Immunosuppressants 1 Flashcards

1
Q

what happens to the cell after CD4 T cell proliferates?

A
  1. may become cytotoxic (IC-2)

or

  1. produce antibodies via B cell/antigen specific B cells (IC-4, IC-5)
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2
Q

what are 2 major side effects/risks of ALL immunosuppressants?

A
  1. increased infection (ALL)

2. increased malignancies/cancer (MANY)

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3
Q

antithymocyte globulin

-class, mech?

A

inhibit T cell (non-specific antibody)

blocks all T cell function,
cytotoxic to/ decreases circulating lymphocytes

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4
Q

antithymocyte globulin

-Tx/ SE?

A

-acute renal transplant rejection

SE: may cause allergic response (due to polyclonal antibodies)
increased risk of infection and malignancy

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5
Q

abatacept

-class, mech?

A

receptor inhibitor
-CD80, CD86

inhibits initial step for binding site of MP and T cell activation affected

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6
Q

abatacept

-Tx, SE?

A
  • RA arthritis

SE: increased risk of infection

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7
Q

belatacept

-class, mech?

A

receptor inhibitor
(CD80, CD86)

affect T cell activation

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8
Q

belatacept

-Tx, SE?

A

-renal transplant

SE: increased risk of infection, assc. with increased malignencies

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9
Q

what ends in ‘-mab’

A

monoclonal antibodies

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10
Q

what do monoclonal antibodies end in?

A

‘-mab’

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11
Q

administration route of monoclonal antibodies?

A

parenterally/ injection

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12
Q

administration route of ‘-mab’ drugs?

A

parenterally/ IV

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13
Q

do monoclonal bodies have more or less specific targets? more or less SE?

A

more specific targets

therefore,
less SE

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14
Q

monoclonal antibodies (‘mab’)- what does the middle of its name tell you?

A

target

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15
Q

what is ‘-li-‘?

A

immune cell (target)

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16
Q

what is ‘tu’?

A

tumor (target)

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17
Q

what are the three monoclonal antibody (‘-mab’) source prefixes?

A

xi
zu
u

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18
Q

what source is ‘-xi-‘?

A

chimeric source

-mouse antibody w/ some human pieces

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19
Q

what source is ‘-zu-‘?

A

humanized

-human ab w/ some mouse pieces

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20
Q

what source is ‘-u-‘?

A

fully human

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21
Q

most antigenic source?

least antigenic source?

A
most= chimeric source (xi)
least= fully human (u)
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22
Q

natalizumab

-class, mech?

A

receptor blocker
-integrin

binds to alpha integrins on CD4 T cell and other immune cells (affects T cell activation)

23
Q

natalizumab

-administration of route, target, source?

A
  • parenterally/ IV
    target: attack immune system (li); monoclonal antibody (mab)
    source: humanized (zu)
24
Q

natalizumab

-Tx, SE?

A
  • Crohn’s + MS

SE: linked w/ progressive multifocal leukoencephalopathe (PML)

increased risk of infection

25
Q

tocilizumab

-class, mech?

A

receptor blocker (IL-6)

binds IL-6 receptors (T cell activation affected)

26
Q

tocilizumab

-administration route, target, source?

A

parenterally/ IV

target: attack immune system (li); monoclonal antibody (mab)
source: humanized (zu)

27
Q

tocilizumab

-Tx, SE?

A

-RA

SE: increased risk of infection

28
Q

ustekinumab

-class, mech?

A

receptor blocker
(IL-12, IL- 23)

binds to interleukins IL-12, IL-23 (T cell activation affected)

29
Q

ustekinumab

-administration route, target, source?

A

parenterally/ IV

target: interleukin (ki); monoclonal antibody (mab)
source: fully human

30
Q

ustekinumab

-Tx, SE?

A

-psoriasis

SE: increased risk of infection

31
Q
  • What is TNF (tumor necrosis factor)?

i. e. receptor, enzyme

A

cytokine (enzyme)

does NOT bind to receptor

32
Q

what monoclonal antibody source is wanted for a little to no immune response?

A

fully human (u)

33
Q

what does TNF do?

A

activator of immune system, central activator

34
Q

etanercept

-class, mech?

A

enzyme inhibitor
-TNF

inhibits activation of T cell by TNF

35
Q

etanercept

-route of administration, other?

A

-subcutaneously

  • used in combo with other immunosupp.
  • $$
36
Q

etanercept

-Tx, SE?

A

RA

SE: increased risk of infection

37
Q

infliximab

-class, mech?

A

enzyme inhibitor
-TNF

binds to TNF (activation of T cell affected)

38
Q

infliximab

-administration route, target, source?

A

-IV

target: immune system; monoclonal antibody
source: chimeric

39
Q

infliximab

-Tx, SE, concern?

A
  • RA, Crohn’s

SE: can cause immune response
-infusion –> itching, hypotension, fever

concern: preexisting infection w/ fungus or TB may become worse

40
Q

infliximab

-why may there be an immune response?

A

b/c it’s chimeric

41
Q

adalimumab

-class, mech?

A

enzyme inhibitor
-TNF

binds TNF (T cell activation affected

42
Q

adalimumab

-administration route, target, source?

A

-IV

target: immune system; monoclonal antibody
source: fully human

43
Q

adalimumab

-Tx, SE?

A

-RA

SE: increased risk of infection

44
Q

certolizumab

-class, mech

A

enzyme inhibitor
-TNF

binds TNF (T cell activation affected)

45
Q

certolizumab

-administration route, target, source?

A

-IV

target: immune system; monoclonal antibody
source: humanized

46
Q

certolizumab

-Tx, SE?

A
  • RA, Crohn’s

SE: increased risk of infection

47
Q

golimumab

-class, mech

A

enzyme inhibitor
-TNF

binds TNF (T cell activation affected)

48
Q

golimumab

-administration route, target, source?

A

-IV

target: immune system; monoclonal antibody
source: fully human

49
Q

golimumab

-Tx, SE?

A

-RA, ulcerative colitis, psoriatic arthritis

SE: increased risk of infection

50
Q

what are 2 ways to block IL-1

A
  1. anakinra (receptor)

2. rilonacept (molecule)

51
Q

anakinra

-class, route of administration?

A

receptor blocker
(IL-1)

-subQ

52
Q

anakinra

-other, contraindications?

A
  • used w/ other immunosuppressants like METHOTREXATE

- contra: should NOT be used w/ TNF inhibitors?

53
Q

why should anakinra NOT be used with TNF inhibitors?

A

b/c almost guaranteed to get infection, suppressing imm. sys too much

54
Q

rilonacept

-class

A

binds to IL-1 molecule