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Moderator: Dr Amit Malhotra
Introduction
 Group of diseases in which primary lesion is most

commonly a papule,
 Usually erythematous, with a variable degree of scaling
on surface
 Plaques form through coalescing of primary lesions
 Both morphology of papule and character of scale give
clues to making a diagnosis
Papulosquamous disorders

Psoriasis
Lichen
Planus

Pityriasis
rosea

Parapsoriasis
eg. small / large
plaque

pityriasis
rubra pilaris

Lichen
nitidus

Pityriasis
lichenoides

Lichen
striatus
Exfoliative
dermatitis

Seborrheic
dermatitis
 Other important papulosquamous diseases
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Mycosis fungoides (cutaneous T-cell lymphoma)
Discoid lupus erythematosus
Subacute cutaneous lupus erythematosus
Tinea corporis
Nummular eczema
Secondary syphilis
Drug eruptions
Erythema dyschromicum perstans
Keratosis lichenoides chronica
Lichen sclerosus
Lichenoid dermatitis
Lichenoid reaction of graft-versus-host disease
Extramammary Paget’s disease
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Common,
Chronic,
Disfiguring,
Inflammatory & Proliferative,
Genetically and environmentally influenced condition of skin and joints
 Unpredictable course
 Remissions & exacerbations

:

Epidemiology

Prevalence 0.1- 3%.
Bimodal age distribution.
Type I – 75%, 15 - 40 Yr of age
Type II ─ >40 Yr of age
No gender predilection.
Develop earlier in women
Winter aggravation frequent.
 Exact cause-unknown
 Genetic predisposition
 Precipitating factors
 Immunopathogenesis
 Epidermal hyperplasia
 Vascular changes

Genetic Background
↓↓
Provocating Factors
↓↓
Exogenous/Endogenous antigens
↓↓
Antigen presentation by APCs
↓↓
T lymphocyte- mediated Immune
response
↓↓
Secretion of cytokines
↓↓
Inflammation & cellular
hyperproliferation
↓↓
Clinical Lesions of psoriasis
Causes and Pathogenesis
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Genetic predisposition - 30% have first degree relative,
Seen in 65% of identical twins,
More frequency of HLA-B 13, HLA-B17, HLA-Cw6 is seen,
9 psoriasis susceptibility loci on different chromosomes have been
identified (PSORS 1-9)
Environmental trigger –
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Trauma
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Infection - streptococcal infection often triggers guttate
and plaque psoriasis. Others are HCV, HIV, HSV, CMV
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Hormonal - Psoriasis frequently improves in pregnancy
and relapse postpartum.
•
Drugs - Antimalarials, beta-blockers, NSAIDs ACEIs and
lithium may worsen psoriasis. withdrawal of systemic
steroids or potent topical steroids.
•
Others – Sunlight, smoking and alcohol intake,
Emotional upset and hypocalcemia
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Obesity - Excess weight increases risk of inverse psoriasis
Disorder of
excessive growth
and
reproduction of
skin cells

Effector cytokine
IL-2,IL-17,IL22,INF-γ and
TNF-α leads to

•Shortening of
cell cycle 8 times
•Proliferative cell
increase 2 times
•Germinative cell
enter growth
fraction100 %

Immune-mediated
disorder
Both of these abnormalities can induce other,
Leading to a vicious cycle of keratinocyte proliferation and inflammatory reaction,
But it is still not clear which is primary defect.
Pathology:
 Hyperkeratosis and parakeratosis with focal orthokeratosis and
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Munro microabscess formation
Near absent granular layer.
Spongiform pustules of kogoj in Malpighian layer
Acanthosis
Rete ridges: elongated and clubbed, branched or fused at their
bases,
Suprapapillary epidermal thinning
Infiltrate: mononuclear leukocyte infiltrates in lower half of
epidermis and in upper dermis and polymorphs in upper
epidermis
Dilated, tortuous papillary blood vessels
Morphology of Chronic plaque psoriasis (psoriasis
vulgaris):
 Well-defined with distinct border.
 Erythematous (salmon pink) papules and plaques

of variable size
 Covered with a silvery white, loosely adherent scales,
accentuated by grating lesions
 Which on removal may reveal punctate bleeding points
(Auspitz sign),
 Isomorphic (koebner)

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phenomenon is positive in 38 –
76% of cases.
Koebner reaction may also be
found in other dermatoses like,
lichen planus, lichen nitidus and
vitiligo.
Reverse koebner phenomenon
may be seen.
Itching is variable.
In Resolving lesions a
peripheral halo around lesion,
woronoff ring may be seen.
Resolved lesion may show post
inflammatory hypomelanosis
Psoriasis vulgaris:
typical plaque
which is welldefined, discoid,
erythematous,
indurated and
surmounted with
loose silvery scales
Psoriasis vulgaris: discoid lesions
become confluent to give rise to
gyrate and polycyclic lesions.

Grattage test and Auspitz sign: accentuation of
scales by grating with a glass slide (StepA) and
finally appearance of bleeding points (Step C).

Woronoff’s ring: vasoconstriction
around active plaques of psoriasis.
 Distribution: B/L symmetrical

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on extensors elbows, knees,
shin, knuckles, sacral areas and
scalp
Sometimes generalized.
Uniformity: plaques tend to
have same features irrespective of
site except on palms and soles,
and flexors.
Patterns seen: plaques are oval
or irregular in shape,
May coalesce together to form
large plaques, gyrate, polycyclic
and geographic plaques.
Central clearing results in
annular lesions.
Follicular, nummular, linear,
circinate pattern may be seen
Clinical variants
Guttate psoriasis
 Commonly seen in Childhood and young
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adults, (1.9% cases)
Streptococcal throat infection usually
precedes onset or flare up
Mildly itchy, small, drop – like, round to
oval, salmon – pink colored, papular
lesions with fine scales appear in crops,
Distributed more or less evenly over body,
on upper trunk and proximal limbs
Palms & soles are spared
Resolve spontaneously or may convert to
plaque form
If lesions enlarged to few cms. to form
coin shaped lesion k/a nummular
psoriasis
Rupioid, elephantine and ostraceous
psoriasis
 Plaques associated with gross hyperkeratosis.
 Rupioid psoriasis - Heaped up scales, so the lesions appear conical.

