Iron Storage and Recycling — MCQs

10 questions

All of the following decrease in iron deficiency anemia except:

Iron metabolism and regulation are important for RBC precursor cells. Which of the following helps in the regulation of iron metabolism but is not specific for iron?

Hepcidin inhibits which of the following?

What is the normal range of ferritin levels in adult males?

Which of the following are characteristic laboratory findings in Iron Deficiency Anemia (IDA)? 1. Low serum ferritin 2. Low transferrin saturation 3. Low serum iron 4. Increased TIBC

Why is blood stored in citrate-phosphate-dextrose considered more beneficial for hypoxic patients compared to blood stored in acidic-citrate-dextrose?

What does hepcidin inhibit?

Which of the following are blood values of Iron Deficiency Anaemia ? 1. Serum iron is less than 30 mg/100 mL 2. Total iron binding capacity is less than 400 µg/mL 3. Percentage saturation is 10% or less 4. Serum ferritin is below 30 µg/mL Select the correct answer using the code given below :

All are increased in IDA except

Q10

According to the WHO criteria, anaemia in infants of 6 months of age is defined as haemoglobin less than:

Iron Storage and Recycling Indian Medical PG Practice Questions and MCQs

Question 1: All of the following decrease in iron deficiency anemia except:

A. Serum iron
B. Ferritin
C. TIBC (Correct Answer)
D. Transferrin saturation

Explanation: ***TIBC*** - In **iron deficiency anemia**, the body attempts to maximize iron absorption and transport, leading to an **increase** in **Total Iron Binding Capacity (TIBC)** [1]. - TIBC reflects the amount of **transferrin** available to bind iron; more transferrin is produced when iron stores are low [1]. *Serum iron* - **Serum iron** measures the iron circulating in the blood bound to transferrin. - In **iron deficiency anemia**, the overall amount of circulating iron is **decreased** due to insufficient iron stores [1]. *Ferritin* - **Ferritin** is a storage protein for iron, reflecting the body's iron stores [2]. - In **iron deficiency anemia**, iron stores are depleted, resulting in a **decreased** serum ferritin level [1]. *Transferrin saturation* - **Transferrin saturation** is the percentage of transferrin binding sites occupied by iron. - In **iron deficiency anemia**, with low serum iron and increased TIBC, the percentage of binding sites occupied by iron is **lowered** [1].

Question 2: Iron metabolism and regulation are important for RBC precursor cells. Which of the following helps in the regulation of iron metabolism but is not specific for iron?

A. Hepcidin
B. DMT-1 (Correct Answer)
C. Ferroportin
D. Ferritin

Explanation: ***DMT-1*** - **DMT-1** (Divalent Metal Transporter 1) facilitates the transport of not only **iron** but also other divalent metals, making it essential for overall metal homeostasis. - It plays a role in the absorption of iron from the **intestine** and release from macrophages, influencing iron availability indirectly. *Hepcidin* - Hepcidin is a **specific** regulator of iron metabolism [2][4], controlling iron absorption and distribution but primarily for **iron regulation**. - It acts defensively against iron overload by inhibiting **ferroportin** [2], specifically targeting iron metabolism. *Ferritin* - Ferritin primarily serves as an **iron storage** protein [1], sequestering excess iron but not involved in its regulatory mechanism in the same context. - It indicates iron levels in the body but does not actively regulate iron metabolism. *Ferroportin* - Ferroportin is an **iron exporter** that helps in the release of iron from cells, particularly in macrophages and enterocytes [2][3], directly linked to iron metabolism regulation. - However, it is **specific for iron** and does not facilitate a broader regulation of other divalent metals. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 658. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 658-659. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 657-658. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, p. 854.

Question 3: Hepcidin inhibits which of the following?

