Dermatology Flashcards
(208 cards)
1
Q
What does it mean if a skin lesion is described as being ‘acral’ in its distribution?
A
Affecting distal areas- hands and feet
2
Q
What dermatological condition do you classically associated with target lesions?
A
Erythema multiforme
3
Q
How do annular and target lesions differ in their appearance?
A
Annular lesions are circle/ ring shaped (usually middle part spared)
Target lesions are concentric rings of varying colour and look like a dartboard / bullseye
4
Q
When assessing the colour of a lesion, can use the term ‘purpura’ to describe a reddish/ purple discolouration of the skin. Name 2 types of purpura?
A
Petechiae and ecchymosis
5
Q
What is key to remember about how lichenification of the skin looks?
A
Roughening of the skin with exaggerated normal skin lines
6
Q
What distinguishes a hypertrophic scar from a keloid scar?
A
Hypertrophic scar = hyperproliferation of scar tissue WITHIN the wound boundary.
Keloid scar = hyperproliferation of scar tissue BEYOND the wound boundary.
7
Q
Striae progress in colour from what.. to what.. to what..?
A
Purple -> Pink -> White
8
Q
What does alopecia areata look like?
A
Well defined patches of hair loss with surrounding normal hair
9
Q
Excess hair growth can be described as hirsutism and hypertrichosis- what is the difference?
A
Hirsutism is androgen-dependent excess hair growth in a female
Hypertrichosis is non-androgen dependent pattern of excessive hair growth
10
Q
What are open and closed comedones more commonly known as?
A
Open comedones- blackheads
Closed comedones- whiteheads
11
Q
The epidermis contains which 4 major cell types?
A
Keratinocytes, Langerhans cells, Melanocytes and Merkel cells
12
Q
Tell me about UVA and UVB
A
UVA- longer wavelength, penetrates deeper and through window glass A = ageing (damages elastic fibres) and carcinogenic
UVB- shorter wavelength causes burning not as carcinogenic
B= burning
13
Q
Outline Fitzpatrick skin types
A
1- always burns, never tans 2- usually burns, sometimes tans 3- sometimes burns, usually tans 4- never burns, always tans 5- brown skin 6- black skin
14
Q
What is the progression from a mole (benign melanocytic naevus) to malignant melanoma?
A
Congenital and acquired melanocytic naevi (benign) -> atypical (dysplastic) melanocytic naevi -> malignant melanoma in situ (Lentigo malinga) -> malignant melanoma
15
Q
What is malignant melanoma in situ called?
A
Lentigo maligna (but note that this is not the same as Lentigo maligna melanoma so do not get them mixed up!)
16
Q
What are seborrhoeic keratoses and how are they classically described?
A
Benign epidermal skin lesions seen in older people. ‘Stuck on’ and ‘warty’ looking appearance.
17
Q
What is the commonest form of skin cancer?
A
Basal cell carcinoma (BCC)
18
Q
What are BCCs also known as?
A
Rodent ulcers
19
Q
Where do you typically see BCCs?
A
Typically on the face in elderly or middle-aged patients. They mainly occur on light-exposed sites, commonly around the nose, the inner canthus of the eyelids and the temple
20
Q
What are some of the risk factors for BCC?
A
UV exposure, history of frequent or severe sunburn in childhood, skin type 1, increasing age, male sex, immunosuppression, previous Hx of skin cancer and genetic predisposition
21
Q
How fast do BCCs grow and do they metastasise?
A
They are a slow growing and locally invasive malignant tumour of the epidermal keratinocytes and only RARELY metastasise
22
Q
What is the most common type of BCC?
A
Nodular
23
Q
How are nodular BCCs classically described?
A
Small skin-coloured papule or nodule that shows fine telangiectasia and a glistening pearly rolled edge and central depression. The superficial branching telangiectasia are characteristic and are seen on dermoscopy as ‘arborizing’
24
Q
What subtype of BCC more commonly occurs in younger patients? And how do these tend to present?
A
Superficial (plaque like). They present most frequently on the trunk as a slowly expanding pink-red patch.
25
When taking a history for a skin lesion, in terms of BCC skin cancer, over what time period does the lesion present?
Takes months-years to present
26
What should you do if you suspect a BCC?
Make a routine referral to dermatology
27
What is the management of a BCC?
If possible, complete excision is the best Tx as this allows a histological check on the adequacy of removal. If excision is difficult, radiotherapy is suitable for those aged >60 years. Often no further investigations/ staging is needed for BCC once they have been excised.
28
Tell me about Mohs micrographic surgery and for what type of BCC is this procedure gold-standard?
Mohs micrographic surgery - excision of the lesion and tissue progressively until specimens are microscopically free of tumour - used for high-risk, recurrent tumours. It also tends to be gold-standard for infiltrative BCC.
29
What is a squamous cell carcinoma?
A locally invasive malignant tumour of the epidermal keratinocytes which has the potential to metastasise
30
What are the risk factors for SCC?
