Iron Deficiency Anemia: Symptoms, Causes, Treatment & Nursing Care

Iron deficiency anemia is a state in which the bone marrow runs out of usable iron and the resulting erythrocytes are too small (microcytic) and too pale (hypochromic) to deliver adequate oxygen. Iron sits at the centre of haemoglobin synthesis, mitochondrial function, neurotransmitter production and immune cell activity, so deficiency injures organ systems beyond the red cell mass and explains why patients describe disproportionate fatigue, exercise limitation and cognitive fog before haemoglobin frankly drops.

Body iron flows in a tight loop. Roughly 1-2 mg is absorbed daily from a Western diet through the duodenum and proximal jejunum, transferrin shuttles it to erythroblasts and storage sites, and macrophages recycle iron from senescent red cells back to plasma. There is no regulated excretion route, so deficiency develops only when intake or absorption fails to keep pace with loss. In iron-replete settings the dominant losses are menstrual and gastrointestinal; in low-income regions hookworm and dietary inadequacy dominate.

Clinicians use a staged framework: depletion of stores (low ferritin, normal haemoglobin), iron-deficient erythropoiesis (low ferritin, low transferrin saturation, still-normal haemoglobin) and overt iron deficiency anemia (low haemoglobin with microcytic indices). Catching the first two stages avoids unnecessary anaemia and makes the search for an underlying cause cleaner; waiting until the haemoglobin drops only adds urgency without adding diagnostic clarity.

Bedside language sometimes lumps every low haemoglobin under “anaemic”, but the management split between mild outpatient work-up and decompensated transfusion-dependent disease is sharp. Map the patient onto stage and severity in seconds; it dictates whether you watch, treat orally, escalate to IV iron or transfuse.

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Two pitfalls to flag early. A “normal” ferritin (50-100 ng/mL) with low transferrin saturation in an inflamed patient still indicates functional iron deficiency and warrants treatment, not reassurance. And the long-running emphasis on a ferritin under 12-15 ng/mL has been superseded—the British Society for Haematology and BSG endorse a 30 ng/mL threshold to capture deficiency before haemoglobin falls and avoid under-diagnosis in pre-menopausal women and pregnancy.

Symptoms are non-specific and often pre-date frank anaemia by months. Patients describe creeping fatigue that does not match their workload, breathlessness on stairs they used to climb without thought, dizziness on standing and a curiously familiar headache pattern. A structured nursing assessment that asks about diet, periods, stool colour, exercise tolerance and pica catches the diagnosis sooner than complaint-led intake alone.

Common adult presentation

• Persistent fatigue with reduced exercise tolerance—an early exercise intolerance often arrives before pallor.
• Exertional shortness of breath and palpitations as compensatory cardiac output rises.
• Headache, dizziness and occasional syncope—worse on standing or after meals.
• Cognitive slowing and reduced concentration that the patient may attribute to ageing, perimenopause or stress.
• Diffuse hair shedding, brittle nails, koilonychia (spoon-shaped nails) and angular cheilitis at the corners of the mouth.
• Smooth, sore tongue with loss of papillae (atrophic glossitis) and a burning quality.
• Pica—craving non-food substances (ice, starch, raw rice, soil)—is highly suggestive when present.
• Restless legs, particularly when ferritin sits under 50 ng/mL.
• Heavy or prolonged menstrual flow, post-menopausal vaginal bleeding, or any change in stool colour, frequency or melaena should be probed actively.

Examination clues

• Conjunctival pallor and pale palmar creases—useful but insensitive at higher haemoglobin values; never substitute for laboratory confirmation.
• Resting tachycardia, soft systolic flow murmur and warm peripheries when anaemia is moderate-to-severe.
• Glossitis, angular cheilitis and koilonychia in chronic disease.
• Abdominal examination targeting tenderness, masses, hepatosplenomegaly and rectal examination when occult bleeding is suspected.
• Pelvic and obstetric history in pre-menopausal women; document menstrual quantification (sanitary product changes per day, flooding, clots, days of bleeding).

