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
Pustular psoriasis?
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
26
Mx of generalised pustular psoriasis?
1) resuscitate ABC 2) Admit 3) Greasy emollients 4) IV support 5) Systemic therapy 6) Avoid or treat concurrent infection 7) ITU if necessary
27
Complications of erythrodermic psoriasis?
Derm emergency: 1) Fluid loss 2) hypothermia 3) infection 4) hypercatabolic state 5) SHOCK Mx same as generalised pustular psoriasis
28
Mx Psoriasis?
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
29
Topical agents in psoriasis?
1) Vitamin D 2) Tar (anti-proliferatives) 3) Dithranol 4) Steroids Only useful in localised disease
30
Systemic agents in psoriasis?
1) Retinoids (acitretin) 2) Fumaric acid 3) Hydroxycarbamide 4) Immunosuppression: - Methotrexate (especially if joint involvement) - Ciclosporin
31
Biologic agents in Psoriasis?
Anti TNF: - Etanercept - Infliximab - Adalimumab Anti IL-12/23: - Ustekinemab
32
5 P's of Lichen Planus
``` Purple (violacious) Planar = flat Polished = Shiny Papular Pruritic ``` (polygonal/pigmented)
33
What is Wickham's striae?
Reticulated lace like lichen planus usually in the mouth, but can be anywhere
34
Lichen planus treatment?
Emollients/soap substitutes Topical: - Super potent steroids - UVB Systemic: - Oral steroids (CF psorarisis - never oral) - Hydroxychloroquine - Immunosuppression
35
Actinic Lichen Planus?
Sun-induced (photodistributed) lichen planus eg. dense hyperpigmentation of face
36
What is the herald patch. What condition is it seen in.
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
37
What is Eczema?
An inflammatory dermatosis characterised by erythema and itching. Histologically shoes spongiosis (fluid building up under skin) + inflammation
38
Causes of eczema?
``` Atopic Contact allergic Contact irritant Seborrhoeic (dandruff) Varicose Asteototic (elderly - dry out) Drug ```
39
Different morphology in eczema?
``` Pompholyx Discoid Lichen Simplex - thickening due to rubbing Lichen Amyloid Nodular prurigo Erythroderma ```
40
What is Atopic eczema?
- 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
41
Exacerbating factors for atopic eczema?
``` Topical irritants Soap Secondary infection: - Staph, viral herpes, tinea House dust mite Animal Moulds Food allergies ```
42
Atopic eczema prognosis?
50% clear by 3 years 66% clear by 6 years 90% clear by 20 years
43
What is pityriasis Alba?
Post-inflammatory hypopigmentation Often in black skin & children
44
What is Pomphoylx?
Episodic visculobullous disorder. A type of eczema Causes tiny blisters on fingers/palms/soles
45
Who gets discoid eczema?
Females aged 15-25 yrs Females and males 55-65 yrs Increased incidence in winter
46
What is lichen simplex chronicus?
Chronic eczema itch-rub cycle leads to lichenification and pigmentation Some excoriation, some scale
47
What is Lichen Amyloid?
same process as Lichen simplex, but leads to deposition of amyloid under skin. Tend to get a hyperpigmented cobblestone type appearance
48
What is Nodular prurigo?
Chronic-itch rub cycle in eczema characterised by very itchy firm lumps, often excoriated to the point of erosion
49
Complications of Atopic eczema?
1) Secondary staph infection | 2) Eczema herpeticum
50
Eczema mx?
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
51
Steroid hierarchy
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
52
Topical Steroids SE?
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
53
Investigation of atopic dermatitis?
Clinical diagnosis so very rarely investigate Biopsy Swab (bacterial/viral) Specific IgE (RAST) testing
54
Classification of nappy rash?
Seborrhaeic dermatitis - sparing of skin folds
55
Seborrheic dermatitis Mx
1) antifungal shampoo 2) corticosteroid scalp application 3) topical steroids 4) Oral ketoconazole/itraconazole
56
What is contact dermatitis?
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)
57
What type of allergic reaction is allergic contact dermatitis
Type IV - delayed cell mediated hypersensitivity
58
Allergic contact dermatitis Dx & Tx
Dx: - History of allergen exposure - Clinical features - Patch testing (2 days with wells on back) Tx: - Allergen avoidance
59
What are the different types of melanocytic naevi?
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
60
Congenital melanocytic naevi
There from birth, and tend to grow with the person. Not likely to become malignant unless greater >20cm (risk greatly increases)
61
What is Beckers Naevus?
stippled/reticular patches of pigmentation, often hairy. Not actually melanocytic- actually a hamaratomatous.
62
Subungal naveus - Linear nail change vs deltoid nail change?
Linear = benign Triangular = melanoma until proved otherwise
63
What is a Spitz Naevus?
Look dark/irregular so easily confused for melanoma. Almost always not cancerous. Normally biopsied to confirm
64
What are seborrhoeic keratosis?
