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Kaizen

Dermatology
Compilation
Edited by : Muhammad Aqlan (Rhazes the 19th)
CAPILLARY HAEMANGIOMA
- Commonest benign vascular tumor
- Cutaneous vs visceral
- Cutaneous subdivided into superficial vs deep

Describe
- Erythematous plaque, with irregular margin,
well-defined, with small erythematous papule
at the right cheek.

Clinical Presentation
- few days after birth, growth for months and years, self limiting but slow
at 10 years, recover with no scar, good prognosis.
- Complication - bleeding, ulceration, infection, impaired vision(ambylopia), airway
obstruction, urinary obstruction

Management
1. Reassurance that this is a benign (watch and wait policy)
2. followup for complication - especially the eye.
3. Hydrosteroid laser to prevent growth - Dye laser (target the endothelial red cell, and less
chance of scarring) or C02 laser destroy it, but cause scarring.
4. Intralesional interferon.
5. PO propanolol 0.5 mg/kg/day and incerase daily by 0,5mg/kg/day until 1.5-2.0 mg/kg/day
(vasoconstrictor effect to shrink tumor)

*Another differential includes carvenous hemangioma - bluish and ill-defined.


PORT - WINE STAIN
Diagnosis and describe
- Macular erythema extending whole
left upper limb and the left part of
the upper chest.
- Well demarcated and irregular margin. Non-raised lesion.

Clinical Presentation
Congenital – increased in VEGF
Capillary proliferation and dilatation within dermis
Not tumor
Developemental defect
Dilated capillary
Do not increase in size
Remain Life long
May be nodular or papular.

Management - Reassurance

*similar lesion in face - Sturge Weber


Syndrome - in paediatrics, at
Port wine stain (PWS) forehead, h/o
It will not regress and persists for life seizure and learning disabilities.
Treat with cosmetic camouflage
If a child has PWS+ epilepsy+ mental retardation+ tram line calcification on skull xray
= Sturge-Weber syndrome
Sturge Weber Syndrome
• Congenital vascular malformation of • Ix
dermis and leptomeningeal capillary and Neuroimaging
venous system in brain and eyes i) CT scan
- calcification
• Clinical features
- hyperdense at malformed site
1. Neurological signs and symptoms
ii) MRI with gadolinium
- seizure
- hyperintense areas at
- neurological deficit
malformed site
- mental retardation
- enlarged contralateral
choroid plexus
2. Ophthalmic manifestation
- conjunctival angioma • Tx
- glaucoma - antiepileptic drug for seizure
- visual field defect (due to vascular
malformation at optic tract or occipital
lobe)
- heterochromia iridis (aggregation of
melanocyte)

3. Dermatological manifestation
- port wine stain
ACNE VULGARIS
Describe
- Papules, and pustule, comedome, [open (blackhead) and
closed (whitehead)]
- Inflammed papulonodular - erythema
- Scar - icepeak/atrophy
- polymorphic lesion
Ddx:
- Nodular acne
Clinical Presentation
Cystic acne
- site - face, shoulder, chest, back. Severe acne
- young people after puberty, rarely at age of 30.

Pathophysiology
- Increase sebum secretion because of androgen hormone .
Sebaceous gland and sebum drain into dark of hair follicle ->
block of opening.
- Propronibacterium acnes - produce lipases enzyme >
hydrolyze TG in sebum > produce FFA > inflammatory cells
go into the dermis > neutrophil migration > comedome >
pustules > papules > nodules
ACNE VULGARIS
2 problems
- psychosocial effects. Another option of oral - oral
- scarring. reitnoid
• No medical treatment to treat scar -
prevention is better than cure. - cannot be used with topical retinoid as it
• Laser surgery - expensive and may cause dryness.
cause loss of epidermis > careful to - completely stop the sebum production
sunlgiht and infection. (reduce sebum production) > skin dry >
dry lip and nasal mucosa.
Treatment - can be control by moisturizer.
- only suppresive and not curative. - Major complication - teratogenic such as
- topical should be continue if oral has still birth, neonatal malformation > need
stopped until acne resolves. advice to avoid pregnancy.
- Topical - for comedome, ex:
benzoylperoxide, retinoid, topical - is an antiandrogen drug - when
a/b. combined with OCP, this is fro female.
- Oral - Doxycycline and Erythromycin
- a presentation of systemic disease such
*see 4-6 months of improvement. as PCOS, Cushing syndrome, late onset
CAH.
KELOID
- Genetic predisposition
- common site - bcg scar, chicken pox scar, acne scar,
surgical scarm sternum, and ear piercing.

