dermatology mind maps

8/16/2019 Dermatology Mind Maps

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" أ ا, و ، ا ا

دزو ، "


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Mapof

Contents

Preface

Primary Lesions

Secondary lesions

Investigations

Red Rash

Urticaria

Types of urticaria

Reactive Erythemas

Eczema

Types of eczema

Bacterial infections Acne Presentation

Rosacea

Alopecia

Hirsutism and Hypertrichosis

Infestations

Scabies

Bullous Diseases

Pemphigus

Pemphigoid

Dermatitis herpetiformis

End


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Primarylesions

Erthyroderma is a generalizedredness of skin that may bescaling (exfoliativeerythroderma) or smooth.

Eczema

Psoriasis

Lichenplanus

Cutaneous

Lymphoma

Erythema is redness caused byvascular dilatation.

Urticaria

cellulitis

A papule is a small solid elevationof skin, less than 0.5 cm indiameter.

Acne

Lichenplanus

A plaque is an elevated area of skin greater than 2 cm in diameter but without substantial depth.

Psoriasis

Pityriasisrosea

A macule is a small flat area, lessthan 5 mm in diameter, of alteredcolour or texture.

Freckles

lentigines

A vesicle is a circumscribedelevation of skin, less than 0.5 cmin diameter, and containing fluid.

Herpes

simplex

Chickenpox

A bulla is a circumscribedelevation of skin over 0.5 cm indiameter and containing fluid.

Pemphigus

Pemphigoid

A pustule is a visible accumulation

of pus in the skin.

Acne

Pustular psoriasis

An abscess is a localizedcollection of pus in a cavity more

The term purpura describes alarger macule or papule of blood in

An ecchymosis (bruise) is a larger extravasation of blood into the skinand deeper structures.

Trauma

Postsurgery

A haematoma is a swelling fromgross bleeding.

A patch is a large macule.Melasma

vitiligo

A burrow is a linear or curvilinear papule, with some scaling, causedby a scabies mite.

Scabies

A comedo is a plug of greasykeratin wedged in a dilated

pilosebaceous orifice. Opencomedones are ‘blackheads’. Thefollicle opening of a closed comedois nearly covered over by skin sothat it looks like a pinhead-sized,ivory-coloured papule.

Telangiectasia is the visibledilatation of small cutaneous bloodvessels.

Rosacea

Topicalsteroids

Horn is a keratin projection that istaller than it is broad.

Poikiloderma is a combination of atrophy, reticulatehyperpigmentation andtelangiectasia.


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Secondarylesions

A scale is a flake arising from thehorny layer. Scales may be seenon the surface of many primarylesions

Psoriasis

Lichenplanus

A keratosis is a horn-likethickening of the stratum corneum.

A crust may look like a scale, butis composed of dried blood or tissue fluid.

Impetigo

Ecthyma

An ulcer is an area of skin fromwhich the whole of the epidermisand at least the upper part of thedermis has been lost. Ulcers mayextend into subcutaneous fat, andheal with scarring.

An erosion is an area of skindenuded by a complete or partialloss of only the epidermis.Erosions heal without scarring.

Eczema

Pemphigus

An excoriation is an ulcer or erosion produced by scratching.

Scabies

Eczema

A fissure is a slit in the skin. Eczema

A sinus is a cavity or channel thatpermits the escape of pus or fluid.

A scar is a result of healing, wherenormal structures are permanentlyreplaced by fibrous tissue.

Acne

Keloid

Atrophy is a thinning of skincaused by diminution of theepidermis, dermis or subcutaneousfat. When the epidermis is atrophicit may crinkle like cigarette paper,appear thin and translucent, andlose normal surface markings.Blood vessels may be easy to seein both epidermal and dermal

atrophy.

Topicalsteroids

Lichensclerosus

Lichenification is an area of thickened skin with increasedmarkings.

Eczema

A stria (stretch mark) is astreak-like linear atrophic pink,purple or white lesion of the skincaused by changes in theconnective tissue.

Steroids

Pregnancy

Pigmentation, either more or lessthan surrounding skin, can developafter lesions heal.

3/23/2011 - Maen K. Abu Househ | Reviewed by Reem Al-qudah - Secondary lesions


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DermatologyInvestigations

Woods light

Diagnosis

Tinea capitis Green on shaft of hair

P.versicolor Golden yellow

Pitrysporum Orange

Erythrasma Coral pink

Pseudomonas Blue

Pigmentarydisorders

Hypopigmentation

Depigmentation

Chalky whiteappearance

Prognosis Hyperpigmentation

Poor enhancement

Poor prognosis

Deep lesion

Goodenhancement

Good prognosis

Superficial lesion

KOHSamples

Skin Scraping

Nail Clipping

Hair Plucked hair

KOH is keratinolytic

We see hyphae and spores

Diascopy

name given to the technique in which aglass slide or clear plastic spoon ispressed on vascular lesions to blanchthem and verify that their redness iscaused by vasodilatation and to unmasktheir underlying colour

Tzanck smear

Herpessimplex

Giant multinucleated cells

Pemphigus Acantholysis

Dermatoscopy

magnifying lens

Patch tests

Prick Test

Biopsy

3/25/2011 - Maen K. Abu Househ | Reviewed by Reem Al-qudah - Dermatology Investigations


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Red Rash

Non-scalyBlanchable

Urticaria


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Urticaria

reactionpatternresultsin

pink,itchy or ‘burning’swellings

Wheals

an elevated whitecompressible evanescentarea produced by dermaloedema. It is oftensurrounded by a redaxon-mediated flare.

Although usually less than2 cm in diameter, somewheals are huge.

