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Equine Clinical Immunology > Chapter 24 Immunosuppressive therapy > Flashcards

Chapter 24 Immunosuppressive therapy Flashcards

1
Q

When does immunosuppressive therapy become necessary?

A

When immune-mediated tissue damage is life-threatening or causes organ dysfunction.

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2
Q

What are the main risks associated with immunosuppressive therapy?

A

Clinical side effects and systemic susceptibility to infections, particularly fungal and viral organisms.

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3
Q

What are some inhibitors of gene expression or transcription used in horses?

A

Corticosteroids.

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4
Q

What drugs inhibit nucleotide synthesis in horses?

A

Azathioprine and methotrexate.

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5
Q

What are some alkylating agents used for immunosuppression in horses?

A

Cyclophosphamide, chlorambucil, and vincristine.

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6
Q

What are phosphatase and kinase inhibitors used in equine immunosuppression?

A

Cyclosporine A, tacrolimus, and rapamycin.

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7
Q

What role do monoclonal antibodies play in immunosuppressive therapy?

A

They target specific B cell molecules.

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8
Q

What is the general effect of glucocorticoids on the immune system?

A

They are potent anti-inflammatory and immunosuppressive drugs.

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9
Q

What are commonly used glucocorticoids in horses?

A

Hydrocortisone, dexamethasone, prednisolone, methylprednisolone, isoflupredone, triamcinolone, beclomethasone, and fluticasone.

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10
Q

What are the common side effects of prolonged glucocorticoid use?

A

Adrenal suppression, hyperglycemia, polyuria/polydipsia, gastrointestinal ulceration, delayed wound healing, growth suppression, osteoporosis, myopathy, hypertension, and hypokalemia.

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11
Q

What mechanism allows glucocorticoids to suppress immune function?

A

They bind to cytosolic glucocorticoid receptors, allowing the receptor to translocate into the nucleus and inhibit transcription factors like NF-kappa B.

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12
Q

What are the two main outcomes of glucocorticoid binding to gene promoters?

A

Transrepression (suppression of other transcription factors) and transactivation (activation of gene transcription).

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13
Q

What is the effect of glucocorticoids on neutrophils?

A

Decreased diapedesis and migration to the site of infection.

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14
Q

What is the effect of glucocorticoids on antigen-presenting cells?

A

Decreased expression of inflammatory cytokines IL-1, IL-6, and TNF-alpha, and lower expression of MHC class II and IL-12 cytokines.

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15
Q

What effect do glucocorticoids have on T cells?

A

They cause profound T cell lymphopenia via inhibition of proliferation, sequestration in the reticuloendothelial system, impaired release from lymphoid tissues, and induction of apoptosis.

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16
Q

What is the role of azathioprine in immunosuppression?

A

It inhibits the synthesis of DNA and RNA, thus inhibiting lymphocyte activation and proliferation.

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17
Q

What are the adverse effects of azathioprine?

A

Leukopenia, anemia, thrombocytopenia, alopecia, dermatitis, and hepatotoxicity.

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18
Q

What is the mechanism of action of cyclophosphamide?

A

It alkylates DNA bases, resulting in mutagenic, cytotoxic, antiproliferative, and chemotherapeutic effects.

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19
Q

What are the adverse effects associated with cyclophosphamide?

A

Anemia, leukopenia, alopecia, and secondary malignancies.

20
Q

What is the mechanism of action of vincristine?

A

It binds to tubulin in the mitotic spindle and prevents purine synthesis, inhibiting cell proliferation.

21
Q

What are the common uses of cyclosporine in horses?

A

Intravitreal treatment of recurrent uveitis and immune-mediated keratitis.

22
Q

What are the potential adverse effects of systemic cyclosporine?

A

Vasoconstriction, hypertension, nephrotoxicity, hepatotoxicity, diarrhea, hyperlipidemia, hyperglycemia, neurotoxicity, and susceptibility to infections.

23
Q

What are the uses of tacrolimus and rapamycin in horses?

A

Tacrolimus has been used topically for hyperkeratosis, and rapamycin’s ocular toxicity and distribution have been studied for potential clinical use.

