Skip to content
MedExams

Iron studies and trace elements

13 DOH Abu Dhabi (HAAD) lab licensing practice questions on Iron studies and trace elements, part of Clinical Chemistry. The first 13 are below; the first 5 with answers and explanations (tap Show answer after you have chosen), the rest in Learn with a free account.

  1. Question 1 · Hard

    A 41-year-old woman with heavy menstrual bleeding and iron deficiency anemia received 1,000 mg of intravenous ferric carboxymaltose 3 days ago. Two months earlier she was given 2 red cell units. Her doctor now orders iron studies to check the response. Results: hemoglobin 99 g/L (9.9 g/dL), serum iron 58 µmol/L (324 µg/dL; reference 9-30), UIBC 6 µmol/L (34 µg/dL), ferritin 940 µg/L (reference 15-150) and CRP 3 mg/L (reference < 5). The serum is not hemolyzed. What is the transferrin saturation, and how is it best interpreted?

    1. A91%; points to hereditary hemochromatosis
    2. B9%; iron deficiency is still present
    3. C91%; raised by the recent iron infusion
    4. D91%; iron overload from the transfusion
    Show answer

    Answer: C · 91%; raised by the recent iron infusion

    TIBC = serum iron + UIBC = 58 + 6 = 64 µmol/L, and transferrin saturation = 58 / 64 x 100 = about 91%. In the days after an intravenous iron dose, iron released from the infused complex saturates transferrin, and ferritin rises as macrophages store the iron, so these results do not reflect body iron stores. Two red cell units add only about 400-500 mg of iron, far too little to cause overload, and hemochromatosis does not appear in a woman who was iron deficient days earlier. Iron studies are best repeated several weeks after the infusion, commonly about 4 weeks; until then the hemoglobin response is the useful measure.

    • A: Her iron deficiency and the infusion explain the result; hemochromatosis does not appear within days.
    • B: This divides the UIBC, not the serum iron, by the TIBC.
    • D: Two units add only about 400-500 mg of iron, far too little to cause overload.
  2. Question 2 · Medium

    Plasma zinc is falsely raised when the sample is:

    1. ADrawn from a patient with low albumin
    2. BHemolyzed or left unseparated for hours
    3. CTaken during an acute-phase response
    4. DCollected in a trace-element-free tube
    Show answer

    Answer: B · Hemolyzed or left unseparated for hours

    Red cells contain roughly ten times as much zinc as plasma, so hemolysis, or zinc leaking from cells during delayed separation, raises the result. Zinc is also easily picked up from rubber stoppers, needles and dust, so trace-element-free (royal blue top) tubes are used. Samples should be separated promptly. Low albumin and the acute-phase response both lower plasma zinc, which makes results hard to interpret in sick patients.

    • A: Most plasma zinc is bound to albumin, so low albumin lowers it.
    • C: The acute-phase response moves zinc into the liver and lowers plasma zinc.
    • D: Trace-element-free tubes prevent contamination rather than cause it.
  3. Question 3 · Hard

    A man who has taken high-dose zinc tablets daily for 2 years has anemia, neutropenia and numb feet. Serum copper is 3 µmol/L (19 µg/dL; reference 11-22 µmol/L), ceruloplasmin 0.08 g/L (reference 0.20-0.60 g/L) and 24-hour urine copper is low. The most likely cause is:

    1. ACopper deficiency from high zinc intake
    2. BMenkes disease
    3. CAcute inflammation lowering ceruloplasmin
    4. DWilson disease with copper overload
    Show answer

    Answer: A · Copper deficiency from high zinc intake

    High zinc intake induces metallothionein in intestinal cells; it binds dietary copper, which is then lost in the stool as the cells are shed, so copper absorption falls. The result is low serum copper, ceruloplasmin and urine copper, and the deficiency causes anemia, neutropenia and a myelopathy that can mimic vitamin B12 deficiency. Wilson disease also lowers ceruloplasmin and total serum copper, but urine copper is high because free copper is in excess. The same zinc effect is used on purpose to treat Wilson disease.

    • B: Menkes disease is an X-linked disorder that presents in infancy.
    • C: Ceruloplasmin is an acute-phase protein and rises, not falls, with inflammation.
    • D: Wilson disease raises 24-hour urine copper, which is low here.
  4. Question 4 · Medium

    Serum iron is 12 µmol/L (67 µg/dL) and TIBC is 60 µmol/L (335 µg/dL). What are the UIBC and transferrin saturation?

    1. AUIBC 48 µmol/L; saturation 20%
    2. BUIBC 72 µmol/L; saturation 17%
    3. CUIBC 48 µmol/L; saturation 25%
    4. DUIBC 48 µmol/L; saturation 80%
    Show answer

    Answer: A · UIBC 48 µmol/L; saturation 20%

    UIBC is the binding capacity still free: TIBC − iron = 60 − 12 = 48 µmol/L (268 µg/dL). Transferrin saturation is iron ÷ TIBC × 100 = 12 ÷ 60 × 100 = 20%. Many analyzers measure iron and UIBC directly and calculate TIBC as their sum. Ferritin is still needed to judge iron stores, because saturation also falls in inflammation.

