define anaemia , its morphological classification and give shortnotes on iron deficency of anaemia , give the answer for the long answer question of physio so that i can achive full marks
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ANAEMIA - Definition, Morphological Classification & Iron Deficiency Anaemia
1. DEFINITION OF ANAEMIA
Anaemia is defined as a reduction of the total circulating red cell mass below normal limits. This reduction in red cell mass decreases the oxygen-carrying capacity of the blood, leading to tissue hypoxia.
In clinical practice, red cell mass is not directly measured. Instead, anaemia is diagnosed by reductions in:
- Haemoglobin (Hb) concentration
- Haematocrit (packed cell volume - ratio of packed RBCs to total blood volume)
- RBC count
These values are adjusted for age and sex. The WHO diagnostic thresholds are:
| Group | Hb threshold (g/dL) |
|---|---|
| Adult men | < 13 g/dL |
| Adult non-pregnant women | < 12 g/dL |
| Pregnant women | < 11 g/dL |
| Children 6-59 months | < 11 g/dL |
(Robbins & Cotran Pathologic Basis of Disease)
2. MORPHOLOGICAL CLASSIFICATION OF ANAEMIA
Morphological classification is based on three red cell characteristics assessed on peripheral blood smear and by red cell indices (MCV, MCH, MCHC, RDW):
Key Red Cell Indices:
| Index | Definition | Normal Range |
|---|---|---|
| MCV (Mean Cell Volume) | Average volume of a single RBC | 80-100 fL |
| MCH (Mean Cell Haemoglobin) | Average mass of Hb per RBC | 27-33 pg |
| MCHC (Mean Cell Hb Concentration) | Hb conc. per unit packed RBCs | 32-36 g/dL |
| RDW (Red Cell Distribution Width) | Coefficient of variation of RBC volume | 11.5-14.5% |
A. MICROCYTIC HYPOCHROMIC ANAEMIA (MCV < 80 fL)
Small, pale red cells - caused by defects in haemoglobin synthesis.
| Cause | Key Feature |
|---|---|
| Iron Deficiency Anaemia | Low serum iron, low ferritin, raised TIBC |
| Thalassaemias | Raised HbA2/HbF; target cells |
| Anaemia of Chronic Disease | Low iron, normal/raised ferritin |
| Sideroblastic Anaemia | Ring sideroblasts in marrow |
| Lead Poisoning | Basophilic stippling |
B. NORMOCYTIC NORMOCHROMIC ANAEMIA (MCV 80-100 fL)
Normal sized, normally coloured cells - diverse aetiology.
| Cause | Key Feature |
|---|---|
| Haemolytic Anaemias (hereditary spherocytosis, G6PD, sickle cell) | Reticulocytosis, splenomegaly |
| Aplastic Anaemia | Pancytopenia, hypocellular marrow |
| Acute Blood Loss | History of trauma/haemorrhage |
| Anaemia of Renal Failure | Low EPO, burr cells |
| Bone Marrow Infiltration | Leukoerythroblastic picture |
C. MACROCYTIC NORMOCHROMIC ANAEMIA (MCV > 100 fL)
Large red cells - caused by impaired DNA synthesis impairing nuclear maturation of erythroid precursors.
i) Megaloblastic (oval macrocytes + hypersegmented neutrophils):
- Vitamin B12 deficiency
- Folate deficiency
ii) Non-megaloblastic:
- Liver disease
- Hypothyroidism
- Alcohol excess
- Myelodysplastic syndrome
- Reticulocytosis (young large RBCs)
3. IRON DEFICIENCY ANAEMIA (IDA) - SHORT NOTES
Iron deficiency is the most common nutritional deficiency in the world and the most frequent cause of anaemia globally. It affects approximately 10% of people in higher-resource countries and 25-50% in lower-resource countries.
(Robbins Basic Pathology)
A. IRON METABOLISM (Essential Background)
- Total body iron: ~2.5 g (women) to 3.5 g (men)
- 80% is in functional pool: haemoglobin, myoglobin, iron-containing enzymes (catalase, cytochromes)
- 15-20% is in storage pool: ferritin and haemosiderin in macrophages of liver, spleen, bone marrow
- Transport: Iron is carried in plasma bound to transferrin (normally 33% saturated)
- Normal serum iron: ~120 µg/dL (men), ~100 µg/dL (women)
- Total iron binding capacity (TIBC): 300-350 µg/dL
- Daily loss: 1-2 mg/day (shed mucosal and skin cells)
- Absorption: Duodenum. Hepcidin (liver peptide) negatively regulates ferroportin - the master regulator of iron absorption
B. AETIOLOGY / CAUSES OF IDA
Iron deficiency develops when iron loss or demand exceeds absorption. Causes differ across populations:
1. Chronic Blood Loss (most important cause in high-income countries):
- GI tract: peptic ulcer, colonic carcinoma, hemorrhoids, hookworm infestation
- Genital tract: menorrhagia, metrorrhagia, endometrial cancer
2. Inadequate Dietary Intake (most important in low-income countries):
- Predominantly vegetarian diets (poor bioavailability of non-heme iron)
- Infants fed exclusively on milk
- Elderly, food-insecure populations
- Note: Heme iron (from meat) is 20% absorbable; non-heme iron only 1-2% absorbable
3. Increased Demand Not Met by Diet:
- Pregnancy (foetal demand)
- Infancy and adolescence (rapid growth)
4. Malabsorption:
- Coeliac disease
- Atrophic gastritis
- Post-gastrectomy states
- Helicobacter pylori gastritis
C. STAGES OF IRON DEFICIENCY (Sequential Development)
| Stage | What Happens | Lab Finding |
