To brief introduction of anemia its cause, classification and management .

1. ANEMIA
AND
DIETARY MANAGEMENT
Presented by
Dev Ram SUNUWAR
M.Sc.Nutrition and dietetics1

2. OUTLINE
 Definition
 Overview of anemia
 Causes of anemia
 Classification
 Dietary management
2

3. DEFINITION
 Anemia from the Greek word ( ναιμία)(an-haîma)
meaning "without blood", is a deficiency of red
blood cells (RBCs) and/or hemoglobin.
 WHO definition: “ a condition in which the
haemoglobin content of blood is lower than normal
as a result of a deficiency of one or more essential
nutrients, regardless of the cause of such
deficiency.
 Anaemia refers to a state in which the level of
haemoglobin in the blood is below the reference
range appropriate for age and sex. ( Davidsons
principle and practice of medicine) 3

4. OVERVIEW
According to WHO
 Worldwide prevalence = over 30% of the world’s population are
anaemic, many due to iron deficiency.
 In developing countries every second pregnant woman and about 40% of
preschool children are estimated to be anaemic.
 40% in young children
 50% of pregnant women and 35% of non-pregnant women affected
 18% adult males
Prevalence of anemia in Nepal
 Anemia affects 35% of all women (close to 48% of pregnant women)
 However, Nepal demonstrated a huge reduction in anemia prevalence
among women between 2001 and 2006 ,Hookworm infestation may be a
particular driver of iron deficiency and anemia in Nepal, particularly in the
Terai, where one study found that 75% of pregnant women had
hookworms, 73% were anemic, and 88% of anemia cases were due to
iron deficiency (Dreyfuss et al. 2000).
 Anemia among women and children still higher:- (35% in women 15-49
years and 46% 6-59 months children anemic (NDHS 2011)
4

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6. CAUSE OF ANEMIA
Decreased or ineffective marrow production
• Lack of iron, vitamin B12 or folate
• Hypoplasia/myelodysplasia
• Invasion by malignant cells
• Renal failure
• Anaemia of chronic disease
Normal marrow production but increased removal
of cells
• Blood loss
• Haemolysis
• Hypersplenism
6

7. Diagnosis of anemia
 Patient history
Dietary habits
Medication
Possible exposure to chemicals and/or toxins
Description and duration of symptoms
 Tiredness
 Muscle fatigue and weakness
 Headache and vertigo (dizziness)
 Dyspnea (difficult or labored breathing) from exertion
 G I problems
 Overt signs of blood loss such as hematuria (blood in urine) or
black stools 7

8. Diagnosis of anemia
 Physical exam
General findings might include
Hepato or splenomegaly
Heart abnormalities
Skin pallor
Specific findings may help to establish
the underlying cause:
In vitamin B12 deficiency there may be signs
of malnutrition and neurological changes
In iron deficiency there may be severe pallor,
a smooth tongue, and esophageal webs
In hemolytic anemias there may be jaundice
due to the increased levels of bilirubin from
increased RBC destruction
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12. IRON-DEFICIENCY ANEMIA
 Clinical Manifestations
 Most common: pallor
 Second most common: inflammation of the tongue
(glossistis)
 Cheilitis=inflammation/fissures of lips
 Sensitivity to cold
 Weakness and fatigue
 Diagnostic Studies
 CBC
 Iron studies Diagnostics:
 Iron levels: Total iron-binding capacity (TIBC), Serum
Ferritin.
 Endoscopy/Colonscopy 12

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17. MANAGEMENT
 Collaborative Care
 Treatment of underlying disease/problem
 Replacing iron
 Diet
 Drug Therapy
 Iron replacement
 Oral iron
 Feosol, DexFerrum, etc
 Absorbed best in acidic environemtn
 GI effects
 Parenteral iron
 IM or IV
 Less desirable than PO
17

