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Dermatology Flashcards

1
Q

What is Pyoderma gangrenosum ?

A

A Rare, non-infectious inflammatory disorder.
It is a neutrophilic dermatosis

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2
Q

what are Neutrophilic dermatoses skin conditions ?

A

skin conditions characterised by dense infiltration of neutrophils in the affected tissue and this is often seen on biopsy

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3
Q

what are the causes of pyoderma gangrenosum?

A

Idiopathic in 50%
IBD
RA or SLE
Haematological conditions (myeloproliferative disorders, lymphoma, myeloid leukaemia, monoclonal gammopathy)
Granulomatosis with polyangiitis
Primary biliary cirrhosis

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4
Q

What are the features of pyoderma gangrenosum?

A

Usually occurs on the lower limb (often at the site of a minor injury)
Usually starts quite suddenly as a small pustule, red bump or blood blister

In the later stages the skin then breaks down resulting in an ulcer which is often painful. The edge of the ulcer is often described as purple, villous and undermined. The ulcer itself may be deep and necrotic

May be accompanied by fever and myalgia

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5
Q

How is pyoderma gangrenosum diagnosed?

A

often made by the characteristic appearance, associations with other diseases, the presence of pathergy, histology results and when other diseases have been ruled out
histology is not specific and can vary depending on the time and site of the specimen but may be helpful in ruling out other causes of an ulcer.

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6
Q

How is pyoderma gangrenosum managed?

A

the potential for rapid progression is high in most patients and most doctors advocate oral steroids as first-line treatment
other immunosuppressive therapy, for example, ciclosporin and infliximab, have a role in difficult cases
any surgery should be postponed until the disease process is controlled on immunosuppression to risk worsening of the disease (pathergy)

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7
Q

What are the different forms of melanoma?

A

Superficial spreading
Nodular
Lentigo maligna
acral lentiginous

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8
Q

What are the features of lentigo maligna?

A

This is a form of melanoma in situ, typically seen in chronically sun-exposed skin, such as the forehead in older people. It classically has the appearance of a freckle, with some suspicious features such as an irregularly shaped border and variable pigmentation. Excision biopsy is preferred.

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9
Q

What are the features of Acral lentiginous melanoma?

A

Acral lentiginous melanoma is a rare form of the condition found under the nails, or the palms or soles. It is more commonly found in African-American and Asian people.

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10
Q

What are the features of desmoplastic melanoma?

A

Desmoplastic melanoma is a very rare form of melanoma. It often involves nerve fibres. Malignant cells in the dermis are surrounded by fibrous tissue and would present more with a flat or raised papule or nodule.

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11
Q

What are the features of nodular melanoma?

A

Nodular melanoma is the most aggressive form, and second commonest. It is found in sun-exposed skin, but generally in younger, middle-aged people, rather than the older people that lentigo maligna melanoma presents in. It typically appears as a red or black lump that bleeds or oozes.

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12
Q

What are the features of superficial spreading melanoma?

A

Superficial spreading melanoma is the most common form, accounting for 70% of cases. It tends to be found on the limbs and torso of young people. It presents as a growing mole with the typical diagnostic features of melanoma including variable pigmentation, irregular borders, increasing size, bleeding, or ulceration.

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13
Q

what are the major and minor diagnostic criteria for melanoma

A

Major
- change in size, shape or colour
Minor
- diameter >/= 7mm, inflammation, oozing or bleeding, altered sensation

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14
Q

How is melanoma treated?

A

excision biopsy
Once the diagnosis is confirmed the pathology reports should be reviewed to determine whether further re-excision of margins is required

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15
Q

What is Hereditary haemorrhagic telangiectasia?

A

Also known as Osler-Weber-Rendu syndrome, hereditary haemorrhagic telangiectasia (HHT) is an autosomal dominant condition characterised by multiple telangiectasia over the skin and mucous membranes.

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16
Q

What are the 4 main diagnostic criteria for hereditary haemorrhagic telangiectasia?

A

> epistaxis : spontaneous, recurrent nosebleeds
telangiectases: multiple at characteristic sites (lips, oral cavity, fingers, nose)
visceral lesions: for example gastrointestinal telangiectasia (with or without bleeding), pulmonary arteriovenous malformations (AVM), hepatic AVM, cerebral AVM, spinal AVM
family history: a first-degree relative with HHT

If they meet 3 or more they are said to have a definite diagnosis

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17
Q

What is a marker for carbamazepine induced Stevens-Johnson syndrome and toxic epidermal necrolysis in Han Chinese?

A

HLA B*1502

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18
Q

What is the predominant cell type involved in Stevens-Johnson syndrome and toxic epidermal necrolysis ?

A

They are delayed-hypersensitivity reaction - thus involving T-Cells

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19
Q

What is Stevens-Johnson syndrome?

A

Stevens-Johnson syndrome is a severe systemic reaction affecting the skin and mucosa that is almost always caused by a drug reaction.

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20
Q

What are the causes of stevens-johnson syndrome?

A

penicillin
sulphonamides
lamotrigine, carbamazepine, phenytoin
allopurinol
NSAIDs
oral contraceptive pill

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21
Q

What is Vitiligo?

A

An autoimmune condition which results in the loss of melanocytes and consequent depigmentation of the skin.

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21
Q

What are the features of Stevens-Johnson syndrome?

A

the rash is typically maculopapular with target lesions being characteristic
may develop into vesicles or bullae
Nikolsky sign is positive in erythematous areas - blisters and erosions appear when the skin is rubbed gently
mucosal involvement
systemic symptoms: fever, arthralgia

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22
Q

What age group does Vitiligo usually develop?

A

20 - 20 years

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23
Q

What conditions are associated with vitiligo?

