My fifth presentation...in slideshare..... This is a precise insight into the popular disease called PSORIASIS....the reasons...classification....diagnosis...and varying therapies.......... Nevertheless, i do sincerely hope that this presentation helps people who are in research work for this disease..or for students, who have this in their curriculum syllabus, or for simple reading............. More ppts will come on the way............ Thanks for reading..............do give ur feedback..in my email address rxvichu623@gmail.com.........ur views and suggestions will be warmly acknowledged.......... For further details, contact me in whatsapp or hike at 8086948729 or in my facebook profile at Rx Vichhu Study well!! Keep rocking!!! @rxvichu :) :)

1. PSORIASIS- A BRIEF OUTLOOK
BY: VISHNU.R.NAIR
THIRD YEAR PHARM.D
NATIONAL COLLEGE OF PHARMACY
KERALA UNIVERSITY OF HEALTH SCIENCES
(KUHS),KERALA STATE

2. A. GENERAL INTRODUCTION:
• Chronic, non-contagious, multi-system, inflammatory disorder
• Characterized by defects in normal cycle of EPIDERMAL
DEVELOPMENT, that leads to epidermal hyper-proliferation, altered
skin maturation, inflammation and vascular alterations
• Aforesaid characteristics often manifest as areas of dry, thickened,
scaling, silvery white and reddened skin
• Psoriatic lesions may hurt, itch and bleed
• Extent of disease can range from a few small plaques to generalized
lesions
• Manifests on the skin of elbows, knees, scalp, genitals, lumbo-sacral
areas, etc.
• In 30% of patients, psoriasis also affects joints………………….

3. B. EPIDEMIOLOGY:
• According to the National Institute of Health (NIH), approximately 2.2%
of US population has psoriasis
• Can begin in any age
• 2-3% of people are affected worldwide
• 10-15% of new cases begin in children younger than 10 years
• Slightly more common in women than in men
• Psoriasis incidence depends on climate and genetic heritage of
population
• Less common in tropics and in dark-skinned people
• Psoriasis prevalence in African Americans is 1.3% compared to 2.5% in
Whites……………………………………..

4. C. CLASSIFICATION OF PSORIASIS:
• PSORIASIS can be classified into 11 types:
1. Chronic stationary psoriasis
2. Plaque psoriasis
3. Guttate psoriasis
4. Inverse psoriasis
5. Pustular psoriasis
6. Erythrodermic psoriasis
7. Scalp psoriasis
8. Nail psoriasis
9. Psoriatic arthritis
10. Oral psoriasis
11. Eruptive psoriasis………………………

5. CONTINUED……………………………
1. CHRONIC STATIONARY PSORIASIS:
- Also known as “PSORIASIS VULGARIS”
- Most common type
- Occurs in:
a. Scalp
b. Extensor surfaces
c. Genitals
d. Umbilicus
e. Lumbosacral regions
f. Retro-auricular regions
2. PLAQUE PSORIASIS:
- Dry scaling patches
- Occurs in:
a. Knees
b. Elbows
c. Scalp
d. Trunk

6. CONTINUED………………………………
3. GUTATTE PSORIASIS:
- Occurs as drop-like dots
- Mainly the aftermath of streptococcal or viral infections (especially Group A beta hemolytic
streptococci)
- Occurs in trunk
4. INVERSE PSORIASIS:
- Occurs as smooth, inflamed lesions
- Occurs in:
a. Flexural surfaces
b. Armpits
c. Groin
d. Skin folds
5. PUSTULAR PSORIASIS:
- Pus like blisters occur
- Non-infectious
- Fluid contains WBCs
- Present on palms and soles

7. CONTINUED……………………………..
6. ERYTHRODERMIC PSORIASIS:
- Exfoliation of fine scales occurs
- Widespread
- Accompanied with severe infection and pain
- Encompasses nearly entire body surface area
7. SCALP PSORIASIS:
- Plaque type lesion occurs
- Affects approximately 50% of patients
8. NAIL PSORIASIS:
- Starts as numerous pits
- May progress to yellowing, crumbling, and thickened nail
- May get sloughed off
9. PSORIATIC ARTHRITIS:
- Inflammation, swelling and joint destruction may occur
- Affects approx. 10-30% of those with skin symptoms

8. CONTINUED……………………………..
10. ORAL PSORIASIS:
- May present as severe CHEILOSIS (inflammation of 1/ both mouth
corners)
- Extends onto surrounding skin
11. ERUPTIVE PSORIASIS:
- Involves upper trunk and extremities
- Mostly seen in younger patients……………………………….