Lesions last less than 24h

Cause

mast cell degranulation

release of histamine

increased capillarypermeability

chronic urticaria

antibodies against (IgE) receptor

direct degranulation

chemical

trauma

complement activation

Divided into

Acute

Chronic

Disease not lesion lastmore than 6 weeks

sudden appearance

pink itchy whealsDifferential

Insect bites

Erythema multiforme

urticarialvasculitis

longer than 24 h,

blanch incompletely

leave bruising

BullousDisease

dermatitisherpetiformis

bullous pemphigoid

Investigations

ESRVasculitis

Eosinophilia

Parasiticinfections

Typesof Urticaria

Course

50% of patients withchronic urticaria andangioedema will beclear in 5 years

50% of those withurticaria only willclear within 6 months


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Typesof

Urticaria

Physical

Cold

areas exposed to cold cycling

reproduced by holding an ice cube, in athin plastic bag to avoid wetting, againstforearm skin for 10 mins

Treatment Avoid ColdProtective clothing

Antihistamines

Solar

IgE-mediated

Investigations

Exclude connectivetissue diseases SLE

CBC, ANA

Treatment

Avoid sun exposureProtective clothing

Sunscreens and sun blocks

Beta-carotene

Antihistamines

Heat

Cholinergic

Anxiety, heat, sexual excitementor strenuous exercise

macules or papules for 10 - 15 min

Treatment

Avoid heat

Minimize anxiety

Avoid excessive exercise

Anticholinergics

Antihistamines

Tranquillizers

Aquagenic

most common type of physical

mast cells releasing extrahistamine after rubbing or

IgE-mediated (type I)

Ingestion

Inhalation

Pharmacological

non-allergic

aspirin

NSAIDs

ACE

morphine

Contact

IgE mediated or pharmacological

most often around the mouth

Foods

foodadditives

Latex allergy

Endogenous

Infection

Viral

hepatitis,infectiousmononucleosis

Bacterial

Mycoplasma

Intestinal parasites

Connective tissue disorders

Hypereosinophilic syndrome

Hyperthyroidism

Cancer

Lymphomas


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ReactiveErythemas

Erythemamultiforme

Causes

Viral infections, especially:Herpes Simplex

hepatitis A, B and C

mycoplasma

Bacterial infections

Fungal infections coccidioidomycosis

Parasitic infestations

Drugs

Pregnancy

Malignancy, or its treatment with radiotherapy

Idiopathic 50%

Presentation

symptoms of an upper

respiratory tract infectionmay precede

annular

non-scaling plaques

Site

Acrofacial

palms, soles

forearms and legs

Face

lesions enlarge and clear centrally

lesion may begin at the same

site as the original onetwo concentric plaques look like a target lesion

Some lesions blister

Stevens-Johnsonsyndrome

is a severe variant

associatedwith

fever

mucousmembranelesions

oralmucosa,lips

conjunctivae

pharynx,

larynx

Course

appear for 1–2 weeks

transiently bygrey or brownpatches

Erythemanodosum

inflammation of thesubcutaneous fat

panniculitis

immunological reaction

Causes

Infections

Bacteria (e.g. streptococci,tuberculosis, brucellosis,leprosy, yersinia)

Viruses

Mycoplasma

Rickettsia

Chlamydia

Fungi (especially coccidioidomycosis)

Drugs (e.g. sulphonamides, oralcontraceptive agents)

Systemic disease (e.g. sarcoidosis,ulcerative colitis, Crohn’s disease,Behçet’s disease)

Pregnancy

Presentation

tender red nodule

Site

shins

Forearms

thighs, face, breasts

painful joints

fever

Course

resolve in 6–8 weeks

walking is difficult

Differential diagnosis

cellulitis or abscess

phlebitis

Chest x-ray

Urticaria


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Eczema

most common skin conditions

Intro

itch

If it does not itch, it isprobably not eczema

in the acutestages

spongiosis

early disease the stratum

corneum remains intact

appears as a red, smooth,oedematous plaque

worsening

oedema becomes more severe

tense blisters appear

may weep plasma

less severeor chronic

scaling

epithelial disruption

Pathogenesis

activated keratinocyte

Increased proliferation of basal cells

secretion of variouscytokines by epidermis

IL-1

IL-8 acts as a chemotacticfactor for neutrophils

Hyperproliferation

thicken

scale

acute stage

spongiosis

intra-epidermal vesicles

larger blisters

Sharply marginated,strong colour

very scaly

Complications

bacterialcolonization

infection

Affects sleep

interfere with

sporting

work

sex lives

Clinicalappearance

Generalfeatures

absence of a sharp margin

epithelialdisruption

coalescingvesiclesbullae

oedematous papuleson pink plaques

intense itching

Acute eczema

Weeping and Crusting

blisteringvesicles

redness, papules and swelling

scaling

Chroniceczema

less vesicular and exudative

more scaly, pigmentedand thickened

lichenification

dry leathery thickened

increased skin markings

secondary to

scratching

rubbing

more likely to fissure


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Types of Eczema

Occupationaldermatitis

second most common occupational disorder

Men

Chemical plant workers

Machine tool setters

Coach and spray painters

Metal workers

Women

Hairdressers

Biological scientists

laboratory workers

Nurses

Catering workers

Allergiccontactdermatitis

Characteristics

delayed(type IV)hypersensitivity

Previouscontact isneeded

specific to one chemical

all skin will react to same allergen

Sensitization persists indefinitely

Desensitization is seldom possible

Well-knownallergens

Metals

Chrome

Cement

Paint

Tatoos

NickelFake jewellery

Jean studs

Cosmetics

Fragrance mix

Medicaments Neomycin

Excess IgE produced as a response to allergen

75% begin before 6 months

90% before age of 5 years

Infancy

On face

Patchy all over the body,sparring napkin area

Weeping and vesicular

Childhood

Knees and elbows flexural areas

Ankles and wrists

Leathery, dry, with excoriations

Adults

Distribution similar to that in childhood

More Lichenification

Major Chronic Itching and scratching

Irritantcontactdermatitis

80% of all casesindustrial cases

occur in children

bubble bath

lip-licking

Cause

Strong irritantsbrief contact

weak irritantsProlonged

Detergents, alkalis, solvents, cutting oilsand abrasive dusts

Past or present atopic dermatitisdoubles the risk of irritant hand eczema

patients with dry or fair skinsare especially vulnerable

Coursereversible in the early stages

Complicationsloss of work.


