Abnormal Iron (Claude)

*Question: What is the hallmark finding in sideroblastic anemia when performing a bone marrow examination with Perl's Prussian Blue stain?
A) Hypersegmented neutrophils
B) Ring sideroblasts
C) Auer rods
D) Megaloblastic changes

*Answer: B) Ring sideroblasts

*Question: Which gene mutation is most commonly associated with inherited X-linked sideroblastic anemia?
A) HFE gene
B) ALAS2 gene
C) Matriptase-2 gene
D) Ferrochelatase gene

*Answer: B) ALAS2 gene

*Question: In X-linked sideroblastic anemia, which vitamin cofactor is used by ALAS2 and may provide modest improvement when given in pharmacologic doses?
A) Vitamin B12
B) Vitamin B6 (pyridoxine)
C) Folic acid
D) Vitamin C

*Answer: B) Vitamin B6 (pyridoxine)

*Question: At which TWO steps does lead poisoning interfere with the heme synthesis pathway?
A) Conversion of ALA to PBG and incorporation of iron into protoporphyrin IX
B) Glycine to ALA and PBG to protoporphyrin
C) Ferritin synthesis and transferrin binding
D) Heme to bilirubin and iron recycling

*Answer: A) Conversion of ALA to PBG and incorporation of iron into protoporphyrin IX

*Question: What is the expected morphology of anemia from acute lead exposure?
A) Microcytic, hypochromic
B) Macrocytic, normochromic
C) Normocytic, normochromic
D) Dimorphic population

*Answer: C) Normocytic, normochromic

*Question: Which classic peripheral blood finding is associated with lead toxicity due to inhibition of pyrimidine-5'-nucleotidase?
A) Target cells
B) Basophilic stippling
C) Howell-Jolly bodies
D) Pappenheimer bodies

*Answer: B) Basophilic stippling

*Question: What chelating agents are commonly used to treat lead poisoning?
A) Deferoxamine and deferasirox
B) Calcium disodium edetate and dimercaprol
C) Penicillamine and trientine
D) EDTA and succimer only

*Answer: B) Calcium disodium edetate and dimercaprol

*Question: Which laboratory tests are helpful in diagnosing lead poisoning by measuring accumulated protoporphyrin?
A) Serum iron and TIBC
B) FEP (Free Erythrocyte Protoporphyrin) and ZPP (Zinc Protoporphyrin)
C) Ferritin and transferrin saturation
D) Reticulocyte count and haptoglobin

*Answer: B) FEP (Free Erythrocyte Protoporphyrin) and ZPP (Zinc Protoporphyrin)

*Question: What is the inheritance pattern of hereditary hemochromatosis (primary hemochromatosis)?
A) X-linked recessive
B) Autosomal dominant
C) Autosomal recessive
D) Mitochondrial inheritance

*Answer: C) Autosomal recessive

*Question: In hereditary hemochromatosis, iron accumulation in which organs is most concerning for cellular dysfunction?
A) Spleen, kidneys, and lungs
B) Liver, pancreas, heart, skin, and pituitary gland
C) Bone marrow, lymph nodes, and thymus
D) Brain, adrenal glands, and gallbladder

*Answer: B) Liver, pancreas, heart, skin, and pituitary gland

*Question: What are the primary screening tests for hemochromatosis?
A) CBC and reticulocyte count
B) Transferrin saturation and serum ferritin
C) Liver biopsy and genetic testing
D) Serum iron and TIBC only

*Answer: B) Transferrin saturation and serum ferritin

*Question: What is the primary treatment for hereditary hemochromatosis?
A) Iron chelation therapy
B) Blood transfusions
C) Phlebotomy
D) Bone marrow transplantation

*Answer: C) Phlebotomy

*Question: How much iron does each unit of transfused RBCs contain in transfusion-related hemosiderosis?
A) 50-100 mg
B) 100-150 mg
C) 200-250 mg
D) 300-400 mg

*Answer: C) 200-250 mg

*Question: Which HFE gene mutation is most commonly associated with classic hereditary hemochromatosis in people of northern European descent?
A) C282Y homozygosity
B) H63D homozygosity
C) S65C mutation
D) Ferroportin mutation

*Answer: A) C282Y homozygosity

*Question: What is the characteristic skin appearance in hereditary hemochromatosis due to hemosiderin accumulation?
A) Pale and jaundiced
B) Golden or bronze color
C) Cyanotic appearance
D) Erythematous rash

