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Question 1

Dietary non-heme iron is absorbed in the intestine as:

Answer 1

C. Fe²⁺

Non-heme iron must be reduced to Fe²⁺ for absorption.

Question 2

The enzyme that reduces Fe³⁺ → Fe²⁺ at the brush border is:

Answer 2

B. DCYTB

DCYTB (Dcytb) is a ferric reductase that facilitates iron absorption.

Question 3

Ferroportin is located on which cell type?

Answer 3

B. Enterocytes

Ferroportin is crucial for iron export from enterocytes into circulation.

Question 4

Hepcidin binding to ferroportin results in:

Answer 4

B. Ferroportin degradation

This process decreases iron absorption and release into the bloodstream.

Question 5

Transferrin’s primary function is to carry iron in the:

Answer 5

B. Plasma

Transferrin transports iron from absorption sites to tissues.

Question 6

The main intracellular iron storage protein is:

Answer 6

B. Ferritin

Ferritin stores iron in a soluble and non-toxic form.

Question 7

Iron absorption increases when body iron stores are:

Answer 7

B. Low

Low iron stores stimulate increased absorption to meet physiological needs.

Question 8

Most daily iron is supplied from:

Answer 8

C. Recycling of senescent RBCs

The body recycles iron from old red blood cells efficiently.

Question 9

The transferrin receptor is highly expressed on:

Answer 9

B. RBC precursors

RBC precursors require high amounts of iron for hemoglobin synthesis.

Question 10

Iron is inserted into protoporphyrin IX by:

Answer 10

B. Ferrochelatase

Ferrochelatase catalyzes the final step in heme synthesis.

Question 11

The earliest laboratory indicator of iron deficiency is:

Answer 11

B. Low ferritin

Ferritin levels drop early in iron deficiency before hemoglobin levels are affected.

Question 12

The most common cause of iron deficiency in adults is:

Answer 12

A. Malabsorption

Malabsorption can lead to insufficient iron uptake from the diet.

Question 13

Which type of blood cell is primarily responsible for blood clotting?

Answer 13

C. Platelets

Platelets are essential for the coagulation process in the body.

Question 14

Iron is inserted into protoporphyrin IX by which enzyme?

Answer 14

B. Ferrochelatase

Ferrochelatase catalyzes the final step in heme synthesis.

Question 15

The earliest laboratory indicator of iron deficiency is:

Answer 15

B. Low ferritin

Ferritin levels reflect the body’s iron stores.

Question 16

The most common cause of iron deficiency in adults is:

Answer 16

B. GI blood loss

Gastrointestinal bleeding is a frequent source of iron loss.

Question 17

Iron deficiency anemia typically shows RBCs that are:

Answer 17

B. Microcytic, hypochromic

This morphology is characteristic of iron deficiency anemia.

Question 18

A high RDW in IDA reflects:

Answer 18

B. Mixed RBC populations

A high RDW indicates variability in red blood cell size.

Question 19

TIBC in iron deficiency is typically:

Answer 19

B. Increased

Total Iron Binding Capacity (TIBC) increases as the body attempts to capture more iron.

Question 20

Serum ferritin in iron deficiency is usually:

Answer 20

C. Low

Low ferritin levels indicate depleted iron stores.

Question 21

Which finding supports iron deficiency over anemia of inflammation?

Answer 21

C. Elevated sTfR

Soluble transferrin receptor (sTfR) levels can help differentiate between these conditions.

Question 22

A symptom strongly associated with iron deficiency anemia is:

Answer 22

B. Pica

Pica is the craving for non-nutritive substances, often seen in iron deficiency.

Question 23

The reticulocyte count in untreated IDA is usually:

Answer 23

B. Low

A low reticulocyte count indicates inadequate red blood cell production.

Question 24

Chronic NSAID use may cause IDA through:

Answer 24

B. GI bleeding

Nonsteroidal anti-inflammatory drugs can lead to gastrointestinal bleeding.