24
Q

What is the effect of glucocorticoids on the CD4:CD8 ratio in horses?

A

Decreases the CD4:CD8 ratio due to a reduction in CD4+ T cells and an increase in CD8+ T cells.

25
Q

What is the effect of fluticasone on heaves-affected horses?

A

Long-term fluticasone treatment had no statistically significant detectable effect on innate and adaptive immune parameters.

26
Q

What is the role of adrenocortical function in glucocorticoid therapy?

A

Parenteral, oral, and aerosolized corticoids reversibly suppress adrenocortical function while the response to ACTH stimulation remains intact.

27
Q

What are the side effects of glucocorticoids on neutrophil phagocytosis?

A

Variable, depending on the experimental system used, but generally results in decreased diapedesis and migration to the infection site.

28
Q

What is the effect of glucocorticoids on eosinophils and basophils/mast cells?

A

Decreased degranulation of these cells.

29
Q

What is the effect of azathioprine on glucocorticoid dosage?

A

Allows reduction in glucocorticoid dose when combined in therapy.

30
Q

What is the effect of cyclophosphamide on B cells?

A

Promotes its application for the treatment of autoantibody-mediated diseases.

31
Q

What is the therapeutic effect of vincristine in immune-mediated thrombocytopenia?

A

It inhibits cell proliferation, resulting in an anti-tumor and immunosuppressive effect.

32
Q

What are the adverse effects of vincristine in horses?

A

Mild neurologic adverse effects (proprioceptive deficits) and ileus.

33
Q

What is the mechanism of action of cyclosporine?

A

It binds to the cytoplasmic receptor cyclophilin, inhibiting calcineurin and preventing the translocation of transcription factors like NFAT to the nucleus.

34
Q

What are the effects of tacrolimus compared to cyclosporine?

A

Tacrolimus is considered to be a more powerful immunosuppressive drug.

35
Q

What are the common clinical uses of cyclophosphamide and vincristine in horses?

A

Treatment of lymphosarcoma, immune-mediated thrombocytopenia, and pemphigus foliaceus.

36
Q

What are the dose-related clinical adverse effects of cyclosporine?

A

Similar to those promoted by cyclosporine, including vasoconstriction, hypertension, nephrotoxicity, hepatotoxicity, diarrhea, hyperlipidemia, hyperglycemia, and neurotoxicity.

37
Q

What is the primary use of corticosteroids in horses?

A

To treat inflammatory, allergic, autoimmune, and neoplastic diseases, and to prevent allograft rejection in transplantation.

38
Q

What is the main benefit of combining different immunosuppressive drugs?

A

Increases effectiveness while allowing the use of doses tolerated by the patient.

39
Q

What is the main goal of immunosuppressive therapy?

A

To manage immune-mediated tissue damage when it is life-threatening or causes organ dysfunction.

40
Q

What is the main mechanism by which glucocorticoids exert their effects?

A

They bind to glucocorticoid receptors, allowing the receptor to translocate into the nucleus and suppress or activate transcription factors.

41
Q

What are the two main categories of glucocorticoid effects?

A

Transrepression (suppression of transcription factors) and transactivation (activation of gene transcription).

42
Q

What are the main adverse effects of prolonged high-dose glucocorticoid treatment?

A

Adrenal suppression, hyperglycemia, gastrointestinal ulceration, osteoporosis, myopathy, and hypertension.

43
Q

What is the role of glucocorticoids in acute phase anti-inflammatory action?

A

They inhibit vasodilation, vascular permeability, chemotaxis, adhesion molecules, and diapedesis.

44
Q

What is the main therapeutic effect of azathioprine?

A

Inhibition of DNA and RNA synthesis, thus preventing lymphocyte activation and proliferation.

45
Q

What is the recommended monitoring for horses on azathioprine?

A

Periodic complete blood cell counts and blood biochemistry tests to monitor for severe leukopenia and hepatotoxicity.

46
Q

What is the mechanism of action of tacrolimus and rapamycin?

A

They bind to the cytoplasmic FK-binding protein (FK-BP), inhibiting calcineurin and preventing the translocation of transcription factors.

Equine Clinical Immunology (32 decks)

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