Scales are firmly adherent to underlying skin (limpet-like)
 Elephantine psoriasis Unusual but very persistent, thickly scaling,
large plaques that sometimes occur on back, limbs, hips
 Ostraceous psoriasis refers to a ring-like hyperkeratotic lesion with a
concave surface, resembling an oyster shell.
Unstable psoriasis
 Phases of disease in which activity is marked and course

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and immediate outcome unpredictable;
Previously stable and chronic form is exacerbated by
inappropriate management and threatens to become
erythrodermic or pustular,
Localized pustular or ill-defined erythematous lesions may
appear spontaneously for first time.
Patients may develop such unstable phases repeatedly,
Settling back again into classical forms of disease.
Withdrawal of intensive systemic or topical corticosteroid
therapy, hypocalcaemia, acute infection, overtreatment
with tar, dithranol or UV irradiation, and severe emotional
upset, may precipitate this condition.
Erythrodermic psoriasis
 Important cause of erythroderma (30%)
 Can evolve from pre-existing plaque psoriasis
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gradually or can occur suddenly
C/f – patient may be febrile and ill,
Generalized itching, intense erythema, and
superficial, fine, white scaling all over body
Edema, fissures, exudation and nail
dystrophy may be present
May lead to protein loss, hypo or
hyperthermia, dehydration, electrolyte
imbalance, renal failure and cardiac failure
Pustular psoriasis
 Localized pustular psoriasis
 (a) palmoplantar pustulosis
 Common in females
 Present as numerous, small, sterile pustules on
erythematous plaques, B/L symmetrically on
palms and soles
 Affected area is dusky red and often scaly.
 Removal of scale leaves a glazed dull-red
surface.
 Fresh pustules are yellow; older ones are
yellow-brown or Dark Brown as pustule dries.
 Desiccated pustule is exfoliated.
 Pustules in all stages of evolution are seen
 (b) acrodermatitis continua of

hallopeau
 Seen in children, more common in
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females.
Fingertips and toes show pustular
lesions over glazed erythema and
scaling
Nails may be destroyed
Osteolysis of distal phalanx can
occur
May evolve into generalized
pustular psoriasis, especially in
elderly
Acrodermatitis continua with destruction of nail plate.
 Generalized pustular psoriasis:
 Triggered by pregnancy, sudden steroid

withdrawal, infections, hypocalcaemia

 Severe form
 Characterized by multiple erythematous

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plaques studded with tiny, sterile pustules
that may coalesce to form lake of pus
Uninvolved skin may shows erythema and
pustules
May a/w fever, arthralgia and malaise
Pustules dry up and form scales or crusts
Lesions develop in crops

(a) acute (von Zumbusch)
(b) of pregnancy (Impetigo herpetiformis)
(c) infantile and juvenile
(d) circinate, annular and linear
(e) localized (not hands and feet).
Acute generalized pustular psoriasis.
Arthropathic psoriasis
 Arthritis is seronegative & inflammatory
 In 70% cases arthritis develops years after skin
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changes
In 10-15% cases precedes skin lesions
RF –ve ,HLA-B7 & B27 commonly found
Involve both peripheral joints & axial skeleton
causing pain, stiffness and swelling
Arthritis mutilans showing
a/w Loss of joint space, periostitis & lysis of
gross digital foreshortening
terminal phalanges
Clinically five type
Asymmetric oligoarthritis - commonest type, <5
joints
Symmetric polyarthritis - rheumatoid-like disease
, >5 joints
DIP joint arthritis ( most characteristic, but
relatively rare),
arthritis mutilans - causes destruction of bones
Spondyloarthritis - axial skeletal involvement,
peripheral oligoarthropathy with sausage-like digital swelling
Variations by site
 Scalp: (50%)
 Diffusely or discreetly involved in form of Well
difined, erythematous plaques with silvery
white, thick scaling, usually no hair loss.
 Sometimes, scaling is asbestos-like, being
firmly adherent to scalp (pityriasis
amiantacea)
 Penis:
 Solitary well-circumscribed reddish plaque
without scales on glans of uncircumcised
male.
 Flexural (inverse) psoriasis (2-6%)
 Lesions present over flexors and intertriginous
areas( axilla, groin, umbilical region,
inframammary folds)
 Extremely erythematous and lack typical
scaling.
 More common in older adults than children
 Difficult to differentiate from seborrhoeic
dermatitis, intertrigo, erythrasma and
candidiasis
 Hands and feet:
 Present as Diffuse hyperkeratotic,
erythematous, plaques on which a fine
silvery scale can be evoked by scratching;
 A Sharply defined edge at wrist or forearm
and absence of vesiculation are helpful.
 On dorsal surface, knuckles frequently
show a dull red thickening of the skin,
 Nails: involved in 25 to 50% of cases.
 Pits, ridges and grooves (psoriasis of nail
matrix)
 Onycholysis, subungual hyperkeratosis
and splinter haemorrhages (involvement
of nail bed or hyponychium)
 Circular areas of discoloration of nail bed
and hyponychium may resemble an ‘oil
drop’ below nail
 Thickened friable nail plate.
Atypical forms
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Digital and interdigital forms.
Verrucous forms - affect legs.
Follicular form - more common in elderly
Lichenoid forms
Linear forms
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As a part of Koebner phenomenon.

 Zonal lesions
 Koebner reaction at site of herpes zoster
 Seborrhoeic psoriasis
 Mucosal lesions
 True mucosal involvement is rare,
 But has been a/w pustular, erythrodermic and plaque form
 Ocular lesions
 Blepharitis, conjunctivitis, keratitis, xerosis, symblepharon,
trichiasis and Chronic uveitis have been recorded.
PITYRIASIS ROSEA
 Is an acute, self limiting skin eruption with distinctive
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and constant course
Incidence: .3-3%
Age: 10-35 years
Sex: M=F
Etiology: Unknown
Infections Picorna virus, HHV 6, HHV 7,
Drug : e.g. Arsenic, Barbiturates, Gold, Bismuth,
Captopril, Ketotifen, Metronidazole, D-penicillamine,
Terbinafine may cause eruption similar to PR
Atopy
CLINICAL FEATURES

