Anemia: Decreased Hemoglobin Content Anemia: Abnormal Hemoglobin RBCs
10 anemia
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Transcript of 10 anemia
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Anemia
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Introduction
• Not a single disease• Results from a number of different pathologies• Defined as a reduction from the normal quantity of
Hb in blood• Who defines anemia as Hb levels less than 13 g/dl for
males and less than 12 g/dl for females• Low Hb levels results in decreased oxygen carrying
capacity of blood
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Epidemiology
• Most common condition resulting in significant morbidity and mortality
• Worldwide: Over 50% of pregnant women and 40 % of infants are anemic
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Aetiology
Two different mechanisms:1. Reduced Hb synthesis (due to lack of nutrient
or bone marrow failure)
Reduced proliferation of precursors or defective maturation of precursors or both
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Aetiology (contd…)
• Increased Hb loss due to haemorrhage (red cell loss) or hemolysis (red cell destruction)
(More than one cause can be found in a patient)
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Normal erythropoiesisPluripotent stem cell
Erythroid burst forming unit
Erythroid colony forming unit Within BM
Erythroblast
Reticulocyte Peripheral blood
Mature red cell
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Normal erythropoiesis (contd…)
• Erythropoietin production si impaired n condictions such as RA, cancer and Sickle cell anemia
• Each day about 2 *1011 erythrocytes enter the circulation
• Normally survive for 120 days
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Normal erythropoiesis (contd…)
• Destroyed by reticuloendothelial system found in spleen and BM
• Iron is removed from haem component of Hb and transported back into bone marrow for reuse
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Normal erythropoiesis (contd…)
• Pyrole ring from globin is excreted as conjugated bilirubin by the liver and the polypeptide portion enters the body’s protein pool
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Clinical manifestations• Mildest form: tiredness and lethargy, reduced
mental performance
• Non-specific signs and symptoms associated with anemia:
Tiredness, Pallor, Fainting, Exertional dyspnea, Tachycardia, Palpitations, Worsening angina, Worsening cardiac failure, Exacerbation of intermittent claudication
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Investigations• No place for blind treatment
• Anemia is a consequence of reduced concentration of Hb in each red cell and/or reduced number of red cells in peripheral circulation
• Imp parameter: Hb concentration of blood, including its size , shape and color, MCV to determine type of anemia
• Bone marrow examination
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Iron deficiency anemia
• Epidemiology: 20% of world’s population
• Cause: diet deficient in iron, parasitic infestations and multiple pregnancies
• Aetiology: Blood loss, GI bleeding (most likely), Haemorrhoids, nosebleeds or postpartum haemorrhage
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Iron deficiency anemia
Causes of Iron deficiency anemia
• Inadequate iron absorptionDietary deficiencyMalabsorption
• Increased physiological demand• Loss through bleeding
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Pathophysiology
• Elimination not controlled physiologically• Homeostasis maintained by controlling iron absorption• Absorption inefficient• Iron bound to haem is better absorbed than iron found
in vegetables• Phosphates and phytates leads to formation of
unabsorbable complex, while ascorbic acid increases iron absoprtiopn
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Pathophysiology (contd…)
• Anemia a result of mismatch between body’s iron requirement and iron absoprtion
• Fortified milk given to children up to the age of 18 months increases Hb levels and improve performance
• Iron malabsoprtion occurs in patients with coleliac disease and in 50% patients following gastrectomy
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Pathophysiology (contd…)
• During pregnancy: dilutional anemia• Some of the increased demand is met by
stopping menstruation
Whatever the cause might be inadequate iron absorption leads
to anemia
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Clinical manifestations
• Pale skin and mucous membrane• Painless glossitis• Angular stomatitis• Koilonychia• Dysphagia• Pica• Atrophic gastritis
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Investigations
• Serum iron, Total iron binding capacity (TIBC) and serum ferritin
• Aim: To correct anemia and replenish iron stores
Important to resolve the underlying cause as far
as possible
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Treatment