Excessive UV exposure, pre-malignant skin conditions (e.g. actinic keratosis), Bowen’s disease, Immunosuppression, smoking, chronic inflammation (long standing leg ulcers, wound scars), genetic conditions
31
How do SCCs present?
Keratitis (e.g. scaly, crusty), ill-defined nodule which may ulcerated. Usually increase in size over weeks-months
32
What is the premalignant form of SCC?
Actinic (solar) keratosis
33
What is SCC in-situ (intraepidermal SCC) known as?
Bowen’s disease
34
What is the management of SCC?
Surgical excision is the Tx of choice- with 4mm margins if lesion <20mm in diameter. If lesion >20mm then margins should be 6mm. Mohs micrographic surgery may be necessary for ill-defined, large, recurrent tumours (high risk patients and in cosmetically important sites). Radiotherapy for large, non-resectable tumours
35
What patient demographic (age/gender) does Bowen’s disease tend to occur in? And what is the risk of it developing into invasive skin cancer
More common in elderly females. There is around a 3% chance of developing invasive skin cancer.
36
What causes actinic keratosis and what are the risk factors for it?
Induced by chronic exposure to UV radiation. Risk factors include: old age, male sex, cumulative sun exposure, fair skin, immunosuppression, genetic factors
37
How do actinic keratoses present?
Small, crusty or scaly, roughened patches of skin, usually <1cm in diameter found on sun-exposed skin (e.g. temples of head) and are often easier to palpate than see.
38
What is the management of actinic keratosis?
5-flurouracil cream (5-FU) in various concentrations applied daily for 1-4 weeks or with salicylic acid (for more hyperkeratotic lesions) for 6-12 weeks is an effective approach.
Other Tx options include: Imiquimod cream, ingenol mebutate gel, cryotherapy
39
What must you warn patients about if you are going to prescribe them 5-FU cream for actinic keratosis?
Warn them about the likely inflammatory reaction during therapy. The skin will become red and inflamed- sometimes topical hydrocortisone is given following 5-FU to settle the inflammation.
40
What is malignant melanoma?
An invasive malignant tumour of the epidermal melanocytes which has the potential to metastasise
41
What are the risk factors for malignant melanoma?
Age, Excessive UV exposure (intermittent exposure sunburn), skin type 1, history of multiple moles or atypical moles, and family history or previous history of melanoma.
42
What is ABCDE in relation to malignant melanoma?
```
Asymmetrical shape
Border irregularity
Colour irregularity
Diameter >6mm
Evolution of the lesion (e.g. change in size/shape)
Symptoms (e.g. bleeding, itching)
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43
In addition to the ABCDE for malignant melanoma, what other checklist can be used to assess a lesion?
Glasgow 7 point checklist which separates major and minor features
44
Describe the Glasgow 7 point checklist for malignant melanoma
Major criteria: change in size, change in shape, change in colour
Minor criteria: diameter >7mm, inflammation, oozing or bleeding, altered sensation (e.g. itch)
45
Name the 4 main subtypes of melanoma
Superficial spreading
Nodular
Lentigo maligna melanoma
Acral lentiginous malignant melanoma
46
What subtype of malignant melanoma is the most aggressive?
Nodular melanoma
47
What is the most common type of malignant melanoma?
Superficial spreading
48
Describe superficial spreading malignant melanoma
Make up 70% of cases. Common mainly on the lower limbs but also the arms, back and chest in young and middle-aged adults, related to intermittent high-intensity UV exposure
49
Describe nodular malignant melanoma
Second commonest. Common on the trunk in young and middle-aged adults, related to intermittent high-intensity UV exposure. Red or black lump or lump which bleeds or oozes.
50
Describe lentigo maligna melanoma
Common on the face in the elderly population, related to long-term cumulative UV exposure
51
Describe acral lentiginous malignant melanoma
Common on the palms, soles and nail beds in elderly population. No clear relation with UV exposure. Is the rest form of melanoma overall but is the commonest form of melanoma in people with dark skin.
52
What is the commonest form of malignant melanoma in people with dark skin?
Acral lentiginous malignant melanoma
53
What is Hutchinson’s sign?
Pigmentation of the nail bed (Subungual pigmentation) affecting the proximal nail fold which suggests melanoma (acral type)
54
What is the management of malignant melanoma?
Suspicious lesions should undergo excision biopsy. The lesion should be removed completely. Once the diagnosis is confirmed the pathology report should be reviewed to determine whether further re-excision of margins is required. Margins of excision is also related to Breslow thickness.
55
What is the most important prognostic factor for malignant melanoma?
The Breslow thickness (depth of abnormal melanocytes within the dermis)
56
When should you offer sentinel lymph node biopsy in malignant melanoma?
If the Breslow depth is >1.0mm
57
What treatment is used for metastatic disease in malignant melanoma?
Chemotherapy
58
What is a keratoacanthoma? And how is it classically described?
