Psoriasis is a chronic non-communicable skin disease of great importance for its challenging treatment among its different types.

2. DEFINITION
Is a chronic non-infectious inflammatory disease of the skin, characterized by well-
defined erythematous plaques bearing large, adherent, silvery centrally attached scales.
CAUSE AND PATHOGENESIS
Keratinocyte hyperproliferation + inflammatory cell infiltrate (neutrophil + TH-1 lymphocytes)
Trigger e.g. trauma, irritant, drug; antigen  immune response
Theory: inflammatory cell mediators  increase Keratinocyte proliferation
EPIDEMIOLOGY
Age
Type I: early onset (75 %) in females (16 years) and in males (22 years)
Type II: late onset (25 %) in males and females (56 years)
Sex
Equal incidence in males and females
Race
High in North American white
Low incidence in American black, West Africans, Japanese, and Eskimos and a very low
incidence or absence in American Indians

3. Epidermal cell kinetics
• ↑ germinative cells entering cell cycle, not ↓ cell cycle time
• Growth fraction 100% in psoriasis vs. 30% in normal skin
•  epidermal turnover <10days vs. 60days in normal skin. Less marked similar changes in nr psoriatic skin
• Mechanism of ↑ hyperproliferation may be due to: cGMP, inducible nitric oxide synthase, arachidonic acid
metabolites, polyamines, calmodulin, plasminogen activator are all ↑ at psoriatic plaques
• INF-γ: normally ↓ growth + ↑ differentiation by phosphorylation and activation of transcription factor
STAT-1α. In psoriasis INF-γ fails to activate STAT-1α
• Transcription factor NFκB activity defective in psoriatic plaques
• Epidermal cell retinoid receptors: RAR (retinoid acid) (defect in signaling)  psoriasis; RXR normal
Altered epidermal maturation
Keratin types: moves from basalis (K5, K14) towards surface (K1, K10); in psoriasis (K6, K16)
Genetic
• Polygenic inheritance: Type I = +ve family history; Type II = -ve family Hx
• 16% one parent vs. 50% two parents; father > mother (Genomic imprinting)
• Non-psoriatic parents have a Child with psoriasis, 10% next child with psoriasis
• 70% monozygotic twins vs. 20% dizygotic
• Early onset psoriasis: psoriasis susceptibility locus (PSOR-1) at 6p21 (close to MHC-I)
near HLA-C & HLA-Cw6. PSOR-1= 50% of total psoriasis, PSOR-2 to 9
• HLA-Cw6: x20 develop psoriasis; Cw6+ 10% develop psoriasis
• HLA weaker link to late-onset psoriasis

4. Inflammation
Unknown antigen (may be immun. Response)  inflammatory cell accumulation
↑ IL and growth factors  many hypotheses:
1. Stimulation (e.g. trauma, infection, drugs, UV)  IL-1, IL-8, IL-18
2. IL-1 up-regulates expression of intercellular adhesion molecule-1 (ICAM-1) and E selectin on dermal
papillary vascular endothelium  lymphocyte function-associated antigen sticks to ICAM-1 
Cutaneous Lymphocyte Antigen (CLA) positive memory T lymphocytes accumulate in the vessels
3. IL-8 from keratinocytes attracts T cell and neutrophils to migrate from papillary vessels into the
epidermis. Then T cells held by adhesion of their lymphocyte function-associated antigen (LFA-1) with
ICAM-1 on keratinocytes
4. Accumulated T cells interacted by Langerhans cell and keratinocytes. Then activated T cells release IL-2,
17, 22, IFN-γ, and TNF-α
5. T-cell further activated by Langerhans cell
6. IL-2  local T cell proliferation
7. IFN-γ, and TNF-α  keratinocytes to express HLA-DR to ↑ their ICAM-1 to produce further IL-6, IL-8,
TGF-α, and TNF-α
8. TGF-α attaches to epidermal growth factor receptors (EGF)  keratinocytes proliferation. IL-6 and TGF-α
 ↑ keratinocyte mitosis

5. • Staph. aureus and some streptococcal exotoxins  T cell proliferation (guttate psoriasis)
• Cyclosporin ↓ TH cell  improves psoriasis
• Neutrophil  microinjuries  default into healing status
• In acute flare of psoriasis: circulating Neutrophils are activated  accumulate in skin after sticking to
endothelial cell  migrate to epidermis till horny layer forming (Munro's) micro-abscesses. This is due to
activated keratinocyte chemotactics (e.g. IL-8, Gro-α, Leukotriene-B4). Scales also contain chemotactics
 visible collection of sub-corneal neutrophils (pustular psoriasis)
The dermis
• Dermal capillary loop  dilated, tortous before epidermal plague formation
• Fibroblast replicate more rapid, produce more glycosaminoglycans