A

type 1 diabetes mellitus
Addison’s disease
autoimmune thyroid disorders
pernicious anaemia
alopecia areata

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24
Q

What are the features of Vitiligo ?

A

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

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25
Q

What is the management of vitiligo?

A

sunblock 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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26
Q

What is Koebner’s phenomenon?

A

It is observed in several skin conditions including vitiligo. It describes the appearance of new skin lesions on areas of the skin that have been traumatized. In vitiligo, this could be due to cuts, burns or abrasions. The underlying mechanism is thought to involve local changes in the immune response or skin environment which provoke melanocyte destruction.

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27
Q

What is the pathophysiology of psoriasis?

A

multifactorial and not yet fully understood
genetic: associated HLA-B13, -B17, and -Cw6. Strong concordance (70%) in identical twins
immunological: abnormal T cell activity stimulates keratinocyte proliferation. There is increasing evidence this may be mediated by a novel group of T helper cells producing IL-17, designated Th17. These cells seem to be a third T-effector cell subset in addition to Th1 and Th2
environmental: it is recognised that psoriasis may be worsened (e.g. Skin trauma, stress), triggered (e.g. Streptococcal infection) or improved (e.g. Sunlight) by environmental factors

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28
Q

what are the subtypes of psoriasis?

A

plaque psoriasis: the most common sub-type resulting in the typical well-demarcated red, scaly patches affecting the extensor surfaces, sacrum and scalp
flexural psoriasis: in contrast to plaque psoriasis the skin is smooth
guttate psoriasis: transient psoriatic rash frequently triggered by a streptococcal infection. Multiple red, teardrop lesions appear on the body
pustular psoriasis: commonly occurs on the palms and sole

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29
Q

What features, non skin, that are found in psoriasis?

A

nail signs: pitting, onycholysis
arthritis

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30
Q

what are the complications of psoriasis?

A

psoriatic arthropathy (around 10%)
increased incidence of metabolic syndrome
increased incidence of cardiovascular disease
increased incidence of venous thromboembolism
psychological distress

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31
Q

where are keloid scars most likely to form?

A

The sternum

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32
Q

What are keloid scars?

A

Keloid scars are a result of an overgrowth of dense fibrous tissue that usually develops after the healing of a skin injury. The scar extends beyond the borders of the original wound, does not regress and tends to recur after excision. The sternum, along with other areas such as shoulders, upper arms and earlobes, is particularly prone to keloid formation due to high tension in these areas.

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33
Q

what are predisposing factors for keloid scars?

A

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

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34
Q

What is the treatment for keloid scars?

A

early keloids may be treated with intra-lesional steroids e.g. triamcinolone
excision is sometimes required but careful consideration needs to given to the potential to create further keloid scarring

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35
Q

What is Seborrhoeic dermatitis?

A

Seborrhoeic dermatitis in adults is a chronic dermatitis thought to be caused by an inflammatory reaction related to a proliferation of a normal skin inhabitant, a fungus called Malassezia furfur (formerly known as Pityrosporum ovale).

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36
Q

What are the features of seborrhoeic dermatitis?

A

eczematous lesions on the sebum-rich areas: scalp (may cause dandruff), periorbital, auricular and nasolabial folds
otitis externa and blepharitis may develop

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37
Q

what conditions are associated with seborrhoeic dermatitis?

A

HIV
Parkinson’s disease

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38
Q

How is scalp seborrheic dermatitis treated?

A

the first-line treatment is ketoconazole 2% shampoo
over the counter preparations containing zinc pyrithione (‘Head & Shoulders’) and tar (‘Neutrogena T/Gel’) may be used if ketoconazole is not appropriate or acceptable to the person
selenium sulphide and topical corticosteroid may also be useful

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39
Q

How is face and body seborrhoeic dermatitis treated?

A

topical antifungals: e.g. ketoconazole
topical steroids: best used for short periods
difficult to treat - recurrences are common

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40
Q

what are common complications of seborrhoeic dermatitis?

A

Otitis externa and blepharitis

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41
Q

what are the two main types of dermatitis?

A

Irritant contact dermatitis
Allergic contact dermatitis?

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42
Q

What is irritant contact dermatitis?

A

Common - non-allergic reaction due to weak acids or alkalis (e.g. detergents). Often seen on the hands. Erythema is typical, crusting and vesicles are rare

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43
Q

What is allergic contact dermatitis?

A

allergic contact dermatitis: type IV hypersensitivity reaction. Uncommon - often seen on the head following hair dyes. Presents as an acute weeping eczema which predominately affects the margins of the hairline rather than the hairy scalp itself. Topical treatment with a potent steroid is indicated

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44
Q

What is the most common skin cancer secondary to immunosupression?

A

Squamous cell carcinoma

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45
Q

what are the risk factors for squamous cell carcinoma?

A

excessive exposure to sunlight / psoralen UVA therapy
actinic keratoses and Bowen’s disease
immunosuppression e.g. following renal transplant, HIV
smoking
long-standing leg ulcers (Marjolin’s ulcer)
genetic conditions e.g. xeroderma pigmentosum, oculocutaneous albinism

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46
Q

What are the features of squamous cell carcinoma?

A

typically on sun-exposed sites such as the head and neck or dorsum of the hands and arms
rapidly expanding painless, ulcerate nodules
may have a cauliflower-like appearance
there may be areas of bleeding

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47
Q

what is the treatment for SCC?

A

Surgical excision with 4mm margins if lesion <20mm in diameter. If tumour >20mm then margins should be 6mm. Mohs micrographic surgery may be used in high-risk patients and in cosmetically important sites.

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48
Q

what are good prognostic features of SCC?

