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Dermatology Flashcards

1
Q

What are 2 topical corticosteroids classified as “Very Potent” in Australian Classifications

A

Betamethasone dipropionate 0.05% in optimised ointment

Clobetasol propionate 0.05% ointment

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2
Q

What are 3 topical corticosteroids classified as “Potent” in Australian Classifications

A

Betamethasone dipropionate 0.05% in standard ointment
Betamethasone valerate 0.1% ointment
Mometasone furoate 0.1% ointment/cream

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3
Q

What are 5 topical corticosteroids classified as “moderate” in Australia

A

Betamethasone dipropionate 0.05% Cream/lotion
Betamethasone valerate 0.05% ointment and vream
Triamcinolone acetonide 0.1% cream
Methylprednisolone aceponate 0.1% ointment/cream/lotion
Clobetasone 0.05% cream

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4
Q

What are 2 topical corticosteroids classified as “Low potency” in Australia

A

Hydrocortisone or hydrocortisone acetate 0.5%, 1% (ointment/cream/lotion)
Desonide 0.05% (ointment/cream/lotion)

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5
Q

Features of different forms of topical corticosteroids

A

Ointments:

  • improve drug absorption due to occluding skin and enhancing hydration
  • greasy, difficult to spread, poor adherence

Creams:

  • combo of 1 or more non-mixable liquids + emulsifying agent
  • less greasy, easy to spread
  • washable in water

Lotions:

  • insoluble preparations dispersed into liquid
  • may need shaking to prepare for use
  • easy to apply
  • can cover extensive areas
  • preferred for children, and hairy skin
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6
Q

Local adverse effects of topical steroids

A
  • Atrophy (skin transparency, brightness, telangiectasia, striae, easy bruising)
  • Rosacea, acne or perioral dermatitis when used on face

Less common:
Hypopigmentation, delayed wound healing, glaucoma (when used around eye), rebound effect when ceased, loss of clinical improvement after period of use, masking or stimulation of cutaneous infections e.g. tinea incognito

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7
Q

Systemic adverse effects of topical corticosteroids

A

Uncommon, associated with prolonged use of high potency steroids in large or denuded areas

  • reversible HPA axis suppression
  • Addisonian crisis on ceasing
  • Cushing’s syndrome
  • DM
  • hyperglycaemia
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8
Q

Diseases likely to be highly responsive to topical corticosteroids

A

Inflammatory conditions on thin skin;

e. g.
- intertriginous psoriasis
- Children’s atopic dermatitis
- other intertrigos

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9
Q

Diseases likely to be moderately responsive to topical corticosteroids

A

Psoriasis
Adult atopic dermatitis
Nummular eczema

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10
Q

Diseases likely to be least responsive to topical corticosteroids

A

Chronic, hyperkeratotis, lichenified or indurated lesions. e.g.

  • palmo-plantar psoriasis
  • lichen planus
  • lichen simplex chronicus
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11
Q

Sites and absorption of topical corticosteroids

A

Palms, soles - poor absorption (0.1-0.8%)
Forearms - poor (1%)
Scalp and intertriginous areas - moderate (4%)
Face - moderate (10%)
Scrotum and eyelids - very high (40%)

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12
Q

Choice of topical corticosteroid vehicle for disesase

A

Ointments: thick, fissured lichenified lesions SHOULD NOT BE USED IN FLEXURAL OR INTERTRIGINOUS areas

Creams: most areas except scalp/hairy skin

Lotions: extensive areas

Solutions, gels, sprays, foams: scalp and hairy skin

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13
Q

Maximum doses of topical corticosteroids in adults

A

Potent: 45g/week

Moderately potent: 100g/week

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14
Q

Maximum duration of topical steroids

A

Face: 2 weeks

Rest of body: 3-4 weeks

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15
Q

Adjunctive treatments with topical corticosteroids

A

Skin care to improve skin’s overall integrity and improve clinical outcome

  • soap-free cleansers
  • moisturisers
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16
Q

Focused history for skin check

A

Presenting complaint - new, changing or concerned lesions
Occupation, sun exposure and sun protection
Personal and family history of NMSC and melanoma
General medical history (current and past)
Drug history (esp. anticoagulants, immunosuppressants)

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17
Q

High risk patients for skin cancer and how frequently should have skin check

A

3 monthly self examination, 12 monthly skin check

  • red hair
  • Type I skin >45y
  • type II skin >65y
  • Family history of melanoma in first degree relative in patients >15y
  • > 100 naevi (>10 atypical)
  • past history of melanoma
  • Past history of NMSC or >20 solar keratoses
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18
Q

Medium risk patients for skin cancer and recommended frequency of skin checks

A

3-6 monthly self-check, 2-5 yearly skin check with doctor

  • Blue eyes
  • Type 1 skin 25-45y
  • Type II skin 45-65y
  • Type 3 skin >65
  • Family history of NMSC
  • Past history of solar keratosis
  • multiple previous episodes of sunburn
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19
Q

Low risk patients for skin cancer and recommended frequency of skin checks

A

Annual self-check, one-off skin check with doctor for assessment of risk and advice regarding skin care

  • Type I skin <25y
  • Type II skin <45y
  • Type III skin <65y
  • Type 4 & 5 skin
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20
Q

Cure rate for solar keratoses with cryotherapy

A

86-99%

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21
Q

Contraindications for cryotherapy

A
  • Lesions with poorly defined margins
  • Lesions >2cm diameter
  • Lesions >3mm deep
  • lesions tethered to underlying structures
  • lesions on ala nasi, eyelids, nasolabial fold and pre-auricular skin
  • recurrent lesions
  • agammaglobuliaemia cryoglobulinaemia
  • blood dyscrasias of unknown origin
  • cold urticaria
  • Raynaud’s disease
  • Pyoderma gangrenosum
  • collagen and autoimmune disease
  • avoid if histology is uncertain
  • can be problematic for patients with Fitzpatrick III-V due to post inflammatory hyperpigmentation and hypopigmentation
  • risk of alopecia on hair bearing skin e.g. beard area
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22
Q

Recommended technique for cryotherapy of solar keratosis

A

1x freeze cycle of 15 seconds, 1mm margin

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23
Q

Expected results after cryotherapy with liquid nitrogen

A

Day 1: red, swollen, blister may develop and may fill with blood - best to leave alone
Days 2-3: Treated area becomes weepy, leave skin open to air if mild and wash with soap and water, if excessive cover with dressing or topical antiseptic
Days 3-4: Area should stop weeping and form scab which usually spontaneously falls off within a week
Should then heal without a scar - may be slightly darker or lighter skin temporarily (may be permanent)

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24
Q

Indications to biopsy a clinical actinic keratosis

A 
"Thickness" on palpation
Pain - particularly on lateral pressure
Bleeding
Rapid growth
Failure of standard topical treatments
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25
Q

recommended biopsy techniques for NMSC

A

Excisional
Punch from CENTRE of lesion if diagnosis required before management, unless ulcerated centre then use more distal site of lesion
- Incisional biopsy may be an option for ulcerated lesions including peripheral and central ulcerated components

Shave biopsy not advised
*BCC tends to be heterogenous and partial punch biopsy may fail to identify aggressive component in 15%

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26
Q

Recommended biopsy technique in pigmented lesions

A

If requires biopsy, excisional biopsy with 2mm clinical margins should be performed
EXCEPT:
- broad lesions on face may consider shave or incisional biopsy if no invasive component on palpation
- large lesions or lesions on functionally sensitive areas e.g. sole of foot - may consider punch or incisional biopsy to confirm diagnosis

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27
Q

Choosing inflammatory lesions to biopsy

A

Generally, choose estalbished lesions, not ones that are so old they have scarring or crust surface
In blistering, pustular or vasculitis conditions, early lesions within 48h of appearance are better

If other lesions available, avoid sites such as:

  • cosmetically sensitive e.g. face
  • areas prone to hypertrophic scarring e.g. shoulders, chest, breast
  • legs as poor healing and venous stasis changes histo
  • high risk areas for infection (axilla and groin)
  • bony prominences or pressure bearing areas

Good areas: thighs, abdo, back, arms

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28
Q

Important info to include on request form for skin biopsy

A 
Patient age and gender
Precise anatomical site of biopsy
morphological description of lesion(s) + any evolution
Distribution of lesions
Clinical impression and differentials
Prior skin biopsy results or diagnoses
Medications if drug eruption is a differential
Other relevant patient clinical history

Specify if ancillary testing required

Provision of dermatoscopic and clinical photographs if possible

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29
Q

Post skin biopsy care

A

Dress with moist occlusive dressing and paraffin ointment and leave alone for 24-48h
After this, gently clean wound daily with warm water and reapply paraffin ointment with non-stick dressing until re-epithelialisation is complete
If sutures present, remove after:
- 5-7 days face
- 12-14 days back and legs
- 7-10 days other areas

