Immune Mediated Flashcards
(28 cards)
Indications for Hemorrhagic or Fe deficiency Anemia
(everything possible, but not required)
- low MCV
- hypochromic
- schistocytes
- acanthocytes, codocytes
Causes of fragmentation hemolysis
- mechanical injury (DIC, caval syndrome, glomerulonephritis)
- endothelial injury (hemangiosarcoma, vasculitis, splenic/hematic disease)
- thermal injury (burns)
- osmotic injury (near drowning)
causes of oxidative RBC damage?
- increased oxidants (drug/toxin)
- acetaminophen, onion, garlic - decreased anti-oxidant (ATP depletion, congenital enzyme deficiency)
Heinz bodies
oxidation of SH groups causes denaturation and precipitation
-> hemolytic anemia
Indications of hemolytic anemia due to oxidative damage
regenerative anemia
heinz bodies
eccentrocytes and pyknocytes
types of hemolytic anemias
- IMHA
- Erythroparasitism
- Heinz body
- RBC metabolic defects (Zn, decreased phosphatemia, envenomation, or congenital)
Mechanism for most IMHA and ITP
Bcell/antibody (IgG, IgM)
Causes of agglutination
- IMHA
- Rouleaux
- cold agglutinations are generally non-pathologic
Hypophosphatemia
severely low (<1-1.5 mg/dL)
ATP depletion causing osmotic fragility and oxidative damage.
associated with insulin (DKA), feeding after starving, hypoparathyroidism
Envenomation
contains phospholipases and hemolysins
- echinocytes, spherocytes, ghosts
- hemolysis
may have blood loss from tissue damage
IMHA indications
regenerative anemia agglutination spherocytes, ghost cells neutrophilia monocytosis
Evans syndrome
IMHA and ITP
IMHA clinical signs
- fever
- organomegaly (spleen, liver, lymph nodes) (due to EMH)
- icterus (not every animal, depends on rate of destruction and how well liver can keep up)
- pigmentemia, pigmenturia, orange feces
- elevated coag times (if in DIC)
Bilirubin
conjugated where?
how is it excreted?
why does IMHA cause icterus?
conjugated in liver
excreted in urine and feces
increased RBC turnover increased bilirubin, causing icteric urine and feces. Once excretory pathways are overwhelmed, you see icteric plasma then MM (when bili >2mg/dL)
Intravascular hemolysis.
What happens to free Hb?
plasma becomes pink (hemoglobinemia)
Haptoglobin binds free Hb and transports it to liver for metabolism.
Hemoglobinuria occurs when haptoglobin is overwhelmed.
Other transport molecules?
Why are they necessary?
Hemopexin (for heme)
Transferrin (for Fe)
Free Heme, Hb, Fe are toxic, so they need an escort. The chaperones consume NO which causes vasoconstriction and platelet clumping. RBC membrane lysis and inflammatory state are also apparent in IV hemolysis.
Difference between IV and EV Hemolysis?
EV / IV Acute to Chronic / Acute Within MPS / Outside conserves Fe, AA / loses / Greater risk of DIC, shock
Cold Agglutination disease
weird neoplasia/ inflammatory conditions produce Ab that are active at colder temperatures (in the extremities)
False negative on Coombs?
may indicate low antibody titer
technical issues
Cat
(not caused by immunosuppression or transfusion!)
Primary IMHA signalment
Cocker Spaniel!
middle aged 2-7 yrs (not geriatric)
IMHA relapse?
common after tapered off of immunosuppresion
factors associated with worse prognosis with IMHA?
IV hemolysis severe hyperbilirubinemia (>10mg/dL)
Acute Zn Toxicosis
can look like IMHA (regenerative anemia, spherocytes, heinz bodies, inflammatory leukogram)
But are Coombs negative!
Hemolysis is due to Zn induced Ab binding and heinz body formation.
Signalment for primary ITP
Cocker spaniel middle aged (same as IMHA) also poodles, sheepdog