemia would be considered a Public Health
Problem if the prevalence of Hb% is below the normal level in
> 5% of the population.
• In normal population, 2.5% of the population would be
below the threshold.
• As Anemia is the most common indicator used to screen for
Iron deficiency, the term anemia, and Iron deficiency anemia
are used interchangeably.
69.
70.
71.
72.
73.
74.
75.
76.
77. NACP (National Anemia Control Programme):
• Pregnant women are regularly screened for anemia
during pregnancy.
• Pregnant women are given 100 tablets of 60 mg
Elemental Iron and 500 μg Folic Acid as prophylaxis
to prevent anemia
• Pregnant Women with Moderate Anemia are given
200 IFA tablets to be taken twice a day.
• Pregnant Women with severe anemia (Hb% < 7gm/dl)
are treated with Parenteral Iron
• Lactating Mothers are provided 60 mg of elemental
Iron and 500 mcg of Folic Acid tablets for 3 months.
79. NEW INITIATIVES
• Even after 3 decades of National Anemia Control Programme
the situation of Anemia among Pregnant women, Lactating
Mothers, Adolescent Girls and Children is not improving, in
fact it is getting worse when we analyze NFHS-2 and NFHS-3
data.
• IFA prophylaxis is not bringing the desired result due to
various reasons.
80. NEW INITIATIVES
• 0n 18-04-2011, a meeting was held in Prime Minister’s Office
on the promotion of consumption of Iron Fortified Iodized Salt
as a measure to deal with malnutrition in the country.
• The meeting was attended by the Principal Secretary to the
Hon Prime Minister, and Officers of the Ministries of Health ,
W&CD, Dept of Industrial Policy and Promotion, Director of
NIN Hyderabad, and Member of PM’s National Council on
India’s Nutritional Challenges
81. • In the above meeting a decision was taken to make use of
Dietary Ferrous Sulfate(DFS) mandatory, Govts should
promote the conumption of DFS through communication
campaigns, mandating its use in Govt sponsored programmes
like ICDS, Mid Day Meals etc., and by supplying DFS
through PDS.
82. • NIN Hyderabad has developed a very cost effective method for DFS.
• MOH & FW, GOI has issued a Gazette Notification for Specification
of DFS in the Country.
• As per NIN average cost of DFS will be Rs 6.85/Kg
• TN is the only State Providing DFS to ICDS, Mid Day Meal and PDS
• TNSC is supplying DFS at Rs 3990/Metric ton and it is costing about
Rs 24.20/year for DFS for the entire Mid Day Meal Programme
• On 21-09-2011, a High Level Meeting was held in Karnataka under
the Chairmanship of Hon CS to address Anemia and implementing
DFS in ICDS, Mid Meal Programme was agreed upon.
83. Conclusion
• 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 anemic patients of any kind in
combinations with appropriate lab investigations and diagnosis before
planning of any treatment.
84. References
• Essentials of medical physiology by Dr.Sembulingam.
• College of Dental Hygienists of Ontario, CDHO Advisory Anemia,
2012-02-01
• Dental and Periodontal Health Status of Beta Thalassemia Major
and Sickle Cell Anemic Patients: A Comparative Study by Jaideep
Singh, Nitin Singh, Amit Kumar, Neal Bharat Kedia, Anil Agarwal
Journal of International Oral Health. Sept-Oct 2013; 5(5):53-8 [
53 ]
85. References contd.
• Blood group and anemia: Exploring a new relationship byBasak
Asim Kumar1 and Maji Kaushik Journal of Public Health and
Epidemiology Vol. 5(1), pp. 43-45, January 2013
• Managing the dental patient with sickle cell anemia: a review of
the literature by Deirdre R. Sams, DDS John B. Thornton,
DMD, MA Paul A. Amamoo, MD PEDIATRIC DENTISTRY:
SEPTEMBER/OCTOBER, 1990 ~ VOLUME 12, NUMBER.
• https://fkilp.iimb.ernet.in/pdf/Healthcare_Anaemia/.../Dr.%20Na
rayana.pdf
86. References contd.
• Special Needs Care in Dentistry for Children Ivonne Ganem,
DMD, MPH
• http://en.wikipedia.org/wiki/Anemia?oldid=664363790
• Iron_deficiency_anemia.jpghttp://upload.wikimedia.org/wikip
edia/commons/f/fc/Iron_deficiency_anemia.jpg
• http://www.flickr.com/photos/euthman/2274260085/ Original
artist: E. Uthman, MD
• http://upload.wikimedia.org/wikipedia/commons/9/91/Symptoms
_of_anemia.png
• “Anemia”.http://www.merriam-webster.com/'‘ Retrieved 7 July
2014
87. Previous Year Questions
• Iron Deficiency Anemia-RGUHS (September 2007) -10
marks.
• Pernicious Anemia-10marks RGUHS (May 2006).
• Vitamin Deficiency in Oral Health- 40 marks.RGUHS (1996)