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30
Q

Duration to leave sutures in for body sites

A

Face: 5-7 days
Back or legs: 12-14 days
Other areas: 7-10 days

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31
Q

Clinical features of cutaenous SCC

A

Enlarging scaly or crusted lumps (usually arise within pre-existing IEC or AK)
May ulcerate
Often tender or painful
Located on sun-exposed sites

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32
Q

Risk factors for cutaneous SCC

A 
Older age, male gender
Previous SCC or other skin cancer
Actinic keratoses
Outdoor occupation or recreation
Smoking
Fair skin, blue eyes, red/blond hair
Previous cutaneous injury, burn, disease
Inherited syndromes (albinism, xeroderma pigmentosum)
Immune suppression/organ transplant
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33
Q

Features of high risk cutaneous SCC

A

Diameter 2cm or more
Location on ear, vermilion of lip, central face, hands, feet, genitalia
Arising in elderly or immune suppressed patient
Histological thickness >2mm, poorly differentiated histology or with invasion of subcut tissue, nerves and blood vessels

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34
Q

Margin for cutaneous SCC excision

A

3-10 mm

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35
Q

Risk factors for BCC

A 
Elderly males
Previous BCC or other skin cancer
Sun damage
Repeated prior episodes of sunburn
Fair skin/blue eyes/ blond/red hair
Previous cutaneous injury, thermal burn, skin disease
Inherited syndromes
- Xeroderma pigmentosum
- Gorlin syndrome
- Rombo syndrome
- Oley syndrome
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36
Q

Clinical features of BCC

A

Slowly growing plaque or nodule
Skin coloured, pink OR pigmented
Spontaneous bleeding or ulceration

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37
Q

Clinical subtypes of BCC

A

Nodular:
- most common
- shiny/pearly nodule with smooth surface
- may have central depression/ulcerations/rolled edges
- blood vessels cross surface
Superficial BCC
- most common type in younger adults
- most common type on upper trunk and shoulders
- slightly scaly, irregular plaque
- think, translucent rolled border
- multiple microerosions
Morphoeic/sclerosing BCC:
- usually in mid-face
- waxy, scar-like plaque with indistinct borders
- may infiltrate cutaneous nerves
Basosquamous carcinoma
- mixed BCC and SCC
- infiltrative growth pattern
- potentially more aggressive than other forms of BCC

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38
Q

Treatment options for BCCs

A

Excision with 3-5mm margin: nodular, infiltrative or mrorphoeic
Moh’s surgery: high risk areas (face around eyes lips and nose)
Superficial skin surgery: shave, curettage and electrocautery
Cryotherapy: suitable for small superficial BCCs on covered areas of trunk and limbs (not head and neck or distal to knee
Photodynamic therapy: low-risk small superficial BCCs, not in sites of high risk of recurrence
Imiquimod: superficial BCCs <2cm
Fluorouracil: small superficial BCCs, high risk of recurrence
Radiotherapy: mainly used if surgery not suitable

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39
Q

Risk factors for melanoma

A

Increasing age
Previous melanoma or NMSC
Many melanocytic naevi
>5 atypical naevi (large or dysplastic on histo)
Strong family history of melanoma (2+ first degree relatives affected)
White skin that burns easily
Parkinson disease

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40
Q

Precursor lesions for melanomas

A

75% arise from otherwise normal-appearing skin

Benign melanocytic naevus
Atypical or dysplastic naevus
Atypical lentiginous junctional naevus or atyipcal solar lentigo
Large congenital melanocytic naevus

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41
Q

Most common sites for melanomas

A

Males: back
Females: legs

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42
Q

Dermoscopic signs of melanoma

A

Disorganised asymmetrical pigment network
Atypical vascular patterns
Blue-grey structures
Multiple colours

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43
Q

Clinical subtypes of melanoma

A

Flat/horizontal growth:

  • superficial spreading
  • lentigo maligna
  • acral lentiginous melanoma

Vertical growth/deeper tissues:

  • nodular
  • mucosal
  • desmoplastic/neurotropic
  • Spitzoid
  • spindle cell
  • ocular
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44
Q

Diagnosis of melanoma

A

Elliptical excisional biopsy with 2mm margin for suspicious pigmented lesions

Special circumstances: deep shave biopsy or punch biopsy

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45
Q

Difference between ephelides and lentignes

A

Ephelides = freckles, inherited condition, not present at birth, no increase in melanocytes, fade in winter months
Lentignes: increased number of melanocytes, do not fade in winter months, may be precursor to other lesions e.g. seb K, naevi

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46
Q

What is solar elastosis

A

Yellow, thickened appearance of skin as a result of sun damage/photo-ageing (also result of smoking)

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47
Q

What is Leser-Trelat sign

A

Eruptive appearance of many seborrhoeic kerkatoses due to underlying malignancy (most commonly gastric adenocarcinoma)

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48
Q

Dermatoscopic clues of seborrhoeic keratosis

A
  • Multiple orange or brown clods
  • White “milia-like” clods
  • Curved thick ridges or furrows forming brain-like (cerebriform) pattern
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49
Q

Treatment options for seborrhoeic keratosis

A 
Cryotherapy
Curettage/electrocauterisation
Laser surgery
Shave biopsy
Chemical peel
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50
Q

Other names that may be used to describe skin tags

A

Papilloma
Acrochordon
Fibroepithelial polyp
Soft fibroma

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51
Q

Treatment options for skin tags

A

Cryotherapy
Excision (often with scissors)
Electrosurgery/diathermy
Ligation

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52
Q

Differentials for skin tags

A

Seborrhoeic keratoses
Viral warts
Molluscum contagiousum

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53
Q

Risk factors for worse/more skin tags

A

Obesity

T2DM

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54
Q

Clinical features of keratoacanthoma

A

Rapidly growing lesion over a few months, starts as small pimple/boil-like lesion but full of solid keratin then grows rapidly
May start at site of minor injury to sun damaged and hair-bearing skin

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55
Q

Cells from which keratoacanthoma arises

A

Hair follicle skin cells

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56
Q

Vascular birthmarks

A

Naevus simplex/Stork Mark: Pink-red on forehead/brow/upper eyelids or nape, self-resolve by 1-3 years

Naevus Flammeus/Port wine stain: If on face may indicate neuro or opthal structural abnormality and require investigations, otherwise darken and thicken overtime. Never fade

Infantile haemangioma/strawberry naevus:
- often unapparent at birth and grow rapidly for several months before gradual involution over several years, treat only if required for severe symptoms (e.g. eyes, airway etc.) with propanolol +/- prednisolone

Venous Malformations: skin coloured, blue or purple swellings anywhere on body, may become more obvious over time, grow in proportion to child’s general growth

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57
Q

Common isolated/local types of telangiectasia

A

Spider telangiectasia: central arteriole and radiating capillaries, arise more often in response to oestrogen (pregnancy, liver disease)
Venous lake: blue or purple compressible papule due to venous dilation, often on lower lip or ear, treat for cosmesis only (sclerotherapy, cryotherapy, IPL, laser)

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58
Q

Features of benign hereditary telangiectasia

A

Inherited autosomal dominant disease
Lesions appear in first years of life, rarely present at birth, more prominent in pregnancy
Widely distributed over face, neck, upper trunk, dorsal hands and knees
As age, increase in size and become paler
NO mucosal involvement
Asymptomatic and DO NOT bleed

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59
Q

Hereditary haemorrhagic telangiectasia

A

Rare inherited disorder presenting usually after 12y with recurrent nosebleeds, telangiectases that develop elsewhere after puberty, mostly on upper half of body INCLUDING MUCOSAL MEMBRANES. May have GI bleeding also

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60
Q

Diagnostic criteria for hereditary haemorrhagic telangiectasia

A
  1. Recurrent nosebleeds
  2. multiple telangiectases on skin and mucous membranes
  3. Involvement of internal organs
  4. affected parent, sibling or child
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61
Q

Malignant vascular tumours

A

Kaposi sarcoma
Angiosarcoma
Intravascular B-cell lymphoma

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62
Q

Risk of a single solar keratosis becoming malignant

A

1/1000 per annum

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63
Q

Treatment for tinea infections

A

anywhere EXCEPT scalp or nails: Topical treatment unless extensive (Canestan, Daktarin, terbinafine creams) until rash completely clears AND THEN FURTHER 2 WEEKS

For scalp or nails: oral terbinafine, fluconazole or itraconazole

+ for macerated lesions make sure kept dry

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64
Q

Clinical presentation of tinea capitis

A

Patchy alopecia
Scalp scaling
Broken hairs at scalp surface/black dots
Kerions (abscess-like lesions that are tender and fluctuant)
Favus (yellow crusts and matted hair)
Wood lamp examination may be useful in some cases

