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Therapeutics > Immunotherapy > Flashcards

Immunotherapy Flashcards

1
Q

too little therapy

A

rejection

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2
Q

too much therapy

A

opportunistic infection

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3
Q

therapy stages

A

induction maintenance rejection

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4
Q

standard regimen

A

TAC + MMF or EC-MPS + Prednisone

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5
Q

secondary acquired immunodeficiencies

A

increase typical and opportunistic infections and cancers

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6
Q

what class needs TDM

A

CNI

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7
Q

Prograf

A

Tacrolimus IR BID DAW

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8
Q

Asatgraf XL

A

Tacolimus ER

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9
Q

Envarsus

A

Tacrolimus ER

70% of IR daily dose

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10
Q

Neoral

A

modified cyclosporine BID

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11
Q

Gengraf

A

modified CYA

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12
Q

Neoral and Gengraf are bioevquivalents and are interchangeable

A

true

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13
Q

Prograf is interchangeable with other TAC generics

A

false

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14
Q

Prograf and Astagraf are equivalent and interchangeable

A

false

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15
Q

Astagraf to Prograf compairson

A

1 mg ER : 1 mg IR

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16
Q

Sandimmune

A

non modified CYA

qd and not interchangeable

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17
Q

CYA AEs

A 
hyperlipidemia 
nephrotoxicity
tremor, HA
HTN
hyperglycemia
gingival hyperplasia
hirsutism
d/v
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18
Q

TAC AEs

A 
N/D
nephrotoxicity
tremor, HA
Insomnia
Hyperglycemia
Hyperlipidemia
HTN
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19
Q

DDI that inhibit CYP3A4

A 
-azole antifungals
antivirals (-VIR)
CCB - diltiazem and verapamil
gastric acid suppressors
grapefruit juice
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20
Q

how would dosing change if there was a DDI inhibiting CYP3A4?

A

higher troughs resulting in lower dosing

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21
Q

how would dosing change if there was a DDI inducing CYP3A4

A

lower troughs resulting in higher dosing

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22
Q

DDI that induce CYP3A4

A

rifampin
caspofungin, terbinafine
phenytoin, phenobarbital, oxcarbazepine
st johns wart

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23
Q

Mycophenolate Mofetil

A

CellCept

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24
Q

MFF is a pro drug delayed release

A

False, it is a prog drug regular release

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25
Q

Mycophenolic Acid Sodium

A

Myfortic

26
Q

MPA is a delayed realse tablet

A

true

27
Q

MPA is highly protein bound: how can that alter other drugs

A

can alter binding of others drugs to albumin

28
Q

MPA MOA

A

inhibit IMPDH - blocking nucleotide synthesis and preventing proliferation of committed T cells

29
Q

Comparison between MMF and MPS

A

1000mg of pro-drug MFF = 720 mg active drug MPS

30
Q

DDI with MPA - enterohepatic recycling

A

CYA > TAC

31
Q

DDI with MPA

A

Acyclovir
COCs
Protein bindning - aspirin + phenytoin

32
Q

MPA AEs

A

GI
Leukopenia
Opportunistic Infections
CNS

33
Q

What AE of MPA has a major impact on adherence

A

severe GI

34
Q

What are the CNS AEs associated with MPA

A

dizziness, insomnia, HA

35
Q

Prednisone - Hydrocortisone comparison

A

5 mg to 20 mg

36
Q

Prednisone - Dexamethasone comparison

A

5 mg to 0.75 mg

37
Q

short acting glucocorticoids have ___ anti-inflammatory properties

A

NONE

38
Q

short acting glucocorticoids have ___ mineralocorticoid activity

A

HIGH

39
Q

intermediate acting glucocorticoids have ___anti-inflammatory and mineral0corticoid activity

A

MODERATE

40
Q

long acting glucocorticoids have ___anti-inflammatory activty

A

HIGH

41
Q

long acting glucocorticoids have ___mineralocorticoid activity

A

NONE

42
Q

Glucocorticoid AEs

A

axillary and lower abdominal striae
steroid induced avascular necrosis
ecchymoses
hyperglycemia

43
Q

depleting induction therapies

A

Thymoglobulin

Alemtuzumab

44
Q

non-depleting induction

A

Interleukin-2 receptor blockers

45
Q

IL-2 receptor blocker

A

Basiliximab

46
Q

Basiliximab

A

Simulect

47
Q

Simulect MOA

A

MoAB against CD25 prevents activation of proliferation

48
Q

AE’s of IL-2 RB

A

minimal due to low potency

n/v/d

49
Q

Anti-thymocyte Globulin (ATG)

A

thymoglobulin

50
Q

thymoglobulin is sourced from animals and therefore could have AEs

A

TRUE - hypersensitivity

51
Q

How is ATG administered

A

IV infusion of 4-6 hours for 2 - 4 daily doses

52
Q

ATG MOA

A

coat hosts Tcells which are destroyed by complement

53
Q

ATG AEs

A

flu-like syndrome = cytokine release syndrome
serum sickness
leukopenia

54
Q

What is used to pre-medicate ATG administration and why

A

diphenhydramine and APAP - cytokine release syndrome

55
Q

Aletuzumab MOA

A

directly against the CD52 surface AG - cytotoxicity and cell lysis

56
Q

Aletuzumab lymphocyte depletetion

A

B cells - 3-12 months

T cells - up to 3 years

57
Q

What is used to pre-medicate aletuzumab

A

IV MEPD 30 mins prior

58
Q

Aletuzumab AEs

A

N/V/D
lymphopenia
increased risk of malignancy and opportunistic infections

59
Q

CNI nephotoxicity

A

acute dose dependent increase in SCr due to afferent arteriolar vasoconstriction

60
Q

As CNI troughs increase….

A

SCr may increase

Therapeutics (3 decks)

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