Question 25

The hallmark mediator of **anemia of inflammation** is:

Answer 25

B. Hepcidin ## Footnote Hepcidin regulates iron metabolism and is elevated in inflammation.

Question 26

AI is typically associated with:

Answer 26

C. Chronic disease ## Footnote Anemia of inflammation often occurs in the context of chronic diseases.

Question 27

Ferritin levels in AI are:

Answer 27

B. Normal or high ## Footnote Ferritin can be elevated due to inflammation.

Question 28

TIBC in AI is usually:

Answer 28

B. Decreased ## Footnote Total Iron Binding Capacity is often reduced in anemia of inflammation.

Question 29

RBC morphology in AI is most often:

Answer 29

C. Normocytic ## Footnote Red blood cells in anemia of inflammation are typically of normal size.

Question 30

Serum iron in AI is:

Answer 30

B. Low ## Footnote Serum iron levels are often decreased in anemia of inflammation.

Question 31

Hepcidin levels in AI are:

Answer 31

B. High ## Footnote Elevated hepcidin levels contribute to iron sequestration.

Question 32

Anemia of inflammation is caused by iron:

Answer 32

C. Sequestration in macrophages ## Footnote Iron is sequestered in macrophages, reducing its availability.

Question 33

A key differentiator of AI from IDA is:

Answer 33

B. TIBC ## Footnote TIBC is typically low in anemia of inflammation and high in iron deficiency anemia.

Question 34

The most common clinical context for AI is:

Answer 34

C. Chronic inflammatory disease ## Footnote Chronic diseases often lead to anemia of inflammation.

Question 35

HH most commonly involves mutation in:

Answer 35

A. HFE gene ## Footnote The HFE gene is associated with hereditary hemochromatosis.

Question 36

HH is characterized by:

Answer 36

B. Excess intestinal iron absorption ## Footnote Hereditary hemochromatosis leads to increased iron absorption from the diet.

Question 37

A typical lab pattern in HH is:

Answer 37

B. High ferritin, high % saturation ## Footnote These lab findings indicate iron overload.

Question 38

The organ most severely affected in untreated HH is:

Answer 38

C. Liver ## Footnote The liver is particularly susceptible to damage from iron overload.

Question 39

HH can lead to which endocrine complication?

Answer 39

B. Diabetes mellitus ## Footnote Iron overload can damage the pancreas, leading to diabetes.

Question 40

The skin of HH patients may appear:

Answer 40

B. Bronze ## Footnote Skin changes, including a bronze discoloration, are common in hemochromatosis.

Question 41

The cornerstone treatment of HH is:

Answer 41

C. Phlebotomy ## Footnote Phlebotomy is used to reduce iron levels in patients with hemochromatosis.

Question 42

HH patients display low levels of:

Answer 42

B. Hepcidin ## Footnote Hepcidin levels are often low in hereditary hemochromatosis.

Question 43

A transferrin saturation >45% suggests:

Answer 43

C. HH ## Footnote High transferrin saturation indicates iron overload conditions.

Question 44

Joint pain in HH commonly affects the:

Answer 44

B. Second and third MCP joints ## Footnote Joint pain is a common symptom in hemochromatosis.

Question 45

Secondary iron overload is most often caused by:

Answer 45

B. Multiple transfusions ## Footnote Repeated blood transfusions can lead to iron overload.

Question 46

Which disease most commonly requires chronic transfusions?

Answer 46

B. Thalassemia major ## Footnote Thalassemia major often necessitates regular blood transfusions.

Question 47

Iron chelation therapy is indicated when:

Answer 47

C. Ferritin >1000 ## Footnote High ferritin levels indicate the need for chelation therapy.

Question 48

The main chelator used for transfusional overload is:

Answer 48

B. Deferoxamine ## Footnote Deferoxamine is commonly used to treat iron overload.

Question 49

Secondary overload affects which organ first?

