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5th year > Dermatology > Flashcards

Dermatology Flashcards

1
Q

What are the components of a derm hx?

A

1) Name/Age Occupation
2) PC
3) Background risk factors/severity markers
4) HPC
5) PmH
6) SH (hobbies/travel) + FH
7) Drug history
8) RS

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2
Q

Rash Hx?

A

1) When, where, evolution
2) Duration, symptoms - is it itchy?
3) Previous episodes
4) exacerbating/relieving factors
5) Other areas affected?
6) Severity markers ie. psoriasis
7) Impact on life/work/psychosocial

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3
Q

Severity markers?

A

Previous treatments eg. UV/Systemic drugs

Hospitilisation

Missing work/School

Social/personal life

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4
Q

Lesional History

A

Different as cancer until proved otherwise:

HPC lesion:
- How it started, how it’s evolving, symptoms, D/C, Bleeding etc

Risk factors:

  • Sun, country of residence, occupation
  • Previous episodes
  • Family Hx
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5
Q

Flat non-palpable lesion

A

Small - Macule

Large - Patch

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6
Q

Raised lesions

A

0.5cm: Nodule

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7
Q

Palpable patch

A

Elevated, flat lesion = Plaque

Can also get an atrophic sunken/flat lesion = plaque

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8
Q

Other descriptive derm terms

A 
Circumscription
Colour
Consistency (soft/hard/firm)
Distribution = Localised vs generalised.
Clustered (HSV)
Dermatomal
Peripheral vs centripetal
Symmetrical?
Flexor vs extensor surfaces
Photodistribution
Monomorphic/pleomorphic
Annular --> Serpiginous 
Discoid (Solid)
Koebnerisation - Psoriasis, LP, viral warts
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9
Q

Fluid filled lesions?

A

Small = Vesicle
Large = Blister
Pus filled = Pustule

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10
Q 
Surface characteristics:
Scale?
Warty?
Ulcerated?
Crusty?
Excoriated?
Lichenification?
A

Scale = Keratotic surface
Warty = Rough/papillomatous surface
Ulcerated = Loss of epidermis (full thickness), partial thickness = erosion
Crusty = Dried Exudate
Excoriated = superficial ulceration secondary to scratching
Lichenification = Flat surfaced epidermal thickening secondary to rubbing
Post-inflam hyperpig.

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11
Q

Ulcer Description?

A

Size, Shape, Location

Edge:

1) Punched out
2) Raised & rolled
3) Sloped
4) Overhanging

Base: Clean, necrotic, sloughy, granulation tissue

Surrounding tissue eg. thick woody hard sclerotic skin = lipodermatosclerosis

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12
Q

Derm investigations?

A 
Dermoscopy
Mycology (scrapings)
Swabs - Microbiology/viral
Biopsy:
- History
- Stains
- Immunofl. studies
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13
Q

3 layers of skin?

A

1) Epidermis: Keratinised stratified squamous epithelium
2) Dermis: collagenous connective tissue
3) Subcutis: Fat layer, nerve endings and blood vessels

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14
Q

Basal cell function?

A

Sit on basement memebrane and produce keratinocytes, which rise to the top as squamous cells. Also produce keratin

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15
Q

Causes of Non-Scarring Alopecia?

A 
Male/Female Pattern alopecia
Telogen Effluvium
Low iron reserves
Alopecia Areata (AI hairloss)
Hyper/hypothyroid

–> follicles still there, so may regrow

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16
Q

Causes of Scarring Alopecia?

A 
Lichen Planus
Lupus
Traction/Traumatic
Folliculitis
Other

Follicles destroyed, so chance of regrowth. Irreversible so need to manage pt expectation!

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17
Q

How to differentiate scarring from non-scarring alopecia?

A

Non Scarring:
- Speed of loss, stress, anaemia, Previous episodes, FH, other diseases

Scarring:
- Itch, redness/scale, previous sclap damage, pain, suppuration

Examination:
Pattern of hair loss
Scarring?
Visible active disease of scalp?

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18
Q

Alopecia Ix?

A

Blood tests - hair loss screen: biotin, ferritin levels etc

Skin biopsy: H&E & Immunoflorence. Biopsy - transverse and longitudinal

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19
Q

What is psoriaris?

A

A common, chronic hereditary condition where you get an inflammatory hyperproliferation of the epidermis. It is a pustular disease and in some forms may be life-threatening

Bimodal age of onset - youth/middle life

T-cell mediated

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20
Q

Psoriasis triggers?

A 
Infection: Strep
Psychological: Stress
Drugs: Steroid withdrawal, B blockers, lithium, antimalarials (chloroquine/hydroxychloroquine), NSAIDs and Ace inhibitors
Trauma : Koebnerisation
Sunburn
HIV
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21
Q

Psoriasis types?