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65
Q

Most common organisms causing tinea

A 
Trichophytum rubrum
Microsporum canis (from cats and dogs)
Trichophytum verrucosum (from farm cattle)
Trichophytum interdigitales
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66
Q

Diagnosis of fungal infections

A

Fungal microscopy and culture PRIOR to antifungal treatment:

  • skin scrapings
  • subungual debris
  • nail clipping
  • plucked hairs
  • scalp scales may be removed with a toothbrush
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67
Q

Predisposing factors to candidal infection

A 
Infancy or elderly
Warm climate
Occlusion e.g. plastic pants, nylon pants, dentures
Broad spectrum antibiotic treatment
High oestrogen (OCP/pregnancy)
Endocrine disorders (Cushing, DM)
Iron or other nutritional deficiencies
General debility e.g. cancer
Immunodeficiency or suppression
Underlying skin disease e.g. psoriasis, lichen planus
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68
Q

Risk factors for ORAL candidiasis specifically

A 
Maternal vaginal yeast infection in newborns
Dry mouth (e.g salivary disease or meds)
Dentures
Smoking 
Inhaled corticosteroids
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69
Q

Prevention of oral candidiasis

A

Good dental/oral hygiene
Warm saline as mouth wash, avoid antiseptic mouth washes
Rinse mouth after inhaled corticosteroids
Clean dentures with anti-candidals BD and store in dry place overnight

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70
Q

Treatment of oral candidiasis

A

Confirm candida before commencing treatment!

Denture-associated, managed with denture hygiene only

If antifungal therapy indicated:
amphotericin lozenges/miconazole gel/nystatin drops
Each is QID dosing for 7-14 days

Discuss with specialist if immunocompromised

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71
Q

Clinical features of CANDIDAL intertrigo

A

Erythematous and macerated plaques with peripheral scaling
+/- superficial satellite papules or pustules
Diagnosis usually clinical

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72
Q

Management of candidal intertrigo

A

Manage predisoposing factors
Topical antifungal e.g. clotrimazole for 2 weeks
If topical treatment impractical or response is poor, PO fluconazole as single dose

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73
Q

Treatment of nappy rash candidiasis

A

Keep child dry, change when wet
Wash hands before and after changing
Avoid plastic pants
Topical antifungal creams

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74
Q

Risk factors for pityriasis versicolor

A

Young adults most frequently M>F
More common in hot, humid climates
Heavy perspiration
May clear in winter months and recur each summer

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75
Q

Cause of pityriasis versicolor

A

Malassezia yeasts, most commonly:

- M globosa, M restrica, M sympodialis

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76
Q

Clinical features of pityriasis versicolor

A

Affects truck, neck and/or arms - uncommon elsewhere

Scaly patches coppery brown OR paler than surrounding skin OR pink

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77
Q

Treatment of pityriasis versicolor

A

Mild disease: topical antifungal creams (azoles or terbinafine creams or shampoos)

Oral antifungals if extensive or topical agents failed: itraconazole or fluconazole for few days oral terbinafine not useful for malassezia

note white marks may persist long after scaling and yeasts gone, further antifungal unhelpful in this case

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78
Q

Recurrent pityriasis versicolor treatment

A

Repeat antifungal treatment when scale recurs

If frequent: antifungal shampoo OR oral antifungal treatment 1-3 days each month

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79
Q

Prevalence of dermatitis

A

Will affect 1 in 5 people at some point in their lives

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80
Q

General treatments for dermatitis

A
  • reduce frequency and duration of bathing (2-3 mins)
  • use lukewarm/tepid water for bathing
  • replace soap with mild soap-free cleanser from chemist
  • wear soft, cool clothes e.g. cotton (avoid coarse fibres e.g. wool or synthetic)
  • avoid irritants (chlorine, sand, grass, dust, detergents etc.) and wash immediately after coming into contact
  • Liberal, regular use of non-perfumed emollients
  • topical steroids
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81
Q

Usual age of atopic dermatitis

A

Most will develop before the age of 2, unusual before 4 months, symptoms worst 2-4y then tend to improve

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82
Q

Distribution of atopic dermatitis rash in infants

A

Often widely distributed, dry, scaly and red
Cheeks often first place affected
Nappy area often spared due to moisture retention

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83
Q

Clinical features of atopic dermatitis in toddlers and pre-schoolers

A

More localised and thickened
Vigorous itching
Extensor surfaces (esp wrists, elbows, ankles, knees)

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84
Q

Clinical features of atopic dermatitis in school-aged children

A

Flexural pattern - mostly elbow and knee creases
Other areas: eyelids, earlobes, neck and scalp
May develop pompholyx
May develop a nummular pattern
mostly improves during school years

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85
Q

Clinical features of atopic dermatitis in adults

A

Often drier and more lichenified than in children
Commonly persistent localised eczema in hands, eyelids, flexures, nipples
Contributes to occupational irritant contact dermatitis

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86
Q

Wet wraps for eczema

A

Layer of corticosteroid under wet layer of clothing or towel for 15-20 minutes

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87
Q

Bleach baths for eczema

A

Indicated to manage recurrent S. aureus infections

twice per week

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88
Q

Clinical features of periorifacial dermatitis

A

Clusters of small papules and surrounding erythema, may be scaly and occasionally vesicles or pustules develop
5-10mm skin adjacent to vermilion unaffected (contrast to contact dermatitis)

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89
Q

Precipitants of periorifacial dermatitis

A 
Topical steroids (esp potent)
Inhaled or intranasal steroids
Thick moisturisers
Sunscreen/cosmetics
Inadequate face-washing
Pregnancy or other hormonal change
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90
Q

Treatment of periorifacial dermatitis

A
  • Avoid oil-based facial creams
  • cleanse face twice daily with mild soap or non-soap cleanser
  • Oral anti-inflammatory antibiotics for 4-8 weeks
  • topical agents not effective and generally best avoided
  • if already on topical steroid, possible flare up on stopping, if necessary continue with weaning onto milder product until weaned off
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91
Q

Age of onset of seborrhoeic dermatitis

A

Infantile: <3 months, resolves by 6-12 months

Adults; tends to begin in late adolescence, prevalence greatest in young adults and elderly

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92
Q

Risk factors for severe adult seborrhoeic dermatitis

A 
Oily skin
Familial tendency to seborrhoeic dermatitis
Family history of psoriasis
Immunosuppression
Neurological and psychiatric disease
Treatment for psoriasis
Lack of sleep and stressful events
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93
Q

Clinical features of pompholyx/vesicular hand dermatitis

A

Intensely itchy crops of skin-coloured blisters on palms and sides of hands and fingers +/- feet

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94
Q

Common trigger of pompholyx

A

Emotional stress (which causes hyperhidrosis)

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95
Q

Cause of seborrhoeic dermatitis

A

Unclear, related to malassezia yeasts

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96
Q

Clinical features of infantile seborrhoeic dermatitis

A

Cradle cap/ armpit or groin fold rash

  • Salmon-pink patches that may flake or peel
  • not very itchy, baby often undisturbed
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97
Q

Clinical features of adult seborrhoeic dermatitis

A

Affects scalp, face (creases around nose, behind ears, within eyebrows) and upper trunk

  • winter flares, improve after sun exposure
  • minimal itch
  • combo oily and dry mid-facial skin
  • ill-defined localised scaly patches or diffuse scale in scalp
  • blepharitis
  • salmon-pink, thin, scaly, ill-defined plaques in skin folds on side of face
  • rash in skin folds
  • superficial folliculitis on cheeks and upper trunk
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98
Q

Treatment of infantile seborrhoeic dermatitis

A

Regular washing of scalp with baby shampoo followed by gentle brushing to clear scales

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99
Q

Treatment of adult seborrhoeic dermatitis

A

Scalp: medicated shampoos with ketoconazole and salicylic acid twice weekly for at least a month
+/- steroid scream applications to reduce itch
- Coal tar cream to scaling areas and remove several hours later with shampoo

Elsewhere: cleanse thoroughly 1-2 times per day using non-soap cleanser
Ketoconazole cream daily for 2-4 weeks
topical steroids or calcineurin inhibitor if required

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100
Q

Age of onset of psoriasis

A

Onset at any age

Bimodal peaks in late teenage years and 50-60yo

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101
Q

How common is psoriatic arthritis in patients with skin psoriasis

A

40% will have associated arthritis

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102
Q

What is Auspitz sign

A

Removal of thick psoriatic scale reveals pinpoint bleeding

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103
Q

Clinical features of chronic plaque psoriasis

A

Well defined, raised red patches with adherent silvery scale
Symmetrical rash
Not as itchy as eczema