Answer 49

C. Liver ## Footnote The liver is typically the first organ affected by iron overload.

Question 50

Cardiac failure from iron overload results from:

Answer 50

B. Iron deposition ## Footnote Iron deposition in the heart can lead to cardiac complications.

Question 51

A clue that overload is secondary, not hereditary, is:

Answer 51

B. Transfusion history ## Footnote A history of transfusions suggests secondary iron overload.

Question 52

Hemosiderosis refers to iron deposition:

Answer 52

B. Without significant tissue damage ## Footnote Hemosiderosis can occur without causing major organ damage.

Question 53

Ineffective erythropoiesis increases iron absorption because:

Answer 53

B. Hepcidin falls ## Footnote Low hepcidin levels lead to increased iron absorption.

Question 54

Secondary overload can occur in liver disease because:

Answer 54

B. Hepcidin is low ## Footnote Low hepcidin levels in liver disease can lead to iron overload.

Question 55

Acute iron toxicity occurs most often in:

Answer 55

B. Young children ## Footnote Young children are particularly vulnerable to iron toxicity.

Question 56

A serum iron >500 µg/dL indicates:

Answer 56

B. Severe iron poisoning ## Footnote High serum iron levels are indicative of iron toxicity.

Question 57

Iron toxicity primarily causes:

Answer 57

B. Metabolic acidosis ## Footnote Iron toxicity can lead to metabolic acidosis.

Question 58

The initial GI symptoms of iron overdose include:

Answer 58

B. Vomiting and diarrhea ## Footnote Gastrointestinal symptoms are common in cases of iron overdose.

Question 59

The antidote for severe iron poisoning is:

Answer 59

B. Deferoxamine ## Footnote Deferoxamine is used to treat severe iron poisoning.

Question 60

A late-stage complication of iron toxicity is:

Answer 60

A. Liver failure ## Footnote Severe iron toxicity can lead to liver damage and failure.

Question 61

In iron poisoning, shock is due to:

Answer 61

B. Free radical injury ## Footnote Free radicals generated by iron toxicity can cause cellular damage.

Question 62

The most dangerous feature of iron toxicity is:

Answer 62

B. Circulatory collapse ## Footnote Circulatory collapse is a critical risk in severe iron toxicity.

Question 63

Radiopaque pills on abdominal X-ray suggest overdose of:

Answer 63

B. Iron tablets ## Footnote Iron tablets are radiopaque and can be seen on X-rays.

Question 64

A temporary “latent phase” in iron toxicity indicates:

Answer 64

B. Impending deterioration ## Footnote A latent phase can precede serious complications in iron toxicity.

Question 65

The first step of **heme synthesis** occurs in the:

Answer 65

C. Mitochondria ## Footnote Heme synthesis begins in the mitochondria of cells.

Question 66

ALA synthase is activated during:

Answer 66

B. Low heme ## Footnote ALA synthase activity increases when heme levels are low.

Question 67

Porphyrinogens are easily:

Answer 67

B. Oxidized ## Footnote Porphyrinogens can be readily oxidized to form porphyrins.

Question 68

Acute porphyrias typically affect the:

Answer 68

A. Liver ## Footnote Acute porphyrias primarily impact liver function.

Question 69

Cutaneous porphyrias cause symptoms triggered by:

Answer 69

B. Sunlight ## Footnote Symptoms of cutaneous porphyrias are often exacerbated by sun exposure.

Question 70

PBG deaminase deficiency causes:

Answer 70

C. AIP ## Footnote Acute Intermittent Porphyria (AIP) is caused by PBG deaminase deficiency.

Question 71

UROD deficiency causes:

Answer 71

B. PCT ## Footnote Porphyria Cutanea Tarda (PCT) is linked to UROD deficiency.

Question 72

Ferrochelatase deficiency causes:

Answer 72

C. EPP ## Footnote Erythropoietic Protoporphyria (EPP) results from ferrochelatase deficiency.

Question 73

CEP is associated with:

Answer 73

B. Severe blistering and erythrodontia ## Footnote Congenital Erythropoietic Porphyria (CEP) leads to significant skin and dental issues.

Question 74

EPP is associated with:

Answer 74

A. Painful burning without blistering ## Footnote Erythropoietic Protoporphyria (EPP) causes pain but typically does not cause blisters.