*Answer: B) Golden or bronze color

*Question: What is the central feature of anemia of chronic inflammation?
A) Absolute iron deficiency with depleted stores
B) Sideropenia with abundant iron stores
C) Hemolysis with reticulocytosis
D) Megaloblastic changes in bone marrow

*Answer: B) Sideropenia with abundant iron stores

*Question: Which cytokine, produced by macrophages during inflammation, stimulates hepcidin production by hepatocytes?
A) TNF-α
B) IL-1
C) IL-6
D) IFN-gamma

*Answer: C) IL-6

*Question: What is the primary mechanism by which hepcidin causes iron sequestration in anemia of chronic inflammation?
A) Inhibits transferrin synthesis
B) Causes internalization and degradation of ferroportin
C) Blocks erythropoietin receptors
D) Increases ferritin breakdown

*Answer: B) Causes internalization and degradation of ferroportin

*Question: In anemia of chronic inflammation, where is iron sequestered despite being unavailable to developing RBCs?
A) In the spleen and lymph nodes
B) In the bone marrow plasma
C) In macrophages and hepatocytes
D) In the kidney tubules

*Answer: C) In macrophages and hepatocytes

*Question: What is the expected hemoglobin level in anemia of chronic inflammation?
A) 5-7 g/dL
B) 8-10 g/dL
C) 11-12 g/dL
D) 12-14 g/dL

*Answer: B) 8-10 g/dL

*Question: What is the typical RBC morphology in uncomplicated anemia of chronic inflammation?
A) Microcytic, hypochromic
B) Macrocytic, normochromic
C) Normocytic, normochromic
D) Dimorphic population

*Answer: C) Normocytic, normochromic

*Question: In anemia of chronic inflammation, what happens to TIBC (Total Iron Binding Capacity)?
A) Remains normal
B) Increases significantly
C) Decreases (low)
D) Fluctuates widely

*Answer: C) Decreases (low)

*Question: Why is TIBC low in anemia of chronic inflammation despite low serum iron?
A) Transferrin is destroyed by inflammation
B) Hepatocyte production of transferrin reflects abundant iron stores
C) Kidney excretion of transferrin increases
D) Iron competes with transferrin binding

*Answer: B) Hepatocyte production of transferrin reflects abundant iron stores

*Question: What is the expected serum ferritin level in anemia of chronic inflammation?
A) Very low (depleted)
B) Low to normal
C) Normal to increased (acute phase reactant)
D) Always extremely elevated

*Answer: C) Normal to increased (acute phase reactant)

*Question: What does an elevated FEP (free erythrocyte protoporphyrin) indicate in anemia of chronic inflammation?
A) Excessive iron incorporation
B) Hemolysis occurring
C) Failure to incorporate iron into heme
D) Vitamin B12 deficiency

*Answer: C) Failure to incorporate iron into heme

*Question: What is the soluble transferrin receptor (sTfR) level in anemia of chronic inflammation?
A) Markedly elevated
B) Normal (reflects normal intracellular iron)
C) Significantly decreased
D) Variable and unreliable

*Answer: B) Normal (reflects normal intracellular iron)

*Question: Which iron-binding protein in neutrophil granules has greater avidity for iron than transferrin?
A) Ferritin
B) Hemosiderin
C) Lactoferrin
D) Hepcidin

*Answer: C) Lactoferrin

*Question: What is the purpose of lactoferrin release during infection?
A) Transport iron to erythroblasts
B) Prevent bacteria from using intracellular iron
C) Stimulate erythropoietin production
D) Decrease hepcidin levels

*Answer: B) Prevent bacteria from using intracellular iron

*Question: In bone marrow iron stains of patients with anemia of chronic inflammation, where is iron visible?
A) In erythroblasts but not macrophages
B) Uniformly distributed throughout
C) In macrophages but not erythroblasts
D) Absent from all cells

*Answer: C) In macrophages but not erythroblasts

*Question: Which inflammatory cytokines impair erythroid progenitor cell proliferation in anemia of chronic inflammation?
A) IL-6 and hepcidin
B) TNF-α, IL-1, and IFN-gamma
C) Erythropoietin and thrombopoietin
D) Lactoferrin and transferrin

*Answer: B) TNF-α, IL-1, and IFN-gamma

*Question: What is the daily iron loss from the body under normal circumstances?
A) 0.5 mg per day
B) 1 mg per day
C) 2-3 mg per day
D) 5 mg per day

*Answer: B) 1 mg per day

*Question: Which mechanism causes iron loss contributing to iron deficiency anemia?
A) Mitochondria of desquamated skin and sloughed intestinal epithelium
B) Respiratory tract secretions
C) Kidney filtration
D) Hepatic metabolism

