Psoriasis is a chronic inflammatory skin disease characterized by well-defined erythematous plaques covered with silvery-white scales. It affects extensor surfaces, scalp, nails and intertriginous areas. The disease has a genetic predisposition and can be triggered by infections, medications, stress and trauma. Pathogenesis involves activation of the immune system including T cells which secrete cytokines leading to abnormal keratinocyte proliferation. Presentations include plaque, guttate, pustular and erythrodermic subtypes. Management involves topical agents, phototherapy and systemic medications such as retinoids, methotrexate and biologics that target cytokines like TNF-α. Complications include psor

2. Introduction of Psoriasis
Psoriasis is a chronic inflammatory, hyperproliferative skin disease. It is
characterized by well-defined, erythematous plaque with silvery-white surface
scale. Distribution includes extensor surfaces (i.e., knees, elbows, and buttocks)
In about 25% of cases, peculiar pitting of nails is seen. Psoriatic arthritis
resembling rheumatoid arthritis is produced in about 5% of cases but
rheumatoid factor is absent. may also involve palms and scalp (particularly
anterior scalp margin). Associated findings include psoriatic arthritis and nail
changes (onycholysis, pitting or thickening of nail plate with accumulation of
subungual debris).

3. History of Psoriasis
 The word psoriasis is derived from Greek word ‘psora’ means itching.
 The Greek physician Galen of perganon (130-200 BC) use the term
Psoriasis vulgaris to refer all dermo and epidermopathies accompanied by
pruiritis.
 Since 1950 local application and systemic medications are used for the
psoriasis.

4. EPIDEMIOLOGY
Psoriasis is the most commonly recognized papulosquamous disease. It occurs in 2 to 3% of the
general population, with considerable variation in different parts of the world.
Lower rates are found in Japanese and psoriasis is rare in West Africans.
It affects male and female patients equally.
Approximately one third of the patients have a positive family history.
Psoriasis has a bimodal peak of onset, at age 22.5 years and again at age 55 years.
The onset of psoriasis before the age of 15 years is associated with a higher prevalence of
positive family history of psoriasis and with more severe disease.
Recent epidemiologic studies have shown that psoriasis is associated with an increased risk of
heart attack and strokes, a relationship that may be related to a chronic inflammatory state.
Psoriasis is also associated in up to 10% of patients with arthritis, which in some cases may be
severe.

5. PATHOBIOLOGY
Psoriasis involves the innate and adaptive immune systems, with abnormal
keratinocyte proliferation. Factors playing a role in the pathogenesis include
activation of antigen-presenting cells and development of TH1 and TH17
cells. Mediators include interleukin-12 (IL-12), IL-23, tumor necrosis factor-α
(TNF-α), and interferon-γ.
Exposure to precipitating factors such as infections (e.g., streptococcal or HIV
infections), stress, or physical injury results in activation of T cells and
generation of cytokines, followed by influx of neutrophils and subsequent
release of inflammatory mediators, which lead to the development of
cutaneous lesions.
Psoriasis has a complex, polygenetic inheritance. Susceptibility genes include
PSORS1 to PSORS9, although PSORS1, mapped to chromosome 6p21.3, is
now considered a major locus for susceptibility to psoriasis.

6. Psoriasis is a multifactorial immunologic disease, both genetic (e.g., human
leukocyte antigen [HLA] types) and environmental factors contribute to risk.
It is not known if the inciting antigens are self or environmental. Sensitized
populations of T cells home to the dermis, including CD4+ TH17 and TH1
cells and CD8+ T cells, and accumulate in the epidermis.
These cells secrete cytokines and growth factors that induce keratinocyte
hyperproliferation, resulting in the characteristic lesions.
Psoriatic lesions can be induced in susceptible persons by local trauma
(Koebner phenomenon), which may induce a local inflammatory response
that promotes lesion development.
GWAS studies have linked an increased risk of psoriasis to polymorphisms in
HLA loci and genes affecting antigen presentation, TNF signaling, and skin
barrier function.
PATHOGENESIS

7. DEREGULATED INFLAMMATORY PROCESS
PATHOPHYSIOLOG
Y
STRESS, GENECTIC, AUTOIMMUNE REACTION AND MEDICATION
CAUSE
HYPERACTIVE OF T-CELLS
EPIDERMIS INFILTRATION AND KERATINOCYTE PROLIFERATION

8. SILVER SCALING OF SKIN
LARGE PRODUCTION OF VARIOUS CYTOKINES ( INTEFERRON,
INTERLEUKIN-12)
SUPERFICIAL BLOOD VESSEL DILATED AND VASCULAR ENGORGEMENT
EPIDERMAL HYPERPLASIA AND IMPROPER CELL MATURATION
FAILS TO RELEASE ADEQUATE LIPIDS WHICH LEAD TO FLAKING,
SCALING PRESENTATION OF PSORIASIS LESION
Cont…

