Dermatology Flashcards

1
Q

What should be included in a dermatological history?

A

History of presenting complaint
Past medical history: systemic disease, history of atopy (triad: asthma, hayfever eczema), history of skin cancer or pre cancer (seborrheic keratosis), history of sunburn/sunbeds/sunvathing, skin type
Social history: work, hobbies, smoking, alcohol (sun exposure, irritants, aggrevating facotrs, LATEX ALLERGY), lived abroad?
Drug history and allergies- regular and recent, systemic and topical - get specific (where/how much/how long for/strength/dosage/hand washing/using other creams at same time (disrupts absorption))
Family hx: autoimmune (inc. vitilligo), skin cancers, atopy
Impact on quality of life: pain, cosmetic appearance -> mental health, treatments (skin thinning, changes to pigmentation)
Presenting complaint: nature - rash vs. lesion
Site
Duration - acute (infection)
Initial appearance and evolution (rash may start with single lesion and spread)
Symptoms (itch/pruritis, pain)
Aggravating and relieving factors - triggers (washing powder, medication, cosmetics)
Previous and current treatments (effective or not) - what, how long, why hasn’t it work (child gets distressed, job is obstructive, treatment causes itching)

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2
Q

How to approach dermatological examination?

A

Inspect, palpate,systemic check (whole skin, hair nails mucous membranes), describe

SCAM:
S- site, size, shape - distrubition (photosensitive, flexural, extensor, genralised) )
C- colour (pigmented (hypo/hyper/de), eryythematous, blanching, purpura) hand configuration (discrete, confluent, linear (psorias, follows line of prev injury), target lesions,))
A - associated changes (e.g. surface features) (exudate/crust, scale, excoriation marks, erosion, ulceration)
M - morphology (raised/flat, fluid filled)

ABCD
Asymmetry
Border (irregular, blurred)
Colour
Diameter

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3
Q

What is a commodome?

A

A comedone is a small black (open) or white (closed) coloured spot which often occur as part of an acne outbreak and develops on the face, neck, chest and back as a result of sebum and keratin blockage of the pilosebaceous unit.

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4
Q

What is alopecia?

A

Ariarta - patchy
Or diffuse
Hair loss

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5
Q

What is hypertrichosis?

A

Excessive hair growth over and above the normal for the age, sex and race of an individual, in contrast to hirsutism, which is excess hair growth in women following a male distribution pattern.

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6
Q

What is hirsuitism?

A

Hirsutism (HUR-soot-iz-um) is a condition in women that results in excessive growth of dark or coarse hair in a male-like pattern — face, chest and back. With hirsutism, extra hair growth often arises from excess male hormones (androgens), primarily testosterone

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7
Q

What is koilonychia?

A

Spoon shaped nail
Associated with iron def. aneamia

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8
Q

What is onycholysis?

A

Thickened nails lifting off the nail bed
Associated with psoriasis

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9
Q

What is clubbing?

A

Clubbing is a physical sign characterized by bulbous enlargement of the ends of one or more fingers or toes

Associated with lung cancer

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10
Q

What is pitting?

A

Small dots in the nail
Associated with psoriasis

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11
Q

What is a macule?

A

Flat, small lesion <1cm,
Discolouration: brown, blue, red or hypopigmented

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12
Q

What is a papule?

A

Superficial elevated solid lesions (<0.5cm)
Varies in colour

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13
Q

What is a vesicle?

A

CIrcular collection of free fluids <1cm

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14
Q

What is a patch?

A

Flat lesion larger than a macule (>1cm)
Circumscribed
Discoloured

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15
Q

What is a plaque?

A

Superfiical lesion which is elevated, solid and flat.
Topped lesion >1cm

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16
Q

What is a nodule?

A

Circular, elevated, solid lesion (>1cm) - larger than a papule

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17
Q

What is a bulla?

A

Circumscribed collection of free fluid >1cm (greater than a vesicle)

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18
Q

What is a pustule?

A

A vesicle containing puss (inflammatory cells)

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19
Q

What is meant by annular?

A

Ring shaped lesion

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20
Q

What is meant by a wheal/urticarial lesion?

A

Odematous, transitory plaque, may last a few hours
May be round, annular or polycyclic

May be associated with angiodema or anaphylaxis

May require bloods and urinalysis to exclude a systemic cause

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21
Q

What is meant by scale?

A

Epidermal thickening, consists of flakes or plates of compacted desquamated layers of stratum corneum

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22
Q

What is meant by crust?

A

Dried exudate on skin

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23
Q

What is erythoderma?

A

Confluent erythema

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24
Q
A

Erosion

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25
Q
A

Palpable purpuric papules

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26
Q
A

Telangiectasia

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27
Q
A

Ulcer

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28
Q
A

Petechiae

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29
Q
A

Scaly papules

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30
Q
A

Annular non scaling plaque

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31
Q
A

Cyst

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32
Q
A

Patch

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33
Q
A

Erythema

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34
Q
A

Gangrene

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35
Q
A

Vesicles

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36
Q
A

Macules

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37
Q
A

Patch

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38
Q
A

Bulla

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39
Q
A

Crust (in impetigo)

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40
Q
A

Eschar

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41
Q
A

Erythoderma

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42
Q
A

Sclaey plaque

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43
Q
A

Pustules

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44
Q
A

Papules

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45
Q
A

Nodule

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46
Q
A

Ecchymosis seen in vasculitis

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47
Q

What is the standar exicisonal shape for removal of a skin lesion?

A

Elliptical shape including saftey margin of normal skin to allow for closure

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48
Q

Risk factors for melanoma?

A

MORE THAN 5 EPISODES OF SUNBURN UNDER 10 YEARS OF AGE
Sun exposure
Sun beds
Immunosupression
Burns easily
Multiple moles (>100)
Atypical naevus syndrome moles
Family history of melanoma
Skin type 1
Previous history of melanoma
Large congenital melanocytic naevus

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49
Q

What do multiple pinpoint bleeding points on a painful callus suggest?

A

Warts

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50
Q

How can a verruca be managed?

A

Duct tape
Topical therapies
Cryotherapy

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51
Q

What is molluscum contagiosum?

A

Shiny smooth papules with central dimple secondary to viral infection . Self limiting but can us antiseptic wash +/- abx if appear infected

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52
Q

How might scabies present?

A

Multiple household members with same condition.
Linear burrows (may be tortuos), rubber nodules, papules, excoriations,

Scabies presents with incredibly itchy small red spots, possibly with track marks where the mites have burrowed.

The classic location of the rash is between the finger webs, but it can spread to the whole body.

History of contact with symptomatic individuals, puritus worse at night

Common sites include fingers, finger webs, wrists, elbows, ankles, feet, nipples and genitals

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53
Q

How long after treatment of scabies will the itchy persist

A

One month

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54
Q

How does bullous phemigoid present?

A

Erythematous rash
Itchy
Papules and plaques
Some annular/targetoid leisions
Tense blisters/bulla on an erythematous base
Preceded by a non-specific itchy rash
Usually effects the trunk and limbs (Mucosal involvement less common)#
Often affecting elderly patients

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55
Q

How does shingles distribute and how does it appear?

A

In a dermatomal distribution
Erthymatous, erosions, crust

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56
Q

How does SSC present?

A

Fast growing
Ulcerated lesion
May have shiny edges and telangiectasia
Bleeding and crust present

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57
Q

What is Bowen’s disease?

A

Type of early skin cancer

Bowen’s Disease appears as an irregular, red, keratinised, scaly plaques classically located on areas of sun exposed skin

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58
Q

How to use steroids in eczema?

A

The general rule is to use the weakest steroid for the shortest period required to get the skin under control. Steroids are very good for settling down the immune activity in the skin and reducing inflammation, but they do come with side effects. They can lead to thinning of the skin, which in turn make the skin more prone to flares, bruising, tearing, stretch marks and enlarged blood vessels under the surface of the skin called telangiectasia. Depending on the location and strength of the steroid there may be some systemic absorption of the steroid. The risks of using steroids need to be balanced against the risk of poorly controlled eczema.

The thicker the skin, the stronger the steroid required. Only weak steroids used very cautiously should be applied to areas of thin skin such as the face, around the eyes and in the genital region. It is best to completely avoid steroids in these areas in children.

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59
Q

How should steroid cream be applied?

A

Emollient should be applied first
Use fairly genourously when active and thinner when improving

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60
Q

What is acne?

A

A chronic inflammatory condition, with or without localised infection disorder of the pilosebaceous units (containing hair follicles and sebaceous glands) causing comedones, papules and pustules to form.

Commodomal - less severe,
Pustular more severe

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61
Q

How might secondary syphillis manifest dermatologically?

A

Secondary syphilis develops as a maculopapular rash covering the torso and limbs as well as the palms and soles.
Patients generally feel very unwell and have lymphadenopathy.

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62
Q

What is the first line treatment of plaque psoriasis?

A

Potent topical corticosteroid + topical vitamin D is the first line treatment for plaque psoriasis.

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63
Q

What psychiatric drug is a common trigger of psoriasis?

A

Lithium

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64
Q

What is contact dermatitis?

A

Contact Dermatitis is a type of Eczema which occurs following exposure to a causative agent.

The rash is typically eczematous and commonly located on the hands in an asymmetrical distribution.

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65
Q

What is Bullous Pemphigoid?

A

Bullous Pemphigoid is an autoimmune blistering skin condition which affects the elderly. It is more common in those with neurological diseases such as Parkinson’s Disease or dementia. Bullous Pemphigoid is caused by autoantibodies against antigens between the epidermis and dermis, resulting in a sub-epidermal split. Initially, it presents as pruritic, tense, fluid-filled bullae (large blisters) on an erythematous base. In the image shown, some of the bullae have ruptured, leaving post-inflammatory hyperpigmentation. The lesions can be localised or widespread, often occurring in skin folds.

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66
Q

What is impetigo and what causes it?

A

Impetigo is a superficial bacterial skin infection, usually caused by the staphylococcus aureus bacteria.

A “golden crust” is characteristic of a staphylococcus skin infection. It is also less commonly caused by the streptococcus pyogenes bacteria.

It occurs when bacteria enter through a break through the skin and is highly contagious.

It can be classified as non-bullous or bullous

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67
Q

How does non-bullous impetigo present?

A

Occurs around the nose or mouth
Exudate from the lesions dries to form a golden crust
Pt not unwell
Common in children

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68
Q

What can be used to treat non-bullous impetigo?

A
  • Topical fusidic acid, antiseptic cream (hydrogen peroxide 1%)
  • Oral flucloxacillin in more wide spread or severe impetigo
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69
Q

How to prevent spread of impetigo?

A

Advise not to touch or scratch lesions
Hand hygine
Avoid shairing face towels and cutlery
Stay off school until lesions have healed (crusted over) - usually 7 to 10 days - or treated with antibiotics for at least 48hrs
If bullous patients should be isolated

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70
Q

How does bullous impetigo occur?

A

Staphylococcus aureus only.
These bacteria can produce epidermolytic toxins that break down proteins that hold skin cells together, causing 1-2cm fluid filled vesicles to form on the skin.

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71
Q

How does bullous impetigo present?

A

Painful ithcy lesions: 1-2cm fluid filled vesicles form, growing in size and then bursting forming a ‘‘golden crust’’
More common in under 2s
Systemic symptoms may occur: fever, lethargy

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72
Q

How is bullous impetigo treated?

A

Flucloxacillin - oral or IV if very unwell or at risk of complications

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73
Q

What is staphylococcus scaled skin syndrome?

A

Complication of bullous impetigo - severe infection with widespread lesions

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74
Q

How can bullous impetigo be investigated?

A

Swabs of the besides can confirm diagnosis bacteria and antibiotic sensitivities

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75
Q

What are the potential (but rare), complications of impetigo.

A

Cellulitis if the infection gets deeper in the skin
Sepsis
Scarring
Post streptococcal glomerulonephritis
Staphylococcus scalded skin syndrome
Scarlet fever

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76
Q

What is folliculitis, how does it present and what causes it?

A

Inflammation of a hair follicle resulting in papules or pustules (pimples).
Most commonly caused by a staphylococcus aureus infection (gram negative folliculitis can occur after prolonged antibiotic treatment for acne)

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77
Q

What is eosinophillic foliculitis? How is it diagnosed and treated?

A

Eosinophilic folliculitis is a sterile folliculitis that is caused by immunosuppression, most commonly due to HIV.
Diagnosis is by skin biopsy, which reveals eosinophils in the skin surface.
Treatment is with HAART and topical corticosteroids.

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78
Q

What is cellulitis?

A

Bacterial soft tissue infection of the dermis and deep subcutaneous tissue

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79
Q

Risk factors for cellulitis?

A

Advancing age
Immunocompromised e.g. diabetic
Predisposing skin condition e.g. ulcers, pressure sores, trauma, lymphoedema

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80
Q

What organisms typicall cause cellulitis?

A

Generally caused by Streptococcus and/or Staphylococcus organisms.

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81
Q

Clinical features of cellulitis?

A

Erythema
Calor (heat)
Swelling
Pain
Poorly demarcated margins
Systemic upset: fever, malaise
Lymphadenopathy
Often evidence of breach in skin barrier e.g. trauma, ulcer, etc

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82
Q

How is cellulitis managed?

A

Blood tests including culture
Skin swab for culture
Oral or IV antibiotics depending on severity - flucloxacillin first line
Mark the area of erythema to aid in detection of rapidly spreading cellulitis
Elevate if possible
Wound debridement may be necessary
Sterile dressing, analgesia

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83
Q
A
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84
Q
A

Folliculitis

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85
Q
A

Cellulitis

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86
Q
A

HSV 1

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87
Q

What is the genital lesion

A

HSV 2

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88
Q
A

Chicken pox

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89
Q
A

Shingles

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90
Q
A

Viral wart

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91
Q

Name the viral lesion

A

Molluscum contagiosum

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92
Q
A

dermatophytosis (ring worm)

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93
Q

What skin infection could this be

A

candidiasis

Candidal intertrigo

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94
Q
A

Scabies

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95
Q

Types of herpes simplex virus?

A

HSV-1 - most common cause of oral herpes (and genital)
HSV-2 causes genital herpes, more likely to cause recurrent anogenital symtpoms

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96
Q

How might genital herpes present?

A

May be entirely asymptomatic

Multiple painful genital ulcers

Dysuria

Vaginal or urethral discharge

Lesions typically crust and heal, at which point virus ceases to be shed from the lesions.

In some cases may have symptoms of fever, malaise, headache and urinary retention.

