MMSC 433 Final Exam | Questions with 100% Verified Answers | Latest Update
Question: 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
Question: transferrin
Answer:
plasma carrier protein for ferrous iron
Question: high iron level regulation
Answer:
-hepcidin is released from hepatocytes
-ferroportin is inactivated, leading to decreased
iron being transported into circulation
Question: low iron level regulation
Answer:
-hepcidin is down regulated by hepatocytes
-ferroportin becomes activated and transports
iron out of the enterocytes and into circulation
Question: ferrous iron
Answer:
the form of iron that is able to be utilized in the body for developing red cells
Question: prussian blue stain
Answer:
stain that is used to identify iron in tissues and bone marrow
,Question: stage 1 iron deficiency (progressive loss of storage iron)
Answer:
-asymptomatic
-RBCs develop normally
-serum ferritin low
Question: 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
Question: 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
Question: 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
,Question: 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
Question: 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
Question: 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
, Question: hereditary hemochromatosis treatment
Answer:
-therapeutic phlebotomy: 500 mL of blood is
removed per week to decrease serum iron
Question: 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
Question: 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
Question: 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
Question: transferrin
Answer:
plasma carrier protein for ferrous iron
Question: high iron level regulation
Answer:
-hepcidin is released from hepatocytes
-ferroportin is inactivated, leading to decreased
iron being transported into circulation
Question: low iron level regulation
Answer:
-hepcidin is down regulated by hepatocytes
-ferroportin becomes activated and transports
iron out of the enterocytes and into circulation
Question: ferrous iron
Answer:
the form of iron that is able to be utilized in the body for developing red cells
Question: prussian blue stain
Answer:
stain that is used to identify iron in tissues and bone marrow
,Question: stage 1 iron deficiency (progressive loss of storage iron)
Answer:
-asymptomatic
-RBCs develop normally
-serum ferritin low
Question: 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
Question: 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
Question: 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
,Question: 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
Question: 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
Question: 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
, Question: hereditary hemochromatosis treatment
Answer:
-therapeutic phlebotomy: 500 mL of blood is
removed per week to decrease serum iron
Question: 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
Question: 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
