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Small Animal Medicine > Immunosuppressive Therapy > Flashcards

Immunosuppressive Therapy Flashcards

1
Q

What is the primary immunosuppressive? What are 5 other secondary ones that can be added on?

A

glucocorticoids - Prednisolone, Dexamethasone

  1. Azathioprine
  2. Cyclosporine
  3. Chlorambucil
  4. Leflunomide
  5. Mycophenolate mofetil
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2
Q

What adjunctive and supportive therapies can be added for immunosuppressive therapy?

A

ADJUVANT = human IVIg, Vincristine, Melatonin

SUPPORTIVE = blood products, antiplatelet therapy

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3
Q

How are immunosuppressive therapies picked?

A
  • expected course and prognosis of disease
  • concurrent diseases
  • safety and efficacy
  • ease of administration and monitoring
  • cost
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4
Q

Why are glucocorticoids a first-line therapy for immunosuppression?

A
  • effective
  • relatively rapid onset
  • cheap
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5
Q

What are 4 immunosuppressive mechanisms of action of glucocorticoids?

A
  1. decreased inflammatory cytokines
  2. decrease antigen presenting
  3. down-regulate Fc receptor expression on macrophages
  4. suppression of T-cell function
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6
Q

What are 7 side effects associated with glucocorticoids?

A
  1. PU/PD, panting, polyphagia
  2. muscle atrophy and weakness
  3. iatrogenic hyperadrenocorticism
  4. vacuolar hepatopathy
  5. infections, sepsis
  6. GI ulceration
  7. hypercoagulability
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7
Q

What are 4 contraindications for the use of glucocorticoids for immunosuppression?

A
  1. diabetes mellitus
  2. infections
  3. hyperadrenocorticism
  4. NSAID therapy —> needs a washout period
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8
Q

How do the doses of Prednisolone and Dexamethasone compare?

A

PREDNISOLONE - 2 mg/kg/day, 50 mg/m^2, dose cap at 50-80 mg/day

DEXAMETHASONE - 7-10x more potent than Prednisone, 0.2-0.3 mg/kg/day (SP = 3 mg/mL)

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9
Q

How are glucocorticoid doses altered once remission is reached? What is done is a patient relapses?

A

decrease 25% every 2-4 weeks for 4-6 months with the goal of discontinuing or getting to the lowest effective dose

return to the original effective dose

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10
Q

What is avoided when decreasing glucocorticoid doses?

A

decreasing other medications

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11
Q

In what 4 situations should other therapies be considered when using glucocorticoids?

A
  1. no or poor response
  2. excessive side effects
  3. long duration of therapy anticipated
  4. corticosteroids contraindiccated

(consider drug availability, patient size, cost, adverse effects, and efficacy —> little to no evidence to support one over the other)

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12
Q

What are 3 mechanisms of actions of Azathioprine?

A
  1. inhibits purine synthesis, which disrupts lymphocyte proliferation
  2. blocks T-cell activation and promotes T-cell apoptosis
  3. decreases antibody synthesis
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13
Q

Is Azathioprine used in cats?

A

not usually —> metabolism relies on thiopurine methyltransferase, which is low in cats

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14
Q

What are the 4 most common side effects associated with Azathioprine? What is commoly monitored?

A
  1. cytopenias - 2-3 months
  2. hepatotoxicity - 1-4 weeks
  3. GI signs - mild and self-limiting
  4. CHRONIC - subclinical anemia (PCV >25-30%)

CBC/Chem

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15
Q

When is Azathioprine hepatotoxicity seen? What. isthe most common sign? How is it solved?

A

concurrent prednisone administration

discordant ALT > ALP, increased BILI

  • dose reduction by 50% —> discontinuing can cause hyperbilirubinemia
  • SAMe can prevent and/or reverse
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16
Q

Why is Azathioprine commonly used? What is it the proposed second-line agent of choice for?

A

has glucocorticoid-sparing effects

IMHA

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17
Q

What onset of Azathioprine have? How is it tapered?

A

slow, takes around 3 weeks

after prednisone, over 2-3 months - 2 mg/kg/day q 48 hr —> 1 mg/kg/day q 48 —> 1 mg/kg twice weekly

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18
Q

What are the 2 mechanisms of action of Cyclosporine? How is it unique?

A
  1. calcineurin inhibitor that decreases IL-2 synthesis
  2. impairs function of T-cells and blunts immune response specific for lymphocytes

NOT CYTOTOXIC = no bone marrow suppression

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19
Q

Cyclosporine drug interactions:

A
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20
Q

What is the most common side effect of Cyclosporine? What else is seen? What is not seen?

A

GI signs

  • hepato/nephrotoxicity
  • gingival hyperplasia
  • hypertrichosis, excessive shedding, papillomatosis
  • opportunistic infections (significant fungal infections)
  • platelet activation - avoid with IMHA?

myelosuppression

21
Q

What onset does Cyclosporine have?

A

days

22
Q

How is therapeutic drug monitoring used for Cyclosporine?

A
  • measurement of blood drug levels - measures build-up
  • pharmacodynamic assays - drug effect on target cells assesses T-cell function and immune response (IL-2)
23
Q

What administrations of Cyclosporine are available? What is not recommended?

A
  • oral microemulsion improves bioavailability - Atopica —> expensive for large dogs
  • injectable, IV - Sandimmune

oil-based, caution with generics

24
Q

What is the mechanism of action of Cyclophosphamide? What is it used for?

