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45 Cards in this Set

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2 causes of anemia associated with iron metabolism
1. faulty heme production
(lack of Fe, defective iron production, or defective PORPHYRIN production)
2. faulty globin synthesis
Etiology of Iron deficiency anemia (IDA)
1. poor diet
2. malabsorption
3. increased demand (pregnancy, etc)
4. blood loss (most common cause)
symptoms of decrease of hemoglobin in body
weakness, fatigue, dizziness
shortness of breath
skin pallor
symptoms of decrease of Fe-containing enzymes in tissues
impaired neutrophil phagocytosis
impaired cell-mediated immunity
neurologic abnormalities
Stages of IDA
1. iron depletion: Fe stores exhausted, normal peripheral blood values & morphology except for slight increase in RDW
2. Fe-deficient erythropoiesis: Fe levels drop, no sideroblasts in marrow
Increased: FEP, TIBC
Decreased: MCV
3. Fe deficiency anemia
decrease in Hb, microcytic hypochromic RBCs
peripheral blood smear features of IDA
Microcytosis, hypochromia, anisocytosis, poikilocytosis
changes in bone marrow in IDA
erythroid hyperplasia in bone marrow, abnormal erythroblasts, decreased hemosiderin, decreased sideroblasts
lab findins of IDA
DECREASED: Hb, Hct, RBC count, Retic count, Serum Fe, ferritin, transferrin saturation
What is hemachromatosis?
condition of Fe overload characterized by high Fe absorption rate