6. PRECIPITATING FACTORS
1. Trauma. at scratches / surgical wounds (Köbner phenomenon)
2. Infection. Tonsillitis due to β-hemolytic streptococci  guttate psoriasis, bacterial antigen act as a
superantigen (no need for cellular presentation)  polyclonat T-cell proliferation. But HIV paradoxically
worsen psoriasis
3. Hormonal. Pregnancy ↓ psoriasis, postpartum relapses it. Hypoparathyroidism  hypocalcemia (rare)
↑ psoriasis
4. Sunlight. Improves psoriasis; 10% worses
5. Drugs. Anti-malarial, β blockers, INF-α, lithium, terbinafen, calcium channel blochers, captopril,
glyburide, granulocyte colony stimulating factor, ILs, and lipid lowering drugs ↑ psoriasis. Steroid
withdrawal ↑ psoriasis
6. Smocking and alcohol. ↑ psoriasis
7. Emotion. Upset ↑ psoriasis
HISTOLOGY
1. Parakeratosis. (nuclei retain in the horny
layer)
2. Epidermal thickening @ rete ridges+ supra-
dermopapillary epidermal thining (Auspitz's
sign)
3. Munro sign.
4. Dermal papillary loops  dilated and
tortuous
5. T cell infiltrate in the upper dermis

7. They begin as red, scaling papules that coalesce to form
round-to-oval plaques, The scale is adherent, silvery white,
and reveals bleeding points when removed (Auspitz's sign).
Early lesion is small macular. Old patches are thick
lamellated (posriasis ostracea). (psoriasis follicularis) tiny
scaly at hair follicle orifice. (p. figurata, annulata, gyrata) for
curved linear pattern. (p. discoidea) for no central
involution. (sebopsoriasis) overlap with seborrhoeic
dermatitis
Psoriasis can develop at the site of physical trauma
(scratching, sunburn, or surgery), the so-called isomorphic
or Köbner's phenomenon.
Woronoff’s ring: concentric red blanch at periphery of
healed psoriatic palgue
Although psoriasis can affect any cutaneous surface,
certain areas are favored and should be examined in all
patients in whom the diagnosis of psoriasis is suspected.
Those areas are the elbows, knees, scalp, gluteal cleft,
fingernails, and toenails.
CLINICAL MANIFESTATIONS

9. Variations in the morphology of psoriasis
Chronic plaque psoriasis
Guttate psoriasis (acute eruptive psoriasis)
Pustular psoriasis
Erythrodermic psoriasis
Light-sensitive psoriasis
HIV-induced psoriasis
Keratoderma blennorrhagicum (Reiter's syndrome)
Variations in the location of psoriasis
Scalp psoriasis
Psoriasis of the palms and soles
Pustular psoriasis of the palms and soles
Pustular psoriasis of the digits
Psoriasis inversus (psoriasis of flexural areas)
Psoriasis of the penis and Reiter's syndrome
Nail psoriasis
Psoriatic arthritis
CLINICAL PRESENTATIONS

10. Chronic plaque psoriasis
Chronic, noninflammatory, well-defined
plaques are the most common
presentation of psoriasis.
Anywhere in the skin.
They enlarge to a certain size and then
tend to remain stable for months or years.
A temporary brown, white, or red macule
remains when the plaque subsides.

17. Guttate psoriasis (<2% of psoriasis)
>30% are <20y;
TYPE Papules 2.0 mm to 1.0 cm
COLOR “Salmon pink”
SHAPE Guttate (Latin: “spots that resemble drops”)
ARRANGEMENT Scattered discrete lesions
DISTRIBUTION Generalized, usually sparing the palms and soles, on the trunk, less on the face,
scalp, and nails
Differential Diagnosis
Multiple Small Scaling Plaques Psoriasiform drug eruption, secondary syphilis, pityriasis rosea

18. Laboratory Examinations
Serologic An increased anti-streptolysin titer
Culture Throat culture for group A b-hemolytic
strept.infection
Course and Prognosis
disappears spontaneously in a few weeks without
Rx.

22. Erythrodermic psoriasis
Generalized erythrodermic psoriasis, like
generalized pustular psoriasis, is a severe, unstable,
highly labile disease that may appear as the initial
manifestation of psoriasis but usually occurs in
patients with previous chronic disease.
Precipitating factors include the administration of
systemic corticosteroids; the excessive use of
topical steroids; phototherapy complications;
severe emotional stress; and preceding illness, such
as an infection.