Recurrent episodes are usually less severe than a primary episode. There may not be a clearly identifiable trigger. The recurrent episode may have a prodromal phase, such as tingling.

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97
Q

Most effective method to diagnose a lesion as HSV

A

The most effective method of diagnosis is to obtain a swab from the base of the ulcer and analyse using nucleic acid amplification tests (NAATs).

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98
Q

How is HSV transmitted?

A

HSV is transmitted from skin-to-skin.

The virus can be shed in the prodromal phase and during phases of recurrence or when displaying clinical symptoms for the first time. Virus can also be shed when the patient is asymptomatic

The current guidance advises patients to abstain from sex during clinical recurrence or when they are experiencing prodromal symptoms. In the case of oral HSV kissing or any skin to skin contact with the lesion should be avoided until completely healed.
There is a risk of transmission to the eye if contact lenses become contaminated

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99
Q

How is genital HSV treated and when should it start?

A

Oral antivirals are the primary treatment for genital herpes simplex infection — treatment should commence within 5 days of the start of the episode, or while new lesions are forming for people with a first clinical episode of genital herpes simplex virus (HSV).

Aciclovir, Valaciclovir, Famciclovir

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100
Q

How is oral HSV-1 infection managed?

A

Usually self limiting
Can reccomend soft diet if eating is painful
NICE advises against prescribing topical anaesthetic or analgesic preparations, mouthwash or lip barrier preparations.
Paracetamol, ibuprofen
Choline salicylate gel for pain control of cold sores can be bought over the counter (this is contra-indicated under the age of 16 due to Reye’s syndrome).

Topical antiviral agents are minimally benificial but can be used if initiated at the onset of symptoms before vesicles appear purchased OTC
Aciclovir 5% (age range is not specified by the manufacturer),

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101
Q

When should oral antiviral agents be considered for oral HSV-1?

A

For immunocompetent individuals, oral antivirals are not routinely indicated for the treatment of cold sores but may be indicated in severe episodes. If possible this should be done from the time of the prodrome - ie before vesicles appear.
Seek specialist advice for people who are immunocompromised (including people with HIV), antivirals may be warrented or even admission.
Aciclovir is active against herpes viruses but does not eradicate them. It can be used as systemic and topical treatment of herpes simplex infections of the mucous membranes and is used orally for severe herpetic stomatitis.
Valaciclovir is an ester of aciclovir. It is licensed for herpes simplex infections of the skin and mucous membranes.

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102
Q

Complications of HSV infection?

A

Dehydration, especially in children.

Recurrent lesions at the same site may occasionally cause atrophy and scarring.

Secondary bacterial infection, including impetigo, can occur.

Eczema herpeticum can complicate atopic eczema.

Bell’s palsy is possibly a complication of herpes simplex infection.

Rare complications include dissemination, herpes encephalitis, meningitis, corneal dendritic ulcers (ocular herpes simplex) and erythema multiforme.

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103
Q

What is Eczema herpeticum?

A

Eczema herpeticum is a rare and serious skin infection caused by one of the herpes viruses. It causes a blistery, painful skin rash. It most often affects children who have eczema

Herpes simplex virus 1 (HSV-1) is the most common causative organism

The eczema causes breaks in the skin which allows the virus in

Considered an emergency as it can spread quickly

Often mistaken for chickenpox, however differes as spots are smaller and closer together

A typical presentation is a patient who suffers with eczema that has developed a widespread, painful, vesicular rash with systemic symptoms such as fever, lethargy, irritability and reduced oral intake. There will usually be lymphadenopathy (swollen lymph nodes).

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104
Q

Eczema Herpeticum management?

A

Antiviral medicine such as aciclovir is usually very successful for treating eczema herpeticum. It may be given as a liquid or a tablet (mild to moderate). For people who are too unwell to take it as a liquid or a tablet, it can be given by a drip intravenously (severe)

Viral swab of vesicles to confirm diagnosis

STEROID CREAM WILL WORSEN

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105
Q

How does eczema herpeticum present?

A

Pt generally unwell with fever
Usually children w history of atopic eczema
Fluid filled vesicles - usually on face or neck
Spreads
Vesicles may weep or become crusted over
Lymphandopathy may be present

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106
Q

What is chickenpox?

A

Chickenpox is caused by the varicella zoster virus (VZV). It causes a highly contagious, generalised vesicular rash. It is common in children. Once a child has had an episode of chickenpox, they develop immunity to the VZV virus and will not be affected again.

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107
Q

When does chicken pox stop being contagious?

A

When the lesions scab over

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108
Q

When does chicken pox start being contagious?

A

A couple of days before rash appears

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109
Q

Clinical features of chickenpox?

A

Widespread, erythematous, raised, vesicular blistering lesions
Rash usually starts on trunk or face and spreads outwards affecting the whole body over 2-5 days
Fever is often the first symptom
Itch
General fatigue and malaise

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110
Q

Intubation period of chicken pox?

A

10 days to 3 weeks

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111
Q

How is chickenpox spread?

A

Chickenpox is highly contagious and spread through direct contact with the lesions or through infected droplets from a cough or sneeze.

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112
Q

Potential complications of chickenpox?

A

Bacterial superinfection
Dehydration
Conjunctival lesions
Pneumonia
Encephalitis (presenting as ataxia)
After the infection the virus can lie dormant in the sensory dorsal root ganglion cells and cranial nerves reactivate later in life as shingles or Ramsay Hunt syndrome.

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113
Q

Advice for pregnant women exposed to chicken pox (and the reasoning behind it)?

A

If they are not immune, varicella zoster immunoglobulins can be given to protect them against the virus after exposure.

Before 28 weeks: potential for congenital varicella syndrome - developmental problem in fetus
Around time of delivery: can lead to life threatening neonatal infection, requires treatment with varicella zoster immunoglobulins and aciclovir

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114
Q

Management of chickenpox?

A

Chickenpox is usually a mild self limiting condition that does not require treatment in otherwise healthy children.

Aciclovir may be considered in immunocompromised patients, adults and adolescents over 14 years presenting within 24 hours, neonates or those at risk of complications.

Complications such as encephalitis require admission for inpatient management.

Symptoms of itching can be treated with calamine lotion and chlorphenamine (antihistamine).

Patients should be kept off school and avoid pregnant women and immunocompromised patients until all the lesions are dry and crusted over. This is usually around 5 days after the rash appears.

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115
Q

What is shingles and which patients is it expected and not expected in?

A

Shingles is a reactivation of the varicella zoster virus which can lie dormant in nerve ganglia following primary infection (chickenpox).

It commonly occurs in the elderly and shingles in young adults should prompt investigation for an underlying immune condition.

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116
Q

How does shingles present?

A

Tingling feeling in a dermatomal distribution
Progression to erythematous papules occuring along one or more dermatones within a few days, which develop into fluid dilled vesicles which then crus over and heal
Fever
Headache
Malise

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117
Q

Potential complications of shingles?

A

Secondary bacterial infection of skin lesions
Corneal ulcers, scarring and blindness if eye involved
Post-herpetic neuralgia
- Pain occurring at site of healed shingles infection
- Can cause neuropathic type pain (burning, pins and needles)
- Can cause allodynia (perception of pain from a normally non-painful stimulus e.g. light touch)

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118
Q

Management of shingles?

A

Oral antiviral (e.g. valaciclovir 1g three times per day for 7 days) if eye involvement or if immunocompromised.
IV antiviral if severe disease
Advise avoiding contact with pregnant women, babies and those who are immunocompromised until the lesions are fully crusted over, as transmission can occur via skin contact

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119
Q

Who should be offered the one off shingles vaccine?

A

Patients in their 70s

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120
Q

What virus causes viral warts?

A

human papillomavirus (HPV)

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121
Q

How can viral warts be classified?

A

Cutaneous (verruca, papiloma)
Mucosal

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122
Q

Who is at increased risk of viral warts?

A

School aged children
Patients with dermatitis (defective skin barrier)
Immunosupressed patients: azathioprine, ciclosporine, HIV

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123
Q

How are viral warts (HPV) spread?

A

Skin to skin contact or autoinoculation (picking or scratchin a ward may cause a subungal wart (under nail) or a wart being spread to another area of skin.
Autoinoculation of the virus in a scratch can result in a line of warts (pseudo-koebnerisation)

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124
Q

HPV incubation period?

A

Up to 12 months depending on amount of virus inoculated

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125
Q

How do cutaneous viral warts appear?

A

Cutaneous viral warts have a hard, keratinous surface.
Tiny red or black dots visible in the wart are papillary capillaries.

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126
Q

How do common warts present?

A

Common warts (verruca vulgaris) present as cauliflower-like papules with a rough, papillomatous and hyperkeratotic surface ranging in size from 1 mm to 1 cm or more. They may be solitary or multiple. Common warts are found most often on the knees, backs of fingers or toes, and around the nails (periungual).

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127
Q

Plantar wart presentations

A

Plantar warts (verruca plantaris) include tender inwardly growing myrmecia on the sole caused by HPV 1, and clusters of superficial less painful mosaic warts due to HPV 2. Myrmecial warts are typically tender with lateral and direct pressure, are surrounded by yellow hyperkeratotic callus-like skin showing accentuated skin markings, but with discontinuation of the skin lines through the actual wart.

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128
Q

Plane wart presentation (verruca plana)

A

Plane warts are typically multiple small flat-topped skin-coloured papules located most commonly on the face, hands, and shins. On the shins and beard-area of the face the virus is often spread by shaving resulting in numerous warts. Plane warts are mostly caused by HPV types 3 and 10.

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129
Q

What is a filiform wart

A

A filiform wart is a cluster of fine fronds emerging from a narrow pedicle base usually found on the face. They are also described as digitate (finger-like).

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130
Q

Complications of cutaneous viral warts

A

Viral warts are infectious to the patient and others
Cutaneous warts can have significant psychosocial effects such as teasing at school, embarrassment, permission refused for swimming lessons.
Periungual warts can cause nail dystrophy and destruction.
Pain due to plantar warts (myrmecia type) interferes with walking and sporting activities, causing knee or hip pain.
In epidermodysplasia verruciformis (rare autosomal recessive condition suscepitable to skin infection) the specific HPV types involved can cause cutaneous squamous cell carcinomas.

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131
Q

Callus vs wart

A

Pinpoint red or black dots (papillary capillaries) are revealed when the wart is pared down. Patent capillaries cause pinpoint bleeding. Plantar corns lack the papillary capillaries.
Location of a plantar wart is not restricted to pressure sites whereas a plantar callus or corn is always at a pressure site.
Tenderness is maximal with lateral pressure for a plantar wart whereas a corn or callus is more tender with direct pressure.

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132
Q

Differential diagnoses for a cutaneous viral wart?

A

Seborrhoeic keratosis
Squamous cell carcinoma
Plantar corn and callus.

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133
Q

Treatment of viral warts?

A

Work by removing virus containing skin - HPV infects the basal cell layer of the epidermis so wards can recur rapidly if the virus has not been eradicated

Topical: salicylic acid or podophyllin containing treaments (remove surface skin cells). Most resolve within 12 weeks of daily applications.
Cryotherapy with liquid nitrogen at one to two week intervals to cause peeling of surface layers for 3-4 months
Electosurgery for large resistant warts

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134
Q

Complications of cataract surgery

A

Endophthalmitis is the most dangerous complication and the first thing any doctor should rule out when
presented with a patient complaining of visual symptoms following intraocular surgery. Patients typically
present within days of surgery with severe pain, loss of vision and hyperaemia. They should be admitted
and seen immediately by an ophthalmologist.
Posterior lens capsule pacification is a relatively common complication of cataract surgery that usually
occurs a few weeks following the operation. The typical patient complains of blurry vision as if their
cataract has returned, and a white opacity may be visible on observation. The condition can be treated
easily with a simple laser procedure which can be carried out as an outpatient.
Other rare complications to be aware of are:
• Retinal detachment
Macular oedema
Glaucoma
• Corneal oedema

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135
Q
A

Eczema herpeticum

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136
Q

The Hazards of Ultraviolet Radiation

A

UV B: sunburn, DIRECT DNA DAMAGE AND CARCINOGENESIS

UV A: Photo ageing! Potentiates UV-B carcinogenesis, Immunological effects

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137
Q

What is an Acquired melanocytic naevus?

A

A melanocytic naevi is a benign skin lesion due to a local proliferation of pigment cells (melanocytes), occuring in childhood.

Evolves in three steps:

Junctional: flat + pigmented (due to melanocytes at the basal layer of the epidermis) - small, flat, and black
Compound: raised + pigmented, hyperkerratotic, and/or hairy (due to melanocytes at the basal layer of the epidermis + deep in the dermis)
Intradermal: raised + pale - usually dome-shaped papules or nodules (due to melanocytes deep in the dermis)

Typical mole appearance

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138
Q

What are congenital naevi?

A

Moles present from birth, tend to be large, pigmented and hairy monitor but not of much concern

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139
Q

What is a dysplastic naevus?

A

An atypical naevus that may resemble a melanoma, by having ‘ABCDE’ features. (ie. Asymmetry, colour changes)
Asymettrical shape
Border irregularity
Colour irregularity
Diameter over 7mm
Evolution of lesion
Symptoms (bleeding, itching)

They may be part of a syndrome called Familial Atypical Multiple Mole-Melanoma (FAMMM) syndrome, where there are multiple naevi (>50) many of which are atypical and an increased risk of melanoma.

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140
Q

What to look for when examining a mole?

A

• A is for asymmetrical shape. Look for moles with irregular shapes, such as two very different-looking halves.
• B is for irregular border. Look for moles with irregular, notched or scalloped borders — the characteristics of melanomas.
• C is for changes in colour. Look for growths that have many colours or an uneven distribution of colour.
• D is for diameter. Look for new growth in a mole larger than about 6mm.
• E is for evolution. Look for change in the mole, includes changes in shape, size and elevation.

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141
Q

Significance of colour in SUPERFICIAL SPREADING MALIGNANT MELANOMA?

A

Black: stratum corneum
Brown: loss of pigment may mean regression, immune system attacking lesion
Grey: papillary dermis
Blue: pigment invading into the deep melanin - concern

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142
Q

Melanoma mimics?

A

Multi component haemangioma
Intracorneal haemorrhage
Subungual haematoma
Benign longitudinal melanonhchia
Pigmented sebkeratosis

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143
Q

What melanoma mimic is this?

A

Multi component haemangioma

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144
Q

What melona mimic is this

A

Intracorneal haemorrhage

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145
Q

T

A
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146
Q

Bowens disease vs Actinic keratosis?

