RBCs Flashcards
basophilic stippling
aggregates of ribosomes that are visualized as small basophilic granules within an RBC
most often seen in immature erythrocytes of ruminants
also seen in immature erthyrocytes of dogs and cats with highly regenerative anemias
lead poisoning
hemoglobin functions
transport O2 from lungs to tissues
transport CO2 from tissues to lungs
buffer hydrogen
Hgb physiology
iron in Hgb molecule must be in the reduced form to bind oxygen
when oxidized-called methemoglobin
too much methemoglobin-mucous membranes cyanotic and blood is brown
iron metabolism
absorbed from intestine-small % in health, during disease increased
transported in blood by transferrin
stored in tissues as hemosiderin or in plasma bound to ferritin
evaluation of iron content of body: serum iron, serum total iron-binding capacity, serum ferritin or bone marrow hemosiderin content
serum iron is low in iron deficiency but also low in conditions where tissue iron is normal or increased
serum ferritin best serum indicator of total body iron content
TIBC-measure of transferrin in blood
Erythrocyte lifespan
dog-120 days
cat-70 days
cow-160 days
horse-145 days
relatively long lived compared to other blood cells
destruction of RBCs
removed by macrophages which attached to RBC membrane
RBC lysed and hemoglobin degraded into heme and globin
Globin–>amino acids
Heme–>iron and bilirubin
bilirubin-released from macrophages into circulation where albumin binds it and transports it to the liver where it is conjugated and excreted in the bile
microcytic RBCs
iron deficiency anemia (chronic blood loss)-related to extra cell division as RBCs mature in marrow
Portosystemic shunts/liver failure-altered iron kinetics
specific breeds-akita, shiba dogs
macrocytic
significantly increased number of young RBCs in circulation
FeLV (no poly)
poodle macrocytosis (rare)
hereditary stomatocytosis
anisocytosis
variation in RBC size
RDW
hypochromic RBCs
associated with significantly increased numbers of reticulocytes in circulation
iron deficiency-Hgb synthesis is impaired
hyperchromic RBCs
almost always an artifact
can’t produce RBCs with too much Hgb
may be free Hgb in plasma (hemoglobinemia) or presence of interfering substances or structures (lipemia, icterus, Heinz bodies)
normal shape for dog
biconcave disk with central pallor
normal shape for cat, pig, horse, cow, sheep
discoid shape with little to no central pallor
normal shape for Llama, camle, bird, reptile
ellitical shape
bird & reptile-nucleated RBCs
poikilocyte
abnormall shapred RBC
may be present in healthy goats, pigs and young cattle
frequently seen in dogs and ruminants with iron deficiency
spherocyte
decreased diameter, decreased ccentral pallor, increased staining intensity
typically have relatively normal cell volumes
suggest immune mediated damage to RBCs
form from partial phagocytosis of RBC membranes by macrophages
associated with blood transfusion, bee sting and zinc toxicity
schistocyte
irregulatly shaped RBC fragment that occurs when RBCs are forced through altered vascular channels, vessels containing fibrin strands or exposed to turublent blood flow
associated wtih DIC, Hemangiosarcoma, vasculitis and +/- iron deficiency
keratocyte
RBC with blister or 2 “hornlike” projections
formed by intravascular trauma or iron deficiency
eccentrocyte
RBC with Hgb shifted to one side and a clear membrane bound area on the opposite side
form from oxidative damage to RBC membranes
may be seen with Heinz bodies
ghost cell
formed from lysis of RBCs
very pale staining cells consisting of an empty RBC membrane
artifactual or pathologic (IMHA, Heniz body hemolysis)
acanthocyte