26. Psoriasis of the scalp
inaccessible for phototherapy and are often
pruritic, which results in lichenification and
koebnerization. It usually does not lead to
hair loss.
Duration Months to years
Symptoms Mild to severe pruritus, which
often causes compulsive and subconscious
scratching
Type Plaques, thick adherent scales
Lichenification, Exudation and fissures,
especially behind the ears
Arrangement Scattered discrete plaques or
diffuse involvement of the entire scalp
(Note: Paradoxically, alopecia is an
uncommon complication)
Differential Diagnosis
Seborrheic dermatitis of the scalp may be
almost
indistinguishable from psoriasis. Some have
called this seborriasis. Tinea capitis,
atopic dermatitis, lichen simplex chronicus
Course and Prognosis
• good; if treated
• Remission occurs after months to years.
• Scratching and rubbing must be avoided to
maintain the remission.

31. Psoriasis of the nails
Pitting. most frequent , tiny, punched-out
depressions on the nail plate surface. They emerge
from under the cuticle and grow out with the nail.
Many other cutaneous diseases may cause pitting
(e.g., eczema, fungal infections, and alopecia areata),
or it may occur as an isolated finding as a normal
variation.
Oil spot lesion. Psoriasis of the nail bed may cause
localized separation of the nail plate. Cellular debris
and serum accumulates in this space. The brown
yellow color observed through the nail plate looks
like a spot of oil.

32. Onycholysis. separation of the nail from the nail bed.
the nail detaches in an irregular manner. The nail
plate turns yellow, simulating a fungal infection.
Subungual debris. This is analogous to fungal
infection; the nail bed scale is retained, forcing the
distal nail to separate from the nail bed.
Nail deformity. Extensive involvement of the nail
matrix results in a nail losing its structural integrity,
resulting in fragmentation and crumbling.

39. Psoriasis of the palms and soles
Superficial red plaques with thick brown scale may be indistinguishable from chronic
eczema. Smooth, deep red plaques are similar to those found in the flexural area
The palms and soles may be the only areas involved. Fingers may develop painful fissures.

46. Psoriasis of the Body Folds (Flexural)
Psoriasis of the body folds (inguinal area, umbilicus, axillae, inframammary, intergluteal fold)
and of the genitalia is especially vulnerable to the development of steroid-induced skin atrophy;
low-potency steroids are recommended but are not very effective. Anthralin and tar
preparations are irritating in these areas. This poses a difficult problem in control. Castellani’s
paint is sometimes useful in genital and perianal psoriasis. The newer topical vitamin D3
preparation, calcipotriene ointment, 50 mg/g, however, is effective in these areas, and there is
no risk of skin atrophy.

50. Palmoplantar pustulosis
chronic, relapsing eruption limited to the palms and soles and characterized by numerous
sterile, yellow, deep-seated pustules that evolve into dusky-red macules.
Age 50 to 60 years
Sex More common in females (4 : 1)
Duration Months
Type Pustules in varying stages of evolution, 2.0 to 5.0 mm, deep-seated, develop into dusky-red
macules and crusts; present in areas of erythema and scaling.
Distribution Localized to palms and soles (Thenar and hypothenar, flexor aspects of fingers,
heels, acral portions of the fingers and toes usually spared.

53. Differential Diagnosis
dermatophytosis (tinea manus, tinea pedis), pustular psoriasis, dyshidrotic eczematous
dermatitis, HSV infection
Laboratory Examinations
KOH Preparations Rule out dermatophytosis.
Bacterial Culture Rule out Staphylococcus aureus
Viral Culture Rule out herpes simplex virus (HSV) infection.
Dermatopathology Edema and exocytosis of mononuclear cells form a vesicle and later many
neutrophils, which form a unilocular spongiform pustule and some acanthosis. Mononuclear
cells at first and later myriads of neutrophils.
Prognosis
years and characterized by unexplained remissions and exacerbations.

54. Light-sensitive psoriasis
Psoriatic patients wait for sunny summer months when, in most
cases, the disease responds predictably to ultraviolet light.
However.
s.t.  sunburned in an anxious attempt to clear the disease
rapidly. As a result of Köebner's phenomenon, guttate lesions or a
painful, diffusely inflamed plaque forms in the burned areas
Plaques subsequently converge onto the clear, previously
protected sites.