A

Actinic keratosis partial dysplasia, Bowens complete
Actinic keratosis has much lower mallignant potential

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147
Q

Typical appearance of seborrheic keratosis?

A

Seborrheic keratosis are typically dull and darkly pigmented, round or oval in shape, and often
appear like a scab of a healing wound. They can be flat or slightly raised. Typically reported as a new skin lesion

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148
Q

Most common dermatological conditions?

A

Eczema
Psoriasis
Acne
Actinic keratosis
Melanoma
SCC
BCC
Lichen planus
Sebhorric warts
Urticaria

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149
Q

What topical treatment can be used to treat acitinic kerratosis or superficial BCC?

A

Efudix

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150
Q

Treatments for moderate acne?

A

Start topical abx: treclin gel, epidura
Topical treatments: benzy peroxide acid
Oral abx: doxycyline - 3 months

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151
Q

Side effects of oral retinoids?

A

Note requires baseline bloods
Dry skin and lips
Dry mucous membranes
Photosensitivity of the skin to sunlight
Depression, anxiety, aggression and suicidal ideation. Patients should be screened for mental health issues prior to starting treatment.
Rarely Stevens-Johnson syndrome and toxic epidermal necrolysis
Teratogenic Fragile skin (avoid waxing)
Slower wound healing
Headaches
Joint pains
Hyperlipidemia

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152
Q

When can oral retinoids be trialed in acne?

A

failure of 3 month course of oral abx

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153
Q

Potential complications of eczema?

A

Eczema herpeticum (rare but serious medical emergency, treated with acyclovir)
Secondary bacterial infection (impetigous eczema)

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154
Q

How should topical steroids be used in eczema flares?

A

Moderate to strong for 5 days
Weaker for 1-2 weeks following

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155
Q

Complications associated with psoriasis?

A

Metabolic syndrome

Nail psoriasis describes the nail changes that can occur in patients with psoriasis. These include nail pitting ( punctate depressions of the nail plate), Onychomycosis (thickening), discolouration, ridging and onycholysis (separation of the nail from the nail bed).

Psoriatic arthritis (occurs in 10 – 20% of patients with psoriasis and usually occurs within 10 years of developing the skin changes. It typically affects people in middle age but can occur at any age)

Psychosocial implications of having chronic skin lesions, which may affect mood, self esteem and social acceptance and cause depression and anxiety.

Other co-morbidities that increase the risk of cardiovascular disease are associated with psoriasis, particularly obesity, hyperlipidaemia, hypertension and type 2 diabetes.

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156
Q

What is basal cell carcinoma?

A

Basal cell carcinoma is the most common form of skin cancer, slow growing, locally invasive mallignant tumour of the EPIDERMAL KERATINOCYTES
Typically presenting as a slow-growing tumour, most commonly of the head or neck. Nodular BCC is the most common subtype, presenting as a shiny nodule with associated telangiectasia, central ulceration and ‘pearly, rolled edges’.
Tend to occur in older individuals
They are associated with a history of sun exposure

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157
Q

What is pyoderma gangrenousum?

A

Pyoderma gangrenosum is a neutrophil dermatosis characterised by the formation of enlarging ulcers, usually on the lower limbs, with a characteristic yellow purulent surface and black/ blue outer edge.
This condition is commonly associated with several systemic diseases (e.g. inflammatory bowel disease); however, it can also be drug-induced (cocaine)

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158
Q

Excisional margin for BCC?

A

4mm

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159
Q

What kind of rash does toxic shock syndrome (staph aureus) present with?

A

Sunburn like

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160
Q

What is impetigo?

A

Impetigo is a contagious bacterial infection that is most commonly seen in the paediatric population. The infection is classically caused by group A Streptococcus and Staphylococcus aureus. Children living in warm, humid climates are most commonly affected.

Skin lesions typically begin as papules and vesicles which eventually break down to give a characteristic golden or honey-coloured crusted appearance. Lesions typically occur on the face and limbs and systemic manifestations are minimal.

Topical treatment can be used for localized disease, however, an oral antibiotic like flucloxacillin should be prescribed for severe infections.

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161
Q

Management of lichen sclerosis?

A

The gold standard management for this condition is topical steroids. A very potent topical steroid is often prescribed as first-line therapy (e.g. clobetasol propionate). In conjunction with this treatment, other conservative measures are often used, including washing the affected area a couple of times per day with water, avoiding restrictive clothing, prompt management of incontinence if present and the application of emollients to alleviate the itch.

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162
Q

How does phemigus vulgaris typically present

A

Easily-burst faccid bullous lesions appear first in the mouth before later appearing on the skin, forming eroisions and crusts. Lesions are often painful. Usualy affecting mucosal areas. It is an autoimmune disease with a peak incidence in the 6th decade that is more prevalent in Ashkenazi Jews. Be aware that it is a medical emergency that is treated with steroids and supportive measures. positive Nikolsky sign

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163
Q

What is positive Nikolsky sign

A

If the test result is positive, the very thin top layer of skin will shear off, leaving skin pink and moist, and usually very tender. A positive result is usually a sign of a blistering skin condition. People with a positive sign have loose skin that slips free from the underlying layers when rubbed.

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164
Q

What is infantile haemangioma

A

infantile haemangioma or ‘strawberry haemangioma’. Strawberry naevi may be present at birth or develop in the first few weeks after birth, they are the most common tumours of infancy. They typically begin as small flat red areas and then develop into raised dimpled lesions. The lesions continue to grow until the child reaches 3-4 years, at which point they begin to regress spontaneously.

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165
Q

What is acne rosacea and how is it managed?

A

This is a condition that typically affects fair-skinned people and is characterised by erythema, telangiectasia, papules and pustules on the forehead, nose, cheeks and often chin. It typically begins with flushing and is often worse after alcohol ingestion, as in this case.

The first-line treatment for acne rosacea is topical metronidazole. Topical azelaic acid can be used if topical metronidazole is not tolerated or fails to improve the condition.

Oral abx (tertracyclines) may be used, topical brimonidine for temporary vasoconstirction may be used, for rhinophyma - surgery or laser ablation.

Advise patients to avoid triggers (spicy food, heat, sunlight, wind, alcohol, hot foods and liquid), wear sun protection and to use bland emollients to mositurise to wash with

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166
Q

How can a topical vitamin d analogue treat psoriasis

A

Increases skin turnover

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167
Q

First line treatment of mild to moderate roseacea

A

Topical Azeliac acid or topical antibiotic such as metronidazole

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168
Q

Most common subtype of BCC?

A

Nodular BCC
Nodular lesion, erythematous with pearly white rolled out lesion, ulcerated center
Spreads into the dermis usually extends over 1mm into the skin
may be well defined, may be symmetrical
Duration - long history, 1-2mm per year, slow growing

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169
Q

What subtype of BCC might be mistaken for a chronic skin condition such as eczema or psoriasis?

A

Superficial-type BCC
Appears as a patch
May have crusting
Erythematous
Serpentine vessels
Superficial BCCs often appear as pink or red dry, scaly spots. They slowly enlarge and may develop a raised edge. Often, people mistake a superficial BCC as a dry patch of skin or a non-itching rash that won’t go away. This subtype of BCC is most often found on the trunk (chest or upper back), arms, or legs.

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170
Q

What type of BCC might be mistaken for a scar?

A

Infiltrative basal cell carcinoma
The cancer grows with a “root system” which is embedded into the dermis of the skin. Because of this root system, infiltrative basal cell carcinomas require certain procedures, including excision or Mohs surgery, to make sure that all of the roots are removed completely
This specific type presents differently than other basal cell skin cancers, in that it forms in thin, small clusters, making it more difficult to spot.
Isolated lesion, no history of trauma to explain a scar
Infiltrating or morpheaform BCCs tend to appear as scar-like growths on the skin. They can be slightly shiny, and sometimes have telangiectasias, sores (erosions), or scabs on their surfaces. These skin changes can be subtle.

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171
Q

Non surgical management of BCC? When would it be used?

A

Chemotherapy creams: Fluorouracil (efudix 5% BD for 4 week), Imiquimod cream (Aldara 5% used 5 days of a week OD for 6 weeks)
Cyrotherapy
Radiotherapy (curative, palliative, adjunct to surgery)
Phototherapy

Only curative for superficial BCC, but may be used if patient declines or is unsuitable for surgery
Small low risk lesions

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172
Q

What might Fluorouracil (efudix) be used to treat?

A

Superficial BCC
Bowens disease
Actinic keratosis

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173
Q
A

Bowens disease

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174
Q
A

Actinic keratosis

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175
Q
A

Superficial BCC

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176
Q
A

Nodular BCC

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177
Q
A

Infiltrive BCC

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178
Q

BCC surgical management

A

Surgical exision
Curettage and cautery
‘Mohs’ micrographic surgery (excision og the lesion and tissue borders are progressively excised until specimens are microscopically free of tumour) - for recurrent, high risk tumours

Direct closure if small (under 1cm) Elliptical excision/excision with flap formation/excision with graft from clavicle

Margin of safety 4mm

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179
Q

SCC typical timeline?

A

Appears in weeks to months (no longer than 6, usually up to 3-4)

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180
Q

Management of SCC?

A

Surgical excision, if not suitable can consider potential palliative or curative radiotherapy
Chemotherapy for large metastic disease

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181
Q

What are the most common skin cancers?

A
  1. BCC
  2. SCC
  3. Malignant melenoma
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182
Q

Most dangerous skin cancers?

A
  1. Malignant melanoma
  2. SCC
  3. BCC
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183
Q

What is an SCC?

A

Squamous Cell Carcinoma
A Cutaneous Squamous Cell Carcinoma (SCC) is a locally invasive malignant tumour of epidermal keratinocytes or its appendages.
SCCs can cause pain, tenderness or bleeding and grow over weeks or months.
SCCs sometimes metastasise, which can be fatal.

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184
Q

Subtypes of melenoma

A

Superficial spreading melenoma
Nodular melenoma
Lentigo maligna melanoma
Acral lentiginous melanoma.

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185
Q

What factors indicate a favourable melenoma prognosis?

A

Symeterical and minimal colour variation most key
Asymptomatic (no itching or bleeding)
Regular boarder
Depth of infiltration

Diameter does not indicate prognosis

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186
Q

How might a melenoma develop?

A

De novo melenoma - New mole in older patient - pleomorphic cells
Melanomas arising from common and congenital nevi - less common, congenital mole changes - composed of roundish, monomorphous cells

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187
Q

Surgical management of mallignant melenoma?

A

Excisional margin with 2mm (more can interfere with sentinel lymph node - false abnormalities)
Radiosensitive dye injected by the scar (entinel lymph node biopsy (SLNB))
Wide local exision potentially later surgery

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188
Q

Which layers of skin are removed when excising a skin cancer to ensure depth clearance?

A

Epidermis, dermis, hypodermis (fat)

Particularly important for SCC and melanoma

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189
Q

Management of melenoma?

A

Excision with 2mm margin and sentiel node biopsy

Second procedure after histology diagnosis if required
Based on the stage, a wider excision margin may be taken around the lesion to ensure the cancer has been removed:

Stage 0 = 0.5cm
Stage I = 1cm
Stage II = 2cm
Stage III and IV are metastatic, so adjuvant immunotherapy or chemotherapy is given.

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190
Q

What tool is used to classify and predict outcome in malignant melenoma?

A

Breslow thickness interpretation

Histology is used to diagnose melanoma and a Breslow thickness is established. The Breslow thickness is the depth of the tumour and is a strong predictor of outcome.

If the Breslow thickness is >1mm a sentinel node biopsy should be carried out, which can look for evidence of metastases and stage the cancer.

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191
Q

What is a superficial spreading melenoma?

A

Subtype of melenoma
Most common
Best prognosis
Typically begins as a dark spot that is asymettric, has irregular boarders, or changes colour
Spread horizontally
Doesn’t tend to infiltrate deeply
Common on lower limbs
Young and middle aged adults
Related to intermittent high intensity UV exposure

It is most likely to develop on the trunk in males, on the legs in females, and on the upper back in both sexes.

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192
Q

What is a nodular melenoma?

A

Subtype of melenoma, starting as a raised spot - dark or light - and grows vertically
Most aggressive form
Usually invasive at time of diagnosis
Common on the trunk
Young and middle aged adults related to intermittent high-intensity UV exposure

The bump is usually black, but it may be:

blue
gray
white
brown
tan
red
the same color as the surrounding skin

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193
Q

What is an acral lentiginous melenoma?

A

Subtype of melenoma
Appears as irregular growth or patch on palms of hands or sole of feet (pain when walking) or under nails
Changes colour and size

Only melenoma that doesn’t have a link to UV raditation
Occurs in the elderly population

An early sign might be an oddly shaped black, gray, tan, or brown mark with irregular borders.

When ALM begins in the nails, it may appear as a streak under the nail. Most cases of ALM on the nails occur on the big toe or thumb.
The surface may be flat, but there may be deep inward growth.
Some tumors involve a loss of color or no change in color.
ALM tumors often take on an irregular shape or color or a rough texture as they grow.
ALM may resemble a plantar wart or a fungal infection.

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194
Q

What is a lentigo maligna and lentio maligna melanoma?

A

Lentigo maligna is an early form of melanoma in which the malignant cells are confined to the tissue of origin, the epidermis, hence it is often reported as ‘in situ’ melanoma.
It occurs in sun damaged skin so is generally found on the face or neck, particularly the nose and cheek. It grows slowly in diameter over 5 to 20 years or longer.
Starts as an irregular shaped tan or brown spot growing slowly over years

Lentigo maligna melanoma is diagnosed when the melanoma cells have invaded into the dermis and deeper layers of skin. Lentigo maligna has a lower rate of transformation to invasive melanoma than the other forms of melanoma in situ (under 5% overall). However, the risk of invasive melanoma is greater in larger lesions, with up to 50% of those with diameter of greater than 4 cm being reported to have an invasive focus.

Common on the face in elderly population, related to long term cumulative UV exposure

May become raised or change colours, can be multipigmented

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195
Q
A

lentigo maligna/lento maligna melenoma

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196
Q
A

Acral lentiginous melanoma

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197
Q
A

Superficial spreading melenoma

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198
Q
A

Nodular melenoma

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199
Q

What features of a skin lesion should be reffered under the 2 week wait pathway for suspected mallignant melenoma?

A

Asymmetry
Border irregularity (melanoma often has a ‘scalloped’ border)
Colour variation (a variegated lesion is one that consists of many colours)
Diameter >6mm
Evolves over time
Additionally an ‘ugly duckling sign’ can be used to identify malignant lesions- any lesion that stands out from the rest should be suspected.