RBC with irregularly spaced surface projections of variable length and diameter
result of altered lipid/cholesterol content of cellular membranes
associated wtih splenic hemangiosarcoma, liver disease, renal disease
Echinocyte
RBC with many short evenly spaced uniform surface projection
artifact-associated with blood film prep and slow drying
pathologic- eletrolyte depletion, renal disease, neoplasia, rattlesnake envenomation, chemotherapy
Codocyte
RBC that has excess membrane
“target cell”
central area of Hgb surrounded by clear ring and an outer rim of Hgb
associated with regenerative anemia in dogs, hepatic and renal dz
Heinz bodies
clumps of denatured Hgb that results from oxidative damage
Wright: appear small eccentric pale structures that often protrube from the cell margin
NMB: dense blue structures
RBCs more susceptible to intravascular and extravascular hemolysis
up to 10% normal in cats
Howell-Jolly bodies
nuclear fragments retained within an RBC
appear small round dark blue inclusions
increased numbres may be seen in regenerative anemias, splenectomy or suppressed splenic function
Siderotic granules (pappenheimer bodies)
iron granules within mitochondria and lysosomes
impaired Heme synthesis, myelodysplasia and ineffective erythropoiesis
nucleated erythrocytes
metarubricytes (metarubricytosis)
never normal to see
present due to toxic, hypoxic or physical damage to bone marrow endothelium
associated with regenerative anemia
should not be used as an indicator of RBC regeneration
other r/o: lead poisoning, chemotherapeutic use, neoplasia or inflammation with marrow space and splenic contraction or dysfunction
Rouleaux
spontaenous association of RBCs in linera stacks
normal in horses
slight amount in cats and some dogs
enhanced with increased plasma proteins
Agglutination
irregular spherical clumps of RBC
grape like clusters
caused by antibody bridging between RBCs
DDx: IMHA
How to differentiate rouleaux from agglunation
small amount of blood and saline are mixed together
rouleaux will disperse
agglutination will stay the same
anemia
not a disease
determine underlying cause
decrease in HCT, [Hgb] or RBC count
bone marrow response to anemia
decreased circulating RBCs–>hypoxmia
Epo producing cells in renal cortex sense hypoxmia–>increased production of Epo
increase in Epo stimulates bone marrow to increase RBC production
when do reticulocytes appear in blood
within 2-3 days
peak within 7 to 10 d
Reticulocytes
show up as RBCs with large blue mats of RNA and mitochondria when stained with New Methylene Blue stain
polychromasia
larger, pink/blue RBCs viewed on a Wright stained blood smear
+1 poly can be normal in dog
reticulocyte count
indicative of regenerative anemia
assessment of bone marrow response
horses and reticulocytes
they do not release reticulocytes into the peripheral circulation
do serial CBCs or bone marrow biopsy
Patient history with anemia
duration of clinical signs (acute vs chronic), exposure to drugs, plants, chemicals, history of blood loss (hematuria, melena, epistaxis), parasite control, etc
physical exam of patient with anemia
icterus, bruisng, petechial or ecchymotic hemorrhages, cyanosis, mucus membrane color, hydration status, evidence of trauma, abdominal distention, etc
acute hemorrhage
HCT and plasma proteins concentration will not decrease until the plasma volume is replaced
over the next 24 to 72 hours, fluid moves into circulation to re-establish blood loss
HCT and plasma protein concentration will decrease
internal or external
What is anemia of blood loss initiated characterized as?
normocytic, normochromic non-regenerative anemia
What can anemia of blood loss become?