DDX
- Cannot be skin tags because it is too big and thick.
Skin tags are small.
- Cannot be SCC because cancer is rapidly growing
nodular lesion which will then ulcerate

Management
- Intralesional steroid- triamcinolone > to inhibit the
fibroblast (synthesize collagen), for once a month, can
cause atrophy if too much.
- dangerous to be given intramuscular - dangerous in
prolong treatment as it may cause depo action.
PHOTOSENSITIVE RASH
• Desribe - Macular erythematous well defined, at face,
sparing the peri-orifice area.
• In SLE (4 out of 11).

• DDX - Cannot be discoid rash because discoid rash


is a raised plaque/nodule, persistent and heals with
scarring. We cannot say SLE because we have to
use criteria in order to diagnose SLE

• Investigation - FBC for pancytopenia, screening by ANA,


specific by anti-dsDNA, but if absent doesnt exclude.
UFEME - proteinuria, hematuria.

• Malar rash - macular, come and go and doesnt cause


scarring.
• Discoid rash - Plaque/Nodules, doesnt but eventually
resolves and cause scar and atrophy.

Management
1. Topical steroid - moderate potency.
2. Try to not go out at 10am and 3pm (max exposure)
3. Wear long sleeves, carry umbrella, wear sunblock,
4. oral? - used in RA - reduce photosensitivity in SLE.
PHOTO DERMATITIS
- A subset of exogenous eczema
- Interaction between sunlight exposure with
substances
- Substances can either be :-
- intake PO of medication eg sulphonamide,
tetracycline.
- substances exposed to skin eg local
anesthetic; local antibiotics
- Clinical features:
- ill defined; scaly; erythematous skin
- at sun exposed areas
- Tx:
- sunscreen
- azathioprine
DERMATOMYOSITIS
Describe
- Macular rash, start with the prominent edema of
the eyelids (heliotrope rash)
- Heliotrope - white people appear purple, and in
dark people, appear reddish.
- involve eyelid and nasolabial fold. Periorbital edema and erythema

Clinical Presentation
- Shawl sign?
- a/w - proximal myopathy - progressive difficulty in
walking. (DDX - myasthenia gravis, ? Cushing )
- Autoimmune connective tissue disease.
- May have u/l diease - paraneoplastic disease in
breast CA/ Colon CA.
Gottron papule
- Dermatomypsitis of the hand.
- In children
- Deposit of calcium (cutaneous calcification on
skin)

Treatment
- Treat the U/L - symptoms will resolve.
- Treat sx of rash - high dose of prednisolone.
*some use azathioprine - action is slow and may
take weeks. Linear erythema at dorsum of finger
- Hydroxychloroquine
DERMATOMYOSITIS
Characteristics:
- Gottron’s papules (erythematous
papules) at knuckles
- Cutaneous calcinosis (white
deposits)
- Erythema at dorsum of hand;
linear erythema of finger dorsum
- Not painful or itchy, patients come
because of proximal weakness

Causes:
- Autoimmune disease causing
weakness of proximal muscles
(shoulder), problems in raising
arms, climbing stairs
- Vasculitis in children (heliotrope
rash)
- Underlying malignancy in 25%
adults (paraneoplastic
phenomenon)

Management:
- Treat the cause (if malignancy )
- Immunosuppressive drugs
Heliotropic rash
VITILIGO
Describe
- depigmentation macules of different
shapes and sizes at the dorsum of fingers
and knuckles.
- middle of lesion - see repigmentation -
normal color of skin can be seen.