*Answer: A) Mitochondria of desquamated skin and sloughed intestinal epithelium

*Question: What is the serum ferritin cutoff that defines iron deficiency in people over 5 years old?
A)

*Answer: C)

*Question: During which life stages is there typically increased iron demand relative to supply?
A) Middle age and elderly
B) Infancy, childhood, and adolescence
C) Young adults only
D) Postmenopausal period

*Answer: B) Infancy, childhood, and adolescence

*Question: Why do infants require more iron per kg of body weight compared to adult men?
A) Higher metabolic rate only
B) Rapid growth, increased blood volume, and muscle development
C) Immature digestive system
D) Maternal antibody breakdown

*Answer: B) Rapid growth, increased blood volume, and muscle development

*Question: What is "functional iron deficiency" in the context of EPO treatment?
A) Absolute depletion of all iron stores
B) Adequate iron stores but cannot be mobilized fast enough for increased RBC production
C) Iron toxicity from excessive supplementation
D) Genetic inability to absorb iron

*Answer: B) Adequate iron stores but cannot be mobilized fast enough for increased RBC production

*Question: Which gastrointestinal disease is a pathologic cause of impaired iron absorption?
A) Irritable bowel syndrome
B) Celiac disease
C) Gastroesophageal reflux disease
D) Peptic ulcer disease

*Answer: B) Celiac disease

*Question: What is IRIDA (Iron-Refractory Iron Deficiency Anemia) caused by?
A) Chronic blood loss
B) Inherited mutations in matriptase-2 gene leading to hepcidin overproduction
C) Dietary insufficiency
D) Autoimmune destruction of iron stores

*Answer: B) Inherited mutations in matriptase-2 gene leading to hepcidin overproduction

*Question: How does decreased stomach acidity contribute to iron deficiency?
A) Destroys dietary iron
B) Reduces conversion of ferric (Fe³⁺) to absorbable ferrous (Fe²⁺) iron
C) Inhibits transferrin synthesis
D) Blocks ferroportin channels

*Answer: B) Reduces conversion of ferric (Fe³⁺) to absorbable ferrous (Fe²⁺) iron

*Question: What is menorrhagia?
A) Absence of menstrual periods
B) Irregular menstrual periods
C) Heavy menstrual bleeding
D) Painful menstruation

*Answer: C) Heavy menstrual bleeding

*Question: In paroxysmal nocturnal hemoglobinuria, how is iron lost leading to deficiency?
A) Through gastrointestinal bleeding
B) Via chronic intravascular hemolysis with iron loss in urine
C) Through excessive menstrual bleeding
D) Via respiratory secretions

*Answer: B) Via chronic intravascular hemolysis with iron loss in urine

*Question: What percentage of total body iron is contained in hemoglobin, intracellular ferritin, and hemosiderin?
A) 50%
B) 70%
C) 90%
D) 100%

*Answer: C) 90%

*Question: In Stage 1 of iron depletion (latent iron deficiency), which compartment is depleted?
A) Functional iron compartment
B) Transport iron compartment
C) Storage iron compartment
D) All compartments equally

*Answer: C) Storage iron compartment

*Question: In Stage 1 iron depletion, which laboratory test is the earliest indicator of declining iron stores?
A) Hemoglobin concentration
B) Serum ferritin
C) TIBC
D) MCV

*Answer: B) Serum ferritin

*Question: What is the prevalence of Stage 1 iron deficiency (storage depletion) in nonpregnant women aged 15-49 years in the U.S.?
A) 5.2%
B) 10.4%
C) 15.1%
D) 20.8%

*Answer: B) 10.4%

*Question: In Stage 2 iron depletion (transport iron depletion), what happens to TIBC?
A) Decreases significantly
B) Remains normal
C) Increases (more transferrin available)
D) Becomes undetectable

*Answer: C) Increases (more transferrin available)

*Question: Why does FEP (free erythrocyte protoporphyrin) increase in Stage 2 iron depletion?
A) Excessive heme breakdown
B) Vitamin deficiency
C) Iron unavailable for heme formation
D) Increased protoporphyrin synthesis

*Answer: C) Iron unavailable for heme formation

*Question: What happens to reticulocyte hemoglobin content in Stage 2 iron depletion?
A) Increases significantly
B) Remains normal
C) Decreases
D) Fluctuates unpredictably

