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ACVIM Specialty 2023 > Immune mediated disease > Flashcards

Immune mediated disease Flashcards

1
Q

What percent of dogs with IMHA display a non-regenerative anemia on presentation?

A

30%

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2
Q

What are non-immune mediated causes of spherocytosis?

A
  • Oxidative damage (zinc, acetaminophen)
  • Pyruvate kinase deficiency
  • Hypersplenism
  • Envenomation
  • Disorders associated with RBC fragmentation (endocarditis, hemangiosarcoma)
  • Dyserythropoiesis
  • Transfusion
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3
Q

How many spherocytes per hpf is supportive of IMHA?

A

> 5 per 100x field = 63% sensitivity, 93% specificity

3-4/hpf = 74% sensitivity and 81% specificity so can be suggestive of IMHA if other causes of spherocytes are eliminated

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4
Q

Is a PCV or hematocrit more reliable in cases of IMHA?

A

PCV - agglutination can falsely decrease the automated hematocrit

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5
Q

How is the saline agglutination test performed?

A

4 drops of saline, 1 drop of blood = 100% specificity

If results are equivocal, can wash the RBCs in saline (1:4 ratio) 3 times and see if agglutination persists

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6
Q

What is another name for a Coombs test?

A

Direct antiglobulin test (DAT)

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7
Q

What is the sensitivity and specificity of a Coombs test for the diagnosis of IMHA?

A

Sensitivity around 80%, specificity 95-100%

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8
Q

How does lipemia affect RBCs?

A

Increases erythrocyte fragility, which can increase artifactual hemolysis

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9
Q

What are the proposed mechanisms for the development of IMHA in dogs infected with B. gibsoni?

A
  • Babesia infects RBCs, which may lead to antibodies targeting the organism destroying the RBC too
  • Oxidative injury may lead to damage of uninfected erythrocytes, exposing antigens that are normally hidden
  • Antibodies form against RBC membranes after silica acid residues are removed
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10
Q

Name two protozoan parasites other than Babesia that can trigger IMHA

A

Rangelia
Theileria

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11
Q

A high level of evidence exists for what organism causing IMHA in cats?

A

Mycoplasma haemofelis

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12
Q

What drug has the highest degree of evidence for inducing IMHA in dogs?

A

Cefazedone

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13
Q

What drug has the highest degree of evidence for inducing IMHA in cats?

A

Propylthiouracil

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14
Q

What are we supposed to call primary IMHA now?

A

Non-associative IMHA

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15
Q

Packed RBC transfusions given to dogs with IMHA should be no older than what? Why?

A
  • 7-10 days
  • Increased age of pRBC was associated with increased risk of mortality in dogs with hemolysis
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16
Q

Why are pRBCs preferred over bovine hemoglobin solutions for dogs with IMHA?

A
  • BHS scavenge nitric oxide, potentially causing vasoconstriction and hypertension
  • BHS exert a greater oncotic pressure, this increasing intravascular volume and hypertension
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17
Q

If a dog with IMHA is started on >2mg/kg/day of prednisone, when should the dose be decreased?

A

Within the first 1-2 weeks, as long as HCT is stable or increasing

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18
Q

What two clinicopathologic abnormalities were identified as predictors of mortality in IMHA patients?

A

Increased bilirubin
Increased BUN/urea

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19
Q

Does the consensus statement recommend IVIG?

A

Only as a salvage measure if a dog is not responding to 1-2 weeks of treatment with 2 immunosuppressive drugs

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20
Q

For IMHA patients, when should the dose of prednisone be tapered and by how much?

A

When the PCV is stable and >30% for 2 weeks after starting treatment, decrease prednisone by 25% (can decrease by up to 50% if on a secondary agent)

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21
Q

What monitoring should be performed while a patient is on azathioprine?

A

CBC and chem every 2 weeks for the first 2 months, then every 1-2 months

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22
Q

When are prophylactic antibiotics recommended for neutropenia?

A

<1000 cells/uL

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23
Q

In patients with severe neutropenia persisting for more than 1 week, what drug can be considered?

A

Recombinant granulocyte colony stimulating factor

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24
Q

What is the relapse rate for IMHA?

A

11-15% based on retrospective studies

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25
Q

Thromboprophylaxis should be provided to all dogs with IMHA except…

A

Dogs with severe thrombocytopenia (<30K)

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26
Q

What antithrombotic drug is recommended first for IMHA? If that isn’t available, what is recommended next?