A

alkylating agent

IMHA —> fallen out of fever for immunosuppression, mostly used for chemotherapy

25
Q

What is the most common adverse effect of Cyclophosphamide?

A

hemorrhagic cystitis

26
Q

What are the 2 mechanisms of action of Chlorambucil? What onset does it have? What species does it work particularly well in?

A
  1. alkylating agent
  2. targets B-cells

slow - takes 2 weeks

cats

27
Q

What is the most common clinical sign associated with Chlorambucil? What are 3 other signs?

A

GI signs

  1. myelosuppression - dose-dependent, monitor CBC
  2. alopecia and poor hair growth in Poodles
  3. neurologic signs in cats
28
Q

What is Chlorambucil used to treat?

A
  • IBD
  • PLE
  • glomerulonephritis

cats
($$$, no generics available)

29
Q

What are the 3 mechanisms of action of Leflunomide?

A
  1. inhibits de novo pyrimidine synthesis
  2. inhibits B and T-cell function and proliferation
  3. suppresses antibody production

myelosuppression!

30
Q

What 4 side effects are associated with Leflunomide?

A
  1. GI - inappetence, vomiting
  2. myelosuppression
  3. cutaneous drug reactions
  4. hepatotoxicity

generally well-tolerated

31
Q

What should be monitored in patients on Leflunomide? What is it used to treat?

A

CBC/Chem (ALT)

  • IMA, ITP, MUE
  • histiocytosis
  • IMPA, pemphigus
  • refractory colorectal polyps
32
Q

What are the 3 mechanisms of action of Mycophenolate mofetil?

A
  1. reversible inhibitor of inosine monophosphate dehydrogenase
  2. inhibits de novo purine synthesis
  3. inhibits lymphocyte proliferation and antibody production
33
Q

What is the most common side effect seen with Mycophenolate mofetil? What else is seen? What needs to be monitored?

A

GI - diarrhea, vomiting, poor appetite, large bowel diarrhea —> common in high doses, can add Metro

  • myelosuppression
  • lymphoma

CBC/Chem

34
Q

What 5 drugs decrease the bioavailability of Mycophenolate mofetil? What drug is avoided?

A
  1. Fluoroquinolones
  2. Metronidazole
  3. PPI, uncoated tablets
  4. glucocorticoids increase metabolism
  5. Cyclosporine

Azathioprine - has similar MOA = more side effects

35
Q

How can Mycophenolate mofetil be used that is different compared to the other second-line drugs?

A

can be used alone in satable disease

36
Q

What are 3 pros and a con to using Mycophenolate?

A
  1. low toxicity
  2. tablet size makes dosing easier for medium to larger dogs (where Cyclosporine would be very expensive)
  3. can be used as a stand alone treatment or in refractory/relapsing disease

can take 2-3 weeks to start working

37
Q

What is the monitoring timeline like for patients in remission?

A
  • improvement in clinical signs and clinicopathologic abnormalities
  • initiate prednisone taper by 25% q 2-4 weeks
  • acceptable maintenance dose or discontinue
  • continue treatment for 3 months
  • taper second line drug in a similar manner
38
Q

How is immunosuppressive relapse approached?

A
  • prednisone + second line drug
  • long-term therapy of low-dose glucocorticoid or second line drug
39
Q

What is human IVIg? What is its mechanism of action?

A

purified IgG pooled from human plasma

blocks Fc receptors, eliminated pathogenic antibodies, inhibits complement, and modulates cytokine synthesis

40
Q

How is human IVIg used for IMHA and ITP?

A

IMHA = short-term stabilization, refractory
- does not reduce transfusion requirements or length of hospitalization

ITP = reduces platelet recovery time and length of hospitalization
- does not increase expense compared to Prednisone alone

41
Q

What are the 4 most common adverse effects associated with human IVIg?

A
  1. hypersensitivity reactions
  2. anaphylaxis
  3. hypercoagulation
  4. renal failure
42
Q

What is Vincristine? What are 2 mechanisms of action? What is it most commonly used for?

A

vinca alkaloid chemotherapy

  1. disruption of intracellular microtubules
  2. cell cycle specific cytotoxicity

adjunctive treatment for ITP

43
Q

How are platelets affected by Vincristine? What does this result in?

A
  • platelets carry vincristine
  • increases megakaryocytopoiesis and thrombosis
  • reduces platelet destruction by intoxicated macrophages

increases platelets within 3-5 days and shortens hospitalization

44
Q

What are the 4 most common side effects associated with Vincristine?

A
  1. perivascular extravasation
  2. neurotoxicity
  3. GI signs
  4. minimally myelotoxic
45
Q

What supportive therapy is preferred in patients undergoing immunosuppressive therapy?

A

transfusions

  • pRBCs**
  • fresh whole blood*
  • plasma, platelets
46
Q

What gastroprotectants are commonly added for patients undergoing immunosuppressive therapy?

A
  • H2 blockers - Famotidine
  • PPIs - Omeprazole
  • Sucralfate
47
Q

What are the 2 most common causes of poor response to therapy?

A
  1. misdiagnosis - underlying etiology not detected, normal variations common in CKCS and Greyhounds
  2. not enough time for a response
48
Q

What medication side effects and disease processes can look like a patient is not responding to therapy?

A
  • failure of PCV to increase
  • recent decrease in PCV
  • non-regenerative anemia (Azathioprine!)

Small Animal Medicine (52 decks)

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