A

Well differentiated tumours
< 20 mm diameter
< 2mm deep
No associated diseases

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49
Q

what are poor prognostic features of SCC?

A

Poorly differentiated tumours
> 20mm in diameter
> 4mm deep
immunosuppression for whatever reason.

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50
Q

What is Bullous pemphigoid?

A

Bullous pemphigoid is an autoimmune condition causing sub-epidermal blistering of the skin. This is secondary to the development of antibodies against hemidesmosomal proteins BP180 and BP230.

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51
Q

What are the features of bullous pemphigoid?

A
  • more common in elderly patients
    features include:
  • itchy, tense blisters around flexures
  • blisters usually heal without scarring
  • typical no mucosal involvement
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52
Q

What would bullous pemphigoid show on skin biopsy?

A

immunofluorescence shows IgG and C3 at the dermoepidermal junction

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53
Q

What is the management of Bullous pemphigoid?

A

referral to a dermatologist for biopsy and confirmation of diagnosis
oral corticosteroids are the mainstay of treatment
topical corticosteroids, immunosuppressants and antibiotics are also used

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54
Q

What is Impetigo?

A

Impetigo is a superficial bacterial skin infection usually caused by either Staphylcoccus aureus or Streptococcus pyogenes. It can be a primary infection or a complication of an existing skin condition such as eczema (in this case), scabies or insect bites. Impetigo is common in children, particularly during warm weather.

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55
Q

what is the incubation period of impetigo?

A

4-10 days

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56
Q

what are the features of impetigo?

A

golden’, crusted skin lesions typically found around the mouth
very contagious

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57
Q

How is impetigo managed?

A

For people who are systemically well and none bullous - hydrogen peroxide 1% cream.

Topical antibiotic creams
topical fusidic acid
topical mupirocin should be used if fusidic acid resistance is suspected
MRSA is not susceptible to either fusidic acid or retapamulin. Topical mupirocin should, therefore, be used in this situation

Extensive disease - oral flucloxacillin or erythromycin if pen allergic

** children should be excluded from school until the lesions are crusted and healed or 48 hours after commencing antibiotic treatment

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58
Q

When is a skin patch test indicated?

A

Skin patch testing is the gold standard for diagnosing contact dermatitis, such as nickel allergy. It involves applying a small amount of various substances, including nickel, to the skin using adhesive patches. The patches are usually left on for 48 hours and then removed. The skin is then examined for signs of an allergic reaction.

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59
Q

What is pemphigus vulgaris

A

Pemphigus vulgaris is an autoimmune disease caused by antibodies directed against desmoglein 3, a cadherin-type epithelial cell adhesion molecule. It is more common in the Ashkenazi Jewish population.

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60
Q

When is a skin prick test indicated?

A

Skin prick tests are typically used to diagnose IgE-mediated allergies, such as food or pollen allergies. They involve pricking the skin with a needle or lancet that contains a small amount of a suspected allergen. A positive result appears as a wheal (a raised, red bump) at the site of testing within 15-20 minutes. However, this method isn’t suitable for diagnosing contact dermatitis because these reactions are not IgE-mediated.

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61
Q

what are the features of pemphigus vulgaris?

A

mucosal ulceration is common and often the presenting symptom. Oral involvement is seen in 50-70% of patients
skin blistering - flaccid, easily ruptured vesicles and bullae. Lesions are typically painful but not itchy. These may develop months after the initial mucosal symptoms. Nikolsky’s describes the spread of bullae following application of horizontal, tangential pressure to the skin
acantholysis on biopsy

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62
Q
A
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63
Q

what is the treatment of pemphigus vulgaris

A

steroids are first-line
immunosuppressants

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64
Q

What is the appearance of Livedo reticularis?

A

purplish, non-blanching reticulated rash caused by obstruction of the capillaries resulting in swollen venules

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65
Q

what can cause Livedo reticularis?

A

Idiopathic
Polyarteritis nodosa
SLE
Cryoglobulinaemia
Antiphospholipid syndrome
Ehlers-Danlos Syndrome
Homocystinuria

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66
Q

what is the most common skin cancer in renal transplant patients?

A

Squamous cell carcinoma of the skin - due to immunosuppression

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67
Q

what are the risk factors for squamous cell carcinoma?

A

excessive exposure to sunlight / psoralen UVA therapy
actinic keratoses and Bowen’s disease
immunosuppression e.g. following renal transplant, HIV
smoking
long-standing leg ulcers (Marjolin’s ulcer)
genetic conditions e.g. xeroderma pigmentosum, oculocutaneous albinism

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68
Q

what are the features of squamous cell carcinoma ?

A

typically on sun-exposed sites such as the head and neck or dorsum of the hands and arms
rapidly expanding painless, ulcerate nodules
may have a cauliflower-like appearance
there may be areas of bleeding

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69
Q

what are the surgical excision boarders for squamous cell carcinoma ?

A

Surgical excision with 4mm margins if lesion <20mm in diameter. If tumour >20mm then margins should be 6mm. Mohs micrographic surgery may be used in high-risk patients and in cosmetically important sites.

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70
Q

What pattern is hereditary haemorrhagic telangiectasia inherited

A

autosomal dominant
Twenty percent of cases occur spontaneously without prior family history.

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71
Q

What is Hereditary Haemorrhagic telangiectasia?

A

Also known as Osler-Weber-Rendu syndrome, hereditary haemorrhagic telangiectasia (HHT) is an autosomal dominant condition characterised by (as the name suggests) multiple telangiectasia over the skin and mucous membranes.

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72
Q

what are the diagnostic features of hereditary haemorrhagic telangiectasia?

