Transplant therapeutics 2 Flashcards
What is a typical dose for prednisone
5-15 mg per day
Who are the patients who would usually receive corticosteriod therapy
multiple rejections on a steroid free regimen, very high risk patients, no induction, patients who are already on steroids
What are the long term side effects of corticosteriods
osteoporosis,diabetes, cataracts, weight gain, hyperlipidemia
How can long term steroid side effects be avoided
a steroid taper
What is the best steroid removal time frame for the least amount of complications
5 to 14 days post transplant
What are the mTOR inhibitors
Sirolimus and Everolimus
T/F: Similiarly mTOrs block IL-2 production just like CNIs
False: Unllike CNIs which block IL-2 production, mTORs block IL-2 signal transduction
What is the MOA of mTORs
mTORs bind to FKBP-12 and complex with mTORs causing no phosphorylation of proteins
What enzyme metabolizes mTORs
CYP3A4 isotype
What enzyme inducers will decrease the levels of mTORs
phenytoin and carbamezapine, rifampin, naficillin
What enzyme inhibotrs will increase the levels of mTORs
ketoconazole, clarithomycin and erythromycin, dilitazem and verapamil, ritonavir
Competition with what CNI can cause complications with mTORs, how, how can this be avoided
cyclosporine, increased sirolimus levels, administer sirolimus 4 hours after cyclosporine
When are mTORs usually started, why
after their wounds are healed, due to lower healing side effects of mTORs
What side effect of mTORs would cause a discontinuation
mouth ulcers
What medication binds to the costimulatory receptor B7 on APCs, what are the consequences of this action
Belatacept, inhibits co-stimulattory signal 2 and promotes T-cell anergy and apoptosis
What are benefits of Belatacept
preserve renal function, improve long term outcomes
What patients avoid Belatacept
Liver patients
What patients can Belatacept only be used in, why
Epistein Barr Virus (EBV) serropositive, could cause PTLD in other patients
What is PTLD
B-cell proliferation due to induced immunosuppresion
What is the best regimen for keeping grafts successful
Triple regimen: CNI, antimetabolite, steroids
What are high risk patient qualities for, what type of antibody induction do they get
Blacks, re-transplants/ Lympho depleting agents (Thymo, Atgam, and Alem)
What type of antibody induction do low risk patients recieve
Basiliximab or no antibody therapy
What is acute tubular necrosis (ATN), what type of anitbody induction do they receive
kidney disorder caused by lack of oxygen to kidney tissue (necrosis), Lympho depleting agents
What are the two best ways to minimize steroid adverse effects, what is the downside
more potent induction and higher levels of CNIs, increased side effects of the CNI medications
