RBC morphology notecards Flashcards
Anisocytosis
This can be due to increased numbers of large RBC or small RBC, or a combination of both. Some degree of anisocytosis is normal in animals.This is the smear equivalent of the red blood cell distribution width (RDW), which is a measure of the variation in RBC volume.
Acanthocytes
Mechanism: Alterations in lipid composition of RBC membrane and fragmentation. Physiologic: Young ruminants (calves). Disorders: ***Hemangiosarcoma (canine), liver disease (canine, feline), DIC (canine), vasculitis (canine), iron deficiency anemia (canine), possible congenital/inherited disorder (canine), various other diseases (e.g. renal, gastrointestinal, cardiac). Largest numbers observed in dogs with hemangiosarcoma.
Agglutination
Mechanism: Mediated by antibody bridging of adjacent RBC. Disorders: Immune-mediated hemolytic anemia (dog, cat, horse). Drugs: Heparin therapy (horses). Differentiate from: Rouleaux formation (does not usually disperse on saline dilution).
Basophilic stippled RBC
Mechanism: Aggregates of RNA due to RBC immaturity or Inhibition of RNA degradation. Does not require intravital dye precipitation to observe in a regularly stained blood smear (Romanowsky stain). Physiologic: Regenerative anemia (ruminants in particular, also dogs and cats but infrequent in the latter).m Pathologic: Lead poisoning (inhibits RNA degradation).
Dacryocytes
Disorders: Iron deficiency (camelids), myelofibrosis (dogs, not a consistent finding).
Drepanocytes
Mechanism: Specific types of hemoglobin form linear polymers under oxygenated states (frequently after blood sample collection). Normal in Deer, Antelope, sheep, mongoose, and genet.
Eccentrocytes
Mechanism: Oxidant-induced cross-linking of RBC membrane. Drugs: Vitamin K1, phenothiazine drenches (horse), new methylene blue, propofol, acetaminophen (cats). Disorders: Copper poisoning (sheep), red maple leaf toxicity (horses), onions (dogs, cats, cattle, horses), Brassica species, e.g. kale (ruminants), zinc toxicity (dog), naphthalene in mothballs (dog), skunk musk (dogs, panda), inherited defects (glucose-6-phosphate dehydrogenase deficiency, flavin adenine dinucleotide deficiency; both in horses), various diseases in dogs associated with oxidant injury (lymphoma, diabetes mellitus, anticoagulant rodenticide toxicosis).
Echinocytes
Mechanism: Expansion of the outer leaflet of RBC membrane, ATP depletion. Artifact: Stored (aged) blood, excess EDTA, increased pH. Drugs: Furosemide (horses), salicylates, phenylbutazone, doxorubicin (small animals). Disorders: Electrolyte depletion, glomerulonephritis, pyruvate kinase deficiency, snake envenomation (rattlesnake, coral snake, viper), burns, bee stings.
Elliptocytes
Three types: Type I (slightly oval), type II (oval), type III (elongate). Normal in camelids.
Ghost RBC
Mechanism: Rupture of RBC membrane, releasing hemoglobin and leaving membrane scaffolds. Artifact:In vitro hemolysis (poor sample collection, freezing of blood, aged RBC). Drugs: DMSO (horse). Diseases: Intravascular hemolytic anemia, due to immune-mediated hemolytic anemia in dogs, Babesia infection, copper poisoning in sheep, zinc toxicity in dogs, Clostridial toxins, hypophosphatemia, acute liver failure in horses, acute transfusion reaction, neonatal isoerythrolysis in horses, ruminants (not an exhaustive list).
Heinz bodies
Indicates oxidant injury. More readily visualized in a reticulocyte (new methylene blue) stain. Mechanism: Precipitated oxidized hemoglobin. Diseases: Oxidant injury (see eccentrocytes for diseases). The hemoglobin of cats is more susceptible to oxidant injury than other species, so low numbers of Heinz bodies are seen in the blood of non-anemic cats. In fact, some non-anemic cats can have many small refractile Heinz bodies due to endogenous (e.g. diabetes mellitus, hyperthyroidism, lymphoma) or exogenous oxidants (e.g. propylene glycol). These small Heinz bodies are called ?endogenous? Heinz bodies. In other species, Heinz bodies are associated with an oxidant-induced hemolytic anemia.
Hypochromic RBC
Mechanism: Decreased or inhibited hemoglobin production. Physiologic: Very young animals (physiologic iron deficiency anemia, easiest to identify in dogs). Mineral/nutrient deficiency: Iron deficiency (blood loss, nutritional deficiency), vitamin B6 deficiency (rare), copper deficiency (leads to iron deficiency), zinc excess. Diseases: Chronic external blood loss, chronic lead poisoning.
Keratocytes
Mechanism: Oxidant or fragmentation injury. Low numbers may be seen in non-anemic cats.
Macrocytes
Not synonymous with macrocytosis (high MCV). Low numbers of macrocytes may be seen without a high MCV (insufficient numbers to increase the MCV above the upper reference limit). Mechanism: Immature RBC (larger than normal), uptake of water, altered DNA metabolism. Artifact: Stored (aged) blood (may be associated with a low mean cell hemoglobin concentration), hyperosmolality (hypernatremia, hyperglycemia with the ADVIA hematology analyzer). Physiologic: Response to regenerative anemia (punctate reticulocytes). Mineral/nutrient deficiency: Vitamin B12 deficiency, folate deficiency, cobalt deficiency, molybdenum excess. Diseases: Feline leukemia virus infection (cats), congenital dyserythropoietic syndromes (poll Hereford), myelodysplastic syndrome, diabetes mellitus (RBC swelling), hyperthyroidism (unknown mechanism).
Microcytes
Difficult to identify true microcytes and RBC are not usually reported as microcytes in animals with MCV below the lower reference limit for that species. This term is rarely or not used at Cornell University, since it is of uncertain relevance and could encompass more diagnostic shapes, such as spherocytes, schistocytes. Identification of the latter specific shapes is more informative.
