Pharmacotherapy of psoriasis

lalchand67 4,589 views 30 slides Nov 02, 2019
Slide 1
Slide 1 of 30
Slide 1
1
Slide 2
2
Slide 3
3
Slide 4
4
Slide 5
5
Slide 6
6
Slide 7
7
Slide 8
8
Slide 9
9
Slide 10
10
Slide 11
11
Slide 12
12
Slide 13
13
Slide 14
14
Slide 15
15
Slide 16
16
Slide 17
17
Slide 18
18
Slide 19
19
Slide 20
20
Slide 21
21
Slide 22
22
Slide 23
23
Slide 24
24
Slide 25
25
Slide 26
26
Slide 27
27
Slide 28
28
Slide 29
29
Slide 30
30

About This Presentation

learning objectives : Pathophysiology of Psoriasis
Common sites with pictures
Pharmacotherapy of Psoriasis
Local Drug therapy
Systemic Drug therapy
Biological therapy
Phototherapy


Slide Content

Dr.Uma Advani
Assistant Professor
Pharmacology,
SMS,MC Jaipur

Introduction
Pathophysiology of Psoriasis
Common sites with pictures
Pharmacotherapy of Psoriasis
Local Drug therapy
Systemic Drug therapy
Biological therapy
Phototherapy

Chronic proliferative epidermal disease .
Affects 1 to 3% of world’s population .
Rapid increase in epidermal transit time.
The time taken for a psoriatic epidermal cell
to travel from the basal layer to the surface
and be cast off is 3 to 4 days , in marked
contrast to the normal 26 to 28 days.
In most cases the disease remains as discrete
localized plaques
Stress and anxiety frequently precede flare
ups of the disease.

Psoriatic lesions are usually erythematous
and sharply circumscribed plaques.
The lesions are covered by silvery white
micaceous scales.
Lesions occur most commonly on the
elbows , knees , scalp, genitalia ,
lumbosacral area and intergluteal cleft.

50% of psoriatic patients will have some degree
of nail involvement
Intense pruritus seen in 30 –40% of patients.
Psoriatic arthritis.
Reduction in the quality of life.

Topical agents (corticosteroids,tar,anthralin,calcipotriol,tazarotene)
Phototherapy
Immunosuppressive agents and retinoids
Biologic agents (Infliximab)
Mild Moderate Severe

Topical therapy
1. Corticosteroids
2. Vitamin D analogues (calcipotriene and
calcitriol)
3. Coal tar
4. Anthralin

Topical therapy
5. Tazarotene
6. Immunomodulators (tacrolimus and
pimecrolimus)
7. Keratolytics –salicylic acid
Drugs used in Psoriasis.

Systemic therapy
1.Methotrexate
2.Acitretin
3.Cyclosporine
4.Mycophenolate mofetil
5.Sulfasalazine
6.6-Thioguanine
7.Tacrolimus
8.Hydroxyurea
Drugs used in Psoriasis.

Biologic therapy
1. Infliximab
2. Etanercept
3. Alefacept
4. Efalizumab
Photochemotherapy
Drugs used in Psoriasis.

Topical Corticosteroids.
Classified according to their potency
(Stoughton Cornell classification) .
High potency steroids like clobetasol,
halobetasol and betamethasone used in
chronic plaque psoriasis.
Used for finite periods of time
Should be used only for small body surface
areas.

Low potency steroids like hydrocortisone
safer
Can be used for long term and also in
infants and children.
ADR: Local tissue atrophy, striae,
suppression of HPA axis, hyperglycemia,
cushingoid features.

Do not abruptly cease topical steroids as
rebound flare is known to occur.
Main role is as an adjunct.
Ointment form considered the clinically
most effective .

Vitamin D analogues
Inhibits keratinocyte differentiation and
proliferation.
Calcipotriene, calcitriol, tacalcitol
Rapidly metabolized locally.
Marked improvement seen after 8 weeks of
therapy.
expensive.

Tazarotene -synthetic retinoid.
Prodrug , metabolized to active tazarotenic
acid.
Modulates keratinocyte proliferation and
differentiation.
Effective for mild to moderate plaque
psoriasis.
Used in combination with steroids to
decrease ADR.

Coal tar
Down regulates epidermal
proliferation rate.
Used in thick plaques and
in scalp psoriasis.
Disadvantages:
burdensome,timeconsuming, unpleasant
odourand staining of skin and clothing.
Can be combined with UVB.

Anthralin
Inhibit DNA synthesis by
intercalating between DNA
strands
Inflammation , irritation and
staining of skin and clothing.
Staining of affected plaques is a
positive response.
Dose to be gradually increased.

Keratolytics-Salicylic acid
Removes scales.
Makes skin smooth .
Decreases hyperkeratosis.
Used in mild cases.
Salicylism-nausea , vomiting, tinnitus and
hyperventilation.

Synthetic analogue of folic acid.
Competitive inhibitor of the enzyme
dihydrofolate reductase.
Inhibits the replication and function of T and B
cells.
Suppresses the secretion of cytokines such as
IL-1, IFN-g, TNF-a.
Indicated in severe psoriasis

Can be given as thrice weekly oral dose.
Nausea , anorexia, headache and alopecia.
Sign of MTX overdose-leukopenia and
thrombocytopenia.
Hepatotoxicity , nephrotoxicity and
pneumonitis.
Avoid all immunosuppressives in active
infection.

Oral retinoid
Active metabolite of etretinate.
Indicated for the treatment of severe
psoriasis.
Combination of acitretin and PUVA is
highly effective.

ADR: hypervitaminoses A, hepatotoxicity,
skeletal changes, hypercholesterolemia and
hypertriglyceridemia.
C/I in pregnancy and in women who are
planning pregnancy within 3 years following
drug discontinuation.

Effective immunosuppressant.
Inhibits the release of inflammatory mediators
from mast cells, basophils and PMN
leukocytes.
Effective in both the cutaneous lesions and also
the arthritic symptoms.

Effective in generalisedpustularpsoriasis
Prolonged use causes nephrotoxicity and
hypertension.
Use for more than two years leads to increased
risk of malignancy.

UVA combined with oral / topical
methoxsalenon alternate days
Immunomodulatory–induces Tcellapoptosis.
Reserved for moderate to severe psoriasis.
Short term adverse effect-mottling,
erythema,burns,blistering,premature aging of
skin,nervousnessand insomnia.
Long term adverse effect-increased risk of skin
cancer.

Thank you.
Tags