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Small Animal Medicine > Hematology - IMHA > Flashcards

Hematology - IMHA Flashcards

1
Q

What is the pathogenesis of IMHA?

A

The immune system produces antibodies that bind to the patient’s own RBCs leading to RBC destruction via intravascular and extravascular hemolysis

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2
Q

What is the most common form of IMHA (think antibody)?

A

IgG mediated - where RBCs are destroyed by macrophages in the liver in the spleen (Extravascular)

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3
Q

How do spheryocytes form?

A

When macrophages consume a piece of the RBC membrane and not the entire thing they leave fragments called spherocytes

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4
Q

IgM activates complement better than ____ which leads to ______ destruction ultimately resulting in ______ hemolysis.

A

IgG; intravascular; intravascular

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5
Q

What are the three etiologies of icterus?

A

Pre-hepatic due to hemolysis, hepatic, and post-hepatic due to biliary obstruction

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6
Q

How do you differentiate between the etiologies of icterus?

A

Obtain minimum database of CBC, chemistry panel, and urinalysis

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7
Q

Why may a dog with IMHA have a non-regenetative anemia at presentation when it is more commonly associated with regenerative anemia?

A

Immune attack at the level of the bone marrow OR early disease

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8
Q

What test is commonly positive in patients with IMHA?

A

Saline agglutination test

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9
Q

What is agglutination in IMHA patients induced by?

A

five-armed IgM or large quantities of IgG

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10
Q

How do you perform a slide agglutination test?

A

Mix 4 drops of saline with 1 drop of anticoagulated whole blood on a slide. Gently agitate and then examine for macroagglutination. Look under microscope for microagglutination

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11
Q

When evaluating a slide agglutination test, what must you look for that is not agglutination due to IMHA?

A

Rouleaux formation

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12
Q

When should a Coomb’s test be performed?

A

Only if there is negative autoagglutination

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13
Q

In an IMHA patient, why would there not be autoagglutination?

A

The anti-RBC antibody levels are too low to cause agglutination

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14
Q

What does the Coomb’s test detect?

A

antibodies or complement attached to RBCs

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15
Q

What is a common CBC finding in patients with IMHA?

A

Very high WBC counts

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16
Q

What is a leukemoid response?

A

Neutrophilic leukocytosis with a left shift

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17
Q

What can cause a leukemoid response?

A

Increased marrow release during strong regenerative RBC response or tissue necrosis

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18
Q

Leukocytosis in dogs with IMHA is correlated with _______ ______.

A

tissue necrosis

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19
Q

What platelet abnormality is associated with IMHA patients?

A

thrombocytopenia

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20
Q

Why do patients with IMHA often have thrombocytopenia?

A

Immune-mediated platelet destruction and disseminated intravascular coagulation (DIC)

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21
Q

True or false: There are no consistent chemistry abnormalities with IMHA.

A

TRUE

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22
Q

What does a biochemistry often reflect in patients with IMHA?

A

dehydration (elevated bilirubin) and hypoxic damage (mild to moderate elevations)

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23
Q

If there is no red in a urinalysis in a patient with IMHA, what does that indicate?

A

there is no intravascular hemolysis

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24
Q

True or False: There is a single definitive test for IMHA.

A

FALSE

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25
Q

Diagnosis of IMHA is based on a number of findings. Name them.

A

Anemia with a HCT of < 25-30%
Evidence of hemolysis
Evidence of antibodies against RBCs
Elimination of underlying causes of anemia
An appropriate response to immunosuppressive therapy

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26
Q

What are some hereditary non-immune causes of hemolysis?

A

Pyruvate kinase deficiency (PK), Phosphofructokinase deficiency (PFK), and hereditary stomatocytosis

27
Q

What are some acquired non-immune causes of hemolysis?

A

Toxins - zinc, onions, garlic
Hypophosphatemia - diabetic ketoacidosis or refeeding syndrome
Microangiopathic hemolytic anemia - DIC or heartworm disease

28
Q

Primary IMHA is what type of hypersensitivity reaction?

A

type 2 hypersensitivity reaction

29
Q

What breeds are predisposed to primary IMHA?

A

Cocker spaniels, Old English Sheepdogs, Poodles, and Dachshunds

30
Q

What is secondary IMHA?

A

An immune response to nonself antigens that have modified or are associated with normal RBC membranes

31
Q

What history/tests are important for secondary IMHA diagnosis?

A

Vaccination history, travel history, flea/tick exposure and prevention, CBC with clinical pathology evaluation, biochemistry panel, UA, abdominal rads, imaging to screen for cancer, test for infectious agents

32
Q

True or false: Animals with IMHA are often hypercoagulable.

