PA14.1-2 | Iron Deficiency Anaemia: Pathogenesis to Lab Diagnosis — Summary & Reflection

REFLECT

Case Challenge — Think Before You Scroll:

A 62-year-old retired farmer presents with 6-month fatigue and mild breathlessness on climbing stairs. He has no obvious symptoms of blood loss — no haematuria, no visible melaena, no vomiting blood. He eats a mixed diet and says he is fine. Examination: pallor, no koilonychia. Hb 9.2 g/dL, MCV 72 fL, MCHC 29 g/dL. Ferritin 8 ng/mL. Serum iron low, TIBC high.

What is your next step before starting oral iron?

Take a moment. Think about the patient's demographic — 62-year-old male. Think about the 'bucket' most likely to be implicated. Think about what you would miss if you simply wrote the iron prescription.

Answer:
This is occult GI blood loss until proven otherwise. A 62-year-old male with new-onset IDA and no dietary explanation has colorectal carcinoma in the differential — and colorectal carcinoma commonly bleeds occultly, without symptoms the patient notices. The workup:
1. Stool for occult blood (x3 samples)
2. Upper GI endoscopy (OGD): exclude peptic ulcer, gastric carcinoma, gastric antral vascular ectasia (GAVE), atrophic gastritis
3. Colonoscopy: exclude colorectal carcinoma, polyps, angiodysplasia — the highest-yield investigation in this age group

Only after GI malignancy is excluded (or identified and referred) do you start iron replacement. Writing a prescription for ferrous sulphate and sending this man home without endoscopy is a clinically dangerous error.

Rule: Unexplained IDA in any adult male or post-menopausal woman = GI malignancy excluded before iron therapy.

KEY TAKEAWAYS

Key takeaways from this SDL:

Epidemiology: IDA is the world's most prevalent nutritional deficiency. In India: 57% of women 15–49 years are anaemic (NFHS-5); the majority is IDA. The burden is greatest in reproductive-age women and children.

Four etiological buckets:
1. Decreased intake (vegetarian diet, infant nutrition, geriatric malnutrition)
2. Decreased absorption (post-gastrectomy, coeliac, atrophic gastritis, H. pylori, PPI overuse)
3. Increased loss — the most common cause; menorrhagia in reproductive women, GI blood loss in older adults
4. Increased demand (pregnancy, lactation, growth spurts)

Pathogenesis: Follows the three-stage model from SDL 1 (storage depletion → transport depletion → frank IDA). At stage 3: insufficient iron for haemoglobin synthesis → microcytic hypochromic RBCs. RDW rises early (before MCV drops).

Clinical features:
- General: pallor, fatigue, exertional dyspnoea, tachycardia
- IDA-specific: koilonychia, angular cheilitis, atrophic glossitis, pica (pagophagia), Plummer-Vinson syndrome (pre-malignant — post-cricoid dysphagia + oesophageal web)
- Paediatric: developmental delay, behavioural changes

Laboratory diagnosis:
- CBC: ↓ Hb, ↓ MCV, ↓ MCH, ↓ MCHC, ↑ RDW
- Iron studies: ↓ serum iron, ↑ TIBC, ↓ transferrin saturation (<15%), ↓ ferritin (<15 ng/mL) — gold standard if no inflammation
- Ferritin trap: false normal in inflammation → use sTfR
- Peripheral smear: microcytic, hypochromic, pencil cells, target cells, anisopoikilocytosis
- Reticulocyte index: low (production failure)
- Bone marrow: erythroid hyperplasia + absent Perls Prussian blue iron (rarely needed)

Management principles:
- Oral iron (ferrous sulphate 200 mg TDS with vitamin C) for 3–6 months AFTER Hb normalises
- IV iron when oral fails/malabsorption/CKD/IBD
- Monitor: retics rise day 3–5, Hb rise 1–2 g/dL at 4 weeks
- Failure to respond → wrong diagnosis or ongoing cause

The cardinal rule: IDA diagnosis is step one. Finding and eliminating the cause is the clinical imperative. Unexplained IDA in adult males and post-menopausal women = exclude GI malignancy before prescribing iron.

Looking ahead: SDL 3 covers the microcytic differentials — thalassemia trait, anaemia of chronic disease, and sideroblastic anaemia. SDL 4 is a dedicated peripheral smear workshop. The H3 capstone IV covers SDL 1+2+3 together — your IDA knowledge is the centre of that capsule.