A. Ferroportin (Correct Answer)
B. Ceruloplasmin
C. Hepheastin
D. DMT-1

Explanation: ***Ferroportin*** - **Hepcidin** is a key regulator of iron homeostasis, primarily by binding to and inhibiting **ferroportin**, the sole known iron export channel from cells. - This binding leads to the **internalization and degradation** of ferroportin, thereby reducing iron release from cells (enterocytes, macrophages, hepatocytes) into the bloodstream and consequently decreasing plasma iron levels. *Ceruloplasmin* - **Ceruloplasmin** is a copper-containing enzyme that acts as a ferroxidase, oxidizing Fe2+ to Fe3+, which is necessary for iron loading onto transferrin. - Hepcidin does not directly inhibit ceruloplasmin; instead, a deficiency in ceruloplasmin can lead to iron accumulation in tissues. *Hepheastin* - **Hephaestin** is a ferroxidase enzyme similar to ceruloplasmin, predominantly found in the intestinal enterocytes, which facilitates iron export from enterocytes. - While hephaestin is involved in iron metabolism, hepcidin directly regulates ferroportin, not hephaestin itself. *DMT-1* - **DMT-1 (Divalent Metal Transporter 1)** is responsible for the uptake of non-heme iron (Fe2+) from the intestinal lumen into the enterocyte. - Hepcidin primarily acts on iron export from cells via ferroportin, rather than on the initial uptake of iron into the enterocytes via DMT-1.

Question 4: What is the normal range of ferritin levels in adult males?

A. 30-300 ng/ml (Correct Answer)
B. 300-500 ng/ml
C. 10-20 ng/ml
D. 500-700 ng/ml

Explanation: ***30-300 ng/ml*** - The normal range for **ferritin levels** in adult males is typically **30-300 ng/ml** (some laboratories report 30-400 ng/ml). - Ferritin is an **iron storage protein**, and its levels reflect the body's iron stores. - Values below 30 ng/ml suggest **iron deficiency**, while values above 300 ng/ml may indicate iron overload or inflammatory conditions. *10-20 ng/ml* - These levels are **significantly low** and indicate **iron deficiency**. - This range is well below the normal threshold and would warrant investigation and likely iron supplementation. - Levels below 15 ng/ml are diagnostic of **iron deficiency** even in the absence of anemia. *300-500 ng/ml* - Levels in this range are considered **elevated** and can indicate iron overload, chronic inflammation, liver disease, or malignancy. - While some laboratories extend the upper limit to 400 ng/ml, persistent elevation above 300 ng/ml warrants further investigation. - Common causes include **hemochromatosis**, **chronic liver disease**, or **inflammatory conditions**. *500-700 ng/ml* - These levels are **significantly elevated** and strongly suggest **iron overload conditions** such as **hemochromatosis**, severe inflammatory states, or hepatocellular injury. - High ferritin levels can be associated with organ damage, leading to conditions like **cirrhosis** or **cardiomyopathy**. - Requires urgent investigation to identify the underlying cause.

Question 5: Which of the following are characteristic laboratory findings in Iron Deficiency Anemia (IDA)? 1. Low serum ferritin 2. Low transferrin saturation 3. Low serum iron 4. Increased TIBC

A. 3 and 4 only
B. 1, 3, and 4 only
C. 1 and 2 only
D. All of the above (Correct Answer)

Explanation: ***All of the above (1, 2, 3, and 4)*** - **All listed parameters are characteristic findings in Iron Deficiency Anemia (IDA):** - **Low serum ferritin** - Indicates depleted iron stores; most specific early marker [1] - **Low serum iron** - Reflects reduced circulating iron availability [1] - **Low transferrin saturation** - Shows decreased percentage of iron-bound transferrin molecules (typically <15%) [1] - **Increased TIBC** - Compensatory increase in total iron-binding capacity as the liver produces more transferrin to capture available iron [1] *Why not just 1, 2, and 3?* - Increased TIBC is also a hallmark finding in IDA, distinguishing it from anemia of chronic disease (where TIBC is typically low) [1] *Why not just 3 and 4?* - Serum ferritin and transferrin saturation are equally important diagnostic parameters [1] *Why not just 1, 3, and 4?* - Low transferrin saturation is a key diagnostic criterion for IDA [1] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 657-660.