Clinical Presentation
-d/t autoimmune destruction in melanocyte.
- site - hand, face, feet.
- a/w u/l - autoimmune, Grave's ds,
Hashimoto ds, pernicious anemia, type DM
1, Addison's disease.
-Cosmetic problem and psycosocial.

Management
1. potent topical steroid, effective for
localized, and not systemic.
2. Phototherapy - UVB - only for very
generalized vitiligo - no Tx available.
*monobenzyl kill melanocyte.
VITILIGO
Characteristic:
Depigmentation of skin

Causes:
- It’s an autoimmune disease
- Systemic diseases (autoimmune
thyroiditis, Addison’s disease,
pernicious anemia, Type I DM)

Management:
- Potent topical steroids (localised)
- Phototherapy (generalised)
NODULAR PRURIGO
Characteristics:
-Usually at extensors of arms and
legs
-Itchy nodules
Cannot be nodular psoriasis
because no erythema or scaling
Cannot be bullous pemphigoid
either

Causes:
- Idiopathic
-CKD - pruritis d/t ureamia > severe
itchy > prurigo
- Systemic disease (CRF,
lymphoma, polycythemia rbra vera,
IDA)
- Common in HIV patients

Management:
- Identify and treat cause
- Potent topical steroid
- Antihistamine
- UVB
NEUROPATHIC ULCER
Ddx:
- Pressure ulcer
- Diabetic Foot Ulcer
- Lepromatous Leprosy

Clues:
- At pressure areas (heel,
lateral side of foot, head of
metatarsals)
- Callus formation
- Damaged joints (Charcot
joint)

investigation - do dextrostix,
DM screening for every 40
years old.
other cause - leprosy?
PYOGENIC GRANULOMA
Diagnosis
- benign lesion
- reactive angioma
- proliferation of the rvascular
endothelium in response to
minor trauma (reactive
hemangioma)
- bleed to touch.
Ddx:
Amelanotic melanoma

Treatment:
- Simple excision - sent to HPE
- Cryotherapy (easier but slower)
-- CARBON DIOXIDE LASER
CHRONIC PARONYCHIA
Chronic Candidal Paronychia

Characteristic:
Swelling and erythema of nail fold because infection (Candida)
enters from nail fold (primary site)
Cannot be Tinea unguium because the dermatophyte infection
enters through distal edge of nail – nailfold normal

Chronic: loss cuticle , abnormal nail fold


Occur in people whose work in demand repeated wetting of hand
(housewives)
Other: DM, poor peripheral circulation, removal cuticle
-Erythema n swelling of nail fold
-Often on 1 side
-Brownish discoloration of nail
-Pus (exudate)
-Nail dystrophy
Causes: candida with 2ry bacteria infection

Management:
Mx: nystatin cream regularly (topical antifungal) - Topical antifungal
apply at nailfold
- Keep hands dry
erythromycin
hygiene
SCABIES
Clues:
- The web spaces of hands – usual site
- Can affect genitalia too.
Sacroptes scabies burrow in tunnel in the epidermis,
Body mount immune response - very itchy.
MOT- Direct contact.
1 month incubation period.
Lesion - described - excoriated papules at the wrist, webspace, along the medial foreamm
axilla, umbilicus, genital area and buttock.
It is a clinical diagnosis.
Secondary infection is common – hence the pus everywhere! :O
Cannot be Lichen simplex because LS is localised plaque

Treatment:
- Apply benzyl benzoate/Lindane/permethrin to whole body except face and scalp for 48h, (rare
to see scabies there) - need to be diluted first.
- repeat after 1 week because medication didnt kill it, so leave 1 week for egg to hatch.
-- if took a bath - need to be reapplied.
- Treat all contacts (family members) - regardless if asymptomatic.
- Oral antibiotic for secondary infection (staph or strep) (Erythromycin)
-antihistamine for itchiness.
SCABIES
TINEA IMBRICATA
• Occur due to tricophytum
cocentricum.
• Polyclic scaling,
• Tribe - immunodefect to the
organism,
• Not itchy - people dont come for
treatment.
• Treatment with oral antifungal or
topical anti-fungal if pregnant.

