According to WHO criteria, anemia is defined as blood hemoglobin concentration <13 g/dL or hematocrit <39% in adult males and Hb <12g/dL or hematocrit <37% in adult females. It can be classified in many ways.

Classification Of Anemia-

Based on mean corpuscular value it can be of following types:

1) Microcytic: defined by MCV <80 fl

2) Normocytic: defined by MCV 80-100 fl (normal) 3) Macrocytic: defined by MCV >100 fl

Causes:

A) Microcytic anemia:

1) Defect in the heme synthesis:
• Iron deficiency anemia (late)
• Anemia of chronic disease
• Sideroblastic anemia

2) Defect in the globin chains:
• Thalassemia

B) Normocytic anemia:

1) Non hemolytic (low reticulocyte index)
• Iron deficiency anemia (early)
• Aplastic anemia
• Chronic kidney disease

2) Hemolytic (high reticuloyte index)
a. Extrinsic:
• Microangiopathic (eg: thrombus)
• Macroangiopathic(eg: mechanical heart valve)
• Infection
• Autoimmune
b. Intrinsic:
i. Enzyme defect:
• G6PD deficiency
• Pyruvate kinase deficiency
ii. Membrane defect:
• Hereditary spherocytosis
• Paroxysmal nocturnal hemoglobinuria
iii. Hemoglobinopathies:
• Sickle cell disease
• HbC disease

C) Macrocytic anemia:

1) Megaloblastic
a) Defective DNA synthesis:
• Folate deficiency
• Vitamin B12 deficiency
• Orotic aciduria

b) Defective DNA repair:
• Fanconi anemia

2) Non megaloblastic
• Diamond Blackfann syndrome
• Liver disease
• Alchoholism
• 5’ Flurouracil

Microcytic hypochromic anemia


Iron Deficiency anemia:


Mechanism of iron absorption in body:
Iron is consumed in heme(animals derived) and non heme(vegetables derived) forms, among which heme form is readily absorbed in the duodenum. The enterocytes in the duodenum then transfer the iron into the bloodstream with the help of transferrin via the ferroportin channels.
Then, from the bloodstream, iron is taken into the liver and bone marrow macropages for storage from where it further takes part in the process of heme synthesis. The stored intracellular iron is bound to a molecule known as Ferritin which futher protects the iron from forming free radicals via the FENTON reaction.


Causes:
• Chronic bleeding (GI loss, menorrhagia)
• Increased demand (pregnancy)
• Malnutrition and breastfeeding infants ( breast milk is devoid of Iron)
• Gastrectomy ( decreased acid level Fe2+ state is converted to Fe3+ state which leads to decreased absorption)
• Hookworm infestation
• GI malignancies and polyps

Stages of iron deficiency:
1) Stage of storage depletion: decreased ferritin, increased TIBC
2) Stage of depletion of serum iron: decreased sr. iron, decreased % saturation
3) Normocytic anemia: bone marrow tries to compensate by production of normal sized RBCs but in less number
4) Microcytic hypochromic anemia: bone marrow gets exhausted and produces RBCs of smaller size and fewer in number

Symptoms/signs:
• Easy fatigability
• Shortness of breath
• Pica eating
• Conjuctival pallor
• Spoon nails (koilonychia)
• Glossitis, cheilosis
• Headache and lightheadedness
• Associated with Plummer Vinson Syndrome (triad of atrophic glossitis, esopgaheal webs and Iron deficiency)

Presents as Iron deficiency anemia, dysphagia and beefy red tongue

Lab findings:
• CBC (decreased Hb% levels)
• Iron profile:
o Ferritin (decreased)
o TIBC (increased)
o Sr. Iron (decreased)
o % saturation (decreased)
• PBS: microcytic hypochromic RBCs with increased RDW (red cell distribution width)
• Increased free erythrocyte protoporphyrin ( heme= iron+protoporphyrin)

Treatment:

Oral iron supplementation (Ferrous sulphate)

Nutritional supplementation of iron rich diets

Treatment of underlying cause

Contributor- Dr. Bidhata Rayamajhi

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