A

1) Chronic plaque psoriasis (commonest)
2) Flexoral psoriasis
3) Psoriatic arthritis/ nail psoriasis (nail dystrophy)
4) Guttate
5) Erythrodermic
6) Pustular
7) Sebo-psoriasis

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22
Q

Chronic plaque psoriasis findings

A 
Chronic, well demarcated (distinguishes from eczema)
Red/pink plaques
Silvery-white scale
Extensor surfaces and scalp
Accounts for 80-90%
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23
Q

Types of psoriatric arthropathy?

A

1) Asymmetric (60-70%)
2) Symmetrical polyarthtropathy (15%)
3) DIP (5%)
4) Destructive (5%) - arthritis mutilans
5) Axial arthritis (5%)

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24
Q

Guttate psoriasis?

A

Post-strep throat
young adults
Shower of scattered discrete lesions
3mm to 1cm lesions, round or slight oval

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25
Q

Pustular psoriasis?

A

1) Localised:
- Palmoplantar common - sterile pustules on erythematous base
- chronic relapsing remitting condition

2) Generalised:
Life threatening - abrupt onset + fever GOOGLE IMAGE. Likely to be secondarily infected

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26
Q

Mx of generalised pustular psoriasis?

A

1) resuscitate ABC
2) Admit
3) Greasy emollients
4) IV support
5) Systemic therapy
6) Avoid or treat concurrent infection
7) ITU if necessary

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27
Q

Complications of erythrodermic psoriasis?

A

Derm emergency:

1) Fluid loss
2) hypothermia
3) infection
4) hypercatabolic state
5) SHOCK

Mx same as generalised pustular psoriasis

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28
Q

Mx Psoriasis?

A

1) Emollients/bath oil/soap substitutes
2) Topical agents:
- Vitamin D
- Tar
- Dithranol
- Steroids
3) Phototherapy
UVA + psoralen = pUVA
4) Systemic agents
5) Biological agents

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29
Q

Topical agents in psoriasis?

A

1) Vitamin D
2) Tar (anti-proliferatives)
3) Dithranol
4) Steroids

Only useful in localised disease

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30
Q

Systemic agents in psoriasis?

A

1) Retinoids (acitretin)
2) Fumaric acid
3) Hydroxycarbamide
4) Immunosuppression:
- Methotrexate (especially if joint involvement)
- Ciclosporin

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31
Q

Biologic agents in Psoriasis?

A

Anti TNF:

  • Etanercept
  • Infliximab
  • Adalimumab

Anti IL-12/23:
- Ustekinemab

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32
Q

5 P’s of Lichen Planus

A 
Purple (violacious)
Planar = flat
Polished = Shiny
Papular
Pruritic

(polygonal/pigmented)

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33
Q

What is Wickham’s striae?

A

Reticulated lace like lichen planus usually in the mouth, but can be anywhere

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34
Q

Lichen planus treatment?

A

Emollients/soap substitutes

Topical:

  • Super potent steroids
  • UVB

Systemic:

  • Oral steroids (CF psorarisis - never oral)
  • Hydroxychloroquine
  • Immunosuppression
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35
Q

Actinic Lichen Planus?

A

Sun-induced (photodistributed) lichen planus eg. dense hyperpigmentation of face

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36
Q

What is the herald patch. What condition is it seen in.

A

Initial lesion in pityriasis rosea post infection.

A week later, several other reactive lesions arise. Browny/orange, lines up down the back ‘christmas tree’ with some scale.

Acute exanthematous eruption
Common in children/young adults
? Viral cause - seasonal variation

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37
Q

What is Eczema?

A

An inflammatory dermatosis characterised by erythema and itching.

Histologically shoes spongiosis (fluid building up under skin) + inflammation

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38
Q

Causes of eczema?

A 
Atopic
Contact allergic
Contact irritant
Seborrhoeic (dandruff)
Varicose
Asteototic (elderly - dry out)
Drug
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39
Q

Different morphology in eczema?

A 
Pompholyx
Discoid
Lichen Simplex - thickening due to rubbing 
Lichen Amyloid
Nodular prurigo
Erythroderma
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40
Q

What is Atopic eczema?

A
  • A chronic itchy relapsing dermatitis

Atopy: phenotypic predisposition to develop asthma, allergic rhinitis and atopic eczema

Increase IgE response and eosinophilia

Increased sensitivity to pruritic stimuli

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41
Q

Exacerbating factors for atopic eczema?

A 
Topical irritants
Soap
Secondary infection:
- Staph, viral herpes, tinea
House dust mite
Animal
Moulds
Food allergies
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42
Q

Atopic eczema prognosis?

