MMSC 433 FINAL | QUESTIONS AND ANSWERS | 2026 UPDATE | WITH COMPLETE
SOLUTIONS.
iron absorption - (ANSWER)-ferric iron is taken in from diet
-ferric iron is reduced by duodenal cytochrome B to become ferrous iron
-ferrous iron is absorbed into enterocytes by DMT 1
-absorbed iron is stored as ferritin, or sent into portal hepatic circulation and carried by transferrin to
developing RBCs
transferrin - (ANSWER)plasma carrier protein for ferrous iron
high iron level regulation - (ANSWER)-hepcidin is released from hepatocytes
-ferroportin is inactivated, leading to decreased iron being transported into circulation
low iron level regulation - (ANSWER)-hepcidin is down regulated by hepatocytes
-ferroportin becomes activated and transports iron out of the enterocytes and into circulation
ferrous iron - (ANSWER)the form of iron that is able to be utilized in the body for developing red cells
prussian blue stain - (ANSWER)stain that is used to identify iron in tissues and bone marrow
stage 1 iron deficiency (progressive loss of storage iron) - (ANSWER)-asymptomatic
-RBCs develop normally
-*serum ferritin low*
stage 2 iron deficiency (exhaustion of iron storage pool) - (ANSWER)-subclinical symptoms
-hemoglobin in retics is decreased, *hemogram appears normal still*
-iron deficiency erythropoiesis is occurring
-hepcidin decreased
-serum iron and ferritin decreased
-RDW, TIBC and sTRs increased
,MMSC 433 FINAL | QUESTIONS AND ANSWERS | 2026 UPDATE | WITH COMPLETE
SOLUTIONS.
-prussian blue stain of BM is negative for iron
stage 3 iron deficiency (frank anemia) - (ANSWER)-patient exhibits fatigue, weakness, pallor, glossitis,
koilonychia and pica
-*H/H decreased*
-*hypochromic/ microcytic anemia*
-FEP, TIBC and sTR increased
-ferritin, hepcidin and serum iron decreased
sideroblastic anemia - (ANSWER)-iron deposits in the mitochondria of erythroblast cells in the bone
marrow interfere with biosynthesis of heme
-caused by genetic inheritance, drugs/ bone marrow toxins (*lead*, antibiotics, chemotherapeutics)
-*ringed sideroblasts* are highly indicative of the disease
-basophillic stippling is common in lead poisoning
-normocytic normochromic cells
iron deficiency anemia (IDA) - (ANSWER)-caused by inadequate intake, increased need or malabsorption
of iron, poor diet or chronic blood loss
-symptoms: fatigue, weakness, pallor, spooning of the nails (koilonychia) and pica
-*H/H decreased*
-microcytic, hypochromic cells
-marked poikilocytosis (target cells, spherocytes, tear drop cells and schistocytes)
-FEP, sTR and TIBC increased
-ferritin, hepcidin and serum iron decreased
anemia of chronic inflammation - (ANSWER)-anemia occurring secondary to underlying condition
(chronic inflammatory disease, chronic infection or malignancy) that causes release of cell products
-hepcidin, lactoferrin and inflammatory cytokines cause decreased iron status and anemia
-low Hgb
,MMSC 433 FINAL | QUESTIONS AND ANSWERS | 2026 UPDATE | WITH COMPLETE
SOLUTIONS.
-*low TIBC* (hepcidin is increased due to acute phase reaction)
-normocytic normochromic anemia
-serum iron decreased
-ferritin (acute phase reactant) and FEP increased
hereditary hemochromatosis (HH) - (ANSWER)-inheritance of mutated HFE gene inhibits production of
hepcidin, leading to constant activation of ferroportin
-increased levels of iron in circulation are exposed to oxygen and produce damaging superoxide ions
-symptoms: begin between 30-40, iron deposits on organs (pancreas), bronzed diabetes, cell death,
release of lysosomal enzymes
-increased serum ferritin and transferrin saturation
-genetic testing reveals mutated HFE gene
hereditary hemochromatosis treatment - (ANSWER)-therapeutic phlebotomy: 500 mL of blood is
removed per week to decrease serum iron
megaloblastic anemia - (ANSWER)-impaired DNA synthesis due to deficiency of Vitamin B12 and/ or
folate leads to decreased number of cell divisions
-produces large macrocytes with immature nuclei
-symptoms: fever, glossitis, loss of appetite, neurologic abnormalities (pins and needles, numbness,
hallucinations and paranoia/ megaloblastic madness)
-pancytopenia
-decreased H/H
-macrocytosis
-increased MCV, high RDW
-hypersegmented neutrophils
-nuclear cytoplasmic asynchrony
_M:E ratio 1:1 to 1:3
-teardrop cells, schistocytes and microspherocytes in PB
, MMSC 433 FINAL | QUESTIONS AND ANSWERS | 2026 UPDATE | WITH COMPLETE
SOLUTIONS.