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200
Q

Basal cell carcinoma risk factors?

A

Type I or II skin (fair skin which always burns and never or rarely tans)
History of frequent or severe previous sun burn
Outdoor occupation or hobbies
Personal or family history of skin cancer
Immunosuppression
Increasing age
Male sex

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201
Q

Management of BCC?

A

Management of a BCC depends on its size, location, type and local guidelines - but the majority are managed surgically. Treatment options include;

Surgical excision with a 4mm margin
Curettage and cautery
Mohs micrographic surgery if the BCC is in a cosmetically sensitive area or appears ill-defined. This involves examining the excised tissue under the microscope as it is removed to ensure all the cancerous cells are removed whilst preserving the maximum amount of healthy tissue.
Cryotherapy
Photodynamic therapy
Radiotherapy is used as an adjunct or if surgery is inappropriate
Topical therapies such as Imiquimod or 5-Fluorouracil

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202
Q

What is Mohs micrographic surgery and when is it used?

A

Mohs micrographic surgery if the BCC is in a cosmetically sensitive area or appears ill-defined. This involves examining the excised tissue under the microscope as it is removed to ensure all the cancerous cells are removed whilst preserving the maximum amount of healthy tissue.

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203
Q

BCC subtypes?

A

Nodular
Superficial spreading
Infiltrative
Pigmented
Cystic
Keratotic

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204
Q

SCC typical appearence?

A

SCCs typically appear as an irregular, ill-defined red keratotic (scaley and crusty) nodule which may ulcerate. They often occur on sun exposed areas of skin such as the face, scalp, ears, hands and shins.

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205
Q

Causes/risk factors of SCC?

A

SCCs are caused by DNA mutations following exposure to ultraviolet (UV) light, certain human wart viruses or other forms of skin damage such as burns. Genetic factors can predispose to these mutations.

Risk factors
Risk factors for the development of SCCs;

Type I or II skin (fair skin which always burns and never or rarely tans)
History of frequent or severe previous sun burn
Outdoor occupation or hobbies
Personal or family history of skin cancer
Immunosuppression, especially following an organ transplant
Smoking
Premalignant skin conditions such as Actinic Keratosis or Bowen’s Disease. (Bowen’s Disease is also known as Intraepidermal SCC or SCC in Situ. It is pre-malignant as tumour cells are confined to the epidermis.)
Increasing age
Male sex

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206
Q
A

SCC

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207
Q

What is Pyogenic Granuloma

A

A Pyogenic Granuloma is a reactive overgrowth of capillary blood vessels. It is a benign lesion, but can cause discomfort and frequent, easy bleeding. Pyogenic Granulomas are relatively common, occurring mostly in children and young adults and in females more often than males.

Pyogenic Granulomas appear as a single, shiny, red nodule of up to 1cm, often described as ““raspberry-like”. This nodule will have grown rapidly from a painless, small, discoloured spot. Pyogenic Granulomas are most commonly located on the fingers and hands.

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208
Q

Presentation of pyogenic granuloma

A

Pyogenic Granulomas appear as a single, shiny, red nodule of up to 1cm, often described as ““raspberry-like”. This nodule will have grown rapidly from a painless, small, discoloured spot.

Pyogenic Granulomas are most commonly located on the fingers and hands.

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209
Q

Causes of pyogenic granuloma?

A

Minor trauma, such as a pin prick
Infection, commonly Staphylococcus aureus
Pregnancy
Some medications, such as oral Retinoids

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210
Q

How are pyogenic granulomas managed and why?

A

The diagnosis of a Pyogenic Granuloma is clinical, but can be confirmed by biopsy and histological examination. This is required to rule out the more sinister differential diagnosis of an Amelanotic Melanoma.

Pyogenic Granulomas can be managed by;

Surgical excision
Laser surgery
Curettage and cautery
Cryotherapy

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211
Q

What gives a blue naveus its colour?

A

A naevus that is blue in colour because the melanocytes are very deep in the skin.

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212
Q

What is a becker naveus?

A

A becker naevus is an irregular, hyperpigmented patch usually affecting the shoulders of males.
During puberty it darkens and becomes hairy.

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213
Q

What is a halo naveus?

A

A halo naevus is melanocytic naevus that is surrounded by a white halo.

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214
Q

What is a spitz naveus?

A

A red, dome-shaped papule that is commonly found on the face of children.

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215
Q
A

Spitz naevus

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216
Q
A

Halo Nevus

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217
Q
A

Beckers Naevus

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218
Q
A

Congenital Melanocytic Naevus

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219
Q

Management of infantile sebhorric dermatitis

A

First line treatment is by applying baby oil, vegetable oil or olive oil, gently brushing the scalp then washing off.

When this is not effective, white petroleum jelly can be used overnight to soften the crusted areas before washing off in the morning.

The next step is a topical anti-fungal cream such as clotrimazole or miconazole, used for up to 4 weeks. Severe or unresponsive cases may need referral to a dermatologist.

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220
Q

Who is typically effected by sebhorric dermatitis and how does it present

A

Seborrhoeic dermatitis is an inflammatory skin condition that affects the sebaceous glands. The sebaceous glands are the oil producing glands in the skin. It affects areas that have a lot of these glands, such as the scalp, nasolabial folds and eyebrows. It causes erythema, dermatitis and crusted dry skin.

In infants it causes a crusted dry flaky scalp, often called cradle cap. It is thought that Malassezia yeast colonisation has a role to play in the development of seborrhoeic dermatitis, and the condition improves with anti-fungal treatment.

This condition most commonly affects babies under 3 months of age, young adults, the elderly and those with a combination of oily and dry skin. It is exacerbated by cold weather and partially relieved by sun exposure. It presents with diffuse scalp scale, blepharitis and scaly skin located in the facial folds (i.e. on either side of the mouth).

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221
Q

Erythema multiforme

A

Erythema multiforme is an uncommon skin rash that is thought to be a hypersensitivity reaction to some medications and infections. It characteristically causes ‘target lesions’ which consist of a central dusky or dark red area with peripheral pink ring and are demonstrated in the image shown. In practice, lesions can have a variable appearance and only a few ‘targets’ may be seen. It is often asymptomatic but can be pruritic. The most common cause is herpes simplex virus but multiple other infections such as typhoid, mycoplasma pneumonia and tuberculosis can trigger it. There are numerous other causes such as medications and inflammatory disorders. It is usually an asymptomatic and self-limiting condition and so treatment is often not needed, although investigations should be considered to investigate an underlying cause.

Mucosal involvement is either absent or limited to only one mucosal surface

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222
Q

What is the minimum length of time recommended to wait between the application of emollients and topical steroids?

A

20-30 mins as to avoid diluting the steroid and affecting its efficacy

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223
Q

What is contact dermatitis?

A

Contact dermatitis is an inflammatory skin condition induced by exposure to an external irritant or allergen. It is a type IV hypersensitivity reaction. The appearance of contact dermatitis is highly variable. It may affect any area of the body and may be any shape. It is often an erythematous and pruritic rash. Lighter skin can become red, and darker skin can become dark brown, purple or grey.

Diagnosis is made clinically or with patch tests in some cases. Type IV hypersensitivity is also known as delayed hypersensitivity, as the reaction typically occurs 24 to 72 hours after antigen exposure. Unlike types I to III, it is not antibody-mediated but T-cell-mediated. It is involved in the processes of contact dermatitis.

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224
Q

When might an infantile/strawberry haemangioma warrant refferal to paediatrics?

A

When strawberry naevi affect the visual axis, they will likely require a referral to paediatrics for further management.

Otherwise no management needed, should stop growing and begin to regress by ages 3-4

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225
Q
A

Molluscum contagiosum

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226
Q

Resolution of mollusom contagiosum?

A

The papules resolve by themselves without any treatment, however this can take up to 18 months. Once they resolve the skin returns to normal. Scratching or picking the lesions should be avoided as it can lead to spreading, scarring and infection.

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227
Q

When might molluscum contagisoum require treatment and what can be done?

A

Rarely, if bacterial superinfection infection occurs in the lesions as a result of scratching, this may require treatment with antibiotics. Options include topical fuscidic acid or oral flucloxacillin.

Immunocompromised patients and those with very extensive lesions or lesions in problematic areas such as the eyelid or anogenital area may require referral to a specialist. Specialist treatment options include:

Topical potassium hydroxide, benzoyl peroxide, podophyllotoxin, imiquimod or tretinoin
Surgical removal and cryotherapy (freezing with liquid nitrogen) is an option but can lead to scarring

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228
Q

Which patients are typically effected by molluscum contagiosum?

A

Children

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229
Q

How does molluscum contagisoum spread?

A

It is spread through direct contact or by sharing items like towels or bedsheets.

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230
Q

Which virus causes molluscum contagiosum?

A

Molluscum contagiosum is a viral skin infection caused by the molluscum contagiosum virus, which is a type of poxvirus.

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231
Q

Common fungal infections by region?

A

Ringworm is a fungal infection of the skin. It is also known as tinea and dermatophytosis. Fungal infections have specific names depending on the area they affect:

Tinea capitis refers to ringworm affecting the scalp (caput meaning head)
Tinea pedis refers to ringworm affecting the feet, also known as athletes foot (pedis meaning foot)
Tinea cruris refers to ringworm of the groin (cruris meaning leg)
Tinea corporis refers to ringworm on the body (corporis meaning body)
Onychomycosis refers to a fungal nail infection

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232
Q

Most common causative organism in dermatophytosis (ringworm)?

A

The most common type of fungus that causes ringworm is called trichophyton

233
Q

Presentation of fungal infections?

A

Ringworm presents as an itchy rash that is erythematous, scaly and well demarcated. There is often one or several rings or circular shaped areas that spread outwards, with a well demarcated edge. The edge is more prominent and red and the area in the centre is more faint in colour.

Tinea capitis can present with well demarcated hair loss. There will also be itching, dryness and erythema of the scalp. This is more common in children than adults.

Tinea pedis (athletes foot) presents with white or red, flaky, cracked, itchy patches between the toes. The skin may split and bleed. This is often the result of sharing changing rooms with someone that has athletes foot and is more likely to occur when feet are sweaty and damp for prolonged periods.

Onychomycosis (fungal nail infections) presents with thickened, discoloured and deformed nails.

234
Q

Management of tinea?

A

Anti-fungal creams such as clotrimazole and miconazole
Anti-fungal shampoo such as ketoconazole for tinea capitis
Oral anti-fungal medications such as fluconazole, griseofulvin and itraconazole
Fungal nail infections can be treated with amorolfine nail lacquer for 6 – 12 months. Resistant cases may need oral terbinafine, however the patient will need their LFTs monitoring before and whilst taking this.
A mild topical steroid can help settle the inflammation and itching. A common combination is miconazole 2% and hydrocortisone 1% cream (Daktacort).
Advice:
Wear loose breathable clothing
Keep the affected area clean and dry
Avoid sharing towels, clothes and bedding
Use a separate towel for the feet with tinea pedis
Avoid scratching and spreading to other areas
Wear clean dry socks every day

235
Q

What is tinea incognito and when does it occur?

A

Tinea incognito refers to a more extensive and less well recognised fungal skin infection that results from the use of steroids to treat an initial fungal infection.

This often occurs when the initial presentation of ringworm was misdiagnosed as dermatitis and a topical steroid was prescribed. The steroid improves the itching and inflammation but accelerates the growth of the fungal infection by dampening the immune response in the local area. When the steroid is stopped the itchy rash caused by the fungus returns and is much worse than previously. It may be less recognisable as ringworm due to a less well-demarcated border and fewer scales, giving rise to the incognito name.

236
Q

Oral candidiasis: presentation, predisposing factors and management?

A

Oral candidiasis is also called oral thrush. It refers to an overgrowth of candida, a type of fungus, in the mouth. This results in white spots or patches that coat the surface of the tongue and palate.

Several common factors can predispose someone to develop oral candidiasis:

Inhaled corticosteroids (particularly with poor technique, not using a spacer and not rinsing with water afterwards)
Antibiotics (disrupt the normal bacterial flora giving candida a chance to thrive)
Diabetes
Immunodeficiency (consider HIV)
Smoking

Treatment options are:

Miconazole gel
Nystatin suspension
Fluconazole tablets (in severe or recurrent cases)

237
Q

Most common causative organism of vaginal candidiasis?

A

The most common is Candida albicans.

238
Q

Predisposing factors for vaginal candisasis?

A

Increased oestrogen (higher in pregnancy, lower pre-puberty and post-menopause)
Poorly controlled diabetes
Immunosuppression (e.g. using corticosteroids)
Broad-spectrum antibiotics

239
Q

Presentation of vaginal candidiasis?

A

The symptoms of vaginal candidiasis are:

Thick, white discharge that does not typically smell
Vulval and vaginal itching, irritation or discomfort

More severe infection can lead to:

Erythema
Fissures
Oedema
Pain during sex (dyspareunia)
Dysuria
Excoriation

240
Q

Management of uncomplicated vaginal candidiasis?

A

A single dose of intravaginal clotrimazole cream (5g of 10% cream) at night
A single dose of clotrimazole pessary (500mg) at night
Three doses of clotrimazole pessaries (200mg) over three nights
A single dose of fluconazole (150mg)

241
Q

What should women treated for thrush be warned about if they are sexual active?

A

Warn women that antifungal creams and pessaries can damage latex condoms and prevent spermicides from working, so alternative contraceptive is required for at least five days after use.

242
Q

Management of recurrent infections

A

Recurrent infections (more than 4 in a year) can be treated with an induction and maintenance regime over six months with oral or vaginal antifungal medications. This is an off-label use.

243
Q

Investigations for vaginal candidiasis?

A

Often treatment for candidiasis is started empirically, based on the presentation.

Testing the vaginal pH using a swab and pH paper can be helpful in differentiating between bacterial vaginosis and trichomonas (pH > 4.5) and candidiasis (pH < 4.5).

A charcoal swab with microscopy can confirm the diagnosis.

244
Q

What is candidal intertrigo?

A

Candidal intertrigo refers to superficial skin-fold infection caused by the yeast, candida.

245
Q

Factors that can trigger candidal intertrigo?

A

The hot and damp environment of skin folds, which is conducive to the growth of candida species, particularly Candida albicans[1]
Increased skin friction [2]
Immunocompromise [3].

246
Q

actors that increase an individual’s risk of developing candidal intertrigo

A

Occlusive clothing, gloves and footwear
Obesity
Excessive sweating (hyperhidrosis)
Incontinence causing irritant contact dermatitis (incontinence-associated dermatitis)
Diabetes mellitus
Immune deficiency conditions, such as human immunodeficiency virus infection (HIV) or immune suppression by medications (chemotherapy, systemic corticosteroids) [2-5].

