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Pharma 2- Semmelweis > B-30. Pharmacotherapy of autoimmune diseases. > Flashcards

B-30. Pharmacotherapy of autoimmune diseases. Flashcards

1
Q

The role of Th1, Th2, Th17, and Tregs

A
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2
Q

What inflammatory pathway does RA, IBD, and psoriasis most likely share?

A

Th-17 T-lymphocyte pathway

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3
Q

How does the AI chronic inflammation most likely occur

A

Surface damage leads to appearance of antigens in the tissue present by APC. APC induce CD4+ T-cell by IL-6 and IL-23 and directly inducing neutrophils via IL-1

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4
Q

Treatment goals of RA

A
  1. Slow down inflammation process (achieve remission)
  2. Relieve symptoms
  3. Prevent joint and organ damage
  4. Improve physical function and overal well being
  5. Reduce long-term complications
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5
Q

Treatment options in RA

A
  • Conventional synthetic disease modifying antirheumatic drugs (CsDMARDs) as soon as possible:
    • Methotrexate (first option)
    • Alternatives cytotoxic drugs
    • short term, tapered glucocorticoid or local steroids
    • If necessary: add biological and so-called targeted synthetic DMARDs
  • In case of ineffeciency other biological and tsDMARDS can be used
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6
Q

Alternative csDMARDs used in RA

A
  1. Leflunomide
  2. Sulfasalazine
  3. Chloroquine
  4. Cyclosporin-A
  5. Cyclophosphamide
  6. Azathioprine/6-mercaptopurine
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7
Q

Non DMARDs used in RA

A
  1. NSAIDs
  2. Corticosteroids
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8
Q

NSAIDs are used in RA to? Long term issues?

A
  • They are also essential in the treatment but only symptomatic: they improve the symptoms, but do not slow the progression (even they could facilitate it)
  • Long term issues are
    • GI ulcerations
    • Cardiovascular risk in RA increased- COX2 inhibition could worsen it
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9
Q

Corticosteriod use in RA? Dosing?

A
  • In acute exacerbation they are the most effective drugs
  • They can also suppress the progression
  • Dosing
    • High dose (transient treatment)
    • Low dose (maintained treatment)
    • Intraarticular local treatment is also used
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10
Q

RA treatment algorithm phase I

A
  • Start methotrexate
  • +Combine with short term glucocorticoids
  • Start Leflunomide or sulfasalazine
  • If the patient goes into remision then lower dose
  • If patient doesn’t go into remission, go to phase II
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11
Q

RA treatment algorithm phase II

A
  • Prognostically unfavorable factors present (RF/CPA/high disease activity/early joint damage)
    • Add a bDMARD or Jack inhibitor
  • Prognostically unfavorable factors not present
    • Change to or add a second conventional synthetic DMARD (Leflunomide, sulfasalazine, methotrexate)
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12
Q

Phase III of RA

A
  • Change the bDMARD
    • Abatacept
    • IL-inhibitor
    • Rituximab
    • (second)TNF-inhibitor
  • Or add a Jak-inhibitor
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13
Q

Biologics used in treatment of RA

A
  • TNF alpha antagonist (infliximab, adalimumab, certolizumab pegol, etanercept, golimumab)
  • CTLA4- containing fusion protein (abatacept)
  • IL-1 receptor antagonist (anakinra)
  • IL-6 receptor antagonisst (tocilizumab, sailumab)
  • CD20 antagonist (rituximab)
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14
Q

Targeted synthetic DMARDS

A
  • Jak inhibitors
    • Tofacinitib
    • Baricitinib
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15
Q

Mild therapeutic approach of IBDs

A
  • Mild
    • 5-aminosalicylic acid (both in CD and UC)
    • Locally applied 5-ASA and glucocorticoids
    • Budesonide (both in CD and UC)
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16
Q

Moderate (or refractory to the mild form of IBD) treatment

A
  • Moderate IBD treatment
    • Oral glucocorticoids (both CD and UC)
    • Azathrioprine/6-mercaptopurine (both in CD and UC)
    • Methotrexate (CD)
17
Q

Severe IBD treatment and if this fails what is next?