A benign epithelial tumour. They are more common with advancing age and rare in young people. Typically 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 within 3 months is common, often resulting in a scar. May be difficult clinically to exclude an SCC so should be urgently excised and removal may prevent scarring.
59
What is the difference between cellulitis and erysipelas?
Cellulitis involves the deep subcutaneous tissue
| Erysipelas is an acute superficial form of cellulitis and involves the dermis and upper subcutaneous tissue
60
What organism is the most common cause of cellulitis/ erysipelas?
Streptococcus pyogenes (a type of group A strep)
61
How does cellulitis present?
Any age, pain is a common feature. The legs followed by the face are the most common sites. Facial involvement tends to be more superficial i.e. erysipelas. Rash is normally unilateral, except on the face where it is occasionally bilateral. Local signs of inflammation. May be systemically unwell with fever, malaise or rigors
62
How is erysipelas clinically distinguished from cellulitis?
Erysipelas is distinguished from cellulitis by a well-defined, red raised border (i.e. the edge is more well-demarcated in erysipelas than in cellulitis).
63
What are the differential diagnoses for cellulitis?
DVT, Gravitational eczema, Contact allergic dermatitis, Panniculitis (including acute lipodermatosclerosis)
64
How might you distinguish cellulitis from gravitational eczema?
Many patients with gravitational eczema are incorrectly diagnosed as having bilateral cellulitis (which is extremely rare)- so if it is bilateral then it is less likely to be cellulitis (which is normally unilateral) and would be more likely to be e.g. gravitational eczema
65
What investigations should you do if you suspect cellulitis?
Skin swabs should be taken, and if present from open areas/ areas of exudate, although in many cases results are negative. If bullseye or abscesses form, culturing the fluid from inside these lesions yields an organism in >90% of cases. Blood cultures for inpatients.
66
Give some circumstances/ examples of when you would admit a patient with cellulitis
Cellulitis associated with marked systemic upset e.g. fever, vomiting, tachycardia and hypotension
Spreading cellulitis that is not responding to oral medication
Lymphangitis
Would also have a lower threshold for admitting those more at risk e.g. infants, very young children, elderly, immunocompromised or sig co-morbidities
67
What is the first-line treatment for uncomplicated cellulitis (and erysipelas)?
Flucloxacillin 500mg QDS for 7-10 days
68
Other than antibiotic Tx, how else would you manage cellulitis/ erysipelas?
Adequate analgesia, (for the lower leg- rest and elevate the affected area where possible to reduce pain, swelling and damage to the venous system), mark out the extent of the cellulitis and review the patient while on Tx.
69
What is the management of recurrent cellulitis and how many attacks of cellulitis per year are needed for this prophylaxis?
Antibiotic prophylaxis should be offered to patients who have two or more attacks of cellulitis per year. Penicillin V should be the first choice.
70
What are some of the complications of cellulitis?
Local necrosis, abscess and septicaemia
Lymphangitis
Deep seated infection e.g. fasciitis and myositis
71
What is lymphangitis?
May be a complication of cellulitis / erysipelas. It presents with a red line originating from the cellulitis and spreading proximally to lymph node along the lymphatic vessels
72
Briefly describe staphylococcal scalded skin syndrome (SSSS)
It is an uncommon, superficial blistering skin condition characterised by widespread erythema and exfoliation, mainly occurring in children <5 years old, although older children and adults can be affected
73
What is SSSS caused by?
Exfoliative toxins (epidermolytic toxins A and B) of some strains of Staphylococcus aureus.
74
How does SSSS tend to present?
Fever and irritability are common, but patients do not appear overly unwell. Macular erythema is followed by diffuse, confluence erythema with bullae which rupture easily. There is marked epidermal exfoliation with the skin peeling off in sheets, leaving exposed moist bright-red tender areas.
75
What is the Nikolsky sign and is it positive or negative in SSSS?
It is when the gentle stroking of the skin causes the skin to separate at the epidermis. In SSSS the Nikolsky sign is positive.
76
How is SSSS differentiated from TEN? - Toxic epidermal necrolysis?
SSSS differs from the more severe, and generally drug-induced TEN, in that the cleavage site in SSSS is INTRAEPIDERMAL, opposed to TEN which involves necrosis of the entire epidermis.
77
How quickly does SSSS present and where on the body does it tend to occur?
Develops within a few hours to a few days and may be worse over the face, neck, axillae or groins. Perioral crusting is also typical.
78
What is the management of SSSS?
Requires prompt recognition and Tx. Same day contact should be made with the on-call dermatologist as hospital admission will almost certainly be required. IV antibiotics. Note: corticosteroids slow down healing and hence are NOT given for SSSS.
79
What is impetigo and what are the 2 main clinical forms?
It is a common contagious superficial bacterial infection of the skin. The 2 main clinical forms are non-bullous impetigo and bullous impetigo
80
Tell me about non-bullous vs bullous impetigo?
Non-bullous impetigo is caused by S.aureus, S.pyogens or a combination of both and accounts for the majority (~70%) of cases- often just referred to as ‘impetigo’.
