Iron deficiency anemia,oral pathology,BDS THIRD YEAR

1. IRON DEFICIENCY
ANEMIA
MANEESHA MENON M
ROLL NO.23

2. Anemia is defined as reduced haemoglobin
concentration in blood below the lower limit of the
normal range for the age and sex of the individual.
ANEMIA
NORMAL VALUES OF Hb
MEN - 14-17.5 g/dL
WOMEN -12.3-15.3g/dL
CHILDREN - 10-15.5g/dL

3. ADULT REFERENCE VALUES OF RED
BLOOD CELLS
Parameter Men Women
Hemoglobin 14-17.5g/dL 12.3-15.3g/dL
Hematocrit 41.5%-50.4% 36.9%-44.6%
Red cell count 4.5-5.9million
cells/microlitre
4.5-5.1million cells/mL
Reticulocyte count 0.5%-1.5%
Mean cell volume[MCV] 80-96fL
Mean cell
hemoglobin[MCH]
27.5-32.2pg
Mean cell hemoglobin
concentration[MCHC]
33.4-35.5g/dL
Red cell distribution
width[RDW]
11.4-14.5

4. 01
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ification
Mechanism common cause
1.Loss of blood
Acute
Chronic
Trauma
Gastrointestinal tract lesions,gynecological
causes,tumors
2.Decreased red cell production
Nutritional deficiency
Inflammation mediated
Erythropoietin deficiency
Immunemediated
Bone marrowinfiltration
Endocrine failures
iron,vitamin B12,folate
Iron deficiency anemia of chronic disease
Renal disease
Aplastic anemia
Primary hematipoietic neoplasms,metastatic
neoplasms
Thyroid,pituitary
ETIOLOGIC CLASSIFICATION

5. p
Mechanism common cause
3.Increased red cell destruction
Membrane alterations[genetic]
Membrane alterations[acquired]
Enzyme deficiencies
Hemoglobin abnormalities
Immunologic abnormalities
Mechanical trauma
Infections of red cells
Toxic/chemical injury
Splenic sequestration
Hereditary elliptocytosis,hereditary
spherocytosis
Hypophosphatemia,paroxysmal nocturnal
hemoglobinuria
G6PD,pyruvate kinase,hexokinase
Thalassemia syndromes,sickle cell
disease,hemoglobinopathies
Hemolytic disease of newborn,transfusion
reactions,drug induced reactions
Disseminated intravasular
coagulation,thrombotic thrombocytopenic
purpura
Malaria
snake venom,lead poisoning
Reticuloendothelial hyperactivity with
splenomegaly

6. Morphologic classification
Type of anemia
based on RBC size
and Hb content
RBC morphology Red cell indices Most common
causes
Normocytic
Normochromic
Normal cell
Normal Hb
Reduction in RBC
number;normal
MCV,MCH and
MCHC
Hemorrhage;hemol
ysis;lack of blood
formation;dilution
of blood with fluid
Macrocytic
normochromic
Large cell
Normal Hb
Increased MCV
and MCH;normal
MCHC
lack of erythrocyte
-maturing factors
Microcytic
normochromic
Small cell
Normal Hb
Reduced MCV and
MH;normal MCHC
Thalassemia
syndromes
Microcytic
hypochromic
Small cell
Reduced Hb
Reduced
MCV,MCH and
MCHC
Iron deficiency

7.  It is a manifestation of severe iron deficiency, caused by depletion of all
available iron stores.
 It is the most common cause of anemia in the world.
 WHO estimates that IDA affects one-fourth of the global population.
 children aged 0-5 years,women of child bearing age group and
pregnant women are at higher risk.
IRON DEFICIENCY ANEMIA

8. • Iron is a vital trace element in the human body.
• The concentrationof iron in the body is approximately 60 parts per
million[ppm].
• Daily loses that range between 1 and 2 mg occur by epithelial shedding
from the mucous membrane and skin;additional physiological loses
occur through blood loss and pregnancy in women.
• The iron required for hemoglobin synthesis is derived from 2 sources-
diet containing iron and recycling of iron from senescent red cells.
IRON

