https://userupload.net/0gv9ijneu7hf Anemia is a condition that develops when your blood lacks enough healthy red blood cells or hemoglobin. Hemoglobin is a main part of red blood cells and binds oxygen. If you have too few or abnormal red blood cells, or your hemoglobin is abnormal or low, the cells in your body will not get enough oxygen.

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2. CONTENTS
• DEFINITION
• CLASSIFICATION
• CLINICAL MANIFESTATION OF ANEMIA
• IRON DEFICIENCY ANEMIA
• MEGALOBLASTIC ANEMIA
2

3. • PERNICIOUS ANEMIA
• APLASTIC ANEMIA
• HAEMOLYTIC ANEMIA
• CONCLUSION
• REFERENCES
3

4. DEFINITION
Abnormal reduction in the number
of circulating red blood cells, the
quantity of hemoglobin and the
volume of packed red cells in a
given unit of blood.
4

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6. Pathophysiologic Classification:
I. Aemia due to blood loss
a. Acute post haemorrhagic anemia
b. Anemia due to chronic blood loss
II. Anemia due to impaired red cell formation
a. Cytoplasmic maturation defects
1. Deficient haem synthesis : Iron deficiency anemia
2. Deficient globin synthesis : Thalassaemic syndromes
b. Nuclear maturation defects
Vitamin B12 & /or Folic acid deficiency : Megaloblastic anemia
6

7. c. Defect in stem cell proliferation & differentiation
1. Aplastic anemia
2. Pure red cell aplasia
d. Bone marrow failure due to systemic diseases (anemia of chronic
disorders)
1. Anemia of inflammation/infections, disseminated malignancy.
2. Anemia in renal disease
3. Anemia due to endocrine & Nutritional deficiences
4. Anemia in liver disease
7

8. e. Bone marrow infiltration
1. Leukaemias
2. lymphomas
3. Multiple myeloma
f. Congenital anemia
1. Sideroblastic anemia
2. Congenital dyserythropoietic anemia.
III. Anemia due to increased red cell destruction (hemolytic
anemias)
1. Intracorpuscular defect
2. Extracorpuscular defect 8

9. MORPHOLOGIC CLASSIFICATION:
Based on red cell size, haemoglobin content & red cell indices
1. Microcytic, hypochromic :
Iron deficiency anemia
Sideroblastic anemia
Thalassaemia
Anemia of chronic diseases
9

10. 2. Normocytic, normochromic
Acute blood loss
Haemolytic anemias
Bone marrow failure
3. Macrocytic normochromic
Megaloblastic anemia
10

11. Clinical manifestation of anemia
Symptoms of anemia
• Tiredness
• Easy fatiguability
• Generalised muscular weakness
• Lethargy
• Headache
In older patients:
• Cardiac failure
• Angina pectoris
• Confusion
• Visual disturbance 11

12. Signs of Anemia :
• Tachycardia, tachypnea, orthostasis
• Pallor
• Jaundice
• Koilonychia or “Spoon nails”
• Splenomegaly, lymphadenopathy
• Petechiae, ecchymoses
• Atrophy of tongue papillae
12

13. IRON DEFICIENCY ANAEMIA
• Iron deficiency is the commonest cause of anaemia worldwide and is
frequently seen in general practice.
• Defective synthesis of haemoglobin, resulting in red cells that are
smaller than normal (microcytic) and contain reduced amounts of
haemoglobin (hypochromic).
• Iron deficiency is usually easily diagnosed from the red cell indices
• A drop in haemoglobin is generally a late feature of iron deficiency
13

14. Iron metabolism
• Iron has a pivotal role in many metabolic processes, and the
average adult contains 3–5 g of iron, of which two-thirds is in the
oxygen carrying molecule haemoglobin.
• A normal Western diet provides about 15·mg of iron daily, of which
5–10% is absorbed (~·1·mg), principally in the duodenum and upper
jejunum, where the acidic conditions help the absorption of iron in
the ferrous form.
14

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16. • Absorption is helped by the presence of other reducing substances,
such as hydrochloric acid and ascorbic acid.
• The body has the capacity to increase its iron absorption in the
face of increased demand, for example, in pregnancy, lactation,
growth spurts and iron deficiency
• Once absorbed from the bowel, iron is transported across the
mucosal cell to the blood, where it is carried by the protein
transferrin to developing red cells in the bone marrow.
16