A
  • Severe IBD treatment
    • IV glucocorticoids
    • TNFalpha antagonist (Infliximab, Adalimumab, Golimumab)
    • Cyclosporine (UC)
    • IL12/IL23 antagonist (Ustekinumab) (CD)
    • Integrin antagonist (Natalizumab, Vedolizumab) (CD)
  • If these treatments fail or in conjuncture with them you migh have to do surgery
18
Q

Glucocorticoids in IBDs

A
  • Usually short term treatment to avoid adverse effects
  • If possible locally acting glucocorticoids (e.g. hydrocortisone enema) or drugs with high first pass metabolism (budesonide controlled release preparations) are preferred
  • If necessary prednisolone (predenisonein theU.S.) per os o rmethylprednisolone (oral or injection) are given
19
Q

Treatment goals in psoriasis

A
  • Successful treatment: decrease in the psoriasis Area and Severity Index (PASI) score of 75% or greater
  • Unsuccessful treatment: improveent is lower than 50% in the PASI score→change in the treatment
20
Q

Drug classes treatments of psoriasis

A
  1. PUVA
  2. Topically applied drugs
  3. Systemically applied drugs
  4. Biologics
21
Q

What is PUVA?

A

UV beam after taking 8-methoxypsoralene orally or applying a cream or bath. The drug makes the plaques photosensitive

22
Q

Topically applied drugs in psoriasis

A
  • Topically applied drugs
    • Glucocorticoid creams alone or with tar or Vit. D3 analogs
      • calcipotriol with betamethasone (cream or gel)
      • or tacalcitol emulsion
    • Retinoids
      • tazaroten
23
Q

Vit. D analogs do what in psoriasis

A

Vitamen D analogs inhibit keratocyte proliferation, used only in localized plaque psoriasis

24
Q

Systemically applied drugs in psoriasis

A
  • Systemically applied drugs
    • Acitretin
    • Immunosuppresive drugs
      • Cyclosporin
      • Methotrexate
      • Leflunomide
    • Dimethyl-fumarate
    • PDE-4 inhibitors
      • Apremilast
    • Biologicals
      • More later
25
Q

Acitretin in psoriasis

A

Inhibits synthesis of keratin precursors, decreases hyperkeratosis

26
Q

Dimethyl-fumarate in psoriasis

A

Stimulates transcription factors

27
Q

Apremilast (PDE-4 inhibitor) function in psoriasis

A

Inhibits expression of TNF-alpha, IL-23, IL-17, and other inflammatory cytokines

28
Q

Mechanism of action and retinoid drugs used in psoriasis

A
  • MOA: Inhibition of cell proliferation and differentiation (they bind to nuclear retinoid receptor RAR and/ or RXR)
  • Drugs
    • Tazaroten (locally applied)
    • Acitretin (systemic)
29
Q

Acitretin (systemic) use, adverse effects

A
  • Can be used in more severe psoriasis
  • Adverse effects may include…
    • Dry mucosa (e.g. xerophtalmia=dry eyes)
    • Iitching
    • Several skin problems (e.g. hairloss, exfoliation, dermatitis, pyogen granuloma)
    • Extremely teratogenic-!!! Getting pregnant must be avoided duringand 3 years after terminating the treatment!!!
30
Q

Biologics used in the treatment of psoriasis

A
  • L-23R antagonists
    • ustekinumab (IL-12R/IL-23R), guselkumab, risankizumab
  • IL-17 antagonists
    • ixekizumab, secukinumab
  • IL-17R antagonist
    • brodalumab
  • TNFalpha antagonists
    • adalimumab, etanercept, infliximab
31
Q

Therapy of mild atopic dermatitis

A
  • Therapy depends on severity
    • Mild form
      • Local creams (emollients, pimecrolimus, glucocorticoids)
      • Systemic steroids only in acute exacerbation for a short time
32
Q

Therapy for more severe forms of atopic dermatits

A
  • More severe forms: systemic drugs
    • Cyclosporin-A
    • Or IL4R/IL3R antagonist dupilumab
33
Q

Treatment options in MS classes

A
  1. Interferons
  2. Glatiramers
  3. Antimetabolites
  4. Leukocyte depletion
  5. T-cell inhibition
  6. B-cell depletion
  7. Other (dimethyl-fumarate)
  8. Improving motoric functions
34
Q

Which interferons are used in in MS

A
  1. INF-B1a
  2. INF-B1b
35
Q

Glatiramers are

A

Mixture of short peptides corresponding myelin building blocks

36
Q

Antimetabolites drugs? how are they taken?

A
  • Taken orally
  • Drugs
    • Teriflunomide (dihyroorotate-dehydrogenase inhbitor)
    • Cladribine (purine analog)
37
Q

Leukocyte depletion drug

A
  • Alemtuzumab- CD53 inhibitor, T and B cell depletion, IV induction treatment
38
Q

Other treatments in MS

A
  • Orally taken Dimethyl-fumarate
    • Nuclear factor (erythroid derived 2)-like 2 (Nrf2) transcription pathway stimulator- increases the level of antioxidant enzymes
39
Q

MS drugs improving motoric function

A
  • Fampridine (4-aminopyridine)- K+-channel blocker

Pharma 2- Semmelweis (43 decks)

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