*Answer: C) Decreases

*Question: In Stage 3 iron deficiency (frank IDA), what is the characteristic RBC morphology?
A) Macrocytic and hyperchromic
B) Normocytic and normochromic
C) Microcytic and hypochromic
D) Target cells and spherocytes

*Answer: C) Microcytic and hypochromic

*Question: What does an increased RDW (red cell distribution width) indicate in iron deficiency anemia?
A) Uniform cell size
B) Increased anisocytosis (unequal RBC sizes)
C) Hemolysis
D) Infection

*Answer: B) Increased anisocytosis (unequal RBC sizes)

*Question: Which clinical sign involves cravings for non-food items like dirt or starch in severe IDA?
A) Glossitis
B) Koilonychia
C) Pica
D) Angular cheilosis

*Answer: C) Pica

*Question: What is koilonychia?
A) Smooth, inflamed tongue
B) Cracks at the corners of the mouth
C) Spoon-shaped nails
D) Pale conjunctiva

*Answer: C) Spoon-shaped nails

*Question: Why are menstruating women at high risk for iron deficiency anemia?
A) Decreased iron absorption
B) Monthly blood loss increases routine iron needs
C) Hormonal effects on iron metabolism
D) Decreased dietary iron intake

*Answer: B) Monthly blood loss increases routine iron needs

*Question: How much iron can be lost during pregnancy and nursing combined?
A) 500 mg
B) 800 mg
C) Nearly 1200 mg
D) Over 2000 mg

*Answer: C) Nearly 1200 mg

*Question: What is march hemoglobinuria?
A) Hemolysis from parasitic infection
B) Exercise-induced hemoglobinuria from foot-pounding trauma
C) Drug-induced hemolytic anemia
D) Autoimmune hemolytic anemia

*Answer: B) Exercise-induced hemoglobinuria from foot-pounding trauma

*Question: How do hookworms (N. americanus, A. duodenale) cause iron deficiency?
A) Compete for dietary iron absorption
B) Attach to intestinal wall and suck blood from gastric vessels
C) Destroy iron-storing hepatocytes
D) Block ferroportin channels

*Answer: B) Attach to intestinal wall and suck blood from gastric vessels

*Question: Why is cow's milk not recommended as a primary iron source for infants?
A) Causes allergic reactions
B) Low in iron content
C) Blocks iron absorption
D) Contains excessive protein

*Answer: B) Low in iron content

*Question: At what age do fetal iron stores typically become depleted, requiring dietary supplementation?
A) 3 months
B) 6 months
C) 9 months
D) 12 months

*Answer: B) 6 months

*Question: In early-stage IDA, which CBC parameter often increases by >15% before hemoglobin decreases?
A) MCV
B) MCH
C) RDW (Red Cell Distribution Width)
D) Platelet count

*Answer: C) RDW (Red Cell Distribution Width)

*Question: What is a common finding in the WBC count in uncomplicated iron deficiency anemia?
A) Leukocytosis
B) Leukopenia
C) Typically normal
D) Left shift with bands

*Answer: C) Typically normal

*Question: Why might thrombocytosis be present in IDA resulting from chronic bleeding?
A) Compensatory mechanism
B) Splenic sequestration
C) Bone marrow hyperplasia
D) Iron stimulates platelet production

*Answer: A) Compensatory mechanism

*Question: What are the backbone diagnostic tests for iron deficiency?
A) CBC and reticulocyte count
B) Biochemical iron studies (iron panel)
C) Bone marrow biopsy
D) Genetic testing

*Answer: B) Biochemical iron studies (iron panel)

*Question: What does TIBC measure?
A) Amount of iron in red blood cells
B) Indirect measure of transferrin and available binding sites for iron
C) Iron stored in liver
D) Daily iron absorption rate

*Answer: B) Indirect measure of transferrin and available binding sites for iron

*Question: How is transferrin saturation calculated?
A) TIBC divided by serum iron
B) Serum iron divided by TIBC
C) Serum ferritin divided by TIBC
D) Hemoglobin divided by serum iron

*Answer: B) Serum iron divided by TIBC

*Question: Under normal conditions, what percentage of transferrin is saturated with iron?
A) 10-15%
B) Approximately 33% (one-third)
C) 50%
D) 75-80%

*Answer: B) Approximately 33% (one-third)

*Question: In IDA, what happens to transferrin saturation?
A) Increases significantly
B) Remains normal
C) Decreases (low)
D) Becomes unmeasurable

*Answer: C) Decreases (low)