May or may not be present

. Located on trunk
Within 10 day of herald patch, secondary plaques appears
Pityriasis rosea: distribution of lesions
on trunk in a typical fir tree appearance.
 Atypical PR (20% of patients), herald patch may be missing or
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confluent with other lesions.
Distribution of rash may be peripheral, and facial involvement
may be seen in children.
Involvement of the axilla and groin (inverse variant)
TYPES of lesion:
 PR gigantea
 PR urticata
 Vesicular
 Pustular
 Purpuric
 Erythema multiforme–like.
Oral lesions of various types have been reported, including
erythematous plaques, hemorrhagic puncta, and ulcers.
LICHEN PLANUS
ETIOPATHOGENESIS
 Not clear, multifactorial
 Infection: may be a/w syphilis, HSV2, HCV, amoebiasis,

and chronic bladder infection
 Psychosomatic: stress and/or anxiety are possibly a/w LP
 Allergic: contact sensitizers and haptens may play a role in
inciting LP
 Immunologically mediated:
 Primary site of immunologic reactivity may be basal

keratinocytes whose new antigen are processed by langerhans
cells and presented to helper / inducer T cells.
 CMI is of primary importance in LP and humoral immunity is
secondary

 Genetic factors: increased incidence of HLA A3, A5, B7,

HLA 28, HLA DR1, DR10, DRB1*0101 is seen
Association of LP
 With diseases of altered or disturbed immunity
 Ulcerative colitis,
 Alopecia areata,
 Vitiligo,
 Dermatomyositis,
 Morphoea
 Lichen sclerosus,
 Systemic lupus erythematosus,
 Pemphigus and paraneoplastic pemphigus,
 Thymoma,
 Myasthenia gravis,
 Hypogammaglobulinaemia,
 Primary biliary cirrhosis
Histology
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Compact hyperkeratosis.
Wedge-shaped hypergranulosis
Irregular acanthosis
Focal increase in thickness of granular
layer and infiltrate corresponds to presence
of Wickham’s striae
Degenerating basal epidermal cells are
transformed into colloid bodies (15–20 µm)
which appear singly or in clumps
Rete ridges may appear flattened or effaced
(‘saw-tooth’ appearance), and focal
separation from dermis may lead to Max
Joseph spaces
Band-like infiltrate of lymphocytes and
histiocytes, admixed with plasma cells
obliterates DEJ.
Epidermal melanocytes are absent or
considerably decreased in number
Pigmentary incontinence with dermal
melanophages is characteristic.
Lichen planus C/f:
 Symptoms: Intensely itchy
 Morphology: Shiny, Flat topped, polygonal, violaceous papules
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of variable size (pinpoint to cms.)
Wickham’s striae: fine whitish reticulated network present
Scaling: Minimal
Grouping: may remain descrete or may be arrnged in groups, in
lines or in circles
Site: Flexures and extremities (Wrists, shins); examine mucosa,
scalp, nails
Distribution: B/L symmetrical
Mucous membrane involvement: Common (30 – 70%)
White streaks forming a lacework on buccal mucosa are
characteristic
koebner phenomenon : common
Papules resolve leaving hyperpigmentation
Clinical variants
Lesional morphology
Hypertrophic LP
Atrophic LP
Guttate LP
Follicular LP (Lichen
planopilaris)
Linear LP
Annular LP
Zosteriform LP
Vesiculobullous LP
Ulcerative (erosive)
LP pigmentosus

Site of involvement
Mucosal (oral, genital)
Palmoplanter
Nail
Scalp
inverse

Special form
Actinic LP
Lichen planus pemphigodes
(30-70%, Oral up to 65%, genital 25%)
SCALP LESIONS
Follicular lesions of LP on scalp subside with
scarring and result in cicatricial (scarring) alopecia
nails show thinning, distal
splitting, tenting of nail plate
and pterygium formation,
pterygium forms due to wingshaped prolongation of
proximal nail fold onto nail bed,
splitting and eventually
destroying nail plate.
Lichenoid drug eruption
 Develop over weeks to month after starting
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therapy
Lesions larger
Scaling prominent but Wickham’s striae
absent
Widely distributed but predilection for
sun-exposed areas, face and upper trunk
Mucous membrane involvement less
common
Residual hyperpigmentation common
Alopecia: common
H/P: focal parakeratosis, focal absence of
granular layer, interface infiltrate is less
dense and pleomorphic, colloid bodies are
more numerous

Drugs
Heavy metals
Antimalarials
Antibiotics
Antitubercular drugs
Diuretics
Antihypertensives
Beta blockers
ACEIs
CCBs
Anticovulsant
NSAIDs
Lipid lowering agents
Isotretinoin
Zidovudine
Ranitidine
Chlorpheniramine
PUVA therapy
Lichen nitidus
 Rarer condition than idiopathic LP
 Seen in children and young adults
 Asymptomatic, monomorphic, tiny (pin point

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to pin head sized), multiple, flat or dome
shaped, skin-colored shiny papules
Wickham’s striae: absent
Usually discrete but may occur in Groups
Seen on forearms, wrists, penis, abdomen,
chest, buttocks and knees
May be seen over palm and soles
Koebnerization may be present
Mucous membrane involvement: uncommon
Healing occurs without scarring and
pigmentary changes
 Intense infiltrate situated