    • B: Adding iron to TIBC gives 72, but UIBC is TIBC minus iron.
    • C: 25% comes from dividing iron by UIBC instead of by TIBC.
    • D: 80% is the unsaturated share (UIBC ÷ TIBC), not the saturation.
  5. Question 5 · Medium

    Serum iron from the same person is 24 µmol/L (134 µg/dL) at 08:00 and 15 µmol/L (84 µg/dL) at 18:00, with no iron tablets taken. Ferritin, TIBC and CRP are normal and unchanged. What best explains the difference?

    1. AAn acute-phase response by the evening
    2. BNormal diurnal variation in serum iron
    3. CIron absorbed from the midday meal
    4. DDeveloping iron deficiency over the day
    Show answer

    Answer: B · Normal diurnal variation in serum iron

    Serum iron has a marked daily rhythm, usually highest in the morning and lower in the late afternoon and evening, and it can differ by 30% or more within a day. Ferritin and TIBC are far more stable, which is why they did not change. For this reason iron studies are best drawn in the morning after an overnight fast and without recent iron tablets. A single serum iron should never be used alone to judge iron status.

    • A: CRP is normal, so there is no acute-phase fall in iron.
    • C: Food iron would raise, not lower, the evening result.
    • D: Iron deficiency develops over weeks, and ferritin is unchanged.
  6. Question 6 · Hard

    A child with beta-thalassemia major receives 2 red cell units every 4 weeks and is not yet on chelation. If each unit carries about 200 mg of iron, ignoring absorption and losses, the iron added to her body in a year is about:

    1. A0.52 g
    2. B2.6 g
    3. C5.2 g
    4. D52 g

    Answer and explanation in LearnFree account

  7. Question 7 · Easy

    The antioxidant enzyme glutathione peroxidase depends on which trace element?

    1. AManganese
    2. BCopper
    3. CZinc
    4. DSelenium

    Answer and explanation in LearnFree account

  8. Question 8 · Hard

    A 16-year-old with beta-thalassemia major on regular transfusions has serum iron 38 µmol/L (212 µg/dL) and UIBC 6 µmol/L (34 µg/dL). What is the transferrin saturation?

    1. A16%
    2. B119%
    3. C14%
    4. D86%

    Answer and explanation in LearnFree account

  9. Question 9 · Hard

    A regularly transfused adult with thalassemia has had a stable ferritin near 1,800 µg/L (ng/mL) for a year on chelation. During a febrile chest infection (CRP 160 mg/L) ferritin is 3,900 µg/L, with transfusions and chelation unchanged. The best interpretation is:

    1. ABody iron has doubled, so chelation has failed
    2. BInflammation has raised ferritin beyond the iron load
    3. CA hook effect has falsely raised the ferritin
    4. DHemolysis in the tube has released ferritin

    Answer and explanation in LearnFree account

  10. Question 10 · Medium

    Serum iron is requested, but the laboratory receives only K2EDTA plasma. A ferrozine iron result on it would be:

    1. AAccurate, as EDTA does not bind iron
    2. BFalsely high, from iron in the EDTA salt
    3. CFalsely low, as EDTA chelates the iron
    4. DFalsely high, as EDTA releases heme iron

    Answer and explanation in LearnFree account

  11. Question 11 · Easy

    In hereditary hemochromatosis, the iron study that usually becomes abnormal first is:

    1. AHemoglobin concentration
    2. BSerum ferritin
    3. CFasting transferrin saturation
    4. DTotal iron-binding capacity

    Answer and explanation in LearnFree account

  12. Question 12 · Medium

    Why is TIBC usually low in iron overload but high in iron deficiency?

    1. AFerritin competes with transferrin for added iron
    2. BLiver transferrin synthesis follows iron stores
    3. CExcess iron damages the TIBC reagent in the assay
    4. DTransferrin is lost in urine when iron is high

    Answer and explanation in LearnFree account

  13. Question 13 · Hard

    A laboratory calculates TIBC from transferrin. Transferrin is 2.0 g/L (200 mg/dL) and serum iron is 10 µmol/L (56 µg/dL). Each transferrin molecule binds two iron atoms, and 1 g/L of transferrin is 12.6 µmol/L. What is the transferrin saturation?

    1. AAbout 25%
    2. BAbout 80%
    3. CAbout 40%
    4. DAbout 20%

    Answer and explanation in LearnFree account

More Clinical Chemistry questions

Answer them one by one, keep your score and see your weak topics in Learn. Signed-out visitors try 25 per exam; sign in with Google to see them all.

Study Clinical Chemistry