9. ETIOLOGY
Dietaryinsufficiency Inadequate absorption Increased requirement
• Inadequate diet
• Malnutrition
•Elderly
•Inadequate dietary iron
content
• Infants[milk has very
little iron content]
• Diets that strictly exclude
meat
• Atrophic gastritis
• Malabsoption
syndrome
• Gastrectomy
• Intestinal resection
or bypass
• Chronic diarrhea
• Dietary components
• Physiological
• Period of active
growth and
development
• Premenopausal
women ,especially
during pregnancy
• Chronic blood loss
gastrointestinal
urinary tract
genital tract
• Chronic disease

10.  The manifestations of IDA are caused by the reduced oxygen-carrying
capacity of blood that leads to tissue hypoxia and physiological
compensatory mechanisms.
 pallor of mucous membrane and skin
 weakness
 shortness of breath on mild exertion
 dizziness
 fast or irrgeular heartbeat
 pounding or whooshing in ears
 headache
Clinical features

12. • several chronic diseases have been associated with IDA-
 Chronic kidney disease
 chronic heart failure
 cancer
 inflammatory bowel disease
 patient may experience fatigue,leg cramps while climbing
stairs,pagophagia,poormental performance,intolerance for cold and
repeated infections.
 Nonavailability of iron to CNS-
• restless leg syndrome
• pica[unusual dietary cravings such as clay].
• Infancy-irreversible cognitive dysfunction.

13. Epithelial defects-
 koilonychia[spoonshaped nails]
 atrophic gastritis
 brittle and longitudnally ridged nails
ORAL MANIFESTATIONS
• Angular chelitis
• diffuse or patchy atrophy of papillae of the tongue leading to a smooth
glossy appearence of the tongue
• lingual varicosity
• xerostomia
• recurrent aphthous ulcers
• burning and tenderness

14. • Hypochromia of RBC-Central pallor increased.
• Anisochromia present.
• Microcytic anisocytic.
• poikilocytosis,pencillike erythrocyte.
• Target cell and reticulocytes present.
• ESR elevated.
• RBC count 30,00,000-40,00,000cells/mm3 of blood.
• Total iron binding capacity-13.1mmol/l.
• Hemoglobin level 4mg/dl/below it.
• MCV and MCH reduced.
• Platelet count increades to 4,50,000/microlitre.
• Increase in erythroid predecessors and absence of stainable iron in the
macrophages as demonstrated by a prussian blue stain.
LABORATORY FINDINGS

15. TREATMENT AND PROGNOSIS
 Oral supplement of 150-180 mg of elemental iron administered in 2 or
3 divided doses per day.
 Intravenous iron therapy in patients who cannot tolerate oral
supplements and those whose daily requirement cannot be met by
the oral route.

16. PLUMMER-VINSON SYNDROME
[PATERSON KELLY SYNDROME]
[SIDEROPENIC DYSPHAGIA]

17. Plummer-
vinson
syndrome
Iron
deficiency
anemia
Oesophageal
webs
Dysphagia

18.  Plummer-vinson syndrome is a rare condition characterised by
iron deficiency anemia in conjunction withmucosal atrophy of the
esophagus and complaint of dysphagia.
 The condition is significant in that it has been associated with a high
frequency of both oral and esophagealsquamous cell
carcinoma;therefore it is considered a premalignant process.

19. • Age - 30-50 years
• Race - Scandinavian or northernEuropean
• Sex-Women
signs and symptoms :
• patients complain of a burning sensation associated with the tongue
and oral mucosa.
• angular cheilitis.
• marked atrophy of lingual papillae,which produces a smooth red
appearence of doral tongue.
CLINICAL AND RADIOGRAPHIC FEATURES

20. • Dysphagia
• An evaluation with endoscopy or esophageal barium contrast
radiographic studies shows the presence of abnormal bands of tissue in
the esophagus,called esophagial webs.
• koilonychia
• other features of anemia
LABORATORY FINDINGS
 Microcytic hypochromic anemia

21. • Dietary iron supplementation
• This therapy usually resolves the anemia ,relieves the glossodynia and
may reduce the severity of the esophageal symptoms.
• Patients with plummer vinson syndrome should be evaluated
periodically for oral,hypopharyngeal and esophageal cancer.
TREATMENT AND PROGNOSIS

22. APLASTIC ANEMIA

23. • Aplastic anemia is pancytopenia[i.e. simultaneous presence of
anemia,leucopenia and thrombocytopenia]that is caused by the
hypocellular bone marrow in the absence of an abnormal infiltrate or
increased reticulin.
• The condition can be fatal and early diagnosis can help with patient
management.
• It comes under the classification of anemia due to defect in stem cell
proliferation and differentiation.