macrocytic, hypochromic regenerative anemia
increased number of reticulocytes
causes of blood loss
trauma
coagulopathies
surgical procedures
parasites
neoplasia
causes of iron deficiency anemia
mature animals: result of chronic blood loss
neonates: poor iron intake and high growth rates
typical cbc findings for iron deficiency anemia
microcytic, normochromic or microcytic, hypochromic
regenerative but in later stages show poor signs of regeneration
hypoproteinemia
Keratocytes, schistocytes, hypochromic RBCs
Low serum ferritin and poor iron stores in bone marrow
thrombocytosis
clinical intravascular hemolysis
within blood vessels or heart
marked RBC damage
marked or rapidly falling anemia
occurs hours to days after insult
reticulocytosis occurs are presentation
Hemoglobinemia
Hemoglobinuria
+/- Hyperbilirubinemia
+/-bilirubinuria
predominantly extravascular hemolysis
macrophages of spleen, liver and bone marrow
mild to marked RBC damage
mild to marked anemia
occurs over days to weeks
reticulocytosis at initial presentation
hyperbilirubinemia
bilirubinuria
haptoglobin
in circulation
binds free Hgb
taken up by hepatocytes when bound to Hgb
causes pink to red color in plasma
Immune mediated hemolytic anemia
typically regenerative
normocytic, normochromic or macrocytic, hypochromic
spherocytes
Positive Coombs’ test
agglutination
inflammatory leukogram
+/-hemoglobinemia/hemoglobinuria
Mycoplasma haemofelis
small blue rod or ring forms on the surface of RBCs
spread through infected blood via blood feeding arthropods
also spread from queen to kittens
mycoplasma haemocanis
small chains of cocci that may branch
usually only causes disase in immunosuppressed dogs or splenectomized animals
Mycoplasma wenyonii (cattle)
Mycoplasmas ovis (sheep, goats)
Mycoplasma haemolamae (llamas, alpacas)
small basophilic structures on RBCs or sometimes free in the background
Anaplasmosis
Rickettsial organism
larger than Mycoplasma but smaller than Howell Jolly bodies
usually around basophilic structures
transmitted by ticks, biting flies and iatrogenically
hemolytic anemia in cattle sheep and goats
Babesiosis
Causes hemolytic anemia
Babesia canis & B. gibsoni (dog)
B. equi (horse)
B. bigemina (ruminants)
piriform
transmitted by tick, direct blood contamination
Theileriosis
Cytauxzoonosis
Feline Heinz body anemia DDx
acetaminophen
onion/garlic
propylene glycol
zinc toxicity
methylene blue
propofol
DM
Hepatic lipidosis
hyperthyroidism
hymphosacroma
canine heinz body anemia DDx
onion/garlic
acetaminophen
zinc toxicity
propylene glycol
propofol
benzocaine
naphthalene
Equine heinz body anemia DDx
red maple leaf ingestion
onion/garlic
ruminant heinz body anemia DDx
Brassica sp (kale, rape, cabbage)
onion/garlic
copper toxicosis
selenium deficiency
Fragmentation Anemia
results from direct physical trauma to RBCs caused by DIC, vasculitis, vascular tumors, etc
increased schistocytes and keratocytes
DDx for nonregenerative anemia
Anemia of inflammation (chronic disease)
Anemia of chronic renal failure
pure red cell aplasia
aplastic pancytopenia
bone marrow replacement
Anemia of Inflammation
Anemia of chronic disease
common
mild to moderate anemia
develops over days to weeks then stabilizes
resolves with correction of underlying cause
normocytic, normochromic non-regenerative
Anemia of inflammation pathophysiology
complex and multifactorial
altered iron kinetics
decreased EPO production
decreased marrow response to Epo
decreased RBC life span
Anemia of CKD
moderate to severe
normocytic, normochromic non-regenerative
result of decreased Epo production
correlates wtih severity of CKD
Pure red cell aplasia
severe normocytic, normochromic non-regenerative anemia
normal leukocyte and platelet numbers
marked decrease in erythroid precursors in bone marrow with normal granulocytic precursors and megakaryocytes
caused by immune mediated destruction of erythroid precursors in bone marrow
occ. spherocytes
direct Coombs’ test infrequently positive
Aplastic pancytopenia
biocytopenia
bone marrow space is replaced by fat
normocytic, normochromic non-regenerative anemia
caused by reversible or irreversible damage to hematopoietic precursors in bone marrow
drugs, toxins, estrogen, infectious agents (parvovirus, FeLV, Ehrlichia canis)
bone marrow replacement
one or more cytopenia
neoplasia & myelofibrosis
Erythrocytosis
aka polycythemia
increased concentration of RBCs in circulation
increased HCT, RBC count and [Hgb]
Relative erythrocytosis
loss of body fluid
splenic conctraction (epinephrine leukogram)
absolute erythrocytosis
primary-polycythemia vera-rare chronic myeloproliferative disorder
secondary appropriate-systemic hypoxemia due to lung dz, cardiac dz or high altitudes; results in increased Epo production
secondary inapproriate-renal ischemia or erythropoietin producing tumor