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immediately below epidermis
and is well circumscribed.
Infiltrate consists of lymphocytes
and histiocytes and few
Langhans’ giant cells
Overlying epidermis is flattened
Liquefaction degeneration of
basal cell
Focally dense infiltrate containing a
Rete ridges at margin of infiltrate few giant cells
are elongated and tend to
encircle it (claw clutching a ball)
Lichen striatus
 Self-limiting, inflammatory, linear dermatitis of
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unknown origin
Develop in lines of Blaschko
Over 50% of cases occur B/w ages of 5 and 15 years,
Females are affected two or three times more.
Small, pink, lichenoid papules, discrete at first but
rapidly coalescing,
Appear suddenly and extend over course of a week or
more to form a dull-red, slightly scaly, Linear band,
usually 2 mm to 2 cm in width,
Parallel linear or zosteriform Patterns may be seen
No Wickham’s striae.
Occur most commonly on one arm or leg, or on neck, but
may develop on trunk.
Involvement of the nails may result in longitudinal
ridging, splitting, Onycholysis or nail loss
Usually no symptoms, pruritic occasionally
Course is variable.
Seborrheic dermatitis
 Chronic dermatitis,
 Red, sharply marginated lesions covered with greasy
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looking scales
Distributed in areas with a rich supply of sebaceous glands,
Dandruff (visible desquamation from scalp surface) appears
to be the precursor of seborrhoeic dermatitis, and this may
gradually progress through redness, irritation and
increasing scaling of scalp to true seborrhoeic dermatitis.
Involve scalp, face, presternal and interscapular regions,
and the flexures.
Lesions tend to be dull or yellowish red in color and
covered with greasy scales.
Clinical pattern of Seborrheic dermatitis
Pityriasis Rubra Pilaris (PRP)
 Uncommon Chronic papulosquamous disorder
 Characterized by reddish orange scaly papules, acuminate
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follicular papules and palmoplanter keratoderma
Etiology
Unknown in most patients.
Familial in a few patients.
Abnormality of vit. A metabolism and Immunological
abnormality, bacterial and viral infections has been blamed
Prevalence: 1 in 5000 population
Age: Occurs in three age groups:
early childhood (upto 10 Yrs0, late childhood (11 – 19
Yrs), adulthood in fifth decade
Gender: adult M=F, children M>F
Classification
 Classical adult type. M/C type, seen in >50% cases, has
cephalocaudal progression, good prognosis, spontaneous
resolution in 80% within 1-3Yrs
 Atypical adult type. 5% of cases, icthyosiform scaling
scalp hair sparse, persists for long time
 Classical juvenile type. Starts in first two Yrs of life, seen
in10% cases, spontaneous resolution in 1-2 Yrs
 Circumscribed juvenile type. Seen on elbows and knees,
seen in 25% of cases
 Atypical juvenile type. begins at birth or in first Yr of life,
erythematous follicular hyperkeratosis and scleroderma
like changes seen in hands and feet, seen in 5% cases,
familial PRP
 HIV associated PRP: shows pustular, acneform and
nodulocystic lesions, elongated follicular plugs are seen
Clinical Features
 Widespread, small, acuminate follicular papules with
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pinkish scales
Coalesce to form plaques with islands of normal skin
Present symmetrically on trunk and limbs
Scalp shows diffuse erythema and scaling
PRP begins at scalp and then descends down to whole
trunk with islands of normal skin
Dorsal aspect of proximal phalanges show follicular
hyperkeratosis, surrounded by erythematous
perifollicular halo
Palpation of lesions give a sensation of nutmeg greater
Scaling is fine and branny
Palms and soles: yellowish orange hyperkeratosis with
painful fissures
Nails: thickened brittle with longitudinal ridging and
splinter hemorrhage
Oral mucosa rarely may show diffuse, lacy white
plaques
Pityriasis Lichenoides
Course: chronic, remissions and relapses
 Etiology Unknown, may be hypersensitivity to infectious agents.
 Clinical Manifestations
 Two clinical patterns recognized:
 Pityriasis lichenoides et varioliformis acuta (PLEVA)
 Constitutional symptoms like fever and arthralgia frequent.
 Polymorphic eruption of multiple, erythematous, edematous papules,

often surmounted by vesicles.
 Pustules/hemorrhagic necrosis may develop
 Lesions heal with hyperpigmented varioliform scars.
 Trunk and flexures of extremities.

 Pityriasis lichenoides chronica (PLC).
 Polymorphic eruption of successive crops of asymptomatic red-brown
papules, which are surmounted by a central, adherent mica-like Scale
 Lesions heal with hypopigmentation.
 Trunk and proximal part of extremities.
pityriasis lichenoides et
varioliformis edematous
papules surmounted with
hemorrhagic crust.
Note scarring

pityriasis lichenoides chronica:
red brown papules surmounted
by mica-like scales. Note
hypopigmentation.
Erythroderma (exfoliative dermatitis )
 Erythroderma is the term applied to any inflammatory skin
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disease that affects more than 90% of body surface.
Incidence: 0.9 per 100 000 population
Age: frequently seen in age group 40–60 years.
Ichthyosiform variant seen in children.
Gender:
Male:female ratio of 2:1
Etiology
Underlying skin diseases: Erythroderma can be a late
manifestation in clinical course of several skin disease
Idiopathic: no underlying cause can be determined.
 Clinical Features
 Extremely itchy.
 In erythroderma secondary to other skin
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diseases, there may be evidence of primary
disease on clinical examination.
Intense erythema and scaling
Scales may be small or large and their color
may vary from white to yellow.
Associated features
Alopecia, Shiny and beveled nails initially,
Dystrophic nails and shedding of nails.
Palmoplantar involvement with massive
hyperkeratosis.
Lymphadenopathy (in 50% of patients),
Hepatomegaly and splenomegaly
(occasionally).
Lesions of underlying disease.
Secondary syphilis
 History of preceding high-risk

sexual contact / genital ulcer
 Maculopapular and
papulosquamous lesions
Associated features
 Mucosal lesions
 Coppery scaly papules on palms and
soles
 Condyloma lata
 Lymphadenopathy
 Serology for syphilis and dark
ground microscopy: positive
Discoid lupus erythematosus (DLE)
 Symptoms: photosensitivity present
 Morphology: annular lesions with central scarring and

an erythematous halo
 Scaling: adherent and prominent
 Typical feature: follicular plugging
 Site: face, ears; scalp, lip
Parapsoriasis
 Parapsoriasis is a controversial term used for a heterogeneous group of













dermatoses.
Small plaque parapsoriasis: benign.
Large plaque parapsoriasis: premalignant
Etiology: Unknown.
Prevalence: Uncommon.
Age: Fifth decade.
Gender: Male preponderance.
Clinical Features
Morphology
Small plaque parapsoriasis
Asymmetrical, yellow-erythematous, scaly plaques, which are small (<5
cm) and have digitating margins.
Predominantly on covered parts of body (abdomen, buttocks, breasts
and flexures).
Runs a chronic course, usually responding to treatment and relapsing
when treatment is stopped.
 Large plaque parapsoriasis
 Initially asymmetrical,
erythematous, scaly plaques , quite
similar to lesions of small plaque
parapsoriasis except being larger (>5
cm) and more erythematous.
 Presence of poikiloderma and
induration in lesions suggestive of
malignant transformation.
 Predominantly on covered parts of
body.
 Course
 Both variants run a chronic course;
over period of time

Large plaque parapsoriasis:
erythematous, scaly, indurated
plaques on covered parts of body.
Morphology of papules/plaques in papulosquamous disorders
Psoriasis

Erythematous papules and plaques

Lichen planus

Violaceous papules with Wickham’s striae

Pityriasis rosea

Annular plaques

Seborrheic dermatitis

Yellowish, follicular papules

Pityriasis rubra pilaris

Erythematous follicular papules

Secondary syphilis

Dusky erythematous papules

Pityriasis lichenoides et
varioliformis acuta

Erythematous edematous papules surmounted
with vesicles/crust

Pityriasis lichenoides
chronica

Erythematous papules surmounted with micalike scales
Characteristics of scales in papulosquamous disorders
Psoriasis