9. D. ETIOLOGY OF PSORIASIS:
1. ENVIRONMENTAL FACTORS:
Include:
- Cold
- Trauma
- Stress increases concentration of neurotransmitters in psoriatic plaques
- Infections:
a. HIV
b. Streptococcal
c. Staphylococcal
- Alcohol
- Drugs:
a. Iodides
b. Steroid withdrawal
c. Aspirin
d. Lithium
e. Beta-blockers
f. Botulinum-A
g. Anti-malarials

10. CONTINUED……………………………
- Chronic gingivitis increases risk of psoriasis
2. GENETIC FACTORS:
- Genetic pre-disposition to obesity
- HLA alleles  HLA-Cw6
- Deletion of LCE (Late cornified envelope) genes LCE3C, LCE3B increases
susceptibility for psoriasis
3. IMMUNOLOGIC FACTORS:
- Increased TNF-alpha activity
- Increased T-cell activity in underlying skin
- For HIV patients  decrease in CD4 T cells causes over-activity of CD8 T
cells  worsening of psoriasis
4. KOEBNER PHENOMENON:
- Refers to psoriatic lesions, that occur at sites of injury to the skin (cut, burn,
scratch/ surgical scar)…………………………………..

11. E. PATHOGENESIS OF PSORIASIS:
• Main function of the skin is protection that is offered by an intact epidermal
layer
• Epidermis consists of 5 layers (from DEEPEST to most SUPERFICIAL):
- STRATUM BASALE
- STRATUM SPINOSUM
- STRATUM GRANULOSUM
- STRATUM LUCIDUM
- STRATUM CORNEUM
• 4 types of cells compose the above layers:
- Keratinocytes (90%)
- Melanocytes (8%)
- Langerhans cells
- Tactile menisci (Merkel cells)

12. CONTINUED…………………………......
.• During epidermal cell cycle new cells formed in stratum basale migrate
towards stratum corneum
• As cells move towards surface they accumulate keratin organelles
disappear
• By the time, the cells reach stratum corneum cells are dead and completely
filled with keratin  this smooth , keratinous layer offers skin its protection
surface cells slough off (exfoliation) and are replaced by underlying cells
• Keratinocytes in basal layer divide approx. once every 2 weeks (in normal
conditions)
• In psoriatic skin epidermal cell cycle is accelerated  cell division in basal
layer occurs every 1.5 days  migration of keratinocytes to stratum corneum
occurs within just 4 days or so rapid movement of cells towards surface 
lack of proper maturations and differentiation of cells stratum corneum is
not fully keratinized epidermal cells build up abnormally and become
scaly epidermal in psoriatic lesions is 3-5 times thicker than normal
blood vessels in dermal papillary layer dilate  inflammatory cells
(neutrophils) infiltrate epidermis………………………………..

13. F. PATHOLOGY ASSOCIATED WITH PSORIASIS:
• Keratinocyte activity becomes abnormal
• Lymphocyte infiltration occurs
• The following markers of epidermal proliferation are increased in psoriasis:
- Keratins (K6, K10, K16, K17)
- Epidermal growth factor receptor
- Ornithine decarboxylase
• The following biochemical markers are associated with differentiation:
- Keratinocyte transglutamase
- Migration inhibitory factor related protein
- Skin derived anti- leukoproteinase
- Involucrin
• Decreased levels of FILAGGRIN (essential for development of stratum corneum is
observed)
• Decrease in differentiation related keratins (K1, K2)
• Keratinocytes also contain a variety of immuno-modulatory cytokines like Interleukins 1,6,8
and TNF (Tumor necrosis factor), that are expressed in different ways in psoriasis…………..