17. • Iron stores comprise ferritin, a labile and readily accessible source of
iron and haemosiderin, an insoluble form found predominantly in
macrophages.
• About 1·mg of iron a day is shed from the body in urine, faeces, Sweat
and cells shed from the skin and gastrointestinal tract.
• Menstrual losses of an additional 20·mg per month and the increased
requirements of pregnancy (500–1000·mg) contribute to the higher
incidence of iron deficiency in women of reproductive age
17

18. Causes of Iron deficiency anaemia
 Inadequate intake of Iron.
 Malabsorption of iron due to hypochlorhydria & diarrhea.
 Increased requirement of iron in a growing child & in
pregnancy.
 Increased loss of iron due to injury, recurrent epistaxis &
peptic ulcer.
 Chronic blood loss such as menustrual & menopausal bleeding
parturition.
 Subtotal or complete gastrotomy.
18

19. Iron Requirements
 Children 1mg per day
 Males 0.5-1mg per day
 Menstruating females 1-2mg per day
 Pregnant females 1.5-2.5mg per day
 An adequate diet contains 15mg of iron, 10% of which is absorbed.
 Normal plasma iron: 80 – 120 μg
19

20. Clinical features :
 Pallor
 Koilonychia
 Fatigue and weakness
 Anxiety
 Irritability
 Sleepiness
 Palpitations
 Hair loss
 Fainting
 Depression
 Breathlessness
20

21. Oral Manifestations
 Pallor of oral mucosa and gingiva.
 Generalized atrophy of oral mucosa both
in tongue and buccal mucosa.
 Redness, soreness or burning of tongue.
 Severe cases fungiform papillae are also
affected leaving the tongue completely
smooth and waxy or glistening in
appearance.
21

22.  Cracking and fissuring at the corner of
mouth.
 Softening of epithelium which leads to
linear ulceration of the skin, extending up
to and beyond the mucocutaneous junction.
 Recurrent aphthous ulceration and candidal
lesions can also occur in iron deficiency
anemia.
 Patient may show slow healing after oral
surgical procedures. 22

23. Paterson–Brown–Kelly syndrome
 P-V syndrome is one of the manifestation
of iron-deficiency anemia
Triad:
 Dysphagia
 Iron deficiency anemia
 Dystrophy of nails (koilonychia) &
glossitis.
PLUMMER–VINSON SYNDROME
23

24. Clinical features
 Cracks / fissures at corner of the
mouth.
 Lemon-tinted pallor of the skin.
 Smooth, red, painful tongue with
atrophy of filiform & alter
fungiform papillae.
24

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26.  Dysphagia occurs due to formation of
webs in esophagus.
 Mucous membranes of oral cavity &
esophagus are atrophic, loss of
keratinization.
 Koilonychia (spoon shaped finger nails)
 Spleenomegaly is seen
26

27. Hematological findings :
 Microcytic & hypochromic & the peripheral smear shows
abnormal forms of RBCs.
 Reduced hemoglobin level, as low as 4g/100ml
 Normal or slightly reduced RBC count.
 MCV, MCH & MCHC are all reduced.
27

28. Bone marrow findings:
 Cellularity – Normal
 Erythropoiesis – normoblastic erythropoiesis with small
polychromatic normoblast.
 Marrow iron – decreases and absence of siderotic granules from
developing normoblast
Biochemical findings:
 Low serum iron level
 Total iron binding capacity is high
 Serum ferritin is low
28

29. TREATMENT
 Treatment of underlying cause.
 Diet : Green leafy vegetables, nuts, dates, meat….
 Iron therapy
a) Oral therapy
Ferrous sulphate 200mg/day
Ferrous fumarate 200mg/day
Ferrous gluconate 300mg/day
29

30. b) Parenteral therapy
Iron dextran (Imferon)
Iron sorbital citrate (Jectofer)
Iron carbohydrate complex (Uniferon)
Blood transfusion:
Transfusion of packed red cells can be given if there is
excessive blood loss, congestive cardiac failure or
immediate replenishment is required.
30