Question 6: Why is blood stored in citrate-phosphate-dextrose considered more beneficial for hypoxic patients compared to blood stored in acidic-citrate-dextrose?

A. The fall in 2,3-DPG is less. (Correct Answer)
B. It has a higher pH level than acidic-citrate-dextrose.
C. It is more effective in oxygen delivery.
D. It has a longer shelf life than acidic-citrate-dextrose.

Explanation: ***The fall in 2,3-DPG is less.*** * **Citrate-phosphate-dextrose (CPD)** better preserves levels of **2,3-bisphosphoglycerate (2,3-DPG)** in stored red blood cells. * Higher 2,3-DPG levels are crucial for **oxygen unloading** from hemoglobin in tissues, which is particularly beneficial for hypoxic patients who need efficient oxygen delivery. *It has a higher pH level than acidic-citrate-dextrose.* * While CPD does maintain a **less acidic pH** than acid-citrate-dextrose (ACD), which is generally favorable for red blood cell viability, the most direct benefit for hypoxic patients relates to 2,3-DPG. * The slightly higher pH indirectly contributes to better 2,3-DPG preservation but isn't the primary reason for improved oxygen delivery. *It is more effective in oxygen delivery.* * While the *consequence* of using CPD is **more effective oxygen delivery** due to better 2,3-DPG preservation, this option describes the outcome rather than the underlying mechanism compared to the more specific answer regarding 2,3-DPG. * The increased efficacy in oxygen delivery is directly attributable to the preserved 2,3-DPG levels. *It has a longer shelf life than acidic-citrate-dextrose.* * The storage solutions primarily impact red blood cell viability and function, but the **shelf life** (typically 21-35 days depending on the anticoagulant/preservative) is generally determined by other factors, including the additive solutions used with the anticoagulant. * While CPD improves red blood cell quality, the primary advantage for hypoxic patients specifically lies in oxygen affinity rather than overall storage duration.

Question 7: What does hepcidin inhibit?

A. Absorption of cobalamine
B. Transfer of iron from enterocytes to blood (Correct Answer)
C. Folic acid synthesis
D. Respiratory oxidase

Explanation: ***Transfer of iron from enterocytes to blood*** - **Hepcidin** is a key regulator of iron homeostasis, primarily functioning to **reduce iron availability**. - It binds to and induces the degradation of **ferroportin**, the only known iron efflux channel found on enterocytes, macrophages, and hepatocytes. - By degrading ferroportin, hepcidin **prevents iron export from enterocytes into the bloodstream**, thereby trapping iron inside cells and reducing circulating iron levels. *Absorption of cobalamine* - **Cobalamin (Vitamin B12)** absorption is a complex process primarily involving **intrinsic factor** produced by gastric parietal cells, and subsequent absorption in the terminal ileum. - Hepcidin has **no direct role** in the absorption or metabolism of cobalamin. *Folic acid synthesis* - **Folic acid** (Vitamin B9) is absorbed primarily in the **jejunum** and its absorption is not regulated by hepcidin. - Hepcidin's role is specifically tied to **iron metabolism**, not the synthesis or absorption of other vitamins. *Respiratory oxidase* - **Respiratory oxidases** are enzymes involved in the electron transport chain, such as **cytochrome c oxidase**. - While iron is a component of some enzymes in the respiratory chain, hepcidin directly regulates **iron transport via ferroportin**, not the activity or synthesis of specific respiratory enzymes.

