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90 Cards in this Set
- Front
- Back
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MCV |
hct / RBC
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MCV
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hct / RBC
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MCH
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hgb/RBC
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MCH
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hgb/RBC
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MCHC
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hgb/hct
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MCHC
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hgb/hct
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HbA
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α2β2
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HbA
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α2β2
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HbA2
common situation this is increased? |
α2δ2 (delta)
beta-thal |
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HbA2
common situation this is increased? |
α2δ2 (delta)
beta-thal |
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HbF
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α2γ2 (gamma)
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HbF
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α2γ2 (gamma)
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HbS
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α2βs2
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HbS
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α2βs2
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What is this called?
What RBC parameters are affected? Causes? |
Spherocyte
Loss of membrane without volume loss MCHC is increased Osmotic fragility is increased HS, warm aiha, old blood, burn, venom, oxidant damage |
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What is this called?
What RBC parameters are affected? Causes? |
Spherocyte
Loss of membrane without volume loss MCHC is increased Osmotic fragility is increased HS, warm aiha, old blood, burn, venom, oxidant damage |
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How is HS inherited & what is the defect?
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AD
Defect in spectrin / ankyrin RBC membrane protein (ankyrin is MOST COMMON, chrom 8) |
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How is HS inherited & what is the defect?
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AD
Defect in spectrin / ankyrin RBC membrane protein (ankyrin is MOST COMMON, chrom 8) |
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Name?
Causes? |
Echinocyte (Burr cell)
ACUTE RENAL FAILURE Acidic environment; sitting in EDTA too long "Prickle cells" of pyruvate kinase deficiency |
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Name?
Causes? |
Echinocyte (Burr cell)
ACUTE RENAL FAILURE Acidic environment; sitting in EDTA too long "Prickle cells" of pyruvate kinase deficiency |
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Name?
How is this different than burr cell? Seen in what 3 classic pictures? |
Acanthocyte (Spur cell)
Irregular, fewer, blunted projections LIVER DISEASE Kx deficiency (McLEOD PHENOTYPE) aB-lipoproteinemia -also in hypothyroid, MDS |
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Name?
How is this different than burr cell? Seen in what 3 classic pictures? |
Acanthocyte (Spur cell)
Irregular, fewer, blunted projections LIVER DISEASE Kx deficiency (McLEOD PHENOTYPE) aB-lipoproteinemia -also in hypothyroid, MDS |
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Name?
Seen in? |
Codocyte (target cell)
too much membrane = decreased osm fragility Seen in: Asplenia IDA Liver disease Hemoglobinopathies |
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Name?
Seen in? |
Codocyte (target cell)
too much membrane = decreased osm fragility Seen in: Asplenia IDA Liver disease Hemoglobinopathies |
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Name?
Classically seen in? |
Bite cell
Seen in cases of oxidative damage (G6PD!!!!!!) (spleen bites out Heinz bodies) |
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Name?
Classically seen in? |
Bite cell
Seen in cases of oxidative damage (G6PD!!!!!!) (spleen bites out Heinz bodies) |
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How to tell normal from pathologic?
Classically seen in? |
Basophilic stippling
- Reticulocytes have small fine blue dots; pathologic states tend to be coarser LEAD POISONING Pyrimidine 5' nucleotidase deficiency MDS Infection Sideroblastic anemia Porphyria |
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How to tell normal from pathologic?
Classically seen in? |
Basophilic stippling
- Reticulocytes have small fine blue dots; pathologic states tend to be coarser LEAD POISONING Pyrimidine 5' nucleotidase deficiency MDS Infection Sideroblastic anemia Porphyria |
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Seen in?
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Howell Jolly bodies
-DNA / nuclear remnant; 3D; peripheral -Spleen normally bites these out Indicate asplenia (functional or real) -SCD, neuroblastoma, IBD, GVHD, ai) |
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Seen in?
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Howell Jolly bodies
-DNA / nuclear remnant; 3D; peripheral -Spleen normally bites these out Indicate asplenia (functional or real) -SCD, neuroblastoma, IBD, GVHD, ai) |
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What are these made of?
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pappenheimer bodies
multiple. See with Howell-Jolly. IRON See with asplenia; iron overload |
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What are these made of?
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pappenheimer bodies
multiple. See with Howell-Jolly. IRON See with asplenia; iron overload |
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What are these and what stain is this?
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Heinz bodies |
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What are these and what stain is this?