Tinea Impricata

-caused by trichophyton concentricum


Stat as small like brown papulovesicle extent centrifugally to produce rosette
concentric scaly ring when coalesce it may cover large area of skin
May have genetic ( commonly among orang asli)
Treatment : griseofulvin, other anti fungal
STEVENS-JOHNSON SYNDROME
Ddx:
- Toxic Epidermal Necrolysis (TEN)

Cannot be Peutz-Jeugher Syndrome


because PJS has blackish nodules,
small crusting on lips, like moles

Characteristic:
Generalized maculopapular rash and
mucosal lesions (oral ulcer, hemorrhagic
crusting over the lip)

Causes:
- Drugs (Antibiotics, NSAIDS, anti-tb,
anti-convulsant, allopurinol)
- Infection (M.pneumoniae)

Management:
- Stop the suspected drug!
- Supportive therapy (Fluid, electrolyte,
Parenteral nutrition, CBD, IO chart)
- IV Immunoglobulin to speed up
recovery (5/7)
- Prevent secondary infection (monitor
V/S, do blood culture)
D/d: SJS, TEN, Pemphigous bullae
STEVENS-JOHNSON
SYNDROME

- Life threatening.
- drug induced hypersensitivity reaction in skin and
mucous membrane.
- Widespread- painful area of detachment and erosion
of mucous membrane. (eyes mouth, resp tract, genital
area)
- May precede prodromal of fever, malaise, coryzal
symptoms and skin pain.

- SJS - <10% of the body surface area detachment.


- SJS -TEN 10-30%
TEN >30%

Mortality rate p SCORTEN parameter.


May involve other organ including the hepatitis or
renal failure.
- clinical diagnosis.
- risk of infection - pneumonia and sepsis.
Steven Johnson Syndrome
Steven Johnson Syndrome vs Toxic
epidermal necrolysis (TEN)
RAYNAUD'S PHENOMENON
• Recurrent reversible vasoconstriction of peripheral arteries
secondary to cold exposure.
• Transient ischemia of digits.
• a/w u/l autoimmune disease such as; systemic sclerosis, mixed
CTD, SLE, and cyroglobulinemia.
• cold exposure - white (vasospasm)> blue (cyanosis) > red
(hyperemia), may a/w pain and numbness.
• Site involved: Fingers, toes, ears, nose, bilateral and symmetrical in
patterns.

• Ddx : vitiligo

Management
1. Keep the peripheries warm.
2. Nifedipine.
3. lloprost.
Alopecia
TINEA CAPITIS
Ddx:
Alopecia arreata
Androgenetic alopecia

Cannot be scalp psoriasis because there is


no scaling/plaque/erythema. Plus,
psoriasis doesn’t cause hair loss.

Cannot be seborrheic dermatitis because


there is no erythema/scaling.

Treatment of T.capitis:
- Oral antihistamine (Chlorphenamine aka
Piriton)
- Oral antifungal (Terbinafine, Itraconazole,
Griseofulvin)

Why oral, not topical?


Because the fungal infection extends deep
inside the hair follicles (until
subcutaneous), so topical cannot penetrate
the depth of it.
ALOPECIA ARRETA
• Autoimmune mediated, attack of hair • Poor prognostic factors
follicles by autoantibodies - childhood onset
• Can affect any areas that bears hairs - atopy history
• Features - family history of autoimmune
- Involves patchy non-scarring loss of disorder
hair - presence of autoantibodies
- exclamation marks hair - nail dystrophy
- alopecia in occipital scalp
• If involve entire scalp = alopecia totalis
(ophiasis)
• If involve whole body – alopecia
universalis