A

4 main diagnostic criteria
3= possible diagnosis
3 or more = definite diagnosis

epistaxis : spontaneous, recurrent nosebleeds
telangiectases: multiple at characteristic sites (lips, oral cavity, fingers, nose)
visceral lesions: for example gastrointestinal telangiectasia (with or without bleeding), pulmonary arteriovenous malformations (AVM), hepatic AVM, cerebral AVM, spinal AVM
family history: a first-degree relative with HHT

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73
Q

what is pompholyx?

A

Pompholyx is a type of eczema which affects both the hands (cheiropompholyx) and the feet (pedopompholyx). It is also known as dyshidrotic eczema.

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74
Q

what are the features pompholyx?

A

small blisters on the palms and soles
pruritic
once blisters burst the skin may become dry and crack

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75
Q

what are the triggers of pompholyx eczema?

A

Humidity
Irritants
Lifestyle - smoking
Drug use - aspirin and COCP
fungal infections

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76
Q

what is the management of pompholyx eczema?

A

cool compresses
emollients
topical steroid

77
Q

what is the treatment of flexoral psoriasis?

A

topical steroid - mild/moderate potency - 1x to 2x daily for max 2 weeks
Vitamin D analogues are not indicted in flexoral psoriais

78
Q

What is the treatment of chronic plaque psoriasis

A

regular emollients
1st Line potent corticosteroid + vitamin D analogue - applied separately morning and evening - for up to 4 weeks
2nd line - Vitamin D analogue BD
3rd line - if no improvement after 8-12 weeks - 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

79
Q

what secondary care options are there for psoriasis

A

Phototherapy - narrowband UV B light - 3x per week, photochemotherapy is also used psoralen + ultraviolet A light (PUVA)

Systemic therapy
oral methotrexate is used first-line. It is particularly useful if there is associated joint disease
ciclosporin
systemic retinoids
biological agents: infliximab, etanercept and adalimumab
ustekinumab (IL-12 and IL-23 blocker) is showing promise in early trials

80
Q

what are the adverse effects of phototherapy?

A

oral methotrexate is used first-line. It is particularly useful if there is associated joint disease
ciclosporin
systemic retinoids
biological agents: infliximab, etanercept and adalimumab
ustekinumab (IL-12 and IL-23 blocker) is showing promise in early trials

81
Q

How is scalp psoriais managed?

A

potent topical corticosteroids used once daily for 4 weeks
if no improvement after 4 weeks then either use a different formulation of the potent corticosteroid (for example, a shampoo or mousse) and/or a topical agents to remove adherent scale (for example, agents containing salicylic acid, emollients and oils) before application of the potent corticosteroid

82
Q

what are examples of vitamin D analgoues?

A

examples of vitamin D analogues include calcipotriol (Dovonex), calcitriol and tacalcitol

83
Q

how do vitamin D analogues work?

A

↓ cell division and differentiation → ↓ epidermal proliferation

84
Q

what is alopecia areata?

A

Alopecia areata is 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

85
Q

what are the treatment options in alopecia arteata?

A

topical or intralesional corticosteroids
topical minoxidil
phototherapy
dithranol
contact immunotherapy
wigs

86
Q

what is a Keratoacanthoma?

A

Benign epithelial tumour

87
Q

what are the features of Keracanthoma?

A

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

88
Q

what is pityriasis Versicolor?

A

Pityriasis versicolor, also called tinea versicolor, is a superficial cutaneous fungal infection caused by Malassezia furfur (formerly termed Pityrosporum ovale)

most commonly affects the trunk
patches may be hypopigmented, more noticible with tan
scale is common
mild pruritus

89
Q

How is pityriasis versicolor managed

A

Ketoconazole shampoo
if failure to respond to treatment - send scraping to confirm diagnosis and oral itraconazole

90
Q

how can alopecia be divided?

A

scarring (destruction of hair follicle) and non-scarring (preservation of hair follicle)

91
Q

what causes scarring alopecia?

A

trauma, burns
radiotherapy
lichen planus
discoid lupus
tinea capitis - carring may develop in untreated tinea capitis if a kerion develops

92
Q

WHat can cause non scarring alopecia?

A

male-pattern baldness
drugs: cytotoxic drugs, carbimazole, heparin, oral contraceptive pill, colchicine
nutritional: iron and zinc deficiency
autoimmune: alopecia areata
telogen effluvium
hair loss following stressful period e.g. surgery
trichotillomania

93
Q

what causes scabies?

A

Scabies is caused by the mite Sarcoptes scabiei and is spread by prolonged skin contact. It typically affects children and young adults.

The scabies mite burrows into the skin, laying its eggs in the stratum corneum. The intense pruritus associated with scabies is due to a delayed-type IV hypersensitivity reaction to mites/eggs which occurs about 30 days after the initial infection.

94
Q

what are the features of scabies?

A

widespread pruritus
linear burrows on the side of fingers, interdigital webs and flexor aspects of the wrist
in infants, the face and scalp may also be affected
secondary features are seen due to scratching: excoriation, infection

95
Q

what is the management of scabies

A

Management
permethrin 5% is first-line
malathion 0.5% is second-line
give appropriate guidance on use (see below)
pruritus persists for up to 4-6 weeks post eradication

Patient guidance on treatment (from Clinical Knowledge Summaries)
avoid close physical contact with others until treatment is complete
all household and close physical contacts should be treated at the same time, even if asymptomatic
launder, iron or tumble dry clothing, bedding, towels, etc., on the first day of treatment to kill off mites.

96
Q

what are the features of BCC?

A

many types of BCC are described. The most common type is nodular BCC, which is described here
sun-exposed sites, especially the head and neck account for the majority of lesions
initially a pearly, flesh-coloured papule with telangiectasia
may later ulcerate leaving a central ‘crater’

97
Q

what is the most important prognostic factor in melanoma?