When the script breaks

Older adults often present with isolated falls, decompensation of heart failure, fresh angina or worsening cognition rather than the textbook fatigue triad. Patients with longstanding mild IDA may attribute symptoms to chronic fatigue syndrome or sleep apnea for years; a single CBC plus ferritin reorders the differential. Endurance athletes can develop sport-related iron loss through gut bleeding, intravascular haemolysis and sweat losses, with ferritin falling well before haemoglobin.

Aetiology shapes the work-up, the conversation and the surveillance plan. Group causes by mechanism: blood loss (most adults), inadequate intake (mostly children, vegans without supplementation), malabsorption (celiac disease, autoimmune atrophic gastritis, post-bariatric, H. pylori, IBD), increased demand (pregnancy, lactation, growth spurts) and combinations. The dominant mechanism in iron-replete settings is chronic, slow gastrointestinal or menstrual blood loss—rarely a single dramatic bleed.

Chronic blood loss

• Heavy menstrual bleeding—use a structured assessment of menorrhagia; consider uterine fibroids, adenomyosis and endometriosis.
• Upper GI loss: peptic ulcer disease, erosive gastritis (NSAID-, aspirin-, alcohol- or stress-related), reflux esophagitis, gastric or oesophageal cancer, vascular ectasia.
• Lower GI loss: colorectal cancer and adenomatous polyps, angiodysplasia, diverticular disease, Crohn disease, ulcerative colitis, haemorrhoids (rarely a sufficient explanation alone).
• Drug-driven loss: chronic aspirin, ibuprofen or naproxen, anticoagulation with warfarin, apixaban or rivaroxaban.
• Tropical infection: hookworm (Necator americanus, Ancylostoma duodenale), schistosomiasis—especially in returning travellers and migrants.
• Frequent blood donation, repeated phlebotomy, intravascular haemolysis (mechanical valves, march haemoglobinuria) and athletic gut microbleeding.

Malabsorption

• Coeliac disease—routine screen with anti-TTG IgA plus total IgA in any unexplained IDA; villous atrophy starts in the duodenum where iron is absorbed.
• Autoimmune atrophic gastritis—loss of gastric acid impairs iron and vitamin B12 absorption; often clusters with autoimmune Hashimoto thyroiditis and hypothyroidism.
• Helicobacter pylori—chronic infection blunts iron absorption and predisposes to ulceration.
• Bariatric surgery (Roux-en-Y, sleeve gastrectomy)—reduced acid plus duodenal bypass disables iron uptake.
• Long-term proton-pump inhibitors (omeprazole, pantoprazole) and high-dose H2 blockers reduce ferric iron solubilisation.
• Inflammatory bowel disease—both active inflammation (ferroportin downregulation) and intestinal blood loss contribute.

Inadequate intake or increased demand

• Restrictive diets without supplementation (vegan, vegetarian, fad-restriction)—plant non-haem iron is far less bioavailable than haem iron.
• Cow’s milk excess in toddlers (>500 mL/day) blocks iron absorption and is a classic preschool cause.
• Pregnancy and lactation—demand rises substantially through gestation; inadequate replacement leads to maternal IDA and infant store depletion.
• Growth spurts in adolescence, particularly in menstruating teenagers.
• Endurance training, repetitive impact (foot-strike haemolysis) and high-altitude training.

Most laboratories run a structured workflow: CBC indices identify a microcytic anaemia, ferritin confirms iron deficiency, transferrin saturation rescues the inflamed phenotype, and a small panel of additional tests targets the underlying mechanism. Resist the urge to over-order panels of zinc, copper, hair mineral analyses or unrequested haemoglobin electrophoresis—they generate noise and delay the search for the cause.

