1|Page
MMSC 433 Final Questions with 100% Verified Answers
UPDATED!!!
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
,2|Page
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
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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*
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-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
MMSC 433 Final Questions with 100% Verified Answers
UPDATED!!!
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
,2|Page
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
,3|Page
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*
, 4|Page
-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