Bullous impetigo is nearly always caused by S.aureus.
81
What age group is most commonly affected by impetigo?
It affects all age groups, but is most common in young children. The non-bullous form is most common in children aged 2-5 years, and bullous impetigo is most common in children under the age of 2.
82
How does non-bullous impetigo present?
Presents with thin-walled vesicles or pustules on an erythematous base (seldom seen O/E as they rupture quickly), which release exudate forming a golden yellow/brown crust. Usually asymptomatic but may be mildly itchy. The area around the mouth and nose is most commonly affected. Mucosal involvement is uncommon.
83
Describe the presentation of bullous impetigo
Most commonly affects infants. Small or large bullae arise over a short period of time. Lesions most often occur on the flexures, face, trunk and limbs. Flaccid fluid-filled vesicles and blisters which can persist for 2-3 days before rupturing, leaving a thin flat yellow/brown crust
84
Outline the management of impetigo (non drug Tx)
Advising on hygiene measures to aid healing and stop infection spreading to other areas of the body and other people. Advising children and and adults to stay away from school/work until the lesions are dry and scabbed over, or, if the lesions are still crusted or weeping, for 48 hours after Abx Tx has started.
85
Outline the management of impetigo (drug Tx)
Treat localised non-bullous infection with topical FUSIDIC ACID (an antibiotic) for 5 days. More extensive, severe or bullous infection may require oral Abx (flucloxacillin for 7 days). Follow up not usually necessary.
86
What is scabies caused by?
The human parasite/ mite: Sarcoptes scabiei - a person with scabies has an average of 10-15 mites
87
Outline the main presenting features of scabies
Intense itch which is characteristically worse at night. Generalised rash with erythema, papular and urticated lesions. Trunk and limbs are predominant sites that are affected. Burrows- are seen as very small irregular tracks which are most common on the sides of the fingers, the webs, the borders of the hands, wrist and feet.
88
What is the characteristic dermoscopic finding in scabies?
The mite have a ‘jet plane’ appearance
89
What is crusted scabies (Norwegian scabies)?
A hyper infestation with thousands or millions or mites present in exfoliating scales of skin (the itch is often less sig than with classical scabies). It develops as a result of an attenuated immune response by the host.
90
What is the treatment of crusted (Norwegian) scabies?
Ivermectin (note: isolation is essential as this form of scabies is highly contagious with huge numbers of mites)
91
In what age group is scabies most common and how does it tend to spread?
Prevalence greatest in people aged 10-19 years. Person-to-person spread occurs predominantly via direct contact with the skin with someone who has scabies.
92
How is the diagnosis of scabies made?
Usually from the Hx and examination, as well as from the history of the family and close contacts. Microscopy of skin scrapings can be used to confirm the diagnosis.
93
What is the management of scabies?
Treat the affected person and all household members, close contacts and sexual contacts with a topical insecticide e.g. permethrin 5% cream, even in the absence of symptoms. Permethrin is safe to use in pregnancy.
94
How should insecticide cream (e.g. permethrin) be applied for Tx of scabies?
The cream should be applied uniformly all over the body from the neck downwards. Every inch of skin must be covered with special attention paid to skin creases, the genitalia and underneath the nails. The face and scalp should only be Tx if they are affected. Wash off after 8-24 hrs (the cream should be re-applied to the hands if they are washed within 8 hrs of first applying the cream). Repeat Tx after 7 days. Contacts mostly only need 1 Tx, but symptomatic contacts require 2 Tx.
95
What types of infection are HSV-1 and HSV-2 typically associated with?
HSV-1 is traditionally associated with orofacial infection, while HSV-2 is traditionally associated with genital infection, although there is considerable overlap in disease manifestations
96
What is herpetic whitlow?
When there is inoculation of herpes simplex virus on the fingertips (small blisters form on the fingers and fleshy area around the fingertips)
97
What is herpes zoster?
Reactivation of varicella zoster virus (VZV) that has remained dormant within dorsal root ganglia, often for decades after the patient’s initial exposure to the virus in the form of varicella (chickenpox), results in herpes zoster (shingles).
98
In what groups of patients is herpes zoster (shingles) more common?
More common in adults, especially the elderly, the unwell and the immunosuppressed.
99
How does herpes zoster (shingles) manifest?
First manifestation of herpes zoster is usually pain (which may be severe), and may be accompanied by fever, headache and malaise. Rash: closely group red papules rapidly becoming vesicular and then pustular which develop in a continuous band in the area of one or occasionally two dermatomes
100
What are some of the complications of herpes zoster infection?
```
Motor involvement
Herpes zoster oticus and Ramsay-Hunt syndrome (peripheral facial nerve palsy accompanied by an erythematous vesicular rash on the ear- herpes oticus)
Herpes zoster ophthalmicus
Disseminated herpes zoster
Postherpetic neuralgia
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101
What is the management of herpes zoster infection?