Core biochemistry

• Complete blood count—microcytic (MCV <80 fL), hypochromic (MCH <27 pg) anaemia with elevated RDW (>14.5%); platelets often modestly elevated as a reactive thrombocytosis.
• Serum ferritin—the single most useful test; below 30 ng/mL confirms deficiency in adults without inflammation.
• Iron studies—serum iron is low, transferrin (or TIBC) is high, transferrin saturation falls below 20%; soluble transferrin receptor adds value when ferritin is unreliable due to inflammation.
• Reticulocyte count—low or normal pre-treatment; reticulocytosis appears within 5-7 days of effective iron therapy.
• Peripheral blood film—microcytic, hypochromic red cells with anisopoikilocytosis, elliptocytes (pencil cells) and target cells when severe; pre-empt the need for haemoglobinopathy review.
• Vitamin B12 and folate—co-deficiency is common, particularly in coeliac disease, autoimmune gastritis and the post-bariatric population (B12, folate).
• Comprehensive metabolic panel—a baseline metabolic panel with creatinine identifies anaemia of CKD and supports IV iron dose calculation.
• Liver function tests—a liver panel screens for chronic liver disease as a confounder of ferritin interpretation.
• Coeliac serology—anti-tissue transglutaminase IgA with total IgA on the same draw as ferritin in any unexplained IDA.
• Faecal occult blood / FIT—a faecal immunochemical test raises pre-test probability of GI loss; do not use a normal FIT to override clinical risk profile when symptoms or risk factors warrant endoscopy.
• Faecal calprotectin—suspect IBD when there is diarrhoea, weight loss or family history; combine with imaging and colonoscopy.

Imaging and endoscopy

Bidirectional endoscopy (esophagogastroduodenoscopy and colonoscopy) is recommended by the British Society of Gastroenterology and American College of Gastroenterology in all men and post-menopausal women with newly identified IDA, and in pre-menopausal women whose anaemia is disproportionate to menstrual loss, who have GI symptoms, family history of colorectal cancer, or who fail oral iron therapy. Capsule endoscopy and CT enterography target the small bowel when bidirectional endoscopy is unrevealing.

Common interpretation traps

• Ferritin elevated by inflammation: infection, malignancy, chronic kidney disease, autoimmune disease and obesity raise ferritin even when iron stores are empty—lean on transferrin saturation under 20% and clinical context.
• Recent blood transfusion: transient rise in haemoglobin that does not reflect underlying iron status; recheck CBC and ferritin 4-6 weeks later before deciding on therapy.
• β-thalassemia trait: microcytic anaemia with disproportionately low MCV relative to mild Hb drop, normal ferritin and high red cell count—confirm with haemoglobin electrophoresis, do not chase iron repletion.
• Anaemia of chronic disease: ferritin normal or high, TSAT low, MCV usually normocytic; treat the underlying disease and consider IV iron when functional deficiency is severe.

The pragmatic chain ward and primary-care teams can run from a single low haemoglobin:

1. Confirm iron deficiency. Ferritin under 30 ng/mL clinches it; ferritin 30-100 ng/mL with TSAT under 20% in inflammation also qualifies.
2. Estimate severity and stability. Hb, postural vitals, presence of bleeding, comorbidity (cardiac, renal, pregnancy)—anyone with active bleeding, haemodynamic instability or Hb under 70 g/L (under 80 g/L with cardiac comorbidity) crosses the transfusion threshold immediately.
3. Ask where the iron went. Menstrual history, dietary screen, NSAID/aspirin/anticoagulant audit, GI symptom review, post-bariatric anatomy, donor history, athletic profile, ethnicity and travel.
4. Choose oral or IV iron. Default to alternate-day oral elemental iron 60-120 mg in stable adults; switch to IV iron at 4-6 weeks of failed response or earlier when the patient meets one of the standard pivot indications below.
5. Match the work-up to risk. Bidirectional endoscopy with celiac serology in adult men and post-menopausal women; structured menstrual evaluation in pre-menopausal women; coeliac serology and H. pylori testing in any unexplained or relapsing case.
6. Recheck CBC at 2-4 weeks, then 4-6 weekly until haemoglobin normalises; document the 2 g/dL by 3-4 week response benchmark in the notes.
7. Continue oral iron 3 months after normalisation until ferritin reaches 50-100 ng/mL, then plan a long-term loss/absorption strategy rather than a one-off course.

