IM9.1-17 | Anaemia — Practice Quiz

Correct. Serum ferritin is the most specific and sensitive marker of iron stores. A ferritin below 12 mcg/L confirms depleted iron stores and is diagnostic of IDA. In the absence of inflammation, a low ferritin alone is sufficient to diagnose IDA without further iron studies.

Serum ferritin < 12 mcg/L is diagnostic of iron deficiency. Serum iron is low, TIBC is elevated (> 400 mcg/dL), and transferrin saturation is < 16% in IDA. However, ferritin is an acute-phase reactant — in concurrent inflammation, ferritin may be falsely normal even in IDA; values up to 50 mcg/L may still represent IDA in inflammatory states.

While serum iron, TIBC, and transferrin saturation are all abnormal in IDA, serum ferritin below 12 mcg/L is the single most specific confirmatory test because it directly reflects body iron stores. Serum iron is subject to diurnal variation and acute changes; ferritin is the definitive store marker.

Correct. Anaemia of chronic disease (ACD) is characterized by a normocytic or mildly microcytic anaemia with low-to-normal serum iron, LOW TIBC (distinguishing it from IDA where TIBC is elevated), and NORMAL or ELEVATED ferritin. The pattern here — low iron, low TIBC, elevated ferritin — in the context of rheumatoid arthritis confirms ACD.

Iron studies pattern: IDA — low ferritin, high TIBC, low transferrin sat (<16%); ACD — normal/high ferritin, LOW TIBC, low-normal transferrin sat; thalassaemia trait — normal ferritin, normal TIBC, normal transferrin sat. The TIBC direction is the key discriminator between IDA and ACD.

The key distinguishing feature between IDA and ACD is TIBC: in IDA, TIBC is elevated (> 400 mcg/dL) because transferrin production increases; in ACD, TIBC is LOW because hepcidin-mediated inflammation suppresses transferrin synthesis. Ferritin is elevated in ACD (an acute-phase reactant) and depleted in IDA.

Correct. G6PD deficiency presents with episodic haemolytic crises triggered by infection, oxidant drugs, or fava beans. The negative Coombs test excludes autoimmune haemolytic anaemia. The tribal Odisha background and infection-triggered onset are classic for G6PD deficiency, the most common RBC enzyme defect in India, particularly prevalent in tribal and malaria-endemic regions.

Haemolytic anaemia is diagnosed by the triad: elevated indirect bilirubin, elevated LDH, and low or absent haptoglobin, with reticulocytosis. Coombs test differentiates immune (positive) from non-immune (negative) haemolysis. G6PD deficiency and sickle cell disease are the two most important hereditary haemolytic anaemias in India; G6PD is X-linked and most common in tribal populations and malaria-endemic zones.

Episodic haemolysis with dark urine after a triggering event (infection, oxidant drugs) with a NEGATIVE Coombs test in a patient from a tribal or malaria-endemic region strongly suggests G6PD deficiency. Autoimmune haemolytic anaemia would show a positive Coombs test. Thalassaemia intermedia is chronic, not episodic, and would present with splenomegaly and characteristic smear findings.

Correct. In macrocytic anaemia with neurological features (subacute combined degeneration of the cord), B12 deficiency must be confirmed BEFORE starting folic acid. If folic acid is given to a B12-deficient patient, it may correct the haematological findings but allow neurological damage to progress unabated — a dangerous trap. Serum B12 must be checked first.

Megaloblastic anaemia: macro-ovalocytes + hypersegmented neutrophils (>5% with 5 lobes or any with 6 lobes) on smear are pathognomonic. B12 deficiency causes BOTH haematological and neurological disease (subacute combined degeneration). Folate deficiency causes haematological changes ONLY. The folic acid trap: administering folic acid alone in B12 deficiency corrects the anaemia but worsens the neuropathy.

The neurological features (peripheral neuropathy, gait difficulty) point to B12 deficiency causing subacute combined degeneration of the cord — folate deficiency does NOT cause neurological disease. Critically, never prescribe folic acid for macrocytic anaemia without first checking serum B12, because folic acid corrects the blood picture but unmasks and worsens subacute combined degeneration in unrecognised B12 deficiency.

Correct. Beta-thalassaemia trait is characterised by a mild microcytic anaemia with a DISPROPORTIONATELY HIGH RBC count (Mentzer index = MCV/RBC < 13 here: 64/6.2 = 10.3), NORMAL or elevated ferritin, and normal TIBC — confirming adequate iron stores. The familial pattern confirms the autosomal inheritance. In contrast, IDA shows a low RBC count and depleted iron stores.

Thalassaemia trait is the second most common cause of microcytic anaemia in India after IDA. Distinguishing features: high RBC count, normal or high ferritin, normal TIBC, Mentzer index (MCV/RBC) < 13. Confirmation is by HPLC (HbA2 > 3.5% in beta-thalassaemia trait). Treatment is NOT iron — iron should not be prescribed unless concurrent IDA is proven.

The key discriminator between IDA and thalassaemia trait is the RBC count and iron studies: thalassaemia trait has a HIGH RBC count (>5.5 million/mcL) with microcytosis and NORMAL iron stores (normal ferritin, normal TIBC). The Mentzer index (MCV/RBC) < 13 suggests thalassaemia; > 13 suggests IDA. Giving iron therapy to a patient with thalassaemia trait is unnecessary and potentially harmful.

Correct. Current evidence supports a RESTRICTIVE transfusion strategy for stable non-cardiac surgical patients: transfuse when Hb falls below 8 g/dL, or if the patient is symptomatic (angina, hypotension, tachycardia attributable to anaemia). A pre-operative Hb of 8.1 g/dL in an asymptomatic patient does not require transfusion; the underlying cause of anaemia should be identified and treated first.

