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
-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
-*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
-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
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
-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
-*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
-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