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Oral iron — first-line for most adults

Ferrous sulfate, ferrous fumarate and ferrous gluconate deliver elemental iron at 20-30% of the salt mass. The pragmatic adult target is 60-120 mg of elemental iron once daily on alternate days—evidence from the Stoffel trials shows that consecutive-day dosing transiently raises hepcidin and blunts absorption of the next dose, while alternate-day single-morning dosing improves fractional absorption with fewer GI side effects.

• Standard adult prescription: ferrous sulfate 200 mg (≈65 mg elemental) once on alternate mornings, taken on an empty stomach with vitamin C-rich juice when tolerated.
• Once-daily dosing remains acceptable when total monthly absorption matters more than minimising symptoms (severe deficiency, pregnancy with limited time to delivery).
• Liquid iron drops for paediatric, post-bariatric or pill-averse patients.
• Avoid co-administration with calcium, antacids, dairy, coffee, tea or PPI within 2 hours; separate from levothyroxine by at least 4 hours.
• Side effect mitigation: reduce frequency, switch salt, try liquid form, take with food (accept lower absorption) before declaring intolerance; warn patients about black stools and metallic taste.

Intravenous iron — second line, with intent

Modern IV iron preparations (ferric carboxymaltose, ferric derisomaltose, iron sucrose, low-molecular-weight iron dextran) are safer than older high-molecular-weight dextran and now permit large single-dose repletion in 15-60 minutes. Indications—per BSG, ASH and ECCO guidance—are well defined; treat them as standard rather than rescue.

• Failed oral iron: no Hb rise of 1 g/dL after 4-6 weeks of adherent therapy with adequate dosing.
• Intolerance: nausea, abdominal pain, constipation or diarrhoea unresolved by alternate-day dosing or salt change.
• Ongoing blood loss outpacing absorption (heavy menorrhagia awaiting gynaecology, recurrent GI bleeding awaiting endoscopy/surgery).
• Malabsorption: active IBD, post-bariatric, atrophic gastritis with chronic PPI exposure.
• Chronic kidney disease—particularly on dialysis or on erythropoiesis-stimulating agents.
• Heart failure with iron deficiency—FAIR-HF and AFFIRM-AHF show symptomatic and rehospitalisation benefits from ferric carboxymaltose even in non-anaemic patients.
• Late pregnancy (after 13-14 weeks) with intolerance, severe anaemia or insufficient time to deliver oral repletion before term.
• Pre-operative anaemia when surgery is within weeks and rapid optimisation reduces transfusion needs.

Red blood cell transfusion

Transfusion treats the symptom of anaemia, not the underlying iron deficiency. AABB 2023 endorses a restrictive haemoglobin threshold of 70 g/L (7.0 g/dL) for haemodynamically stable hospitalised adults, and 80 g/L (8.0 g/dL) in adults with pre-existing cardiovascular disease, undergoing orthopaedic surgery or cardiac surgery. Symptomatic anaemia, ongoing bleeding or haemodynamic instability override these numbers. Always pair transfusion with iron repletion to address the underlying deficit; blood transfusion administration protocols (consent, identity check, baseline observations and post-transfusion observation) should be followed without shortcut.

Treat the cause, not just the lab

• Stop or substitute culprit drugs (NSAIDs, aspirin, unmonitored anticoagulants) where clinically reasonable.
• Eradicate H. pylori with triple or quadruple therapy when positive.
• Refer for gynaecology evaluation and consider tranexamic acid or hormonal options for menorrhagia.
• Initiate gluten exclusion when coeliac serology and biopsy confirm disease.
• Endoscopic clipping, coagulation or surgical resection for an identified bleeding lesion.

