Immunotherapy Flashcards
too little therapy
rejection
too much therapy
opportunistic infection
therapy stages
induction maintenance rejection
standard regimen
TAC + MMF or EC-MPS + Prednisone
secondary acquired immunodeficiencies
increase typical and opportunistic infections and cancers
what class needs TDM
CNI
Prograf
Tacrolimus IR BID DAW
Asatgraf XL
Tacolimus ER
Envarsus
Tacrolimus ER
70% of IR daily dose
Neoral
modified cyclosporine BID
Gengraf
modified CYA
Neoral and Gengraf are bioevquivalents and are interchangeable
true
Prograf is interchangeable with other TAC generics
false
Prograf and Astagraf are equivalent and interchangeable
false
Astagraf to Prograf compairson
1 mg ER : 1 mg IR
Sandimmune
non modified CYA
qd and not interchangeable
CYA AEs
hyperlipidemia nephrotoxicity tremor, HA HTN hyperglycemia gingival hyperplasia hirsutism d/v
TAC AEs
N/D nephrotoxicity tremor, HA Insomnia Hyperglycemia Hyperlipidemia HTN
DDI that inhibit CYP3A4
-azole antifungals antivirals (-VIR) CCB - diltiazem and verapamil gastric acid suppressors grapefruit juice
how would dosing change if there was a DDI inhibiting CYP3A4?
higher troughs resulting in lower dosing
how would dosing change if there was a DDI inducing CYP3A4
lower troughs resulting in higher dosing
DDI that induce CYP3A4
rifampin
caspofungin, terbinafine
phenytoin, phenobarbital, oxcarbazepine
st johns wart
Mycophenolate Mofetil
CellCept
MFF is a pro drug delayed release
False, it is a prog drug regular release
Mycophenolic Acid Sodium
Myfortic
MPA is a delayed realse tablet
true
MPA is highly protein bound: how can that alter other drugs
can alter binding of others drugs to albumin
MPA MOA
inhibit IMPDH - blocking nucleotide synthesis and preventing proliferation of committed T cells
Comparison between MMF and MPS
1000mg of pro-drug MFF = 720 mg active drug MPS
DDI with MPA - enterohepatic recycling
CYA > TAC
DDI with MPA
Acyclovir
COCs
Protein bindning - aspirin + phenytoin
MPA AEs
GI
Leukopenia
Opportunistic Infections
CNS
What AE of MPA has a major impact on adherence
severe GI
What are the CNS AEs associated with MPA
dizziness, insomnia, HA
Prednisone - Hydrocortisone comparison
5 mg to 20 mg
Prednisone - Dexamethasone comparison
5 mg to 0.75 mg
short acting glucocorticoids have ___ anti-inflammatory properties
NONE
short acting glucocorticoids have ___ mineralocorticoid activity
HIGH
intermediate acting glucocorticoids have ___anti-inflammatory and mineral0corticoid activity
MODERATE
long acting glucocorticoids have ___anti-inflammatory activty
HIGH
long acting glucocorticoids have ___mineralocorticoid activity
NONE
Glucocorticoid AEs
axillary and lower abdominal striae
steroid induced avascular necrosis
ecchymoses
hyperglycemia
depleting induction therapies
Thymoglobulin
Alemtuzumab
non-depleting induction
Interleukin-2 receptor blockers
IL-2 receptor blocker
Basiliximab
Basiliximab
Simulect
Simulect MOA
MoAB against CD25 prevents activation of proliferation
AE’s of IL-2 RB
minimal due to low potency
n/v/d
Anti-thymocyte Globulin (ATG)
thymoglobulin
thymoglobulin is sourced from animals and therefore could have AEs
TRUE - hypersensitivity
How is ATG administered
IV infusion of 4-6 hours for 2 - 4 daily doses
ATG MOA
coat hosts Tcells which are destroyed by complement
ATG AEs
flu-like syndrome = cytokine release syndrome
serum sickness
leukopenia
What is used to pre-medicate ATG administration and why
diphenhydramine and APAP - cytokine release syndrome
Aletuzumab MOA
directly against the CD52 surface AG - cytotoxicity and cell lysis
Aletuzumab lymphocyte depletetion
B cells - 3-12 months
T cells - up to 3 years
What is used to pre-medicate aletuzumab
IV MEPD 30 mins prior
Aletuzumab AEs
N/V/D
lymphopenia
increased risk of malignancy and opportunistic infections
CNI nephotoxicity
acute dose dependent increase in SCr due to afferent arteriolar vasoconstriction
As CNI troughs increase….
SCr may increase