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Heinz bodies
See with reticulin stain - don't see with Wright Giemsa Represent oxidized hemoglobin: G6PD, unstable hgb, 3deletion alpha thal Bite cells have them bitten out |
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Rouleaux
secondary to large proteins: fibrinogen, immunoglobulin |
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Rouleaux
secondary to large proteins: fibrinogen, immunoglobulin |
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How is this different than rouleaux?
causes? How to correct? What indices will be changed? |
Autoagglutination
RBC clumping COLD AGGLUTININS (IgM autoantibody: EBV, mycoplasma) Correct by warming increased MCV, decreased RBC |
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How is this different than rouleaux?
causes? How to correct? What indices will be changed? |
Autoagglutination
RBC clumping COLD AGGLUTININS (IgM autoantibody: EBV, mycoplasma) Correct by warming increased MCV, decreased RBC |
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Babesia
Babesia parasites resemble Plasmodium falciparum, however Babesia has several distinguishing features: the parasites are pleomorphic (vary in shape and size), can be vacuolated, and do not produce pigment. Can be extracellular |
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Babesia
Babesia parasites resemble Plasmodium falciparum, however Babesia has several distinguishing features: the parasites are pleomorphic (vary in shape and size), can be vacuolated, and do not produce pigment. Can be extracellular |
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Vector for babesia?
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IXODES DAMMINI (same as Lyme)
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Vector for babesia?
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IXODES DAMMINI (same as Lyme)
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Fast migrating Hb?
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J N I H Barts
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Fast migrating Hb?
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J N I H Barts
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Alkaline hgb electrophoresis
What are the bands? |
AFSC
A Fat Santa Claus |
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Alkaline hgb electrophoresis
What are the bands? |
AFSC
A Fat Santa Claus |
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What classically migrates with S in alkaline?
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S D G Lepore
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What classically migrates with S in alkaline?
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S D G Lepore
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What classically migrates with C on alkaline?
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C E O A2
Also C-Harlem |
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What classically migrates with C on alkaline?
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C E O A2
Also C-Harlem |
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What does the star represent?
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Fast migrating hemoglobins (JNIHBarts)
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What does the star represent?
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Fast migrating hemoglobins (JNIHBarts)
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What is a classic slow-migrating hemoglobin on alkaline?
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Constant Spring
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What is a classic slow-migrating hemoglobin on alkaline?
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Constant Spring
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Acid hb electrophoresis. What are the bands?
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F A S C
Lots migrate with A... |
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Acid hb electrophoresis. What are the bands?
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F A S C
Lots migrate with A... |
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The patient is in lane 1. There was an abnormal hemoglobin on alkaline gel in the C lane. What is it?
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Hemoblobin E.
The abnormal hemoglobin migrates as Hb C on cellulose acetate and as Hb A in acid agar. Diagnosis : Hb E trait (heterozygote for Hb E) Comment : Hb E is very common among southeast Asians. |
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The patient is in lane 1. There was an abnormal hemoglobin on alkaline gel in the C lane. What is it?
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Hemoblobin E.
The abnormal hemoglobin migrates as Hb C on cellulose acetate and as Hb A in acid agar. Diagnosis : Hb E trait (heterozygote for Hb E) Comment : Hb E is very common among southeast Asians. |
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African American with jaundice after fava beans
disease? Inheritance? Triggers? |
G6PD
10% Af Amer (wildtype is type B***) Susceptible to oxidative damage; Heinz bodies, hemolysis RETICULOCYTES ARE NORMAL XR (boys) Triggers: fava beans, sulfa drugs, antimalarials, infxn (hepatitis, pna, thyroid) COOMBS TEST IS NEGATIVE G6PD protects against malaria! |
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African American with jaundice after fava beans
disease? Inheritance? Triggers? |
G6PD
10% Af Amer (wildtype is type B***) Susceptible to oxidative damage; Heinz bodies, hemolysis RETICULOCYTES ARE NORMAL XR (boys) Triggers: fava beans, sulfa drugs, antimalarials, infxn (hepatitis, pna, thyroid) COOMBS TEST IS NEGATIVE G6PD protects against malaria! |
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Thal minor
Inheritance? Clues? |
One damaged Beta chain
AR chrom 11 Microcytic anemia with increased RBC (MCV/RBC<13) HbA2 > 3.5% (vs IDA!!) |
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Thal minor
Inheritance? Clues? |
One damaged Beta chain
AR chrom 11 Microcytic anemia with increased RBC (MCV/RBC<13) HbA2 > 3.5% (vs IDA!!) |
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Thal major, a.k.a...?
Population? Inheritance? Clues? Clues? |
Cooley's anemia
2 damaged B chains AR, Chrom 11, Mediterranean Marked anisopoikilocytosis Splenomegaly, death < 20y |
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Thal major, a.k.a...?
Population? Inheritance? Clues? Clues? |
Cooley's anemia
2 damaged B chains AR, Chrom 11, Mediterranean Marked anisopoikilocytosis Splenomegaly, death < 20y |
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Inheritance of alpha thal?