9. Etiology of Psoriasis
(1)Unknown
(2)Genetic
 Some factor may aggravated the condition such as:-
 Trauma
• Psoriatic lesions can appear at sites of skin trauma, such as scratches or surgical wounds (Kobner
isomorphic phenomenon)
 Infection
• β-hemolytic streptococcal throat infections often precede guttate psoriasis.
• Severe psoriasis may be the initial presentation of HIV infection.
 Sunlight
• sun exposure, mainly due to Kobnerisation at sites of sunburn or polymorphic light eruption.
 Drugs
• Antimalarials, β-adrenoceptor antagonists (β-blockers), lithium, NSAIDs and anti-TNF-α drugs.
 Psychological factors
• Anxiety and stress may exacerbate psoriasis.
 Smoking and Alcohol
 Obesity
 Hormonal changes

10. Types of Psoriasis
1) Plaque psoriasis
2) Guttate psoriasis
3) Inverse psoriasis
4) Pustular psoriasis
• Localised
• Grneralised
5) Local forms of psoriasis
• Palmoplanter
• Scalp
• Nail (psoriatic onychodystrophy)
6) Psoriatic arthritis

12. Plaque Psoriasis
 Most common type affects
approximately 85%.
 Features pink, well defined
plaques with silver scale.
 Lesion may be single or
numerous.
 Plaque may involve large areas
of skin.
 Classically affects elbows,
Knees, buttocks and scalp.

13. Guttate psoriasis
 Guttate psoriasis usually occurs after viral or
bacterial (most commonly streptococcal)
infection.
 This is most common in children and
adolescents.
 It is commonly associated with HLA Cw6.
 Individual lesions are droplet-shaped, small
(usually less than 1 cm in diameter),
erythematous, scaly and numerous.
 An episode of guttate psoriasis may clear
spontaneously or with topical treatment within
a few months, but UVB phototherapy is often
required and is highly effective.
 Guttate psoriasis often heralds the onset of
plaque psoriasis in adulthood.

14. Inverse or flexural
psoriasis
 psoriasis that occurs in skinfold
areas such as the groin, axilla,
and inframammary folds.
 It appears as an erythematous,
somewhat shiny patch because
of the constant friction in the
involved areas, scales are
usually absent.
 May cause diagnostic difficulty
when genital or perianal region
is affected in isolation.

15.  Generalized pustular psoriasis is uncommon, unstable and life-threatening. It
will often emerge in the context of plaque disease and the onset is usually
sudden, with large numbers of small sterile pustules on aerythematous
background, often merging into sheets, with waves of new pustules in
subsequent days.
 The patient is usually febrile and systemically unwell, and this must be dealt
with as a medical emergency.
Pustular psoriasis
Pustular psoriasis may be generalized or localized.
 Localised pustular psoriasis of the palms and soles (palmoplantar pustulosis) is
more common, chronic and closely associated with smoking; small, sterile
pustules and erythema develop and resolve with pigmentation and scaling.
 A localised form of sterile pustulosis of a few digits (acropustulosis) can also
occur.
 It is unclear whether these localised forms of pustulosis are truly psoriatic.

16. Erythrodermic psoriasis
 Generalized erythema covering entire
skin surface.
 May evolve slowly from chronic plaque
psoriasis or appear as eruptive
phenomenon.
 Patients may become febrile,
hypo/hyperthermic and dehydrated.
 Complication include cardiac failure,
infections, malabsorption and anemia.
 Relatively uncommon

17. Palmoplantar psoriasis
 Can be hyperkeratotic or pustular.
 May mimic dermatitis look for
psoriatic manifestations elsewhere to
aid diagnosis.
 Possibly aggravated by trauma.

18. Scalp psoriasis
 Varies from minor scaling with
erythema to thick hyperkeratotic
plaques.
 May extend beyond hairline.
 Patient scratching may produce
asymmetric plaques.

19. Nail psoriasis
 May be present in patients with any type of
psoriasis.
 Can take several forms:-
 Pitting:- Discrete, well circumscribed
depressions on nail surface.
 Subungual hyperkeratosis:- Silvery white
crusting under free edge of nail with some
thickening of nail plate.
 Onycholysis:- Nail separates from nail bed
at free edge.
 Oil drop sign:- Pink/red colour change on
nail surface.

20. Psoriatic Arthritis
 Five to 30% of patients with psoriasis
may also have psoriatic arthritis,
which may precede the appearance of
cutaneous lesions 95% of these
patients present with peripheral
asymmetrical oligoarthritis involving
the interphalangeal joints of the hands
and feet, while 5% have exclusively
axial or skeletal disease.
 Psoriatic arthritis has been associated
with HLAB57, although some studies
have also reported HLA-Cw6 in more
than 50% of all persons with this
disease.

