RBC disorders
Pernicious anemia
o Decreased serum B12
o Hypersegmented neutrophils
o Abnormal schillings test corrected by adding intrinsic factor
o Increased Homocysteine
o Increased serum gastrin
o Neurological findings- decreased vibratory sensation (posterior column
disease)
o Autoantibodies against parietal cells and intrinsic factor
Drugs
o Oral contraceptives
Cause hypertension, increased T4, & decrease reabsorption of
monoglutamates in jejenum
o Methotexate
Reversibly inhibits dihydrofolate reductase= folic acid deficiency
Suppresses bone marrow= leukopenia and thrombocytopenia
Used in Tx of arthritis
o Indomethacin
Aplastic anemia
o Systemic corticosteroids
Increases neutrophil count by inhibiting neutrophil adhesion molecule
activation
o Trimethoprim/sulfamethoxazole
Blocks dihydrofolate reductase and can cause macrocytic anemia w/
hyperseg neutrophils
Schillings test
o Abnormal test+ intrinsic factor= pernicious anemia
o Abnormal test + pancreatic extract= pancreatic insufficiency
o Abnormal test + antibiotic= bacterial overgrowth
o Normal test= malabsorption of B12 in terminal ileum
o Crohns disease would be abnormal w/ no correction
Involves terminal ileum- why B12 cant be absorbed
Ciliacs disease
o Involves duodenum (reabsorbs iron) and jejunum (reabsorbs folic acid)= iron
deficiency and microcytic and macrocytic cells or a dimorphic RBC population
and combined anemia
Hereditary spherocytosis
o Increased RBC osmotic fragility
o Calcium bilirubinate stones
o RBCs w/ a defect in spectrin
o Increased MCHC
o RBCs with no central area of pallor; presence of polychromasia
o Normal serum ferritin
o Increased unconjugated bilirubin
Deficiency in B12
o Vegans are susceptible
o Atrophic gastritis of body and fundus- destruction of parietal cells leading to
pernicious a.
o Bacterial overgrowth in bowel- destroy intrinsic factor-B12 complex
o Gastrectomy, chronic pancreatitis, removal of ileum increases risk
o Treating w/ folate can correct
Megaloblastic anemia, glossitis, pancytopenia
CAN NOT correct neurological deficits
Folate deficiency
o Overuse in pregnancy
o Acute leukemia
o Phenytoin- blocks intestinal conjugase conversion of poly to monoglutamate
o Contraceptives block absorption of monoglutamate in jejunum
o Alcohol increases risk
Lead
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G6PD deficiency
o XR disease
Heinz bodies
Decreased RBC glutathione
Worsed by sulfur drug
Primarily intravascular
Bite cells
poisoning
Coarse basophilic stippling
Increase blood Pb levels
Increased RBC protoporphyrin levels
Ringed sideroblasts
Microcytic anemia
Increased serum ferritn- increased iron due to death of ringed sideroblasts
and reuptake
o Densities in epiphyses
o Increased levels of ALA causes encephalopathy by increasing vessel
permeability
Exudate
o Peripheral neuropathies, (claw hand, wrist drop) visible deposits in
epiphyses, learning disabilities, Abdominal colic, proximal renal tubular
acidosis
Hemochromatosis
o Autosomal recessive iron overload disorder
o Inverse relationship between ferritin and transferrin synthesis
o Decreased TIBC
o Increased Serum iron, ferritin, percent saturation
Alpha thalassemia
o Normal serum iron, ferritin, percent saturation, a nd TIBC
o Problem with globin, not iron
o Normal RDW; Increased RBC count
o Normal Hgb electrophoresis
Beta
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Hemosiderosis
o Iron overload due to multiple transfusions
o Decreased TIBC
o Increased serum iron, ferritin, and percent saturation
Warm AIHA
o Positive direct coombs test- IgG and C3
o Unconjugated hyperbilirubinemia- extravascular hemolysis
o Positive serum antinuclear antibody test
Erythroid hyperplasia
o High altitude resident
o Blood loss over 1 week
minor thalassemia
Abnormal Hgb electrophoresis
Increased A2, F; Decreased HgbA
Normal to high RBC count
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Intravascular
o Microangiopathic hemolytic
o G6PD
Intrinsic
o Paroxysmal nocturnal hemoglobinuria
Intrinsic w/ membrane defect and activation of complement pathway
o Cold autoimmune
Anemia
o Decreased O2 content
o Tissue hypoxia
o Normal PaO2 and oxygen saturation
Extramedullary hematopoiesis
o Myelofibrosis
o B-thalassemia major
Wright-giemsa stain
o Intraerythrocytic malarial parasites
o Remnants of nuclear material- Howell Jolly bodies
o Coarse basophilic stippling
Pure RBC aplasia
o Involves destruction of erythroid stem cells
o Seen in very brisk hemolytic anemias (sickle, spherocytosis) and w/
thymomas
o Paravirus infection
Complement mediated hemolytic anemias
o Paroxysmal
o Warm AI- IgG, C3
Spherocytes are most often seen in AI hemolytic anemia when macrophages bites
of some RBC membrane
Bite cell indicated oxidant injury to RBCs; macrophage removes Heinz bodies
attached to RBC membrane leaving a defect; Distinctive finding for G6PD
Heinz body is detected using surpavital stain and shows clumps of denatured
hemoglobin
Tear drop cells are markers for bone marrow fibrois or thalassemia