31. MEGALOBLASTIC ANEMIA
• Megaloblastic anemia is hematological disorder caused due to
impared DNA synthesis
• Characterized by distinctively abnormal hemopoietic
precursors in bone marrow in which nuclear maturation is
delayed relative to that of cytoplasm
• Deficiency of Vitamin B12 & Folate or both, resulting in
disordered cell proliferation leading to Megaloblastic anemia.
31

32. Vitamin B12
 Important for pyrimidine synthesis in the production of DNA.
 Deficiency - delay in nuclear maturation and cell division.
 Only Dietary source are foods of animal origin ( fish, egg,
cheese, milk)
 Vit B12 is synthesised in the human large bowel by bacteria
but is not absorbed, thus, humans are entirely dependent on
dietary source.
 Vit B12 is stored in liver
 The stores may last for 3 years
 Daily requirement is 1-2mg/day
32

33. Vitamin B12 absorption
 Absorbed from the lower ileum
 Facilitated by gastric intrinsic factor, a glycoprotein
synthesised by the parietal cells in the stomach which forms
complex with vitamin B12.
 Complex is carried to special binding sites in the ileum which
takes up the complex and releases vit B12 in the ileal cells &
intrinsic factor is freed.
 After absorption, vit B12 binds to a carrier protein in the
plasma, is transported to tissues.
33

34. Vitamin B12 deficiency :
 Etiology:
A) Inadequate dietary intake
B) Malabsorption
1) Gastric causes - pernicious anaemia, Gasterectomy
2) Intestinal causes - tropical sprue, crohn’s disease
3) Removal of B12 from intestines – Fish tape worm infestation
34

35. Oral Manifestations
• Sore painful tongue, glossitis and
glossodynia.
• Tongue is inflamed and is beefy red in
color.
• Painful and burning lingual sensation occur.
• Small shallow ulcers resembling aphthous
ulcers on the tongue with atrophy of
papillae with a loss of normal muscle tone is
called as 'hunter's glossitis. 35

36.  Important in DNA synthesis
 Dietary sources- eggs, green vegetables, liver, nuts
 Absorbed in the jejumun
 Daily requirement
Males age 14 and older: 400 mcg/day
Females age 14 - 50: 400 mcg/day plus 400 mcg/day from
supplements or fortified foods
Females age 50 and over: 400 mcg/day
 Stored in the liver (4-6 months supply)
FOLIC ACID
36

37. Function of folate
To synthesize DNA, RNA and to repair
Aiding rapid cell division and growth
To produce healthy red blood cells
It is important for pregnant women to have enough folic acid to
prevent major birth defects of her baby's brain or spine
37

38. Causes of folate deficiency
 Inadequate dietary intake
1. Alcoholism
2. Malnutrition
3. Excessive cooking
 Inadequate absorption
1. Tropical sprue
2. Non-tropical sprue
3. Drugs : Phenytoin, barbiturates, methotrexate
 Increased requirement – infancy, pregnancy, lactation
 Others : Hemodialysis, hemolytic anemia
38

39. Clinical manifestations :
• Fatigue
• Weakness
• Bodyache
• Vertigo
• Beefy tongue
• Diarrhoea
• Anorexia
• Weight loss
39

40. Laboratory findings
A) General laboratory findings:
1) Blood picture and red cell indices:
a) Haemoglobin – reduced
b) Red cell – macrocytic.
- anisocytosis, poikilocytosis.
c) Reticulocyte count – low
40

41. d) Red cell indices– MCV increased
MCH increased,
MCHC normal or reduced
e) Leucocytes – hyper segmented neutrophils
f) Platelets – moderately reduced
2) Bone marrow findings:
a) Cellularity – hypercellular with decreased myloid-
erythroid ratio
b) Erythropoiesis – erythroid hyperplasia, megaloblasts with
fenestrated chromatin network
c) Gaint metamyelocytes may be present
41

42. 3) Biochemical findings:
a) Serum Vit B12 is reduced in Vit B12 deficiency
b) Serum folate is reduced in folate deficiency
c) Rise in the serum unconjugated bilirubin and LDH
d) Serum iron and ferritin may be normal or elevated
e) Urinary formiminoglutamate (FIGLU) levels increased
f) Red cell folate is reduced in folate deficiency
42