• Tx
- intralesional/ systemic corticosteroids
(to suppress autoimmunity)
- phototherapy with PUVA (also to
suppress immunity)
HERPES ZOSTER (SHINGLE)

Characteristics:
- Blister, bullous, vesicular eruption
- Unilateral
- Within a dermatome (maxillary
branch of trigeminal nerve)
- Self-limiting within few weeks

Treatment:
Oral Acyclovir to reduce severity of
disease and complication
(post-herpetic neuralgia)
ACANTHOSIS NIGRICANS
Ddx:
Pseudoacanthosis nigricans

- Occur at hyperpigmentation skin at back of neck,


skin fold (neck, axilla)
Can be also. with obesity which release insulin GF
that leads to epidermal hyperplasia
Uncommon in peri-oral areas, if present then must
suspect malignancy

Causes:
- Endocrine : DM, Cushing, acromegaly,
hyperthyroidism
- Obesity : pseudoacanthosis
- Drugs
- Internal malignancy

Treatment:
Treat the underlying cause!
MOLLUSCUM CONTAGIOSUM

Describe
-papules and nodules with central
depression -> looks like chessy
white subtances.
Cannot be chicken pox because CP
is generalised!

Characteristics:
- Localised because viral inoculation
is only at that site
- Self-limiting (6-12 months)
- Contagious!

Treatment:
- children - leave it alone.
- older child - treat with Cryotherapy
URTICARIA
Characteristics:
-Smooth, raised plaque
-Itchy
-No secondary change like scaling
- Edema at the dermis.
Cannot be eczema because there is no
erythema/oozing/scaling
Cannot be tinea corporis because TC is annular
lesion and has scaling

Causes:
Urticaria/pityriasis rosea/annular sarcoidosis
- Food (seafood, nuts, dairy milk)
- Drugs (aspirin, antibiotic)
- Infections (Strep throat, tonsilitis, worm
infestation, chronic URTI)
- Physical causes are RARE (cold, pressure)

Management:
- Symptomatic (oral non-sedating
antihistamine)
- Find cause and avoid triggering factors
PALMAR ERYTHEMA
This is JUST Palmar Erythema,
haha

Causes:
- CLD
- RA
- Pregnancy
- Hyperthyroidism
PSORIASIS
Characteristics:
- Nail involvement in psoriasis –
psoriatic nail
- Erythematous scaly plaque
- Nail signs : pitting, onycholysis
- Typical presentation, you must not
get this wrong okay!

Management:
- Assess severity and extent of
disease
- Topical (steroid, calcipotriol),
systemic (methotrexate, oral
retinoids) or phototherapy (UVB)

Don’t use cyclosporine because


nephrotoxic!
ICHTHYOSIS
Ddx:
- Atopic xerosis
- Asteatotic eczema

Characteristics:
- Generalised scaling of both legs
- Lichenification at ankle
- Very dry skin

Treatment:
Apply moisturizers/olive oil/emollients
effectively after bath

Ichthyosis Vulgaris
• 1)Congenital disease of hereditary origin
• Autosomal dominant
• Dryness over extensors of arms and legs
• Thickening of palms and soles
• Sparing of the cubital and popliteal fossa (flexures)
• Rough ,thick, large coarse and scaly skin (fish skin disease)
• Acquired type
• Occur in pts with CRF, IDA, thyroid disease, nutritional def, Hansen’s
disease, malignancy
• Drugs : nicotinamide, Chlorfazemine
• D/d : atopic eczema
SHINGLES

Shingles: acute self limiting vesicular eruption in


a dermatomal distribution
d/t recrudescence of varicella zoster
Cx:
-ophthalmic dz: corneal ulcers or scars
-motor palsy: Ramsay hunt syndrome
-post-herpetic neuralgia
-disseminated herpes zoster