Pregnancy and the antenatal period

Iron demand rises through gestation; maternal IDA increases the risk of preterm birth, low birth weight, postpartum haemorrhage tolerance reduction and infant store depletion. WHO defines anaemia in pregnancy as haemoglobin under 110 g/L in the first and third trimester and under 105 g/L in the second; UK and US guidance similarly screen at booking and again in the second and third trimester. Oral iron is first line from booking; intravenous iron is appropriate from the second trimester for intolerance, severe anaemia or insufficient time to delivery. The U.S. Preventive Services Task Force’s current statement notes insufficient evidence to recommend universal pregnancy screening in low-risk asymptomatic adults but explicitly endorses screening when anaemia or risk factors are present.

Children and adolescents

IDA in toddlers usually reflects cow’s milk excess and dietary inadequacy; treat with oral iron drops, dietary diversification and a 500 mL daily milk cap. Iron deficiency without overt anaemia in this age group is associated with adverse cognitive and motor developmental outcomes—treat even when haemoglobin is borderline. Adolescents, particularly menstruating teenagers and athletes, tolerate alternate-day iron well; anchor on ferritin under 30 ng/mL with symptomatic fatigue rather than waiting for haemoglobin to fall.

Chronic kidney disease and dialysis

KDIGO 2012 endorses an iron status target of ferritin above 100 ng/mL with TSAT above 20% before considering ESA escalation; many haemodialysis units use IV iron preferentially because of impaired absorption and ongoing dialyser losses. Pair IV iron with erythropoiesis-stimulating agents and monitor phosphate when ferric carboxymaltose is used repeatedly.

Inflammatory bowel disease

ECCO recommends IV iron as first-line for moderate-to-severe IBD-related anaemia, in active disease, in patients intolerant of oral iron, and when ferritin is under 100 ng/mL with TSAT under 20%. Oral iron may aggravate gut inflammation and is poorly absorbed when active disease is present.

Heart failure

FAIR-HF and AFFIRM-AHF demonstrated symptomatic and rehospitalisation benefit from intravenous ferric carboxymaltose in heart failure patients with iron deficiency (ferritin under 100 ng/mL, or 100-300 ng/mL with TSAT under 20%) regardless of haemoglobin. ESC 2023 and AHA/ACC 2022 guidelines incorporate IV iron repletion as a quality marker in iron-deficient patients with reduced ejection fraction.

Pre-operative optimisation

Identify and correct IDA at least 4-6 weeks before elective major surgery to reduce transfusion exposure. Use IV iron when oral therapy will not deliver in time; expect a 1.5-2 g/dL Hb rise within 2-3 weeks of single-dose ferric carboxymaltose 1000 mg.

• Lab cadence: CBC plus reticulocyte count at 2-4 weeks of oral iron, then 4-6 weekly until haemoglobin normalises; recheck ferritin at 3 months to confirm replenishment. Post IV iron, recheck CBC at 4 weeks and ferritin at 8-12 weeks (interpret with caution because of acute-phase ferritin rise).
• Drug-interaction guard: separate iron from levothyroxine, fluoroquinolones, tetracyclines, methyldopa, bisphosphonates and PPIs by at least 2-4 hours; reconcile via structured medication reconciliation on every admission and discharge.
• Transfusion stewardship: avoid transfusing for IDA without source control or iron repletion plan—transfusion does not refill stores.
• IV iron safety: consent must include hypersensitivity risk (rare with modern preparations), Fishbane reaction (transient pruritus, flushing, chest tightness without true anaphylaxis), and the risk of transient hypophosphataemia with ferric carboxymaltose; a baseline phosphate and symptom-directed recheck after repeat dosing is standard. Have anaphylaxis kit, oxygen, suction and emergency drugs (including hydrocortisone) immediately available during infusion.
• Adherence and counselling: warn about black stools, mild metallic taste, transient nausea; agree a fixed routine (e.g. alternate mornings 30 minutes before breakfast) the patient can sustain.
• Co-management: chase the cause—gynaecology for menorrhagia, gastroenterology for endoscopy and IBD, dietitian for vegan or post-bariatric diets, primary care for surveillance.
• Statin and cardiac comorbidity: manage atorvastatin and antiplatelet/anticoagulant therapy thoughtfully when GI loss is suspected; bridging or temporary withdrawal needs senior input rather than a unilateral decision.
• Documentation: record diagnosis with mechanism, current Hb, ferritin, treatment plan, expected response and next CBC date in a single line for handover via structured nursing handoff; specify when the GI work-up is due so it does not lapse.
• Specialist referral: haematology for refractory IDA, pancytopenia, suspicion of myelodysplasia, paediatric or pregnancy complications, and any patient where bidirectional endoscopy is unrevealing despite recurrent IDA.