A
  1. Unfractionated heparin with individual dose adjustment
  2. LWM heparin OR oral Xa inhibitor recommended second
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27
Q

How long should antithrombotics be continued in IMHA patients?

A

Until the patient is in remission and off prednisone OR until they have been in remission for 6 months with no other risk factors for thrombosis

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28
Q

In a retrospective study, what dog breeds were predisposed to developing PIMA?

A

Whippets, Miniature Dachshunds, Lurchers

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29
Q

What percent of dogs with PIMA ultimately responded to treatment? What was associated with improved survival?

A
  • Erythroid regeneration in 88%, remission in 62%
  • Corrected reticulocyte percentage >0.2 associated with improved survival
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30
Q

Cell free DNA was increased in dogs with IMHA compared to controls. What might cause this increase and why is it concerning?

A
  • May be caused by cell death and release of neutrophil extracellular traps
  • Cell free DNA has prothrombotic properties
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31
Q

What is a hallmark feature of bone marrow histopathology in dogs with PIMA?

A

Rubriphagocytosis

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32
Q

Dogs with PIMA develop a regenerative response after a median of how many days of immunosuppression? When is remission achieved?

A

Regeneration: 30 days
Remission: 60 days

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33
Q

What drug is capable of inhibiting canine complement-mediated hemolysis in vitro?

A

C1-esterase inhibitor

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34
Q

What cardiac biomarker is increased in dogs with IMHA on presentation and decreases with treatment?

A

Troponin I

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35
Q

Primary IMHA is most commonly diagnosed in what age cat?

A

2-6 years of age

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36
Q

What were negative prognostic indicators in cats with IMHA?

A

Higher bilirubin, older cats

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37
Q

What is IgG4 related disease?

A

Diffuse IgG4 positive lymphoplasmacytic infiltrates lead to increased serum concentrations of IgG4, peripheral eosinophilia, tumorous swellings, obliterative phlebitis, and fibrosis

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38
Q

What arm of the immune system mediates most autoimmune diseases?

A

Th2 cells - results in the production of autoantibodies

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39
Q

What antibody class is involved in most cases of IMHA? What is its half life?

A

IgG - half life is one week

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40
Q

How do glucocorticoids affect gene transcription?

A
  • Enter the cell by passive diffusion
  • Interact with glucocorticoids receptors in the cytosol
  • Leads to a conformational change in the receptor and release of an activated complex => nucleus
  • Activated complex binds to short DNA sequences called glucocorticoid response elements => modification of gene transcription
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41
Q

Name 5 ways that glucocorticoids suppress the immune system

A
  1. Inhibit production and release of cytokines, chemokines
  2. Impair macrophage activity by influencing the expression and function of Fc receptors
  3. Decrease macrophage antigen processing/presentation
  4. Reduce the numbers of lymphocytes
  5. Decrease migration of inflammatory cells from the blood into tissues
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42
Q

Describe the mechanism of action of cyclosporine

A
  1. Enters the cytosol and complexes with cyclophilin
  2. This complex then binds and inhibits calcineurin, thus inhibiting calcineurin’s calcium-stimulated phosphatase
  3. Without this dephosphorylation, NFAT is not activated
  4. NFAT is needed for nuclear transcription of cytokines, like IL-2
  5. IL-2 is needed for the activation and proliferation of T cells => inhibits T cell function
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43
Q

What enzyme metabolizes cyclosporine in the liver?

A

Cytochrome P450

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44
Q

When measuring blood cyclosporine levels, when should samples be obtained?

A

Peak - 2 hours after dosing
Trough - right before the next dose

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45
Q

What is the active metabolite of azathioprine?

A

6-mercaptopurine

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46
Q

What is the mechanism of action of azathioprine?

A

Purine analogue
- 6 mercaptopurine resembles adenine and guanine, so it is alternately inserted during the S phase of cell division
- Leads to ribonucleic acid miscoding => disruption of RNA and DNA synthesis and mitosis

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47
Q

Why are lymphocytes more sensitive to inhibition of purine and pyrimidine synthesis?

A

Lymphocytes lack a salvage pathway for the synthesis of purines and pyrimidine and are reliant on de novo synthesis of these nucleotides (unlike other cell lines)

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48
Q

What breed has lower thiopurine methytransferase activity and is therefore at higher risk of azathioprine toxicity?