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104
Q

Nail changes associated with psoriasis

A

Pitting, onycholysis, subungal hyperkeratosis

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105
Q

Less common forms of psoriasis (6)

A 
Guttate psoriasis
Psoriasis of palms and soles
Pustular psoriasis
Flexural psoriasis
Erythrodermic psoriasis
Infantile psoriasis
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106
Q

Clinical features of guttate psoriasis

A

Typically presents in teens or early 20s after a streptotoccal sore throat
May be florid outbreak of small plaques, especially on trunk and proximal limbs

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107
Q

Clinical features of psoriasis of palms and soles

A

Well defined edge of involved skin adjacent to normal skin

Back of the hands and web spaces unlikely to be involved

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108
Q

Clinical features of pustular psoriasis

A

Mostly on palms and soles (can occur on body)
Mix of new and old pustules (look like small brown dots)
HIGH CORRELATION WITH SMOKING

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109
Q

Clinical features of flexural psoriasis

A 
Usually lacks scale due to moisture
Well defined border (in contrast to intertrigo and eczema)
No pustules (in contrast to thrush)
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110
Q

Clinical features of erythrodermic psoriasis

A

Appears rapidly when oral steroids have been stopped
Patient typically very unwell - unable to regular temperature or fluid
Entire skin surface red and scaly
Skin is hot, but patient often hypothermic

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111
Q

Clinical features of infantile psoriasis

A

May involve nappy area, axillae, neck, umbilicus
Child not distressed as little or no itch
Difficult to distinguish from seborrhoeic dermatitis

112
Q

Common drug triggers for psoriasis

A

Lithium
Beta blockers
NSAIDs

113
Q

Treatment of psoriasis

A 
General health:
- smoking cessation
- diet
- weight control
- avoid excessive alcohol
General skin measures:
- avoid scratching/rubbing/picking
- regular moisturiser
- short tepid showers
Specific treatments;
- topical corticosteroids
- topical calcipotriol
- dithranol
- tar cream
Systemic treatments
- phototherapy
- MTX
- cyclosporin
- biological agents
114
Q

Good initial management routine for psoriasis

A
  • Quick tepid shower with soap substitute
  • weekly bath with bath oil or oatmeal
  • Sorbolene with 10% glycerine in the morning
  • betamethasone 0.05% ointment at night
    +/- short term intermittent treatment with ointment containing calcipotriol and betamethasone

Continue for 1 month, if good response continue with just moisturiser, if poor response consider adding further agents

115
Q

Use of dithranol ointment

A

Used for psoriasis
Temporarily stains skin, permanently stains clothes
Apply carefully to plaque only and wash off after half an hour
avoid on face and flexures

116
Q

Management of psoriasis on face or flexures

A

1% hydrocortisone (cream on moist areas, ointment on dry)

Calcipotriol may be used by more likely to cause irritation - may be appropriate to alternate with steroid

117
Q

Management of infantile psoriasis

A

Usually responds well to bland emollients only (e.g. sorbolene)

118
Q

Management of scalp psoriasis

A

Apply tar cream at night and wash out in morning 1-2x per week
Apply a steroid lotion on the other days

119
Q

Management of nail psoriasis

A

Can be very resistant to treatment
Steroid lotion to cuticle and under the end of the nail each night
Apply moisturiser several times a day to nail
Slow response (months)

120
Q

When to refer psoriasis to specialist

A
  • extensive psoriasis (>10-20% BSA) that is not controlled
  • diagnostic uncertainty
  • significant associated arthritis
  • rapidly progressive psoriasis, acute erythrodermic psoriasis or generalised pustular psoriasis (emergency)
  • difficult to treat sites not responding to initial treatment (face, genitals, palms, soles)
  • Psoriasis unresponsive to topical therapies
  • major physical and/or psychological disability associated with the disease
121
Q

Associated comorbidities of psoriasis

A 
Hypertension
Obesity
Hyperlipidaemia
Heart disease
Diabetes
Inflammatory bowel disease
Lymphoma
Depression
122
Q

Epidemiology of rosacea

A

Most commonly affects fair skinned, blue eyed Europeans or Celtics
Symptoms typically peak 30-50y
More common in females, however phymatous rosacea more common in males

123
Q

Clinical features of rosacea

A

Primary: persistent erythema of central face >3 months

Other findings:

  • flushing
  • telangiectasia
  • oedema
  • inflammatory papules
  • pustules
  • ocular symptms
  • rhinophyma or hyperplasia of connective tissue
124
Q

4 primary subtypes of rosacea

A

Erythrotelangiectactic (vascular) rosacea:

  • flushing and vasodilation overtime leads to permanent erythema and telangiectasia
  • central face most affected, ears, neck and upper chest can also be affected

Papulopustular rosacea

  • persistent or episodic developement of inflammatory papules and pustules, often on central face +/- background ETR
  • typically in middle-aged women

Phymatous rosacea

  • hyperplasia of skin due to chronic inflammation
  • nose most commonly affected (rhinophyma)
  • most common in older men
  • significant telangiectasia can be present over affected areas

Ocular rosacea:

  • may precede skin symptoms
  • blepharitis and conjunctivitis are most common findings
125
Q

Common triggers for rosacea (12)

A 
Emotional stress
hot or cold weather
Sun exposure
Wind
Exercise
Hot drinks
Alcohol
Spicy foods
Dairy products
Hot baths or showers 
Certain skin care products/cosmetics
Medications
126
Q

Treatment of rosacea

A

General measures:

  • identify triggers and avoid/keep journal to identify triggers
  • sun protection
  • soap-free and abrasive free cleansers
  • moisturise if skin is dry
  • avoid abrasive materials, pat dry with towel for better absorption of moisturiser
  • cosmetics with green or yellow tint to conceal redness

First-line:

  • metronidazole cream or gel + azelaic acid
  • topical ivermectin can be added for inflammation +/- briminotide for erythema

If rhinophyma: isotretinoin (specialist)

+/- topical/oral antibiotics (doxycycline) for inflammatory lesions

127
Q

What is acne conglobata and acne fulminans

A

Acne conglobata is a rare form of nodulocystic acne characterised by interconnecting abscesses and sinuses

Acne fulminans is a very rare and severe acute form of acne conglobata associated with systemic symptoms

128
Q

Superficial lesions in acne

A

Open and closed uninflamed comedomes (whiteheads and blackheads)
Papules
Pustules

129
Q

Deeper lesions in acne

A

Nodules (large painful red lumps)

Pseudocysts (cyst-like fluctuant swellings)

130
Q

Secondary lesions in acne

A 
Excoriations
Erythematous macules (red marks from recently healed spots, mostly seen in fair skin)
Pigmented macules (dark marks from old spots, mostly affecting dark skin)
131
Q

How long do individual acne lesions last

A

<2 weeks for superficial lesions

Deeper papules and nodules may last several months

132
Q

Grading severity of acne:

A

By total lesion count or inflammatory lesion count:
Mild: <30 total (<15 inflam)
Moderate: 30-125 total (15-50 inflam)
Severe: >125 total, >50 inflam OR >5 pseudocysts

133
Q

Treatment of mild acne

A

Topical antiacne (benzoyl peroxide and/or tretinoin or adapalene gel)
Low dose COCP
Antiseptic or keratolytic washes containing salicylic acid
Light/laser therapy

134
Q

Treatment of moderate acne

A

As for mild + doxycycline 50-200mg per day for 6 months (erythromycin or trimethoprim if doxycycline intolerant)
Anti-androgen therapy (cyproterone or spironolactone) for women not responding to low-dose COCP, esp if have PCOS
Isotretinoin if persistent or treatment resistant

135
Q

Treatment of severe acne

A

Refer to dermatologist (urgently if systemic symptoms suggestive of acne fulminans)
Oral isotretinoin usually recommended
Oral antibiotics often used in higher than normal doses

136
Q

General measures for acne control

A

Skin care: no picking/popping, no routine need for moisturiser, oil-free make up and sunscreen - ensure sun protection

Diet: balanced healthy diet, no evidence for specific diets

137
Q

How long before a clinical effect will be apparent with acne management

A

Antibiotics: should see effect within 6 weeks

COCP: at least 3 months before any visible effect, peak effect after 6 months

138
Q

Management of cellulitis

A

WITHOUT systemic features: oral antibiotics for 5-10 days, elevation, rest, and adequate fluid intake

WITH systemic illness: IV antibiotics, fluids
Change to orals once fever settles, rash regressing +/- CRP reducing

139
Q

Risk factors for pitted keratolysis

A

moist skin
therefore occupational factors, hot humid weather, occlusive footwear, hyperhidrosis

Diabetes
advanced age
Immunodeficiency
thickened skin of palms and soles

140
Q

Clinical features of pitted keratolysis

A

Smelly feet
White area on forefoot or heel with clusters of punched out pits that may coalesce to form crater-like lesions - more dramatic appearance when skin is wet

May cause itch or soreness when walking, usually asymptomatic

141
Q

Treatment of pitted keratolysis

A

Clindamycin 1% lotion for 10 days

142
Q

What is erythrasma

A

A common bacterial infection of skin folds under arms, in the groin and between the toes, caused by corynebacterium.