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AR chrom 16
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Inheritance of alpha thal?
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AR chrom 16
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Why is beta-thal picked up in the first year of life while alpha-thal is diagnosed in utero?
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Because B thal can make HbF, which is normal at birth. Beta chain production (and hence hgb A) is not predominant right away.
vs. Alpha thal: alpha chain is required for all types of hgb |
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Why is beta-thal picked up in the first year of life while alpha-thal is diagnosed in utero?
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Because B thal can make HbF, which is normal at birth. Beta chain production (and hence hgb A) is not predominant right away.
vs. Alpha thal: alpha chain is required for all types of hgb |
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Hgb types in B thal minor
Major? |
HbF < 5%
HbA2 4-10% Major: HbF 90% |
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Hgb types in B thal minor
Major? |
HbF < 5%
HbA2 4-10% Major: HbF 90% |
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1-deletion alpha thal
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silent carrier
slight decreased MCV, MCH |
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1-deletion alpha thal
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silent carrier
slight decreased MCV, MCH |
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2 deletion alpha thal
Does it matter if it is -/- a/a or -/a -/a? |
"alpha thal trait"
Mild microcytic anemia -/- a/a seen in Chinese -/a -/a in African Americans matters for inheritance |
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2 deletion alpha thal
Does it matter if it is -/- a/a or -/a -/a? |
"alpha thal trait"
Mild microcytic anemia -/- a/a seen in Chinese -/a -/a in African Americans matters for inheritance |
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3-deletion alpha thal
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get tetramers. microcytic anemia. Heinz bodies. Splenomegaly.
HbH (4 beta chains) (GOLF BALLS) and HbBarts (gamma x 4)(normally in HbF) -both have HIGH affinity for O2 |
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3-deletion alpha thal
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get tetramers. microcytic anemia. Heinz bodies. Splenomegaly.
HbH (4 beta chains) (GOLF BALLS) and HbBarts (gamma x 4)(normally in HbF) -both have HIGH affinity for O2 |
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4-deletion alpha thal
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No alpha chains.
HbBarts (tetrameric gamma) Fatal Hydrops fetalis |
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4-deletion alpha thal
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No alpha chains.
HbBarts (tetrameric gamma) Fatal Hydrops fetalis |
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Hemoglobin that is made of 2 alpha chains and 2 delta-beta fusion chains?
What does it mimic? |
Hemoglobin Lepore
Mimics thal trait (B thal minor) |
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Hemoglobin that is made of 2 alpha chains and 2 delta-beta fusion chains?
What does it mimic? |
Hemoglobin Lepore
Mimics thal trait (B thal minor) |
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delta-beta thalassemia
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deletion of both delta and beta chains on chrom 11
heterozygous (~thal minor) or homozygous (~thal intermedia) also known as "F thalassemia" since there are no A or A2 hemoglobins produced (since no delta or beta), they have only F |
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delta-beta thalassemia
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deletion of both delta and beta chains on chrom 11
heterozygous (~thal minor) or homozygous (~thal intermedia) also known as "F thalassemia" since there are no A or A2 hemoglobins produced (since no delta or beta), they have only F |
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How to tell hereditary persistance of fetal hemoglobin vs. delta-beta thal?
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Both have increased HbF!!!!!!
BUT delta-beta thal will have decreased total hemoglobin resulting in a low MCV, low MCHC, high normal to elevated erythrocyte counts and often low or low normal HbA2. In contrast, in HPFH the total amount of hemoglobin produced is sufficient to prevent these abnormalities |
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How to tell hereditary persistance of fetal hemoglobin vs. delta-beta thal?
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Both have increased HbF!!!!!!
BUT delta-beta thal will have decreased total hemoglobin resulting in a low MCV, low MCHC, high normal to elevated erythrocyte counts and often low or low normal HbA2. In contrast, in HPFH the total amount of hemoglobin produced is sufficient to prevent these abnormalities |
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Heterozygous beta thal
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Heterozygous beta thal
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nice graphic
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nice graphic
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name the lanes
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Lanes 1 and 5 are hemoglobin standards.
Lane 2 is a normal adult. Lane 3 is a normal neonate. Lane 4 is a homozygous HbS individual. Lanes 6 and 8 are heterozygous sickle individuals. Lane 7 is a SC disease individual. |
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name the lanes
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Lanes 1 and 5 are hemoglobin standards.
Lane 2 is a normal adult. Lane 3 is a normal neonate. Lane 4 is a homozygous HbS individual. Lanes 6 and 8 are heterozygous sickle individuals. Lane 7 is a SC disease individual. |
