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RA PHARM Flashcards

1
Q

describe the structure of abatacept (IV/SC)

A

fusion protein: human CTLA4/IgG1 Fc fragment

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2
Q

MOA of abatacept (IV/SC)

A

binds CD80 and CD86 (B7) on APCs & prevents T-Cell co stimulatory signal engaging with CD28 (B7 receptor) on T-cells

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3
Q

structure of adalimumab(SC)

A

TNF-alpha monoclonal antibody

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4
Q

MOA adalimumab (SC)

A

binds TNF-alpha, blocks its interaction with the p55 & p75 cell surface receptors

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5
Q

structure of anakinra (SC)

A

recombinant human IL-1 receptor antagonist (IL-1Ra)

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6
Q

moa of anakinra (SC)

A

copmetitively inhibits IL-1alpha & IL-1beta binding to IL-1 type 1 receptor (IL-1R1)

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7
Q

structure of infliximab (IV)

A

chimeric (mouse-human) IgG1k mAb against TNF-alpha

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8
Q

MOA of infliximab (IV)

A

binds to and neutralizes both soluble and transmembrane TNF-alpha

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9
Q

structure etanercept (SC)

A

extracellular ligand-binding portion of human p75 TNF receptor linked to part of human IgG Fc (2:1 ratio p75/Fc)

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10
Q

moa etanercept (SC)

A

endogenous p75 acts as a TNF antagonist, drug binds to and inactivates TNF but does not affect TNF production or serum levels

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11
Q

structure of golimumab (SC)

A

human TNF alpha ab

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12
Q

moa of golimumab (SC)

A

binds to and neutralizes both soluble and transmembrane TNF alpha

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13
Q

structure of certolizumab (SC)

A

Fab fragment of humanized TNF-alpha ab

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14
Q

MOA of certolizumab

A

neutralizes membrane associated and soluble human TNF-alpha

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15
Q

rituximab (IV) structure

A

chimeric (mouse-human) IgG-1k mAb against b-cell CD20

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16
Q

MOA rituximab (IV)

A

Fab binds CD20 & Fc domain recruits immune effector functions to mediate B-cell lysis (complement-dependent cytotoxicity, ADCC, induction of apoptosis)
-sensitizes drug-resistant human B-cell lymphoma cell lines to cytotoxic chemotherapy

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17
Q

structure of tocilizumab (IV)

A

human IL-6 receptor-inhibiting mAb

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18
Q

MOA of tocilizumab (IV)

A

binds to both soluble (serum & synovial fluid) & membrane bound IL-6 receptors & inhibits signaling

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19
Q

which RA drug can cause SJS or toxic epidermal necrolysis?

A

rituximab

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20
Q

which RA drug has maltose in it and why does it matter?

A

Abatacept IV, important because it can complicate blood glucose tests

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21
Q

which RA drug requires you to check a serum lipid profile?

A

tocilizumab (tociLIPIDmab)

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22
Q

which RA drug requires you to use reliable contraception while taking the drug and avoid pregnancy for 4-6 months after therapy?

A

rituximab (IgG crosses placenta)

Rituximab–>RELIABLE contraception

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23
Q

which RA drugs have CHF or hypotension/angina/dysrhythmia as an adverse effect?

A 
Infliximab
Golimumab
Adalimumab
Rituximab
(C-IGAR)
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24
Q

Blood dyscrasias requiring CBCs have been reported with which RA drugs?