A

50% clear by 3 years
66% clear by 6 years
90% clear by 20 years

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43
Q

What is pityriasis Alba?

A

Post-inflammatory hypopigmentation

Often in black skin & children

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44
Q

What is Pomphoylx?

A

Episodic visculobullous disorder. A type of eczema

Causes tiny blisters on fingers/palms/soles

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45
Q

Who gets discoid eczema?

A

Females aged 15-25 yrs
Females and males 55-65 yrs
Increased incidence in winter

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46
Q

What is lichen simplex chronicus?

A

Chronic eczema itch-rub cycle leads to lichenification and pigmentation

Some excoriation, some scale

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47
Q

What is Lichen Amyloid?

A

same process as Lichen simplex, but leads to deposition of amyloid under skin.

Tend to get a hyperpigmented cobblestone type appearance

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48
Q

What is Nodular prurigo?

A

Chronic-itch rub cycle in eczema characterised by very itchy firm lumps, often excoriated to the point of erosion

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49
Q

Complications of Atopic eczema?

A

1) Secondary staph infection

2) Eczema herpeticum

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50
Q

Eczema mx?

A

1) Emollients/soap substitutes/bath oils
2) Topical anti-inflammatories (Steroids/Tacrolimus)
3) phototherapy:
- pUVA
- UVB
4) Systemic agents:
- Systemic steroids
- Azathioprine
- Ciclosporin A
5) other agents

(treat infection)

+ avoid provoking factors
+ Anti-histamines for itching

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51
Q

Steroid hierarchy

A

Mild: hydrocortisone

Moderate: Clobetasone (Eumovate)

Beclomethasone (Propaderm)

Potent: Bethametasone (Betnovate)

Super potent: Clobetasol (dermovate)

nb. Start at appropriate level - DO NOT have to start at bottom and work way up

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52
Q

Topical Steroids SE?

A

1) Potential systemic absorption - only complication is addisonian crisis on stopping
2) Tachyphylaxis
3) Skin Atrophy
4) Tinea incognito - red scaly plaque mistaked for eczema
5) May cause acne or perioral dermatitis
6) Skin changes eg. telangiectasia

nb. Steroid sparing alternative - topical tacrolimus

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53
Q

Investigation of atopic dermatitis?

A

Clinical diagnosis so very rarely investigate

Biopsy

Swab (bacterial/viral)

Specific IgE (RAST) testing

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54
Q

Classification of nappy rash?

A

Seborrhaeic dermatitis - sparing of skin folds

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55
Q

Seborrheic dermatitis Mx

A

1) antifungal shampoo
2) corticosteroid scalp application
3) topical steroids
4) Oral ketoconazole/itraconazole

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56
Q

What is contact dermatitis?

A

Inflammation due to interaction of external agent and skin

  • Non-immunological irritant in 80% (would irritate most people)
  • Immunological allergic in 20% (only in those with sensitivity)
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57
Q

What type of allergic reaction is allergic contact dermatitis

A

Type IV - delayed cell mediated hypersensitivity

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58
Q

Allergic contact dermatitis Dx & Tx

A

Dx:

  • History of allergen exposure
  • Clinical features
  • Patch testing (2 days with wells on back)

Tx:
- Allergen avoidance

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59
Q

What are the different types of melanocytic naevi?

A

Junctional naevus - band of melanocytes clumped together. Relatively Flat

Intradermal naevus - Melanocytes migrate down into dermis, so tend to be deeper, pushing up, often with hair follicles. Shiny, dome shaped, but no surface changes. Can be any colour (pink/black/blue)

Compound naevus - combination of junctional and intradermal + epidermal changes - rough warty appearance because of epidermal involvement

Congenital melanocytic naevi

Beckers Naevus

Epidermal naevus - Warty change, often swirling following embryological growht lines

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60
Q

Congenital melanocytic naevi

A

There from birth, and tend to grow with the person.

Not likely to become malignant unless greater >20cm (risk greatly increases)

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61
Q

What is Beckers Naevus?

A

stippled/reticular patches of pigmentation, often hairy. Not actually melanocytic- actually a hamaratomatous.

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62
Q

Subungal naveus - Linear nail change vs deltoid nail change?

A

Linear = benign

Triangular = melanoma until proved otherwise

63
Q

What is a Spitz Naevus?

A

Look dark/irregular so easily confused for melanoma. Almost always not cancerous. Normally biopsied to confirm

64
Q

What are seborrhoeic keratosis?

A

Benign, warty/papillomatous lesion.

  • Age >30
  • Pale to dark brown
  • ‘stuck on’ appearance
  • Waxy/greasy
  • Keratin cysts within
65
Q

What is a dermatofibroma?