57. Generalized acute pustular psoriasis (von zumbusch)
This can be a life-threatening medical problem with an abrupt onset. The skin
involvement is distinctive and starts with a burning erythema that spreads in hours
to result in large areas of fiery-red skin. Pinpoint pustules then appear in clusters,
peppering the red areas of skin; these pustules become confluent and form “lakes”
filled with purulent fluid. Fever, generalized weakness, severe malaise, and a leukocytosis
are prominent features in almost every patient. Impetigo herpetiformis is
generalized acute pustular psoriasis with hypercalcemia occurring in pregnancy.
Age Adults, rarely children
Onset of Lesions The constellation of fiery-red erythema followed by formation
of pustules and “lakes” occurs over a period of less than 1 day. Waves of pustules
may follow each other; as one set dries, another will appear.
Skin Symptoms Marked burning, tenderness
Constitutional Symptoms
ACUTE Headache, chills, feverishness, marked fatigue, severe malaise

60. Physical Examination
Patient is Frightened, “toxic”, Vital Signs Fast pulse, rapid breathing, fever that may be high
Type burning erythema  clusters of tiny nonfollicular and very superficial pustules
confluent, forming “lakes” of pus. Removal of the top yields superficial, oozing erosions, and
there will be crusting.
Distribution Generalized, but especially involving the flexural areas and the anogenital regions
Hair and Nails become thickened, and there is onycholysis; subungual “lakes” of pus lead to
shedding of nails; hair loss of the telogen defluvium type developing in 2 or 3 months may occur.

61. Differential Diagnosis
Widespread Erythema with Pustules The abrupt onset and the typical evolution of erythema
followed by pustulation are highly characteristic.
Generalized herpes simplex has umbilicated pustules,
Generalized pustular drug eruptions (e.g., after furosemide, amoxicillin/clavulanic acid, and
other drugs) may be clinically indistinguishable and patients are less toxic.
Laboratory Examinations
Large spongiform pustules resulting from the migration of neutrophils from the capillaries in the
dermal papilla, where they aggregate within the interstices of the degenerated and thinned
keratinocytes
Bacterial Culture Of Tissue Rule out S. aureus infection.
Hematologic Polymorphonuclear leukocytosis as high as 20,000 WBC

62. Pathogenesis
The fever and leukocytosis probably result from the marked increase in the number of
polymorphonuclear cells that invade the dermis and release their chemical mediators. This
causes inflammation and necrosis of cells (leukocytes and keratinocytes). These patients are
often brought to the emergency rooms of hospitals.
Course and Prognosis
Relapses and remissions may occur over a period of years. May evolve into or be
followed by psoriasis vulgaris.

63. Seborrhoeic-like psoriasis
Overlap with seborrhoeic dermatitis.
Face, submammary, scalp, flexure, axillae
Moist erythematous, with yellowish greasy soft scales
Napkin psoriasis
2-8m of age
Bright red sharp border at the diaper area
If cleared may reappear in adulthood
Acrodermatitis continua of Hallopeau
Acral red plague studded with pustules
Nail float over lakes of pus  anonychia
Hyperkeratosis, painful and taper fingertips

64. Impetigo herpitiformis
Generalized pustular psoriasis of pregnancy
Begin flexural  flare to generalise
Rx: early compatible delivery after prednisolone 1mg/kg/day
Keratoderma psoriasis (Reiter syndrome)
Tendency for thicker keratotic lesion
Positive for HLA-B27
After a bout of urethritis or enteritis

65. Psoriatic arthritis
Rheumatoid factor is usually negative. At any age, peak 20-40y; women = men.
5%-8% of psoriasis, but up to 53% of psoriatic have arthralgia. Nail involvement >80% vs. 30% of
patients with uncomplicated psoriasis.
following trauma. pregnancy improves 80% of cases.
Diagnosis.
Although tests for antinuclear antibody (ANA) levels, ESR, WBC, and uric acid are elevated
Rheumatoid factor levels are typically normal
Clinical Features.

68. Asymmetric arthritis.
The most common pattern is an asymmetric arthritis involving one or
more joints of the fingers and toes. Usually one or more proximal
interphalangeal (PIP), distal interphalangeal (DIP),
metatarsophalangeal, or metacarpophalangeal joints are involved.
During the acute phase, the joint is red, warm, and painful.
soft-tissue swelling on either side of the joint (“sausage finger”)
and restricts mobility.
HLA-DR7 is increased in this group with peripheral arthritis
Symmetric arthritis.
Resembling rheumatoid arthritis, but the rheumatoid factor is
negative.
Distal interphalangeal joint disease.
With psoriatic nail disease. Chronic but mild, is not disabling
Arthritis mutilans.
Osteolysis, Gross deformity and subluxation digital telescoping,
producing the “opera glass” deformity.
Ankylosing spondylitis.
HLA-B27 and spondylitis is well known. The strongest association is in
males with sacroiliitis 1/3 of cases of psoriasis. usually asymmetrical