24. ETIOLOGICAL CLASSIFICATION
Acquired Genetic and inherited
Idiopathic
• stem cell defects
Known causes
• Drugs,dosedependent and
reversible
• Chloramphenicol
• thyroid medicines
• phenytoin
• Chlorpromazine
• sulfonylurea
Viral infections
• Hepatitis virus
• HIV virus
• Epstein-Barr virus
Physical agents
• Radiation
Other conditions
• Pregnancy
• Anorexia
• Fanconi anemia
• Dyskeratosis congenita

25. • The exact pathogenesis is unclear.
• Three main mechanisms have been found to lead to hypocellular bone
marrow.
 Direct damage to bone marrow by exposure to toxic substances is the
common cause of bone marrow failure.
• It is most often iatrogenic as a result of exposure to chemotherapeutic
agents or radiation.
• The effects on bone marrow are dose dependent and transient at
conventional doses.
PATHOGENESIS

26.  Germline defects can cause marrow failure as a result of specific loss of
function.
• These are inherited and manifests in childhood.
• All cells and organs are affected ,they manifests physical anomalies
including multiple organs.
• Fanconi anemia mutations reduce hematopietic stem cells ability to
repair DNA.
 Immune mediated destruction of hematopoietic progenitors can lead to
bone marrow suppression.
 T cell mdaited destruction may develop spontaneously or often an
immunogenic alteration by exposure to physical,chemical,biological
agents.
• Seronegative hepatitis,eosinophilic fascitis and thymoma are
associated with aplastic anemia but have been labelled idiopathic.

27. • Age - Any age group
• Sex- both genders
• Usually insidious in origin.
• Higher incidence rate in asia,2-3 times more common in East Asians.
• Increased incidence in Asian population is related to environmental
factors since the increase was not found in Asians living in united states.
• Rare in western populations.
CLINICAL FEATURES

28.  Anemia and its symptoms like mild progressive weakness and
fatigue,pallor,palpitaions.
 Thrombocytopenia-petechiae,ecchymoses,bleeding .
 Frequent and recurrent infections ,chills and fever due to neutropenia.
 Hemorrhage from skin or mucosal bleeding ,nose,gum,bowel and visual
disturbance caused by retinal bleeding.
 Infections in mouth and throat.
CLINICAL MANIFESTATIONS

29.  Mucosal pallor.
 Spontaneous gingival bleeding.
 Mucosal petechiae.
 Purpura
 Ecchymoses.
 Gingival hyperplasia
 mucosal ulceration with minimal erythema at margins
due to deficiency of leukocytes.
ORAL MANIFESTATIONS

30. • Total blood counts in the early stages of the disease may show single
cell line suppression ,most commonly affecting thrombocytes leading to
thromboytopenia.
• All cell lines except lymphocytes are affected -Pancytopenia and
reduced Hb level.
• Reticulocytopenia in conjunction with anemia.
• Erythrocytic macrocytosis,anisopoikilocytosis and neutrophils with
toxic granules.
• platelets are reduced in number and size.
LABORATORY FINDINGS

31.  An empty marrow picture.
 Marrow is hypocellular with prominent for spaces variable number of
hematopoietic cells.
 Normal production of all cell lines is suppressed.
 Areas with abnormal erythropoiesis.
BONE MARROW CHANGES

32. Requires atleast 2 of the following criteria to be fulfilled-
1. Hb count less than 10g/dL
2. Platelet count less than 20,000/microlitre
3. Neutrophil count less than 500/mm3
TREATMENT
Involves steps-
I. to identify and discontinue causative drugs.
II. rule out genetic and hereditary causes by screening for approximately
50 genes that cause germline mutations that lead to bonemarrow
failure.
III. stage of the disease
• Bone marrow replacement
• Immune mediated aplastic anemia treatment.
DIAGNOSIS

33. An intensified National Iron plus initiative
Ministry of Health and Family welfare ,Government of INDIA.

34. Reference-
1.SHAFERS TEXTBOOK OF ORAL PATHOLOGY
2.NEVILLE TEXTBOOK OF ORAL AND MAXILLOFACIAL PATHOLOGY