A

In malignant melanoma, the most important prognostic marker is the Breslow thickness, which measures the depth of invasion of the melanoma into the skin. This measurement directly correlates with the risk of metastasis; deeper tumours are more likely to have spread to lymph nodes or distant organs.

98
Q

what is Pellagra

A

Pellagra is a caused by nicotinic acid (niacin) deficiency. The classical features are the 3 D’s - dermatitis, diarrhoea and dementia.
Pellagra may occur as a consequence of isoniazid therapy (isoniazid inhibits the conversion of tryptophan to niacin) and it is more common in alcoholics.

99
Q

what are the features of Pellagra?

A

dermatitis (brown scaly rash on sun-exposed sites - termed Casal’s necklace if around neck)
diarrhoea
dementia, depression
death if not treated

100
Q

what are the features of SJS?

A

the rash is typically maculopapular with target lesions being characteristic
may develop into vesicles or bullae
Nikolsky sign is positive in erythematous areas - blisters and erosions appear when the skin is rubbed gently
mucosal involvement
systemic symptoms: fever, arthralgia

101
Q

How quickly would SJS start after antibiotics and anticonvulsants

A

Abx - 1 weeks - 1month
anticonvulsants 2 months

102
Q

How does SJS initially present?

A

SJS presents initially with a prodromal illness of intermittent fevers, myalgia and a sore throat. After a few days, a painful, erythematous skin rash develops abruptly over the trunk and arms. Blisters then appear and merge to form sheets of detached skin. Mucosal involvement is prominent and severe with at least two mucosal surfaces becoming involved. In this case, the patient developed conjunctivitis and painful ulcerations on the lips.

103
Q

how does lupus vulgaris present

A

it is a form of cutaneous tuberculosis caused by Mycobacterium tuberculosis. It presents as reddish-brown plaques with an apple jelly appearance on diascopy.

104
Q

How does necrobiosis lipoidicia diabeticorum present?

A

it is associated with diabetes
Necrobiosis lipoidica diabeticorum typically presents as well-defined, yellow-brown plaques with atrophic centres and telangiectasia.

105
Q

what is Granuloma Annulare

A

papular lesions that are often slightly hyperpigmented and depressed centrally
typically occur on the dorsal surfaces of the hands and feet, and on the extensor aspects of the arms and legs

associated with diabetes

106
Q

what is dermatitis herpetiformis?
features
diagnosis
management

A

Dermatitis herpetiformis is an autoimmune blistering skin disorder associated with coeliac disease. It is caused by deposition of IgA in the dermis. More than 90% of patients exhibit small bowel biopsy findings consistent with some degree of gluten-sensitive enteropathy.

Features
itchy, vesicular skin lesions on the extensor surfaces (e.g. elbows, knees, buttocks)

diagnosis: skin biopsy - direct immunofluorescence shows deposition of IgA in a granular pattern in the upper dermis

Management - gluten free diet, dapasone

107
Q

what is eczema herpeticum?

A

Eczema herpeticum describes a severe primary infection of the skin by herpes simplex virus 1 or 2.

It is more commonly seen in children with atopic eczema and often presents as a rapidly progressing painful rash.

108
Q

what are the features of eczema herpeticum?

A

monomorphic punched-out erosions (circular, depressed, ulcerated lesions) usually 1-3 mm in diameter are typically seen.

109
Q

How is eczema herpeticum managed?

A

As it is potentially life-threatening children should be admitted for IV aciclovir.

110
Q

what are the features of lichen planus?

A

itchy, papular rash most common on the palms, soles, genitalia and flexor surfaces of arms
rash often polygonal in shape, with a ‘white-lines’ pattern on the surface (Wickham’s striae)
Koebner phenomenon may be seen (new skin lesions appearing at the site of trauma)
oral involvement in around 50% of patients: typically a white-lace pattern on the buccal mucosa
nails: thinning of nail plate, longitudinal ridging

111
Q

what causes lichenoid drug eruptions?

A

gold
quinine
thiazides

112
Q

what is the management of lichen planus

A

potent topical steroids are the mainstay of treatment
benzydamine mouthwash or spray is recommended for oral lichen planus
extensive lichen planus may require oral steroids or immunosuppression

113
Q

what is side effect of minocycline?

A

Minocycline can cause irreversible skin pigmentation and is now considered a second line drug in acne

114
Q

how is acne classified?

A

mild: open and closed comedones with or without sparse inflammatory lesions
moderate acne: widespread non-inflammatory lesions and numerous papules and pustules
severe acne: extensive inflammatory lesions, which may include nodules, pitting, and scarring

115
Q

how is mild to moderate acne managed?

A

a 12-week course of topical combination therapy should be tried first-line:
a fixed combination of topical adapalene with topical benzoyl peroxide
a fixed combination of topical tretinoin with topical clindamycin
a fixed combination of topical benzoyl peroxide with topical clindamycin
topical benzoyl peroxide may be used as monotherapy if these options are contraindicated or the person wishes to avoid using a topical retinoid or an antibiotic

116
Q

how is severe acne managed?

A

a 12-week course of one of the following options:
a fixed combination of topical adapalene with topical benzoyl peroxide
a fixed combination of topical tretinoin with topical clindamycin
a fixed combination of topical adapalene with topical benzoyl peroxide + either oral lymecycline or oral doxycycline
a topical azelaic acid + either oral lymecycline or oral doxycycline

117
Q

when should tetracyclines be avoided?

A

tetracyclines should be avoided in pregnant or breastfeeding women and in children younger than 12 years of age. Erythromycin may be used in pregnancy

118
Q

why is minocycline now considered less appropriate for the treatment of acne?