Atopic eczema

Allergic contact dermatitis

Treatment

Avoidance

Protection

Topical steroids


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Types of Eczema

SeborrhoiecEczema

Presentation

Affect hair area

Greasy yellowish scales

most common in adult males

may affect infants

Sites

red scaly or exudative eruption

scalp, ears

face, eyebrows

associated withchronic blepharitisand otitis externa

Dry scaly lesions

presternal

interscapular areas

papules or pustules on the trunk

Intertriginous lesionsarmpits, umbilicusgroins, or under spectacles or hearing aids

Cause

not obviously related to seborrhoea

run in some families

affecting those with a tendency to dandruff

overgrowth of yeast

early sign of AIDS

Complications

Furunculosis

Intertriginous lesions

Addedcandidainfection

Treatment

Suppressive

Topical imidazole

Topical Li

DiscoidEczema

Causes

Reaction to bacterial Ag

Chronic stress

Not really known

P t ti

Limbs of middle aged males

Multiple lesions

Coined shapedold age

Localizedneurodermatitis

skin is damaged as a result of repeatedrubbing or scratching

habit or in response to stress

Presentation

single, fixed, itchy,lichenified plaque

Site

neck in women

legs in men

anogenital area

Treatment

Potent topical steroids

occlusive bandaging

break the scratch–itch cycle

Napkin(diaper)dermatitis

irritant in origin

aggravated by the use of waterproof plastic pants

Cause

faecal enzymes

ammonia

prolonged contact

overgrowth of yeasts

Presentation

glazed and sore erythema

sparing of the skin folds

Complications

Superinfection with Candida albicansvesicopustules appearing around theperiphery of the main eruption

satellite lesions "pustules

around the rash"


infantile seborrhoeic eczema

candidiasis

Treatment

keep this area clean and dry

increase the napkin free time

superabsorbent napkins

Protective ointments

topical imidazole


14/38Bacterial

i f ti

Erythrasma

Overgrowth

diphtheroid skin flora

symptom-free

macular wrinkled

slightly scaly pink, brown or macerated white areas

Site

armpits

groins

between the toes

In diabeticslarger areas of the trunk may be involved

On Woods light examinationcoral pink fluoresce

Treatment

Topicalfusidic acid

miconazole

Streptococcalinfections

Erysipelas

first warningoften malaise

shivering and a fever

skin becomes red

well-defined advancing edge

Blisters may develop on the red plaques

not extending beyond the dermis

If untreated can be fatal

responds rapidly to systemic penicillin

Causative organisms enter via skin split

Episodes can affect the same arearepeatedly and so lead to persistentlymphoedema

Minor tinea pedis maycause recurrent Erysipelas

inflammation of the skin occurs at a

deeper level than erysipelas

subcutaneous tissues are involved

area is more raised and swollen

erythema less marginated than in erysipelas


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Staphylococcalinfections

Staphylococcus aureus

not part of the resident flora

Carriage

Mostly nostrils

perineum

armpits

Impetigo

caused by

staphylococci

streptococci

Types

bulloustype

staphylococci

Exfoliativetoxins desmoglein 1

toxin islocalized bullous impetigo

Not local scalded skin syndrome

crusted ulcerated type

beta hemolyticstreptococcus

highly contagious

Presentation

the erosion is at the stratum corneum

thin-walled flaccid clear blister

may become pustular

Rupture leaving yellow exudate and crust

Multiple lesion Around face

heals without scarring

Courseclear even without treatment

Complicationsacute glomerulonephritis

Differential

diagnosis

Recurrentimpetigo search for scalp lice

Investigationand

Gram stain and culture

Systemic antibiotics cefalexin

(boils)

acute pustular infection of a hair follicle

causeStaphylococcus aureus

predisposing factors

source (carrier)

host ( low immunity as DM and systemic steroids)

route (skin disease, minor trauma)

Presentationand course

mainly adolescent boys

tender red nodule

enlarges

May discharge pus

leave a scar Fever and enlarged draining nodes are rare

Most patients have one or two boils only

appearance of many

suggests a virulentstaphylococcus

Scalded

skinsyndrome

Erythema and tenderness

followed by the loosening of large areas of overlyingepidermis

Occurs mostly in children

Cause

Exfoliative toxins

affects desmoglein 1

Organism is localized but the toxin is widespread

Affects only stratum corneum

Differentialdiagnosis

toxic epidermalnecrolysis

full thickness

In adults

usually drug induced

Toxicshocksyndrome

Cause

staphylococcal toxin

Follow overgrowth of staph in vagina

Associated with using tampons.

Presentation

fever

rash

widespread erythema

circulatory collapse

desquamationFingers

Hand


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Varicellazoster

Varicella

spread by the respiratory route

Presentationandcourse

Slight malaise

itchy

papules

clear vesicles pink base

pustules

next few days the lesionscrust and then clear

sometimes leavingwhite depressed scars

Sitecentripetal

Mostly on trunk

Second attacks are rare

Complications

Pneumonitis

Secondary infectionof skin lesions

Haemorrhagic or lethal chickenpox

Scarring


Smallpox

InvestigationsTzanck smear

Herpes zoster

result of the reactivationvaricella-zoster

virus that has remained dormant in asensory root ganglion

Occur in

old age

Hodgkin’s disease

AIDS

leukaemia

patients with zoster can transmit the virus to others

Presentation

start with a burning pain

followed by erythema

grouped, sometimes blood-filled, vesicles

over a dermatome

clear vesicles quickly become purulent

a few days burst and crust

leaving depressed depigmented scars

characteristically unilateral

Affects commonly

thoracic segments

ophthalmic division

trigeminal nerve

Complications

Secondary bacterial infection

Motor nerve involvement

ocular muscles,

facial muscles

diaphragm

bladder

Zoster of the

ophthalmicdivisioncorneal ulcers and scarring

Persistent neuralgic pain

b f th happendicitis


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Herpessimplex

Cause

type Iusually extragenital

type IImainly on the genitals

route of infection

through mucous membranes

or abraded skin.