Transfusion thresholds: stable hospitalised patients — Hb < 7 g/dL (restrictive); post-cardiac surgery or high-risk cardiovascular disease — Hb < 8 g/dL. The patient's symptoms and haemodynamic status (not just the number) determine the need. Transfuse whole blood only in acute haemorrhage; packed red cells (PRBCs) are the component of choice for chronic anaemia.

A restrictive transfusion threshold (Hb < 8 g/dL, or symptomatic) is appropriate for most stable hospitalised patients including those undergoing elective orthopaedic surgery. There is no evidence that maintaining Hb > 10 g/dL improves outcomes in stable, asymptomatic patients. Transfusion carries real risks (infection, transfusion reactions, fluid overload) and should never be prescribed without a clear indication.

Correct. The Anaemia Mukt Bharat (AMB) programme, launched in 2018, is India's comprehensive anaemia prevention strategy covering six population groups including pregnant and lactating women. Under AMB, pregnant women receive daily iron-folic acid supplementation (180 tablets — one per day throughout pregnancy and 180 days postpartum). WIFS is specifically for adolescent girls and boys.

Anaemia Mukt Bharat (2018): six population groups, six interventions (IFA supplementation, deworming, fortified foods, dietary diversification, delayed cord clamping, behaviour change communication). Pregnant women — 180 tablets IFA (180 mg elemental iron + 0.5 mg folic acid). WIFS — weekly IFA for adolescent girls (100 mg iron + 500 mcg folic acid). Target: reduce anaemia prevalence by 3% per year.

Anaemia Mukt Bharat (AMB) is the umbrella programme launched in 2018 covering six beneficiary groups: children 6-59 months, children 5-9 years, adolescents 10-19 years, pregnant and lactating women, and women of reproductive age. WIFS (Weekly Iron Folic Acid Supplementation) is specifically for school-going and out-of-school adolescents. Antenatal IFA falls under AMB.

Correct. A pain crisis in sickle cell disease with Hb at baseline does NOT require transfusion. Transfusion in sickle cell disease increases viscosity and can worsen vaso-occlusion. The standard management of an uncomplicated painful crisis is hydration (IV fluids), analgesia (WHO pain ladder), oxygen if hypoxic (SaO2 < 95%), folic acid supplementation, and treatment of any precipitant. Transfusion is reserved for aplastic crisis, acute chest syndrome, splenic sequestration, or pre-operatively.

Sickle cell disease in India: most prevalent in tribal populations of Chhattisgarh, Jharkhand, Odisha, Maharashtra, and Gujarat. Indications for transfusion: aplastic crisis (Hb drop >2 g/dL below baseline + reticulocytopenia), splenic sequestration, acute chest syndrome, stroke. Hydroxyurea is a long-term disease-modifying agent (increases HbF), not used acutely.

In sickle cell disease, routine transfusion for pain crisis is NOT indicated when Hb is at or near baseline. Increasing Hb by transfusion raises blood viscosity and can paradoxically worsen vaso-occlusion. Transfusion is indicated for: aplastic crisis, acute chest syndrome, priapism, stroke, pre-operative preparation, or splenic sequestration. Exchange transfusion is used for stroke or acute chest syndrome, not routine pain crisis.

Correct. The anaemia of CKD is primarily a normocytic, normochromic anaemia caused by reduced erythropoietin (EPO) production by the failing kidneys. EPO is synthesised in peritubular fibroblasts and is the primary driver of erythropoiesis. As GFR declines below 30 mL/min, EPO production is progressively impaired. This is a hypo-proliferative anaemia (low reticulocyte count with normal iron stores).

Anaemia of CKD: normocytic, normochromic, hypo-proliferative (low RPI); begins at GFR < 60, significant at GFR < 30. Primary mechanism: EPO deficiency. Secondary contributors: iron deficiency (from GI blood loss, dialysis losses), folate loss (dialysis), shortened RBC lifespan from uraemic toxins. Treatment: correct iron stores first, then ESA (erythropoietin or darbepoetin) if Hb < 10 g/dL in symptomatic patients.

In CKD, the primary mechanism of anaemia is erythropoietin deficiency — the diseased kidneys cannot produce adequate EPO to stimulate bone marrow erythropoiesis. This results in a normocytic normochromic anaemia with a low reticulocyte count (hypo-proliferative pattern) and normal or elevated iron stores. Treatment is with erythropoiesis-stimulating agents (ESAs) once iron stores are optimised.

Correct. Conjunctival pallor is the single most sensitive and reproducible clinical sign for detecting anaemia on examination. Studies show sensitivity of approximately 70-80% for Hb < 9 g/dL. The palpebral conjunctiva lacks melanin and overlies a vascular bed that directly reflects haemoglobin concentration. Palmar crease pallor is specific but less sensitive and is affected by skin pigmentation.

The four sites for clinical pallor assessment in decreasing sensitivity: palpebral conjunctiva > tongue > palmar creases > nail beds. Conjunctival pallor: sensitivity ~70% for Hb < 9 g/dL. Palmar crease pallor: when the creases are as pale as the surrounding skin, Hb is almost certainly < 7 g/dL (high specificity). Assess all four sites; the conjunctivae should be everted gently for examination.

Among the four standard sites for pallor assessment (conjunctivae, palms, tongue, nail beds), conjunctival pallor is the most sensitive because the palpebral conjunctiva is non-pigmented and its vascular supply directly reflects systemic haemoglobin. Palmar crease pallor is highly specific when present (almost always means Hb < 7 g/dL) but less sensitive. Nail bed and tongue pallor are less reliable, especially in darker skin tones.