Hematology: Erythrocyte Abnormalities Flashcards
Effects of radiation on bone marrow
Which cells affected first?
Leukopenia–>especially neutrophils- why? shortest lifespan
Bone marrow gets damaged–>DNA damage, ROS–> unable to replace n’phils–> susceptible to infection
platelets affected next, can’t clot–> bleeding
Eventual anemia, intestinal tract, and skin epithelia destroyed.
Anemia
a reduction in erythrocyte number and or the hemoglobin concentration i.e. decreased RBC, HCT/PCV and or Hb
Not a final diagnosis- must look for underlying cause
Anemia isn’t a disease, it’s a clinical finding.
Clinical features of acute anemia
Pallor
tachycardia
muscular weakness
subnormal temperature
coma
death
Clinical features of chronic anemia
fatigue/lethargy
exercise intolerance
tachycardia
fainting
pallor
cardiac (haemic) murmur- develop murmur d/t change in blood viscosity (decrease in rbcs, decrease in viscosity, more turbulence)
Causes of anemia
1) decreased number of erythrocytes entering the blood i.e. decreased production/bone marrow issue
or
2) increased number of erythrocytes exiting the blood
decreased O2–>kidneys detect hypoxia–>increased EPO–>bone marrow increases RBC production.
If BM is functioning normally, increased numbers of reticulocytes appear in blood=regeneration (replacing damaged or lost rbcs)
NB: it takes 3-5 days for this to occur
Types of anemia
Non-regenerative: decreased production
can be due to primary BM disorder, or secondary BM disorder (i.e. renal failure, not enough EPO, not stimulating BM)
Regenerative: increased exit or turnover of RBCs
can be due to: 1) hemolysis (increased destruction of RBCS) a) intravascular or b) extravascular
or 2) hemorrhage a) internal or b) external
How do we tell if anemia is regenerative?
** increased number of reticulocytes in blood (nb not in horses)
Macrocytic hypochromic: increased MCV (because reticulocytes are larger), decreased MCHC because reticulcytes are bigger, Hb concentration is decreased, but not the AMOUNT of Hb.
increased polychromasia (abnormally high number of RBCs in blood) /increased anisocytosis (RBCs are of unequal size)
Sometimes see normoblasts
Basophilic stippling (cattle): tend to see blue/black dots on RBCs.
Hemorrhagic anemia
blood loss
Acute: after accidents or sx
Chronic: bleeding from ulcers, neoplasms or parasites
Coagulopathies: e.g. rodenticide
Internal: animal isn’t losing all red cells to outside world, macrophages can mop up and save iron.
external: less iron, less red-cells–> may have impact on BMs ability to make new RBCs.
Blood findings in hemorrhagic anemia
Normal in first few days–> pre-regenerative
Regenerative: polychromasia (increased number of RBCs in blood due to presence of reticulocytes)
Anisocytosis: difference in red blood cell size (reticulocytes bigger than rbcs)
Howell Jolly body: nuclear remnants in circulating erythrocytes (nb: presence usually signifies damaged spleen)
Thrombocytosis: increase in number of platelets in circulation–> reactive response
Neutrophilia: due to stimulation, stress and inflammation
All of these result in macrocytic hypochromic–> i.e. increased mean cell volume.
Degree of regeneration in hemorrhagic anemia factors
Degree of regeneration depends on:
severity of blood loss
location of bleeding: internal vs. external– in internal bleeding, iron is available for Hb synthesis= greater regeneration
Proteins: not just red cells being lost–> hypoproteinemia (classicaly a panhypoproteinemia).
Hemolytic anemia
two important features:
1) reduced red blood cell survival time
2) iron from destroyed erythrocytes is retained in the body
Blood picture: markedly regenerative and additional finidings depend on pathogenesis.
Methods of red cell destruction in hemolytic anemia
1) extravascular lysis (phagocytosis)- mostly in spleen
2) intravascular lysis- RBCs being destroyed in the bloodstream.
Extravascular lysis of RBCs
Phagocytosis of red cells–> spleenic englargement
Iron and globin is reused
Haem–> biliverdin–>bilirubin (not h2o soluble)
Bilirubin transported by albumin (jaundice)
In liver, bilirubin and glucuronide are conjugated (h2o soluble)–> bile
nb: herbivores may have yellowish plasma anyway (don’t confuse with jaundice).