*Question: What percentage of free erythrocyte protoporphyrin exists as zinc protoporphyrin (ZPP)?
A) 25%
B) 50%
C) 75%
D) >95%

*Answer: D) >95%

*Question: What is the advantage of measuring soluble transferrin receptor (sTfR) compared to ferritin?
A) Less expensive to perform
B) Less affected by inflammation and anemia
C) More widely available
D) Provides faster results

*Answer: B) Less affected by inflammation and anemia

*Question: When measuring sTfR in iron deficiency, what happens to the levels as the disease progresses?
A) Levels decrease progressively
B) Levels remain constant
C) Levels increase (cells seek more iron)
D) Levels fluctuate unpredictably

*Answer: C) Levels increase (cells seek more iron)

*Question: Is bone marrow biopsy routinely indicated for suspected uncomplicated iron deficiency?
A) Yes, always required for diagnosis
B) No, not routinely indicated
C) Only in children
D) Only in elderly patients

*Answer: B) No, not routinely indicated

*Question: What stain is used to assess iron in bone marrow specimens?
A) Wright-Giemsa stain
B) Perl's Prussian Blue stain
C) Gram stain
D) PAS stain

*Answer: B) Perl's Prussian Blue stain

*Question: In early iron deficiency, what happens to the myeloid:erythroid (M:E) ratio in bone marrow?
A) Increases significantly
B) Remains normal
C) Decreases due to increased erythropoiesis
D) M:E ratio is not affected

*Answer: C) Decreases due to increased erythropoiesis

*Question: What characteristic finding is seen in polychromatic normoblasts in iron-deficient bone marrow?
A) Megaloblastic changes
B) Nuclear-cytoplasmic asynchrony (mature nucleus, immature cytoplasm)
C) Hypersegmentation
D) Increased mitotic figures

*Answer: B) Nuclear-cytoplasmic asynchrony (mature nucleus, immature cytoplasm)

*Question: What is the standard oral prescription for iron supplementation in IDA?
A) Ferric chloride
B) Iron dextran
C) Ferrous sulfate
D) Carbonyl iron

*Answer: C) Ferrous sulfate

*Question: What are common side effects of oral ferrous sulfate supplementation?
A) Headache and dizziness
B) Nausea, constipation, and black tarry stool
C) Rash and itching
D) Joint pain and fever

*Answer: B) Nausea, constipation, and black tarry stool

*Question: What is the typical duration of iron supplementation treatment for IDA?
A) 2-4 weeks
B) 2-3 months
C) 6 months or longer
D) 1 year minimum

*Answer: C) 6 months or longer

*Question: What is an advantage of oral bovine lactoferrin compared to ferrous sulfate?
A) More rapid absorption
B) Reduced/tolerable intestinal side effects with equal effectiveness
C) Lower cost
D) Once-weekly dosing

*Answer: B) Reduced/tolerable intestinal side effects with equal effectiveness

*Question: In which conditions is intravenous iron dextran administration used?
A) Patient preference for IV therapy
B) Impaired iron absorption (gastric achlorhydria, celiac disease, IRIDA)
C) All cases of IDA
D) Pediatric patients only

*Answer: B) Impaired iron absorption (gastric achlorhydria, celiac disease, IRIDA)

*Question: What is a notable risk associated with intravenous iron dextran administration?
A) Tissue necrosis at injection site
B) Increased risk of anaphylactic or allergic reactions
C) Permanent discoloration
D) Immediate hemolysis

*Answer: B) Increased risk of anaphylactic or allergic reactions

*Question: When are RBC transfusions warranted in the treatment of IDA?
A) In all cases of IDA
B) When ferritin is

*Answer: C) Rarely, only when hemoglobin is dangerously low

*Question: Within how many days does the hemoglobin content of reticulocytes correct after starting iron therapy?
A) Within 1 day
B) Within 2 days
C) Within 5 days
D) Within 10 days

*Answer: B) Within 2 days

*Question: When does the reticulocyte count begin to increase after starting iron treatment?
A) Within 1-2 days
B) Within 5-10 days
C) After 2 weeks
D) After 1 month

*Answer: B) Within 5-10 days

*Question: When is the anticipated rise in hemoglobin typically observed after starting iron therapy?
A) Within 3-5 days
B) Within 1 week
C) Within 2-3 weeks
D) After 2 months

*Answer: C) Within 2-3 weeks

*Question: How long does it take for hemoglobin levels to return to normal with iron therapy?
A) 2 weeks
B) 1 month
C) About 2 months
D) 6 months