14. G. SIGNS AND SYMPTOMS:
• Worsening of a long term erythematous scaly area
• Sudden onset of many small areas of scaly redness
• Pain, especially in cases of:
- Erythrodermic psoriasis
- Traumatized plaques
- Joints affected by psoriatic arthritis
• Pruritus , especially in the case of:
- Eruptive psoriasis
- Guttate psoriasis
• Afebrile state, except in cases of:
- Pustular psoriasis
- Erythrodermic psoriasis
• Dystrophic nails
• Long term rash, with recent presentation of joint pain
• Stiffness, pain, throbbing, swelling/tenderness of joints

15. CONTINUED……………………………….
• OCULAR MANIFESTATIONS:
- Corneal dryness
- Blepharitis (eyelid inflammation)
- Chronic non-specific conjunctivitis
- Keratoconjunctivitis sicca (inflammation of cornea and
conjunctiva)………………………………….

16. H. COMPLICATIONS:
• Secondary infections
• Possible increased lymphoma risk
• Possible increased risk of cardiovascular and Ischemic heart disease
• Psoriatic arthritis
• Mitral valve prolapse……………………………….

17. I . DIAGNOSIS:
1. LAB STUDIES:
- Normal ESR (Erythrocyte sedimentation rate) , except in conditions of:
a. Pustular psoriasis
b. Erythrodermic psoriasis
- Increased uric acid levels, especially in pustular psoriasis
- Fluid from pustules is sterile, with neutrophilic infiltrate
- Perform fungal studies:
Important in cases of hand and foot psoriasis, that seem to be worsening
with the use of topical steroids
- CBC (Complete blood counts)

18. CONTINUED………………………………
2. OTHER TESTS:
a. Dermatologic biopsy:
- Biopsy of skin lesion may reveal:
• Basal cell hyperplasia
• Proliferation of sub-epidermal vasculature
• Absence of normal cell maturation
• Keratinization
b. Joint X-Ray:
- Facilitates psoriatic arthritis diagnosis
c. Bone scan:
- Helps in early joint identification
d. Conjunctival impression cytology:
- May reveal squamous metaplasia, neutrophil clumping, or snake-like chromatin
e. AUZPITZ sign:
Scales on being removed small blood droplets appear within a few
seconds……………………….

19. J. MANAGEMENT OF PSORIASIS:
Here, we will discuss:
• GOALS OF THERAPY
• TREATMENT PLAN
• PHARMACOTHERAPY
• NON-PHARMACOTHERAPY (PATIENT COUNSELLING
TIPS)………………………………………..

20. A. GOALS OF THERAPY:
- To alleviate signs and symptoms
- To reduce irritations, pain and discomfort
- To focus on strict drug regimen and medication adherence
- To avoid progression into complications
- To improve QOL (Quality of Life)…………………………..

21. B. TREATMENT PLAN :
- Psoriasis is a chronic problem
- Consultation for follow-up with a dermatologist/ rheumatologist is appropriate
- Severity of psoriasis can be classified as follows :
a. Mild: less than 2% of body surface area (BSA) affected
b. Moderate : 2-10 % of BSA affected
c. Severe: >10% of BSA affected (Remember : Palm of patient’s hand= 1% of BSA)
- Treatments for more advanced psoriasis include:
a. Narrow band UV ‘B’ light
b. Psoralen with UV ‘A’
c. Light retinoids : Isotretinoin (ACCUTANE), Acitretin (SORIATANE)
d. MTX (Methotrexate)
e. Cyclosporine
f. Infliximab , etc……………………
- According to American Association of Dermatology (AAD) guidelines:
Recommend treatment with MTX, cyclosporine, and Acitretin, considering their
contraindications and drug interactions with other medications, as will be
discussed………………………

22. C. PHARMACOTHERAPY:
1. TOPICAL CORTICOSTEROIDS;
- Decreases plaque formation
- Possess anti-inflammatory activities
- Cause profound and varied metabolic activities
- Modify body’s response to diverse stimuli
- Available in various strengths
- Application regimen: 2-4 times daily for maintenance
- ADRs:
a. Local tissue atrophy
b. Hypopigmentation
c. Fine hair growth
d. Contact dermatitis
e. Adrenal suppression