21.  It will vary according to types of at psoriasis. Initially the first sign of
psoriasis is often red spots on the body.
The patches of skin
 Dry, swollen and inflammed Covered with silver white flakes Raised and
thick skin.
 Other symptoms of psoriasis includes:- Pain, itching and burning.
 Restricted joint motion or pain Cracked and bleeding skin.
 Dandruff on scalp
 Pus filled blisters Genital lesions in males.
 Pitting, small depression on the surface of the nail Yellow, dicsolored nail
Koebner phenomenon
 Arthriti
COMMON CLINICAL MANIFESTATIONS

23. 1)Auspitzsign(Grattage test):- Removing
the scale reveals a smooth, red, glossy
membrane with tiny punctate bleeding
point.
2) Rich red color:- often referred to as
'salmon pink‘. This quality of color is of
special diagnostic value to differentiate
psoriasis from eczema in lesions on the
palms, soles and scalp.
3) Candle grease sign
4) Koebner’s or Isomorphic phenomenon
5) Holo or Woronoff sign
Signs of psoriasis

24. PASI Score (Psoriasis Area and Severity Index)
■It is a method to estimate severity of psoriasis in order to evaluate the clinical
efficacy of new treatments
■Psoriatic plaques are graded based on three criteria: redness (R), thickness (T),
and scaliness (S)
■Severity is rated on a 0-4 scale (0 for no involvement up to 4 for severe
involvement)
■The highest PASI score is 12; the lowest is 0

26. Diagnostic Investigations
 Collect history
 Physical examinations
 Skin biopsy :- under local anesthesia
 Blood and radiography test was done to rule out psoriatic arthritis
 TLC ,ESR, C- Reactive protein, Serum calcium, Serum uric acid.
 Immunoglobulin
 Anti-nuclear antibody
 Nail dipping and skin scraping
 Throat swab

27. Localised patches/plaques Guttate Flexural Erythrodermic Palmoplantar
Tinea Pityriasis rosea Tinea Eczema Tinea
Eczema Drug eruption Eczema Cutaneous T-cell
lymphoma
Superficial basal cell carcinoma
and Bowen’s disease
Secondary
syphilis
Candidiasis Pityriasis rubra
pilaris
Seborrhoeic dermatitis
Cutaneous T-cell lymphoma
(mycosis fungoides)
Seborrhoeic
dermatitis
Lichen planus
Drug
DIFFERENTIAL DIAGNOSIS

28. Complications
Infection
Fluid and electrolyte imbalance
Low self esteem
Depression
Stress
Metabolic syndrome (increased blood pressure, high blood sugar, excess
body fat around the waist, and abnormal cholesterol levels)
Hypertension
Joint damage

29. Management of psoriasis
Therapy includes
1) Topical medications
2) UV-based treatment
3) Systemic drugs
 For mild disease, topical therapy with topical corticosteroids(e.g.,
triamcinolone ointment, 0.1% twice daily for 1 to 2 weeks).
 Calcipotriene cream (0.005%, twice daily as needed).
 Tazarotene gel (0.05%, once or twice daily as needed), used alone or in
combination, is effective.

30. UV-based treatment
In patients who have widespread lesions, NB-UVB isthe best option, whereas
PUVA should be considered for patients in whom NB-UVB therapy has failed.
Systemic drugs
For patients with recalcitrant disease, oral medications such as
Methotrexate (7.5 to 15 mg/week)
Acitretin (25 to 50 mg/day)
Cyclosporine (3 to 5 mg/kg/day)
Hydroxyurea (1 g/day)
Mycophenolate mofetil (1 to 2 g/day) have all been used with success.

31. Topical agents Photo(chemo)
therapies
Systemic agents Intensive inpatient or
day-patient care
Emollients
tars
UVB Retinoids Topical agents and
photo(chemo)therapie
s under medical
supervision
dithranol
vitamin D
agonists,
PUVA Immunosuppressants, e.g.
methotrexate, ciclosporin,
mycophenolate,
hydroxycarbamide
retinoids, excimer laser Immunomodulators, e.g.
fumaric acid esters
corticosteroids Biological
immunosuppressants, e.g.
infliximab, etanercept,
adalimumab
Treatment categories in psoriasis

32. BIOLOGIC
AGENTS
DOSE/DURATION MONITORING SIDE EFFECTS
TNF-α
INHIBITORS
Etanercept
(Enbrel)
50 mg SC twice a week for 12 wk, then
50 mg SC weekly indefinitely
PPD CBC, LFT Injection site reaction,
infection
Infliximab
(Remicade)
5-10 mg/kg IV at weeks 0, 2, 6, then
every 8 wk indefinitely
PPD CBC, LFT Infusion reaction,
sepsis, lupus-like
syndrome, aplastic
anemia (rare)
Adalimumab
(Humira)
80 mg SC at week 0, 40 mg at wk 1,
then 40 mg every 2 wk indefinitely
PPD CBC, LFT Injection site reaction,
infection
ANTI-CD2
Alefacept (Amevive) 15 mg IM weekly for 12-16 wk; consider a
second course after a 12-wk interval
CD4 Infection
ANTI–IL-12/23
Ustekinumab (Stelara) SC at weeks 0, 4, then every 12 wk 100 kg: 90
mg indefinitely
PPD Infection
BIOLOGIC AGENTS FOR PSORIASIS