A
  • Insect bite/pimple fibroses into a hard/firm papule.
  • Palpate to feel. press from either side and centre with dimple ‘dimple sign’

Often mistaken for melanoma

66
Q

What are the indicators of sun damage?

A

1) Actinic keratosis
2) Solar Lentigines
3) Freckles
4) Favre-Racouchot - sun dmg so bad you start forming cysts and blackheads over face
5) Solar elastosis (histological thickened skin) - whitening of collagen
6) Freckles

67
Q

Risk factors for Skin cancer?

A

1) Sun exposure/Occupation
2) Fitzpatrick Skin type 1-3
3) Radiotherapy
4) Phototherapy
5) High risk pt groups:
- 100 moles
- Immunosuppressed
6) FH

68
Q

Features SCC?

Subtypes?

A

SCC produce keratin therefore abnormal keratotic lesions (dyskeratotic)

Well/moderately/poorly differentiated

69
Q

What is Actinic (solar) keratosis

A

Dysplasia - redness, ill defined clumps of dyskeratotic keratin caused by sun dmg. Premalignant SCC.

Full thickness = CIS = bowen’s disease

70
Q

What is Bowen’s disease?

A

SCC in situ. Full thickness dysplasia

well circumscribed erythematous scaly plaque.

Differentials include eczema and psoriasis.

Solitary/few

Asymptomatic

71
Q

BCC subtypes?

A

Nodular

Superficial

Morphoeic/infiltrative (most dangerous subtype - ill defined therefore poorly defined borders)

Pigmented

72
Q

BCC features

A

Arise from basal layer (produce other cells) so not very keratotic. Commonest human cancer

Rarely invades

Pearlescent
Telangiectasia
Rolled border

AKA rodent ulcer

73
Q

Nodular BCC

A

classical BCC - Raised, rolled edge with central ulceration. Pearlescent. Sometimes has overlying telangiectasia

74
Q

Infiltrative BCC

A

Slightly pearlescent. Difficult to see when tumour ends and skin begins. Need to biopsy

High risk tumour

75
Q

SCC features

A 
Keratotic/Ulcerated
Rapid growth
\+- Painful
Increased risk in transplant recipients
Metastatic potential higher on head and neck
76
Q

What is Lentigo Maligna?

A

Irregular mole/freckle

In-situ melanoma
Pre-malignant

Face, elderly, sun damaged skin

Irregular pigmented macules, variagation in pigment, blurring of border

77
Q

Lentigo maligna Mx?

A

Surgical Excision IS best option.

Topical:
5-FU
Immiquimoid
Cryotherapy
Photodynamic therapy
78
Q

Malignant Melanoma features

A 
ABCD
Asymmetrical (in 2 plains)
Border (irregular, growing)
Colour (>2 colours, odd colours, variagation of pigment)
Diameter (anything growing)

Skin markings lost
Rapid growth
May Ulcerate

79
Q

What is Hutchingson’s sign?

A

Sub-ungal melanoma coming through skin fold

80
Q

Prognostic factors in melanoma?

A

1) Breslow thickness
2) Ulceration (bad)
3) Mitotic index
4) Sentinal Node Biopsy (if Breslow > 1mm)

81
Q

What is Breslow thickness?

A

Depth from top to bottom in mm. 5 yr survival:

4mm = 25%

surrogate marker for how active the tumour is (mitotic rate)

82
Q

How do you do a sentinel node biopsy

A

WLE of melanoma + biopsy.

If melanoma >1mm, sentinel node biopsy. Radioactive blue dye around scar, then WLE, then geiger counter to find sentinel node + send to lab to see if tumour is in there or not. If tumour in there, has already metastasised, so has gone from stage I to stage III.

83
Q

Melanoma Tx

A 
Surgical:
Narrow excision and Histology
Then Wide local Excision
Plus:
Breslow >1mm sentinal node
Breslow
84
Q

Tx of non-melanoma skin cancer

A

Non-surgical (superficial disease)

1) Topicals
- Imiquimoid
- 5-FU
2) Photodynamic therapy - Cream soaks into tumour, light activates into toxin
3) Cryotherapy

Deeper disease

4) Radiotherapy
5) Surgery:
- Excision
- Curettage and cautery
- Mohs Surgery (Gold standard)

85
Q

What is Moh’s surgery?

A

A surgical procedure used to treat non-melanoma skin cancer.

Has the best cure rate with good tissue preservation.

Used for high risk BCC; those which are infiltrative, in high risk areas(head/neck/near eye) and recurrent. In young patients etc.

Not used much for SCC as harder to visualise under microscope

1) Anaesthetise + slice out tumour and freeze
2) look at biopsy straight away under microscopy and check margins
3) If cut margins encroaches on tumour, go back and excise some more + check again

86
Q

Aetiology of acne?