Vital signs

• Heart rate via manual pulse assessment—watch for resting tachycardia and new arrhythmia, especially in older adults.
• Blood pressure with a postural set when symptomatic—postural drop suggests acute volume loss.
• Respiratory rate and SpO₂—hypoxia is unusual unless anaemia is severe or coexisting cardiopulmonary disease.
• Temperature—fever may indicate infection driving an inflammatory ferritin rise or a complication of treatment.
• Capture trends with structured vital sign monitoring rather than single snapshots.

Targeted assessment

• Conjunctival pallor, palmar crease pallor, glossitis, angular cheilitis, koilonychia.
• Capillary refill and peripheral perfusion as adjunct markers of severity.
• Stool colour, frequency and presence of melaena or fresh PR bleeding.
• Menstrual diary, sanitary product change frequency, clot size and post-coital or intermenstrual bleeding.
• Weight, peripheral oedema, exercise tolerance and any new chest pain or weakness.
• Cognition and mood baseline with structured head-to-toe assessment on admission.

Red flags requiring escalation

• Fresh haematemesis, melaena or large-volume PR bleeding with tachycardia or postural drop.
• New or worsening angina, breathlessness at rest or pulmonary oedema.
• Hb <70 g/L with symptoms, or <80 g/L with cardiac comorbidity.
• Suspected anaphylaxis or severe Fishbane reaction during IV iron infusion (urticaria, hypotension, dyspnoea, chest tightness)—stop the infusion, escalate, manage per anaphylaxis pathway.
• Pregnancy with Hb <70 g/L, breathlessness at rest, fetal growth concerns or active bleeding.
• Cold intolerance, profound fatigue, syncope or hypothermia in a frail patient who may also be hypothyroid—escalate sooner rather than later.

Untreated or under-treated

• Cardiovascular: demand-related angina, decompensated heart failure, atrial fibrillation, perioperative ischaemia.
• Pregnancy: preterm birth, low birth weight, increased maternal morbidity from bleeding, infant iron-deficiency anaemia and developmental impact.
• Cognitive and developmental: impaired attention, working memory and motor development in infants and toddlers; cognitive slowing in adults.
• Functional: reduced exercise capacity, restless legs syndrome, hair shedding, persistent fatigue.
• Underlying disease progression: missed colorectal cancer, untreated coeliac disease, untreated peptic ulcer or H. pylori—each compounds long-term morbidity.

From treatment

• Oral iron: GI upset, constipation, transient nausea, dark stools, dental staining with liquid forms, accidental paediatric iron overdose (a leading cause of paediatric poisoning fatalities).
• IV iron: extravasation skin staining, hypersensitivity (rare), Fishbane reaction, transient hypophosphataemia (especially with ferric carboxymaltose).
• Transfusion: alloimmunisation, volume overload, transfusion-associated lung injury, infection—use restrictive thresholds and pair with iron repletion to avoid recurrent transfusion dependency.
• Iron overload from over-zealous repletion in haemoglobinopathies or unrecognised hereditary haemochromatosis; check baseline studies before long courses.