note: NOT assoc. w/ anemia!
Etiology of Hemachromatosis
1. PRIMARY idiopathic (inherited)
2. Chronic transfusion therapy
Pathophysiology of hemachromatosis
excess Fe deposits accumulate & interfere w/ normal cellular function
Lab findings of hemachromatosis
DECREASED: normal or low TIBC
INCREASED: Serum Fe, serum ferritin, transferrin saturation
what is sideroblastic anemia?
group of disorders characterized by abnormalities of HEME metabolism
Pathophysiology of sideroblastic anemia
1. Fe absorption is normal but UTILIZATION is impaired
2. Fe present but not incorporated into hemoglobin
3. Positive Fe balance, yet anemia still exists
Unique characterics of sideroblastic anemia
1. ringed sideroblasts in bone marrow
2. dimorphic peripheral blood picture
classifications of sideroblastic anemia
1. Idiopathic (primary) - idiopathic refractory anemia w/ dyserythropoiesis, abnormal Fe utilization, PRE-Leukemia
2. secondary -
disturbance in enzymes regulating heme synthesis (alcoholism, malignancies, etc)
visual characteristics of secondary sideroblastic anemia
poikilocytosis, inclusions, basophilic stippling, dimorphism in peripheral blood
lab findings in secondary sideroblastic anemia
DECREASED: TIBC (can be normal too)
INCREASED: serum Fe, transferrin, FEP
what is anemia of chronic disease (AOD)/anemia of inflammation (AOI)
anemia caused by a long term chronic disease, 2nd most common anemia in western world
Pathophysiology of AOD/AOI
caused by decrease of Fe flow to bone marrow (by blockage?)
erythropoietin not stimulated
shortened RBC survival: changes to rbc surfaces, hyperactive macrophages, intramedullary destruction
suppression of erythropoiesis:
release of IL-1
Effect of IL-1 on body in situation of AOD
IL-1 inhibits erythroid stem cell proliferation. Activates neutrophilic response w/ release of lactoferrin. Aids release of tissue necrosis factor (TNF)
Clinical findings of AOI/AOD
1. general symptoms of anemia
2. generally present in mild form
Lab findings of AOD/AOI
Polychromasia, Anisocytosis (P b4 A)
DECREASED: serum Fe, TIBC, transferrin saturation, sideroblasts in marrow
INCREASED: serum ferritin
what is a megaloblastic anemia
group of disorders which have characteristic of macrocytosis. Caused by impairment of DNA synthesis, resulting in abnormal erythrocyte, GRANULOCYTE, & MEGAKARYOCYTE maturation
megaloblastic vs. non-megaloblastic macrocytosis
nonmegaloblastic macrocytosis results if RBCs are released too early from marrow (acute blood loss, hemolysis, alcoholism)
classification of megaloblastic anemia (3)
1. due to folic acid deficiency
2. due to vitamin B12 deficiency
3. due to unresponsiveness to folic acid or B12
Mechanism of megaloblastic transformation
unbalanced growth of developing cells in bone marrow due to impaired DNA synthesis w/o assoc. impairment of RNA/protein synthesis. disparity between nucleus & cytoplasm called NUCLEAR-CYTOPLASMIC ASYNCHRONISM
nutritional aspects of Folic Acid deficiency
SOURCES: leafy veggies, liver, kidney, yeast, mushrooms, dairy, eggs
DAILY REQ: narrow margin between what is required and what is intaked
BODY STORES: depleted within months if no new source
INTESTINAL ABSORPTION: most in proximal jejunum
Etiology of folic acid deficiency
1. inadequate dietary intake (folate is destroyed when heated during cooking)
2. increased requirements of Folic acid
3. impaired absorption
4. drug inhibition: alcoholism, oral contraceptives, anti-cancer drugs
Clinical features of folic acid deficiency
1. general signs of anemia
2. glossitis
3. insidious onset
4. diarrhea/steatorrhea (fatty stool)
5. weight loss
visual findings of peripheral blood in folic acid deficiency
hypersegmented neutrophils
large, hypogranular bands
decreased, enlarged platelets
oval macrocytes
Howell-jolly bodies, baso. stip., cabot rings
polychromatophilia, nucleated RBCs
lab findings in folic acid deficiency
DECREASED: Hb, Hct, RBC count, retic count (RPI<2), pancytopenia
Changes in bone marrow in folic acid deficiency
2. megaloblastic changes
a. loose, open chromatin in RBC precursors
b. Giant bands & metamyelocytes
c. giant megakaryocytes
Specific features of folic acid deficiency
decreased serum and red cell folate
NORMAL B12 levels
treated w/ folic acid
INCREASED FIGLU (intermed. in glutaminic acid synthesis)
nutritional aspects of Vitamin B12 deficiency (sources, daily req., body stores, absorption)
SOURCES: liver, meat, milk, eggs, fish
Daily requirements: 3-5ug, plenty in all but vegan diets
Body stores: enough for few years
absorption: occurs in ileum and requires INTRISIC FACTOR (IF) & TRANSCOBALAMIN II (TC II)
etiology of B12 deficiency
1. impaired absorption:
several problems, main is Pernicious anemia
2. microorganism competition: tapeworms, bacteria in blind loop syndrome
3. defects in transport proteins:
hereditary deficiency of TCII
abnormal TC II
4. dietary deficiency
What is Pernicious anemia?
megaloblastic anemia caused by absence of IF secondary to gastric atrophy. B12 can't be absorbed w/o it. most common B12 deficiency
Clinical features of B12 deficiency
1. same as folic acid deficiency
2. addition of NEUROLOGIC abnormalities:
parasthesias, gait abnormality, difficulty w/ fine motor coordination
Lab findings of B12 deficiency
same as seen in folic acid deficiency and megaloblastic anemia in general.
SPECIFIC features: decreased serum B12
responsive to B12 therapy
increased methylmalonic acid
causes of megaloblastic anemia to be unresponsive to B12 or folate therapy
1 antimetabolic drugs
2. Congenital deficiencies
a. hereditary orotic aciduria
b. Leysch-Nyhan syndrome
c. errors of folate metabolism
3. unexplained disorders
a. myelodysplastic syndrome (preleukemia)
b. erythroleukemia
causes of macrocytosis WITHOUT megaloblastic changes
1. Alcoholism
2. liver disease

some overlap, lipids build up on RBC surface w/ no way to metabolise them

3. reticulocytosis
Characteristics of macrocytosis
1. ROUND, not oval macrocytes
2. less pronounced macrocytes
3. no super segs
4. no pancytopenia
5. absence of megaloblastic anemia signs: jaundice, glossitis, neuropathy
Etiology of macrocytosis
there is an increase in membrane lipids
there is a delay in blast maturation
chemsitry tests useful in differential Dx of macrocytosis
LDH, bilirubin, serum B12, serum and red cell folate levels, gastric analysis, SCHILLING TEST, BONE MARROW EXAMINATION
what is Schilling test?
differentiates B12 deficiency resulting from malabsorption, dietary inadequacy, or lack of IF.