A
  • Androgens
  • Sebacious gland over-activity
  • Comedome and cyst formation
  • Colonisation of follicle with Propinobacter.acnes
  • Inflammation

Blackheads = Open comedones (Oxidised)

Whiteheads = Closed

87
Q

What is Acne Rosacea?

A

Acne + redness
–> vasodilation of blood vessels + telangiectasia

  • Tx: Metronidazole cream
  • Oral tetracycline
  • Oral retinoid (at a lower dose than for acne)
88
Q

Acne Classification?

A

Mild
Moderate
Severe –> Scarring is straight away severe

Comedonal
Inflammatory
Mixed

89
Q

Acne Treatments:

A

Topical:

  • Benzoyl peroxide
  • Antibiotics
  • Retinoids (normal desquamation + reduce inflammatory response

Systemtic:

  • Antibiotics
  • Anti-androgens (in women)
  • Isotretinoin
90
Q

Tx of comedomal acne?

A

1st choice usually topical retinoids:

- Adapalene, Tretinoin, Isotretinoin

91
Q

Tx of mild papular-pustular acne?

A

Combine topical retinoids and topical Antimicrobials

  • Adapalene/isotretinoin
  • Benzoyl peroxide/antibiotics eg. clindamycin
92
Q

Tx of moderate inflammatory acne

A

Oral abx + topical retinoids

Eg. Tetracyclines, minocycline, lymecycline

93
Q

Alternative oral tx for females with moderate acne?

A

Co-cyprinderol (dianette) - should be reserved for moderate to severe acne +- evidence of androgenisation (hirsutism, adiposity, irregular menses)

nb. Spironolactone also has anti-androgen effects and can be used in both men and women

94
Q

Tx of severe Acne?

A

Oral Isotretinoin

Sx: Dry skin, dry eyes
Hoarse Voice
Cheilitis
Headache
Arthritis/Myalgia
TERATOGENICITY
Adverse psychiatric effects - mood swings, depression, suicide

NEED to make sure they are not pregnant (pregnancy test), informed about and taking contraception

95
Q

What is a blister?

A

A cicumscribed skin lesion containing fluid

Blister/Bulla >5mm in diameter

Vesicle

96
Q

Causes of blistering?

A

1) Inflammatory eg. Pompholyx Eczema
2) Immunobullous diseases eg. Pemphigoid/pemphigus
3) Infectious: bullous Impetigo/varicella, bullous cellulitis
4) Extrinsic causes: Trauma/burns
5) Other causes. eg. Drugs, metabolic (porphyria)

97
Q

Pemphigoid?

A

DEEP Autoimmune bullous disease caused by antibodies against cells that holds epidermis to basement membrane

Common in older pts
May begin with urticarial plaques
Later, Tense, round blisters
Oral mucosa rarely involved
May be widespread
98
Q

Course and complications of bullous pemphigoid

A

Course: Usually self-limiting and treatment (minimal immunosuppressive therapy) can be stopped around 2 years

Complications: discomfort, loss of fluid from ruptured bullae

99
Q

Pemphigus vulgaris?

A

Chronic SUPERFICIAL autoimmune bullous disorder.

  • Highly aggressive (100% mortality without Tx)
  • Begins in oral mucosa
  • Flaccid vesicles and superficial EROSIONS
  • +ve Nikolsky (describes the spread of bullae following application of horizontal, tangential pressure to the skin). Pull the skin next to a blister and the epidermis comes off
100
Q

Antibodies in Pemphigus vs Pemphigoid

A

Pemphigus: antibodies directed against desmoglein 3, a cadherin-type epithelial cell adhesion molecule that holds cells to EACH OTHER.

Pemphigoid: antibodies against hemidesmosomal proteins BP180 and BP230 that hold epidermis to BASEMENT MEMBRANE. Immunoflorescence shows IgG and C3 at the dermoepidermal junction

Immunoflorescence: Pemphigus : Ab all around epidermis (Chicken wire)
Pemphigoid : Ab on basement membrane

101
Q

Pemphigus vulgaris Tx and complications

A

Tx:
- Aggressive immunosuppression eg. Pred, mycophenolate

Complications:

  • Overwhelming sepsis
  • Drug side effects
  • Fluid loss/heat loss etc.
102
Q

What is Dermatitis Herpetiformis?

A

AI blistering condition associated with coeliac disease formed by depositoon of IgA in dermis

Intensely pruritic vesicular eruption. Begins in early adult life, affecting mostly whites.

Symmetrically distributed papules and vesicles

Mx;
gluten free diet
Dapsone

103
Q

Erythema multiforme? Causes?