A

minocycline is now considered less appropriate due to the possibility of irreversible pigmentation

119
Q

how long can you continue abx treatment (oral and topical) for acne?

A

6 months

120
Q

what should be co-prescribed with oral abx in the treatment of acne?

A

a topical retinoid (if not contraindicated) or benzoyl peroxide should always be co-prescribed with oral antibiotics to reduce the risk of antibiotic resistance developing. Topical and oral antibiotics should not be used in combination

121
Q

what is a complication of long-term abx use in the treatment of acne and what is the treatment for this complication?

A

Gram-negative folliculitis may occur as a complication of long-term antibiotic use - high-dose oral trimethoprim is effective if this occurs

122
Q

when is a referral to dermatology for acne indicated?

A

the following patients should be referred to a dermatologist:
patients with acne conglobate acne: a rare and severe form of acne found mostly in men that presents with extensive inflammatory papules, suppurative nodules (that may coalesce to form sinuses) and cysts on the trunk.
patients with nodulo-cystic acne
referral should be considered in the following scenarios:
mild to moderate acne has not responded to two completed courses of treatment
moderate to severe acne has not responded to previous treatment that includes an oral antibiotic
acne with scarring
acne with persistent pigmentary changes
acne is causing or contributing to persistent psychological distress or a mental health disorder

123
Q

what are the features of erythemaha nodosum?

A

inflammation of subcutaneous fat
typically causes tender, erythematous, nodular lesions
usually occurs over shins, may also occur elsewhere (e.g. forearms, thighs)
usually resolves within 6 weeks
lesions heal without scarring

124
Q

what are the causes of arythema nodosum?

A

Infection - streptococci, TB, brucellosis
Systemic disease - sarcoidosis, IBD, Behcet’s disease
Malignancy/lymphoma
drugs - penicillins, sulphonamides, COCP
pregnancy

125
Q

What is actinic Keratoses?

A

Actinic, or solar, keratoses (AK) is a common premalignant skin lesion that develops as a consequence of chronic sun exposure

126
Q

What are the features of Actinic keratoses?

A

small, crusty or scaly, lesions
may be pink, red, brown or the same colour as the skin
typically on sun-exposed areas e.g. temples of head
multiple lesions may be present

127
Q

what is the treatment of Actinic keratoses ?

A

prevention of further risk: e.g. sun avoidance, sun cream
fluorouracil cream: typically a 2 to 3 week course. The skin will become red and inflamed - sometimes topical hydrocortisone is given following fluorouracil to help settle the inflammation
topical diclofenac: may be used for mild AKs. Moderate efficacy but much fewer side-effects
topical imiquimod: trials have shown good efficacy
cryotherapy
curettage and cautery

128
Q

what is Molluscum contagious?

A

a common skin infection caused by molluscum contagiosum virus (MCV), a member of the Poxviridae family

129
Q

How is Molluscum contagiousum transmitted?

A

ransmission occurs directly by close personal contact, or indirectly via fomites (contaminated surfaces) such as shared towels and flannels. The majority of cases occur in children (often in children with atopic eczema), with the maximum incidence in preschool children aged 1-4 years.

130
Q

what is the appearance of molluscum contagiosum?

A

characteristic pinkish or pearly white papules with a central umbilication, which are up to 5 mm in diameter. Lesions appear in clusters in areas anywhere on the body (except the palms of the hands and the soles of the feet).

131
Q

How is molluscum contagiousum managed?

A

Reassure people that molluscum contagiosum is a self-limiting condition.
Spontaneous resolution usually occurs within 18 months
Explain that lesions are contagious, and it is sensible to avoid sharing towels, clothing, and baths with uninfected people (e.g. siblings)
Encourage people not to scratch the lesions. If it is problematic, consider treatment to alleviate the itch
Exclusion from school, gym, or swimming is not necessary

f lesions are troublesome or considered unsightly, use simple trauma or cryotherapy, depending on the parents’ wishes and the child’s age:
Squeezing (with fingernails) or piercing (orange stick) lesions may be tried, following a bath. Treatment should be limited to a few lesions at one time
Cryotherapy may be used in older children or adults, if the healthcare professional is experienced in the procedure
Eczema or inflammation can develop around lesions prior to resolution. Treatment may be required if:
Itching is problematic; prescribe an emollient and a mild topical corticosteroid (e.g. hydrocortisone 1%)
The skin looks infected (e.g. oedema, crusting); prescribe a topical antibiotic (e.g. fusidic acid 2%)

For people with eyelid-margin or ocular lesions and associated red eye urgent referral to an ophthalmologist
Adults with anogenital lesions should be referred to genito-urinary medicine, for screening for other sexually transmitted infections

132
Q

what does streptococcus pyogenes cause?

A

This is a frequent cause of infections in children, including pharyngitis and impetigo.

133
Q

what does Trichophyton rubum cause?

A

This is a common cause of fungal skin infections such as tinea corporis. This typically presents with a single circular patch with erythema and scaling. Multiple lesions can develop and may coalesce

134
Q

what skin disorder is associated with gastric cancer?

A

Acanthosis nigrans

135
Q

What skin condition is associated with lymphoma?

A

Acquired ichthyosis
erythroderma

136
Q

what cancers is acquired hypertrichosis languinosa associated with ?

A

GI and Lung Ca

137
Q

what cancers are associated with dermatomyositis

A

ovarian and lung

138
Q

what skin disorder is pancreatic cancer related to

A

migratory thrombophlebitis

139
Q

what skin condition in glucagonoma related to?

A

Necrolytic migratory erythema

140
Q

what skin condition is myeloproliferative disorders related to?

A

Pyoderma gangrenosum

141
Q

what skin condition is related to oesophageal cancer

A

Tylosis

142
Q

what is Rosacea?