Silvery scales
Collarette of scales on leading edge

Pityriasis rosea
Seborrheic dermatitis

Greasy scales

Pityriasis lichenoides
chronica

Mica-like, adherent scales
Guide to Diagnosing Papulosquamous Disorders

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Guide to Diagnosing Papulosquamous Disorders

  • 2. Introduction  Group of diseases in which primary lesion is most commonly a papule,  Usually erythematous, with a variable degree of scaling on surface  Plaques form through coalescing of primary lesions  Both morphology of papule and character of scale give clues to making a diagnosis
  • 3. Papulosquamous disorders Psoriasis Lichen Planus Pityriasis rosea Parapsoriasis eg. small / large plaque pityriasis rubra pilaris Lichen nitidus Pityriasis lichenoides Lichen striatus Exfoliative dermatitis Seborrheic dermatitis
  • 4.  Other important papulosquamous diseases • • • • • • • • • • • • • Mycosis fungoides (cutaneous T-cell lymphoma) Discoid lupus erythematosus Subacute cutaneous lupus erythematosus Tinea corporis Nummular eczema Secondary syphilis Drug eruptions Erythema dyschromicum perstans Keratosis lichenoides chronica Lichen sclerosus Lichenoid dermatitis Lichenoid reaction of graft-versus-host disease Extramammary Paget’s disease
  • 5.      Common, Chronic, Disfiguring, Inflammatory & Proliferative, Genetically and environmentally influenced condition of skin and joints  Unpredictable course  Remissions & exacerbations : Epidemiology Prevalence 0.1- 3%. Bimodal age distribution. Type I – 75%, 15 - 40 Yr of age Type II ─ >40 Yr of age No gender predilection. Develop earlier in women Winter aggravation frequent.
  • 6.  Exact cause-unknown  Genetic predisposition  Precipitating factors  Immunopathogenesis  Epidermal hyperplasia  Vascular changes Genetic Background ↓↓ Provocating Factors ↓↓ Exogenous/Endogenous antigens ↓↓ Antigen presentation by APCs ↓↓ T lymphocyte- mediated Immune response ↓↓ Secretion of cytokines ↓↓ Inflammation & cellular hyperproliferation ↓↓ Clinical Lesions of psoriasis
  • 7. Causes and Pathogenesis • • • • • Genetic predisposition - 30% have first degree relative, Seen in 65% of identical twins, More frequency of HLA-B 13, HLA-B17, HLA-Cw6 is seen, 9 psoriasis susceptibility loci on different chromosomes have been identified (PSORS 1-9) Environmental trigger – • Trauma • Infection - streptococcal infection often triggers guttate and plaque psoriasis. Others are HCV, HIV, HSV, CMV • Hormonal - Psoriasis frequently improves in pregnancy and relapse postpartum. • Drugs - Antimalarials, beta-blockers, NSAIDs ACEIs and lithium may worsen psoriasis. withdrawal of systemic steroids or potent topical steroids. • Others – Sunlight, smoking and alcohol intake, Emotional upset and hypocalcemia • Obesity - Excess weight increases risk of inverse psoriasis
  • 8. Disorder of excessive growth and reproduction of skin cells Effector cytokine IL-2,IL-17,IL22,INF-γ and TNF-α leads to •Shortening of cell cycle 8 times •Proliferative cell increase 2 times •Germinative cell enter growth fraction100 % Immune-mediated disorder Both of these abnormalities can induce other, Leading to a vicious cycle of keratinocyte proliferation and inflammatory reaction, But it is still not clear which is primary defect.
  • 9. Pathology:  Hyperkeratosis and parakeratosis with focal orthokeratosis and        Munro microabscess formation Near absent granular layer. Spongiform pustules of kogoj in Malpighian layer Acanthosis Rete ridges: elongated and clubbed, branched or fused at their bases, Suprapapillary epidermal thinning Infiltrate: mononuclear leukocyte infiltrates in lower half of epidermis and in upper dermis and polymorphs in upper epidermis Dilated, tortuous papillary blood vessels
  • 10.
  • 11. Morphology of Chronic plaque psoriasis (psoriasis vulgaris):  Well-defined with distinct border.  Erythematous (salmon pink) papules and plaques of variable size  Covered with a silvery white, loosely adherent scales, accentuated by grating lesions  Which on removal may reveal punctate bleeding points (Auspitz sign),
  • 12.  Isomorphic (koebner)      phenomenon is positive in 38 – 76% of cases. Koebner reaction may also be found in other dermatoses like, lichen planus, lichen nitidus and vitiligo. Reverse koebner phenomenon may be seen. Itching is variable. In Resolving lesions a peripheral halo around lesion, woronoff ring may be seen. Resolved lesion may show post inflammatory hypomelanosis
  • 13. Psoriasis vulgaris: typical plaque which is welldefined, discoid, erythematous, indurated and surmounted with loose silvery scales Psoriasis vulgaris: discoid lesions become confluent to give rise to gyrate and polycyclic lesions. Grattage test and Auspitz sign: accentuation of scales by grating with a glass slide (StepA) and finally appearance of bleeding points (Step C). Woronoff’s ring: vasoconstriction around active plaques of psoriasis.
  • 14.  Distribution: B/L symmetrical       on extensors elbows, knees, shin, knuckles, sacral areas and scalp Sometimes generalized. Uniformity: plaques tend to have same features irrespective of site except on palms and soles, and flexors. Patterns seen: plaques are oval or irregular in shape, May coalesce together to form large plaques, gyrate, polycyclic and geographic plaques. Central clearing results in annular lesions. Follicular, nummular, linear, circinate pattern may be seen
  • 15. Clinical variants Guttate psoriasis  Commonly seen in Childhood and young       adults, (1.9% cases) Streptococcal throat infection usually precedes onset or flare up Mildly itchy, small, drop – like, round to oval, salmon – pink colored, papular lesions with fine scales appear in crops, Distributed more or less evenly over body, on upper trunk and proximal limbs Palms & soles are spared Resolve spontaneously or may convert to plaque form If lesions enlarged to few cms. to form coin shaped lesion k/a nummular psoriasis
  • 16. Rupioid, elephantine and ostraceous psoriasis  Plaques associated with gross hyperkeratosis.  Rupioid psoriasis - Heaped up scales, so the lesions appear conical. Scales are firmly adherent to underlying skin (limpet-like)  Elephantine psoriasis Unusual but very persistent, thickly scaling, large plaques that sometimes occur on back, limbs, hips  Ostraceous psoriasis refers to a ring-like hyperkeratotic lesion with a concave surface, resembling an oyster shell.