18. IRON-DEFICIENCY ANEMIA
MANAGEMENT
 Diet counseling—foods rich in iron
 Provide periods of rest
 Supplemental iron
 Discuss diagnostic studies
 Iron therapy for 2-3 months after the hemoglobin
levels return to normal
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21. Guidelines for oral iron and folate therapy to treat severe anaemia
Age Group Dose Duration
< 2 years 25 mg iron + 100-400μg folic acid daily 3 months
2-12 years 60 mg iron + 400μg folic acid daily 3 months
Adolescents and adults,
including pregnant
women
120 mg iron + 400μg folic acid daily 3 months
 After completing 3 months of therapeutic supplementation, pregnant women and
infants should continue preventive supplementation regimen.
 Children with Kwashiorkor or marasmus should be assumed to be severely anaemic.
However, oral iron supplementation should be delayed until the child regains
appetite and starts gaining weight, usually after 14 days
Source: Rebecca J. Stoltzfus and Michele L. Dreyfuss, Guidelines for the use of Iron
Supplements to Prevent and Treat Iron Deficiency Anaemia, INACG, WHO and UNICEF,
1998
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23. FOOD FORTIFICATION
 Ministry of Health and Population (MoHP) has also started
home fortification programs in Nepal with multiple
micronutrient powders (MNPs) under the World Health
Organization’s guidelines
 This does not ask for a change in food habits as the
powders are sprinkled on the food that the children usually
eat.
 This has also helped a timely initiation of complementary
food. This program has targeted children completing 6
months.
 Simultaneously, the second anemia control plan 2012–
2016 is being formulated by MoHP addressing anemia
among all strata, particularly the most vulnerable ones like
children of 6-23 months young, children of 6-59 months,
adolescents, pregnant women's 23

24. MEGALOBLASTIC ANEMIAS
 Characterized by large RBCs
which are fragile and easily
destroyed
 Common forms of
megaloblastic anemia
1. Cobalamin deficiency
2. Folic acid deficiency
24
This picture shows large, dense,
oversized, red blood cells (RBCs)
that are seen in megaloblastic
anemia.

25. COBALAMIN (VITAMIN B12) DEFICIENCY
 Cobalamin Deficiency--formerly known as
pernicious anemia
 Vitamin B12 (cobalamin) is an important water-
soluble vitamin.
 Intrinsic factor (IF) is required for cobalamin
absorption
 Causes of cobalamin deficiency
 Gastric mucosa not secreting IF
 GI surgery loss of IF-secreting gastric mucosal cells
 Long-term use of H2-histamine receptor blockers
cause atrophy or loss of gastric mucosa.
 Nutritional deficiency
 Hereditary defects of cobalamine utilization
25

26. COBALAMIN (VITAMIN B12) DEFICIENCY
 Clinical manifestations
 General symptoms of anemia
 Sore tongue
 Anorexia
 Weakness
 Parathesias of the feet and hands
 Altered thought processes
 Confusion  dementia
26

27. COBALAMIN DEFICIENCY
DIAGNOSTIC STUDIES
 RBCs appear large
 Abnormal shapes
 Structure contributes to erythrocyte destruction
 Schilling Test: a medical investigation used for
patients with vitamin B12 deficiency. The purpose
of the test is to determine if the patient has
pernicious anemia.
27

28. COBALAMIN DEFICIENCY
 Collaborative Care
 Parenteral administration of cobalamin
 ↑ Dietary cobalamin does not correct the anemia
 Still important to emphasize adequate dietary intake
 Intranasal form of cyanocobalamin (Nascobal) is
available
 High dose oral cobalamin and SL cobalamin can use be
used
28

29. FOLIC ACID DEFICIENCY
 Folic Acid Deficiency also causes megablastic
anemia (RBCs that are large and fewer in number)
 Folic Acid required for RBC formation and maturation
 Causes
 Poor dietary intake
 Malabsorption syndromes
 Drugs that inhibit absorption
 Alcohol abuse
 Hemodialysis
29

30. FOLIC ACID DEFICIENCY
 Clinical manifestations are similar to those of
cobalamin deficiency
 Insidious onset: progress slowly
 Absence of neurologic problems
 Treated by folate replacement therapy
 Encourage patient to eat foods with large amounts
of folic acid
 Leafy green vegetables
 Liver
 Mushrooms
 Oatmeal
 Peanut butter
 Red beans 30

31. THALASSEMIA
 Etiology
 Autosomal recessive genetic disorder of inadequate
production of normal hemoglobin
 Found in Mediterranean ethnic groups
 Clinical Manifestations
 Asymptomatic  major retardation  life
threatening
 Splenomegaly, hepatomegaly
 No specific drug or diet are effective in treating
thalassemia
 Thalassemia minor
 Body adapts to ↓ Hb
 Thalassemia major
 Blood transfusions with IV deferoxamine (used to
remove excess iron from the body)
31