|---|---|---|
| Stage I - Storage Depletion | Iron stores exhausted | ↓ Serum ferritin; absent bone marrow iron (Prussian blue stain) |
| Stage II - Transport Depletion | Iron supply to marrow falls | ↓ Serum iron; ↑ Transferrin (TIBC); ↓ Transferrin saturation |
| Stage III - Functional Deficiency | Hb synthesis impaired | Microcytic hypochromic anaemia appears; ↑ ZPP (zinc protoporphyrin); ↑ EPO |
D. PATHOGENESIS
- Iron stores depleted → serum ferritin falls + bone marrow macrophages lose stainable iron
- Serum iron falls → transferrin (TIBC) rises as a compensatory response
- Insufficient iron for haem synthesis → erythroid precursors produce small RBCs with less haemoglobin
- Result: Microcytic hypochromic anaemia
- Impaired function of other iron-containing proteins: myoglobin (muscle fatigue), cytochromes (reduced immunocompetence), neurotransmitter enzymes (cognitive impairment)
E. CLINICAL FEATURES
General features of anaemia:
- Pallor (skin, conjunctiva, nails, tongue)
- Fatigue, weakness, listlessness
- Dyspnoea on exertion
- Tachycardia, palpitations
- Headache, poor concentration
Features specific to IDA (due to epithelial and enzyme effects):
- Koilonychia - spoon-shaped nails (flattening, thinning)
- Angular stomatitis / cheilosis - cracking at corners of mouth
- Glossitis - smooth, painful tongue
- Plummer-Vinson / Paterson-Kelly syndrome - post-cricoid dysphagia (upper oesophageal web) + IDA + glossitis
- Pica - compulsion to eat non-food items (dirt, clay, ice - pagophagia)
- Reduced immunocompetence
- Impaired work capacity and cognitive performance in children
F. LABORATORY FINDINGS
| Investigation | Finding in IDA |
|---|---|
| Haemoglobin | Decreased |
| MCV | Decreased (< 80 fL) |
| MCH | Decreased |
| MCHC | Decreased |
| RDW | Increased (anisocytosis) |
| Serum ferritin | Decreased (first to fall - best early marker) |
| Serum iron | Decreased |
| TIBC | Increased (compensatory) |
| Transferrin saturation | Decreased (< 16%) |
| Serum EPO | Elevated (but marrow response blunted) |
| Platelet count | Often elevated |
| Zinc protoporphyrin (ZPP) | Elevated |
| Bone marrow iron (Prussian blue) | Absent (gold standard) |
| Reticulocyte count | Low/normal (hypoproliferative) |
Comparison with other microcytic anaemias:
| IDA | β-Thalassaemia trait | Anaemia of Chronic Disease | Sideroblastic | |
|---|---|---|---|---|
| Serum iron | ↓ | N/↑ | ↓ | ↑ |
| TIBC | ↑ | N | N/↓ | ↓ |
| % Saturation | ↓ | N | ↓ | ↑ |
| Ferritin | ↓ | N/↑ | N/↑ | ↑ |
| HbA2 | N/↓ | ↑ | N | N |
(Henry's Clinical Diagnosis and Management by Laboratory Methods)
G. PERIPHERAL BLOOD SMEAR - MORPHOLOGY
The characteristic findings on peripheral smear:
- Microcytes - smaller than normal RBCs (< 6 µm)
- Hypochromia - increased area of central pallor (> 1/3 of cell diameter)
- Anisocytosis - variation in RBC size (raised RDW)
- Poikilocytosis - variation in shape: pencil cells (elongated elliptocytes), target cells
- Thrombocytosis - raised platelet count is common
Note: In early IDA, microcytosis appears first; hypochromia is a feature of more advanced disease.
(Robbins Basic Pathology)
H. TREATMENT
1. Identify and Treat the Underlying Cause (mandatory - as IDA is a symptom, not a disease in itself)
2. Oral Iron Replacement (first-line):
- Ferrous sulphate 200 mg TDS (provides ~60 mg elemental iron per tablet) - taken on an empty stomach for better absorption
- Duration: 3-6 months after Hb normalises to replenish stores
- Expected response: Reticulocytosis at 5-7 days; Hb rise ~1-2 g/dL per week
- Side effects: Nausea, constipation, dark stools
3. Parenteral Iron (IV/IM - when oral fails or is not tolerated):
- Malabsorption, non-compliance, inflammatory bowel disease
- Ferric carboxymaltose, iron sucrose, low molecular weight iron dextran
4. Blood Transfusion:
- Only in severe, symptomatic anaemia (Hb < 7 g/dL) or haemodynamic compromise
I. IMPORTANT POINTS TO REMEMBER (Examiner's Favourite!)
- IDA is a symptom of another underlying disease in well-nourished adults - always investigate the cause (e.g., colon cancer causing occult GI bleeding)
- Serum ferritin is the first parameter to fall and the best marker of early iron deficiency
- Bone marrow iron stain (Prussian blue) is the gold standard for diagnosing iron deficiency
- Persons often die with IDA but virtually never of it
- Platelet count is paradoxically elevated in IDA
- Microcytosis precedes hypochromia in the development of IDA
- IDA vs ACD: In ACD, ferritin is normal or raised (it is an acute phase protein) and TIBC is normal or low - opposite to IDA
Sources:
- Robbins & Cotran Pathologic Basis of Disease (10th ed.) - Chapter 14: Diseases of Red Cells
- Robbins & Kumar Basic Pathology - Chapter 10: Hematopoietic and Lymphoid Systems
- Henry's Clinical Diagnosis and Management by Laboratory Methods - Chapter 33
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