Treatment is recommended in adults to prevent progression of the eruption and reduce complications including the development of post herpetic neuralgia. Standard Tx in adults: aciclovir 800mg PO 5 times a day for 7 days.
102
What are the 3 main groups of organism that cause superficial fungal infections?
Dermatophytes (tinea/ ringworm), yeasts (candidiasis, Malassezia), moulds (e.g. aspergillus)
103
What is tinea?
Tinea is a common fungal infection caused by a dermatophyte. The most common organism in the UK is Trichophyton rubrum (except on the scalp).
104
How does tinea tend to present in general?
A rash that is asymmetrical and/or has a leading edge which is erythematous and scaly. Usually itchy.
105
Describe tinea corporis
Tinea infection of the trunk and limbs - itchy circular or annular lesions with a clearly defined, raised and scaly edge is typical
106
What is tinea cruris?
Tinea infection of the groin and natal cleft, very itchy
107
What is tinea pedis?
Aka athletes foot. Moist scaling and fissuring in the toe webs, spreading to the sole and dorsal aspect of the foot
108
What is tinea incognito and what does lesson does it teach about treatment for tinea?
(Inappropriate Tx of the tinea infection with topical or systemic corticosteroids), ill-defined and less scaly lesions.
109
How does candidiasis present?
Candidal skin infection- white plaques on mucosal areas, erythema with satellite lesions in flexures
110
Tell me the key points about pityriasis versicolor
Yeast infection with Malassezia furfur. Causes scaly pale/brown patches on upper trunk that fail to tan on sun exposure (so usually noticed after a holiday), usually asymptomatic. Ketoconazole shampoo is used to treat it.
111
What is the causal agent of viral warts?
Human papillomavirus (HPV)
112
Describe molluscum contagiosum
Infection caused by the pox virus. Majority of cases occur in children. Typically presents with characteristic pinkish/ pearly white papules with a central umbilication up to 5mm diameter. Lesions appear in clusters in areas anywhere on the body (except palms and soles)
113
What is the management of molluscum contagiosum?
Self care advice: reassure that it is a self limiting condition, and spontaneous resolution usually occurs within 18 months. Lesions are contagious so avoid sharing towels, clothing etc. Encourage people not to scratch lesions. No need to exclude from school, gym etc. Tx not usually recommended.
114
What should you consider in an adult who presents with molluscum contagiosum?
Consider HIV infection
115
Tell me about eruptive xanthomas
A metabolic early warning sign. Present as widespread, symmetrical, yellow-red papular rash. Extracellular lipid deposition. Associated with uncontrolled hypertriglyceridaemia. Risk of pancreatitis.
116
Tell me about carotenaemia and how is it differentiated from e.g. jaundice?
A clinical condition characterised by yellow pigmentation of the skin and increased beta-carotene levels in the blood. Differentiated from jaundice if the sclera are normal. Increased carotenoids in diet.
117
Describe flexural acanthosis nigricans
The term describes symmetrical, brown velvety plaques that are often found on the neck, axilla and groin
118
Name some causes of acanthosis nigricans
GI cancer, diabetes mellitus, obesity, PCOS, acromegaly, Cushing’s disease, hypothyroidism
Also: familial, Prader-Willi syndrome, drugs: OCP, nicotinic acid
119
What does lipodermatosclerosis look like? (Hint: key term)
‘Inverted champagne bottle’ legs
120
What is lipodermatosclerosis ?
It is a chronic inflammatory condition characterised by subcutaneous fibrosis and hardening of the skin on the lower legs. Also known as sclerosing panniculitis.
121
What causes lipodermatosclerosis?
It is associated with immobility and obesity and results from underlying venous insufficiency. The resulting venous HTN causes an increase of leucocytes within the veins which migrate to the surrounding tissues, they become activated, inducing a chronic inflammatory state.
122
Lipodermatosclerosis results from underlying venous insufficiency, what are other features of chronic venous insufficiency?
Hyperpigmentation of the skin from haemosiderin deposition, atrophie Blanche, varicose veins, venous eczema and venous ulcers.
123
What is the Mx of lipodermatosclerosis?
Physical activity (walking) should be encouraged to increase the functionality of the calf muscle pump. Weight reduction is effective as obesity is a factor. Mechanical compression therapy using compression stockings/socks is the mainstay of Tx. Elevation of the legs can help reduce oedema and pain.
124
Describe the presentation of erythema nodosum
Inflammation of subcutaneous fat, typically causes tender, erythematous nodular lesions. Usually occurs over shins, but may occur elsewhere. Leave bruise like discolouration as they resolve. Lesions do not ulcerate and resolve without atrophy or scarring
125
What causes erythema nodosum?
It is a hypersensitivity reaction to a variety of stimuli. Causes include: infection, systemic disease (sarcoidosis, IBD, Behcets), malignancy/lymphoma, drugs, COCP, pregnancy and leprosy
126
How does pyoderma gangrenosum present?