43. Treatment:
1. Treatment of B12 deficiency
a) Diet : Non vegetarian food, diary products
b) Replacement therapy : 1000ugB12 I.M once a week for 8 weeks
2. Treatment of folic acid deficiency
a) Diet : green leafy vegetables, nuts, meat
b) Replacement therapy : 5mg/day for 2-4 months
c) Folinic acid 15 mg/day used in patients on treatment with
methotrexate or trimethoprim
43

44. PERNICIOUS ANEMIA
(Addison’s anemia, Biermer anemia, Hunter –Addison anemia)
 The term pernicious anemia should be reserved for patients who
have B12 deficiency secondary to intrinsic factor deficiency.
 It occurs due to atrophy of gastric mucosa resulting in failure to
secrete the still unidentified ‘intrinsic factor’
 It is autoimmune disorder, because autoantibodies to gastric
parietal cells are often found in patients.
44

45. Clinical features
 Males > Females.
 Triad of symptoms present are:
-- Generalized weakness.
-- Sore painful tongue.
-- Numbness / Tingling of extremities.
45

46.  Exhibit yellow tinge on the skin & sclera.
 Paresthetic sensations of the
extremities.
 Weakness, stiffness, difficulty in
walking, drowsiness,
 In-coordination or loss of vibratory
sensation.
 Degeneration of myelin sheaths, loss of
nerve fibers.
46

47. Oral manifestations
• Glossitis is common symptom.
• Painful & burning sensation of the tongue
• Tongue is inflamed “Beefy red”.
• shallow ulcers occur on tongue.
• Characteristically, glossitis, glossodynia &
glossopyrosis
• Gradual atrophy of the papillae of the tongue leading
to “Bald tongue”. known as Hunter’s glossitis
Moeller’s glossitis.
47

48. Laboratory findings
 RBC count is decreased
 Macrocytosis is present – a chief characteristic blood.
 Poikilocytosis, a variation in shape.
 WBC count & MCH decreased
 Bone marrow shows great number of immature red cells
 Achlorhydria or lack of gastric hydrochloric acid
secretion is a constant feature
 Schilling test detects the absence of intrinsic factor48

49. Treatment
 Lifelong Vitamin B12 replacement therapy.
 Standard dosage is 100mg IM every 30 days.
 Occasionally blood transfusions
49

50. HAEMOLYTIC ANEMIA
Haemolytic anemia is defined as anemia resulting from an
increase in the rate of red cell destruction.
Classification:
I. ACQUIRED (EXTRACORPUSCULAR)
A. Antibody: Immunohaemolytic anaemias
1. Autoimmune haemolytic anaemia (AIHA)
i) Warm antibody AIHA
ii) Cold antibody AIHA
2. Drug-induced immunohaemolytic anaemia
3. Isoimmune haemolytic anaemia50

51. B. Mechanical trauma: Microangiopathic haemolytic anaemia
C. Direct toxic effects: Malaria, bacterial, infection and other
agents
D. Acquired red cell membrane abnormalities: paroxysmal
nocturnal haemoglobinuria (PNH)
E. Splenomegaly
II. HEREDITARY (INTRACORPUSCULAR)
A. Abnormalities of red cell membrane
1. Hereditary spherocytosis
2. Hereditary elliptocytosls (hereditary ovalocytosis)
3. Hereditary stomatocytosls 51

52. B. Disorders of red cell interior
1. Red cell enzyme defects (Enzymopathies)
i) Defects in the hexose monophosphate shunt: G6PD deficiency
ii) Defects in the Embden-Meyerhof (or glycolytic) pathway:
pyruvate kinase deficiency
2. Disorders of haemoglobin (Haemoglobinopathies)
i) Structurally abnormal haemoglobins: sickle syndromes
other haemoglobinopathies
ii) Reduced giobln chain synthesis: thalassaemias
52

