Immunosuppressants 1 Flashcards

(54 cards)

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
tocilizumab -class, mech?
receptor blocker (IL-6) binds IL-6 receptors (T cell activation affected)
26
tocilizumab -administration route, target, source?
parenterally/ IV target: attack immune system (li); monoclonal antibody (mab) source: humanized (zu)
27
tocilizumab -Tx, SE?
-RA SE: increased risk of infection
28
ustekinumab -class, mech?
receptor blocker (IL-12, IL- 23) binds to interleukins IL-12, IL-23 (T cell activation affected)
29
ustekinumab -administration route, target, source?
parenterally/ IV target: interleukin (ki); monoclonal antibody (mab) source: fully human
30
ustekinumab -Tx, SE?
-psoriasis SE: increased risk of infection
31
* What is TNF (tumor necrosis factor)? | i. e. receptor, enzyme
cytokine (enzyme) **does NOT bind to receptor**
32
what monoclonal antibody source is wanted for a little to no immune response?
fully human (u)
33
what does TNF do?
activator of immune system, central activator
34
etanercept -class, mech?
enzyme inhibitor -TNF inhibits activation of T cell by TNF
35
etanercept -route of administration, other?
-subcutaneously - used in combo with other immunosupp. - $$
36
etanercept -Tx, SE?
RA SE: increased risk of infection
37
infliximab -class, mech?
enzyme inhibitor -TNF binds to TNF (activation of T cell affected)
38
infliximab -administration route, target, source?
-IV target: immune system; monoclonal antibody source: chimeric
39
infliximab -Tx, SE, concern?
- RA, Crohn's SE: can cause immune response -infusion --> itching, hypotension, fever concern: preexisting infection w/ fungus or TB may become worse
40
infliximab -why may there be an immune response?
b/c it's chimeric
41
adalimumab -class, mech?
enzyme inhibitor -TNF binds TNF (T cell activation affected
42
adalimumab -administration route, target, source?
-IV target: immune system; monoclonal antibody source: fully human
43
adalimumab -Tx, SE?
-RA SE: increased risk of infection
44
certolizumab -class, mech
enzyme inhibitor -TNF binds TNF (T cell activation affected)
45
certolizumab -administration route, target, source?
-IV target: immune system; monoclonal antibody source: humanized
46
certolizumab -Tx, SE?
- RA, Crohn's SE: increased risk of infection
47
golimumab -class, mech
enzyme inhibitor -TNF binds TNF (T cell activation affected)
48
golimumab -administration route, target, source?
-IV target: immune system; monoclonal antibody source: fully human
49
golimumab -Tx, SE?
-RA, ulcerative colitis, psoriatic arthritis SE: increased risk of infection
50
what are 2 ways to block IL-1
1. anakinra (receptor) | 2. rilonacept (molecule)
51
anakinra -class, route of administration?
receptor blocker (IL-1) -subQ
52
anakinra -other, contraindications?
- used w/ other immunosuppressants like METHOTREXATE | - contra: should NOT be used w/ TNF inhibitors?
53
why should anakinra NOT be used with TNF inhibitors?
b/c almost guaranteed to get infection, suppressing imm. sys too much
54
rilonacept -class
binds to IL-1 molecule