A

a chronic skin disorder of unknown aetiology

143
Q

what are the features of Rosacea?

A

typically affects nose, cheeks and forehead
flushing is often first symptom
telangiectasia are common
later develops into persistent erythema with papules and pustules
rhinophyma
ocular involvement: blepharitis
sunlight may exacerbate symptoms

144
Q

what is the management of Rosacea?

A

Simple measures - recommended daily application of a high factor suncream

predominant erythema/flushing
- topical brimonidine gel (if predominant flushing and limited telangiectasia)
-can be used as required -temporarily reduces redness

Mild to moderate papules and/or pustules
- topical ivermectin is first line (alternatives include topical metronidazole or topical azelaic acid)
Moderate to severe papules and/or pustules
- combination of topical ivermectin + oral doxycycline

145
Q

what Is brimonidine gel?

A

brimonidine is a topical alpha-adrenergic agonist

146
Q

when should a referred be made for Rosacea?

A

symptoms have not improved with optimal management in primary care
laser therapy may be appropriate for patients with prominent telangiectasia
patients with a rhinophyma

147
Q

What are the differential diagnosis for skin lesion on the skins?

A

erythema nodosum
pretibial myxoedema
pyoderma gangrenosum
necrobiosis lipoidica diabeticorum

Erythema nodosum
symmetrical, erythematous, tender, nodules which heal without scarring
most common causes are streptococcal infections, sarcoidosis, inflammatory bowel disease and drugs (penicillins, sulphonamides, oral contraceptive pill)

Pretibial myxoedema
symmetrical, erythematous lesions seen in Graves’ disease
shiny, orange peel skin

Pyoderma gangrenosum
initially small red papule
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

Necrobiosis lipoidica diabeticorum
shiny, painless areas of yellow/red skin typically on the shin of diabetics
often associated with telangiectasia

148
Q

what is toxic epidermal necrolysis?

A

potentially life threatening skin disorder - most commonly seen secondary to a drug reaction

The skin develops a scalded appearance over the extensive area
Mucosal involvement

149
Q

what are the features of toxic epidermal necrolysis?

A

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

150
Q

What are the drugs known to cause toxic epidermal necrolysis?

A

phenytoin
sulphonamides
allopurinol
penicillins
carbamazepine
NSAIDs

151
Q

What is the management of toxic epidermal necrolysis?

A

stop precipitating factor
supportive care - often requires ITU
IVIG is first line
other options include - immunosuppressive agents (ciclosporin and cyclophosphamide) and plasmapheresis

152
Q

when is venous ulceration typically seen?

A

Venous ulceration is typically seen above the medial malleolus

153
Q

What are the investigations for venous ulceration?

A

ABPI - important for non healing ulcers
Normal ABPI - 09-1.2
Values less that 0.9 indicate arterial disease (values above 1.3 may also indicate arterial disease, in the form of false-negative results secondary to arterial calcification (e.g. In diabetics)

154
Q

what is the management of venous ulcers?

A

compression bandaging
oral pentoxifylline, a peripheral vasodilator, improves healing rate
small evidence base supporting use of flavinoids
little evidence to suggest benefit from hydrocolloid dressings, topical growth factors, ultrasound therapy and intermittent pneumatic compression

155
Q

What are examples of mild, moderate, potent and very potent steroids?

A

Mild - Hydrocortison 0.5-2.5%
Moderate - Betamethasone valerate 0.025% (Betnovate RD), Clobetasone butyrate 0.05% (Eumovate)
Moderte - Fluticasone propionate 0.05% (Cutivate), Betamethasone valerate 0.1% (Betnovate)
Very potent - Clobetasol propionate 0.05% (Dermovate)

156
Q

What is the appearance of Acanthuses nigricans?

A

ymmetrical, brown, velvety plaques that are often found on the neck, axilla and groin.

157
Q

What is the pathophysiology of acanthuses nigricans?

A

type 2 diabetes mellitus
gastrointestinal cancer
obesity
polycystic ovarian syndrome
acromegaly
Cushing’s disease
hypothyroidism
familial
Prader-Willi syndrome
drugs - combined oral contraceptive pill , nicotinic acid

158
Q

what is more typical of malignant acanthosis nigrans?

A

Symptoms of pruritis and the presence of more extensive lesions involving the palms, soles and mucosa is more typical of malignant acanthosis

159
Q

what medications can exacerbate psoriasis?

A

trauma
alcohol
drugs: beta blockers, lithium, antimalarials (chloroquine and hydroxychloroquine), NSAIDs and ACE inhibitors, infliximab
withdrawal of systemic steroids

Streptococcal infection may trigger guttate psoriasis.

160
Q

What is erythema multiforme?

A

a hypersensitivity reaction that is most commonly triggered by infections

161
Q

What are the features of erythema multiforme?

A

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

162
Q

What are the causes of erythema multiforme?

A

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

163
Q

what is erythema multiforme major?

A

The more severe form, erythema multiforme major is associated with mucosal involvement.

164
Q

what is the most appropriate anti-histamine for lorry driver?

A

loratadine

(cetirizine can be drowsy)

165
Q

What is the Hirsutism ?

A

androgen-dependent hair growth in women

166
Q

what is hypertrichosis?

A

ndrogen-independent hair growth

167
Q

what are the causes of hirsutism ?

A

PCOS
Cushing’s syndrome
congenital adrenal hyperplasia
androgen therapy
obesity: thought to be due to insulin resistance
adrenal tumour
androgen secreting ovarian tumour
drugs: phenytoin, corticosteroids

168
Q

how is Hirsutism assessed?