A

Giant Schnauzers

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49
Q

What breed has higher thiopurine methytransferase activity and therefore may need higher doses of azathioprine to be effective?

A

Alaskan Malamute

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50
Q

What is the active metabolite of mycophenolate mofetil?

A

Mycophenolic acid

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51
Q

What is the mechanism of action of mycophenolate?

A

Inhibits inosine monophosphate dehydrogenase - enzyme necessary for de novo purine synthesis

  • Inhibits both B and T cell proliferation/clonal expansion in the S phase of the cell cycle
  • Suppresses B cell antibody formation
  • Induces apoptosis of activated T cells
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52
Q

What isoform of inosine monophosphate dehydrogenase is primarily affected by mycophenolate?

A

Type 2 isoform (5 fold greater affinity) - found in activated lymphocytes

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53
Q

What nucleotide is primarily depleted by inhibition of inosine monophosphate dehydrogenase?

A

Guanosine

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54
Q

What is the mechanism of action of leflunomide?

A

Reversibly inhibits dihydro-orotate dehydrogenase - enzyme needed for de novo pyrimidine synthesis

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55
Q

What is the mechanism of action of alkylating agents?

A
  • Cross-link DNA, thus interfering with DNA replication and RNA transcription
  • Toxic to both resting and dividing cells (cell cycle nonspecific)
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56
Q

Name 2 alkylating agents that are commonly used for immune suppression in veterinary medicine

A
  • Chlorambucil
  • Cyclophosphamide
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57
Q

What metabolite of cyclophosphamide results in sterile hemorrhagic cystitis?

A

Acrolein

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58
Q

What drug has a primary immunosuppressive effect against macrophages?

A

Liposomal clodronate

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59
Q

What glucocorticoid has negligible mineralocorticoid activity and may be preferred in situations where water retention is detrimental?

A

Dexamethasone

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60
Q

In the bone marrow, how long does it take for erythroid precursors to differentiate into mature RBCs?

A

5-7 days

61
Q

What is the half life of a RBC in dogs and cats?

A

Dogs: 100-120 days
Cats: 75 days

62
Q

What causes excessive Heinz body formation?

A

Oxidative damage that denatures hemoglobin

63
Q

Why are excessive Heinz bodies detrimental?

A

Increase RBC rigidity, thus increasing susceptibility to hemolysis

64
Q

What is this abnormality?

A

Heinz body

65
Q

Name two toxins that may result in Heinz body anemia in dogs?

A

Zinc, onions, acetaminophen

66
Q

Name 3 conditions in cats that can increase the number of Heinz bodies present

A
  • Diabetes mellitus
  • Hyperthyroidism
  • Lymphoma
67
Q

How does hypophosphatemia result in hemolysis?

A

Decreased RBC ATP stores, leading to decreased membrane stability, increased osmotic fragility and increasing susceptibility to hemolysis

68
Q

Name 2 genetic erythrocyte enzyme deficiencies that cause impaired erythrocyte energy metabolism => hemolytic anemia

A

Pyruvate kinase deficiency
Phosphofructokinase deficiency

69
Q

In dogs with pyruvate kinase deficiency, progression iron overload from continuous hemolysis may lead to what?

A

Hemosiderosis and liver fibrosis

70
Q

What causes sporadic hemolysis crises in dogs with phosphofructokinase deficiency?

A

Exercise-induced hyperventilation alkalemia

71
Q

What cell line gives rise to hemophagocytic histiocytic sarcoma? What are the cells positive for on immunophenotyping?

A

Macrophages
CD11/CD18

72
Q

What feline blood type develops high-titer antibodies against the other blood type in the first 3 months of life?

A

Type B cats develop anti-A antibodies that are hemolyzing and hemagglutinating

73
Q

What is the effect of anesthesia on feline hematocrit?

A

Causes up to a 25% drop in hematocrit - don’t measure during anesthesia

74
Q

What cells produce erythropoietin in the kidney?

A

Peritubular interstitial cells of the inner renal cortex and outer medulla

75
Q

What inflammatory cytokine increases the production of hepcidin?

A

IL-6, primarily

76
Q

How does hypocobalaminemia lead to anemia?