143
Q

Clinical features of erythrasma

A

well-defined pink or brown patches with fine scaling and superficial fissures +/- mild itch
Occurring in skin folds, mostly groin, axillae or interdigital spaces

144
Q

Management of erythrasma

A

Fusidate sodium 2% ointment topically BD for 14 days
OR
PO clarithromycin 1g PO as single dose

Usually self-limiting

145
Q

Epidemiology of impetigo

A 
Most common in children (boys>girls) with peak during summer
Risk factors:
- scabies
- atopic dermatitis
- skin trauma
146
Q

Bacteria involved in impetigo

A

Most commonly staph aureus

In non-bullous impetigo and remote indigenous communities: usually strep pyogenes

147
Q

Clinical features of impetigo

A

Usually affects exposed areas (face and hands)
Single or multiple irregular crops of irritable superficial plaques that extend as they heal, forming annular lesions
Bullous: small vesicles evolving into bullae with honey coloured fluid
Non-bullous impetigo: starts as pink macule -> vesicle or pustule then honey coloured cursted erosion

148
Q

What is ecthyma

A

Punched out necrotic ulcerated lesion secondary to non-bullous impetigo

149
Q

Management of impetigo in non-remote settings

A

Cleanse wound using moist soaks to gently remove crusts
Localised sores: mupirocin 2% to crusted areas TDS for 7days

Mulitple sores or recurrent infection:

  • di/flucloxacillin 12.5mg/kg up to 500mg TDS for up to 10 days (stop earlier if infection resolved)
  • cephalexin or bactrim if hypersensitive

Bactrim if non-responsive

150
Q

Management of impetigo in remote/indigenous communities

A

As s. pyogenes more frequently the pathogen involved:
- benzathine penicillin IM stat
OR
- bactrim BD for 5 days (or higher dose daily for 5 days)
See guidelines for dosages

151
Q

When should leprosy be considered as a differential

A

With any hypopigmented skin patches, particularly if altered sensation present, and in ATSI patients from Northern Australia, or migrants from higher risk countries (Brazil, India, Myanmar, Nigeria and Indonesia) - pacific islands and other developing countries are higher risk than most of Australia

152
Q

Skin changes in syphilis

A

Primary: chancre on genitals, anus or mouth.

  • non-tender, well defined margin with indurated base
  • multiple chancres in 30%
  • spontaneously heals within a few weeks even if untreated

Secondary:

  • generalised rash over trunk (may only involve palms and soles)
  • nonpruritic
  • subtle OR rough, re-brown papules or patches appearing more obvious with physical activity or heat
  • may have patchy alopecia
  • may have condylomata lata (warthy growths) in ano-genital area
153
Q

Management of viral warts

A

1/3 will spontaneously resolve within 3 months, 2/3 within 2 years
Initial treatment should be salicylic acid (best evidence)
Second line is cryotherapy with paring down of wart

154
Q

Duration of exclusion for molluscum

A

No exclusion period required. Advise to avoid sharing towels or bathing together to reduce spread to siblings

155
Q

Management of molluscum

A

Most children do not require treatment, complete resolution will occur when immune response develops in 3 months to 3 years (usually 6-9 months)

Secondary eczema may require treatment

156
Q

Clinical features of molluscum

A

firm, pearly, dome-shaped papules with CENTRAL UMBILICATION
usually 1-3mm but up to 1-2cm
Presentation can often be propted by development of eczema in surrounding skin, obliterating the primary lesions

157
Q

Clinical features of chicken pox.

A

Begins as itchy red papules progressing to vesicles -> crusted lesions
Begins on stomach, back and face then spreads to rest of body, can arise inside the mouth
Lesions at different stages present simultaneously
May have systemic symptoms (high fever, URTI symptoms, headahce, vomiting, diarrhoea)

158
Q

Exclusion period for chicken pox

A

Until ALL blisters have formed scabs (usually 5-10 days)

159
Q

Clinical features of measles

A 
Prodromal phase: 10-12 days after exposure. Fever, malaise, anorexia, conjunctivitis, cough, coryza. Koplik spots (blue-white spots on inside of mouth opposite molars)
Exanthem phase ( 24-48h after prodrome): red non-itchy maculopapular rash. Begins on face and behind ears with cephalocaudal spread to entire body within 24-36 hours). Associated high fever >40. Fades 3-4 days after onset.
160
Q

Diagnosis of measles

A

In Australia as it is seen so infrequently, diagnosis required lab confirmation:
Viral NPS or blood serology

161
Q

Clinical features of rubella

A

25-50% are so mild there are few or no signs or symptoms

Mild fever, URTI symptoms, malaise
Tender/swollen glands almost always accompany the rash (most commonly postauricular, occipital and posterior cervical chain)
Forchheimer sign: pinpoint or larger petechiar on soft palate and uvula during prodromal period
Rash: cephalocaudal spread from face, usually not as widespread as measles, pink/light red spots 2-3mm in size
Lasts up to 5 days (avg 3 days)
May or may not be itchy
As passes, affected skin may shed in flakes

162
Q

Clinical features of roseola

A 
Often few or no signs or symptoms
Typically:
- high fever (up to 40) for 3-5 days
- URTI symptoms
- Irritability, tiredness
- Rash on day 3-5, as fever subsides : small, blanching rose-pink or red raised spots 2-5mm, mainly on trunk, non-itchy and painless. May fade within few hours or persist up to 2 days
Main complication is febrile seizures
163
Q

Clinical presentation of parvovirus B19

A

Non-specific viral prodrome (mild headache, fever)
Rash few days later: initially firm red cheeks feel burning hot for 2-4 days, then pink rash develops on limbs and sometimes trunk (lace-like or network pattern)
Most prominent in first few days, can persist for up to 6 weeks (at least intermittently) most obvious when warm

164
Q

Other name for parvovirus B19 illness

A

erythema infectiosum

165
Q

Epidemiology of roseola

A

Affects most children before the age of 1 (6m-3y)

166
Q

Primary HSV1 infection presentation

A 
most often gingivostomatitis in child 1-5yo
Fevers, may be high
Restlessness
Excessive dribbling
Foul breath
Painful eating and drinking
Red swollen gums, bleed easily
Whitish vesicles -> yellow ulcers on tongue, throat , palate and inner cheeks
Localised tender lymphadenopathy
Recovery usually complete within 2 weeks
167
Q

Common locations for HSV infections

A

(Face/lips, genitals)
Thumb sucker - thumb
Health care worker: herpetic whitlow (paronychia)
Rugby player: scrum pox (blisters on one cheek)

168
Q

Most common sites for HSV2 infections

A

Males: glans, foreskin, shaft (anal in MSM)
Females: vulva and in vagina, painful to urinate. Infection of cervix may cause severe ulceration

169
Q

Management of herpes simple infections

A

Mild primary infection: supportive +/- topical anaesthetic
Severe primary: oral antivirals
Mild recurrence: topical aciclovir 4 hourly for 5d from first sign of recurrence
Severe recurrence: oral antivirals

If immunocompromised or not tolerating oral, discuss with infectious disease specialist

170
Q

Pregnancy specific pruritic diseases

A

Cholestasis of pregnancy
Prurigo of pregnancy (papular dermatitis of pregnancy)
Pruritic urticarial papules and plaques of pregnancy (AKA polymorphous eruption of pregnancy)
Pemphigoid gestationis

171
Q

Clinical features of pemphigoid gesationis

A

(rare)
Onset at any stage of pregnancy/postpartum, most common in 2nd T
Itchy papules mainly affecting abdo, INCLUDING umbilicus. may appear as grouped or annular red papules, plaques and blisters

172
Q

Clinical features of pruritic urticarial papules and plaques of pregnancy

A

Onset in 3rd T, more common in primips and multiple pregnancies
Itchy red papules and plaques first appearing in straie then spreading to trunk and proximal limbs, SPARING umbilicus

173
Q

Management of pruritic urticarial papules and plaques of pregnancy

A

Emollients
Medium potency topical steroids
Sedative oral antihistamines for relief of symptoms
Systemic steroids if severe cases

174
Q

Clinical presentation of prurigo of pregnancy

A

Scattered itchy papules developing at any stage of pregnancy

Should be managed with emollients (topical steroids may help INDIVIDUAL lesions but not the rash as a whole)

175
Q

Clinical presentation of pruritus gravidarum/cholestasis of pregnancy

A

Unexplained itch in 2nd or 3rd T with no rash present.