247
Q

Candidial intertrigo presentation?

A

Candidal intertrigo classically presents as erythematous and macerated plaques with peripheral scaling. There are often associated superficial satellite papules or pustules [2,5,6].

248
Q

Management of candidal Intertrigo

A

Predisposing factors should be addressed primarily, such as weight loss, blood glucose control, and avoidance of tight clothing
Patients should be advised to maintain cool and moisture-free skin. This may be aided by regular use of a drying agent such as talcum powder, especially if infection is recurrent
Topical antifungal agents such as CLOTRIMAZOLE cream are recommended as first-line pharmacological treatments
Severe, generalised and/or refractory cases may require oral antifungal treatments such as fluconazole or itraconazole

249
Q

How long after initial infestation does a rash appear in scabies?

A

It can take up to 8 weeks for any symptoms or rash to appear after the initial infestation.

250
Q

What parasite causes scabies?

A

Sarcoptes scabiei (tiny mites)

251
Q

Management of scabies?

A

Treatment is with permethrin cream (Lyclear) or malathion (Prioderm). This needs to be applied to the whole body, completely covering skin. It is best to do this when the skin is cool (i.e. not after a bath or shower) so that a layer of cream remains on top of the skin and does not get absorbed. The cream should be left on for 8 – 12 hours and then washed off. This should be repeated a week later to kill all the eggs that survived the first treatment and have now hatched.

Oral ivermectin as a single dose that can be repeated a week later is an option for difficult to treat or crusted scabies.

Antihistamines may be used to relieve itch

Scabies is contagious to all household and close contacts. When one person is diagnosed, all household and close contacts should also be treated in exactly the same way, even if asymptomatic. This is because they may be infected and not yet have symptoms.

All clothes, bedclothes, towels and other materials in contact with scabies need to be washed on a hot wash to destroy the mites. Thorough hoovering of carpets and furniture is also essential.

Itching can continue for up to 4 weeks after successful treatment. Crotamiton cream and chlorphenamine at night at night can help with the itching.

252
Q

What is crusted/noweigan scabies?

A

Crusted scabies is also known as Norwegian scabies. It is a serious infestation with scabies in patients that are immunocompromised. These patient may have over a million mites in their skin. They are extremely contagious. Rather than individual spots and burrows, they have patches of red skin that turn into scaly plaques. These can be misdiagnosed as psoriasis. Immunocompromised patients may not have an itch as they do not mount an immune response to the infestation. They may need admission for treatment as an inpatient with oral ivermectin and isolation.

253
Q

What are head lice and how do they present?

A

Head lice are the Pediculus humanus capitis parasite, which causes infestations of the scalp, most commonly in school aged children.

Head lice are commonly known as nits, however nits are egg shells that have hatched or contain unviable embryos and not the lice themselves.

Head lice are spread by close contact with someone that has head lice, usually in schools or amongst family members. Transmission is by head to head contact or by sharing equipment like combs or towels.

Presentation
Infestation causes an itchy scalp. Often the nits (eggs) and even lice themselves are visible when examining the scalp.

254
Q

Management of head lice?

A

Dimeticone 4% lotion can be applied to the hair and left to dry. This is left on for 8 hours (i.e. overnight), then washed off. This process is repeated 7 days later to kill any head lice that have hatched since treatment.

Special fine combs can be used to systematically comb the nits and lice out of the hair. They can be used for detection combing to check the success of treatment. NICE clinical knowledge summaries recommend The Bug Buster kit.

255
Q

Which common skin condition is this?

A

Eczema

256
Q

What is eczema (basic pathophysiology)?

A

Eczema is a chronic atopic condition caused by defects in the normal continuity of the skin barrier, leading to inflammation in the skin.

The simplified pathophysiology is that eczema is caused by defects - loss of function of various varients of the protein filaggrin - in the barrier that the skin provides. Tiny gaps in the skin barrier provide an entrance for irritants, microbes and allergens that create an immune response, resulting in inflammation and the associated symptoms.

257
Q

Typical presentation of eczema?

A

Eczema usually presents in infancy with dry, red, itchy and sore patches of skin over the flexor surfaces (the inside of elbows and knees) and on the face and neck.

Patients with eczema experience periods where the condition is well controlled and periods where the eczema is more problematic, known as flares.

258
Q

Maintenace management in eczema?

A

The key to maintenance is to create an artificial barrier over the skin to compensate for the defective skin barrier. This is done using emollients that are as thick and greasy as tolerated, used as often as possible, particularly after washing and before bed. Patients should avoid activities that break down the skin barrier, such as bathing in hot water, scratching or scrubbing their skin and using soaps and body washes that remove the natural oils in the skin. Emollients or specifically designed soap substitutes can be used instead of soap and body washes when showering or washing hands.

259
Q

Environmental factors that can affect eczema?

A

Some patients find certain environmental factors play a role in making their eczema symptoms worse or better. For example, it may completely resolve on holiday in warm, humid countries, only to flare on returning to the cold air in the UK. Environmental triggers, such as changes in temperature, certain dietary products, washing powders, cleaning products and emotional events or stresses can also play a role.

260
Q

Management of eczema flares?

A

Flares can be treated with thicker emollients, topical steroids, “wet wraps” (covering affected areas in a thick emollient and applying a wrap to keep moisture locked in overnight) and treating any complications such as bacterial or viral infections. Very rarely IV antibiotics or oral steroids might be required in very severe flares.

Other specialist treatments in severe eczema include zinc impregnated bandages, topical tacrolimus, phototherapy and systemic immunosuppressants, such as oral corticosteroids, methotrexate and azathioprine.

261
Q

Thin emmolients for eczema?

A

E45
Diprobase cream
Oilatum cream
Aveeno cream
Cetraben cream
Epaderm cream

262
Q

Thick, greasy emmolients used to treat eczema?

A

50:50 ointment (50% liquid paraffin)
Hydromol ointment
Diprobase ointment
Cetraben ointment
Epaderm ointment

263
Q

Topical steroid ladder

A

The steroid ladder from weakest to most potent:

Mild: Hydrocortisone 0.5%, 1% and 2.5%
Moderate: Eumovate (clobetasone butyrate 0.05%)
Potent: Betnovate (betamethasone 0.1%)
Very potent: Dermovate (clobetasol propionate 0.05%)

264
Q

Bacterial infection in eczema

A

Opportunistic bacterial infection of the skin is common in eczema. The breakdown in the skin’s protective barrier allows an entry point for infective organisms. The most common organism is staphylococcus aureus. Treatment is with oral antibiotics, particularly flucloxacillin. More severe cases may require admission and intravenous antibiotics.

265
Q

Rash in eczema herpeticum

A

The rash is usually widespread and can affect any area of the body. It is erythematous, painful and sometimes itchy, with vesicles containing pus. The vesicles appear as lots of individual spots containing fluid. After they burst, they leave small punched-out ulcers with a red base.

266
Q

Acne vulgaris pathophysiology?

A

Acne results from increased production of sebum, trapping of keratin (dead skin cells) and blockage of the pilosebaceous unit. This leads to swelling and inflammation in the pilosebaceous unit. Androgenic hormones increase the production of sebum, which is why acne is exacerbated by puberty and improves with anti-androgenic hormonal contraception. Swollen and inflamed units are called comedones.

The Propionibacterium acnes bacteria is felt to play an important role in acne. This is a bacteria that colonises the skin. It is thought that excessive growth of this bacteria can exacerbate acne. Many of the treatments of acne aim to reduce these bacteria.

267
Q

Lesions in acne vulgaris

A

Macules are flat marks on the skin
Papules are small lumps on the skin
Pustules are small lumps containing yellow pus
Comedomes are skin coloured papules representing blocked pilosebaceous units
Blackheads are open comedones with black pigmentation in the centre
Ice pick scars are small indentations in the skin that remain after acne lesions heal
Hypertrophic scars are small lumps in the skin that remain after acne lesions heal
Rolling scars are irregular wave-like irregularities of the skin that remain after acne lesions heal

268
Q

Management of acne vulgaris?

A

No treatment may be acceptable if mild
Topical benzoyl peroxide reduces inflammation, helps unblock the skin and is toxic to the P. acnes bacteria
Topical retinoids (adapalene) and oral (chemicals related to vitamin A) slow the production of sebum (women of childbearing age need effective contraception)
Combination gels: Epiduo gel (adapalene with benzoyl peroxide)
Topical antibiotics such as clindamycin, erythromycin,(prescribed with benzoyl peroxide to reduce bacterial resistance)
Spironolactone
Oral antibiotics such as lymecycline, doxycycline - caution can induce sun sensitivity
Oral contraceptive pill can help female patients stabilise their hormones and slow the production of sebum
Oral retinoids for severe acne (i.e. isotretinoin) is an effective last-line option, although it is only prescribed by a specialist after other methods fail. This needs careful follow-up and monitoring and reliable contraception in females. Retinoids are highly teratogenic.

269
Q

What is the most effective COCP in management of acne? Why can’t it be used long term?

A

Co-cyprindiol (Dianette) is the most effective combined contraceptive pill for acne due to it’s anti-androgen effects. It has a higher risk of thromboembolism, so treatment is usually discontinued once acne is controlled and it is not prescribed long term.

270
Q

Excessive growth of what bacteria colonising the skin might exaccerbate acne?

A

Propionibacterium acnes

271
Q

How long before falling pregnant must a patient stop taking isotretinoin (Roaccutane)?

A

One month

272
Q

Mechanism of action of oral retinoids such as isotretinoin (Roaccutane)

A

Reducing production of sebum, reducing inflammation and reducing bacterial growth

273
Q

What is psoriasis?

A

Psoriasis is a chronic autoimmune condition that causes recurrent symptoms of psoriatic skin lesions. There is a large variation in how severely patients are affected with psoriasis. There appears to be a genetic component but no clear genetic inheritance has been established. Around a third of patients have a first degree relative with psoriasis. The symptoms start in childhood in a third of patients.

274
Q

What chronic condition is this?

A

Psoriasis

275
Q

What causes psoriasis?

A

Autoimmune process

Patches of psoriasis are dry, flaky, scaly, faintly erythematous skin lesions that appear in raised and rough plaques, commonly over the extensor surfaces of the elbows and knees and on the scalp.

These skin changes are caused by the rapid generation of new skin cells, resulting in an abnormal buildup and thickening of the skin in those areas.

276
Q

Signs specific to psoriasis?

A

Auspitz sign: small points of bleeding when plaques are scraped off

Koebner phenomenon: refers to the development of psoriatic lesions to areas of skin affected by trauma

Residual pigmentation of the skin after the lesions resolve

277
Q

What is Auspitz sign?

A

Auspitz sign refers to small points of bleeding when plaques are scraped off in psoriasis

278
Q

What is Koebner phenomenon?

A

Koebner phenomenon refers to the development of psoriatic lesions to areas of skin affected by trauma

279
Q

Types of psoriasis?

A

Plaque psoriasis is the most common form of psoriasis in adults.

Guttate psoriasis is the second most common form of psoriasis and commonly occurs in children. Guttate psoriasis is often triggered by a streptococcal throat infection, stress or medications.

Pustular psoriasis is a rare severe form of psoriasis

Erythrodermic psoriasis is a rare severe form of psoriasis

Seborrhoeic (naso-labial and retro-auricular)

280
Q

What is plaque psoriasis?

A

Plaque psoriasis features the thickened erythematous plaques with silver scales, commonly seen on the extensor surfaces and scalp. The plaques are 1cm – 10cm in diameter. This is the most common form of psoriasis in adults.

281
Q
A

Plaque psoriasis

282
Q

What condition is this (hint, peadiatric patient post strep throat infection)

A

Guttate psoriasis

283
Q

What is guttate psoriasis?

A

Guttate psoriasis is the second most common form of psoriasis and commonly occurs in children.
It presents with many small raised papules across the trunk and limbs.

The papules are mildly erythematous and can be slightly scaly.

Over time the papules in guttate psoriasis can turn into plaques.

Guttate psoriasis is often triggered by a streptococcal throat infection, stress or medications. It often resolves spontaneously within 3 – 4 months.

284
Q

What triggers guttate psoriasis?

A

Guttate psoriasis is often triggered by a streptococcal throat infection, stress or medications. It often resolves spontaneously within 3 – 4 months.

285
Q

What is pustular psoriasis?

A

Pustular psoriasis is a rare severe form of psoriasis where pustules form under areas of erythematous skin. The pus in these areas is not infectious. Patients can be systemically unwell. It should be treated as a medical emergency and patients with pustular psoriasis initially require admission to hospital.

286
Q

What rare but serious skin condition is this?

A

Pustular psoriasis

287
Q

What is erythrodermic psoriasis?

A

Erythrodermic psoriasis is a rare severe form of psoriasis with extensive erythematous inflamed areas covering most of the surface area of the skin. The skin comes away in large patches (exfoliation) resulting in raw exposed areas. It should be treated as a medical emergency and patients require admission.

288
Q

What rare severe dermatological condition is this?

A

Erythrodermic psoriasis

289
Q

What might precipitate erythrodermic psoriasis?

A

Infections
Low calcium
Withdrawal of oral corticosteroids (prednisone)
Withdrawal of excessive use of strong topical corticosteroids
Strong coal tar preparations
Certain medications including lithium, antimalarials and interleukin II
Excessive alcohol consumption

290
Q

Erythrodermic psoriasis is a dermatological emergency, what complications can it cause?

A

Dehydration
Heart failure
Infection
Hypothermia
Protein loss and malnutrition
Oedema (swelling), particularly of lower legs
Death

291
Q

Management of erythrodermic psoriasis?

A

Hospitalisation for supportive care including intravenous fluids and temperature regulation
Bland emollients and cooling wet dressings
Bed rest
Treatment of complications (for example antibiotics, diuretics (water tablets), nutritional support)
Low-dose methotrexate, ciclosporin or acitretin
Individual cases have been reported to have successful outcomes with biologic agents,

292
Q

Triggers of pustular psoriasis?

A

Sudden withdrawal of injected or oral corticosteroids
Drugs such as lithium, aspirin, indomethacin, iodide and some beta-blockers
Infection
Pregnancy.

293
Q

Characteristic of pustular psoriasis?

A

Generalised pustular psoriasis is characterised by recurrent acute flares.

Initially, the skin becomes dry, fiery red and tender.
Within hours, 2–3 mm pustules appear.
After a day, the small pustules coalesce to form lakes of pus
These dry out and peel to leave a glazed, smooth surface on which new crops of pustules may appear.
Successive crops of pustules may appear and erupt every few days or weeks.