A

Features
target lesions
initially seen on the back of the hands / feet before spreading to the torso
upper limbs are more commonly affected than the lower limbs
pruritus is occasionally seen and is usually mild

If symptoms are severe and involve blistering and mucosal involvement (eye/mouth) the term Stevens-Johnson syndrome is used.

Causes
viruses: herpes simplex virus (the most common cause),
idiopathic
bacteria: Mycoplasma, Streptococcus
drugs: penicillin, sulphonamides, carbamazepine, allopurinol, NSAIDs, oral contraceptive pill, nevirapine
connective tissue disease e.g. Systemic lupus erythematosus
sarcoidosis
malignancy

104
Q

Erythema multiforme causes

A

Causes
viruses: herpes simplex virus (the most common cause),
idiopathic
bacteria: Mycoplasma, Streptococcus
drugs: penicillin, sulphonamides, carbamazepine, allopurinol, NSAIDs, oral contraceptive pill, nevirapine
connective tissue disease e.g. Systemic lupus erythematosus
sarcoidosis
malignancy

105
Q

what is toxic epidermal necrolysis?

Features?

A

Toxic epidermal necrolysis (TEN) is a potentially life-threatening skin disorder that is most commonly seen secondary to a drug reaction. In this condition the skin develops a scalded appearance over an extensive area. Some authors consider TEN to be the severe end of a spectrum of skin disorders which includes erythema multiforme and Stevens-Johnson syndrome

Features
systemically unwell e.g. pyrexia, tachycardic
positive Nikolsky’s sign: the epidermis separates with mild lateral pressure

Drugs known to induce TEN
phenytoin
sulphonamides
allopurinol
penicillins
carbamazepine
NSAIDs

Management
stop precipitating factor
supportive care, often in intensive care unit
intravenous immunoglobulin has been shown to be effective and is now commonly used first-line
other treatment options include: immunosuppressive agents (ciclosporin and cyclophosphamide), plasmapheresis

106
Q

Drug causes of TEN

A 
Drugs known to induce TEN
phenytoin
sulphonamides
allopurinol
penicillins
carbamazepine
NSAIDs
107
Q

Mx of TEN

A 
Stop precipitating factor
Nurse on burns unit
Supportive care
Fluid balance
Nutrition
temperature
Prevent infection
IV IG
108
Q

Golden Crust?

Tx?

A

Impetigo (Staph aureus)

Tx
Topical Potassium permanganate Soaks
Topical Fusicidic/ Flucloxacillin

109
Q

Commonest cause of abscess

A

Staph - another form of impetigo

110
Q

Cellulitis causes?

Tx

A

Staph OR Strep pyogenes

Therefore IV Fluclox

Clari in pen allergic

If severe: IV benpen + fluclox

111
Q

Single infectious bullae?

A

staph toxin blistering

112
Q

Staph scalded skin syndrone aka Staph toxic shock syndrome

A

Superficial desquamation caused by staph infection

113
Q

Tinea diagnosis + Tx

A

Ix: Card scrapings + look under microscope for hypae

Woods lamp - tinea lights up under lamp

Tx: Topical antifungal eg.. Terbinafine, ketoconazole, itraconazole

Topical ketoconazole shampoo should be given for first 2 weeks to reduce transmission

Systemic:
eg. Griseofulvin, terbafine

114
Q

Tinea incognito

A

Hidden serpiginous edge Tinea + steroid –> Swells up and expands, filling up with pustules

115
Q

Tinea in feet? Head? Trunk, legs/arms? Groin?

A

Tinea pedis
Tinea capitis (get very rampant occipital lymph nodes with scalp infection)
Tinea corporis
Tinea Cruris

116
Q

What is a kerion?

A

A large raised, pustular, spongy/boggy mass eg. on the scalp, formed by untreated tinea capitis.

117
Q

Skin fold lesions - some erosion

A

Cutaneous candidiasis
–> INTERTRIGO

but also:

  • Genital
  • Folliculitis
  • Nappy dermatitis
  • Nails
  • Chronic mucocutaneous candidiasis
118
Q

Hyperpigmented lesions around chest, young man just back from holiday. Worse in sunshine

A

Pityriasis versicolor,

is a superficial cutaneous fungal infection caused by Malassezia furfur

Features
most commonly affects trunk
patches may be hypopigmented, pink or brown (hence versicolor)
scale is common
mild pruritus
Predisposing factors
occurs in healthy individuals
immunosuppression
malnutrition
Cushing's

Management
topical antifungal. NICE Clinical Knowledge Summaries advise ketoconazole shampoo as this is more cost effective for large areas
if extensive disease or failure to respond to topical treatment then consider oral itraconazole

119
Q

scabies tx?

A

Topical permethrin/malthione
- Head to toe, wash 24 hrs later, repeat a week later to kill eggs when they hatch

Treat contacts

Can also use systemic (immunocompromised) ivermectin

120
Q

Viral wart cause?