Raised blood levels of bile acids and/or liver enzymes.

176
Q

What is telogen effluvium and how does it present

A

Shedding of telogen hair - occurs 2-6 months after an event that stops active hair growth (childbirth, fever, weight loss, haemorrhage, surgery, illness or psychological stress, medications (OCP, anticoagulatns, anticonvulsants))

177
Q

Normal hair growth cycle

A

Anagen: actively growing hair (most of them)
Catagen: in-between phase of 2-3 weeks when growth stops and follicle shrinks (1-3% of hairs at any time)
Telogen: resting phase for 1-4 months (up to 10% of hairs in a normal scalp at any one time)

178
Q

What is anagen effluvium

A

Shedding of hair in anagen phase:
Caused but: autoimmune disease, mediations (e.g. CTx), inherited/congenital conditions)

If caused by a drug/toxin can return to normal within 3-6 months

179
Q

Inflammatory skin conditions that can damage or destroy the hair bulb

A

Localised alopecia areata
Localised infection e.g. tinea capitis
Severe local skin disease (psoriasis, seborrhoeic dermatitis, eczema, lupus, T-cell lymphom)
Generalised skin disease e.g. erythroderma

180
Q

Systemic causes of hair loss

A

Cause reversible patchy hair thinning, poor hair quality and bald patches.

Causes: 
Iron deficiency
Hypothyroidism
SLE
Syphilis
Severe acute or chronic illness
181
Q

Risk factors for alopecia areata

A 
Family history of same or other autoimmune conditions
Personaly hsitory of thyroid disease, vitiligo or atopic dermatitis
Chromosomal disorders (e.g. Down Syndrome)
182
Q

Diagnosis of alopecia areata

A

Clinical

Should also be worked up for atopy, vitiligo, thyroid disease and other autoimmune conditions

183
Q

Patterns of alopecia areata

A

Patchy:

  • affects any hair-bearing area mostly scalp, brows, lashes and beard
  • 3 stages: sudden loss of hair, enlargement of bald patch(es), regrowth of hair
  • regrowing hairs often initially white or grey and may be curly when previously straight

Alopecia totalis:
- all or nearly all scalp hair is lost

Alopecia univeralis
- all hair on entire body is lost

Diffuse:

  • sudden diffuse thinning of scalp hair
  • positive hair pull test
  • persisting hair turns grey (Turning white overnight)
  • may be confused with telogen effluvium
184
Q

Treatment of alopecia areata

A

If limited hair loss of recent onset:
- potent topical corticosteroid 3-4 months (betamethasone 0.05% cream/lotion/optimised vehicle 1-2x per day)

If extensive or topical treatment not successful within few weeks

185
Q

Treatment of trichotillomania

A

In children: usually benign and self-limiting, will usually outgrow it. If response to significant stress at home or school may need to refer to psychologist/psychiatrist

In adults; usually psychopathological, refer to psychologist/psychiatrist

186
Q

Definition of hirsutism

A

Male pattern of secondary or post-pubertal hair growth occurring in women (moustache and beard areas, + more hair on limbs and trunk)

187
Q

Causes of hirsutism

A

Genetic (early onset)

Late onset may be due to hyperandrogenism:

  • PCOS
  • insulin resistance
  • obesity
  • androgenic medications
  • Cushing syndrome
  • Congenital adrenal hyperplasia
  • tumour of adrenal gland or ovary
188
Q

Assessing severity of hirsutism

A

Ferriman-Gallwey visual scale (score of 0-4 re: amount of hair present in different areas of body)

189
Q

Investigations to perform for hirsutism

A

Free androgen index
- if high, DHEA (elevated if adrenal origin) and androstenedione (elevated if ovarian origin)
If premature adrenarche, early onset of family history of CAH: 17-OHP
If cushingoid: urine and serum cortisol
If menstrual disorder:
LH, FSH, prolactin

General: TFT, glucose, lipids, imaging if indicated by symtpoms

190
Q

Treatment of hirsutism

A

Treatment of underlying cause (e.g. metformin if PCOS)

hormonal treatment: spironolactone, OCP, cyproterone

191
Q

Definition of hypertrichosis

A

Excessive hair growth above normal for age, sex and race - can develop all over body or isolated to small patches

192
Q

Causes of hypertrichosis

A

Generalised acquired causes:

  • porphyria cutanea tarda
  • malnutrition (e.g. .anorexia nervosa)
  • malignancy
  • drugs (ciclosporin, phenytoin, androgenic steroids, minoxidil)

Localised:

  • increased vascularity
  • repetitive rubbing or scratching (lichen simplex)
  • application of plaster cast (temporary)
  • repeated application of potent topical steroid, PUVA, iodine
  • long eyelashes (trichomegaly) can arise from local bitanoprost
193
Q

Treatment of hypertrichosis

A

Hair removal, treatment of underlying cause if identified

194
Q

What is lichen simplex

A

AKA neurodermatitis, a localised area of chronic, lichenified eczema/dermatitis

195
Q

Cause of lichen simplex

A

Not entirely understood
Follows repetitive scratching and rubbing secondary to chronic localised itch
(primary itch can be caused by all types of dermatitis, psoriasis, lichen planus, fungal infection, insect bite, neuropathy)

196
Q

Clinical presentation of lichen simplex

A

Solitary plaque well circumscribed, linear or oval in shape and markedly thickened
Intensely itchy

Often unilateral, affecting patient’s dominant side (back of scalp/neck, scrotum or vulva, wrists and forearms, lower legs)

+/-: exagerrated skin markings, dry or scaly surface, leathery induration, broken-off hairs, pigmentation, scratch marks

Clinical appearance can be atypical - skin scrapings and biopsy may be necessary

If no known underlying skin problem/infection, consider neuropathy

197
Q

treatment of lichen simplex

A

Treat symptoms and underlying cause
Potent tropical steroids until plaqu resolves (4-6 weeks), reduce potency or frequency once lichenification resolves
Moisturise, antihistamines PRN for itch

Treat underlying primary condition

198
Q

Dermatological emergencies

A

Angioedema
Steven Johnson syndrome/ toxic epidermal necrolysis
Staphylococcal TSS
Necrotising fasciitis

199
Q

Cause of staphylococcal toxic shock syndrome

A

Staph aureus produces exotoxins causing massive cytokine secretion by T cells -> fever, hypotension and multi-organ failure

200
Q

Risk factors for staphylococcal TSS

A

Relatively rare as most adults have protective antibodies to exotoxin

  • most common in healthy people 20-50y
  • recent childbirth, miscarriage or abortion
  • foreign bodies e.g. nasal packing for epistaxis or wound packing after surgery
  • post surgical wound
201
Q

Clinical presentation of staphylococcal TSS

A

2-3 day prodrome of malaise
Fever, chills, nausea, abdominal pain
Rapid onset generalised erythema with desquamation, fever, hypotension and multisystem failure
Rash begins on trunk and spreads peripherally to palms and soles

202
Q

Management of staphylococcal TSS

A

Aggressive supportive management of hypotension
Obtain cultures
Treat with beta-lactamase resistant antibiotic (fluclox, benPen, cephazolin if non-immediate hypersensitivity or vancomycin if MRSA or immediate hypersensitivity)

203
Q

Common causes of angioedema

A

Often idiopathic
Medications: especially ACE-i, NSAIDs, penicillins, radiographic contrast
Allergens
Physical agents (cold, vibration)

204
Q

What is exfoliative erythroderma

A

AKA Red Man Syndrome

Generalised scaly erythematous skin eruption of >90% of skin surface

205
Q

Causes of exfoliative erythroderma

A 
Often idiopathic
Can be related to underlying dermatoses
Drug reaction (sulphonamides, penicillin, antimalarials, anticonvulsatns, allopurinol)
Cutaneous T-cell lymphoma or leukaemia
Paraneoplastic syndrome
Dermatomyositis
206
Q

Presentation of exfoliative erythroderma

A

Initially pruritus
Malaise and fever -> leading to excessive vasodilatation
Scaly erythematous rash covering >90% of skin surface

207
Q

Management of exfoliative erythroderma

A

Determine cause and address, stop ALL unnecessary medications
Supportive therapy: hydration, nutrition, electrolyte monitoring and replacement, cardiac monitoring, temperature support
Skin care: emollients and compresses, topical corticosteroids
Antihistamines for pruritus
Antibiotics if signs of infection

208
Q

Types of necrotising fasciitis

A

Type I: staph aureus, mixed anaerobes, gram neg bacilli, enterococci - most commonly seen in elderly or diabetics
Type II: Group A strep - affects all ages including healthy people
Type III: clostridia - follows significant injury or surgery, results in crepitus