Typically on the lower limbs. Initially a small red papule but later deep, red, necrotic ulcers with a violaceous border. Painful, rapidly progressing, blue/purpled-edged ulceration at site of minor injury
127
What is the management of pyoderma gangrenosum?
First line is oral steroids
128
What is melasma?
A chronic skin disorder that results in symmetrical, blotchy, brownish facial pigmentation. The causes are complex but sun exposure and sun damage is the most important avoidable risk factor
129
What is vitiligo?
An autoimmune condition which results in the loss of melanocytes and consequent depigmentation of the skin. Results in symmetrical well-defined patches of hypopigmentation in an acral distribution (the peripheries tend to be most affected)
130
Tell me about alopecia areata
A presumed autoimmune condition causing localised, well demarcated patches of hair loss. At the edge of the hair loss there may be small broken ‘exclamation mark’ hairs
131
What tool may be used to assess the severity of hirsutism?
The Ferriman-Gallwey visual scale
132
What is necrotising fasciitis?
A rapidly spreading infection of the deep fascia with secondary tissue necrosis
133
What causes necrotising fasciitis?
Group A haemolytic streptococcus or a mixture of anaerobic and aerobic bacteria. Risk factors include abdominal surgery and medical comorbidities e.g. diabetes, malignancy.
134
How does necrotising fasciitis present?
Sever pain, erythematous, blistering and necrotic skin. Systemically unwell with fever and tachycardia. Presence of crepitus (subcutaneous emphysema). X Ray may show soft tissue gas (although absence should not exclude diagnosis)
135
What is the management of necrotising fasciitis?
Urgent referral for extensive surgical debridement and IV antibiotics
136
Describe eczema herpeticum- what is it often a complication of?
Widespread eruption of extensive crusted papules, blisters and erosions. Systemically unwell with fever and malaise. A serious complication of atopic eczema (or less commonly other skin conditions).
137
What is eczema herpeticum caused by?
Herpes simplex virus (HSV) 1 or 2
138
What is the management of eczema herpeticum?
Antivirals (e.g. aciclovir) and antibiotics for any secondary bacterial infection
139
What is ‘erythroderma’?
Means ‘red skin’ - exfoliative dermatitis which involves at least 90% of the skins surface
140
What are the causes of erythroderma?
Previous skin disease (e.g. eczema, psoriasis), lymphomas and leukaemias, drugs (e.g. sulphonamides, gold, sulphonylureas, penicillin, allopurinol, captopril) and idiopathic
141
What is the management of erythroderma?
Treat the underlying cause, where known. Emollients and wet wraps to maintain skin moisture. Topical steroids may help to relieve inflammation.
142
What is the main precipitating factor / most common cause of erythema multiforme?
Herpes simplex virus (HSV)
143
What is erythema multiforme and what are the features?
An acute self-limiting inflammatory condition. It is a hypersensitivity reaction which is most commonly triggered by infections. Classic target lesions initially seen on the back of the hands/ feet before spreading to the torso. Mucosal involvement is absent or limited to only one mucosal surface.
144
What is Stevens-Johnson syndrome characterised by?
Mucocutaneous necrosis with at least two mucosal sites involved. Skin involvement may be limited or extensive. Drugs or combinations of infections or drugs are the main associations. The extensive necrosis distinguishes Stevens-Johnson syndrome from erythema multiforme.
145
What are the key points to remember about toxic epidermal necrolysis (TEN)?
Usually drug induced, characterised by extensive skin and mucosal necrosis accompanied by systemic toxicity. The skin develops a scaled appearance over an extensive area. Positive Nikolsky’s sign.
146
What is the management of TEN?
Intravenous Ig has been shown to be effective and is now commonly used first-line, but also need to: stop precipitating factor, full supportive care to maintain haemodynamic equilibrium (often in ICU)
147
In children, what is the most common cause of urticaria?
A preceding viral infection
148
What is the management of urticaria?
Antihistamines
149
What is dermatitis herpetiformis a cutaneous manifestation of?
Coeliac disease
150
What is a pyogenic granuloma?
An overgrowth of blood vessels which forms red nodules, usually following trauma
151
At what point would ultrasound be necessary in the diagnosis of a lipoma?
If the lipoma is >5cm
152
Tell me about erythema ab igne
Caused by infrared radiation and is commonly associated with hot water bottles and open fires. Characterised by a reticulated area of hyperpigmentation or erythema with telangiectasia. Tx is removal of the heat source.
153
Tell me about lichen planus
Itchy papular rash most common on the palms, soles, genitalia and flexor surfaces of arms. Rash often polygonal in shape, ‘white lace’ pattern on surface (Wickham’s striae).
154
How do you treat lichen planus?
Topical steroids are the mainstay of Tx
155
In terms of topical steroid treatment, when might you use a cream vs an ointment?
Steroid cream often used for wet/moist lesions, whereas ointment often used more commonly in dry skin conditions
156
What determines the strength of a topical steroid Tx?