A

Ferriman-Gallwey scoring system: 9 body areas are assigned a score of 0 - 4, a score > 15 is considered to indicate moderate or severe hirsutism

169
Q

what are the causes of hypertrichosis?

A

drugs: minoxidil, ciclosporin, diazoxide
congenital hypertrichosis lanuginosa, congenital hypertrichosis terminalis
porphyria cutanea tarda
anorexia nervosa

170
Q

What is the management of hirsutism?

A

advise weight loss if overweight
cosmetic techniques such as waxing/bleaching - not available on the NHS
consider using combined oral contraceptive pills such as co-cyprindiol (Dianette) or ethinylestradiol and drospirenone (Yasmin). Co-cyprindiol should not be used long-term due to the increased risk of venous thromboembolism
facial hirsutism: topical eflornithine - contraindicated in pregnancy and breast-feeding

171
Q

What is dermatitis artefacta?

A

Dermatitis artefacta is a rare psycho-dermatological condition characterised by self-inflicted skin lesions. Patients typically deny that these are self-induced.

172
Q

what are the risk factors for dermatitis artefacts?

A

dermatitis artefacta is strongly associated with personality disorder, dissociative disorders and eating disorders
the prevalence of dermatitis artefacta is up to 33% in patients with bulimia or anorexia

173
Q

what are the clinical features of dermatitis artefacta?

A
  • linear/geometric lesions that are well-dermacated from normal skin.
  • mechanisms of injuries may (scratching with fingernails or other objects, burning skin with cigarettes) or chemical (deodorant spray)
  • skin lesions typically are described to appear suddenly e.g. overnight
  • commonly affected areas are the face and hands
  • despite severity of the lesions, patients may be nonchalant, displaying ‘la belle indifference’
174
Q

What are the differentials for dermatitis artefacts?

A

cutaneous T-cell lymphoma, pyoderma gangrenosum, basal cell carcinoma, lichen planus, psoriasis

other factitious disorders e.g. Munchausen syndrome (self-inflicting is not limited to the skin), malingering (self-inflicting for secondary gain e.g. to avoid work or to gain compensation)

175
Q

What are the adverse effects if Isotretinoin?

A

teratogenicity - females MUST be taking contraception
low mood
dry eyes and lips
raised triglycerides
hair thinning
nose bleeds

176
Q

what is the initial step wise approach for the management of psoriasis?

A

regular emollients may help to reduce scale loss and reduce pruritus
f
irst-line: NICE recommend:
a potent corticosteroid applied once daily plus vitamin D analogue applied once daily
should be 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

Phototherapy - narrowband ultraviolet B light is now the treatment of choice. If possible this should be given 3 times a week
photochemotherapy is also used - psoralen + ultraviolet A light (PUVA)
adverse effects: skin ageing, squamous cell cancer (not melanoma)

177
Q

What is the management of systemic psoriasis?

A

oral methotrexate is used first-line. It is particularly useful if there is associated joint disease
ciclosporin
systemic retinoids
biological agents: infliximab, etanercept and adalimumab
ustekinumab (IL-12 and IL-23 blocker) is showing promise in early trials

178
Q

how is scalp psoriasis managed?

A

topical corticosteroids used once daily for 4 weeks
if no improvement after 4 weeks then either use a different formulation of the potent corticosteroid (for example, a shampoo or mousse) and/or a topical agents to remove adherent scale (for example, agents containing salicylic acid, emollients and oils) before application of the potent corticosteroid

179
Q

How is face, flexural and genital psoriasis managed?

A

NICE recommend offering a mild or moderate potency corticosteroid applied once or twice daily for a maximum of 2 weeks

180
Q

what are examples of vitamin D analogues and how do they work ?

A

calcipotriol (Dovonex), calcitriol and tacalcitol
they work by ↓ cell division and differentiation → ↓ epidermal proliferation

181
Q

Facts about VD analogues?

A

adverse effects are uncommon
unlike corticosteroids they may be used long-term
unlike coal tar and dithranol they do not smell or stain
they tend to reduce the scale and thickness of plaques but not the erythema
they should be avoided in pregnancy
the maximum weekly amount for adults is 100g

182
Q

What is melasma?

A

Melasma is a benign but relatively common skin condition which can appear in pregnancy. In this situation it may resolve a few months after delivery

183
Q

what is atopic eruption of pregnancy?

A

is the commonest skin disorder found in pregnancy
it typically presents as an eczematous, itchy red rash.
no specific treatment is needed

184
Q

What is polymorphic eruption of pregnancy?

A

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

185
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

186
Q

What is Mastocytosis?

A

Mastocytosis is caused by abnormal accumulation of mast cells. This can occur in the skin only (cutaneous mastocytosis, which occurs mostly in children) or in other organs (systemic mastocytosis, which occurs mainly in adults). Systemic mastocytosis is caused by the accumulation of mast cells in the bone marrow, liver, spleen, lymphatics, skin and other organs. Organ infiltration and mast cell degranulation can lead to a wide range of features including abdominal symptoms (pain, nausea, vomiting, diarrhoea, malabsorption), hepatosplenomegaly, anaemia, myalgia, arthralgia, fatigue and mood disturbance. Systemic mastocytosis can also lead to mast cell leukaemia.

187
Q

what are the features of Systemic mastocytosis?

A

urticaria pigmentosa - produces a wheal on rubbing (Darier’s sign)
flushing
abdominal pain
monocytosis on the blood film

188
Q

how is mastocytosis diagnosed?

A

raised serum tryptase levels
urinary histamine

189
Q

What skin disorders are associated with TB?

A

lupus vulgaris (accounts for 50% of cases)
erythema nodosum
scarring alopecia
scrofuloderma: breakdown of skin overlying a tuberculous focus
verrucosa cutis
gumma

MRCP (18 decks)

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