FTR

o Exposure to blood products at some time for antibodies to develop; common

in multiparous women who commonly have fetomaternal bleeds during
delivery
o Patients should receive leukocyte poor blood
o Patient anti-HLA antibodies are directed against donor leukocytes; Mature
RBCs lack HLA antigen on their surface
HTR
o Antibody directed against an antigen on donor RBC
o Delayed hemolytic transfusion reaction
o Type 2 HSR
o Extravascular hemolysis- macrophage removal of RBCs
Possible ruptured spleen
o Positve tilt test= volume depletion
o Common w/ lower left ribcage injuries
o Normal saline uncovers RBC deficit
o Peritoneal lavage= intraabdominal bleeding
Most common cause of jaundice in first 24 hrs is ABO HDN
o Spherocytes in babies blood
o Rh incompatibility
o T2HSR
o ABO incompatibility protects against Rh sensitization, but mother should still
receive Rh immune globulin. Mothers anti-A IgM will destroy babies D
antigen + cells before shes able to develop antibodies
Rh HDN
o No risk during 1st pregnancy
o Severe anemia requiring blood transfusion
o Positive direct coombs test
o Unconjugated hyperbilirubinemia
o Extravascular hemolysis of fetal RBCs by maternal anti-A,B, IgG antibodies
ABO HDN
o Can affect first kid
o Spherocytes in newborns peripheral blood
o Positive direct coombs test
o Unconjugated hyperbilirubinemia
o Sequence is
Anti-A,B IgG in maternal serum
Fetal RBCs with anti-A,B-IgG antibodies on surface
Phagocytosis of fetal RBCs in fetal splenic macrophages
Conjugation of bilirubin in maternal liver
Jaundice in baby
A major crossmatch
o Does not guarantee survival of the infused donor RBCs
o Does not prevent patient antibodies developing against donor RBC antigens;
in fact, it is very likely the patient will, because most patients do not receive
blood from identical twin

Blood group facts

o Duodenal ulcers are more common in blood group O patients
o Gastric adenocarcinomas are usually seen in group A patients
o AB are universal recipients; O is universal donor
o 1:300 chance of becoming HIV+ from needle stick of positive patient
o HBV has greatest viral load in blood of all viruses; HBV common in Iv drug
users
o Anti-CMV is most commonly encountered antibody
o CMV is the most common infection transmitted by a blood transfusion
Bone marrow transplants and newborns particularly prone to infection
in lungs
Hepatitis risk from infusion of:
o Cryoprecipitate, FFP, Packed RBCs
o HCV is most common cause of transfusion hepatitis; HCV screening relatively
new
Malaria
o Absence of a Duffy blood group antigen (attachment site) protects against P.
vivax
o Mutations that help against Plasmodium falciparum
Sickle cell
G6P deficiency
B-thalassemia

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
o
o
o
o
o
o

G6PD deficiency
o XR disease
Heinz bodies
Decreased RBC glutathione
Worsed by sulfur drug
Primarily intravascular
Bite cells

Macroangiopathic intravascular hemolytic anemia

o Decreased plasma haptoglobin
o Schistocytes
o Hemoglobinuria
o Decreased serum ferritin
o Aortic stenosis MCC

Sickle cell anemia

o Step pneumonia (G+) common; reason for pneumovax
o Aseptic necrosis of femoral head- salmonella- osteomyelitis
o Acute chest syndrome w/ infiltrates and hypoxemia- MC death for adults
o Dactylitis by 6-9 months
o Iron overload due to multiple transfusions
o Septicemia due to step MC death in children

Iron deficient anemia

o Decreased serum iron, ferritin, and percent saturation
o Increased TIBC
o Positive stool guiac
o Over 50= cancer, stool guaic

Anemia of chronic disease

o Decreased serum iron, TIBC, percent saturation

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

o Increased serum ferritin

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
o
o
o

Autoimmune hemolytic anemia

o Spherocytes
o Polychromasia
o Corrected reticulocyte under 3%
o Unconjugated hyperbilirubinemia- macrophage destruction of RBCs coated
by IgG and C3b
o Autoantibodies against Rh with methyldopa use
o T2HSR
o Extravascular hemolytic

Hemosiderosis
o Iron overload due to multiple transfusions
o Decreased TIBC
o Increased serum iron, ferritin, and percent saturation

Anemia related to type 2 hypersensitivity

o Patient on penicillin- IgG antibody against drug on RBC membrane
o Patient w/ SLE

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

Normocytic anemias w/ corrected reticulocyte under 3

minor thalassemia
Abnormal Hgb electrophoresis
Increased A2, F; Decreased HgbA
Normal to high RBC count

o
o
o
o
o

Blood loss under 1 week

Iron deficiency- early before it becomes microcytic
Anemia of chronic disease
Chronic renal failure
Aplastic anemia

Normocytic w/ count over 3

o Hereditary spherocytosis- extravascular
Intrinsic w/ defect in ankyrin
o G6PD- mostly intravascular
o Cold autoimmune- mostly intravascular due to IgM
o Microangiopathic hemolytic- intravascular

Extravascular hemolytic anemia

o Warm autoimmune
Extrinsic w/ IgG against altered Rh
o Heriditary spherocytosis
Spherocytes

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

o Cold AI- IgM

o Quinidine-induced (T3HSR)
Sideroblastic anemia
o Requires bone marrow exam for diagnosis
Ringed sideroblasts

Polychromasia is an increase in blue-staining cells falsely increasing reticulocyte

count
o Takes 2-3 days to become mature; divide by 2

Howell Jolly body- remnant of nucleus in RBC removed by splenic macrophages

normally
o Presence indicates absent or dysfunction spleen

Spherocytes are most often seen in AI hemolytic anemia when macrophages bites
of some RBC membrane

Rouleau indicated increase in fibrinogen in inflammation; stack of coin effect;

fibrinogen is an acute phase reactant synthesized and released in acute or chronic
inflammation; Roulea increases erythrocyte sedimentation rate

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

Marker cells indicate hemoglobinopathy or macrocytes in alcoholic liver disease;

bulges in center

Hypersegmented neutrophils is a marker for folate or B12

Schistocytes is marker for thrombi or AS

Tear drop cells are markers for bone marrow fibrois or thalassemia

Macroovalocyte is egg shaped and classic finding in folate or B12