53. SICKLE CELL ANEMIA
 Autosomal recessive genetic blood disorder with
overdominance.
 This is the most common type of
hemoglobinopathy in which there is a substitution
of amino acid glutamine on position 6 present in
the chain of the HbA, by valine; giving rise to an
abnormal Hb, i.e. hemoglobin S.
 In homozygous individuals, whole of HbA is
replaced by HbS and this is known as 'sickle cell
disease’ and in heterozygous individuals, only 50%
of HbA is replaced by HbS and this is known as
'sickle cell trait'.
53

54.  It is chronic hemolytic blood disorder
characterized by abnormal hemoglobin
(deoxygenated hemoglobin) which under low
oxygen tension, results in sickling of cell.
 When HbS is deoxygenated, it forms structures
know as 'tactoids' which distort the RBC
membrane and produce characteristic sickle
shaped cell which are destroyed by RE cells.
 Sickle cells increase blood viscosity and tend to
reduce blood flow leading to thrombosis and
tissue infarction.
54

55. Clinical Features
• Common in females
• Clinical manifestations begin only after several months as fetal
Hb protects against sickling phenomenon.
• Fatigue, weakness and shortness of breath.
• Severe abdominal pain, muscle and joint pain, at high temperature
which may result in circulatory collapse also occur.
• Painless hematuria.
55

56. • Increased susceptibility to infection. Most of people may expire
before the age of 40 years.
• Hyperplasia of marrow in first year of life expands the marrow
cavity producing bossing of the skull, prominent malar bones and
protuberant teeth.
• Sickle cell crisis — There is a long quit spell of hemolytic
latency occasionally punctuated by exacerbations called as
sickle cell crisis.
56

57. Oral Manifestations
 Oral mucosa will show pallor and jaundice.
 Delayed eruption and hypoplasia of the dentition.
 Prone to develop osteomyelitis. This may be due to hypovascula-
rity of the bone marrow secondary to thrombosis.
 Paresthesia of mental nerve which may be secondary to
occlusion involving the nerves and blood supply.
 Mongoloid facies with high cheek bones and bimaxillary
proganthism is present. It is due to marrow hyperplasia
resulting in an increase in hard palate length and palate alveolar
ridge angle
57

58.  Significant bone changes are seen
dental radiographs
 Mild to severe generalized
osteoporosis .
 loss of trabeculation of the jaw
bones – stepladder defect
 Appearance of large, irregular
marrow spaces.
 No alterations in Laminadura or PDL.
58

59. Laboratory findings
 RBC count  up to 10,00,000/mm3.
  Hb level concentration 6-9 g/dl
 Blood smear shows typical sickle-shaped red cell.
 Presence of howell-jolly bodies
 Hb electrophoresis – no normal HbA, more of HbS.
 Reticulocyte count is raised.
59

60. Treatment
 Prevention of episode by avoiding the precipitating factors
 Folic acid supplement (5mg/daily)
 Prophylactic antibiotics are given.
 Blood transfusion should be given during crisis only
60

61. Dental Considerations :
 Do not prolong or carry out extensive dental procedures
involving the soft tissues unless absolutely necessary, as with
chronic anemia there is slow healing.
 Keep dentition as healthy as possible because there are
always chances that any infection might precipitate an
aplastic crisis
 Avoid using general anesthesia or when used, it is imperative
to avoid episodes of hypoxia because of the cerebral or
myocardial thrombosis which might result.
61

62. THALASSEMIA
'Cooleys anemia', 'Mediterranean anemia' and 'erythroblastic anemia'.
 Inherited autosomal recessive blood disorders that originated
in the Mediterranean region.
 Genetic defect, which could be either mutation or deletion,
results in reduced rate of synthesis or no synthesis of one of
the globin chains that make up hemoglobin
 This can cause the formation of abnormal hemoglobin
molecules, thus causing anemia
62

63. Types :
1. Alpha thalassemia :There is reduction or absence of alpha chain
synthesis.
2. Beta thalassemia : There is reduction or absence of beta chains.
3. Thalassemia major or homozygous thalassemia :
Occurs when the patient is homozygous. It is also called as
Cooley's anemia.
63

64. a. Hemoglobin H disease :very mild form of the disease in which
the patient may live relatively normal life.
b. Hemoglobin Bart disease : infants are stillborn or die shortly
after birth
4. Thalassemia intermedia—It is group of disorders
characterized by clinical manifestations between major and
minor.
5. Thalassemia minor or thalassemia trait—Occurs when the
patient heterozygous.
64

