Immunosuppressive Therapy Flashcards
What are some of the side effects of glucocorticoid administration?
(PU/PD, panting, polyphagia, muscle atrophy/weakness, iatrogenic hyperadrenocorticism, vacuolar hepatopathy, infections/sepsis, GI ulceration, and hypercoagulability)
When are glucocorticoids contraindicated?
(Diabetes mellitus (GCs disrupt diabetic regulation, can use steroids but need to stop ASAP), infections, hyperadrenocorticism (can use steroids by need to stop ASAP), and when already using NSAIDs (optimally would have a washout period))
Why is there a prednisone dose cap for patients of greater weights?
(Bc at a certain point (maybe 60-80 mg/kg) immunosuppression does not become more effective and you’re just giving them worse side effects)
Optimally you would keep a patient that has reached clinical remission on their full dose of steroid for how long?
(2 weeks)
How are glucocorticoids tapered?
(Once clinical remission is achieved, the dose is tapered by 25% every 2-4 weeks, so it will take 4-6 months, taper to discontinue or the lowest effective dose)
What should you do if your patient relapses during a glucocorticoid taper?
(Return to the original effective dose)
(T/F) Azathioprine is minimally used in cats.
(T, metabolism issue that we don’t need to know the specifics of)
What are some of the side effects of azathioprine?
(Myelosuppression (cytopenias, chronic subclinical anemia), hepatotoxicity, and GI signs)
If you are giving a patient glucocorticoids and azathioprine for immune suppression, what should you be looking for on CBC/chem to indicate they are experiencing the hepatotoxicity side effects of azathioprine and not side effects of the steroids?
(Elevated ALT (steroids increase ALP so if ALT is sky high compared to ALP = hepatotoxicity) and increased bilirubin (steroids never cause this))
What should you do if your patient on azathioprine experiences hepatotoxicity?
(It depends, if no hyperbilirubinemia decrease the dose by 50%, if yes hyperbilirubinemia discontinue)
(T/F) Azathioprine is dosed at 2 mg/kg q24h for 2 weeks and is then tapered to 2 mg/kg q48h, regardless of the clinical signs the patient is showing.
(T)
How does cyclosporine differ from other immunosuppressive drugs?
(Cyclosporine impairs function of T-cells rather than actually reducing the production of T-cells = not myelosuppressive)
What are some of the side effects of cyclosporine?
(GI signs (primary side effect), hepatotoxicity and nephrotoxicity (not common unless giving high doses), gingival hyperplasia, hypertrichosis, excessive shedding, papillomatosis, and opportunistic infections (particularly fungal))
How do the doses for cyclosporine differ with non-life threatening/chronic inflammatory vs acute life threatening immune mediated diseases?
(Non-life threatening/chronic inflammatory → 5 mg/kg SID, acute life threatening → 5-10 mg/kg BID)
Why is therapeutic drug monitoring necessary when using cyclosporine?
(The immunosuppression induced by cyclosporine is animal dependent so you need to make sure the dose you’re giving is actually immune suppressing them)