Severity of disease, what the pt has tried before, body site (need for potent steroid for hands and soles of feet), age (neonate vs elderly)
157
What are the 4 major features involved in acne aetiology?
Androgen-induced seborrhoea, comedone formation, colonisation of the pilosebaceous duct with P.acnes, and production of inflammation
158
What areas of the body does acne commonly affect?
The face, upper back and chest
159
How does acne present? (Generally)
It presents with lesions which can be non-inflammatory (open and closed comedones)- seen in mild acne, inflammatory (papules, pustules, nodules and cysts)- seen in moderate or severe acne, or a mixture of both
160
What are some of the complications of acne?
Scarring, post-inflammatory hyperpigmentation or depigmentation and psychosocial problems such as depression and anxiety
161
What is pomade acne?
Caused by hair pomades, with comedonal and papulopustular acne on the forehead and temples
162
What (2) types of scarring can you get in acne?
Atrophic (ice pick) or keloid scarring
163
What self care measures should you recommend as part of acne Tx?
Avoid over cleaning the skin (which may cause dryness and irritation)- acne is not caused by poor hygiene
Avoid heavy makeup and use non-comedogenic makeup, cleaners and/or emollients with a pH close to the skin if needed
Avoid picking and squeezing spots which may increase the risk of scarring
164
What is the Tx ladder for acne? (Ladder of escalation)
Self care advice
Topical Tx: Benzoyl peroxide, topical retinoids (e.g. adapalene)
Systemic Tx: Oral Lymecycline (an Abx)
Dianette (a COCP which can improve acne)
Isotretinoin (Roaccutane)- a type of retinoid
165
Tell me the key considerations relating to isotretinoin (Roaccutane)
More potential side effects than Abx, SE’s include: skin changes (dry skin commonly), nosebleeds and dry eyes, increased sensitivity to the sunlight, liver and lipid abnormalities. Cant get pregnant during Tx or for up to 1 month after Tx, depression. Drug interactions: alongside tetracyclines can increase the risk of BIH (benign intracranial hypertension).
166
How is isotretinoin prescribed/ given?
Do a blood test before commending Tx with isotretinoin and after 1 month. Usually given for 4-6 months. Dose calculated by weight of patient
167
What is the maximum length of time that you can give oral antibiotics for the Tx of acne?
3 months maximum
168
Can you give oral antibiotics alone for the Tx of acne?
No- a topical retinoid or benzoyl peroxide should always be co-prescribed with oral antibiotics to reduce the risk of antibiotic resistance
169
With regards to acne treatment, what are the indications for referral to dermatology for consideration of Tx with isotretinoin?
Non-response to two different courses of antibiotics, or scarring
170
What is rosacea?
A chronic relapsing skin condition affecting the face, characterised by recurrent episodes of facial flushing, erythema, telangiectasia, papules and pustules.
171
What are the 4 main types of rosacea?
Erythematotelangiectatic
Papulopustular
Phymatous
Ocular
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What are some of the triggers for rosacea?
Extremes of temperature, sunlight, strenuous exercise, stress, spicy foods, alcohol and hot drinks. Triggers should be avoided where possible
173
How is flushing/ transient erythema linked to rosacea?
Flushing / transient erythema are signs of pre-rosacea- so onset of rosacea is often preceded by a history of episodic flushing
174
What is the management of mild or moderate papulopustular rosacea?
Topical metronidazole
175
In general, how does eczema present?
As ill-defined, red, slightly lichenified patches mostly flexural in distribution (worse on knees, hands, head and neck)
176
Outline topical steroid therapy and the potencies
Mild - hydrocortisone
Moderate- Clobestone butyrate (Eumovate)
Potent- betamethasone valerate (Betnovate)
Very potent- Clobetasol propionate (Dermovate)
177
Name a sedating antihistamine which may be given to help improve sleep in eczema (i.e. due to itch at night)
Chlorphenamine
178
What is the most common type of eczema and when does it tend to present?
Atopic eczema- usually develops by early childhood and resolves during teenage years (but may recur)
179
What are some other types of eczema other than atopic eczema?
Discoid eczema, contact dermatitis, varicose eczema, seborrhoeic dermatitis, pompholyx eczema
180
What is the distributional presentation of atopic eczema in the infant, child and adult?
More common on the face and extensor aspects of the limbs in infants, and the flexor aspects in children and adults
181
What causes atopic eczema?
Causes not fully understood, but a positive family history of atopy is often present. A primary genetic defect in skin barrier function (loss of function variants of the protein filaggrin) appears to underlie atopic eczema
182
What secondary changes may you see in eczema?
Chronic scratching and rubbing may lead to excoriation and lichenification
183
Outline the management of atopic eczema
General measures- avoid known exacerbating factors, frequent emollients +/- bandages (wet and dry wraps) and soap substitute
Topical therapies- topical steroids for flare-ups, topical immunomodulators (e.g. tacrolimus) can be used as steroid-sparing agents
Oral therapies- anti-histamines, antibiotics for secondary bacterial infections and antivirals for secondary herpes infection
184
Give some complications of atopic eczema
Secondary bacterial infection (crusted weepy lesions) - usually caused by Staph aureus
Secondary viral infection- particularly eczema herpeticum which is caused by HSV
185
What is pompholyx eczema?
