Exam 7 L. 2

Question 1

IMHA pathogenesis

Answer 1

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

Question 2

Coombs’ test

Answer 2

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)

Question 3

WBC counts and IMHA

Answer 3

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

Question 4

Urinalysis

Answer 4

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

Question 5

Hereditary causes of hemolysis

Answer 5

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!

Question 6

Acquired causes of hemolysis

Answer 6

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

Question 7

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

Answer 7

Cocker spaniel (one third of all cases)!!

Usually middle-aged female dogs

Question 8

Secondary cause of IMHA

Answer 8

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

Question 9

IMHA in cats

Answer 9

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

Question 10

Hypercoagulable?

Answer 10

Animals with IMHA are often hypercoagulable

• increased D- dimers, reduced anti-thrombin, shortened PTT/PT
• thromboelastography (TEG) is probably the best we have

Question 11

Thromboemboli in IMHA

Answer 11

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

Question 12

IMHA - immunosuppression

Answer 12

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

Question 13

Immunosuppression - glucocorticoids

Answer 13

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!

Question 14

Azathioprine

Answer 14

Do not use in cats!!

Immunosuppressive drug, use every other day

Question 15

Cyclosporine

Answer 15

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

Immunosuppressive

Question 16

Anti-thrombotics

Answer 16

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

Question 17

Number 1 cause of death in IMHA?

Answer 17

Thromboembolic disease

Question 18

Recovery from IMHA

Answer 18

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

Question 19

Poor prognostic indicators with IMHA

Answer 19

1) thrombocytopenia
2) hyperbilirubinemia
3) hypoalbuminemia

Question 20

IMHA long-term therapy

Answer 20

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