A

Deficiency of B12 inhibits purine and thymidylate synthesis => impaired DNA synthesis within erythroblasts => erythroblast apoptosis

77
Q

What is ferritin?

A

The soluble storage form of iron in tissues
- Positive acute phase protein
- Representative measure of total body iron stores in health

78
Q

What is transferrin? How is it measured?

A
  • Main protein in the blood that binds and transports iron
  • Measured indirectly and reported as total iron binding capacity
  • Negative acute phase protein
79
Q

Describe how an iron panel would look in a case of iron-deficiency anemia

A
  • Serum iron level: low
  • Ferritin level: low
  • Transferrin (TIBC): normal to increased
  • Iron saturation (serum iron/TIBC): less than 20%
  • Bone marrow iron: low
80
Q

Describe how an iron panel would look in a case of anemia of inflammation or chronic disease?

A
  • Serum iron: low
  • Ferritin: increased
  • Transferrin (TIBC): normal to low
  • Iron saturation: normal to low
  • Bone marrow iron: normal to high
81
Q

What is the lifespan of a platelet in circulation?

A

6-10 days

82
Q

What cat breed develops Chediak-Higashi syndrome? What coat color occurs along with the disease?

A

Persians - blue smoke coat color due to partial albinism

83
Q

What is Chediak-Higashi syndrome?

A

Primary immunodeficiency
- Recurrent neutropenia, neutrophil function defects, and platelet function defects
- Neutrophils and eosinophils contain abnormally fused granules

84
Q

What causes Pelger-Huet anomaly?

A
  • Autosomal dominant disorder
  • Defective terminal granulocyte maturation leading to abnormal appearance but normal function
85
Q

What dog breed is over-represented for Pelger-Huet anomaly?

A

Australian Shepherds

86
Q

What is the appearance of granulocytes in Pelger-Huet anomaly?

A

Hyposegmented nuclei with mature chromatin

87
Q

What causes leukocyte adhesion deficiencies, specifically type I LAD?

A
  • Mutations in leukocyte adhesion proteins that prevent normal adherence and migration of WBC through the endothelium
  • Type I = defect in the beta-2 integrin subunit (CD18)
88
Q

Type I LAD has been described in what dog breed?

A

Irish Setters

89
Q

What clinicopathologic abnormalities are observed in type I LAD?

A
  • Marked peripheral neutrophilia with nuclear hypersegmentation
  • Absence of neutrophils in tissues on biopsy
90
Q

What are the clinical signs of type I LAD?

A

Puppies present with omphalitis followed by lymphadenopathy, low body weight, and febrile infections

91
Q

What causes trapped neutrophil syndrome and what abnormalities are seen on a CBC and bone marrow biopsy?

A
  • Neutrophils cannot leave the bone marrow normally
  • Peripheral neutropenia with a degenerative left shift, marked monocytosis
  • Myeloid hyperplasia in the bone marrow with increased mature neutrophils
92
Q

Trapped neutrophil syndrome is autosomal recessive in what dog breed?

A

Border Collies

93
Q

What phenotypic abnormality can be seen in Border Collies with trapped neutrophil syndrome?

A

Craniofacial deformity

94
Q

Pyruvate kinase deficiency in dogs causes what changes to the bone marrow?

A
  • Progressive myelofibrosis and osteosclerosis => bone marrow failure
  • Likely due to iron overload and effects of prolonged increased erythropoiesis
95
Q

What causes X-linked severe combined immunodeficiency?

A

Mutation in the common interleukin 2 receptor gamma chain - affects developing thymocytes

96
Q

X-SCID is found in what dog breeds?

A

Cardigan Welsh Corgi and Basset Hound

97
Q

What are the clinical signs of X-SCID?

A

Stunted growth, recurrent or chronic infections as maternal antibody production declines, dysplastic thymus, hypoplastic or absent lymphoid tissues

98
Q

What clinicopathologic abnormalities are present with X-SCID?

A

Rare peripheral T lymphocytes, increased B lymphocytes

99
Q

What causes autosomal recessive severe combined immunodeficiency?

A

Defective recombination events during T and B lymphocyte maturation - mutation in the catalytic subunit of DNA-dependent protein kinase

100
Q

Autosomal recessive severe combined immunodeficiency has been described in what dog breed?

A

Jack Russel Terrier

101
Q

What clinicopathologic abnormalities are present in autosomal recessive severe combined immunodeficiency?