  • 17. Unstable psoriasis  Phases of disease in which activity is marked and course      and immediate outcome unpredictable; Previously stable and chronic form is exacerbated by inappropriate management and threatens to become erythrodermic or pustular, Localized pustular or ill-defined erythematous lesions may appear spontaneously for first time. Patients may develop such unstable phases repeatedly, Settling back again into classical forms of disease. Withdrawal of intensive systemic or topical corticosteroid therapy, hypocalcaemia, acute infection, overtreatment with tar, dithranol or UV irradiation, and severe emotional upset, may precipitate this condition.
  • 18. Erythrodermic psoriasis  Important cause of erythroderma (30%)  Can evolve from pre-existing plaque psoriasis     gradually or can occur suddenly C/f – patient may be febrile and ill, Generalized itching, intense erythema, and superficial, fine, white scaling all over body Edema, fissures, exudation and nail dystrophy may be present May lead to protein loss, hypo or hyperthermia, dehydration, electrolyte imbalance, renal failure and cardiac failure
  • 19. Pustular psoriasis  Localized pustular psoriasis  (a) palmoplantar pustulosis  Common in females  Present as numerous, small, sterile pustules on erythematous plaques, B/L symmetrically on palms and soles  Affected area is dusky red and often scaly.  Removal of scale leaves a glazed dull-red surface.  Fresh pustules are yellow; older ones are yellow-brown or Dark Brown as pustule dries.  Desiccated pustule is exfoliated.  Pustules in all stages of evolution are seen
  • 20.  (b) acrodermatitis continua of hallopeau  Seen in children, more common in     females. Fingertips and toes show pustular lesions over glazed erythema and scaling Nails may be destroyed Osteolysis of distal phalanx can occur May evolve into generalized pustular psoriasis, especially in elderly Acrodermatitis continua with destruction of nail plate.
  • 21.  Generalized pustular psoriasis:  Triggered by pregnancy, sudden steroid withdrawal, infections, hypocalcaemia  Severe form  Characterized by multiple erythematous          plaques studded with tiny, sterile pustules that may coalesce to form lake of pus Uninvolved skin may shows erythema and pustules May a/w fever, arthralgia and malaise Pustules dry up and form scales or crusts Lesions develop in crops (a) acute (von Zumbusch) (b) of pregnancy (Impetigo herpetiformis) (c) infantile and juvenile (d) circinate, annular and linear (e) localized (not hands and feet). Acute generalized pustular psoriasis.
  • 22. Arthropathic psoriasis  Arthritis is seronegative & inflammatory  In 70% cases arthritis develops years after skin           changes In 10-15% cases precedes skin lesions RF –ve ,HLA-B7 & B27 commonly found Involve both peripheral joints & axial skeleton causing pain, stiffness and swelling Arthritis mutilans showing a/w Loss of joint space, periostitis & lysis of gross digital foreshortening terminal phalanges Clinically five type Asymmetric oligoarthritis - commonest type, <5 joints Symmetric polyarthritis - rheumatoid-like disease , >5 joints DIP joint arthritis ( most characteristic, but relatively rare), arthritis mutilans - causes destruction of bones Spondyloarthritis - axial skeletal involvement, peripheral oligoarthropathy with sausage-like digital swelling
  • 23. Variations by site  Scalp: (50%)  Diffusely or discreetly involved in form of Well difined, erythematous plaques with silvery white, thick scaling, usually no hair loss.  Sometimes, scaling is asbestos-like, being firmly adherent to scalp (pityriasis amiantacea)  Penis:  Solitary well-circumscribed reddish plaque without scales on glans of uncircumcised male.  Flexural (inverse) psoriasis (2-6%)  Lesions present over flexors and intertriginous areas( axilla, groin, umbilical region, inframammary folds)  Extremely erythematous and lack typical scaling.  More common in older adults than children  Difficult to differentiate from seborrhoeic dermatitis, intertrigo, erythrasma and candidiasis
  • 24.  Hands and feet:  Present as Diffuse hyperkeratotic, erythematous, plaques on which a fine silvery scale can be evoked by scratching;  A Sharply defined edge at wrist or forearm and absence of vesiculation are helpful.  On dorsal surface, knuckles frequently show a dull red thickening of the skin,  Nails: involved in 25 to 50% of cases.  Pits, ridges and grooves (psoriasis of nail matrix)  Onycholysis, subungual hyperkeratosis and splinter haemorrhages (involvement of nail bed or hyponychium)  Circular areas of discoloration of nail bed and hyponychium may resemble an ‘oil drop’ below nail  Thickened friable nail plate.
  • 25. Atypical forms      Digital and interdigital forms. Verrucous forms - affect legs. Follicular form - more common in elderly Lichenoid forms Linear forms  As a part of Koebner phenomenon.  Zonal lesions  Koebner reaction at site of herpes zoster  Seborrhoeic psoriasis  Mucosal lesions  True mucosal involvement is rare,  But has been a/w pustular, erythrodermic and plaque form  Ocular lesions  Blepharitis, conjunctivitis, keratitis, xerosis, symblepharon, trichiasis and Chronic uveitis have been recorded.
  • 26. PITYRIASIS ROSEA  Is an acute, self limiting skin eruption with distinctive        and constant course Incidence: .3-3% Age: 10-35 years Sex: M=F Etiology: Unknown Infections Picorna virus, HHV 6, HHV 7, Drug : e.g. Arsenic, Barbiturates, Gold, Bismuth, Captopril, Ketotifen, Metronidazole, D-penicillamine, Terbinafine may cause eruption similar to PR Atopy
  • 27. CLINICAL FEATURES May or may not be present . Located on trunk
  • 28. Within 10 day of herald patch, secondary plaques appears
  • 29. Pityriasis rosea: distribution of lesions on trunk in a typical fir tree appearance.
  • 30.
  • 31.  Atypical PR (20% of patients), herald patch may be missing or     confluent with other lesions. Distribution of rash may be peripheral, and facial involvement may be seen in children. Involvement of the axilla and groin (inverse variant) TYPES of lesion:  PR gigantea  PR urticata  Vesicular  Pustular  Purpuric  Erythema multiforme–like. Oral lesions of various types have been reported, including erythematous plaques, hemorrhagic puncta, and ulcers.