virus may become latent

Complications

Herpes encephalitis or meningitis

Disseminated herpes simplex

Eczema herpeticum

recurrent dendritic ulcers leading tocorneal scarring

erythema multiforme

Treatment

sunblock

Aciclovir cream

cut down thelength of attacks

used in the first 24 hrs

when the firstsymptoms appear

tingling

burning

oral aciclovir

for those with

widespread or systemicinvolvement

Presentation

Primary infection

type I

most common

in children

acute gingivostomatitis

Vesiclessoon turning into ulcers

scattered over the lips

With

malaise

headache

fever

enlargedcervicalnodes

lasts about 2 weeks

herpeticwhitlow

direct inoculation of the virus

pus-filled blisters on a fingertip

Primary

type II

usually transmitted sexually

cause multiple and painful

genital or perianal blisterswhich rapidly ulcerate

Recurrent

strike in roughly the same place each time

precipitated by

respiratory tract infections

ultraviolet radiation

menstruation

stress

sites

face

lips

genitals

Starts with

Tingling

burning

pain

Then

erythema

clusters of tense vesicles

Crusting occurs within 24–48 h

whole episode lasts about 12 days

3/25/2011 - Maen K. Abu Househ | Reviewed by Reem Al-qudah - Herpes simplex


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Dermatophyteinfections

(Tinea )

Presentation

Tineapedis

(athlete’s foot)

most common type of fungal infection

Risk sharing of wash places

threepatterns

Soggy interdigital scaling, particularly inthe fourth and fifth interspace

diffuse dry scaling of the soles

Recurrent episodes of vesication

Tineaof thenails

associated with tinea pedis

initial changes occur at the free edge of the nail

Changes

Nail becomes crumbly

Yellow Discoloration

Subungual hyperkeratosis

Onycholysis

Separation of the nailplate from its bed

Tineaof

thehands

usually asymmetrical

associated withtinea pedis

unilateral onychomycosispowdery scale in the creases

Tineaof thegroin

common

affects men more

sometimes unilateral

upper inner thigh is involved

lesions expand slowly

sharply demarcated plaques withperipheral scaling

scrotum is usually sparedfew vesicles or pustules can occur

Tinea of the

plaques with scaling and erythema mostpronounced at the periphery

Investigations

Wood’slight

In Tinea Capitis

Green fluorescenceon the hair shaft

Not present in all cases

The most common causeTrichophyton tonsuransgives negative result

SkinScrapingscaly margin

ClippingCrumbly area

Treatment

Local

for minor skin infections

imidazole

miconazole

clotrimazole

terbinafine

Systemic

Indications

Tinea Capitis

Tinea of the nail

Widespreadinfections

Resistant infections

Terbinafine

Itraconazole

Griseofulvin

Drug of choice inTinea Capitis

Cause

Trichophyton – skin, hair and nail infectionsMicrosporum – skin and hair

Epidermophyton – skin and nails

Spread either

Animal to humanzoophilic

Human to humananthopophilic


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FungalInfections

Pityriasisversicolor

Cause

old name: tinea versicolor

regarded as non-infectious

Pityrosporum orbicularecommensal yeasts

Overgrowth

Carboxylic acids released by theorganisms inhibit the increase inpigment production by melanocytes

Presentation

superficial scaly patches

fine wrinkling

slightly itchy

fawn or pink on non-tanned skin

paler than the surrounding skinafter exposure to sunlight

Siteupper trunk

can become widespread

Untreated lesions persist

Treatmentslow to regain their former colour


Vitiligo

border is clearly definedscaling is absent

lesions are larger

Affect limbs and face more

depigmentation ismore complete

Investigations

Scrapings KOH

branched hyphaeand spores

‘spaghetti andmeatballs’appearance

wood's light golden yellow

Treatment topical preparationimidazole group

Candidiasis

Candida albicans is a classic opportunistic pathogen

predisposingfactors

obesity

moisture

maceration

immobility

diabetes

pregnancy

use of broad-spectrum antibiotics

contraceptive pill

Immunosuppression

Leucopenia

Thymic tumours

Low serum iron

Endocrinopathy

Immersion in water

Cold hands

Poor hygiene

Presentation

Oral candidiasis

whitish adherent plaque witherythematous base, in denture wearers

Candida intertrigo

in body folds, erythema and macerationwith satellite papulopustules

Genital candidiasis

Paronychia

Acuteusually bacterial

Staph. Aureus

chronic

Candida

proximal and sometimes the lateral nail folds

cuticles are lost

small amounts of pus can be expressed

nail plate becomes ridged and discoloured

Predisposing factors

wet work

poor peripheral circulation

vulval candidiasis

systemic and topical antifungal

Chronic mucocutaneous candidiasis

Systemic candidiasis

InvestigationSwabsculture

Treatment

Predisposing factors should be sought and eliminated

Amphotericin, nystatin and the imidazole

3/25/2011 - Maen K. Abu Househ | Reviewed by Reem Al-qudah - Fungal Infections


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Psoriasis

Intro

chronic, non-infectious, inflammatory

well-defined salmonpink plaques bearing largeadherent silvery centrally attached scales

Affects white people mainly

Cause

genetic predisposition

one affected parent has a 16%

rises to 50% if both

environmental trigger

hidden antigens

keyabnormalities

hyperproliferationof keratinocytes

excessive number of germinative cellsenter the cell cycle

growth fraction is almost100% compared with 30%in normal skin

turnover timeis greatlyshortened

Normally30-60 days

Becomes10 days

inflammatory cell infiltrate

neutrophils

lymphocytesTh17

T1

Histology

Parakeratosisnuclei retained in the horny layer

Irregular thickening of the epidermis

Epidermal polymorphonuclear leucocyte infiltrates

Munro

in stratumcorneum

Dilated and tortuous capillary loops in the dermal papillae

T-lymphocyte infiltrate in upper dermis

Distal arthritis Most charecteristic

Usually diagnosed clinically

Biopsy

Throat swabbing for

beta-haemolytic streptococci

guttate psoriasis

Skin scrapings and nail clippingsFungal infections

Arthropathy

Precipitatingfactors

Trauma

Köbner phenomenon

Induction of new lesion in normalskin by trauma or scratching

+ve in

Warts

Psoriasis

Lichen planus

Vitiligo

Infection

beta-haemolytic streptococci

guttatepsoriasis

HIVexplosive forms

Hormonal

improves in pregnancy

in postpartumhave a rebound

hypothyroidism

hypocalcemia

SunlightImproves

Drugs

Antimalarials, beta-blockers

withdrawal of systemicsteroids or potent

topical steroids‘rebound’