Look for icterus in mucosal membranes, sclera. where there’s more elastic fibers, that’s where you see jaundice.
Intravascular lysis
Lysis of RBCs in the circulation–>free Hb in the blood–> hemoglobinemia
Free Hb–>+haptoglobins–>phagocytosis–>jaundice (if amount exceeds phagocytic capability)
Saturation of haptoglobins–>Hb appears in kidneys–>Hemoglobinuria–>toxic nephrosis
Hematuria: post centrifugation- red cells sediment at bottom
Hemoglobinuria: post centrifugation, whole sample stays red.
Causes of hemolytic anemia
Inherited: phosphofructokinase deficiency of springer spaniels; pyruvate kinase deficiency of basenjis; NB inherited hemolytic anemia is REALLY rare.
Acquired: much more common- Infectious agents, oxidative compounds and toxins, fragmentation (increased mechanical trauma), immune-mediated.
Infectious hemolytic anemia
mycoplasma spp, babesiosis
blood picture of mycoplasma hemofelis infxn: small reddish magenta dots in blood cells. macs try to remove these cells. can trigger immune-mediated destruction as well.
blood picture of babesia divergens in cattle: pear-shaped bilobed organism in red cells; causes intravascular lysis–> hemoglobinuria.
Toxic and oxidative hemolytic anemia
Oxidative agents in drugs can reduce glutathione levels on RBCs
Haem iron can be oxidized to methaemoglobin (chocolately brown color to blood)
Oxidative damage to hemoglobin causes Heinz body formation–> destoryed by intra- or extravascular lysis.
heinz body: inclusions within rbcs composed of denatured hemoglobin.
Heinz bodies
inclusions on RBCs of denatured hb
nb: completely healthy and normal cats have heinz bodies
see heinz bodies in GI disease, diabetes, hyperthyroidism in cats
rarely seen in dogs except in onion/garlic poisoning.
easier to see on new methylene blue stain.
Causes of toxic/oxidative hemolytic anemia
cooper poisoning (ruminants)
paracetamol (cats especially)
onions
zinc
brassicas (rape and kale)
red maple (horses)
snake venoms
Fragmentation hemolytic anemia
RBCs subjected to excessive trauma
features of intravascular lysis may be present
Schistocytes ( shredded red cells) and acanthocytes (intact red cells, but irregularly shaped (spiculated)
small vessel disorders: microangiopathic
large vessel disorders
valve lesion: stops heart valve from closing–> increased turbulence–>red cells bash against each other–> mechanical trauma
metastatic cancer (lungs): tumours disrupt capillary network–> increased mech. trauma to red cells.
thrombus in blood vessel: impeded blood flow in that blood vessel–> mechanical trauma of red cells trying to squeeze past thrombus.
Immune-mediated hemolytic disorders
Blood group incompatabilities: blood transfusion reaction (naturally occuring ABs to other blood groups); neonatal isoerthyrolysis
Immune-mediated hemolytic anemia generated against self-antigen/own red cells
Isoerthyrolysis
hemolytic disease of the newborn
Maternal blood group ABs are absorbed from colostrum, destroying neonate’s RBCs.
This occurs when mother’s blood group is different to the new born’s AND the mother has been previously sensitised to that blood grup (i.e. she’s developed ABs to foal’s red cell type, either from previous pregnancy, or vax, or blood products).
Dam with sensitization to foreign antigens–>formation of alloantibodies–>neonate ingests colstrum and absorbs antibodies which are dictate against own blood type–> destruction of RBCs–>occur via phagocytosis or intravascular lysis.
How to avoid isoerythrolysis
indirect coomb’s test if mare has ABs against stallions RBCs. if sensitized, attach another AB to cause agglutination. if she does have ABs, can stop foal getting colostrum from mom.
signs develop 12-48 hours after birth.
IMHA in adults
primary/autoimmune (idiopathic)
secondary: under-lying trigger; i.e. drugs/toxins, infectious agents, neoplasia, vaccines?
Dogs often primary/idiopathic
other species uncommon and usually secondary.