  • 32.
  • 34. ETIOPATHOGENESIS  Not clear, multifactorial  Infection: may be a/w syphilis, HSV2, HCV, amoebiasis, and chronic bladder infection  Psychosomatic: stress and/or anxiety are possibly a/w LP  Allergic: contact sensitizers and haptens may play a role in inciting LP  Immunologically mediated:  Primary site of immunologic reactivity may be basal keratinocytes whose new antigen are processed by langerhans cells and presented to helper / inducer T cells.  CMI is of primary importance in LP and humoral immunity is secondary  Genetic factors: increased incidence of HLA A3, A5, B7, HLA 28, HLA DR1, DR10, DRB1*0101 is seen
  • 35. Association of LP  With diseases of altered or disturbed immunity  Ulcerative colitis,  Alopecia areata,  Vitiligo,  Dermatomyositis,  Morphoea  Lichen sclerosus,  Systemic lupus erythematosus,  Pemphigus and paraneoplastic pemphigus,  Thymoma,  Myasthenia gravis,  Hypogammaglobulinaemia,  Primary biliary cirrhosis
  • 36. Histology          Compact hyperkeratosis. Wedge-shaped hypergranulosis Irregular acanthosis Focal increase in thickness of granular layer and infiltrate corresponds to presence of Wickham’s striae Degenerating basal epidermal cells are transformed into colloid bodies (15–20 µm) which appear singly or in clumps Rete ridges may appear flattened or effaced (‘saw-tooth’ appearance), and focal separation from dermis may lead to Max Joseph spaces Band-like infiltrate of lymphocytes and histiocytes, admixed with plasma cells obliterates DEJ. Epidermal melanocytes are absent or considerably decreased in number Pigmentary incontinence with dermal melanophages is characteristic.
  • 37. Lichen planus C/f:  Symptoms: Intensely itchy  Morphology: Shiny, Flat topped, polygonal, violaceous papules          of variable size (pinpoint to cms.) Wickham’s striae: fine whitish reticulated network present Scaling: Minimal Grouping: may remain descrete or may be arrnged in groups, in lines or in circles Site: Flexures and extremities (Wrists, shins); examine mucosa, scalp, nails Distribution: B/L symmetrical Mucous membrane involvement: Common (30 – 70%) White streaks forming a lacework on buccal mucosa are characteristic koebner phenomenon : common Papules resolve leaving hyperpigmentation
  • 38. Clinical variants Lesional morphology Hypertrophic LP Atrophic LP Guttate LP Follicular LP (Lichen planopilaris) Linear LP Annular LP Zosteriform LP Vesiculobullous LP Ulcerative (erosive) LP pigmentosus Site of involvement Mucosal (oral, genital) Palmoplanter Nail Scalp inverse Special form Actinic LP Lichen planus pemphigodes
  • 39.
  • 40.
  • 41.
  • 42. (30-70%, Oral up to 65%, genital 25%)
  • 43.
  • 44. SCALP LESIONS Follicular lesions of LP on scalp subside with scarring and result in cicatricial (scarring) alopecia
  • 45. nails show thinning, distal splitting, tenting of nail plate and pterygium formation, pterygium forms due to wingshaped prolongation of proximal nail fold onto nail bed, splitting and eventually destroying nail plate.
  • 46. Lichenoid drug eruption  Develop over weeks to month after starting        therapy Lesions larger Scaling prominent but Wickham’s striae absent Widely distributed but predilection for sun-exposed areas, face and upper trunk Mucous membrane involvement less common Residual hyperpigmentation common Alopecia: common H/P: focal parakeratosis, focal absence of granular layer, interface infiltrate is less dense and pleomorphic, colloid bodies are more numerous Drugs Heavy metals Antimalarials Antibiotics Antitubercular drugs Diuretics Antihypertensives Beta blockers ACEIs CCBs Anticovulsant NSAIDs Lipid lowering agents Isotretinoin Zidovudine Ranitidine Chlorpheniramine PUVA therapy
  • 47. Lichen nitidus  Rarer condition than idiopathic LP  Seen in children and young adults  Asymptomatic, monomorphic, tiny (pin point        to pin head sized), multiple, flat or dome shaped, skin-colored shiny papules Wickham’s striae: absent Usually discrete but may occur in Groups Seen on forearms, wrists, penis, abdomen, chest, buttocks and knees May be seen over palm and soles Koebnerization may be present Mucous membrane involvement: uncommon Healing occurs without scarring and pigmentary changes
  • 48.  Intense infiltrate situated     immediately below epidermis and is well circumscribed. Infiltrate consists of lymphocytes and histiocytes and few Langhans’ giant cells Overlying epidermis is flattened Liquefaction degeneration of basal cell Focally dense infiltrate containing a Rete ridges at margin of infiltrate few giant cells are elongated and tend to encircle it (claw clutching a ball)
  • 49. Lichen striatus  Self-limiting, inflammatory, linear dermatitis of            unknown origin Develop in lines of Blaschko Over 50% of cases occur B/w ages of 5 and 15 years, Females are affected two or three times more. Small, pink, lichenoid papules, discrete at first but rapidly coalescing, Appear suddenly and extend over course of a week or more to form a dull-red, slightly scaly, Linear band, usually 2 mm to 2 cm in width, Parallel linear or zosteriform Patterns may be seen No Wickham’s striae. Occur most commonly on one arm or leg, or on neck, but may develop on trunk. Involvement of the nails may result in longitudinal ridging, splitting, Onycholysis or nail loss Usually no symptoms, pruritic occasionally Course is variable.
  • 50. Seborrheic dermatitis  Chronic dermatitis,  Red, sharply marginated lesions covered with greasy    looking scales Distributed in areas with a rich supply of sebaceous glands, Dandruff (visible desquamation from scalp surface) appears to be the precursor of seborrhoeic dermatitis, and this may gradually progress through redness, irritation and increasing scaling of scalp to true seborrhoeic dermatitis. Involve scalp, face, presternal and interscapular regions, and the flexures. Lesions tend to be dull or yellowish red in color and covered with greasy scales.
  • 51. Clinical pattern of Seborrheic dermatitis
  • 52.