23. CONTINUED………………………………
- Drugs:
a. TRIAMCINOLONE ACETONIDE (TRIDERM, PEDIADERM):
• Treats inflammatory dermatosis responsive to steroids
• Drug, has 2 anti-inflammatory actions:
i. Suppresses PML (poly- morphonuclear leucocytes)
ii. Reverses capillary permeability
* Mild potency
• First drug of choice for most patients
b. BETAMETHASONE (DIPROLENE , ALPHA TREX):
• Same actions as in (a)
• Drug of choice if psoriasis is resistant to milder
forms………………………………

24. CONTINUED………………………………
2. OPHTHALMIC CORTICOSTEROIDS:
- Control conjunctival, corneal and anterior chamber inflammation
- Delay vascularization
- Drugs include:
a. PREDNISOLONE ACETATE OPHTHALMIC ( OMNIPRED, PRED
FORTE):
• Same actions as that of topical ones
• In case of bacterial infections  use along with anti-infective agents
• Dosing may be reduced
• Do not prematurely discontinue therapy
b. DEXAMETHASONE OPHTHALMIC (MAXIDEX, OZURDEX):
• Same action…………………..

25. CONTINUED……………………………….
3. COAL TAR ( DHS-TAR, THERAPLEX T):
- Inexpensive
- Use as 0.5-33%
- Available as OTC , in the form of shampoos, lotions, creams, foams
- Mainly useful in hair-bearing areas
- 1% conc. Can also be used to control lesions
- Mainly useful when used in combination with topical corticosteroids
- ADRs:
a. Staining potential
b. Skin irritation
c. Photosensitivity
- Application regimen:
a. Apply at bedtime
b. Allow to remain as such until morning
- Anti-pruritic
- Anti-bacterial
- Inhibits deregulated epidermal proliferation and dermal infiltration

26. CONTINUED……………………………….
- Does not injure normal skin when applied widely
- Increases usefulness of phototherapy
- Generally used as 2nd line drug therapy, due to messy application (except
shampoos)……………………………

27. CONTINUED……………………………..
4. KERATOLYTIC AGENTS:
- Remove scales
- Smoothen skin
- Treat hyperkeratosis
- Drug removes thick scale allows topical corticosteroids and other
medications to better reach target tissues  better results achieved
- Mainly effective on scalp
- Many OTC preparations can be used for this, most of which contain
SALICYLIC ACID
- Lactic acid, ammonium lactate and urea are the other ingredients that
may be applied too
- Urea preparations stronger than 30% require a prescription
- Anthralin is also considered to be in the anti-psoriatic therapeutic class

28. CONTINUED……………………………….
- ADRs:
a. Skin irritation
b. Salicylism (with salicylic acid)
c. Staining potential
d. Inflammation
- Strength : 0.1-1.0%
- Application regimen: same as that of COAL TAR
ANTHRALIN (DRITHO-CRÈME, ZITHRANOL):
- Decreases cell proliferation rate
- Drug possesses chemically reducing properties upsets oxidative
metabolic processes decreased epidermal
mitosis………………………

29. CONTINUED…………………………….
5. VITAMIN D ANALOGS:
- Used in the following patients:
a. Lesions resistant to topical therapy
b. Lesions on face
c. Exposed areas, where skin thinning can cause cosmetic problems
- Used as ointments, solutions and foams
- Mainly used for scalp treatments
- Strength: 0.005%
- Application regimen:
a. Once or twice daily
b. Not more than 100g of vehicle base/week (for 8 weeks)
- ADRs:
a. Skin irritation
b. Hypercalcemia risk

30. CONTINUED………………………………
- Drugs:
a. CALCITRIOL OINTMENT (VECTICAL):
• Less irritating
b. CALCIPOTRIENE (DOVONEX, CALCITRENE):
• Synthetic Vitamin D3 analog
• Regulates skin cell production and development
• Used in treatment of moderate plaque psoriasis
• No long term skin thinning/ systemic effects
• Also used in combination with BETAMETHASONE as topical
ointment, foam, / solution ,as
a. Calcipotriene: 0.005%
b. Betamethasone : 0.064%
• Expensive therapy………………………………….

