RBC Anomalies

ANOMALIES ILLUSTRATION OF CELL RED CELL DESCRIPTION OF DEFECT OR ASSOCIATED

TYPE OR CELL CHANGES DISEASE
MORPHOLOGY
RED CELL HEMOGLOBIN CONTENT
I) Anisocytosis
-Variation in size
-Microscopic: assess easily
-Qualitative: MCV and RDW
Normocytic Normocytic  6-8 um There may be marked
 Biconcave disc variations in size and
appearance with shape, but these are such
central pallor to equalize one another.

Microcytic Microcytic  <6um Abnormally small RBC  Iron deficiency

 MCV = <80fL containing a low anemia
 Failure of Hgb concentration of  Thalassemia
Synthesis hemoglobin.

Macrocytic Macrocytic  >8um Increase of hemoglobin  Megaloblastic

 MCV = >100fL in individual RBC and anemia
reduction in the number  Liver disease
of RBC  Alcoholism
 Impaired DNA
synthesis
 Stress
erythropoiesis
 Excess surface
membrane

II) Anisochromia
 -Variation in color, Hgb content
-Microscopic: base on central pallor
-MCHC = 32-36 g/dL
Normochromic  Central pallor
that is 1/3 of
cell
 MCHC = 32-36
g/dL

Hypochromic  Central pallor  Iron deficiency

exceeds 1/3 of anemia
cell  Thalassemia
 MCHC=
<32g/dL
 Reduced Hgb
content
Hyperchromic  Central pallor is  Spherocytosis
<1/3 of cell
 MCHC=
>36g/dL

RED CELL SHAPE

I) Poikilocytosis
-Variation in shape
-Normal : Biconcave, “Doughnut appearance” (like krispy kreme )

Acanthocyte Spur cell  Spheroid Defectin the lipid or  End stage liver
 3-12 irregular protein composition of disease
spikes red cell membrane.  Pyruvate kinase
 Increase ratio of Focal changes in the deficiency
cholesterol to membrane skeleton.  Abetalipoprotene
lecithin mia
Echinocyte Burr cell  10-30 scalloped Surface area of the outer  Uremia
short projection lipid monolayer  Cirrhosis
 ATP depletion increases relative to the  Hepatitis
 Hypertonic inner monolayer.  Chronic renal
solution disease
 Drying

Codocyte Target cells,  Thin peripheral Disproportional increase  Hemoglobinophat

Mexican hut cell rim of Hgb in the ratio of surface ies
 Clear area membrane area to  Thalassemia
 “Bull’s eye” volume.  Post-splenectomy

Dacrocyte Tear drop cell  Tear drop Erythrocyte stretching  Myeloid

shaped/pear during blood film metaplasia
shaped preparation.  Hypersplenism
 Single
elongated
point/tail
 Squeezing and
fragmentation
during splenic
passage
Depranocyte Sickle cell  Crescent shaped Polymers are elongated  Sickle cell anemia
cells in oxygenated state.
 Lacks zone of Changes are seen in
central pallor blood exposed for more
 Polymerization than a few seconds to
of atmospheric oxygen.
deoxygenated
Hgb
Elliptocyte Ovalocytes  Rod/cigar Defect in red cell  Herediatry
shaped membrane. elliptocytosis
 Polymerization  Iron deficiency
of Hgb anemia
 Hereditary  Infectious
annemias
 Thalassemia
Schistocyte Schiztocyte  Helmet cell RBC damage by fibrin  Disseminated
 RBC fragments during coagulation. intravascular
 Variable shape coagulation
and size  Microangiopathic
 Excess hemolytic anemia
fragmentation
 Altered BV
 Prosthetic heart
valve
Spherocyte Sphere shaped  Smaller in Low surface area to  Hereditary
diameter volume ration; spherocytosis
 Concentrated Defective membrane  Immunehemolytic
Hgb anemia
 No visible
pallor
 Hereditary
Stomatocyte Bowl shaped  Normal sized Increase in the volume  Herediatry
cell of the RBC, decrease in stomatocytosis
 Central slit-like the surface area.  Rh null disease
area
 “Mouth” cell
 Increased
sodium
permeability
Red Cell Inclusion
Howell-Jolly
bodies