  • 53. Pityriasis Rubra Pilaris (PRP)  Uncommon Chronic papulosquamous disorder  Characterized by reddish orange scaly papules, acuminate         follicular papules and palmoplanter keratoderma Etiology Unknown in most patients. Familial in a few patients. Abnormality of vit. A metabolism and Immunological abnormality, bacterial and viral infections has been blamed Prevalence: 1 in 5000 population Age: Occurs in three age groups: early childhood (upto 10 Yrs0, late childhood (11 – 19 Yrs), adulthood in fifth decade Gender: adult M=F, children M>F
  • 54. Classification  Classical adult type. M/C type, seen in >50% cases, has cephalocaudal progression, good prognosis, spontaneous resolution in 80% within 1-3Yrs  Atypical adult type. 5% of cases, icthyosiform scaling scalp hair sparse, persists for long time  Classical juvenile type. Starts in first two Yrs of life, seen in10% cases, spontaneous resolution in 1-2 Yrs  Circumscribed juvenile type. Seen on elbows and knees, seen in 25% of cases  Atypical juvenile type. begins at birth or in first Yr of life, erythematous follicular hyperkeratosis and scleroderma like changes seen in hands and feet, seen in 5% cases, familial PRP  HIV associated PRP: shows pustular, acneform and nodulocystic lesions, elongated follicular plugs are seen
  • 55. Clinical Features  Widespread, small, acuminate follicular papules with           pinkish scales Coalesce to form plaques with islands of normal skin Present symmetrically on trunk and limbs Scalp shows diffuse erythema and scaling PRP begins at scalp and then descends down to whole trunk with islands of normal skin Dorsal aspect of proximal phalanges show follicular hyperkeratosis, surrounded by erythematous perifollicular halo Palpation of lesions give a sensation of nutmeg greater Scaling is fine and branny Palms and soles: yellowish orange hyperkeratosis with painful fissures Nails: thickened brittle with longitudinal ridging and splinter hemorrhage Oral mucosa rarely may show diffuse, lacy white plaques
  • 56. Pityriasis Lichenoides Course: chronic, remissions and relapses  Etiology Unknown, may be hypersensitivity to infectious agents.  Clinical Manifestations  Two clinical patterns recognized:  Pityriasis lichenoides et varioliformis acuta (PLEVA)  Constitutional symptoms like fever and arthralgia frequent.  Polymorphic eruption of multiple, erythematous, edematous papules, often surmounted by vesicles.  Pustules/hemorrhagic necrosis may develop  Lesions heal with hyperpigmented varioliform scars.  Trunk and flexures of extremities.  Pityriasis lichenoides chronica (PLC).  Polymorphic eruption of successive crops of asymptomatic red-brown papules, which are surmounted by a central, adherent mica-like Scale  Lesions heal with hypopigmentation.  Trunk and proximal part of extremities.
  • 57. pityriasis lichenoides et varioliformis edematous papules surmounted with hemorrhagic crust. Note scarring pityriasis lichenoides chronica: red brown papules surmounted by mica-like scales. Note hypopigmentation.
  • 58. Erythroderma (exfoliative dermatitis )  Erythroderma is the term applied to any inflammatory skin         disease that affects more than 90% of body surface. Incidence: 0.9 per 100 000 population Age: frequently seen in age group 40–60 years. Ichthyosiform variant seen in children. Gender: Male:female ratio of 2:1 Etiology Underlying skin diseases: Erythroderma can be a late manifestation in clinical course of several skin disease Idiopathic: no underlying cause can be determined.
  • 59.
  • 60.  Clinical Features  Extremely itchy.  In erythroderma secondary to other skin        diseases, there may be evidence of primary disease on clinical examination. Intense erythema and scaling Scales may be small or large and their color may vary from white to yellow. Associated features Alopecia, Shiny and beveled nails initially, Dystrophic nails and shedding of nails. Palmoplantar involvement with massive hyperkeratosis. Lymphadenopathy (in 50% of patients), Hepatomegaly and splenomegaly (occasionally). Lesions of underlying disease.
  • 61. Secondary syphilis  History of preceding high-risk sexual contact / genital ulcer  Maculopapular and papulosquamous lesions Associated features  Mucosal lesions  Coppery scaly papules on palms and soles  Condyloma lata  Lymphadenopathy  Serology for syphilis and dark ground microscopy: positive
  • 62. Discoid lupus erythematosus (DLE)  Symptoms: photosensitivity present  Morphology: annular lesions with central scarring and an erythematous halo  Scaling: adherent and prominent  Typical feature: follicular plugging  Site: face, ears; scalp, lip
  • 63. Parapsoriasis  Parapsoriasis is a controversial term used for a heterogeneous group of             dermatoses. Small plaque parapsoriasis: benign. Large plaque parapsoriasis: premalignant Etiology: Unknown. Prevalence: Uncommon. Age: Fifth decade. Gender: Male preponderance. Clinical Features Morphology Small plaque parapsoriasis Asymmetrical, yellow-erythematous, scaly plaques, which are small (<5 cm) and have digitating margins. Predominantly on covered parts of body (abdomen, buttocks, breasts and flexures). Runs a chronic course, usually responding to treatment and relapsing when treatment is stopped.
  • 64.  Large plaque parapsoriasis  Initially asymmetrical, erythematous, scaly plaques , quite similar to lesions of small plaque parapsoriasis except being larger (>5 cm) and more erythematous.  Presence of poikiloderma and induration in lesions suggestive of malignant transformation.  Predominantly on covered parts of body.  Course  Both variants run a chronic course; over period of time Large plaque parapsoriasis: erythematous, scaly, indurated plaques on covered parts of body.
  • 65. Morphology of papules/plaques in papulosquamous disorders Psoriasis Erythematous papules and plaques Lichen planus Violaceous papules with Wickham’s striae Pityriasis rosea Annular plaques Seborrheic dermatitis Yellowish, follicular papules Pityriasis rubra pilaris Erythematous follicular papules Secondary syphilis Dusky erythematous papules Pityriasis lichenoides et varioliformis acuta Erythematous edematous papules surmounted with vesicles/crust Pityriasis lichenoides chronica Erythematous papules surmounted with micalike scales
  • 66. Characteristics of scales in papulosquamous disorders Psoriasis Silvery scales Collarette of scales on leading edge Pityriasis rosea Seborrheic dermatitis Greasy scales Pityriasis lichenoides chronica Mica-like, adherent scales