*Answer: C) About 2 months

*Question: After hemoglobin normalizes, how long must iron therapy continue to replenish storage pools?
A) 1-2 weeks
B) 1 month
C) 3-4 months
D) 1 year

*Answer: C) 3-4 months

*Question: What is seen in the peripheral blood smear during iron therapy recovery?
A) Uniform microcytic cells
B) Biphasic population (microcytic old cells and normocytic young cells)
C) Macrocytic cells only
D) Target cells

*Answer: B) Biphasic population (microcytic old cells and normocytic young cells)

*Question: What is the alternate name for anemia of chronic inflammation due to its unifying pathophysiologic factor?
A) Anemia of chronic disease
B) Inflammatory anemia
C) Secondary anemia
D) Anemia of chronic inflammation (correct term)

*Answer: D) Anemia of chronic inflammation (correct term)

*Question: Which patient population is most commonly affected by anemia of chronic inflammation?
A) Children and adolescents
B) Hospitalized patients
C) Athletes
D) Pregnant women

*Answer: B) Hospitalized patients

*Question: In anemia of chronic inflammation, what finding is seen on bone marrow iron staining that reflects maldistribution?
A) No iron in any cells
B) Iron in erythroblasts only
C) Iron in macrophages but not in erythroblasts
D) Uniform iron distribution

*Answer: C) Iron in macrophages but not in erythroblasts

*Question: Why is the elevation of hepcidin during inflammation potentially beneficial initially?
A) Stimulates RBC production
B) Iron sequestration decreases iron available to bacteria
C) Increases transferrin synthesis
D) Enhances iron absorption

*Answer: B) Iron sequestration decreases iron available to bacteria

*Question: What is the long-term consequence of chronically high hepcidin levels?
A) Iron overload in tissues
B) Increased hemolysis
C) Diminished RBC production
D) Splenomegaly

*Answer: C) Diminished RBC production

*Question: During chronic inflammation, what is the most significant cause of anemia?
A) Shortened RBC lifespan
B) Impaired ferrokinetics
C) Decreased EPO production
D) Increased destruction

*Answer: B) Impaired ferrokinetics

*Question: In chronic inflammation with coexisting iron deficiency, what is the expected RBC morphology?
A) Normocytic, normochromic
B) Macrocytic, normochromic
C) Microcytic, hypochromic
D) Dimorphic population only

*Answer: C) Microcytic, hypochromic

*Question: What additional CBC abnormalities might be seen in anemia of chronic inflammation?
A) Pancytopenia
B) Leukocytosis and thrombocytosis
C) Isolated thrombocytopenia
D) Leukopenia only

*Answer: B) Leukocytosis and thrombocytosis

*Question: In which form of hereditary hemochromatosis may symptoms appear in the teenage years?
A) Classic HH (HFE mutation)
B) Juvenile HH (hepcidin/hemojuvelin mutations)
C) Ferroportin disease
D) Transferrin receptor mutation

*Answer: B) Juvenile HH (hepcidin/hemojuvelin mutations)

*Question: By what age do patients with classic hereditary hemochromatosis (HFE mutation) typically accumulate 20-30 g of iron?
A) Age 20-30
B) Age 30-40
C) Age 40-60
D) Age 70-80

*Answer: C) Age 40-60

*Question: Why do men show earlier phenotypic expression of hereditary hemochromatosis than women?
A) Men absorb more dietary iron
B) Women lose iron through menstruation/childbirth, delaying accumulation
C) Men have larger livers
D) Genetic penetrance is higher in men

*Answer: B) Women lose iron through menstruation/childbirth, delaying accumulation

*Question: Which dietary factors can increase iron absorption in hereditary hemochromatosis?
A) Calcium and phosphorus
B) Ascorbic acid and alcohol
C) Fiber and phytates
D) Zinc and copper

*Answer: B) Ascorbic acid and alcohol

*Question: What is "bronzed diabetes" in the context of hereditary hemochromatosis?
A) Diabetes with kidney complications
B) Diabetes mellitus due to pancreatic iron accumulation with skin bronzing
C) Type 1 diabetes with hyperpigmentation
D) Gestational diabetes with liver involvement

*Answer: B) Diabetes mellitus due to pancreatic iron accumulation with skin bronzing

*Question: What cancer risk is increased in hereditary hemochromatosis due to iron-generated free radicals?
A) Pancreatic cancer
B) Hepatocellular carcinoma (HCC)
C) Lung cancer
D) Colon cancer

*Answer: B) Hepatocellular carcinoma (HCC)