294
Q

What might flares of generalised pustular psoriasis result in?

A

Fever and chills (or hypothermia)
A headache
Rapid pulse rate
Loss of appetite and nausea
Thirst and dehydration
Muscle weakness
Leg swelling.

295
Q

Complications of generalised pustular psoriasis?

A

Secondary bacterial infection
The blood count may show anaemia, neutrophilia, lymphopenia
Raised inflammatory markers such as C-reactive protein (CRP)
Disturbed protein and electrolyte balance, low albumin, low calcium and low zinc
High-output cardiac failure
Renal and liver impairment
Protein-losing enteropathy
Peripheral neuropathy
Malabsorption of nutrients and therapeutic drugs.

296
Q

Management of generalized pustular psoriasis?

A

Generalised pustular psoriasis can be life-threatening, so hospitalisation is usually required. The aim is to prevent further fluid loss, stabilise body temperature and restore electrolyte imbalance. Specialist care is essential.

Affected areas are treated with bland topical compresses using emollients and low potency topical steroid creams.

Systemic medications may include:

Antibiotics for confirmed or suspected infection
Acitretin
Systemic corticosteroids (cautiously)
Ciclosporin (cautiously)
Methotrexate
Colchicine
Biologic agents including infliximab, etanercept, ustekinumab, adalimumab, and anakinra.

297
Q

Psoriasis presentation in children compared to adults?

A

In children the distribution and presentation of psoriasis may differ from adults. Guttate psoriasis (Presenting with many small raised erythematous, slightly scaly papules across the trunk and limbs, which can turn into plaques over time, often resolves spontaneously within 3 – 4 months) is more common in children, often triggered by a throat infection.

Plaques of psoriasis are likely to be smaller, softer and less prominent.

298
Q

Management of psoriasis?

A

Management depends on the severity of the condition. Psoriasis in children is usually managed and followed up by a specialist. It can be difficult to treat and psychosocial support is very important. The treatment options include:

Topical steroids
Topical vitamin D analogues (calcipotriol) Tazarotene gel (vit A),Enstilar foam (calcipotriol & Betnovate combination )​
Topical dithranol
Topical calcineurin inhibitors (tacrolimus) (usually only used in adults)
Phototherapy with narrow band ultraviolet B light is particularly useful in extensive guttate psoriasis (children)
Where topical treatments fail with severe and difficult to control psoriasis, systemic treatment under the guidance of an experienced specialist. This might include methotrexate, cyclosporine, retinoids or biologic medications.

Oral immunosuppressants –Methotrexate , ciclosporin ,mycophenolate ​

Biologics injectable eg Humira (adalimumab) oral ( aprimilast )

Potent steroid+vitamin D analogues:
Dovobet (gel)
Enstilar (spray)

299
Q

Nail changes in psoriasis?

A

Nail pitting ( punctate depressions of the nail plate),
Onychomycosis (thickening),
discolouration,
ridging and
onycholysis (separation of the nail from the nail bed).

300
Q

What nail change associated with psoriasis is this?

A

Onychomycosis (thickening)

301
Q

What psoriatic nail change is this?

A

onycholysis (separation of the nail from the nail bed)

302
Q

What psoriatic nail change is this?

A

Pitting

303
Q

What is urticaria?

A

Urticaria are also known as hives.
Swelling involving the superficial dermis, riasing the epidermis, itchy wheals
They are small itchy lumps that appear on the skin. They may be associated with a patchy erythematous rash. This can be localised to a specific area or widespread. They may be associated with angioedema and flushing of the skin. Urticaria can be classified as acute urticaria or chronic urticaria.

304
Q

Pathophysiology of urticaria?

A

Urticaria are caused the release of histamine and other pro-inflammatory chemicals by mast cells in the skin.
This may be part of an allergic reaction in acute urticaria or an autoimmune reaction in chronic idiopathic urticaria.

305
Q

Causes of acute urticaria?

A

Acute urticaria is typically triggered by something that stimulates the mast cells to release histamine. This may be:

Allergies to food, medications or animals
Contact with chemicals, latex or stinging nettles
Medications
Viral infections
Insect bites
Dermatographism (rubbing of the skin)

306
Q

Sub classification of urticaria?

A

Chronic idiopathic urticaria describes recurrent episodes of chronic urticaria without a clear underlying cause or trigger.
Chronic inducible urticaria describes episodes of chronic urticaria that can be induced by certain triggers
Autoimmune urticaria describes chronic urticaria associated with an underlying autoimmune condition, such as systemic lupus erythematosus.

307
Q

Triggers of chronic inducible urticaria?

A

Sunlight
Temperature change
Exercise
Strong emotions
Hot or cold weather
Pressure (dermatographism)

308
Q

Antihistamine of choice to treat urticaria?

A

Fexofenadine

309
Q

Management of urticaria?

A

Antihistamines (fexofenadine)
Oral steroids can be trialled short term
Speciallist refferal if severe to consider:
Anti-leukotrienes such as montelukast
Omalizumab, which targets IgE
Cyclosporin

310
Q

What is staphylococcal scalded skin syndrome, what bacteria causes it and how?

A

Staphylococcal scalded skin syndrome (SSSS) is a condition caused by a type of staphylococcus aureus bacteria that produces epidermolytic toxins.

These toxins are protease enzymes that break down the proteins that hold skin cells together.
When a skin infection occurs and these toxins are produced, the skin is damaged and breaks down

311
Q

What age range affected by staphylococcus scolded skin syndrome and why?

A

This condition usually affects children under 5 years. Older children and adults have usually developed immunity to the epidermolytic toxins.

312
Q

How does staphylococcus scolded skin syndrome prsent?

A

A red rash with wrinkled tissue or paper-like consistency

Typically starts on the face and flexural regions (groin, axillae, and neck), then spreads rapidly to other parts of the body including the arms, legs, and trunk.

Following the rash, the formation of large fluid-filled blisters

Frequently occur in areas of friction (such as axillae, groin, and buttocks), the centre of the face and body orifices (such as the nose and ears).
Fluid contents range from a sterile cloudy fluid to frank yellow pus.

Blisters easily rupture leading to the top layer of the skin (epidermis) peeling off easily, often in large sheets.

Exposure of the underlying, moist, reddish tissue leaves the skin with a burned-like appearance.

Gentle rubbing of the skin causes exfoliation (Nikolsky sign is positive).

Systemic symptoms include fever, irritability, lethargy and dehydration. If untreated it can lead to sepsis and potentially death.

313
Q

SSSS management?

A

Most patients will require admission and treatment with IV antibiotics. Fluid and electrolyte balance is key to management as patients are prone to dehydration. When adequately treated, children usually make a full recovery without scarring.

314
Q

What serious condition is this?

A

Staphylococcal scalded skin syndrome

315
Q

SSSS complications?

A

Scarring
Loss of bodily fluids and salts leading to dehydration and electrolyte imbalance
Hypothermia
Secondary infections such as sepsis, cellulitis, and pneumonia
Renal failure.

316
Q

How is SSSS diagnosed?

A

Skin swabs can be taken from the suspected source of infection and/or the blister fluid to confirm the presence of S. aureus. However, these can frequently be negative given the condition is toxin mediated.
Blood cultures are undertaken when sepsis is of concern.
Tzanck smear
Skin biopsy is occasionally undertaken to exclude other causes of blisters, and occasionally is a justification for frozen section histology
SSSS reveals non-inflammatory intra-epidermal splitting at the granular layer.

317
Q

SSSS diferential diagnosis?

A

Steven–Johnsons syndrome/Toxic Epidermal Necrolysis (SJS/TEN)
Bullous impetigo
Drug hypersensitivity reaction
Viral exanthem
Thermal burns.

318
Q

Suitable abx for SSSS?

A

flucloxacillin
MRSA: vancomycin

319
Q

Presentation and management of seborrhoeic dermatitis of the slap?

A

Mild seborrhoeic dermatitis of the scalp presents with flaky itchy skin on the scalp (dandruff). More severe cases cause more dense oily scaly brown crusting. This commonly occurs in adolescents and adults rather than children.

First line treatment is with ketoconazole shampoo, left on for 5 minutes before washing off. Topical steroids may be used if there is severe itching. It often reoccurs after successful treatment.

320
Q

Seborrhoeic Dermatitis of the Face and Body - presenation and management?

A

Seborrhoeic dermatitis of the face and body presents with red, flaky, crusted, itchy skin. It commonly affects the eyelids, nasolabial folds, ears, upper chest and back.

First line treatment is with an anti fungal cream, such as clotrimazole or miconazole, used for up to 4 weeks. Localised inflamed areas may benefit from a topical steroids, such as hydrocortisone 1%.

Severe or unresponsive cases should be referred to a dermatologist or paediatrician.

321
Q

What is Pityriasis rosea?

A

Pityriasis rosea a generalised, self limiting rash that has an unknown cause. It often occurs in adolescents and young adults. It may be caused by a virus such as human herpes virus (HHV-6 or HHV-7), but no definitive causative organism had been established.

322
Q

Presentation of pityriasis rosea?

A

There may be prodromal symptoms prior to the rash developing. These include headache, tiredness, loss of appetite and flu-like symptoms.

The rash starts with a characteristic herald patch. This is a faint red or pink, scaly, oval shaped lesion that is 2cm or more in diameter, usually occurring somewhere on the torso. It appears 2 or more days prior to the rest of the rash. If you suspect pityriasis, ask and look for a herald patch. Most, but not all, patients have a herald patch.

The rash consists of widespread faint red or pink, slightly scaly, oval shaped lesions, usually less than 2 cm in diameter. On the torso they can be arranged in a characteristic “christmas tree” fashion, following the lines of the ribs.

In dark skinned patients the lesions can be grey coloured, lighter or darker than their skin colour.

Other symptoms may be present:

Generalised itch
Low grade pyrexia
Headache
Lethargy

323
Q

This patch appears two days preceeding a more widespread rash of faint red or pink, slightly scaly, oval shaped lesions, usually less than 2 cm in diameter. What is it called and whatt conidtion is it a feature of?

A

Herold patch
Pityriasis Rosea

324
Q

Course of disease: Pityriasis Rosea?

A

The rash resolves without treatment within 3 months. It can leave a discolouration of the skin where the lesions were, however these will also resolved within another few months.

325
Q

What is the management of pityriasis rosea?

A

There is no treatment for the rash. It will resolve spontaneously without any long term effects. Patient education and reassurance is all that is required. It is not contagious and they can continue all their normal activities.

They may require symptomatic treatment if bothered by itching. This may include emollients, topical steroids or sedating antihistamines at night to help with sleep (e.g. chlorphenamine).

326
Q

Dermatological conditions in which a disproportional immune response causes epidermal necrosis?

A

Stevens-Johnson Syndrome (less than 10% of the body, Widespread erythematous or purpuric macules or flat atypical targets)
Toxic epidermal necrolysis (over 10% of body without spots, 30% with spots, Widespread purpuric macules or flat atypical targets)

327
Q

What happens to the epidermis in SJS and TEN?

A

Blistering and shedding of top layer of skin

328
Q

Causes of SJS/TEN?

A

Note: Risk increased by certain HLA genetic types

Medications

Anti-epileptics
Antibiotics
Allopurinol
NSAIDs

Infections

Herpes simplex
Mycoplasma pneumonia
Cytomegalovirus
HIV

329
Q

How does SJS present?

A

Patients usually start with non-specific symptoms of fever, cough, sore throat, sore mouth, sore eyes and itchy skin. (Prodromal illness)

They then develop a purple or red rash that spreads across the skin and starts to blister.

A few days after the blistering starts, the skin starts to break away and shed leaving the raw tissue underneath.

Pain, erythema, blistering and shedding can also happen to the lips and mucous membranes. Eyes can become inflamed and ulcerated.

It can also affect the urinary tract, lungs and internal organs.

330
Q

Prodromal illness in SJS?

A

Fever > 39 C
Sore throat, difficulty swallowing
Runny nose and cough
Sore red eyes, conjunctivitis
General aches and pains.

331
Q

Rash in SJS?

A

There is then an abrupt onset of a tender/painful red skin rash starting on the trunk and extending rapidly over hours to days onto the face and limbs (but rarely affecting the scalp, palms or soles). The maximum extent is usually reached by four days.

The skin lesions may be:

Macules — flat, red and diffuse (measles-like spots) or purple (purpuric) spots
Diffuse erythema
Targetoid — as in erythema multiforme
Blisters — flaccid (ie, not tense).
The blisters then merge to form sheets of skin detachment, exposing red, oozing dermis. The Nikolsky sign is positive in areas of skin redness. This means that blisters and erosions appear when the skin is rubbed gently.

332
Q

Symptoms caused by mucosal involvement in SJS/TEN?

A

Eyes (conjunctivitis, less often corneal ulceration, anterior uveitis, panophthalmitis) — red, sore, sticky, photosensitive eyes

Lips/mouth (cheilitis, stomatitis) — red crusted lips, painful mouth ulcers

Pharynx, oesophagus — causing difficulty eating

Genital area and urinary tract — erosions, ulcers, urinary retention

Upper respiratory tract (trachea and bronchi) — cough and respiratory distress

Gastrointestinal tract — diarrhoea.

333
Q

SJS complications?

A

Dehydration and acute malnutrition
Infection of skin, mucous membranes, lungs (pneumonia), septicaemia (blood poisoning)
Acute respiratory distress syndrome
Gastrointestinal ulceration, perforation and intussusception
Shock and multiple organ failure including kidney failure
Thromboembolism and disseminated intravascular coagulopathy.

334
Q

SJS vs TEN?

A

Stevens-Johnson Syndrome (less than 10% of the body, Widespread erythematous or purpuric macules or flat atypical targets)

Toxic epidermal necrolysis (over 10% of body without spots, 30% with spots, Widespread purpuric macules or flat atypical targets)

335
Q

Why is skin biopsy usually required in SJS and TEN?

A

Skin biopsy is usually required to confirm the clinical diagnosis and to exclude staphylococcal scalded skin syndrome (SSSS) and other generalised rashes with blisters.

336
Q

SJS abnormalities on bloods and urinalysis?

A

Anaemia occurs in virtually all cases (reduced haemoglobin).
Leucopenia (reduced white cells), especially lymphopenia (reduced lymphocytes) is very common (90%).
Neutropenia (reduced neutrophils), if present, is a bad prognostic sign.
Eosinophilia (raised eosinophil count) and atypical lymphocytosis (odd-looking lymphocytes) do not occur.
Mildly raised liver enzymes are common (30%), and approximately 10% develop overt hepatitis.
Mild proteinuria (protein leaking into the urine) occurs in about 50%. Some changes in kidney function occur in the majority.