Mx:
-Mild: symptomatic, rest, analgesia, calamine lotion
-Severe: Oral acyclovir and prednisolone
HERPES ZOSTER OPTHALMICUS
Herpes zoster ophthalmicus
-vesicular lesion over V1 (trigeminal nerve) dermatome
-swelling of upper eyelid
-conjunctivitis
-keratitis
-painful eye

Herpes Zoster Ophthalmicus


Affect the ophthalmic branch of trigeminal nerve
Can also get lesion at tip of nose when affect the nasociliary division of
ophthalmic branch
Can get visual impairment when involve eyes
Tx: Acyclovir

Complication:1) Post-Herpetic Neuralgia which is persistence of pain, occur for


a month
2) secondary infection

Tx: Carbamazepine - 50% of pts more than 50 yrs old develop post-herpetic
neuralgia
LEPROMATOUS LEPROSY

-thickening and foldings of forehead skin


-nodules at forehead and ear
-loss of eyebrow
*All above are typical appearance of lepromatous leprosy (leonine facies)
-if only have forehead lesion, d/d is acromegaly, actinic reticuloid
-confirm diagnosis with slit skin smear, skin biopsy
Leprosy can be divided into
•Tuberculoid -few skin lesion, few thickened nerve, early lost of sensation, no glove n stockings appearance
•Lepramatous - multiple skin lesion, multiple thickened nerve, late lost of sensation, + glove n stockings
appearance
Tx: Dapsone, Chlorfazemine, RifampiciN

Predilection: nv. And dermis


TL: hypopigmented center/ erythematous raised plaque, anesthetic, nv. Thickening, ms. atrophy, dry, hairless
LL: multiple lesions in macules, papules, nodules, plaques at face, arms, legs, buttocks
madarosis (loss of eyebrows) nasal stuffiness. Leonine: thickened furrowed appearance , sensation is
usually not impaired
ant. Chambers invasion🡪 glaucoma and cataract

Cx:
-TL: Peripheral neuropathy🡪 insensate🡪 bone damage of foot or hand🡪 shortening of toes & fingers
-LL: nasal damage🡪 saddle nose defect
-ichthyosis, leg ulcers (Lucio’s reaxn) & testicular atrophy
-contractures of hand and feet

Tx
LL: rifampicin, dapsone, clofazemine 2 yrs until skin smears negative
TL: rifampicin and dapsone for 6-12 mths
TUBERCULOID LEPROSY

Leprosy
TL: hypopigmented center/ erythematous raised plaque, anesthetic, nv.
Thickening, ms. atrophy, dry, hairless
LL: multiple lesions in macules, papules, nodules, plaques at face, arms,
legs buttocks.

A/W - madarosis (loss of eyebrows) nasal stuffiness. Leonine: thickened


furrowed appearance , sensation is usually not impaired. ant. Chambers
invasion🡪 glaucoma and cataract
Hansen’s disease ( Leprosy) affecting radial n ulnar nerve
- There is Claw Hand for left hand with wasting of thenar n hypothenar muscles
On palpation - thickening of the radial nerve or ulnar nerve
VIRAL WART OF THE FINGERS

Viral wart of fingers


Warts can be divided
Cutaneous surfaces- involve hands, fingers n face-
HPV 1,2,4
Mucosal surfaces-genital warts- HPV 6-sexually
transmitted- oncogenic
Tx:1) topical salicylic acid for young children
2) cryotherapy for adults
3) podophylline for genital warts

Resolve within 2 yrs in 65%, 6mths in 30%


Cx: Condyloma acuminate - penile wart
-epidermodysplasia verruciformis: generalized
-painful
Diff Dx
-Molluscum contangiosum
-plantar corns
-Granuloma annulare
-Condyloma acuminata
VIRAL WART
• ETIO?
• RX?
• ADVICE?
PITYRIASIS VERSICOLOR

Infection and overgrowth of commensal


yeast Pityrosporum orbiculare
-chronic asymptomatic, fungal infection
Recurs!