Cigarette smokingand alcohol

Palmoplantar Pustular Psoriasis

Emotionexacerbations


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PsoriasisPresentation

Commonpatterns

Plaquepattern

most common type

well demarcated

pink or red

large, centrally adherent,silverywhite, polygonal scales

Symmetrical sites

elbows

knees

lower back

scalp

Guttatepattern

children and adolescents

Triggered by streptococcal tonsillitis

‘drop-shaped’

small round red macules

Then scales develop

Scalp

Areas of scaling are interspersed with normal skin

overflows just beyond the scalp margin

Significant hair loss is rare

Nails

Thimble pitting

onycholysis separation of the nail from the nail bed

subungual hyperkeratosis

Oil drop sign

Splinter hemorrhage

Flexures

submammary, axillary and anogenital

not scaly

glistening sharply demarcatedred plaques with fissuring.

most common in women and elderly

negative auspitz sign

Palms and soles

poorly demarcated

Less erythematous

painful fissures on fingers

pustules

negative auspitz sign

Lesscommonpatterns

Napkinpsoriasis

psoriasiform spreadoutside the napkin

Acute generalizedpustular psoriasis

recurrent episodesof pustulation

Erythrodermicpsoriasis

withdrawal of potent topical or systemic steroids

skin becomes universallyand uniformly red

Malaise

shivering

Erythroderma

generalized redness of skinthat may be scaling (exfoliativeerythroderma)

Causes

Eczema

Psoriasis

cutaneous lymphoma

Drug allergy

Complications

Sepsis

Dehydration

poor thermal control

high output heart failure

Auspitz sign

appearance of punctatebleeding spots when psoriasisscales are scraped off

3/12/2011 - Maen K. Abu Househ | Reviewed by Reem Al-qudah - Psoriasis Presentation


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PsoriasisTreatmentand DDx

Treatment

Explanation and reassurance

TopicalTreatment

Vitamin D analogue

Calcipotriol

Tacalcitol

mild to moderatepsoriasis

retinoids Tazarotene

corticosteroids

‘limitedchoice’ areas

face, ears,genitalsandflexures

patients who cannot usevitamin D analogues

unresponsivepsoriasis

scalp,palms andsoles

minor localized psoriasis

Salicylic acid short periods

Dithranol

Coal tar

UV

S/E Acute Phototoxicity

Skin cancer

Systemic

When Severe

photochemotherapy

retinoids Acitretin

methotrexate Liver failure

ciclosporinS/E

Renal failure

HTN

hydroxyurea

Sulfasalazine

never use systemic steroids for psoriasis

Combinedresistant cases


Discoideczema

less well defined

exudative or crusted

lack thick scales

Don't favor extensor surfaces

Seborrhoeiceczema

more diffuse

less lumpy

overflowing the scalpmargins and interspersedwith normal skin in psoriasis

not so sharply marginated

Sitesear, face, eyebrows

Pityriasisrosea

confused with guttate psoriasis

lesions are oval

run along rib lines

Christmas tree

Scaling is of collarette type

herald plaque

confined to the upper trunk

2ndry syphilis

Cutaneous t-cell lymphoma

Tinea

unguium

more asymmetrical

obvious tinea of neighboring skin

Pitting is not seen

Nails are crumbly and discoloured

3/12/2011 - Maen K. Abu Househ | Reviewed by Reem Al-qudah - Psoriasis Treatment and DDx


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Lichen

planus

mediated immunologically

genetic susceptibility

associated withautoimmune disorders

alopecia areata

vitiligo

ulcerative colitis

5p's

plain

purple

pruritic

papule

polygonal

papules

violaceous

intensely itchy

flat-topped

on extremitieswrists

legs

Wickham’sstriae

white streaky pattern on thesurface of these papules

in mouth

lacy lines

dots

white plaques

Ulcers SCCInvestigations

Course

Individual lesions may last for many months

hypertrophic variantFor many years

As lesions resolve

become darker

flatter

leave discretebrown or greymacules

Treatment

difficult

if drugs are suspectedStop them

Systemic steroid

extensive involvement

nail destruction

painful and erosive oral

photochemotherapyreduce pruritus

Resistant cases

Oral ciclosporin

acitretin

AntihistaminesFor itching

Mucousmembrane

Usually asymptotic

If symptomaticTopical

corticosteroid

tacrolimus


25/38

Pityriasisrosea

Cause reactivation of

herpes virus 7

herpes virus 6.

Presentation

Common during winter

affects children and young adults

second attacks are rare

At first herald or ‘mother’ plaque

larger than later lesions

Rounder

Redder

more scaly

After several days

smaller plaques appear

On trunk mainly

also on neck and extremities

plaques

are oval

salmon pink

delicatescaling

adherent peripherally

collarette scales

configuration

Christmas tree

axes run down andout from the spine

along the linesof the ribs


tinea corporis

pityriasis versicolor

guttate psoriasis

secondary syphilis

drug eruption

gold

captopril

Treatment

No Cure

For itching

topical steroid

calamine lotion

Sunlight

UVB

ointment reduces scaling

Course

herald plaque precedes the generalized eruption

Subsequent lesions enlarge

systemic symptoms such as aching and tiredness

eruption lasts 2–10 weeks

resolves spontaneously

leaving hyperpigmented patches

3/12/2011 - Maen K. Abu Househ | Reviewed by Reem Al-qudah - Pityriasis rosea


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Hyper pigmentation

PIGMENTED

Pi: Post-inflammatory

Lichen planus

Eczema

Secondary syphilis

Systemic sclerosis

Lichen and macular amyloidosis

Cryotherapy

G: Genetic

Freckles

seen most often in thered-haired or blond person

sharply demarcated

brown–ginger macules

usually less than 5 mm

become darker with sun exposure

Histopathology

Increased melanin isseen in the basal layer

without any increase in thenumber of melanocytes

without elongationof the rete ridges

No treatment needed Only sunscreens

Lentigines

light or dark brown macules

1 mm to 1 cm

irregular outline

Simpleandsenile

Simple inchildren

On areas notexposed to sun

on mucousmembranes

Senileor

solar

after middle age

on the backs of the hands

on the face

"liver spots"

