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Bloc F - Defense > Apr4 M2-DMARDS > Flashcards

Apr4 M2-DMARDS Flashcards

1
Q

biologic drugs treat what

A

inflammatory diseases

like RA, and asthma with anti-IgE

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2
Q

first biologic drug made

A

human insulin

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3
Q

3 types of biologic drugs

A
  • substances nearly identical to endogenous signaling proteins
  • monoclonal Abs
  • receptor constructs (fusion proteins. name = RECEPTOR DECOYS) based on naturally-occurring R linked to the Ig frame (soak up the ligand for endogenous Rs)
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4
Q

omalizumab (anti-IgE) effect in asthma (>12 yrs old, not controlled with CSs)

A
  • binds IgE and removes it from circulation
  • no adverse allergic effects of asthma caused by IgE
  • no more signal to basophils, B cells, etc.
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5
Q

newer future biologic drugs in asthma do what

A
  • target IL-4, IL-5 and IL-13 or their receptors
  • can block the ligands or the receptors
  • shuts down eosinophils and basophils
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6
Q

DMARD meaning and disease using it the most

A

disease modifying antirheumatic drugs

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7
Q

RA pathogenesis

A
  • related to genetic but initiating event unknown
  • presence of a rheumatoid factor: is an IgM that binds different IgGs
  • rheumatoid factor is produced by B cells in synovial fluid (of joints) and serves as a marker of RA
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8
Q

what rheumatoid factor does in RA

A
  • RF complexes trigger complement = tissue damage
  • RF attracts PMNs and macrophages
  • PANNUS: PMNs + macrophages + fibroblasts from scar tissue accum in joint
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9
Q

what pannus does in asthma

A

produces IL-1 and TNF-alpha causing proliferation and bone resorption by osteoclasts from macrophages

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10
Q

important principle in RA management

A
  • act EARLY and AGGRESSIVELY (progresses most rapidly in first two years)
  • joint damage is an EARLY phenomenon of RA
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11
Q

role of CSs in RA

A
  • use to transition slowly to the DMARD

- use flare up phases of the disease

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12
Q

new therapeutic strategies in RA

A

triple therapy: methotrexate + biologic drugs

not the DMARDs only triple therapy, we use biologics nowadays

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13
Q

effect of DMARDs in RA

A
  • less joint damage and deformity
  • less radiographic progression
  • less long-term disability
  • can arrest or slow RA progression (joint erosion on XR)
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14
Q

1st generation DMARDs are what + good and bad

A

gold compounds like aurothioglucose

  • good = accum macrophages + interfere with migration and phago
  • bad = toxicity bc get colitis + weekly IM injections
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15
Q

2nd generation DMARDs: what + good and bad

A

cytotoxic B and T cell inhibitors like methotrexate and leflunomide
-good = S phase blocker (of pyrimidine synthesis)
+ prevents B and T cell prolif RF not produced
-bad = effects on proliferating cell populations

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16
Q

methotrexate effect

A
  • inhibits dihydrofolate reductase which produces tetrahydrofolate, an important cofactor in prod of purines
  • immunosuppressive and anti-cancer drug
  • inhibits AICAR
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17
Q

(EXAM) REAL reason for which we use methotrexate in RA

A

inhibits the enzyme AICAR, involved in the de novo synthesis of purines

18
Q

(EXAM) which mechanism of action of methotrexate is the most important one in RA

A

AICAR inhibition (bc is the most important one at the low dose of mtx we give in RA)

19
Q

(imp?) mechanism of action of mtx related to AICAR and what AICAR does

A

Methotrexate’s principal mechanism of action at the low doses used in the rheumatic diseases probably relates to inhibition of aminoimidazolecarboxamide ribonucleotide (AICAR) transformylase and thymidylate synthetase, with secondary effects on polymorphonuclear chemotaxis.

20
Q

what hydroxychloroquine does and mechanism of action

A
  • classical anti-malarial drug
  • useful as DMARD
  • interferes with cellular ability to degrade and process proteins
21
Q

main mtx and hydroxychloroquine side effects

A

mtx: oral ulcers, BM toxicity, infection, malignancy, NOT during pregnancy
hydroxy: retina damage, nausea, diarrhea

22
Q

sulfasalazine active component and mech of action in RA

A
  • cleaves into salcitylate and sulfinpyradone (active ingredient)
  • sulfinpyradone mech of action not understood
23
Q

sulfasalazine prob

A
  • SE: malaise, nausea, hypersensitivity rx, headaches, dizziness
  • microbiome issues similar to Abx. can’t use in c.diff
24
Q

newer DMARD and side effects

A
  • leflunomide

- SE like all DMARDS: diarrhea, nausea, malaise, htn, alopecia, rash, malignancy, infection

25
Q

examples of biologic drugs

A
  • TNF-a inhibitors (receptor decoy or Ab against TNF-a)
  • IL-1 inhibitors
  • T cell costimulatory blockade
  • B cell depletion
26
Q

critical cytokine found in most people in RA and why

A
  • TNF-alpha

- triggers IL-1, IL-6 and IL-8 release

27
Q

was we block TNF-a in RA

A
  • humira (receptor decoy), binds TNF-a around
  • non soluble forms of the R bind TNF-a
  • engineered R floating around and binding TNF-a
28
Q

the diff TNF-inhibitors

A
  • infliximab and adalimumab = Abs against TNF

- etanercept = soluble R decoy

29
Q

TNF-a i side effects

A
  • infection
  • malignancy
  • autoimmune probs
  • CHF
  • neurologic
30
Q

IL-1 fct in the body

A

drives fever in the brain + produced in a lot of tissues as autacoid or autocrine

31
Q

how IL-1 inhibited

A
  • Ab to IL-1 R

- decoy ligands

32
Q

IL-1 i SE

A
  • infection*

- headaches, neutropenia, infusion rx

33
Q

T-cell co stim blockade (abatecept) does what

A

blocks coreceptor CD80 or CD86 on APC so you lose T cell activation

34
Q

SE of abatecept and biologics seen

A
  • infection
  • COPD exacerbation
  • malignancy
  • infusion rx
35
Q

immunity in RA: what happens

A
  • *T cell mediated**
  • APC presents unknown Ag to T cell
  • CD4 th starts rx in genetically predisposed people
36
Q

why act on B cell depletion in RA

A
  • B cells can act as APCs
  • B cell produces rheumatoid factor
  • B cell releases cytokines
  • stops doing all that*
37
Q

B cell depletion therapy in RA done with what

A

rituximab, anti-CD20

38
Q

molecules that ARE NOT BIOLOGICS but may be an alternative

A

Jak (J associated kinase) inhibitors

  • downstream of many cytokines
  • block them = block cytokines more downstream so block more of the immune response
39
Q

jaki drug used in RA added to DMARD and bio drug mix

A
  • tofacitinib (Xeljanz)

- used in autoimmune diseases

40
Q

principle of treatment in RA nowadays (real way you should treat)

A
  • start early and aggressively*
  • start with DMARD (mtx)
  • add biologic (mtx + bio)
  • add 2nd line biologic (mtx + 2 biologics)

Bloc F - Defense (57 decks)

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