209
Q

Most common site for necrotising fasciitis

A

Lower leg

210
Q

Risk factors for necrotising fasciitis

A

Diabetes
Peripheral vascular disease
Immunosuppression

211
Q

Clinical presentation of necrotising fasciitis

A 
Diffuse swelling of affected skin area -> developement of bullae which rapidly become burgundy in colour
Severe pain
indurated oedema
Skin hyperaesthesia
Crepitation
Muscle weakness
Foul-smelling exudate
212
Q

Management of necrotising fasciitis

A

Aggressive management of sepsis
Surgical debridement of necrotic tissue
Broad spectrum antibiotics unless causative agent definitively identified

213
Q

What are Stevens-Johnson Syndrome and Toxic epidermal necrolysis

A

Both represent a spectrum of drug-induced or idiopathic mucocutaneous reaction patterns characterised by skin tenderness, erythema, epidermal necrosis and desquamation

214
Q

Common medications responsible for SJS/TEN

A

Sulfonamides
Anticonvulsants
Allopurinol
NSAIDs

Note drug administration typically precedes rash by 1-3 weeks

215
Q

Clinical presentation of SJS/TEN

A

Prodrome: fever, stinging eyes, sore throat, odynophagia, coryza and cough, general aches and pains
Rash: development of dusky erythematous macules that progress to flaccid blisters, 2+ mucous membranes typically involved with erythema/erosions(buccal, genital, occular)

<10% of eridermis sloughs off in SJS
>30% in TEN

216
Q

Mortality of TEN and SJS

A

TEN: 30%
SJS: 5%

217
Q

Management of SJS/TEN

A 
Identify and remove offending medication
Admit to burn unit if necessary
IV fluids
Electrolyte and temperature maintenance
Ophthal assessment
Skin care: wound dressings oral hygiene (chlorhex rinses)
Antihistamine
Antibiotics in case of super infection
218
Q

How does scabies spread?

A

Person-to-person only
20 minutes of close contact required (e.g. holding hands, sexual contact)
Household contacts highest risk of transmission

Note may be a delay of up to 6 weeks from first infestation to beginning of symptoms

219
Q

Presentation of classical scabies

A

Often multiple household members have same

Papules/burrows in typical locations (web spaces, wrists, buttocks breasts, genitals)
Intensely itchy
Secondary bacterial infection in up to 90% (surrounding erythema, yellow crusting or pus)

220
Q

Clinical presentation of Norwegian/crusted scabies

A

(hyperinfestation of millions of mites causing hyperkeratosis)
Plaques and extensive scale
Deep fissures in severe case
May not be itchy

221
Q

Diagnosis of scabies

A

Usually clinical
If atypical appearance: ink from pen over burrow entrance will track along burrow
Or dermatoscope will show “delta sign”

Crusted scabies usually requires confirmation with skin scrapings

222
Q

Management of scabies

A

ALL household contacts need to be treated at the same time

<2 months: crotamiton

> 2 months: permethrin 5% cream, apply to whole body and wash off after 8 hours, if symptoms persist, repeat in 7-14 days

Second line: benzyl benzoate 25% left for 24h then washed, diluted for children, repeat once after 7-14 days

Third line: oral ivermectin, 2 doses 7 days apart, if >5y, non-pregnant, not breastfeeding and failure to respond to topical treatment

223
Q

Management of crusted scabies

A

Discuss with specialist
Combination of topical scabicides, oral ivermectin and topical keratolytics

LOTS OF SHEDDING SCABIES therefore very infectious
Treatment sometimes requires hospital admission for isolation and intensive treatment

224
Q

Treatment of head lice

A

Children <2y: wet combing - put hair conditioner on, then comb sections with fine tooth comb and wipe conditioner + lice onto tissue. Daily for few days after last louse is found
Children >2y: pediculicides (OTC)

Exclusion from school only until appropriate treatment is commenced

225
Q

Management of body lice

A

As live in clothing not body, only need treatment of body if infestation is widespread (same as headlice treatments)

Otherwise environmental measures only:

  • laundering clothes and linen with hot washes and hot tumble-drying
  • ironing with hot iron
  • dry cleaning
  • topical insecticide spray applied to clothing, especially seams
226
Q

Treatment of pubic lice

A

Same treatments as head lice, apply to ALL hairy areas from neck to knees and repeat 7 days later
Sexual partners need to be treated, even if asymptomatic

227
Q

What is latrodectism

A

Red back spider bite envenomation

228
Q

Clinical presentation of red back spider bite envenomation (latrodectism)

A

Bite may not be felt, rarely leaves fang mark, erythema not always present

Localised sweating and piloerection (25% of patients)
Pain typically increasing over about 1 hour - may radiate proximally along affected limb
Systemic effects (uncommon)
- hypertension
- agitation/irritability
- priapism
- patchy paralysis
- paraesthesia
- fasciculations
- cardiac effects
229
Q

Management of red back spider envenomation

A

Antivenom if signs of systemic envenomation OR pain not controlled with simple analgesia/requiring repeated doses of opiates

230
Q

Spiders which cause necrotising arachnidism

A

Recluse spider
NOT associated with white tailed spider (common myth)
In Australia necrotising arachnidism is very uncommon, there is more likely to be an underlying infective, inflammatory or traumatic cause that needs to be investigated

231
Q

Skin conditions related to diabetes mellitus

A

Diabetic dermopathy/shin spots: pigmented, slightly indented scaly patches on shins often bilaterally

Diabetic bullae (rare) spontaneous, develop on hands and feet

Diabetic stiff skin/cheiroarthropathy: waxy, thickened, yellow skin - restricting mobility of joints of hands

232
Q

Skin changes of hypothyroidism

A 
Carotanaemia - yellowish hue to skin
Eczema craquele
Sparse and brittle hair
Dry skin
Loss of hair in outer third of eyebrows
233
Q

Skin changes of hyperthyroidism

A 
Nail changes: thyroid acropachy (distorted and overgrown nails) +/- onycholysis
Generalised pruritus
Urticaria
Fine, soft and thinned scalp hair
Flushing of face and hands

Grave’s only:
Pretibial myxoedema (reddish, tender swellings nodules and plaques on shins, calves and feet, prominent hair follicles give orange peel or warty appearance)
Exophthalmos

234
Q

Skin changes of Cushing Syndrome

A 
Purpura/easy bruising
Purple Striae over abdomen
Telangiectatic cheeks
Fragile skin, poor wound healing
Acne
Hirsutism
Clitoral hypertrophy
Male-pattern baldness in females
235
Q

Skin changes of Addison’s disease

A

Generalised hyperpigmentation

Women may have loss of androgen-stimulated hair (pubic and underarm hair)

236
Q

Clinical features of mammary Paget’s disease

A 
Chronic eczema-like rash of nipple and adjacent areolar skin
Itchy, burning rash on and around nipple
Skin may be broken and sore from scratching
\+/-"
- redness
- swelling
- oozing nipple 
- discharge
- ulceration
- inversion of the nipple

Usually only unilateral

237
Q

Clinical features of extramammary Paget’s disease

A

Chronic eczema-like rash
Intense itching
pain and bleeding secondary to scratching
Thickened plaques may form

Most often occurs on vulva in middle aged women
(also occurs on axilla and anogenital area in males)

238
Q

Skin changes associated with liver dsiease

A

Telangiectasia
Spider naevi
Palmar erythema
Terry nails (proximal leukonychia and pink distal nail plate)

haemochromatosis: bronze hyperpigmentation of skin

Wilson disease:

  • Kayser-Fleisher rings
  • pigmentation over skin
  • blue lunulae (half-moons) on nails
239
Q

Skin changes associated with coeliac disease

A

Dermatitis herpetiformis:
- intensely itchy herpetiform vesicles within erythematous or urticated plaques.
Symmetrical distribution over extensor surfaces and buttocks

240
Q

Skin conditions associated with inflammatory bowel disease

A

Oral ulcers
Erythema nodosum (tender red subcutaneous nodules on shins)
Pyoderma gangrenosum (irregularly undermined necrotic ulcers on lower legs)
Swelling of oral cavity
Cutaneous polyarteritis notosa
Acute neutrophilic dermatosis/Sweet syndrome

241
Q

Skin changes in vitamin B12 deficiency

A

Angular cheilitis
Hunter glossitis (atrophic, red, painful tongue)
Hair depigmentation
Hyperpimgenation

242
Q

Skin changes in vitamin C deficiency

A

(Scurvy)

  • enlarged hyperkeratotic hair follicles on posterolateral arms
  • abnormal hair development
  • swelling of gums, erythema
  • splinter haemorrhages in nails
243
Q

Skin changes secondary to vasculitides

A

Depends on size of inflamed blood vessel;
Capillaritis
- pigmented purpura
- petechiae resolving with haemosiderin staining