A 
Certolizumab
Anakinra
Rituximab
Tocilimumab
(BLOOD CART)
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25
Lupus-like syndrome has been reported with which RA drugs?
``` Adalimumab Certolizumab Infliximab Etanercept (ACEi) ```
26
upon entry into the cell MTX undergoes _____________ which serves to retain the drug in the cell
polyglutamation
27
how is MTX eliminated?
via the kidney in a process involving tubular secretion (competes w/ probenecid
28
how is MTX metabolized?
hepatic metabolism with enterohepatic recirculation, which increases half-life
29
what are the pulmonary toxicities of MTX therapy?
potentially fatal acute or chronic interstitial pneumonitis & pulm. fibrosis which may not be reversible
30
which pregnancy category is MTX?
X
31
if you are taking MTX you may have severe GI toxicity that may occur if you had PUD or ulcerative colitis especially when given with __________
NSAIDs
32
Sulfasalazine MOA
beneficial effects result primarily from the anti-inflamm. properties of mesalamine, an inhibitor of PG and LT production
33
sulfasalazine is metabolized to what 2 active components by bacteria in the colon?
sulfapyridine (a sulfonamide) | mesalamine (inhibits PG & LT production)
34
what is an important contraindication to sulfasalazine?
known hypersensitivity to mesalamine, salicylate, or sulfonamide drugs
35
which nonbiological DMARD has hematotoxicity including a potentially fatal blood dyscrasia
sulfasalazine
36
Name the nonbiologic DMARDs
MTX Sulfasalazine Leflunomide Hydroxychloroquine
37
Leflunomide MOA
produces active metabolite A771726 that inhibits dihydroorotate dehydrogenase (DHODH) an enzyme located in cell mitochondria that catalyzes a key step in de novo pyrimidine synthesis - T-cell, B-cell cell-cycle stopped and interaction stopped, Ig prod. is suppressed - drug is cytostatic not cytotoxic
38
what is the name of the active primary metabolite of leflunomide?
A771726
39
A77 1726 is the active primary metabolite of leflunomide and it inhibits what enzyme?
dihydroorate dehydrogenase (DHODH)
40
where is DHODH located in the cell?
in the mitochondria
41
A77 1726 inhibits DHODH in the mitochondria of what kind of cells?
B-cells, and T-cells causing their cell cylce to be stopped
42
which drug has a major metabolite that has a uricouric (increase the excretion of uric acid) effect?
Leflunomide w/ A77 1726
43
what pregnancy category is leflunomide?
X
44
how does Hydroxychloroquine work?
increases intracellular vacuole pH and alters processes such as protein degradation by acid hydrolases in the lysosome, assembly of macromolecules in the endosomes, and PTM of proteins in Golgi can't make MHC II drug diminishes formation of MHC complexes required to stimulate CD4 Tcells & results in decreased immune resopnse against autoantigenic peptides
45
what are the indications for hydroxychloroquine
prophylaxis of malaria, RA, SLE
46
``` which non-biological DMARD has these adverse effects: contraindicated in ocular disease hepatic disease or alcoholism blood dyscrasias CNS toxicity ```
hydroxychloroquine
47
in addition to suppressing signs and symptoms of RA ______________ appear to have disease modifying effects at least in early RA
glucocorticoids
48
the disease-modifying effects of _______________probaby persist after discontinuation of therapy
glucocorticoids
49
Glucocorticoid therapy has a place, even in a tight control and treat to target strategy based on _______________
MTX
50
The risk of adverse effects of ___________________ is often overestimated.
low-dose glucocorticoids
51
for low & medium dose glucocorticoids adverse effects are generally __________
mild
52
administration of low-dose glucocorticoids in accordance w/ physiological ________________ may bring efficacy and safety benefits.
circardian rhythms
53
what time of the day would you give exogenous prednisone to improve clinical outcomes?
at night as endogenous cortisol levels begin to rise
54
there is clinical data that shows if you give glucocorticoids in accordance with circadian rhythms you can actually reduce ________________________ as compared to conventional predisone.
hypothalmic-pituitary-adrenal suppression
55
the majority of the anti-inflamm. effects of glucocorticoids occur via the ___________receptors.
cytosolic GC receptors
56
what happens when the cytosolic GC receptors are activated?
1. upregulate or downregulate protein synth. by binding to specific DNA-binding sites (GC-responsive elements) 2. neg. intefere w/ NFkB, activator protein-1 (AP-1), and nuclear factor for activated T-cells (NF-AT)
57
explain how GCs cause transrepression of pathways involved in the pathogenesis of RA
a. reduced synth. of pro-inflamm. cytokines: TNF-alpha, IL-1, IL-6 b. reduced pro. of receptor activator of nuclear factor kappa B ligand (RANKL) which finally supports the generation of osteoclasts, responsible for bone resorption and erosions in RA
58
The pattern of glucocorticoid adverse effects is dependent upon what 2 things?
both cumulative and daily dose employed
59
giving GCs with what drugs may increase the risk of adverse effects?
DMARDs
60
Which pts taking steroids should undergo intense monitoring b/c increased risk of adverse effects?
pts taking medium or high glucocorticoid doses
61
What are the exceptions to the rule that says that you don't have to monitor carefully pts taking low dose GCs?
screening for osteoporosis pretreatment assessments of fasting blood glucose levels risk factors for glaucoma presence of ankle edema
62
if you are taking GCs, which does a better job of maintaining bone density, bisphosphonate drugs or calcium supplementation?
bisphosphonate drugs
63
how do medium-high dose GCs cause increased risk of CV adverse events?
adversely impacting lipid profiles, BG regulation, insulin prod. & resistance, & by increasing obesity
64
what is the relationship b/w risk of infection and glucocorticoid use?
dose-dependent
65
which glucocorticoids have no mineralocorticoid activity and don't promote salt and water retention?
Tramcinolone (intermediate acting), betamethasone, dexamethasone (long-acting)
66
which NSAID drug has the lowest risk of GI tox?
ibuprofen
67
which 2 drugs are highest in global sales among NSAIDs?
diclofenac & ibuprofen
68
which NSAID has a very short half life?
diclofenac
69
which NSAID has a very long half life?
piroxicam
70
which parenteral NSAID is recovered in excreta and has the highest risk of GI toxicity?
ketorolac
71
which 2 NSAIDs are considered COX-2 selective?
celecoxib | diclofenac
72
what are some ways to reduce GI toxicity with NSAIDs?
take with food H2 receptor antagnoist PPIs
73
why do you get GI toxicity with NSAIDs?
when you inhibit COX you prevent the formation of PGE2 & PGF2alpha which stimulate mucus production-->too much gastric acid secretion-->epigastric distress
74
how could a pt taking a prescribed aspirin regiment increased their risk of CV adverse events?
if you took an NSAID it might compete for inhibition of COX and prevent the irreversible inhibition by aspirin thereby shifting the balance towards pro-aggregatory condition
75
which drug is considered cardioprotective and one of the safest NSAIDs to take?
naproxen
76
about what percentage of drug induced liver injury is caused by NSAIDs?
10%
77
what happens when you give NSAIDs in the setting of acute renal toxicity or compromised kidney function?
you inhibit PGs which cause vasodilation and maintain renal blood flow leading to : reversible renal ischemia, reduced GFR (acute renal failure)
78
which drugs decrease renal clearance of lithium & MTX potentially leading to toxicity?
NSAIDs
79
which tests do you have to order for adults taking chronic NSAID therapy?
LFTs serum creatinine/BUN stool guaic CBC
80
of all the NSAIDs which has the most adverse effects?
indomethacin
81
which drugs can antagonize the beneficial effects of uricosuric drugs?
salicylates
82
how can you reduce the symptoms of Nausea, dyspepsia, abdominal pain, heartburn and gastritis when taking aspirin?
take it with food, use H2 blocker or PPI
83
what is Reye's syndrome?
when a child takes aspirin during a viral infection, fatal fulminating hepatitis with cerebral edema

MUSCULOSKELETAL/RHEUM (8 decks)

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