31. CONTINUED……………………………….
6. TOPICAL RETINOIDS:
- Odorless and colorless aqueous gel formulations
- No long term skin damage
- No withdrawal symptoms
- Avoid in pregnancy
- TAZAROTENE ( TAZORAC FABIOR, AVAGE):
• Retinoid prodrug enters body converted to active form modifies differentiation and
proliferation of epithelial tissue
• Anti-inflammatory
• Immuno-modulatory
• Strength: 0.05, 0.1%
• Application regimen: Once or twice daily, up to 12 weeks
• ADRs:
a. Pruritus
b. Burning
c. Erythema……………………………

32. CONTINUED……………………………….
7. ANTI-METABOLITES:
- Inhibit cell growth and proliferation
- METHOTREXATE (TREXALL, RHEUMATREX):
a. Drug inhibits dihydrofolate reductase enzyme DHFA wont be
converted to THFA  Nucleotides and thymidylate synthesis wont
occur DNA synthesis, repair and cellular replication obstructed
b. Mainly effective against actively proliferating tissues
c. Used in people who are non-responsive to the above drugs
d. Contraindicated in pregnancy, liver, and renal problems.
e. ADRs:
• Bone marrow toxicity
• Hepatotoxicity
f. Dose: 2.5-5 mg orally BID, thrice weekly……………….

33. CONTINUED……………………………….
8. IMMUNOMODULATORS:
• Regulate key factors responsible for inflammatory response
• Drugs include:
a. TACROLIMUS TOPICAL 0.1% (PROTOPIC):
- Used for psoriasis affecting face
- Less effective than steroids
- More ADRs associated with it, thus less used
- Interferes with IL-2, and IL-8 production
- Dose: 0.05-0.1 mg/kg/day
- ADRs:
i. Paresthesia
ii. Tremor
iii. Palpitations
b. CYCLOSPORINE (SANDIMMUNE):
- 11-amino acid cyclic peptide
- Natural fungi product

34. CONTINUED……………………………….
- drug inhibits Helper T-cell formation depresses cell mediated immune responses
- Drug binds to cyclophilin (intracellular protein) prevents formation of IL-2 Prevents
recruitment of activated T-cells
- Dose: 3mg/kg/day (maintenance therapy)
- ADRs:
i. Paresthesia
ii. Musculoskeletal pain
iii. Nephrotoxicity
c. ALEFACEPT ( AMEVIVE):
- Recombinant dimeric fusion protein
- Drug binds to CD2 on memory effector T-lymphocytes inhibits activation of these
cells decreases number of these cells
- Mainly used for moderate-severe psoriasis
- Given i.m
- ADR: Lymphopenia, injection site reactions
- Dose: 15 mg i.m every week, for 12 weeks…………………………..

35. CONTINUED…………………………….
9. TNF INHIBITORS:
- Neutralize TNF-alpha effects
- Drugs include:
1. INFLIXIMAB (REMICADE):
- Chimeric antibody
- Drug binds to both soluble and transmembrane TNF-alpha molecules
neutralizes TNF-Alpha effects
- Used for chronic severe plaque psoriasis and for psoriatic arthritis
- Dose: 5mg/kg i.v infusion (every 8 weeks)
2. ETANERCEPT (ENBREL):
- Recombinant human TNF-Alpha receptor protein, fused with Fc portion of
IgG1
- Same MOA as that of infliximab
- ADR: injection site reactions
- Dose: 25 mg twice weekly (s.c)

36. CONTINUED……………………………
3. ADALIMUMAB (HUMIRA):
- Fully human anti-TNF alpha monoclonal antibody
- Same MOA and ADR as that of infliximab and etanercept
- Dose: 80 mg s.c……………………………………….

37. CONTINUED………………………………
10. PHOSPHODIESTERASE-4-ENZYME
INHIBITORS:
APREMILAST (OTEZLA):
- Drug inhibits phosphodiesterase-4-enzyme increases cyclic AMP
levels  affects cytokines and chemokine synthesis  anti-
inflammatory effects
- Mainly used for moderate-severe plaque psoriasis
- Dose: 30 mg PO BID
- ADRs:
a. Upper respiratory tract infections
b. Headache…………………………….