• Folic acid use during pregnancy• Prophylaxis in menorrhagia, after partial
gastrectomy and in some low birth weight infants
• Continue for 6 months to both correct anemia and replenish body stores
• Standard treatment: 200 mg three times a day
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Treatment (contd…)
• It takes 1 to 2 weeks for Hb level to rise to 1 g/dl
• N and abdominal pain occurs in some patients• Alternative salts of iron are tried• Absorption is 15% of intake during the first 2-3
weks but falls off to an average of 5% thereafter
• Modified release oral preparations also available
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Treatment (contd…)
• There is little place for parenteral iron• In renal patients, a regular weeks dose is often
given and patients’ serum ferritin monitored to check for iron overload
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MEGALOBLASTIC ANEMIA
• They are macrocytic anemia (raised MCV)• Abnormality in the maturation of
haemopoietic cells in the bone marrow• Two causes: Folate deficiency and Vit. B12
deficiency anemia• Pernicious anemia is a specific disease caused
by malabsorption of Vit B12
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Aetiology
Folate deficiency anemia
• Readily available in normal diet (Fruit, green vegetables and yeast)
• Folate deficiency either due to folic acid deficiency anemia or increased folate utilization
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Aetiology (contd…)
Vitamin B12 deficiency anemia • Inadequate intake or malabsorption (dueto
removal of distal ileum)• Dietary source: Food of animal origin• Daily requirements: 1-2 micrograms
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Pathophysiology
• Common: inhibition of DNA synthesis in maturing cells
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Folate deficiency anemia
Dietary folate Gut
Folate monoglutamate
Methyltetrahydrofolate monoglutamate
Tetrahydrofolate monoglutamate Bone
Tetrahydrofolate polyglutamate marrow
Folate co-enzymes Dihydrofolate Polyglutamate
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Pathophysiology of Vit. B12 deficiency anemia
• Absorption occurs by an active process• Enzyme in the stomach release Vit. B12 from protein complexes• One molecule of Vit. B12 combine with one molecule of
glycoprotein (called intrinsic factor)• There are specific receptors in the distal ileum for intrinsic
factor-Vit B12 complex• Vit B12 enters the ileal cell and is then transported through the
blood attached to transport proteins• A total gastrectomy always leads to Vit. B12 deficiency• Onset of anemia is usually delayed
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Pathophysiology of pernicious anemia
• Autoimmune in origin• Patients typically have a gastric atrophy and no or
virtually no intrinsic factor secretion• Two different intrinsic factor antibodies have been
produced in serum of patients with pernicious anemia
• Gastric parietal antibodies found (in 90% patients)
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Clinical manifestations• Glossitis• Angular stomatitis• Altered bowel habit• Anorexia• Mild jaundice• Insiduous onset• Sterility• Bilateral peripheral neuropathy• Melanin skin pigmentation• Fever
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Investigations
Folic acid deficiency anemia
• Symptomless initially• Large oval red cells• Anisocytosis and poikilocytosis• Thrombocytopenia
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Investigations (contd…)
Vit B12 deficiency anemia
• Serum Vit B12 level• Serum folate level• Measuring absorption of Vit. B12 (by Schilling
test)• Parietal cell antibodies (not accurately
diagnostic)
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Treatment
• Necessary to establish whether the patient with megaloblastic anemia has Vit. B12 deficiency or folic acid deficiency or both
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Treatment of folate deficiency anemia
• Replacement therapy• Duration of treatment depends on cause• Changes in dietary habit or removal of any
precipitating factor• Normal daily requirement approx. 100 micrograms
per day• Dose: 5-15 mg per day for 4 months• Parenteral folic acid treatment not normally required
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Treatment of folate deficiency anemia during pregnancy
• Folate requirement increases in pregnancy and is higher in twin pregnancies
• Prophylaxis with folate ( 350-500 micrograms) frequently given during pregnancy
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Treatment of Vit. B12 deficiency anemia
• Require life long replacement therapy• Transfusion not normally given• If emergency transfusion deemed necessary, packed cells may
be given• Diuretics also given• Definite diagnosis should be made before starting treatment• Std. treatment: Hydroxocobalamin 1 mg IM repeated five
times at 3 day intervals to replenish body stores, followed by maintenance dose, usually 1 mg IM every 3 months.
