IMHA, ITP, and IMPA Flashcards
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
What do pale mm indicate? (4 things)
Anemia
Shock
Vasoconstriction
Hypothermia
Life span of erythrocytes
100-120 days (dogs) 90 days (cats)
What bloodcell morphology suggests IMHA?
Spherocytes
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)
IgG vs. IgM hypersensitivity
IgG mediated: IMHA, not as serious IgM
IgM: patient is sicker, complement mediated usually, poor prognosis
Primary autoimmune hemolytic anemia
Idiopathic (genetic?)
Usually middle aged
True autoantibody with specificity for a self antigen or the RBC membrane
Secondary immune mediated hemolytic anemia (IMHA)
Antibody has specificity for an infectious agent or drug that is associated with RBC surface
Underlying disease occuring
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
Intravascular Hemolysis
IgM and IgG bind to RBC membrane
Complement attack complex on RBC -> cell lysis
Hemoglobinemia and hemoglobinuria!
Very ill patient
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
Other causes of hemolysis: non immune mediated
Oxidant damage (onion, garlic, zinc)
Intrinsic RBC deficit
Mechanical injury (DIC, heartworm, splenic disease)
Other Immune Mediated Anemias
Non-regenerative IMHA
Acquired pure red cell aplasia
Transfusion reaction
Neonatal isoerythrolysis
Chronic anemia no inflammation
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
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
IMHA Acute Clinical Signs (3 major)
Intravascular hemolysis (icterus, hemoglobinemia, hemoglobinuria)
Pyrexia
Vomiting (decrease appetite)
IMHA Chronic Clinical Signs (3 major)
Pale mm (weakness, lethargy, tachycardia)
Hepatosplenomegaly
Lymphadenomegaly
Heart murmur (S3) - loss of viscosity, atrial kick/push
Petechiae
Pigmenturia
IMHA: CBC Findings
Anemia: usually regenerative, can be non-regenerative (bone marrow) Hemoglobinemia/hemoglobinuria Autoagglutination Spherocytosis Thrombocytopenia Leukocytosis +/- left shift
What is Evan’s Syndrome?
IMHA and immune mediated thrombocytopenia
IMHA: Chemistry Findings
Hyperbilirubinemia Elevated liver enzymes Hypoalbuminemia (negative acute phase protein) Elevated BUN Hypokalemia Abnormal coagulation Bilirubinuria/Hemoglobinuria
IMHA: Diagnosis
Diagnosis of exclusion
Thoracic radiographs
Abdominal ultrasound
Serologic tests for infectious diseases
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
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