Clinical features
- hyper/hypo pigmentation of skin
- +/- scales formation

Ix
- skin scraping + microscopy with KOH
(spaghetti and meatball appearances –
hyphae)

Tx:
-imidazole cream
-selsun (selenium sulphide) shampoo
-itraconazole
SCLERODERMA

Scleroderma-systemic sclerosis

A multisystem disease characterised by


inflammatory, vascular and sclerotic change
of skin and internal organs (lung, heart, GIT)
-types:
1.limited (acrosclerosis): anticentomeric Ab.
-CREST syndrome (calcinosis cutis,
raynauds, esophageal dysfx, sclerodactyly,
telangiectasia)
2.Diffuse
-early internal involvement: synovitis
-rapid onset and diffuse

Face: telangiectasia & diffuse


hyperpigmentation, microstomia, small sharp
nose, thinning of lips, radial perioral furrowing
Cx: dysphagia, pulmonary fibrosis
multiple, bilateral, cutaneous,
ERYTHEMA NODOSUM color changes. Subside in 3-6
wks
Causes:
-bacterial: strep
-sarcoid
-Drugs: sulfonamides
-deep fungal: dermatphytes
-viral/ chlamydial
-enteropathies
-malignancis: lymphoma,
leukemia
Red nodules🡪 bluish fluctuant
🡪 yellowish bruise-like
Ant. Shin, fever malaise,
Erythematous nodules with black patches chills, arthralgias
on the skin
Diagnosis: erythema nodosum with
post-inflammatory hyperpigmentation.
Erthythema nodusum-strep infection,
sulphamomides, Tb or connective ts.
disorder
Atopic xerosis-dry scaling skin
Give emollients-aqueous cream, olive oil
Don’t give topical steroid

Atopic xerosis-lichenification
NEUROFIBROMATOSIS
-autosomal dominant
-café au lait macules in 1st 3yrs
-neurofibromata nodules, late adolescence
-lisch nodules: pigmented hamartomas of
iris
A/w: hpt pheochromocytomas, brain tumor
astrocytoma, patho. # of bone cyst, mental
retardation, short stature, precocious
puberty
Dx is by 2 of the following:
1.Café au lait spot >6 of 1.5cm in adult/ >5
of 0.5cm in child. <5y.o.
2. Freckles in axillary and inguinal region
3.at least 2 nf of any type / 1 plexiform Neurofibromatosis type 1
neurofibroma Café au lait spot-at least 6 spots,
4.Bilateral optic nv gliomas 15mm in adult, 5mm in
5.Sphenoid wing dysplasia/ thinning of long children,neofibroma, +ve family
bone cortex history,Leish nodule,bone
6.2/> Lisch nodules lesion(pseudoarthrosis)
7. 1st degree relative
Adenoma sebaceum aka Facial Angiofibroma TUBEROUS SCLEROSIS
- Cutaneous sign for tuberous sclerosis

Tuberous sclerosis-multiple hyperpigmentation nodules& papules, starts at 4 years age,facial angiofibroma,come


with seizure/fits

Inherited disorder of skin and nervous system.


Characteristic : epilepsy, mental retardation, rash resembling acne, noncancerous tumour of brain, kidney, retina
and heart
Autosomal dominant
A.k.a epiloia
Angioma? sjorgen petal? Periungual fibroma
- Pt may have epilepsy+ mental retardation+ periungual fibroma

-auto. Dominant, programmed hyperplasia of the ectodermal and mesodermal cells


Early signs: seizures, mental retardation, early white spots
-hypomelanotic macules( ashleaf/ confetti)
-adenoma sebaceum= angiofibroma
-shagreen patch: plaques, c.t. naevi, cobblestone
-periungual fibroma- koeners tumor