Question 8: Which of the following are blood values of Iron Deficiency Anaemia ? 1. Serum iron is less than 30 mg/100 mL 2. Total iron binding capacity is less than 400 µg/mL 3. Percentage saturation is 10% or less 4. Serum ferritin is below 30 µg/mL Select the correct answer using the code given below :

A. 1, 3 and 4 (Correct Answer)
B. 1, 2 and 4
C. 1, 2 and 3
D. 2, 3 and 4

Explanation: ***1, 3 and 4*** - In **iron deficiency anemia**, **serum iron** levels are typically **less than 30 µg/dL** [1] (or 30 mg/100 mL), indicating a reduced iron supply. - The **percentage saturation** of transferrin with iron falls to **10% or less** [1] because there is insufficient iron to bind to the available transferrin. - **Serum ferritin**, which reflects iron stores, is significantly **reduced, usually below 30 ng/mL** (or 30 µg/mL) [1]. *1, 2 and 4* - While options 1 and 4 are correct, option 2 stating **total iron binding capacity (TIBC) less than 400 µg/mL** is incorrect. - In iron deficiency, the body attempts to increase iron absorption by producing more transferrin, leading to an **elevated TIBC** [1] (often >400 µg/dL). *1, 2 and 3* - Although options 1 and 3 are correct for iron deficiency anemia, option 2, which states **TIBC is less than 400 µg/mL**, is false. - **TIBC is elevated** in iron deficiency, reflecting an increased capacity for iron binding due to increased transferrin. *2, 3 and 4* - While options 3 and 4 are correct, option 2, suggesting **TIBC is less than 400 µg/mL**, is inaccurate. - **TIBC** is typically **increased** in iron deficiency anemia as the body tries to maximize any available iron.

Question 9: All are increased in IDA except

A. Transferrin saturation (Correct Answer)
B. TIBC
C. Soluble transferrin receptor
D. Erythropoietin

Explanation: ***Transferrin saturation*** - In **iron deficiency anemia (IDA)**, there is insufficient iron to saturate transferrin, leading to a **decreased** transferrin saturation. This is the exception among the given options. - Transferrin saturation is calculated as (serum iron / TIBC) x 100, and both **serum iron** and its percentage saturation are low in IDA. *TIBC* - **Total iron-binding capacity (TIBC)** is typically **increased** in IDA as the liver produces more transferrin in an attempt to capture more iron [1]. - This elevated TIBC reflects the body's compensatory mechanism to maximize available iron uptake. *Soluble transferrin receptor* - **Soluble transferrin receptor (sTfR)** levels are **elevated** in IDA because iron-deficient erythroblasts upregulate the production of transferrin receptors on their surface as they try to scavenge more iron. - The elevated sTfR is a sensitive and specific marker for **iron deficiency**, particularly useful in differentiating IDA from anemia of chronic disease [1]. *Erythropoietin* - **Erythropoietin (EPO)** levels are **increased** in IDA due to the kidney's response to the decreased oxygen-carrying capacity of the blood (anemia) [1]. - EPO stimulates the bone marrow to produce more red blood cells, which exacerbates the demand for iron, often leading to further iron depletion if iron stores are low.

Question 10: According to the WHO criteria, anaemia in infants of 6 months of age is defined as haemoglobin less than:

A. 115 gm/litre
B. 110 gm/litre (Correct Answer)
C. 100 gm/litre
D. 105 gm/litre

Explanation: ***110 gm/litre*** - According to the **World Health Organization (WHO)** criteria, anaemia in infants aged **6-59 months** is defined as a haemoglobin concentration of less than 110 g/L (11.0 g/dL). - This threshold is used for **population-based screening** and **public health interventions** to identify and manage anaemia in young children. *100 gm/litre* - A haemoglobin level of less than 100 g/L (10.0 g/dL) in infants typically indicates **moderate to severe anaemia**, but the WHO threshold for defining anaemia in this age group is higher. - This value would represent a more pronounced degree of anaemia, often warranting immediate investigation and treatment. *105 gm/litre* - While 105 g/L is close to the threshold, the **WHO standard** for defining anaemia in infants aged 6-59 months specifically sets the cut-off at 110 g/L. - Using 105 g/L might underestimate the prevalence of anaemia or delay interventions for children who are considered anaemic by the official criteria. *115 gm/litre* - A haemoglobin level of 115 g/L (11.5 g/dL) in an infant of 6 months is generally considered **within the normal range** and does not meet the WHO criterion for anaemia. - This value would typically indicate a healthy haemoglobin status, and therefore, would not prompt a diagnosis of anaemia.

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