A

Severe lymphopenia, decrease serum globulins, marked lymphoid hypoplasia (spleen, thymus, LN)

102
Q

What causes cyclic hematopoiesis (or cyclic neutropenia)?

A

Autosomal recessive defect in trafficking of lysosomal membrane proteins

103
Q

Cyclic hematopoiesis has been reported in what dog breed?

A

Gray Collies - grey coat color results from defect in melanocytes

104
Q

What clinicopathologic abnormalities are found in cyclic hematopoiesis?

A

Neutropenia that occurs every 2 weeks

105
Q

What abnormalities are found with common variable immunodeficiency?

A

Hypogammaglobulinemia, absence of B cells in lymph nodes, lymphocyte function deficits

106
Q

What breeds are affected by common variable immunodeficiency and what infection do they commonly get?

A

Miniature Dachshunds and Cavaliers
Pneumocystis carinii pneumonia

107
Q

What causes primary myelodysplastic syndrome?

A

Clonal disorders arising from mutations within hematopoietic stem and progenitor cells - as they are clonal, they are technically neoplastic disorders

108
Q

What histopathologic changes on a bone marrow biopsy may increase the suspicion for primary MDS over secondary causes?

A

Increased immature precursors, higher percentages of dysplastic cells, megaloblastic erythroid precursors

109
Q

Cyclosporine and prednisone suppressed expression of what inflammatory cytokines? Which drug suppressed them more?

A

IL-2 and IFN-gamma
Cyclosporine was more suppressive

110
Q

What percent of dogs develop GI side effects from mycophenolate? What was the median time to onset?

A

25%, 10 days after starting the drug

111
Q

What percent of dogs develop cytopenias from mycophenolate?

A

4%

112
Q

What effect did 5-7 days of steroid administration have on cardiac changes in cats?

A
  • Increased median left atrial and ventricular dimension
  • No difference in absolute concentration of NT-proBNP but increased individual percentage change (60% of cats had a NT-proBNP that increased by 60% after treatment)

Suggests plasma volume expansion with steroids

113
Q

What effect does desmopressin have on PU/PD in dogs receiving high dose glucocorticoids?

A

Decreased water intake, increased USG BUT caused hyponatremia

114
Q

What dose of leflunomide is recommended and what dose increases the risk of side effects?

A

Recommended: 2mg/kg/day
Side effects: 3-4 mg/kg/day

115
Q

What percent of dogs on immunosuppressive therapy develop opportunistic fungal infections? When do they occur?

A
  • 13% overall - but 20% of dogs on cyclosporine developed them compared to 4% of dogs on other immunosuppressives
  • Median of 43 days after starting treatment
116
Q

Where do dogs on immunosuppressive therapy develop opportunistic fungal infections?

A

Majority are skin lesions, common on the distal extremities

117
Q

What are the most common opportunistic fungal infections in dogs on immunosuppressives?

A

Soil saprophytes - phaeohyphomycoses and hyalohyphomycoses

118
Q

In a retrospective study comparing mycophenolate/pred vs cyclosporine/pred, which group had better outcomes? Adverse effects?

A
  • Similar outcomes (hospitalization time, 30 and 60 day survival)
  • Cyclosporine technically had more adverse events, but it was 9 vs 11 dogs
119
Q

In dogs with primary ITP, what clinical sign was associated with decreased survival to discharge?

A

Melena

120
Q

In dogs with primary ITP, did anti-platelet antibodies correlate with response to treatment? With relapse?

A
  • Persistence or percentage of APA was NOT associated with treatment response/survival
  • But recurrence of APA WAS associated with relapse
121
Q

What percent of dogs with primary ITP survive to discharge? What percent relapse and in what time frame?

A

89% survive to discharge
31% relapse, median of 79 days

122
Q

In dogs with primary ITP that experienced a relapse, what percent experienced a second relapse?

A

50% - dogs that have relapsed once should be more closely monitored

123
Q

Administration of what immunosuppressive drug increases the risk of neutropenia after vincristine in dogs with ITP?

A

Cyclosporine (OR 13)

124
Q

In dogs with ITP, when does neutropenia develop after giving vincristine?

A

2-14 days, median 5 days

125
Q

Do the immature platelets released after vincristine administration function as mature platelets?