A

HPV

121
Q

Cold sore organism + Ix?

A

HSV
–> blister fluid PCR

Tx with acyclovir

122
Q

Eczema herpeticum optic risk?

A

Stellate ulcer of eye –> blinds you

123
Q

Molluscum cause + characteristic finding?

A

Pox virus

  • self limiting
  • Central dimpling
  • Often clustered

Tx:
Cryotherapy
Immiquimod

124
Q

Kaposi’s sarcoma cause?

A

HHV-8

125
Q

Granulomatous infectious papular erythematous rash

A

Mycobacteria

also Lupus vulgaris TB

126
Q

Annular erythematous plaque which keeps growing, in a man who has just returned from philiipines. Stick a pin in it and he feels no pain. What is it?

A

M.leprii

127
Q

Eczema distribution in 10 month old?

Young Children?

Older Children?

A

Face & trunk

Extensor surfaces

Typical distribution: flexor surfaces + creases of face and neck

128
Q

Causes of acantosis nigricans?

A 
gastrointestinal cancer
diabetes mellitus
obesity - Most common caused. linked to inuslin resistance
polycystic ovarian syndrome
acromegaly
Cushing's disease
hypothyroidism
familial
Prader-Willi syndrome
drugs: oral contraceptive pill, nicotinic acid
129
Q

Where are Keloid scars most likely to form?

A

Keloid scars are tumour-like lesions that arise from the connective tissue of a scar and extend beyond the dimensions of the original wound

Predisposing factors
ethnicity: more common in people with dark skin
occur more commonly in young adults, rare in the elderly
common sites (in order of decreasing frequency): STERNUM, shoulder, neck, face, extensor surface of limbs, trunk

Keloid scars are less likely if incisions are made along relaxed skin tension lines*

Treatment
early keloids may be treated with intra-lesional steroids e.g. triamcinolone
excision is sometimes required

130
Q

Acne rosacea Tx?

A

Acne rosacea treatment:
mild/moderate: topical metronidazole
severe/resistant (if plaques): oral tetracycline

131
Q

What is a Rhinophyma?

A

Rhinophyma is a condition causing development of a large, bulbous, ruddy nose associated with granulomatous infiltration, commonly due to untreated rosacea

132
Q

NICE first line tx of psoriasis?

A

Emolliants, bath oils, soap substitutes

first-line: NICE recommend a potent corticosteroid applied once daily plus vitamin D analogue applied once daily (applied separately, one in the morning and the other in the evening) for up to 4 weeks as initial treatment
second-line: if no improvement after 8 weeks then offer a vitamin D analogue twice daily
third-line: if no improvement after 8-12 weeks then offer either: a potent corticosteroid applied twice daily for up to 4 weeks or a coal tar preparation applied once or twice daily
short-acting dithranol can also be used

133
Q

What is a keratoacanthoma?

A

Keratoacanthoma is a benign epithelial tumour. They are more frequent in middle age and do not become more common in old age (unlike basal cell and squamous cell carcinoma)

Features - said to look like a volcano or crater
initially a smooth dome-shaped papule
rapidly grows to become a crater centrally-filled with keratin

Spontaneous regression of keratoacanthoma within 3 months is common, often resulting in a scar. Such lesions should however be urgently excised as it is difficult clinically to exclude squamous cell carcinoma. Removal also may prevent scarring.

134
Q

Organism in fungal nail infections?

A

Trichophyton rubrum

Onychomycosis is fungal infection of the nails. This may be caused by
dermatophytes - mainly Trichophyton rubrum, accounts for 90% of cases
yeasts - such as Candida
non-dermatophyte moulds

135
Q

What is lichen sclerosis?

A

sclerosus: itchy white spots typically seen on the vulva of elderly women

136
Q

Erythema nodosum causes

A

Causes
infection: streptococci, TB, brucellosis
systemic disease: sarcoidosis, inflammatory bowel disease, Behcet’s
malignancy/lymphoma
drugs: penicillins, sulphonamides, combined oral contraceptive pill
pregnancy

137
Q

Athlete’s foot cause and treatment

A

Athlete’s foot is also known as tinea pedis. It is usually caused by fungi in the genus Trichophyton.

Features
typically scaling, flaking, and itching between the toes

Clinical knowledge summaries recommend a topical imidazole (eg. topical miconazole), undecenoate, or terbinafine first-line

eg. topical miconazole

138
Q

Verrucas?