A

TRUE

33
Q

Why is hypercoagulability difficult to diagnose in IMHA patients?

A

Because they have increased D-dimers, reduced antithrombin, and shortened aPTT and PT times

34
Q

What is the most common complication of IMHA?

A

pulmonary thromboembolism

35
Q

What plays a role in the formation of pulmonary emboli in IMHA patients?

A

Stasis of blood, vascular endothelial injury, and hypercoagulability

36
Q

What is the mortality rate in IMHA patients and why?

A

High mortality rate of 50% is related to pulmonary thromboembolism and DIC

37
Q

What are the five principles of treatment of IMHA?

A

Provide supportive care, treat tissue hypoxia, treat secondary cause if present, prevent hemolysis with immunosuppressive therapy, and deter formation of thrombi

38
Q

What supportive care is recommended for patients with IMHA?

A

Maintain hydration and GI protection/support

39
Q

When are IV fluids indicated in IMHA patients?

A

For patients with hemoglobinuria to prevent pigment nephropathy

40
Q

True or False: Oxygen therapy is recommended in IMHA patients.

A

False - it does not help with anemia

41
Q

Transfusions are needed in what percentage of IMHA patients?

A

70-90% of patients

42
Q

What is the mainstay of therapy for IMHA?

A

glucocorticoids

43
Q

What is the preferred glucocorticoid for IMHA?

A

Prednisone at immunosuppresive doses - can give dexamethasone initially if oral medications cannot be tolerated

44
Q

How do glucocorticoids work in the face of IMHA?

A

They decrease macrophage phagocytosis of antibody-coated RBCs and in the long-term mimimize autoantibody production by B ccells

45
Q

How quickly does it take to see a response to glucocorticoids in IMHA patients?

A

3-7 days

46
Q

What are the side effects associated with glucocorticoid use in IMHA treatment?

A

PU/PD, polyphagia, secondary infections due to immunosuppression, muscle weakness, diabetes melitus, GI ulceration, and panting

47
Q

When is a second immunosuppressive drug indicated in IMHA patients?

A

If the PCV is not stabilized or transfusion dependent for greater than 7 days
Severe disease
Larger dog due to the side effects

48
Q

True or False: you should always use steroids as part of front-line therapy because they are the most rapidly acting drug choice.

A

TRUE

49
Q

What are some 2nd immunosuppressive drug options?

A

Azathioprine, Cyclosporine, Mycophenolate mofetil, and Leflunomide

50
Q

How does azathioprine work?

A

It is converted into 6-mercaptopurine which inhibits purine synthesis. Purines are needed for DNA and RNA synthesis. This suppresses T cell proliferation and function

51
Q

What are the side effects of azathioprine?

A

bone marrow suppression, hepatopathy, and pancreatitis

52
Q

True or False: You should not use azathioprine in cats.

A

TRUE

53
Q

What does cyclosporine do?

A

It inhibits T cell function by preventing T cell IL-2 production, which is necessary for T cell activation

54
Q

What type of IMHA can cyclosporine be used in and why?

A

nonregenerative IMHA because it is not myelosuppressive

55
Q

What are the side effects of cyclosporine?

A

Anorexia, diarrhea, gingival hyperplasia, papillomatosis, and hirsutism

56
Q

Aside from glucocorticoids, what immunosuppressive ‘agents’ could be used in IMHA cases?

A

Splenectomy and plasmapheresis

57
Q

What is plasmapheresis?

A

The removal of components of plasma that is thought to cause disease and replace the remainder of the plasma

58
Q

What antithrombotics can be used in IMHA patients?

A

Aspirin, Clopidogrel, and heparin

59
Q

How does asprin work as an antithrombotic?

A

Ultralow-dose aspirin inhibits platelet aggregation without inhibiting beneficial effects of prostaglandins

60
Q

How does Clopidogrel work as an antithrombotic?

A

It inhibits P2Y12 ADP receptor on platelets

61
Q

How does heparin work as an antithrombotic?

A

It binds to antithrombin allowing it to inhibit FII and Fxa

62
Q

True or False: All heparin doses are the same for dogs with IMHA.

A

False - you need to do individualized dosing - every dog is different

63
Q

When should you begin to taper glucocorticoids?

A

when PCV is normal

64
Q

If the CBC is normal, but what percentage should you taper the glucocorticoid dose and how often?

A

Taper the dose by 25% every 3 weeks if the CBC was normal

Small Animal Medicine (100 decks)

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