IMHA, ITP, and IMPA Flashcards by Brittany Jermalovic

Acute vs Chronic Anemia Clinical Signs (broad)

Acute: sudden “loss” of RBCs so will have clinical signs. Total solids are low.

Chronic: patients are “used” to having anemia therefore may not have any drastic signs. Total solids may not be low

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What do pale mm indicate? (4 things)

Anemia
Shock
Vasoconstriction
Hypothermia

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Life span of erythrocytes

100-120 days (dogs)
90 days (cats)

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What bloodcell morphology suggests IMHA?

Spherocytes

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Pathogenesis IMHA

Type II hypersensitivity; development of antibodies that react against erythrocyte antigens

IgG mediated

Extravascular hemolysis

Antigens can be self-antigens or exogenous antigens (erythrocyte parasite)

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IgG vs. IgM hypersensitivity

IgG mediated: IMHA, not as serious IgM

IgM: patient is sicker, complement mediated usually, poor prognosis

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Primary autoimmune hemolytic anemia

Idiopathic (genetic?)

Usually middle aged

True autoantibody with specificity for a self antigen or the RBC membrane

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Secondary immune mediated hemolytic anemia (IMHA)

Antibody has specificity for an infectious agent or drug that is associated with RBC surface

Underlying disease occuring

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Extravascular Hemolysis

Coating with IgG and IgM

No hemoglobinemia or hemoglobinuria!

Phatocytosis with macrophage-phagocytosis system (usually in liver, spleen, bone marrow)

Results in:
Spherocytosis
Bilirubinemia

More common

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Intravascular Hemolysis

IgM and IgG bind to RBC membrane

Complement attack complex on RBC -> cell lysis

Hemoglobinemia and hemoglobinuria!

Very ill patient

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Secondary IMHA Pathogenesis: Causes

RBC parasite (Babesia)

Drugs (sulfonamide, cephalosporins, penicillins)

Neoplasia (lymphosarcoma, hemangiosarcoma)

Toxins

Infections (Ehrlichiosis, Leptospirosis, Dirofilariasis, Rickettsioses, etc.)

Other immune mediated disease
Idiopathic

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Other causes of hemolysis: non immune mediated

Oxidant damage (onion, garlic, zinc)

Intrinsic RBC deficit

Mechanical injury (DIC, heartworm, splenic disease)

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Other Immune Mediated Anemias

Non-regenerative IMHA
Acquired pure red cell aplasia
Transfusion reaction
Neonatal isoerythrolysis

Chronic anemia no inflammation

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Predisposition for IMHA; genetic influence

Middle age dogs
Female > Male
Seasonal? (May-June)

Cocker Spaniel, Border Collie, Poodle, Bichon Frise, Old English Sheepdog, Irish Setter, Miniature Schnauzer

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IMHA Clinical Signs

Peracute (hours), Acute (more hours to days), or Chronic

Lethargy, anorexia, weakness/exercise
Syncope
Vomiting
MM pallor (pale)
Increased respiratory rate/effort 
Icterus, bilirubinuria
Shock
Tachycardia
Petechiae

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IMHA Acute Clinical Signs (3 major)

Intravascular hemolysis (icterus, hemoglobinemia, hemoglobinuria)

Pyrexia

Vomiting (decrease appetite)

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IMHA Chronic Clinical Signs (3 major)

Pale mm (weakness, lethargy, tachycardia)

Hepatosplenomegaly
Lymphadenomegaly

Heart murmur (S3) - loss of viscosity, atrial kick/push

Petechiae
Pigmenturia

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IMHA: CBC Findings

Anemia: usually regenerative, can be non-regenerative (bone marrow) 
Hemoglobinemia/hemoglobinuria
Autoagglutination 
Spherocytosis
Thrombocytopenia
Leukocytosis +/- left shift

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What is Evan’s Syndrome?

IMHA and immune mediated thrombocytopenia

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IMHA: Chemistry Findings

Hyperbilirubinemia 
Elevated liver enzymes
Hypoalbuminemia (negative acute phase protein)
Elevated BUN
Hypokalemia 
Abnormal coagulation 
Bilirubinuria/Hemoglobinuria

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IMHA: Diagnosis

Diagnosis of exclusion

Thoracic radiographs
Abdominal ultrasound
Serologic tests for infectious diseases

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Immune mediated disease Treatment

Suppression of immune system!

Glucocorticoids: 2 mg/kg PO q24 (DO NOT exceed 60 mg)

Azathioprine (can get liver and bone marrow suppression)

Cyclosporine (expensive, can give with Ketoconozole to make it last longer)

Others:
Lefunomide
Mycophenolate mofetil
Human immune globulin

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Glucocorticoid Treatment:

Length and Weaning

Patients will have to be on glucocorticoids for at least 3 weeks (may be on for rest of life)

Takes 2 weeks to start working

Weaning:
Once PCV gets to normal range wait 2-4 weeks until tappering by 25%, monitor PCV and if it maintains can continue tappering by 25% every 2-4 weeks

IMHA: Treatment Principles

Prevent or decrease risk for thromboembolic disease (aspirin, clopidogrel, heparin)

Support tissue oxygenation (blood products; packed red blood cells is best)

Primary hemostasis disruption includes...