-Howell jolly bodies (DNA remnants) and cabot rings (figure 8)
-increased bilirubin and LDH
G6PD deficiency - (ANSWER)-decrase in G6PD enzyme causes underproduction of NADPH, leading to
inability to reduce glutathione for detox of H2O2
-H2O2 oxidizes hemoglobin in the RBCs, leading to formation of *heinz bodies*
-can be induced by oxidative drugs
-symptoms: jaundice, anemia, hyperbilirubinemia
-N/N anemia
-anisocytosis, poikilocytosis
-spherocytes and schistocytes in PB
-*heinz bodies seen with crystal violet*
-G6PD activity decreased
-fluorescent spot test negative
hereditary spherocytosis (HS) - (ANSWER)-proteins in the RBC membrane disrupt *vertical* interactions
and destabilize the lipid bilayer, causing loss of membrane material that leads to formation of
spherocytes
-mutations in genes for *ankyrin*, alpha and beta spectrin or protein 4.2 lead to increased membrane
permeability to Na+ and K+, leading to cellular dehydration
-splenic conditioning: abnormal RBCs are targeted by macrophages and lead to anemia
-HS triad: N/N anemia, jaundice and splenomegaly
-*spherocytes* and polychromasia in PB
-increased MCHC and RDW
-increased osmotic fragility
-EMA binding test: low fluorescence
-autohemolysis test: 10-50%, decreased in presence of glucose
SOLUTIONS.
iron absorption - (ANSWER)-ferric iron is taken in from diet
-ferric iron is reduced by duodenal cytochrome B to become ferrous iron
-ferrous iron is absorbed into enterocytes by DMT 1
-absorbed iron is stored as ferritin, or sent into portal hepatic circulation and carried by transferrin to
developing RBCs
transferrin - (ANSWER)plasma carrier protein for ferrous iron
high iron level regulation - (ANSWER)-hepcidin is released from hepatocytes
-ferroportin is inactivated, leading to decreased iron being transported into circulation
low iron level regulation - (ANSWER)-hepcidin is down regulated by hepatocytes
-ferroportin becomes activated and transports iron out of the enterocytes and into circulation
ferrous iron - (ANSWER)the form of iron that is able to be utilized in the body for developing red cells
prussian blue stain - (ANSWER)stain that is used to identify iron in tissues and bone marrow
stage 1 iron deficiency (progressive loss of storage iron) - (ANSWER)-asymptomatic
-RBCs develop normally
-*serum ferritin low*
stage 2 iron deficiency (exhaustion of iron storage pool) - (ANSWER)-subclinical symptoms
-hemoglobin in retics is decreased, *hemogram appears normal still*
-iron deficiency erythropoiesis is occurring
-hepcidin decreased
-serum iron and ferritin decreased
-RDW, TIBC and sTRs increased
,MMSC 433 FINAL | QUESTIONS AND ANSWERS | 2026 UPDATE | WITH COMPLETE
SOLUTIONS.