Prevention is most useful in well-defined high-risk groups. Pregnancy, infancy, adolescence with menstruation, frequent blood donors, post-bariatric patients, dialysis patients, IBD cohorts and chronic NSAID users all benefit from structured supplementation strategies and surveillance rather than reactive treatment when haemoglobin tips into anaemia. Universal screening of asymptomatic non-pregnant adults is not endorsed by USPSTF, but case-finding remains appropriate when symptoms or risk factors arise. Counsel pregnant women, athletes and adolescents on dietary iron quality (haem iron from meat, fortified cereals, legumes plus vitamin C), and reinforce alternate-day low-dose supplementation in those at greatest risk.

Most adults achieve haemoglobin normalisation within 6-12 weeks of effective oral iron and ferritin replenishment within 3-6 months. IV iron delivers a faster trajectory—a 1.5-2 g/dL haemoglobin rise is typical within 2-3 weeks of a single 1000 mg ferric carboxymaltose infusion. Long-term outlook is dictated by the underlying cause: a treated source (resected polyp, healed ulcer, eradicated H. pylori, gluten exclusion, gynaecology intervention) closes the loop, while ongoing menstrual or GI loss without source control predicts relapse despite repeated repletion. Mortality directly attributable to IDA is low; morbidity and the missed-cancer signal in inappropriately reassured adults are where the real damage sits.

Subtle deterioration

The IDA patient who decompensates rarely arrives in florid shock. Watch the cumulative drift: a heart rate that has crept from 78 to 102 over three days, a persistent “off” feeling that the patient downplays, a ferritin trending down on outpatient bloods, and a stool diary that quietly admits to occasional dark stools. None alone triggers a rapid response, but pattern recognition reaches for the IV access, group-and-screen and senior review before the call.

Communication friction

Patients told they are “a bit anaemic” often interpret it as benign and miss the urgency of the GI work-up. Use lay framing—“we need to find where the iron is going, not just put it back”—and explicitly explain that bidirectional endoscopy looks for an early treatable cancer. Counter influencer-driven advice (mega-dose vitamin C, herbal blood tonics, denigration of medical iron) with calm physiology rather than confrontation.

Bedside checklist

• Confirm the iron schedule the patient can sustain—alternate mornings beats a perfect daily plan abandoned by week three.
• Audit interacting drugs and supplements: calcium, antacids, PPI, levothyroxine, fluoroquinolones, bisphosphonates.
• Set a clear next-step diary entry: when is the next CBC? Who is doing the colonoscopy? Has coeliac serology been added?
• Document dose, salt, brand, last Hb, last ferritin, last endoscopy result and any interacting drug introduced this admission for handover.

Initial bundle: ABCDE primary survey, IV access via large-bore peripheral cannulation, paired bloods (CBC, urea, group-and-screen, crossmatch when bleeding, coagulation, lactate, troponin if cardiac symptoms), structured specimen collection with documented timing, oxygen if SpO₂ <94%, withhold further antiplatelet/anticoagulant agents pending senior review, escalate to gastroenterology, obstetrics or cardiology by clinical context. Anchor transfusion at AABB thresholds, and continue iron repletion planning beyond the acute window so the patient does not bounce back.

These NCLEX-style clinical judgment practice items focus on the nursing priorities for this condition — recognise cues, escalate red flags, take safe action and evaluate outcomes (NCSBN Clinical Judgment Measurement Model) — through Priority FIRST, SATA, deterioration trends, multi-patient triage, ordered response, matrix matching and cloze completion on the topic of iron deficiency anemia diagnosis, alternate-day oral iron stewardship, IV iron triggers, transfusion thresholds and GI bleed escalation—matched to Clinical Judgment Measurement Model layering of cues before action.