32. ANEMIA OF CHRONIC DISEASE
 Underproduction of RBCs, shortening of RBC survival
 2nd most common cause of anemia (after iron deficiency
anemia
 Generally develops after 1-2 months of sustained
disease
 Causes
 Impaired renal function
 Chronic, inflammatory, infectious or malignant
disease
 Chronic liver disease
 Folic acid deficiencies
 Splenomegaly
 Hepatitis 32

33. APLASTIC ANEMIA
 Characterized by Pancytopenia
 ↓ of all blood cell types
 RBCs
 White blood cells (WBCs)
 Platelets
 Hypocellular bone marrow
 Etiology
 Congenital
 Chromosomal alterations
 Acquired
 Results from exposure to ionizing radiation, chemical
agents, viral and bacterial infections
33

34. APLASTIC ANEMIAEtiology
 Low incidence - Affecting 4 of every 1 million persons
 Manageable with erythropoietin or blood transfusion
 Can be a critical condition
 Hemorrhage
 Sepsis
Clinical Manifestations
Gradual development
Symptoms caused by suppression of any or all bone marrow
elements
General manifestations of anemia
Fatigue/ Dyspnea, Pale skin
Frequent or prolonged infections
Unexplained or easy bruising
Nosebleed and bleeding gums
Prolonged bleeding from cuts
Dizziness headache
34

35. APLASTIC ANEMIA
 Treatment
 Identifying cause
 Blood transfusions
 Antibiotics
 Immunosuppressants (neoral, sandimmune)
 Corticosteroids (Medrol, solu-medrol)
 Bone marrow stimulants
 Filgrastim (Neupogen)
 Epoetin alfa (Epogen, Procrit)
 Bone marrow transplantation
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36. ANEMIA CAUSED BY BLOOD LOSS
 Acute Blood Loss
 Chronic Blood Loss
36

37. ACUTE BLOOD LOSS
 Result of sudden hemorrhage
 Trauma, surgery, vascular disruption
 Collaborative Care
1. Replacing blood volume
2. Identifying source of hemorrhage
3. Stopping blood loss
Chronic Blood Loss
 Sources/Symptoms
 Similar to iron deficiency anemia
 GI bleeding, hemorrhoids, menstrual blood loss
 Diagnostic Studies
 Identifying source
 Stopping bleeding
 Collaborative Care
 Supplemental iron administration
37

38. ANEMIA CAUSED BY INCREASED
ERYTHROCYTE DESTRUCTION
 Hemolytic Anemia
 Sickle Cell disease
 Acquired Hemolytic Anemia
 Hemochromatosis
 Polycythemia
38

39. HEMOLYTIC ANEMIA
 Destruction or hemolysis of RBCs at a rate that
exceeds production
 Third major cause of anemia
 Intrinsic hemolytic anemia
 Abnormal hemoglobin
 Enzyme deficiencies- G6PD deficiencies
 RBC membrane abnormalities
 Extrinsic hemolytic anemia
 Normal RBCs
 Damaged by external factors
 Liver
 Spleen
 Toxins
 Mechanical injury (heart valves) 39

40. SEQUENCE OF EVENTS IN HEMOLYSIS
40
Fig. 30-1

41. ACQUIRED HEMOLYTIC ANEMIA
 Causes
 Medications
 Infections
 Manifestations
 S/S of anemia
 Complications
 Accumulation of hemoglobin molecules can obstruct
renal tubules  Tubular necrosis
 Treatment
 Eliminating the causative agent
41

42. SICKLE CELL ANEMIA
 First described in Chicago in 1910 by James
Herrick as an inherited condition that results
in a decrease in the ability of red blood cells
to carry oxygen throughout the body
 A serious condition in which red blood cells
can become sickle-shaped
 Normal red blood cells are smooth and
round. They move easily through blood
vessels to carry oxygen to all parts of the
body.
 Sickle-shaped cells don’t move easily
through blood. They’re stiff and sticky and
tend to form clumps and get stuck in blood
vessels.
 The clumps of sickle cell block blood flow in
the blood vessels that lead to the limbs and
organs. Blocked blood vessel can cause
pain, serious infection, and organ damage.
42