A type of eczema that causes tiny blisters to erupt across the palms of the hands
186
What is seborrhoeic dermatitis?
A common, chronic or relapsing form of eczema that mainly affects the sebaceous gland-rich regions of the scalp, face and trunk
187
What are the clinical features of infantile seborrhoeic dermatitis?
Affects babies under 3 months and usually resolves by 6-12 months of age. Causes cradle cap (diffuse, greasy scaling on scalp). The rash may spread to affect armpit and groin folds (a type of napkin dermatitis). There are salmon pink patches that may flake or peel. It is not especially itchy.
188
What are the clinical features of adult seborrhoeic dermatitis?
Tends to begin in late adolescence, prevalence is greatest in young adults and the elderly. Affects scalp, face (creases around the nose, behind ears, within eyebrows) and upper trunk.
189
What is bullous pemphigoid?
A blistering skin disorder which usually affects the elderly
190
Where does the split in the skin occur in bullous pemphigoid? Thus, what are the characteristics of the blisters in this condition?
Sub-epidermal split. This creates tense, fluid-filled blisters (on an erythematous base). They are generally clear blisters but can be cloudy or blood stained.
191
What is the management of bullous pemphigoid?
Vast majority of pts need urgent referral to secondary care and those with widespread blistering may require admission. General measures- wound dressings when required, monitor for signs of infection. Topical therapies for localised disease -topical steroids i.e. dermovate cream is very effective for localised disease.
192
What investigations may you use to diagnose bullous pemphigoid?
Blood tests- indirect immunofluorescence- circulating pemphigoid antibodies (BP180 antibodies) are present in approx 3/4 of patients. Skin biopsies -direct immunofluorescence. Two biopsies are required- one of lesion/ blister and one of peri-lesional skin. Shows antibodies along the basement membrane that lie between the epidermis and dermis.
193
What is pemphigus vulgaris?
A blistering skin disorder which usually affects the middle-aged
194
Where does the split in the skin occur in pemphigus vulgaris? And thus what are the characteristics of the blisters in this condition?
Intra-epidermal split which results in flaccid and easily ruptured blisters which form erosions and crusts
195
In which population is pemphigus vulgaris more common?
The Ashkenazi Jewish population
196
What is a difference between bullous pemphigoid and pemphigus vulgaris in terms of mucosal involvement?
Mucosal involvement is less common in bullous pemphigoid, however pemphigus vulgaris usually affects mucosal areas (which can precede skin involvement). Oral mucosal involvement is seen in 50-70% of patients.
197
What is psoriasis?
A systemic, immune-mediated (autoimmune) inflammatory skin disease, which typically as a chronic relapsing-remitting course and may have nail and joint involvement. It is due to hyper-proliferation of keratinocytes and inflammatory cell infiltration
198
What is the most common type/form of psoriasis?
Chronic plaque psoriasis - plaques are symmetrical and tend to be on extensor surfaces
199
What other forms of psoriasis are there? (Other than chronic plaque psoriasis)?
Localised pustular psoriasis (of the palms and soles) - sometimes called palmar-plantar psoriasis.
Guttate psoriasis
Nail psoriasis
Erythrodermic and generalised pustular psoriasis
200
What type of psoriasis is characterised by ‘raindrop lesions’?
Guttate psoriasis
201
What is a well known factor that provokes guttate psoriasis?
Infection- streptococcal infection especially of the throat
202
What factors are associated with the onset or exacerbation of psoriasis?
Infection e.g. streptococcal and guttate psoriasis
Drugs
Trauma (psoriasis can occur at the site of skin injury- Koebner phenomenon)
Hormonal changes and pregnancy
Stress
Smoking and alcohol
203
Outline the management of psoriasis
Avoid known precipitating factors. Offer Tx with topical preparations such as emollients (to reduce scales), corticosteroids, vitamin D analogues, coal tar preparation and short-contact dithranol (for large plaque psoriasis) depending on the person’s preferences, cosmetic acceptability and practical aspects of application
204
What Tx option may be used for extensive psoriasis disease?
Phototherapy
205
What are the complications of psoriasis?
Erythroderma, psychological and social effects
206
What are the dangers/ side effects of prolonged/ potent topical corticosteroid therapy?
Skin atrophy, striae and rebound symptoms
207
What is the management of fungal infections? (I.e. name a common topical antifungal agent)
Terbinafine cream
208
What drugs can trigger / exacerbate psoriasis?
Beta blockers, lithium, antimalarials (chloroquine and hydroxychloroquine), NSAIDs, ACE inhibitors, infliximab and corticosteroid (systemic steroid) withdrawal