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Sideroblastic anemias
• Group of conditions diagnosed by finding ring siderobalst in the BM
• Both hereditary and acquired forms present
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Aetiology
• In hereditary forms, there is X chromosome linked pattern of inheritance
• Both autosomal dominant and autosomal recessive families present
• Defect: Reduced activity of the enzyme 5-aminolevulinate synthase (ALAS)
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Pathophysiology
• Examination of BM shows number of erythroblasts that have iron granules surrounding the cell nucleus (known ad ring sideroblast)
• Low levels of ALAS in hereditary forms• Drugs and toxins: Alcohol, Isoniazid in slow
acetylators, Dose of Chloramphenicol over 2 g
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Clinical manifestations
• Develop on infancy or childhood• Severe or mild anemia• Splenomegaly• Idiopathic forms tends to develop insiduously
(middle age or later)• Many becoem asymptomatidc for long
periods
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Investigations
• In heriditary fomrs: red cells in peripheral blood are hypochromic and microcytic
• Increased iron stores in BM• Serum iron and ferritin high• In acquired forms: Peripheral blood has hypochromic
cells which may be either normocytic or macrocytic• Common finding: Presence of sideroblast in BM
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Treatment
• For hereditary forms: 200 mg daily Pyridoxine• Frequent blood transfusion required in
unresponsive patients• Desferrioxamine given i.v or s.c• Oral Vit. C
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Hemolytic anemias
• Reduced life span of erythrocytes• Imbalance between rate of destruction and
rate of production• Presence of both genetic and acquired
disorders
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Aetiology of Sickle cell anemia
• They have a different form of Hb (Hb S)• Patients with homozygous Hb S develop many
problems including anemia• Sickle cell trait is usually asymptomatic• The offspring from a father with a trait and a mother
with a trait has a 1 in 4 chance of having sickle cell disease
•
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Aetiology of Thalassaemias
• No alpha chain production or reduced production of a chain
• Heterozygotes are symptomless
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Aetiology of G6PD deficiency
• Large variants of G6PDdeficiency• It is an enzyme involved in the production of
reduced glutathione
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Pathophysiology of Sickle cell disease
• Membrane of red cells containing Hb S is damaged (lead to IC dehydration)
• Polymerization of Hb S occurs when the patients blood is deoxygenated
• These two processes lead to crescent-shaped cells (known sickle cell)
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Pathophysiology of Sickle cell disease (contd…)
• Sickle cells are less flexible than normal cells• This leads to local tissue hypoxia• Anemia results from an increased red cell
destruction
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Pathophysiology of Thalassemia
• Reduced or absent production of globin beta chain• Leads to relative excess of alpha chain, when
unpaired become unstable and precipitate in red cell precursors
• Ineffective erythropoiesis• In alpha thalassemia, deficiency of alpha chain leads
to an excess of beta or gamma chains
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Pathophysiology of Thalassemia (contd…)
• Erythropoiesis is less affected but Hb produced is unstable when the cells are in circulation and precipitate as the cells grow older
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Pathophysiology of G6PD deficiency
• Essential for the production of reduced form of NADPF in RBC
• NADPH is needed to keep gluthathione in reduced form
• Glutathione helps RBC deal with oxidative stress
• In G6PD deficiency Hb becomes oxidised and Heinz bodies are form
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Clinical manifestations
• Malaise• Fever
Abdominal pain• Dark urine• Jaundice
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Clinical manifestations of Sickle cell anemia
• Chronic anemia, arthralgia, fatigue, splenomegaly. Crisis precipitated by infection, fever. Dehydration, hypoxia or acidosis. Severe pain is a common feature.
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Clinical manifestations of thalassemia
• Causes Erythropoietin production to increase andresulst in expansion of BM
• Bone deformity and growth retardation• Spleen becomes enlarged
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Clinical manifestations of G6PD deficiency
• Two forms• This form is self-limiting
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Treatment
• Sickle cell anemia: prophylactic antibiotics (Penicillin V 250 mg b.d), pneumococcal vaccine, hydroxyurea is effective.
• Thalassemia: transfusion, desferroxamine and deferiprone
• G6PD deficiency: causative oxidising agent stopped and general supportive measures adopted. No specific drug treatment for this disorder