65. Alpha Thalassemia :
 Alpha chains of hemoglobin are required not only for HbA but also for
HbF, which is the main hemoglobin type in fetal life.
 Therefore, major type of alpha thalassemia is incompatible with life
and results in hydrops fetalis and intrauterine death of fetus.
Bata Thalassemia :
 Hemolysis is not primarily due to lack of B-globin chains but it is
because of the free alpha chains which form insoluble aggregates
that precipitate within the RBCs and cause damage to the cell
membranes
65

66. Clinical Features :
 Pallor of skin , fever, chills, prominent cheek bone and mild
hepatosplenomegaly.
 Deposition of iron in various organs (due to multiple transfusions)
leads to signs and symptoms of organ failure.
 Most patients die in childhood due to anemia and cardiac failure.
 Mongoloid appearance : Bone marrow hyperplasia in early life may
produce frontal head bossing and there may be marked
overdevelopment of malar bone which is associated with a short
nose having a depressed bridge giving the appearance of mongoloid.66

67. Oral Manifestations
• There is excessive overgrowth of maxilla causing excessive
lacrimation and nasal stuffness.
• Oral mucosa is pale and has a lemon yellow tint because of
chronic jaundice.
• Rodent faces—There is marked over development of maxilla
associated with hyperplasia of alveolar process, which results in
anterior open bite and prominent cheek bone producing
characteristic 'rodent facies'.
67

68. • The maxillary teeth are protrudes with
spacing between them with a short
upper lip due to a lag between the
growth of the maxilla and the growth
of upper lip.
• Chip munk fades—There is also saddle
nose, prominent malar bone and
pneumatization of maxillary sinus. As a
result of these skeletal changes, the
upper lip is retracted giving the child a
'chip munk' facies.
68

69. Radiographs
• Inner & outer plates are poorly defined.
• Bristle like “crew-cut” or “hair-on-end”
appearance of the surface of the skull.
• Osteoporosis is present.
• intra oral radiograph shows peculiar
trabecular pattern, resulting in a “salt &
pepper” effect.
• Thinning of laminadura & circular
radiloucencies in the alveolar bone
69

70. Laboratory findings
 Pronounced anemia of hypochromic microcytic type.
 Red cells exhibit poikilocytosis & anisocytosis.
 “Target” cells with a condensing of coloring matter in the
center of the cell.
 Reticulocyte count is increased
 Platelet count is normal
70

71. • MCV, MCH, MCHC are significantly reduced
• WBC’S count increased to 10,000-25,000/mm3.
• Bone marrow cells show cellular hyperplasia
• Serum bilirubin & fecal & urinary urobilinogen are elevated
because of severe hemolysis.
71

72. Treatment:
• Blood transfusion
• Splenectomy indicated when there is severity of anemia
• Chelating agent- iron overload can be reduced by regular
use of chelating agents like desferrioxamine therapy
• Folic acid owing to increase erythropoiesis
72

73. APLASTIC ANEMIA
 Characterized by a general lack of bone marrow activity.
 Affects RBC’s, WBC’s & platelets resulting in pancytopenia.
 Two chief forms :
1. Primary : it is the disease of unknown origin which occurs most
frequently in young adults, develops more rapidly and usually
terminates fatally
2. Secondary aplastic anemia : it has known etiology occurs at any
age and presents better prognosis.
73

74. Etiology
 Drugs : Methotrexate, Chloramphenicol, Sulpha drugs
 Toxic chemicals : Benzene derivatives, insecticides, arsenicals
 Infections : viral hepatitis, AIDS
 Miscellaneous : Irradiation, Pregnancy..
74

75. Clinical features
 Severe weakness with dyspnea ,
 Exhibit skin Pallor
 Numbness & tingling of extremities
 Edema is present.
 Petechiae in the skin and mucous membrane occur, due to
platelet deficiency.
 Nutropenia leads to a decreased resistance to infection.
75

76. Oral manifestations
 Petechiae, purpuric spots or frank
hematomas of oral mucosa.
 Spontaneous gingival hemorrhage is
present , relating to blood platelet
deficiency.
 Due to nutropenia :  Resistance to
infections leading to ulcerative lesions
of oral mucosa & pharynx.
76