337
Q

Illness severity score in SJS/TEN?

A

SCORTEN is an illness severity score that has been developed to predict mortality in SJS and TEN cases.

338
Q

SJS/TEN differntials?

A

Other severe cutaneous adverse reactions (SCARs) to drugs (eg, drug hypersensitivity syndrome)
Staphylococcal scalded skin syndrome and toxic shock syndrome
Erythema multiforme, particularly erythema multiforme major (with mucosal involvement)
Mycoplasma infections
Bullous systemic lupus erythematosus
Paraneoplastic pemphigus

339
Q

SJS/TEN management

A

SJS and TEN are medical emergencies and patients should be admitted to a suitable dermatology or burns unit for treatment.

Good supportive care is essential, including nutritional care, antiseptics, analgesia and ophthalmology input.

Treatment options include steroids, immunoglobulins and immunosuppressant medications guided by a specialist.

Give pain relief as pain can be severe

Temperature maintenance — as body temperature regulation is impaired, the patient should be in a warm room (30–32C)

Hospital admission with reverse isolation and sterile handling procedures

340
Q

Symptoms of DRESS syndrome?

A

Drug hypersensitivity syndrome is a specific, severe, unexpected reaction to a medicine, which affects several organ systems at the same time. It typically causes a combination of:

High fever
Morbilliform eruption
Haematological abnormalities
Lymphadenopathy
Inflammation of one or more internal organs.

Drug hypersensitivity syndrome is sometimes also called drug reaction with eosinophilia and systemic symptoms (DRESS), and drug-induced hypersensitivity syndrome (DIHS).

341
Q

Severe cutaneous adverse reaction (SCAR) syndromes?

A

DRESS syndrome ( drug reaction with eosinophilia and systemic symptoms )
Acute generalised exanthematous pustulosis (AGEP)
Stevens–Johnson syndrome / toxic epidermal necrolysis (SJS/TEN)

342
Q

Which drugs can cause DRESS syndrome?

A

The most common drugs to cause this reaction are a number of anticonvulsant drugs (particularly carbamazepine, phenobarbital, and phenytoin), the anti-gout drug, allopurinol, olanzapine, and the sulphonamide group of antibiotics.

343
Q

DRESS syndrome: pathophysiology

A

Drug hypersensitivity syndrome is a delayed T cell-mediated reaction.

Tissue damage is due to cytotoxic T cells and cytokine release.

There is a genetic predisposition to drug hypersensitivity syndrome.
A defect in the way the liver metabolises drugs may be responsible.
Re-activation of human herpesvirus 6 (HHV6, the cause of roseola) or Epstein-Barr virus (EBV) may also be important.

344
Q

How does DRESS syndrome present?

A

Drug hypersensitivity syndrome usually develops over several days, with onset 2-8 weeks after starting the responsible medicine.

A high fever of 38–40 C is usually noticed first. This is quickly followed by a widespread skin rash. Characteristics of the rash are diverse.

Morbilliform eruption affects 80% of cases, with varying morphology including targetoid lesions, blisters and pustules
Erythroderma or exfoliative dermatitis (involving > 90% body surface area) may follow in about 10%
Facial swelling affects 30%
Mucosal involvement affects 25% (lips, mouth, throat, genitalia)
The rash can last many weeks.

345
Q

After how long does DRESS syndrome occur?

A

2-8 weeks following initiation of drug

346
Q

What very serious derm condition is this?

A

Drug erruption in DRESS syndrome?

347
Q

Systemic involvement in DRESS syndrome?

A

Enlarged lymph nodes in several sites (75%)
Haematological disorders: raised white count (or less often, reduced white count), eosinophilia (in 30% this is > 2.0 x 109/L), atypical lymphocytes, thrombocytopenia, anaemia, haemophagocytic syndrome
Liver enlargement, hepatitis, and rarely hepatic necrosis with liver failure. Abnormal liver function tests are found in most patients
Kidneys are affected in about 10%, and is usually a mild interstitial nephritis. Renal failure is rare.
Inflammation of the heart (myocarditis) or pericarditis causing chest pain, breathlessness, and lowered blood pressure
Lung involvement causes shortness of breath and cough (interstitial pneumonitis, pleuritis, pneumonia and acute respiratory distress syndrome)
Neurological involvement may lead to meningitis and encephalitis, polyneuritis, causing headache, seizures, coma, and palsies
Gastrointestinal symptoms: gastroenteritis, pancreatitis, bleeding and dehydration. In severe cases, acute colitis and pancreatitis can occur, and chronic enteropathy may follow.
Endocrine abnormalities: thyroiditis and diabetes
Myositis
Uveitis.

348
Q

How can DRESS syndrome be life threatening?

A

Causes of death from drug hypersensitivity syndrome include:

Acute liver failure causing coagulation problems, jaundice, and impaired consciousness
Multiorgan failure
Fulminant myocarditis
Haemophagocytosis.

349
Q

Clinical triad used to diagnose DRESS syndrome?

A

High fever
Extensive skin rash
Organ involvement

Supported by deranged LFTs and eosinophilia

350
Q

What will be seen in skin biopsy in DRESS syndrome?

A

Skin biopsy usually shows dense infiltration of inflammatory cells, including lymphocytes and eosinophils, extravasated erythrocytes, and oedema.

351
Q

Investigating DRESS syndrome?

A

Blood count and coagulation studies
Biochemical tests: at least liver function, renal function, muscle enzymes
Viral serology: hepatitis B, C, EBV, CMV, HHV-6
Endocrine function: thyroid, glucose levels
Genetic susceptibility tests.
Urinalysis is undertaken to assess renal damage
Skin biopsy
Cardiac and pulmonary evaluation may include electrocardiograph (ECG), echocardiogram, and chest X-ray. Scans may be performed to evaluate the liver, kidneys, and brain depending on clinical findings and the results of initial tests.

352
Q

Management of DRESS syndrome?

A

Systemic corticosteroids (eg, prednisone) are generally used in the more severe cases of drug hypersensitivity syndrome with significant exfoliative dermatitis, pneumonitis, and/or hepatitis

Supportive management and close monitoring

Ciclosporin?

Additional treatment may include intravenous immunoglobulin, plasmapheresis, and immunomodulatory drugs such as cyclophosphamide, mycophenolate, and rituximab.

Supportive treatment for the skin rash may include:

Dressings
Topical steroids
Emollients
Oral antihistamines.

Abx if secondary infection

353
Q

What should a patient who has recovered from DRESS syndrome be warned about

A

More at risk of developing autoimmune disease
Risk of relapse

354
Q

Cutaneous features of erythema multiforme?

A

Cutaneous lesions develop at the peripheries before spreading centrally.
Distribution is usually symmetrical with a preference for extensor surfaces.
May be painful, pruritic, or swollen.
Early lesions present as round, erythematous papules which later develop into target lesions.
Target lesions consist of three concentric rings of colour variation:
A central, dusky area of epidermal necrosis
Surrounded by a lighter oedematous area
With a peripheral erythematous margin.
Atypical lesions may be present with typical lesions. Atypical lesions are raised with poorly defined borders and/or fewer zones of colour variation.
In severe disease, up to hundreds of lesions may be present in different developmental stages, at times making it difficult to identify characteristic lesions.

355
Q

Prodromal symptoms in erythema multiforme?

A

Many patients report prodromal symptoms including fatigue, malaise, myalgia, or fever. These likely represent the course of precipitating illness rather than true prodrome.

356
Q

Erythema multiforme mucosal features?

A

Lesions develop as blisters, which then break to reveal shallow erosions with a white overlying pseudo-membrane.
Erythema multiforme favours oral membranes, but may also present with urogenital and, rarely, ocular lesions.
Mucous membrane involvement can be painful and significantly limit oral intake; lesions may precede or follow cutaneous lesions.

357
Q

Complications of erythema multiforme?

A

Cutaneous lesions resolve without scarring, though hyperpigmentation may persist for several months.

Ocular involvement can lead to more serious complications including:

Keratitis
Conjunctival scarring
Uveitis
Permanent visual impairment.

358
Q

How long does it take for erythema multiforme to resolve?

A

Symptoms are expected to self-resolve within 4 weeks from onset (or up to 6 weeks in severe disease).

359
Q

Acute generalised exanthematous pustulosis

A

Acute generalised exanthematous pustulosis, or AGEP, is an uncommon pustular drug eruption characterised by superficial pustules.

Over 90% of cases of AGEP are provoked by medications, most often beta-lactam antibiotics (penicillins, cephalosporins and quinolones)

Typically, AGEP starts on the face or in the armpits and groin and then becomes more widespread. It is characterised by the rapid appearance of areas of red skin studded with pinhead-sized sterile pustules. There tends to be more disease in skin folds. Facial swelling often arises.

Oral lesions affect about 20% of patients with AGEP.

The onset of AGEP is usually within 2 days of exposure to the responsible medication.

Can lead to severe systemic symptoms (10%)

360
Q

What is necrotizing fasciitis?

A

Necrotising fasciitis is a life-threatening infection of the subcutaneous soft tissue with secondary tissue necrosis, with spread along the fascial planes but not the underlying muscle.

361
Q

Presentation of necrotising fasciitis?

A

Patients present with rapidly spreading cellulitis and are systemically very unwell - fever, tachycardia.

Blistering and necrotic skin

Severe pain

There is often a history of risk factors i.e. a cutaneous portal of entry for the bacteria (trauma/surgery(abdominal)/co-morbidities(diabetes and malignancy).

On physical examination the affected region will be blistering and erythematous. In early stages mild oedema may be the only sign. There will either be severe pain or anaesthesia over the site of cellulitis. In advanced cases, the skin may be grey, with overlying crepitus (subcutaneous emphysema). The patient is typically pyrexial, tachycardic, tachypnoeic, and hypotensive.

X-ray may show soft tissue gas

362
Q

Most common types of necrotising fascitis?

A

The most common are type 1 (polymicrobial infection with anaerobes) and type 2 (monomicrobial infection with group A streptococci).

363
Q

Management of necrotizing fasciitis?

A

Management is with haemodynamic support, urgent debridement surgery, and broad-spectrum antibiotics. Radiography or CT/MRI can confirm the diagnosis, but should not delay surgery.

364
Q

Emollients: Examples, quanitity, indications, side effects?

A

Examples: Aqueous cream, emulsifying ointment, liquid paraffin and white soft paraffin in equal parts
Quantitiy: 500g per tub
Indications: To rehydrate the skin and re-establish a surface lipid layer.
Useful for dry scaling conditions
Side effects: Reactions may be irritant or allergic

365
Q

How much steroid cream is in a tube typically?

A

30g - enough to cover the whole body once

366
Q

Indication of steroids in dermatology?

A

Allergic and immune reactions, inflammatory skin conditions, bullous and blistering disorders, connective tissue disorders, vasculaitis

Anti inflammatory and anti proliferative effects

367
Q

Side effects of topical steroids?

A

Skin atrophy
Telangiectasia
Striae
Acne or perioral dermatitis
Allergic contact dermititis
May mask, cause or exaccerbate skin infections

368
Q

Side effects of oral corticosteroids?

A

Cushing’s syndrome
Immunosupression
Hypotension
DM
Osteoperosis
Cataract
Steroid induced psychosis

369
Q

Derm indications for oral aciclovir?

A

Viral infections due to herpes simplex and herpes zoster virus

370
Q

Side effects of aciclovir?

A

GI upset
Raised liver enzymes
Reversable neurological reactions
Haematological disorders

371
Q

Classifications of oral anti-histamines and examples of them?

A

Nonsedatives:
Fexofenadine
Cetirizine
Loratadine

Sedative anti-histamines:
Chlorphenamine
Hydroxyzine

372
Q

Indications for anti histamines in derm and mechanism of action?

A

Type 1 hypersentivity reactions and eczema
Block histamine receptors from producing an anti-pruritic effect

373
Q

Side effects of sedative anti-histamines?

A

Antichollenergic effects: dry mouth, blurred vision, urinary retention, constipation

374
Q

Examples of topical antibiotics?

A

Fusidic acid
Mupirocin (Bactroban)
Neomycin

375
Q

When might topical antbiotics be used?

A

Bacterial skin infections
Acne vulgaris

376
Q

Topical abx side effects?

A

Local skin irritation/allergy
Fusidic acid - abx resitance

377
Q

Examples of topical antiseptics (treatment and prevention of skin infection)?

A

Chlorhexidine
Cetrimide
Povidone-iodine

378
Q

What might oral retinoids such as isotretinoin and acitretin be used to treat?

A

Acne
Psoriasis
Disorders of keritisation

379
Q

How long before starting Isotretinoin should effective contraception be practiced?

A

One month

380
Q

For how long after stopping acitretin must a patient not get pregnant (practice effective contraception)

A

Three years

381
Q

Examples of biological therapies used in dermatology?

A

Monocloncal antibodies: Infliximab, adalimumab, ustekinumab
Fusion antibody proteins: Etanercept
Recombinant human cytokines and growth factors (interlukins)

382
Q

Dermatoloigcal conditions in which biologic therapy may be used?

A

Psoriasis
Atopic dermatitis
Hidradenitis suppurativa

383
Q

Side effects of biologics?

A

Local: resness, swelling, brusing at site of injection
Systemic: allergic reaction, antibody formation, flu-like symptoms, infections,, hepaitis, demyelinating disease, HF, blood problems, lymphome, SSC+BCC

384
Q

Erythema nodosum

A

Erythema nodosum is an uncommon skin condition that causes dusky red/blue tender nodules due to inflammation of the underlying subcutaneous tissue. It is most commonly found on the shins and calves and is frequently symmetrical. The image shown demonstrates the typical features of erythema nodosum with poorly demarcated edges and the dusky blue/red colouration. Erythema nodosum has many causes including some infections, malignancies and inflammatory bowel disease. It can also occur in pregnancy, as in this case in this scenario. It is usually self-limiting.

Discrete tender nodules which may become confluent, appear for 1-2 weeks and leave a bruise-like discoloration as they resolve.

Lesions do not ulcerate and resolve without atrophy or scarring

385
Q
A

Erythema nodosum

386
Q

BCC risk factors?

A

UV expoxusre
History of frequent or severe sunburn in child hood
Skin type 1
Increasing age
Male
Previous history of skin cancer
Immunosupression
Genetic predisposition

387
Q

Where does BCC most commonly occur?