Benign, warty/papillomatous lesion. - Age >30 - Pale to dark brown - 'stuck on' appearance - Waxy/greasy - Keratin cysts within
65
What is a dermatofibroma?
- 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
What are the indicators of sun damage?
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
Risk factors for Skin cancer?
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
Features SCC? Subtypes?
SCC produce keratin therefore abnormal keratotic lesions (dyskeratotic) Well/moderately/poorly differentiated
69
What is Actinic (solar) keratosis
Dysplasia - redness, ill defined clumps of dyskeratotic keratin caused by sun dmg. Premalignant SCC. Full thickness = CIS = bowen's disease
70
What is Bowen's disease?
SCC in situ. Full thickness dysplasia well circumscribed erythematous scaly plaque. Differentials include eczema and psoriasis. Solitary/few Asymptomatic
71
BCC subtypes?
Nodular Superficial Morphoeic/infiltrative (most dangerous subtype - ill defined therefore poorly defined borders) Pigmented
72
BCC features
Arise from basal layer (produce other cells) so not very keratotic. Commonest human cancer Rarely invades Pearlescent Telangiectasia Rolled border AKA rodent ulcer
73
Nodular BCC
classical BCC - Raised, rolled edge with central ulceration. Pearlescent. Sometimes has overlying telangiectasia
74
Infiltrative BCC
Slightly pearlescent. Difficult to see when tumour ends and skin begins. Need to biopsy High risk tumour
75
SCC features
``` Keratotic/Ulcerated Rapid growth +- Painful Increased risk in transplant recipients Metastatic potential higher on head and neck ```
76
What is Lentigo Maligna?
Irregular mole/freckle In-situ melanoma Pre-malignant Face, elderly, sun damaged skin Irregular pigmented macules, variagation in pigment, blurring of border
77
Lentigo maligna Mx?
Surgical Excision IS best option. ``` Topical: 5-FU Immiquimoid Cryotherapy Photodynamic therapy ```
78
Malignant Melanoma features
``` 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
What is Hutchingson's sign?
Sub-ungal melanoma coming through skin fold
80
Prognostic factors in melanoma?
1) Breslow thickness 2) Ulceration (bad) 3) Mitotic index 4) Sentinal Node Biopsy (if Breslow > 1mm)
81
What is Breslow thickness?
Depth from top to bottom in mm. 5 yr survival: 4mm = 25% surrogate marker for how active the tumour is (mitotic rate)
82
How do you do a sentinel node biopsy
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
Melanoma Tx
``` Surgical: Narrow excision and Histology Then Wide local Excision Plus: Breslow >1mm sentinal node Breslow ```
84
Tx of non-melanoma skin cancer
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
What is Moh's surgery?
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
Aetiology of acne?
- Androgens - Sebacious gland over-activity - Comedome and cyst formation - Colonisation of follicle with Propinobacter.acnes - Inflammation Blackheads = Open comedones (Oxidised) Whiteheads = Closed
87
What is Acne Rosacea?
Acne + redness --> vasodilation of blood vessels + telangiectasia - Tx: Metronidazole cream - Oral tetracycline - Oral retinoid (at a lower dose than for acne)
88
Acne Classification?
Mild Moderate Severe --> Scarring is straight away severe Comedonal Inflammatory Mixed
89
Acne Treatments:
Topical: - Benzoyl peroxide - Antibiotics - Retinoids (normal desquamation + reduce inflammatory response Systemtic: - Antibiotics - Anti-androgens (in women) - Isotretinoin
90
Tx of comedomal acne?
1st choice usually topical retinoids: | - Adapalene, Tretinoin, Isotretinoin
91
Tx of mild papular-pustular acne?
Combine topical retinoids and topical Antimicrobials - Adapalene/isotretinoin - Benzoyl peroxide/antibiotics eg. clindamycin
92
Tx of moderate inflammatory acne
Oral abx + topical retinoids Eg. Tetracyclines, minocycline, lymecycline
93
Alternative oral tx for females with moderate acne?
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
Tx of severe Acne?
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
What is a blister?
A cicumscribed skin lesion containing fluid Blister/Bulla >5mm in diameter Vesicle
96
Causes of blistering?
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
Pemphigoid?
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
Course and complications of bullous pemphigoid
Course: Usually self-limiting and treatment (minimal immunosuppressive therapy) can be stopped around 2 years Complications: discomfort, loss of fluid from ruptured bullae
99
Pemphigus vulgaris?
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
Antibodies in Pemphigus vs Pemphigoid
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
Pemphigus vulgaris Tx and complications
Tx: - Aggressive immunosuppression eg. Pred, mycophenolate Complications: - Overwhelming sepsis - Drug side effects - Fluid loss/heat loss etc.
102
What is Dermatitis Herpetiformis?
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
Erythema multiforme? Causes?