A

Secondary to the human papilloma virus
Firm, hyperkeratotic lesions
Pinpoint petechiae centrally within the lesions
May coalesce with surrounding warts to form mosaic warts

139
Q

Corn and calluses

A

A corn is small areas of very thick skin secondary to a reactive hyperkeratosis
A callus is larger, broader and has a less well defined edge than a corn

140
Q

Keratoderma

A

May be acquired or congenital
Describes a thickening of the skin of the palms and soles
Acquired causes include reactive arthritis (keratoderma blennorrhagica)

141
Q

Pitted keratolysis

A

Affects people who sweat excessively
Patients may complain of damp and excessively smelly feet
Usually caused by Corynebacterium
Heel and forefoot may become white with clusters of punched-out pits

142
Q

Palmoplantar pustulosis

A

Crops of sterile pustules affecting the palms and soles
The skin is thickened, red. Scaly and may crack
More common in smokers

143
Q

Juvenile plantar dermatosis

A

Juvenile plantar dermatosis Affects children. More common in atopic patients with a history of eczema
Soles become shiny and hard. Cracks may develop causing pain
Worse during the summer

144
Q

What is Pemphigoid gestationis?

A

pruritic blistering lesions

often develop in peri-umbilical region, later spreading to the trunk, back, buttocks and arms

usually presents 2nd or 3rd trimester and is rarely seen in the first pregnancy

oral corticosteroids are usually required

145
Q

What is Polymorphic eruption of pregnancy

A

Polymorphic eruption of pregnancy
pruritic condition associated with last trimester
lesions often first appear in abdominal striae
management depends on severity: emollients, mild potency topical steroids and oral steroids may be used

NOT associated with blistering - think pemphigoid gestationis

146
Q

Pyoderma gangrenosum?

A

initially small red papule, often on shin

later deep, red, necrotic ulcers with a violaceous border
idiopathic in 50%, may also be seen in inflammatory bowel disease, connective tissue disorders and myeloproliferative disorders

147
Q

Vitiligo? Features, assoicated conditions and management

A

Vitiligo is an autoimmune condition which results in the loss of melanocytes and consequent depigmentation of the skin. It is thought to affect around 1% of the population and symptoms typically develop by the age of 20-30 years.

Features
well demarcated patches of depigmented skin
the peripheries tend to be most affected
trauma may precipitate new lesions (Koebner phenomenon)

Associated conditions
type 1 diabetes mellitus
Addison's disease
autoimmune thyroid disorders
pernicious anaemia
alopecia areata

Management
sun block for affected areas of skin
camouflage make-up
topical corticosteroids may reverse the changes if applied early
there may also be a role for topical tacrolimus and phototherapy, although caution needs to be exercised with light-skinned patients

148
Q

Causes of Steven’s Johnson

A 
Causes
idiopathic
bacteria: Mycoplasma, Streptococcus
viruses: herpes simplex virus, Orf
drugs: penicillin, sulphonamides, carbamazepine, allopurinol, NSAIDs, oral contraceptive pill
connective tissue disease e.g. SLE
sarcoidosis
malignancy
149
Q

Causes of hirsuitism

A 
Polycystic ovarian syndrome is the most common causes of hirsutism. Other causes include: 
Cushing's syndrome
congenital adrenal hyperplasia
androgen therapy
obesity: due to peripheral conversion oestrogens to androgens
adrenal tumour
androgen secreting ovarian tumour
drugs: phenytoin
150
Q

Causes of hypertrichosis?

A 
Causes of hypertrichosis
drugs: minoxidil, ciclosporin, diazoxide
congenital hypertrichosis lanuginosa, congenital hypertrichosis terminalis
porphyria cutanea tarda
anorexia nervosa
151
Q

Granuloma anulare?

A

Idiopathic, annular plaque, raised purple/red/nodular edge

Tx:

  • Emolliant soap substitutes
    1) Topical steroids/ Intralesional steroids
    2) photo therapy
    3) Systemic medications eg. methotrexate
152
Q

Differentiating feature between acne and acne rosacea?

A

Acne will have comedomes (blackheads)

153
Q

Cutaneous vasculitis?

A

Purple/pruritic patches/plaques
Central vesiculation and necrosis

DISTRIBUTION is the defining feature

Ix:

1) Urinalysis (blood/protein)
2) BP (rule out kidney involvement)
3) (Skin biopsy - not always necessary)
4) Vaculitis screen

To differentiate primary from secondary causes?

  • FBC, LFT, U+E
  • Urinalysis
  • ESR CRP
  • Autoantibodies - ANA, ENA, RhF, ANCA, dsDNA , C3 C4, Pr3, MPo
  • Infection (Hep B, C) , ASOT, mycoplasma

2 most common cause of vasculitis:

  • Drugs
  • Sepsis
154
Q

How to differentiante TEN from staph scalded skin syndrome

A

Mucosal involvement - Pts with scalded syndrome never have mucosal involvement

5th year (14 decks)

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