increase in the number of melanocytesN: Nevi | Nutrition

Malabsorption

TE:TraumaandExogenous

Melasma

acquired

symmetrical hypermelanosis

on sun-exposed skinface

well defined

edges may be scalloped

common in women

becomes darker after exposure to the sun

causes

Pregnancy

sunlight

oral contraceptives

thyroid dysfunction

photosensitizing drugs

Treatment

sunscreen

bleaching agentshydroquinone

D: DrugsPhotosensitizing drugs

Melanin

phenylalanine>>

Tyrosine>>

Phaeomelanins

trichochromes

Eumelanins

Melanin is made within melanosomes

Melanocytes inject melanin to nearby keratinocytes

all together for Epidermal melanin unit

Blacks

Don't have more melanocytes

melanocytes produce more and larger melanosomes

broken down less rapidly

Control of skin color

Melanin

Oxyhaemoglobin

Carotene


27/38

Hypopigmentation

A: Autoimmune Vitiligo

Causecell-mediated autoimmune attack

Trauma and sunburn can precipitate both types

typescommon generalized

acrofacial variant

starts after the second decade

family history in 30%

Associated with

DM 1

thyroid disorders

pernicious anaemia

rare segmental

Clinicalcourse

Generalizedtype

sharply defined

symmetrical

Sites

backs of the hands

wrists

fronts of knees

neck

around body orifices

hair of the scalp and beardmay depigment too

Köbner phenomenon

Induction of new lesion in n ormalskin by trauma or scratching

+ve in

Vitiligo

Warts

Psoriasis

Lichen planus

occasionally, they repigmentspontaneously from the hair follicles

Segmentaltype Spontaneous repigmentation occurs more often


depigmenting chemicals

Pityriasis versicolor

Post-inflammatory

leprosy

Treatment

Sun avoidance and screeningpreparations

topical corticosteroidfor 1–2 months

strength should be gradually tapered

calcineurin inhibitors tacrolimus ointment

PUVA

transplant

extensive vitiligo

completely and irreversibly

depigmented bymonobenzyl

hydroquinone

Pi: Post-inflammatory

Eczema

Pityriasis alba

Psoriasis

Sarcoidosis

Lupus erythematosus

Lichen sclerosus et atrophicus

Cryotherapy

G: Genetic Albinism

oculocutaneous albini sm

defect in the synthesis or packaging of melanin in the melanocyte

little or no melanin is made

AffectsIris

Skin

whole epidermis is white

have poor sight, ph otophobiaand a rotatory nystagmus

Phenylketonuria

Chediak–Higashi syndrome:

M: MalignancyMalignant melanoma

E: EndocrineHypopituitarism

N:Halo naevus

T:Trauma

D: Drugshydroxychloroquine

A PIGMENTED

3/18/2011 - Maen K. Abu Househ | Reviewed by Reem Al-qudah - Hypo pigmentation


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Acne

Intro

disorder of the pilosebaceous apparatus

lesions

comedones

papules

pustules

nodules

Cysts

Scars

Prevalence

Nearly all teenagers

clears by the age of 23–25

years in 90% of patients

Pathogenesis

Poral occlusion

Bacterialcolonization of duct Propionibacterium acnes

Dermal inflammation

Increased Sebum secretion rate

Presentation

Investigations

Culturesexclude a pyogenic infection

Hormones

LH LH:FSH 2.5:1

FSH

dehydroepiandrosteronesulphate

androstenedione

17-hydroxyprogesterone

urinary free cortisol

Imaging

Pelvic U/S

CT

MRI

Treatment

Accordingto severity

Mildcomedones

ModeratePapules

Pustules

Severe

Nodules

Cysts

Scars

Mild

Topical

Retinoids

Isotretinoin

Adapalene

Tazarotene

Azelaic acid

Moderate

Topical and systemic

Topicalantibiotics

clindamycin

erythromycin

zinc &

erythromycin

Systemic

systemicantibiotics

Tetracycline

Minocycline

Doxycycline

S/E

GIT upset

Photosensitivity

Hepatotoxicity

Teeth staining

dental hypoplasia

Pigmentation

Increased ICP

contraindicatedin children andpregnancy

Hormonal

In all females

High estrogen low progesterone

Diane-35 Anti androgens

just given for females

ketoconazoleantiandrogen

spironolactoneantiandrogen

metforminFor PCOS

Systemic

Depression


29/38

AcnePresentation

Common type

Site

Face

Upper trunk

Seborrhoea

Open comedones

closed comedones

papules, nodulesand cysts

Depressed or hypertrophic scarring

hyperpigmentation can follow

Conglobate

‘ball’

Severe form

Nodules

Cysts

Scar

abscesses or cysts withintercommunicating sinuses

leaves deeply pitted or hypertrophic scars

Fulminans

conglobate acne

+

fever

joint pains

High (ESR)

Infantile

soon after birth

common in maleshirsutism

Congenital adrenal hyperplasiaambiguous genitalia

salt-wasting

Druginduced

dominated by papulopustules

suddenly

E.G..

Corticosteroids

androgens

anabolic steroids

gonadotrophins

oralcontraceptives

Progesteronecontaining

lithium

iodides

bromides

anticonvulsants

Androgen-secretingtumours

Systemicvirilization

clitoromegaly

deepening of voice

breast atrophy

Cutaneous virilization


30/38

Rosacea

Intro

2 Types

papulopustular

erythematotelangiectatic

affects theface of adults

usually women

peak incidence is in the thirties

Cause

Still Unknown

Demodex folliculorum

Helicobacter pylori

Seen in those who flush easily

Warmth

spicy food

alcohol

embarrassment

Sites

centre of forehead

cheeks

nose

chin

periorbital and perioral areas are spared

Intermittent flushing

followed by a fixed erythema and telangiectases.