-prussian blue stain of BM is negative for iron
stage 3 iron deficiency (frank anemia) - (ANSWER)-patient exhibits fatigue, weakness, pallor, glossitis,
koilonychia and pica
-*H/H decreased*
-*hypochromic/ microcytic anemia*
-FEP, TIBC and sTR increased
-ferritin, hepcidin and serum iron decreased
sideroblastic anemia - (ANSWER)-iron deposits in the mitochondria of erythroblast cells in the bone
marrow interfere with biosynthesis of heme
-caused by genetic inheritance, drugs/ bone marrow toxins (*lead*, antibiotics, chemotherapeutics)
-*ringed sideroblasts* are highly indicative of the disease
-basophillic stippling is common in lead poisoning
-normocytic normochromic cells
iron deficiency anemia (IDA) - (ANSWER)-caused by inadequate intake, increased need or malabsorption
of iron, poor diet or chronic blood loss
-symptoms: fatigue, weakness, pallor, spooning of the nails (koilonychia) and pica
-*H/H decreased*
-microcytic, hypochromic cells
-marked poikilocytosis (target cells, spherocytes, tear drop cells and schistocytes)
-FEP, sTR and TIBC increased
-ferritin, hepcidin and serum iron decreased
anemia of chronic inflammation - (ANSWER)-anemia occurring secondary to underlying condition
(chronic inflammatory disease, chronic infection or malignancy) that causes release of cell products
-hepcidin, lactoferrin and inflammatory cytokines cause decreased iron status and anemia
-low Hgb
,MMSC 433 FINAL | QUESTIONS AND ANSWERS | 2026 UPDATE | WITH COMPLETE
SOLUTIONS.
-*low TIBC* (hepcidin is increased due to acute phase reaction)
-normocytic normochromic anemia
-serum iron decreased
-ferritin (acute phase reactant) and FEP increased
hereditary hemochromatosis (HH) - (ANSWER)-inheritance of mutated HFE gene inhibits production of
hepcidin, leading to constant activation of ferroportin
-increased levels of iron in circulation are exposed to oxygen and produce damaging superoxide ions
-symptoms: begin between 30-40, iron deposits on organs (pancreas), bronzed diabetes, cell death,
release of lysosomal enzymes
-increased serum ferritin and transferrin saturation
-genetic testing reveals mutated HFE gene
hereditary hemochromatosis treatment - (ANSWER)-therapeutic phlebotomy: 500 mL of blood is
removed per week to decrease serum iron
megaloblastic anemia - (ANSWER)-impaired DNA synthesis due to deficiency of Vitamin B12 and/ or
folate leads to decreased number of cell divisions
-produces large macrocytes with immature nuclei
-symptoms: fever, glossitis, loss of appetite, neurologic abnormalities (pins and needles, numbness,
hallucinations and paranoia/ megaloblastic madness)
-pancytopenia
-decreased H/H
-macrocytosis
-increased MCV, high RDW
-hypersegmented neutrophils
-nuclear cytoplasmic asynchrony
_M:E ratio 1:1 to 1:3
-teardrop cells, schistocytes and microspherocytes in PB
, MMSC 433 FINAL | QUESTIONS AND ANSWERS | 2026 UPDATE | WITH COMPLETE
SOLUTIONS.
-Howell jolly bodies (DNA remnants) and cabot rings (figure 8)
-increased bilirubin and LDH
G6PD deficiency - (ANSWER)-decrase in G6PD enzyme causes underproduction of NADPH, leading to
inability to reduce glutathione for detox of H2O2
-H2O2 oxidizes hemoglobin in the RBCs, leading to formation of *heinz bodies*
-can be induced by oxidative drugs
-symptoms: jaundice, anemia, hyperbilirubinemia
-N/N anemia
-anisocytosis, poikilocytosis
-spherocytes and schistocytes in PB
-*heinz bodies seen with crystal violet*
-G6PD activity decreased
-fluorescent spot test negative
hereditary spherocytosis (HS) - (ANSWER)-proteins in the RBC membrane disrupt *vertical* interactions
and destabilize the lipid bilayer, causing loss of membrane material that leads to formation of
spherocytes
-mutations in genes for *ankyrin*, alpha and beta spectrin or protein 4.2 lead to increased membrane
permeability to Na+ and K+, leading to cellular dehydration
-splenic conditioning: abnormal RBCs are targeted by macrophages and lead to anemia
-HS triad: N/N anemia, jaundice and splenomegaly
-*spherocytes* and polychromasia in PB
-increased MCHC and RDW
-increased osmotic fragility
-EMA binding test: low fluorescence
-autohemolysis test: 10-50%, decreased in presence of glucose