77. Laboratory findings
 RBC count is remarkably reduced to 10,00,000cells/mm3.
 The absolute granulocyte count is particularly low with relative
lymphocytosis.
 Thrombocytopenia results in a prolonged BT; CT remains normal.
 Clot retraction is poor; tourniquet test (capillary fragility test)
is positive.
 The classical finding is that of pancytopenia along with
reduction of absolute reticulocyte count
77

78. Treatment
• Withdrawal of the etiological agent
• Supportive therapy—it is in the form of antibiotics and
transfusion.
• Hemopoiesis—stimulation of hemopoiesis by androgens.
• Bone marrow transplantation—it can be useful in some cases.
• Antifibrinolytic agents—gingival bleeding can be reduced by using
systemic antifibrinolytic agents such as aminocaproic acid or
transexamic acid and local treatment.
78

79. Anemia due to abnormalities of RBC membrane
Hereditary spherocytosis :
Red blood cells are excessively permeable to sodium ion.
The osmostic fragility of red cells is abnormal in these
conditions. It will lead to loss of cell membrane and
gradually the cell becomes spherical in shape and are
destroyed by spleen, giving rise to hemolytic anemia.
79

80. Clinical features :
• Age—symptoms are usually present in childhood.
• Symptoms—there is mild to moderate hepato- splenomegaly,
jaundice and anemia.
• A hemolytic and aplastic crisis may be precipitated by infection
or may occur with any cause. Such patients will have shivering,
fever, marked weakness, vomiting, abdominal pain, dyspnea and
palpitation.
80

81. Hematological findings :
• The peripheral smear shows presence of spherocytes.
• Reticulocyte count is increased.
• Hb ranges from 5 to 12 gm/dl.
Management :
• Splenectomy is the treatment of choice but should be done
after the child is 6 years old.
• Folic acid 5 mg daily.
81

82. ISOIMMUNE HEMOLYTIC ANEMIA
Erythroblastosis fetalis :
• It occurs due to isoimmune antibodies.
• It is also called as Hemolytic Disease of Newborn (HDN).
• Congenital hemolytic anemia due to Rh incompatibility
results from destruction of fetal blood brought about by a
reaction between maternal and fetal blood factors
82

83. Pathogenesis :
• It occurs due to inheritance, by the fetus, of a blood factor
from the father that acts as a foreign antigen to mother.
• The transplacental transfer of this antigen, actually
transplacental leak of red cells, from fetus to mother results
in immunization of mother and formation of antibodies.
• When the fetal red cells cross placenta they may stimulate the
production of maternal antibodies against the fetal antigens.
83

84. • Some of these antibodies then cross into fetal circulation and
cause the destruction of fetal red cells.
• If the father is Rh positive and the mother is Rh negative,
fetus inherits Rh positive antigens, which may act as antigen to
the mother and immunize her with resultant antibody formation.
• The problem is complicated by Rh antigens which are termed as
C, D and E. Out of this, D antigen is the strongest and is
responsible for the clinical manifestations of erythroblastosis
fetalis.
84

85. Clinical features :
• Some infants are stillborn.
• Symptoms : anemia with pallor, jaundice, edema resulting in
fetal hydrops.
85

86. Oral manifestations :
Teeth—Deposition of blood pigment in enamel and dentin of
developing teeth giving them a green, brown or blue hue..
Enamel hypoplasia—it is also reported occurring in some cases of
erythroblastosis fetalis and usually involves the incisal edges of the
anterior teeth and middle portion of the deciduous cuspid and first
molar crown. There is ring like defect called as Rh hump’
86

87. Laboratory findings
• RBCs count may vary less than 1,000,000 cells /cubic mm
• Large number of normoblasts and nucleated RBC
• The icterus index is very high and may reach a level of 100
units
87

88. Management:
• Antenatal—maternal sensitization is prevented by the
administration of 300 mg of Rh antiglobulin after
amniocentesis has been done.
• Management of affected fetus can be done by intensive
plasmapheresis of mother during pregnancy in order to
remove maternal antibodies or by intravenous transfusion of
blood into the fetus to prevent fetal anemia.
• Postnatal—in infants exhibiting only anemia, fresh packed
RBCs are given to correct anemia.
88