Small vessel vasculitis:
- palpable purpura

Medium vessel:

  • nodules
  • livedo reticularis

Large vessel infrequently results in cutaneous features

244
Q

Epidemiology of lichen sclerosus

A

Most common in women >50y
10x more common in women than men
15% of patients have a family member with same condition
May follow or co-exist with another skin condition (e.g. lichen simplex, psoriasis etc. 0
Often personal or family history of other autoimmune conditions

245
Q

Clinical features of lichen sclerosis

A

Mostly occurs on vulva

  • non hair-bearing inner areas
  • can be localised or extensively involve perineum, labia minora and clitoral head
  • NEVER involves vaginal mucosa
  • extremely itchy and/or sore
  • may have painful fissuring of posterior fourchette
  • can cause adhesions and scarring
246
Q

Diagnosis of lichen sclerosus

A

Usually requires biopsy unless experienced physician

247
Q

treatment of lichen sclerosus

A

General:
- wash 1-2 x per day with soap free (or no) cleanser)
- avoid tight clothing, rubbing or scratching
- manage incontinence
- emollients to relieve dryness and itch
Topical steroid ointment
- encourage to use mirror to apply directly to affected skin
- can take months for skin to return to normal
Other therapy:
- intravaginal oestrogen (reduces symptoms of atrophic vulvovaginitis)
- systemic treatments if severe or resistant

248
Q

Complications of lichen sclerosus

A

Associated with increased risk of SCC and other cancers of vulva, penis and anus

249
Q

Three principles to ulcer/wound management

A
  1. Define the aetiology
  2. Control modifiable factors affecting healing
  3. Select appropriate local environmental management
250
Q

Most common chronic wounds seen in GP

A

Leg ulcers (venous, arterial, mixed)
Pressure wounds
Skin tears

251
Q

Cause of venous leg ulcers

A

Breakdown of venous circulation -> increased venous pressure -> pitting oedema -> reduced perfusion to skin -> insufficient supply for healing to occur after trauma -> ulcer development

252
Q

Clinical presentation of venous ulcers

A
  • Commonly on gaiter area (lower 1/3 of leg)
  • irregular shape
  • pitting oedema
  • haemosiderin staining of surrounding skin
  • typical surrouding skin changes of venous eczema or atrophy blanche
253
Q

Most common risk factors for venous ulcers

A

Obesity
Past DVT
Poor mobility

254
Q

General treatment of venous ulcers

A

Graduated compression therapy (toe to knee) - ensure exclude arterial involvement first with ABI
Lower limb exercise
Address occupational factors (Rarely, surgery)

255
Q

Clinical presentation of arterial ulcers

A
  • commonly below ankles and foot/toes
  • Punched out/sharply defined margins
  • base covered in slough
  • skin often shiny and friable
    +/- other signs of ischaemia:
  • ischaemic pain esp at night
  • intermittent claudication
  • dusky/white foot on elevation
  • sluggish capillary refill
  • low ABI
  • weak/absent pulses
  • known peripheral vascular disease
256
Q

Treatment of arterial ulcers

A 
Surgical is mainstay:
- angioplasty
- stenting
- bypass grafting
- amputation
Pain control!
DO NOT APPLY COMPRESSION
257
Q

Treatment of mixed leg ulcers

A

(15-25% of leg ulcers)
Determine if predominant cause is venous or arterial and treat it
**Depending on degree of arterial problem, graduated compression may be contraindicated, in this instance it is difficult to address the venous component of the problem and thus difficult to treat

258
Q

How to simply reduce risk of skin tears

A

Applying moisturising lotion BD to patients in nursing homes

259
Q

Treatment of skin tears

A

If possible, replace the flap, carefully holding in place with a few adhesive strips (no tension) and cover with silicone foam dressing and 1-2 layers of tubular compression to apply mild pressure
Review after 3 days and redress avery 5-7 days

260
Q

General factors that affect wound healing

A 
Arterial and venous circulation
Anaemia
Immune function
Comorbidities (DM, RA)
Age-related skin changes
Balanced nutritious diet
Mechanical stress (pressure, friction, shearing forces)
Debris (slough, necrotic tissue, eschar, scab, sutures)
Dessication
Maceration
Temperature (optimum 37 degrees)
Infection
Chemical stress (e.g. topical agents/antiseptics, smoking, steroids/NSAIDS, other drugs)
261
Q

Principles of LOCAL wound management

A

Tissue (if non-viable, debride)
Inflamation/infection(only treat with Abx if signs of invasive infection)
Moisture (correct dressing for optimal environment)
Edge/epithelialisation (if advancing or undermining, reconsider diagnosis and use advanced therapies)

262
Q

Correct dressings to use for very dry wounds/minor burns

A

Hydrogels

  • increase wound moisture
  • use for dry, scabbed, necrotic/escharotic wounds and minor burns
  • usually require secondary dressings in form of foams
    e. g. Aquaclear (sheet) or solosite (amorphous hydrogel comes in a tube)
263
Q

Appropriate dressings for nil-to-low exudate wounds

A

Films

  • neither absorb nor donate moisture
  • semi-permeable, transparent and flexible
  • maintains a moist environment and encourages sutolysis (keeps exudate within local environment)
    e. g. Opsite, Tegaderm
264
Q

Appropriate dressings for low-to-moderate exudate wounds and ulcers

A

Hydrocolloids:
- combine with exudate to form soft, moist gel that keeps wound bed hydrated
- encourage autolysis and aid removal of slough
E.g. duoderm (sheets, pastes), comfeel (sheets, pastes, powders)

265
Q

Appropriate dressings for moderate-to-high exudate wounds

A

Foams:
- highly absorbent, non-adherent, insulating and cushioning
- used in exuding wounds to maintain moisture without maceration
e.g. Lyofoam, Mepilexx (foam sheet with soft silicone)
Absorbent fibre dressings
- absorbs exudate and maintains moist environment
- calcium alginates have haemostat properties
- need foams as secondary dressings
- e.g. Kaltostat (alginate sheet or rope) Melgisrob (alginate rope), Aquacel (hydrofirbe sheet, rope)

266
Q

When to use activated charcoal as a dressing

A

(with or without silver)

On malodorous wounds to absorb odour and bacteria

267
Q

What dressing to use on malodorous wounds

A

Activated charcoal +/- silver

268
Q

When are non-adherent dressings used

A

Mainly as protective dressings for minor lacerations or healed wounds e.g. Mepitel (soft silicone mesh) or Jelonet (paraffin tulle)

269
Q

When are negative pressure dressings required

A

Complicated exudating wounds (much more expensive than standard wound care

270
Q

What is hidradenitis suppurativa?

A

AKA acne inversa, a chronic inflammatory disease of the skin in intertriginous areas characterised by multiple inflammatory nodules, abscesses, sinuses, fistulas and scarring. Related to follicular occlusion.

271
Q

Prevalence of hidradenitis suppurativa

A

Approx 1%

F:M ratio 3:1

272
Q

Inflammatory diseases associated with hidradenitis suppurativa

A

Pyoderma gangrenosum
Spondyloarthropathies
Crohn’s disease

273
Q

Comorbidities associated with hidradenitis suppurativa

A 
Obesity
Acne
hyperlipidaemia
depression
insulin resistance
PCOS
diabetes
hypertension
keratosis pilaris
smoking
274
Q

Follicular occlusion tetrad consists of:

A

Hidradenitis suppurativa
Dissecting cellulitis
Acne conglobata
Pilonidal sinus

275
Q

Clinical presentation of hidradenitis suppurativa

A

Multiple (and often recurrent or chronic) lesions in intertriginous areas, including:

  • Comedomes
  • Painful nodules
  • Abscesses
  • Sinus tracks
  • Fistulae
  • Scarring

Lymphoedema can occur secondary to lymph node scarring and subsequent obstruction

276
Q

Management of hidradenitis suppurativa`

A

General measures:

  • loose fitting clothing
  • smoking cessation
  • healthy eating
  • weight loss (if appropriate)

Topical therapy:

  • topical antiseptic when bathing (benzoyl peroxide 5% wash, antibacterial soap)
  • topical clindamycin 1% BD for up to 3 months

Oral therapy:

  • antibiotics (doxy or mino 50-100mg daily, or erythromycin if tetracyclines contraindicated)
  • COCP - ideally one containing cyproterone (i.e. Brenda, Dianne etc. ) OR desogestrel (Marvelon), drospiernone (Yaz) or gestodene (Minulet)
  • spironolactone: severe disease only, start at 25-50mg daily

Biological agents:
- severe disease, refer to derm

Surgical:

  • acute abscess I/D - likely to worsen scarring
  • after review by derm ?wide local excision, deroofing etc.

GP ACRRM (14 decks)

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