Lesions

papules

papulopustules

plaques

nodules

has no comedones or seborrhoea

Eye

blepharitis

conjunctivitis

keratitis

hyperplasia of thesebaceous glandsand connective


Acne

no erythema andtelangiectases

comedones

Involves face, backand shoulders

Seborrhoeic eczema

perioral dermatitis

systemic lupus erythematosus

photodermatitis

flushing

menopausal symptoms

Superior vena

caval obstruction

Treatment

avoidance of exacerbating factors + sunscreens

papulopustular rosacea

tetracyclines

Erythromycin

Topical metronidazole

stubbornrosacea

systemicmetronidazole

isotretinoin

Erythematotelangiectaticrosacea

vascular lasers

rhinophymas

surgical excision

cryotherapy


31/38

Alopecia

localizedanddiffuse

Localized

Scaringandnon-scaring

Scaring

Loss of openhair follicles

Burns

radiodermatitis

Aplasia cutis

Kerion

carbuncle

Cicatricial basalcell carcinoma

lichen planus

lupus erythematosus

sarcoidosis

non-scaring

Alopecia areata

Androgenetic

Hair-pulling habit

Traction alopecia

non-inflammatorytinea capitis

diffuse

Telogen effluvium

Endocrine

hypopituitarism

hypo- or hyperthyroidism

hypoparathyroidism

high androgenic states

Drug-induced

antimitotic agents

retinoids

anticoagulants

vitamin A excess

oral contraceptives

Androgenetic

Iron deficiency

Severe chronic illness

Malnutrition

Diffuse type of alopecia areata

Alopeciaareata

autoimmuneT-cells

Associated with

thyroid disease

vitiligoatopy

affects 10% of those with Down’s syndrome

Presentation

patch of hair loss

With no scaring

Skin colored

Not scaly

Well defined margin

No specific arrangement

Distribution is variable

Scalp

beard

eyelashes

eyebrows

Pathognomonic

‘exclamation-mark’hairs

broken hair that is4 mm long , lesspigmented andthinner proximally

Course

unpredictable

poor prognosticfeatures

onset before puberty

association withatopy or Down’ssyndrome

unusually widespread

involvement of thescalp margin

Recurrent

more than 3 months duration

nail envolvement


Intradermal/intralesional Corticosteroid

Topical corticosteroids


32/38

Hirsutism

Causes

Adrenal

Cushing syndrome

androgen producing tumors

congenital adrenal hyperplasia

Ovarian

androgen producing tumors

Poly cysticovariansyndrome

serum testosterone

LH:FSH 2.5:1

sex hormone-binding globulin

dehydroepiandrosteronesulphate (DHEA-S)

androstenedione

Pelvic U/S

lipid profilefasting glucose

Drugs

Racial / Familial

idiopathic

Presentation Excess hair

on beard

chestshoulder-tips

around the nipples

male pattern of pubic hair

Investigations

doneif

occurs in childhood;

features of virilization

sudden or recent onset

menstrual irregularity

or cessation

serum testosterone

LH:FSH2.5:1

sex hormone-binding globulin

dehydroepiandrosterone sulphate

androstenedione

17-alpha hydroxyprogestrone

prolactin

Pelvic U/S

Transvaginal ovarian ultrasound

lipid profile

fasting glucose

Treatment

decrease weight and exercise

underlying disorder must be treated

waxing or shaving

Plucking should probably be avoided

Laser

Oral antiandrogens

electrolysis

3/15/2011 - Maen K. Abu Househ | Reviewed by Reem Al-qudah - Hirsutism


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Infestations

Head lice

still common

10% of children

few or no symptoms

peak between the ages of 4 and 11

more common in girls than boys

Cause

about 10 adult lice3–4 mm in length

greyish

Eggs (nits) stuck to the hair shafts

Spread

head-to-head contact

shared combs or hats

Presentation

andcourse

main symptom is itching

is mainly aroundthe sides andback of thescalp

later it spreadsgenerally over

the scalptake several months to develop

Scratching and secondary infection soon follow

hair becomes matted and smelly

Draining lymph nodes often enlarge

ComplicationsSecondary bacterial


recurrent impetigo Search for lice

crusted eczema Search for lice

Topical

Malathion

carbaryl

now uncommon

Spreadinfested bedding or clothing

Presentationand course

Self-neglect is usually obvious

widespread itching

Results in excoriations and crusts

Pubiclice

Spreadsexual contact

Presentation

Severe itching in the pubic area

followed by

eczematization

secondary infection

small blue–grey macules

shiny translucent nits are less obviousthan those of head lice

spread most extensively in hairy malesand may even affect the eyelashes

InvestigationsCoexistant STD

Treatment

Carbaryl

permethrin

malathion

Infestation of the eyelashes isparticularly hard to treat

Lice

P. humanus capitisHead lice

P. humanus corporisBody lice

Phthirus pubisPubic lice


34/38

Scabies

Cause

Incubation for 1 month

Sarcoptes scabiei hominis

Adult mites are 0.3–0.4 mm long

Transmission

close bodily contact

fertilized female

produce two or three oval eggs

turn into sexually mature mites in 2-3 weeks.

ItchCaused by sensitization to the mites or their products

Presentation

first infestation

For 4–6 weeks no itching

thereafter Severe itching

bad at night

Many people itch

second attack

itching starts within a day or two

victims already have immunity

Result

excoriated

eczematized

urticarial papules

Sites of burrows

sides of the fingers

finger webs

sides of the hand

wrists

elbows, ankles and feet

nipples and genitals

Only in infancy does scabies affect the face

On the genitals, burrows are associated witherythematous rubbery nodules

Coursepersists indefinitely unless treated

Complications

Secondary infection

with pustulation

glomerulonephritis

Persistent itchy red nodules

Venereal disease

Crusted (Norwegian) scabies

crusted eruption

vast numbers of mites

INmental retardation

immunosuppression

Differential diagnosisOnly scabies shows characteristic burrows

Treatment

treat all members of the family and sexual contactstoo, whether they are itching or not

scabicide

permethrin

malathion

Applied with paintbrush

second application, a week after the first

Residual itching may last for several days,or even a few weeks

calamine lotion

Ordinary laundering deals satisfactorily with clothingand sheets. Mites die in clothing unworn for 1 week.