A

Yes based on expression of P-selectin (CD62P) - marker of alpha granule release

126
Q

What type of hypersensitivity reaction is thought to be involved in the development of non-erosive IMPA?

A

Type III hypersensitivity - immune complex deposition in the joint space, leading to neutrophil activation. Antigens may come from systemic circulation OR within the joint space itself

127
Q

Describe type I hypersensitivity

A

IgE is bound to mast cells via the Fc portion. An allergen binds to and cross links the IgE molecules => mast cell degranulation

128
Q

Describe type II hypersensitivity

A

IgG mediated cytotoxic hypersensitivity
- Cells are destroyed by bound antibodies, either through activation of complement or by a cytotoxic T cell with an Fc receptor for the antibody (ADCC)

129
Q

Describe type IV hypersensitivity

A

Cell mediated - Th1 cells secrete cytokines that activate macrophages and cytotoxic T cells

130
Q

In rheumatoid arthritis (erosive IMPA), what antibody has been found along the joint surface?

A

Antibodies against type II collagen

131
Q

In rheumatoid arthritis (erosive IMPA), what characterizes the chronic persistent synovitis that occurs?

A
  • Perivascular accumulation of mononuclear cells - possible type IV hypersensitivity
  • T lymphocytes, macrophages, and fibroblasts release matrix-degrading enzymes (MMPs, etc) => cartilage damage
132
Q

How long can it take for the erosive lesions in rheumatoid arthritis to appear on x-rays?

A

Up to 6 months - dogs with apparently non-erosive form should be re-evaluated

133
Q

What are rheumatoid factors?

A

Antibodies directed against immunoglobulins (IgM, IgM, IgA)

134
Q

What percent of dogs diagnosed with rheumatoid arthritis are positive for rheumatoid factors?

A

75%

135
Q

Idiopathic IMPA can be subcategorized into 4 types. Name them

A
  1. Type 1 = no underlying disease
  2. Type 2 = reactive (infectious/inflammatory disease distant from the joints)
  3. Type 3 = enteropathic
  4. Type 4 = neoplasia-related
136
Q

Why might GI disease lead to the development of IMPA?

A

Increased intestinal permeability may increase the amount of potential antigens accessing the blood stream => stimulates immune complex formation

137
Q

What virus has been implicated in the development of IMPA, either after infection or vaccination?

A

Canine distemper virus

138
Q

What dog breed may be predisposed to vaccine induced polyarthritis?

A

Akitas - 10% of puppies developed joint pain and cyclic fevers after vaccination

139
Q

What dog breed may be predisposed to polyarthritis after receiving sulfonamides?

A

Dobermans

140
Q

In cases of drug induced polyarthritis, clinical signs typically resolve within how many days of discontinuing the drug?

A

2-7 days

141
Q

What is the typical signalment and presenting complaint of a dog with steroid responsive meningitis-arteritis?

A
  • Medium to large breed, <2 years of age
  • Acute onset neck pain, fever, lethargy
142
Q

What does CSF analysis show in dogs with SRMA?

A

Inflammation, specifically increased IgA, and increased protein

143
Q

Describe the pathogenesis of Shar Pei fever

A
  • Shar Peis have an increased production of hyaluronic acid (HA) by dermal fibroblasts (leads to appearance)
  • Degradation of HA by trauma/oxidative damage => smaller fragments that mimic microbial surface proteins
  • Leads to the release of IL-1beta, IL-6, and inflammation
144
Q

What is the mechanism of action of colchicine?

A

Thought to impair the release of serum amyloid A from the liver by binding to hepatocyte microtubules and preventing amyloid secretion

145
Q

What cell type is more common in the synovial fluid of dogs with erosive IMPA compared to non-erosive IMPA?

A

Lymphocytes

146
Q

What joints are most commonly affected by erosive IMPA?

A

One paper says carpal joints

147
Q

What marker of oxidative stress is found in anemic dogs (all causes of anemia)?

A

Decreased glutathione peroxidase activity

148
Q

In dogs with IMHA undergoing necropsy, what percent displayed evidence of thrombus formation?

A

50-80%, depending on the study

149
Q

What are the mechanisms driving hypercoagulability in IMHA patients? What is not responsible?

A
  • Increased tissue factor expression
  • Platelet activation
  • Procoagulant microparticles
  • Neutrophil NETs

NOT: antiphospholipid antibodies

ACVIM Specialty 2023 (38 decks)

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