89. • Splenectomy—it results in striking and permanent improvement,
both in anemia and symptoms. After splenectomy, daily penicillin
250 mg 12 hourly is given to avoid infections.
• Blood transfusion—severe hemolytic crisis needs blood
transfusion.
• Folic acid should be given 5 mg orally to support increased
erythropoiesis
89

90. AUTOIMMUNE HEMOLYTIC ANEMIA
• Antibodies are formed the against the red cells antigens and
there is immune mediated destruction of RBCs.
• These antibodies, depending on thermal characteristics, are
divided into
1. Warm antibodies
2. Cold antibodies
90

91. Warm autoimmune haemolytic anaemia
• Occur at any age and in either sex.
• Disease may occur without any apparent cause (idiopathic), but 20-
25% patients develop this disorder as a complication of underlying
disease i.e. chronic lymphatic leukaemia, lymphoma, systemic lupus
erythematosis (SLE).
• It may occur in association with drugs (alpha methyldopa).
• Thermal optimum of 37’c
91

92. Clinical features :
• Symptoms vary with severity of the disease and its cause.
• Vomiting
• Fever
• Hepatosplenomegaly
92

93. Investigations :
• Mild to moderate chronic anaemia.
• Reticulocytosis.
• Spherocytosis and polychromasia on blood film examination.
• Positive Direct Coomb's (antiglobin) test for warm antibodies on
red cells.
• Positive Indirect Coomb's (antiglobin) test for warm antibodies
in the serum.
93

94. Management :
• Drug therapy - Oral prednisolone 40-60 mg daily may be
given to suppress antibody formation and continued for 4-
6 weeks.
• Blood transfusion is not necessary except in life
threatening situations.
• Splenectomy is considered if response to steroids fails.
94

95. Cold autoimmune haemolytic anaemia
• Cold agglutinins induce haemolysis at low temperature by
binding the complement on the red cells.
• Thermal optimum of 4’c.
• It occurs in two conditions.
1. Idiopathic cold agglutinin disease
2. Cold agglutinin type disease
95

96. Idiopathic cold agglutinin disease :
• It occurs mainly in the Elderly.
• Raynaud's phenomenon (intense vasospasm of peripheral arteries
on exposure to cold leading to tricolour response - paleness,
cyanosis and redness) and acrocyanosis occurs when a person is
exposed to cold.
• Characteristic findings demonstrate increased red cells turnover
and agglutination on the blood film which is reversed on warming.
• Cold agglutinins are present in high titres.
• The antiglobin test is always positive and demonstrates
complement binding.
96

97. • Treatment consists of keeping the extremities warm.
• Transfusion should he avoided as far as possible.
• Steroids and splenectomy have no role.
• Immunosuppressive therapy may help to decrease levels
of antibody in severe cases.
97

98. Cold agglutinin type disease :
It occurs on 2 conditions:
• Infection with mycoplasma pneumonia or infectious
mononucleosis. This is self limiting haemolysis.
• Paraxysmal cold haemoglobinuria. Seen in association
with syphilis or certain viral infection such as mumps
& measles.
98

99. CONCLUSION
 Anaemia although preventable is a global problem
 Anaemia still is the commonest cause of maternal mortality and
morbidity in spite of easy diagnosis and treatment
 Anaemia can be due to a number of causes, including certain diseases
or a shortage of iron, folic acid or Vitamin B12.
 The most common cause of anemia in pregnancy is iron deficiency.
 The youth needs to be educated about diet, sanitation and personal
hygiene
99

100. REFERENCES
• ABC of clinical haematology by Drew Provan. 3rd edition.
• Textbook of oral pathology by Shafer 4th edition
• Practical Medicine by P.J Mehta 18th edition
• Text book of Clinical Medicine by S.N Chugh
• Burket’s textbook of Oral medicine by Malcom A Lynch
10th edition
• Essentials of medical physiology by Sambulingum K and
Sambulingum prema 3rd edition
• Text book of Medical Physiology by Guyton and Hall 10th
edition
100

101. 101

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