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
Erythema multiforme causes
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
what is toxic epidermal necrolysis? Features?
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
Drug causes of TEN
``` Drugs known to induce TEN phenytoin sulphonamides allopurinol penicillins carbamazepine NSAIDs ```
107
Mx of TEN
``` Stop precipitating factor Nurse on burns unit Supportive care Fluid balance Nutrition temperature Prevent infection IV IG ```
108
Golden Crust? | Tx?
Impetigo (Staph aureus) Tx Topical Potassium permanganate Soaks Topical Fusicidic/ Flucloxacillin
109
Commonest cause of abscess
Staph - another form of impetigo
110
Cellulitis causes? Tx
Staph OR Strep pyogenes Therefore IV Fluclox Clari in pen allergic If severe: IV benpen + fluclox
111
Single infectious bullae?
staph toxin blistering
112
Staph scalded skin syndrone aka Staph toxic shock syndrome
Superficial desquamation caused by staph infection
113
Tinea diagnosis + Tx
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
Tinea incognito
Hidden serpiginous edge Tinea + steroid --> Swells up and expands, filling up with pustules
115
Tinea in feet? Head? Trunk, legs/arms? Groin?
Tinea pedis Tinea capitis (get very rampant occipital lymph nodes with scalp infection) Tinea corporis Tinea Cruris
116
What is a kerion?
A large raised, pustular, spongy/boggy mass eg. on the scalp, formed by untreated tinea capitis.
117
Skin fold lesions - some erosion
Cutaneous candidiasis --> INTERTRIGO but also: - Genital - Folliculitis - Nappy dermatitis - Nails - Chronic mucocutaneous candidiasis
118
Hyperpigmented lesions around chest, young man just back from holiday. Worse in sunshine
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
scabies tx?
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
Viral wart cause?
HPV
121
Cold sore organism + Ix?
HSV --> blister fluid PCR Tx with acyclovir
122
Eczema herpeticum optic risk?
Stellate ulcer of eye --> blinds you
123
Molluscum cause + characteristic finding?
Pox virus - self limiting - Central dimpling - Often clustered Tx: Cryotherapy Immiquimod
124
Kaposi's sarcoma cause?
HHV-8
125
Granulomatous infectious papular erythematous rash
Mycobacteria also Lupus vulgaris TB
126
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?
M.leprii
127
Eczema distribution in 10 month old? Young Children? Older Children?
Face & trunk Extensor surfaces Typical distribution: flexor surfaces + creases of face and neck
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Causes of acantosis nigricans?
``` 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 ```
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Where are Keloid scars most likely to form?
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
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Acne rosacea Tx?
Acne rosacea treatment: mild/moderate: topical metronidazole severe/resistant (if plaques): oral tetracycline
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What is a Rhinophyma?
Rhinophyma is a condition causing development of a large, bulbous, ruddy nose associated with granulomatous infiltration, commonly due to untreated rosacea
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NICE first line tx of psoriasis?
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
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What is a keratoacanthoma?
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.
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Organism in fungal nail infections?
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
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What is lichen sclerosis?
sclerosus: itchy white spots typically seen on the vulva of elderly women
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Erythema nodosum causes
Causes infection: streptococci, TB, brucellosis systemic disease: sarcoidosis, inflammatory bowel disease, Behcet's malignancy/lymphoma drugs: penicillins, sulphonamides, combined oral contraceptive pill pregnancy
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Athlete's foot cause and treatment
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
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Verrucas?
Secondary to the human papilloma virus Firm, hyperkeratotic lesions Pinpoint petechiae centrally within the lesions May coalesce with surrounding warts to form mosaic warts
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Corn and calluses
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
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Keratoderma
May be acquired or congenital Describes a thickening of the skin of the palms and soles Acquired causes include reactive arthritis (keratoderma blennorrhagica)
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Pitted keratolysis
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
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Palmoplantar pustulosis
Crops of sterile pustules affecting the palms and soles The skin is thickened, red. Scaly and may crack More common in smokers
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Juvenile plantar dermatosis
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
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What is Pemphigoid gestationis?
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
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What is Polymorphic eruption of pregnancy
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
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Pyoderma gangrenosum?
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
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Vitiligo? Features, assoicated conditions and management
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
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Causes of Steven's Johnson
``` 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 ```
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Causes of hirsuitism
``` 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 ```
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Causes of hypertrichosis?
``` Causes of hypertrichosis drugs: minoxidil, ciclosporin, diazoxide congenital hypertrichosis lanuginosa, congenital hypertrichosis terminalis porphyria cutanea tarda anorexia nervosa ```
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Granuloma anulare?
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
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Differentiating feature between acne and acne rosacea?
Acne will have comedomes (blackheads)
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Cutaneous vasculitis?
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
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How to differentiante TEN from staph scalded skin syndrome
Mucosal involvement - Pts with scalded syndrome never have mucosal involvement