IMHA, ITP, and IMPA Flashcards

1
Q

Acute vs Chronic Anemia Clinical Signs (broad)

A

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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2
Q

What do pale mm indicate? (4 things)

A

Anemia
Shock
Vasoconstriction
Hypothermia

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3
Q

Life span of erythrocytes

A
100-120 days (dogs)
90 days (cats)
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4
Q

What bloodcell morphology suggests IMHA?

A

Spherocytes

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5
Q

Pathogenesis IMHA

A

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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6
Q

IgG vs. IgM hypersensitivity

A

IgG mediated: IMHA, not as serious IgM

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

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7
Q

Primary autoimmune hemolytic anemia

A

Idiopathic (genetic?)

Usually middle aged

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

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8
Q

Secondary immune mediated hemolytic anemia (IMHA)

A

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

Underlying disease occuring

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9
Q

Extravascular Hemolysis

A

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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10
Q

Intravascular Hemolysis

A

IgM and IgG bind to RBC membrane

Complement attack complex on RBC -> cell lysis

Hemoglobinemia and hemoglobinuria!

Very ill patient

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11
Q

Secondary IMHA Pathogenesis: Causes

A

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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12
Q

Other causes of hemolysis: non immune mediated

A

Oxidant damage (onion, garlic, zinc)

Intrinsic RBC deficit

Mechanical injury (DIC, heartworm, splenic disease)

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13
Q

Other Immune Mediated Anemias

A

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

Chronic anemia no inflammation

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14
Q

Predisposition for IMHA; genetic influence

A

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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15
Q

IMHA Clinical Signs

A

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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16
Q

IMHA Acute Clinical Signs (3 major)

A

Intravascular hemolysis (icterus, hemoglobinemia, hemoglobinuria)

Pyrexia

Vomiting (decrease appetite)

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17
Q

IMHA Chronic Clinical Signs (3 major)

A

Pale mm (weakness, lethargy, tachycardia)

Hepatosplenomegaly
Lymphadenomegaly

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

Petechiae
Pigmenturia

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18
Q

IMHA: CBC Findings

A
Anemia: usually regenerative, can be non-regenerative (bone marrow) 
Hemoglobinemia/hemoglobinuria
Autoagglutination 
Spherocytosis
Thrombocytopenia
Leukocytosis +/- left shift
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19
Q

What is Evan’s Syndrome?

A

IMHA and immune mediated thrombocytopenia

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20
Q

IMHA: Chemistry Findings

A
Hyperbilirubinemia 
Elevated liver enzymes
Hypoalbuminemia (negative acute phase protein)
Elevated BUN
Hypokalemia 
Abnormal coagulation 
Bilirubinuria/Hemoglobinuria
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21
Q

IMHA: Diagnosis

A

Diagnosis of exclusion

Thoracic radiographs
Abdominal ultrasound
Serologic tests for infectious diseases

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22
Q

Immune mediated disease Treatment

A

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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23
Q

Glucocorticoid Treatment:

Length and Weaning

A

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

24
Q

IMHA: Treatment Principles

A

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

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

25
Q

Primary hemostasis disruption includes…

A

Platlets, von Will.

Surface bleeding: mucous membranes and GI tract

26
Q

Secondary hemostasis disruption includes…

A

Fibrin-strong
Not enough clotting factors

Bleed into cavities (thorax, abdomen, etc.)
Ex. Rodenticide toxicity

27
Q

Immune-mediated thrombocytopenia (ITP, IMTP) Pathogenesis

A

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

28
Q

ITP Primary

A

Idiopathic (genetic?)

True autoantibody with a specificity for self antigen of the platelet membrane

29
Q

ITP Secondary

A

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

30
Q

ITP Clinical Disease

A
Hyphema (blood collection in anterior of eyes)
Retinal hemorrhage
Ecchymoses
Sclera petechia
Petechiae 
Melena
Hematochezia 

Tachycardia, tachypnea
Weakness, lethargy
Hematuria

31
Q

Bleeding/hemorrhage vs. ITP

A

Autoagglutination -> immune mediated, spherocytes

Bleeding/hemorrhage: TS will be decreased

32
Q

ITP Pathogenesis (3 main)

A

Decreased production (infiltrative, toxic, infectious)

Increased consumption (DIC, vasculitis)

Sequestration

33
Q

Top DfDx of Severe Thrombocytopenia (number)

A

Severe thrombocytopenia = <40,000

DfDx:
Immune mediated
DIC

34
Q

ITP CBC Findings

A

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

35
Q

ITP Chemistry Findings

A

Normal unless there has been hemorrhage causing hypoproteinemia

Abnormalities of IMHA if present

36
Q

ITP Urinalysis Findings

A

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

37
Q

ITP Diagnosis

A

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

38
Q

ITP Treatment

A

Same as IMHA for immunosuppression

Vincristine
Minimally increases pletelet count
Accelerated fragmentation of megakaryocytes
Impaired platelet destruction 
Reduce degree of phagocytosis
39
Q

Immune-mediated polyarthritis: Pathogenesis

A

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

40
Q

Infectious Polyarthritis

A
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)

41
Q

Immune-Mediated Polyarthritis Forms

A

Erosive form (uncommon) - poor prognosis

Non-erosive forms (most common)

42
Q

Immune-Mediated Polyarthritis Erosive Form

A

Rheumatoid arthritis (painful and debilitating)

Periosteal proliferative arthritis

Long term pain no matter what you do

Permanent joint destruction can occur

43
Q

Immune-Mediated Polyarthritis Non-erosive Forms

A

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

44
Q

Immune-mediated Polyarthritis: Non-erosive Type I

A

Idiopathic; no underlying disease

45
Q

Immune-mediated Polyarthritis: Non-erosive Type II

A

Reactive - distant infeciton

46
Q

Immune-mediated Polyarthritis: Non-erosive Type III

A

Enteropathic

47
Q

Immune-mediated Polyarthritis: Non-erosive Type IV

A

Neoplasia-related

48
Q

Immune-mediated Polyarthritis Signalment

A

Medium to large-breed dogs

Young to middle aged (usually young)

Retrievers, Spaniels, German Shepherds

49
Q

Immune-mediated Polyarthritis Clinical Signs

A
Variable:
Fever (waxing and waning) 
Lameness, stiffness (pain) - can see shifting limb lameness
Back, neck pain
Lethargy (painful)
Joint swelling, joint pain
50
Q

Immune-mediated Polyarthritis CBC

A

Inflammatory leukogram +/- left shift

Thrombocytopenia

Anemia of chronic disease (normocytic, normochromic)

51
Q

Immune-mediated Polyarthritis Chemistry

A

Hypoalbuminemia (negative acute phase protein)

Proteinuria

52
Q

Immune-mediated Polyarthritis Diagnostic

A

Arthrocentesis (usually of peripheral joints)

Suppurative inflammation

May be tin or discolored (should usually be straw colored and stringy)

53
Q

Immune-mediated Polyarthritis Diagnosis

A

Rule out other diseases

Radiographs
Serology
Blood, urine, joint fluid cultures

54
Q

Immune-mediated Polyarthritis Treatment

A

Immunosuppressive drug therapy

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

55
Q

Clotting factors that require Vitamin K

A

II, VII, IX, X