Platlets, von Will. Surface bleeding: mucous membranes and GI tract

Secondary hemostasis disruption includes...

Fibrin-strong Not enough clotting factors Bleed into cavities (thorax, abdomen, etc.) Ex. Rodenticide toxicity

Immune-mediated thrombocytopenia (ITP, IMTP) Pathogenesis

Type II hypersensitivity disorder: development of antibodies that react against platelet antigens

ITP Primary

Idiopathic (genetic?) True autoantibody with a specificity for self antigen of the platelet membrane

ITP Secondary

Antibody has specificity for an infectious agent or drug that is associated with platelet surface Drug/infectious agent changes surface of membrane and the body attacks platelet thinking it is foreign

ITP Clinical Disease

``` Hyphema (blood collection in anterior of eyes) Retinal hemorrhage Ecchymoses Sclera petechia Petechiae Melena Hematochezia ``` Tachycardia, tachypnea Weakness, lethargy Hematuria

Bleeding/hemorrhage vs. ITP

Autoagglutination -> immune mediated, spherocytes Bleeding/hemorrhage: TS will be decreased

ITP Pathogenesis (3 main)

Decreased production (infiltrative, toxic, infectious) Increased consumption (DIC, vasculitis) Sequestration

Top DfDx of Severe Thrombocytopenia (number)

Severe thrombocytopenia = <40,000 DfDx: Immune mediated DIC

ITP CBC Findings

Profound thrombocytopenia Neutrophilic leukocytosis with possible left shift Anemia of chronic disease

ITP Chemistry Findings

Normal unless there has been hemorrhage causing hypoproteinemia Abnormalities of IMHA if present

ITP Urinalysis Findings

Normal unless bleeding into bladder (potential cavity to lose blood to)

ITP Diagnosis

Exclusion of other causes of thrombocytopenia Normal PT, PTT excludes DIC and Vitamin K rodenticide toxicity Negative results for infectious disease (60x to rule out tick borne disease) Negative imaging results

ITP Treatment

Same as IMHA for immunosuppression ``` Vincristine Minimally increases pletelet count Accelerated fragmentation of megakaryocytes Impaired platelet destruction Reduce degree of phagocytosis ```

Immune-mediated polyarthritis: Pathogenesis

Type III Hypersensitivity (immune-complex disease) Antibody + antigen (small) Small antigen settles in joints to the basement membrane resulting in an inflammatory response Multiple joints often involved

Infectious Polyarthritis

``` Bacterial infection (usually a single joint unless bacteria is being spread hematogenously) Staph, Strep, E. coli, Pasteurella ``` Rickettsial Infection Rocky Mountain Spotted Fever Ehrlichioses Lyme disease Mycoplasma Viral (Calcivirus) Protozoal (Toxoplasma)

Immune-Mediated Polyarthritis Forms

Erosive form (uncommon) - poor prognosis Non-erosive forms (most common)

Immune-Mediated Polyarthritis Erosive Form

Rheumatoid arthritis (painful and debilitating) Periosteal proliferative arthritis Long term pain no matter what you do Permanent joint destruction can occur

Immune-Mediated Polyarthritis Non-erosive Forms

Idiopathic polyarthritis, vaccine induced, drug induced, steroid-responsive meningitis-arteritis, juvenile-onset polyarthritis of Akitas and Chinese Shar Pei

Immune-mediated Polyarthritis: Non-erosive Type I

Idiopathic; no underlying disease

Immune-mediated Polyarthritis: Non-erosive Type II

Reactive - distant infeciton

Immune-mediated Polyarthritis: Non-erosive Type III

Enteropathic

Immune-mediated Polyarthritis: Non-erosive Type IV

Neoplasia-related

Immune-mediated Polyarthritis Signalment

Medium to large-breed dogs Young to middle aged (usually young) Retrievers, Spaniels, German Shepherds

Immune-mediated Polyarthritis Clinical Signs

``` Variable: Fever (waxing and waning) Lameness, stiffness (pain) - can see shifting limb lameness Back, neck pain Lethargy (painful) Joint swelling, joint pain ```

Immune-mediated Polyarthritis CBC

Inflammatory leukogram +/- left shift Thrombocytopenia Anemia of chronic disease (normocytic, normochromic)

Immune-mediated Polyarthritis Chemistry

Hypoalbuminemia (negative acute phase protein) Proteinuria

Immune-mediated Polyarthritis Diagnostic

Arthrocentesis (usually of peripheral joints) Suppurative inflammation May be tin or discolored (should usually be straw colored and stringy)

Immune-mediated Polyarthritis Diagnosis

Rule out other diseases Radiographs Serology Blood, urine, joint fluid cultures

Immune-mediated Polyarthritis Treatment

Immunosuppressive drug therapy Secondary issue? Treat the underlying disease with glucocorticoids and may clear the disease

Clotting factors that require Vitamin K

II, VII, IX, X