Exam 7 L. 2 Flashcards Preview

Small Animal Medicine > Exam 7 L. 2 > Flashcards

Flashcards in Exam 7 L. 2 Deck (20):

IMHA pathogenesis

Most common form is IgG mediated, where RBCs are destroyed by macrophages in the liver and spleen (extravascular)

IgM activates complement more efficiently than IgG, with destruction occurring in the vessels (intravascular, process)
- *intravascular hemolysis has been associated with a poorer prognosis*


Coombs' test

1) perform only if NEGATIVE auto-agglutination
-anti-RBC antibody levels are too low to cause agglutination
2) Coombs' test is the direct anti-globulin test
-detects antibodies or complement attached to RBCs
-moderate sensitivity ==> false negatives (negative result does not exclude IMHA diagnosis)


WBC counts and IMHA

Very high WBC counts (up to 100,000/ul) commonly occur with IMHA

Note: IMHA patients often have THROMBOCYTOPENIA due to
-immune mediated platelet destruction (immune thrombocytopenia - ITP)
-**when ITP and IMHA are present together ==> Evan syndrome**



If the urine is not red, it indicates there is no intravascular hemolysis (i.e. No free hemoglobin release)


Hereditary causes of hemolysis

Breeds such as Basenji's, Spring/Cocker Spaniels, Alaskan malamute's, miniature schnauzer cannot make enough ATP to keep the red blood cell stable-they become fragile!


Acquired causes of hemolysis

1) toxins (zinc, onion, garlic, acetaminophen, propylene glycol-cats)
-pennies minted after 1982 contain zinc!
2) hypophosphatemia
3) Microangiopathic hemolytic anemia (DIC, heartworm disease)
-direct shearing injury to RBCs


What breed of dog is most predisposed to developing antibody against its own red blood cells?

Cocker spaniel (one third of all cases)!!

Usually middle-aged female dogs


Secondary cause of IMHA

Immune response to nonself antigens that have modified or are associated with normal RBC membranes
i.e. antibody develops versus penicillin, which for example in the patient share structure similarities to a red blood cell protein and causes IMHA against the RBC


IMHA in cats

Secondary IMHA is the most common form of hemolytic anemia in cats (IMHA is usually due to a primary cause in dogs



Animals with IMHA are often hypercoagulable
- increased D- dimers, reduced anti-thrombin, shortened PTT/PT
- thromboelastography (TEG) is probably the best we have


Thromboemboli in IMHA

High mortality rate in IMHA (50%) is related to PTE and DIC**
(pulmonary thromboembolism is a common complication of IMHA)


IMHA - immunosuppression

1) glucocorticoids are the mainstay of therapy for IMHA!!
2) immunosuppressive doses of prednisone (2-4 mg/kg/day - divided)
- divide prednisone dose by 7 to get dexamethasone dose** -- give dex initially if oral meds can't be tolerated


Immunosuppression - glucocorticoids

1) most rapidly acting immunosuppressive available
-decreases macrophage phagocytosis of antibody coated RBCs
-*takes 3 to 7 days to see a response!*

**Always use steroids w/ IMHA as part of front-line therapy because they are the fastest acting drug choice!**



Do not use in cats!!

Immunosuppressive drug, use every other day



Not myelosuppressive so can be used with non-regenerative IMHA!




They may be important in improving survival rates of IMHA, but we don't have much evidence nor doing those which anti-thrombotic to use


Number 1 cause of death in IMHA?

Thromboembolic disease


Recovery from IMHA

1) Guarded
2) complete response takes weeks to months, lifelong therapy required in some
3) IMHA can relapse (15%)
4) 50:50 survival rate


Poor prognostic indicators with IMHA

1) thrombocytopenia
2) hyperbilirubinemia
3) hypoalbuminemia


IMHA long-term therapy

1) when PCV normal ==> begin to taper glucocorticoids
2) taper dose by 25% every 3-4 weeks if CBC normal (PCV stable, no spherocytes or autoagglutination)
3) once reach 0.5 mg/kg/day prednisone switch to every other day, then stop
4) steroid withdrawal takes 2-4 months, minimum