38. CONTINUED……………………………
11. INTERLEUKIN INHIBITORS:
- IL-17 Plays key role in the pathogenesis of plaque psoriasis
- SECUKINUMAB (COSENTYX):
• Human IgG1 monoclonal antibody
• Selectively binds to and neutralizes pro-inflammatory cytokine 17-A
• Mainly used in severe plaque psoriasis
• Given s.c
• Dose: 300 mg s.c once monthly
• ADRs:
a. Infections
b. Nasopharyngitis……………………….

39. CONTINUED……………………………..
12. ANTI-PSORIATIC AGENT, SYSTEMIC:
USTEKINUMAB (STELARA):
-Human monoclonal antibody
- Drug  acts against IL-12 and IL-23 Interferes with T-cell
differentiation and activation  blocks cytokine cascades
- Given for moderate to severe plaque psoriasis
- Newest available biologic agent
- Dose: 45 mg s.c at 0, 4, 12 weeks
- ADRs:
a. Upper respiratory infection
b. Nasopharyngitis
c. Injection site erythema…………………………..

40. CONTINUED………………………………
13. OPHTHALMIC AGENTS, MISCELLANEOUS:
ARTIFICIAL TEARS (HYPO TEARS, MURINE TEARS):
- Used to treat dry eye irritation
- Different types available OTC
- Classified into:
a. Preserved tears:
• Used in mild cases
• Include: GenTeal, Refresh Tears, Tears Naturale II
b. Non- preserved tears:
• Used in severe cases
• Include: Refresh, Refresh Plus, Hypo Tears PF
- Contain equivalent to 0.9% NaCl
- Used to maintain ocular tonicity
- Stabilize and thicken pre-corneal tear film
- Prolong tear film break up time
- ADRs: Blurred vision, eye pain, headache……………

41. CONTINUED……………………………..
14. INJECTABLE CORTICOSTEROIDS:
- i.m route not preferred for corticosteroids since increased risk of
flares upon withdrawal
- Used for isolated plaques (psoriatic nails)
- Injected intra- lesionally / in nail/ matrix
TRIAMCINOLONE (KENALOG, ARISTOSPAN):
- Same corticosteroid action
- Long lasting result
- Dose: 0.4 ml injected into nail bed and matrix
- Used to improve psoriatic dystrophy……………………..

42. CONTINUED………………………………
15. LIGHT THERAPY (PHOTOTHERAPY):
PUVA (PSORALENS + UVA LIGHT):
- Valuable role in treatment of stable moderate- severe psoriasis
- Psoralens:
. Drugs  activated by long wavelength UV light (320-400 nm) interferes with DNA
synthesis decreases epidermal turnover
. Include :
• 8-MOP (Methoxy psoralen)
• 5-MOP
. Taken orally 2 hour before UVA light exposure
. Eyes are protected due to cataract risks
. Patients are given sunglasses to wear for 12 hours after treatment
. Given twice a week, for 6 week period
. ADR:
- Nausea
- Long term cutaneous malignancy………………………………….

43. D. NON-PHARMACOTHERAPY AND
PATIENT COUNSELLING TIPS:
• Focus on medication adherence
• Focus on follow-ups, or consultations, as advised by doctors
• People who take methotrexate, should focus on takin folic acid supplements to
avoid risk of anemia
• Stress reduction
• CLIMATOTHERAPY:
“ Relocation of a patient to a different climate, so as to aid recovery from /
management of a condition”
• Adequate sunshine exposure
• Use of moisturizers
• Patients, who are on corticosteroid therapy, should report about pigmentation
if noted………………………..

44. BIBLIOGRAPHY:
• CLINICAL PHARMACY AND THERAPEUTICS by ROGER WALKER
• MEDSCAPE
• PATHOPHYSIOLOGY AND TREATMENT OF PSORIASIS BY BRYAN ADAMS
(PHARM.D)
• www.healthline.com
• www.drugs.com

45. THANK YOU !!!   