A/w:
-CNS hamartomas🡪 seizures
-cardiac rhabdomyomas
-eye: grey/ yellow retinal plaques
Tuberous sclerosis-multiple hyperpigmentation nodules& papules, starts at 4 years age,facial angiofibroma,come
with seizure/fits
LICHEN SIMPLEX
• Lichenification of skin due to persistent
excoriation
• Can have an underlying etiologies eg
atopic dermatitis
• Clinical features
- irregular areas of lichenification with
prominent skin markings
- scaliness (white in color)
- some hyper pigmented crust within rash
• Tx
- emmolients
- TCS or intralesional CS
- TCI eg tacrolimus
- kiv antibiotics if superimposed with
bacterial infection
Well demarcated
erythematous
E. MULTIFORME
maculopapular lesion • Type IV hypersensitivity skin reaction
towards various triggers
• Acute self limiting disease
• Triggers :
- viral : HSV; EBV
- bacterial : mycoplasma pneumoniae
- drugs : sulfa drugs; anticonvulsant eg
phenytoin
• Clinical features:
- target lesion
- arcuate lesion
- Well demarcated erythematous
Target lesion maculopapular lesion
• Ix : a clinical diagnosis
Erythema multiforme major • Mx
-Involve mucosa - discontinue triggers
- analgesics
Erythema multiforme minor - PO antihistamine
- No mucosal involvement *can consider TCS
INFANTILE SEBORRHIEC
DERMATITIS

2 peak age – young and 25-35


onset is very soon after birth
area : flextural,scalp,neck,face,perineum
prognosis: resolve spontaneously, few months
+atopic dermatitis
persist in childhood
onset later
area: X affect flextural,others same
theory: child crawling-friction
prognosis : resolved by age 12 longer course,
0% develop persist as localised

Irritant dermatitis
X involve skin folds
d/d include saboerrhic dermatitis, candidiasis
( involve skin folds ), psoriasis, erythema + papules
ESCHAR

• Clinical features :
- Painless; non-pruritic
necrotic tissue
- black discoloration scab
• Ddx
- in scrub typhus
- and Anthrax
- burns
FIXED DRUG ERUPTION
AUSPITZ SIGN
Auspitz sign:
Slight scratching of a
scaly lesion reveals
punctate bleeding
points🡪 psoriasis
PITYRIASIS ALBAWHICH

- is a form of eczema ( atopic


dermatitis-white papule)
- white color hypopigmentation,
- a form of eczema
-Start off as mild erythema, then
lead to hypopigmented macule
Usually affect the cheeks
-Ix
- clinical diagnosis
- must rule out other ddx with
hypopigmented macule
eg pityriasis versicolor; vitiligo
-Mx
- emmolients
- TCS / TCI
TINEA INCOGNITO
-Partially treated fungal infection (with
topical corticosteroids.
-Symptoms are being supressed but
the fungus are spreading

- Rx: oral anti fungal eg miconazole


TENIA IMBRICATA
• Chronic superficial mycosis, caused by
tricophyton concentricum.
• A subset of Tinea corporis.
• Endemic in SEA, Central and South
America, Southwest Pacific.
• Often presented with multiple annular
rash, with concentric scales, associated
with pruritus.
Predominantly affecting trunks and
upper and lower limbs.
• Ix : skin scraping and
- examination under microscope with
KOH 10% (look for hyphae)
- culture and sensitivity
• Treated either with
- systemic antifungal (for extensive
lesion) or
- topical antifungal (for localised lesion).
ADENOMA SEBACEUM
KERATOACANTHOMA
- Eg Big nodule over
forehead of old lady.
- Rolled edges with
central keratin plug
- Colour changes seen
- Ddx: SCC
- Intervention:
- don’t do cryotherapy
(cuz slow progression
and may have
metastasis)
- sent for HPE TRO SCC

Predilection sites:
- head and neck
- forearms
- hands
ACITINIC KERATOSIS
- Thin small patchy
yellow plaque over
scalp of and oldman.
- Asymptomatic
- Premalignant
lesion(may
transform into SCC)
- Due to chronic sun
exposure
- Intervention:
cryotherapy
- Lesion over right/left upper eyelid
BCC
- Rolled up edge
- Intervention: MOHS, send to plastic surgery
- Don’t do cryotherapy cuz site of lesion not suitable.(only suitable for superficial BCC)

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