MMSC 433 exam 1 with complete solution
iron absorption
-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 ...
MMSC 433 exam 1 with complete solution
iron absorption
-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
plasma carrier protein for ferrous iron
high iron level regulation
-hepcidin is released from hepatocytes
-ferroportin is inactivated, leading to decreased iron being transported into circulation
low iron level regulation
-hepcidin is down regulated by hepatocytes
-ferroportin becomes activated and transports iron out of the enterocytes and into circulation
dietary iron sources
red meat, legumes, dark leafy vegetables, whole grains
ferrous iron
the form of iron that is able to be utilized in the body for developing red cells
prussian blue stain
stain that is used to identify iron in tissues and bone marrow
thomas plot
a chart that is used to compare soluble transferrin receptors/ log ferritin to hemoglobin
concentration of reticulocytes to identify the iron status of the patient
-iron status is used to correlate to certain diseases/ anemias
stage 1 iron deficiency (progressive loss of storage iron)
-asymptomatic
-RBCs develop normally
-serum ferritin low
stage 2 iron deficiency (exhaustion of iron storage pool)
-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)
-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
, -iron deposits in the mitochondria of erythroblast cells in the bone marrow interfere with
biosynthesis of heme
-caused by genetic inheritance of 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)
-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
-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)
-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
-therapeutic phlebotomy: 500 mL of blood is removed per week to decrease serum iron
megaloblastic anemia
-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
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