Burrows are

grey–white

slightly scaly

Linear or cervelinear papules

Pathognomonic for Scabies

3/19/2011 - Maen K. Abu Househ | Reviewed by Reem Al-qudah - Scabies


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BullousDiseases

Location of bullae

Subepidermalbulla

tend to be tense

intact

may contain blood

Intra-epidermalbulla

within the pricklecell layer

thin roofs

rupture easily

leave an oozingdenuded surface

Subcornealbulla

beneath the

stratumcorneum

thinner roofs

rupture more easily

Infections

impetigo

Ecthyma

herpes simplex

herpes zoster

vesicular tinea pedis

Acute dermatitis

epidermolysis bullosaGenetic

bullous lupus erythematosus

Porphyria cutanea tarda

Blisters in diabetes and renal disease

Autoimmune

Pemphigus

Pemphigoid

Dermatitis herpetiformis

drugsPenicillamine

cold and friction injury

3/16/2011 - Maen K. Abu Househ | Reviewed by Reem Al-qudah - Bullous Diseases


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Pemphigoid

Intro Autoimmune

mainly affecting the elderly

Cause

IgG mediate

Bind to

At Basement membrane

BP230

BP180

Complement is then activated

Usually no precipitating factorsBut UV play a part

Presentation

chronic

itchy

blistering

Lesion

smooth, itching red plaques

in which tense vesicles and bullae form

flexures are often affected

Nikolsky test is negative

high risk

old age

need for high steroid dose

low serum albumin levels

Courseself-limiting

treatment can often be stopped after 1-2 years

Complication

much discomfort

loss of fluid

S/E of Systemic steroids andimmunosuppressives


Investigations

Biopsy

subepidermal blister

filled with eosinophils

Directimmunofluorescence

linear band of IgG and C3 alongthe basement membrane

Indirect immunofluorescence

antibodies that bind to

normal skin at thebasement membrane

in 70% of patients

titre does not correlate with clinicaldisease activity

Treatment

Mildpotent topical steroids

acute phaseprednisolone or prednisone

dosage is reduced as soon as possible

Immunosuppressives

3/16/2011 - Maen K. Abu Househ | Reviewed by Reem Al-qudah - Pemphigoid


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Pemphigus

severelife-threatening

it affects middle age

Types

pemphigus vulgaris

3/4 of cases

Pemphigus vegetans rare

common in AshkenaziJews, Mediterraneans and Indian

superficial pemphigus

generalized foliaceus

localized erythematosus

Drug eruptionpenicillamine

paraneoplasticpemphigus

thymoma

Castleman’s tumour

lymphoma

Cause All are autoimmune

IgG mediated

main antigensdesmoglein 3

desmoglein 1

Presentation

Pemphigusvulgaris

flaccid blistersOn skin

Trunk

flexures

scalp

In mouth

Most patients develop the mouth lesions first

blisters rupture easily

Leaves widespread painful erosions

Positive Nikolsky sign

Shearing stresses on normal skincan cause new erosions

also positive in toxic epidermal necrolysis

Vegetans variant

heaped-up, cauliflower-like weeping areasare present in the groin and body folds

pemphigusfoliaceus

Blisters so superficialrupture so easily

Dominated more by weeping and crusting erosions than by blisters

pemphigus erythematosus

facial lesions

pink, rough and scaly

patient is in poor health bcoz of the diseases it self

Course

Course is prolonged

mortality rate15%

1/3 go into remission after 3 years

Superficial pemphigus is less severe

Complications

Due to high dose of steroids and immunosuppressives

severe oral ulcers make eating painful

dehydration and electrolytes imbalance


Widespreaderosions

pyoderma

impetigo

ecthyma

epidermolysis bullosa

Mouth ulcers

Aphthous ulcer

Behçet’s disease

herpes simplex infection

Scalp erosionsbacterial or fungal infections

Investigations

Biopsy

vesicles are intra-epidermal

Acantholysis

rounded keratinocytes floating freelywithin the blister cavity


intercellular epidermaldeposits of IgG and C3

Indirectimmunofluorescence

serum from a patient with pemphigus containsantibodies that bind to the desmogleins in thedesmosomes of normal epidermis

ELISA

titre of these antibodiescorrelates loosely with clinical activity

Tzank smear acantholysis

Treatment

In superficial pemphigus

small doses of systemic corticosteroids

topical corticosteroids

high doses of systemic steroids

mmunosuppressives

azathioprine

gold salts

cyclophosphamide

mycophenylate mofetil

plasmapheresis

intravenous immunoglobulin

Dapsone

3/16/2011 - Maen K. Abu Househ | Reviewed by Reem Al-qudah - Pemphigus


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Dermatitisherpetiformis

Intro

chronic

very itchy

secondary eczematous dermatitis

'dermatitis'

subepidermal vesicles

erupt in groups

‘herpetiformis’

Cause

Autoimmune

Antibodiesagainst

epidermaltransglutaminase

Always associatedwith Gluten-sensitiveenteropathy

Can be asymptomatic

patchy

involves only theproximal smallintestine

Other serum antibodies

tissue transglutaminase

reticulin

gliadin

endomysium

Presentation

mainly affects adults

extremely itchy

grouped vesicles

often broken byscratching

shows only groupedexcoriations

urticated papules

Site

elbows

knees

buttocks

shoulders

secondary eczematous dermatitis develops

Course

Prolonged unless treated

Resolves later than enteropathy withGluten free diet

Complications

diarrhoea

abdominal pain,

anaemia

malabsorption

Small bowel lymphomas

Decreased risk withGluten free diet

Investigations

Biopsy

subepidermal blister

neutrophils packing theadjacent dermal papillae


granular deposits of IgA

C3

in the dermal papillae

Serum antibody tests

anti-endomysial antibodies

tissue transglutaminase

Treatment

dapsone

sulfapyridine

gluten-free diet

Resolves later than enteropathy withGluten free diet

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