43. NORMAL AND SICKLE RED BLOOD CELLS
IN BLOOD VESSELS
43
Figure A shows normal red blood cells flowing freely in
a blood vessel. The inset image shows a cross-section
of a normal red blood cell with normal hemoglobin.
Figure B shows abnormal, sickled red blood cells clumping and
blocking the blood flow in a blood vessel. The inset image shows a
cross-section of a sickled red blood cell with abnormal strands of
hemoglobin.
Source from http://www.nhlbi.nih.gov/health/dci/Diseases/Sca/SCA_WhatIs.html

44. Genetics
 2 copies of the gene for
Hb (each parent)
 HbS –
Recessive
 S=Sickle
 A=Normal
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46. SIGNS AND SYMPTOMS
 Individual signs and symptoms
varies. Some have mild symptoms,
others have very severe symptoms
and may be hospitalized for treatment
 Present at birth, many infants doesn’t
show signs until after 4 months of
age
 Anemia: Fatigue (tiredness), pale
skin and nail beds, jaundice, and
shortness of breath
 Pain (Sickle Cell Crisis): Sudden
episode of pain throughout the body.
Common sites: bones, lungs,
abdomen, and joints. Lack of blood
flow can cause pain and organ
damage. 46

47. Medical Complications
1. pain episodes
2. strokes
3. increased infections
4. leg ulcers
5. bone damage
6. yellow eyes or
jaundice
7. early gallstones
8. lung blockage
9. kidney damage and
loss of body water in urine
10. painful erections in men
(priapism)
11. blood blockage in the spleen
or liver (sequestration)
12. eye damage
13. low red blood cell counts
(anemia)
14. delayed growth 47

48. TREATMENT & PREVENTION
 Taking the folic acid (folate) daily to help make new red
cells
 Drinking plenty of water daily (8-10 glasses for adults)
 Identify what can trigger the “Crisis” such as stress,
avoid extremes of heat and cold weather
 Maintain healthy lifestyle habits
 Eating healthy
 Avoid dehydration
 Exercise regularly
 Get enough sleep and rest
 Avoid alcohol and don’t smoke
 Regular medical checkups and treatment are important
48

49. SIDEROBLASTIC ANEMIA
 Sideroblastic anemias, a group of heterogeneous
disorders, produce a common defect-failure to use
iron in Hb synthesis, despite the availability of
adequate irons stores.
 Disease that interfere with production of heme. May
be microcytic and hypochromic
49

50. ETIOLOGY
 Hereditary
 X- linked (isolated/ genetic syndrome) autosomal
 Acquired
 Drugs (chloramphenicol, isoniazid)
 Heavy metals (e.g. lead)
 Chemotherapeutics agents
50

51. SIGNS AND SYMPTOMS
 Non specific clinical effects,
 Anorexia, weakness, fatigue, dizziness, pale skin
and mucous membrane and occasionally enlarged
lymph node
 Heart and liver failure may developed from
excessive iron accumulation in these organs
causing angina, slight jaundice and
hepatosplenomegaly
 Hereditary sideroblastic anemia is associated with
increased GI absorption of iron causing sign of
hemosiderosis.
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52. TREATMENT
 Hereditary sideroblastic anemia usually respond to
several weeks treatment with high doses of
pyridoxine
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55. REFERENCES
 Advance text book on food & nutrition vol -2, Dr. M.
Swaminathan
 Davidsons principle and practice of medicine 22nd
edition; Brian R. Walker, Nicki R. Colledge, Stuart
H. Ralston, Ian D. Penman
 Hematologic System, Oncologic Disorders &
Anemias, Dr Ibrahreem Bashayreh, RN, PhD
 Sickle cell anemia, Gregg Selke, Ph.D. 11/28/06
 NDHS 2011
55

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57. CLASSIFICATION
Anemias may be classified morphologically based on the average size of the cells and
the hemoglobin concentration into:
1. Normochromic, normocytic anemia (normal MCHC, normal MCV).These
include:
 anemias of chronic disease
 hemolytic anemias (those characterized by accelerated destruction of
RBC's)
 anemia of acute hemorrhage
 aplastic anemias (those characterized by disappearance of RBCs
precursors from the marrow)
2. Hypochromic, microcytic anemia (low MCHC, low MCV).These include:
 iron deficiency anemia
 thalassemias
 anemia of chronic disease (rare cases)
3. Normochromic, macrocytic anemia (normal MCHC, high MCV).These include:
 vitamin B12 deficiency
 folate deficiency
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