A

Head and neck

388
Q

BCC: Prognosis and complications

A

Local tissue invasion and destruction
Depends on tumour sizem site, type, growth pattern, histological sbutype, failure of previous treatment/recurrence and immunosupresison

389
Q

SCC risk factors

A

UV expoxusre
History of frequent or severe sunburn in child hood
Skin type 1
Increasing age
Male
Previous history of skin cancer
Immunosupression
Genetic predisposition
Long standing non healing lesion

390
Q

Prognosis of SCC

A

Depends on the tumor size, site, histological pattern, depth of invasion, perineural involvement and immunosuppression

391
Q

Stage 1 melanoma?

A

T<2mm thick N0 M0

392
Q

Stage 2 melanoma

A

T>2mm thick, N0, M0

393
Q

Stage 3 mallignant melanoma?

A

N>1, M=0

394
Q

Stage 4 mallignant melenoma?

A

M>1

395
Q

What might cause urticaria?

A

Idiopathic,
Food (e.g. nuts, sesame seeds, shellfish, dairy products)
Drugs (e.g. penicillin, contrast media, NSAIDs, morphine, ACEi,
Insect bites,
Contact (latex)
Viral
Parasite
Autoimmune
Heridatry angiodema

396
Q

Pathophysiology of urticaria?

A

Local increase in permeability of capilaries and small venules
A large number of inflammatory mediators (including prostaglandins, leukotrienes, and chemotactic) play a role but histamine derived from skin mast cells appear to be the major mediator
Local mediator release from mast cells can be induced by immunological or non-immunological mechanisms

397
Q

Urticaria vs angiodema vs anaphylaxis?

A

Urticaria: swelling involving the SUPERFICIAL DERMIS, riasing the epidermis (itchy wheals)
Angiodema: deeper swelling involving the dermis and subcutaneous tissue - swelling of tounge and lips
Anaphylaxis: bronchospasam, facial and laryngeal odema, hypotension, may present initially with urticaria and angiodema

398
Q

Management of urticaria?

A

Anithistamines
Corticosteroids for severe acute angiodema

399
Q

Management of angiodema?

A

Corticosteroids

400
Q

Implications of urticaria vs angioedema?

A

Urticaria is normally uncomplicated
Angioedema and anaphylaxis can lead to asphyxia, cardiac arrest and death

401
Q

Infections that can cause erythema nodosum?

A

Group A beta-haemolytic steprococcus
Primary tuberculosis
Chlamydia
Leprosy

402
Q

What distinguishes Stevens-Johnson syndrome from erythema miltiforme?

A

Steven’s Johnson Syndrome is characterized by mucocutaneous necrosis with at least two muscosal sites involved. Extensive necrosis.

403
Q

What is seen on histopathology in SJS?

A

Epitheilial necrosis with few inflammatory cells

404
Q

Histopathology findings in TEN?

A

Full thickness epidermal necrosis with subepidermal detachment

405
Q

What is acute meningococcemia?

A

A serious communicable infection transmitted via respiratory secretions, bacteria get into the circulating blood.

Gram negative doplococcus Neisseria meningitdis is the causative organism.

Presents with features of menigitis, septicemia (hypotension, fever, myalgia) and a typical rash:
Non blanching purpiric rash on the trunk and extermities which may be preceded by a blanching maculopapular rash, and can rapidly progress to ecchymoses, hemorrhagic bullae and tissue necrosis

406
Q

Potential complications of acute meningococcemia?

A

Progression to ecchymoses, hemorrhagic bullae and tissue necrosis
Septicaemic shock
DIC
Multiorganfailure and death

407
Q

Management of acute meningococcaemia?

A

Abx: benzylpenicillin
Prophylatic abx (e.g. rifampicin) for close contacts ideally within 14 days of exposure

408
Q

What is erythroderma, its causes, presentation, management, complications?

A

Exfoliative dermatitis involving at least (90% of the skin surface.
Caused by previous skin disease (e.g. eczema, psoriasis), lymphoma, drugs (e.g. sulphonamides, gold, suphonylureas, penicillin, allopurinol, captopril) and idiopathic
Presents with inflamed skin, edematous and scaly, systemically unwell with lymphadenopathy and malaise
Managed by treating the underlying cause, where known, emollients and wet-wraps to maintain skin moisutre, topical steroids may help to relieve inflammation
Complications can include secondary infection - fluid loss and electrolyte imbalance, hypothermia, high-output cardiac failure, capillary leak syndrome

409
Q

What is kaposi’s varicelliform eruption more commonly known as?

A

Eczema herpeticum

410
Q

Complications of eczema herpeticum?

A

Herpres hepatitis
Encephalitis
Disseminated intrvascular coagulation (DIC)
Death (rarely)

411
Q

What is erysipelas and how is it distinguishable from cellulitis?

A

An acute superfical form or cellulitis and involves ther dermis and UPPER (as opposed to deep) subcutaneous tissue

Well-defined, red raised border
Patients more likely to be systemically unwell

412
Q

Causative organisms in cellulitis and erysipelas?

A

Streptococcus pyogenes and staphylococcus aureus

413
Q
A

erysipelas

414
Q

How does staphylococcal scalded skin syndrome present?

A

Develops within a few hours to a few days, and may be worse over the face, neck, axillae or groins
A scald like skin appearence is followed by a large flaccid bulla
Perioral crusting is typical
There is intraepidermal blistering in this condition
Lesions are very painful
Sometimes the eruption is more localised
Recovery is usally 5-7 days

415
Q

Management of SSSS?

A

Abx (flucloxacillin, erythromycin, or appropriate cephalosporin)
Analgesia

416
Q

Three main groups of fungal skin infection?

A

Dermatophytes (tinea/ringworm)
Yeasts (e.g. candidasis, malassezia)
Moulds (aspergillus)

417
Q

Tinea corporis appearance

A

Tinea infection of the trunk and limbs - itchy, circular or annular lesions with a clearly defined raised and scaly edge is typical

418
Q

Tinea cruris

A

Tinea infection of the groin and natal cleft - very itchy, similar to tinea corporis (itchy circular or anullar lesions with a clearly definied raised and scaley edge)

419
Q

Tinea pedis

A

Atheletes foot - moist scailing and fissuring in the toewebs, spreading to the sole and dorsal aspect of the foot

420
Q

Tinea mannum

A

Tine infection of the hand - scailing and drying in the pamar creases

421
Q

Tinea capitis

A

Scalp ringworm
Patches of broken hair, scailing and inflammation

422
Q

Tinea unguium

A

Infection of the nail - yelow discolouration, thickened and crumbly nail

423
Q

Tinea incognito

A

Inappropriate treatment of tinea infection with topica; or systemic corticosteroids - ill defined and less scaly lesions

424
Q

Candidiasis

A

White plaques on mucosal areas, erythema with satellite lesions in flexures

425
Q

Pityriasis/Tinea versicolor

A

Infection with Malassezia furfur
Scaly pale brown patches on upper trunk that fail to tan on sun exposure
Usually asymptomatic

426
Q

How can fungal infections be diagnoses?

A

Skin scrapings
Hair or nail clippings (dermatophytes)
Skin swabs (yeasts)

427
Q

What is terbinafine cream

A

Topical antifunga

428
Q

When might an oral antifungal agents such as itraconazole be used?

A

Severe, widespread or nail fungal infections

429
Q

Why should topical steorids not be used in fungal infection?

A

Can lead to tinea incognito

430
Q

Predisposing factors to fungal infection

A

Moist environment - incontinence, sweating, not drying skin properly
Immunosupression -steroids, DM,

431
Q

How might eczema patches appear in highly pigmented skin?

A

Grey/brown (as opposed to erythematous)

432
Q

What does chronic scartching in eczema ead to?

A

Lichenification

433
Q

Nail signs in eczema?

A

Pitting and ridging

434
Q

Topical immunomodulators that may be used in eczema?

A

Tacrolimus, pimecrolimus

435
Q

What immunosupressants may be used in severe non-responive cases of eczema?

A

Azathioprine
Ciclosporin
Methotrexate

436
Q

When might acne present with hyperpigmented macules?

A

Inflmmatory lesions may appear this way in highly pigmented skin
May aso signifiy ongoing inflamation

437
Q

Complications of acne vulgaris?

A

Post inflammatory hyperpigmentation, scarring, deformity, psycholoigcal and social effects

438
Q

Precipitating factors to psoriasis?

A

Infection (e.g. tonsilitis)
Trauma (Koebner phenomenom)
Drugs (lithium)
Stress
Alcohol

439
Q

How is bullous phemigoid managed?

A

General measures - wound dressings where required, mointor for signs of infection
Topical therapies for localised disease - topical steroids
Oral therapise for widespread disease = oral steroids, combination of ora tetracycline and nicotinamide, immunosupressive agents (azathioprine, mycophenolate mofetil, methotrexate)

440
Q

How is phemigus vulgaris managed?

A

General measures: wound dressings where required, monitor for signs of infection, good oral care (if oral mucosa involved)
Oral therapies - high dose oral steroids, immunosupressive agents (e.g. methotrexate, azathioprine, cyclophosphamide, mycophenolate mofetil, other)

441
Q

Vitiligo

A

An aquired depigmenting disorder where there is a complete loss of pigment cells (melanocytes)
Thought to have autoimmune aetiology, where the innate immune system causes destruction of loss of melanocytes, leading to loss of pigment formation in the skin
Presentation: any age, single or multiple patches or depigmentation, often symettrical
Common sites are exposed areas such as face hands and feet, as well as body folds and genitalia
Favours sites of injury - Koebner phenomenon
Mx: Minimise skin injury, topical treatments such as steroids and calcineurin inhibitors, phototherapy such as UVB therapy, oral immunosupressants such as methotrexate, ciclosporin, mycophenolate mofetil

442
Q

Melasma

A

An aquired chornic skin disorder where there is increased pigmentation in the skin
Thought to be due to genetic predisposition and triggered by factors such as sun exposure, hormonal changes such as pregnancy and contraceptive pills
The pigmnetation is caused by and overproduction of pigment (melanin) by pigment cells (melanocytes)
Presents with brown macules (freckle like spots) or larger patches with an irregular border
Symettrical distribution
Common sites include forhead cutaneous upper lips and cheeks
Mx: Lifelong sun protection, discontinuation of hormonal OCP, cosmetic camouflage, topical treatments that aim at inhibiting the formation of new melanin such as hydroquinone, azelaic acid, kojic acid, vit C

443
Q

Venous ulcers

A

Often painful, worse on standing
History of venous disease (varicose veins, DVT)
Typically occur in the malleolar area (more common over the medial than lateral malleolus)
Lesions are large, shallow, irregular ulcers with exudative and granulating bases
Associated features include warm skin, normal peripheral pulses, leg oedema, haemosiderin and melanin deposition (brown pigment), lipodermatoclerosis, and atrophie blanche (white scarring with dilated capillaries)
ABPI withh be normal 0.8-1

444
Q

What type of ulcer is this and what features suggest it?

A

VENOUS

-Malleolar areas
- Large
- Shallow
- Irregular
- Exudative and granulating base
- Surrounding hyperpigmentation (haemosiderin and melanin deposition)
- Skin appears hard surrounding (lipodermatosclerosis)
- White scarring with dilated capilaries (atrophie blanch)

445
Q

Arterial ulcer

A

Painful ulcers (especially at night, worse when legs elevated)
History of arterial disease (atheroslerosis)
Occur at pressure and trauma sites, e.g. pretibial, supramalleolar and at distal points.
Small, sharply definied deep ulcers, with necrotic base
Cold skin, weak or absent peripheral pulses, shiny pail skin, loss of hair
ABPI<0.8
Dopple studies and angigraphy may be performed
Managed by vascular reconstruction - COMPRESSION BANDAGING IS CONTRAINDICATED

446
Q

What type of ulcer is this and which features suggest that?

A

ARTERIAL
At pressure area, distal point
Relatively small
Sharply defined
Deep
Partially necrotic base
Shiny pale skin surrounding
Hair loss surrounding

447
Q

Neuropathic ulcer

A

Often painless, abnormal sensation, history of diabetic or neurological disease
Occur at pressure sites such as soles, heels, toes, metatarsal heads, scaram
Variable in size and depth
Have a granulating base
May be surrounded by a hyper keratotic lesion (callus)
ABPI<0.8 implies a neuroischaemic ulcer
X-ray to exclude osteomyelitis
Wound debridement, regular repositioning to manage

448
Q

What type of ulcer is this and what features suggest this?

A

NEUROPATHIC ULCER
Occuring at a pressure site
Granulating base
Surrounded by hyperkeratotic lesion (e.g. callus)

449
Q

What is meant by lichen nitidus pattern?

A

Lichen nitidus is an uncommon inflammatory skin condition that usually presents with tiny skin-coloured bumps
Can be the pattern which eczema presents in darker skin

450
Q

How might acute eczema differ from more chronic eczema?

A

Vesicular and exudative

451
Q

Possible investigations in eczema?

A

Patch testing
Serum IgE levels
Skin swab

452
Q

How might scabbies be investigated?

A

Skin scrabe, extraction of mite and view under microscope

453
Q

Associated features of scabies?

A

Secondary eczema and impetigo

454
Q

Common sites of occurence in lichen planus?

A

Forarms, wrist and legs
May occur on oral mucosa (always examine)

455
Q

What is lichen planus?

A

Lichen planus (LP) is a chronic inflammatory condition affecting the skin and mucosal surfaces. There are several clinical types:

Cutaneous lichen planus
Mucosal lichen planus
Lichen planopilaris (scalp)
Lichen planus of the nails
Lichen planus pigmentosus
Lichenoid drug eruption.

456
Q

How do lichen planus lesions appear?

A

Violaceous *Iliac) flat-topped paules or hyperpigmented papules (in darker skin)
Symmetrical distrubtion - Note that lichen planus in darker skin types has a typical purplish tinge

457
Q

Associated features - lichen planus?

A

Nail changes and hair loss
Lacy white streaks on the oral mucosa and skin lesions (Wickham’s striae)

458
Q

How might lichen planus be managed?

A

Corticosteroids
Antihistamines

459
Q

Examples of changing pigmented lesions:

A

Benign: Melanocytic naevi, sebhorric wart
Mallignant: Malignant melanoma

460
Q

How does the location of mallignant melenoma tend to differ in women and men?

A

Women: legs
Men: trunk

461
Q

Seborrheic warts

A

Warty greasy papules or nodules
Stick on appearence with well definied edges
Commonly occur on the face ad trunk in middle aged or elderly patients
Often multiple, asymptomatic, may be managed if symptomatic with:
Curette and caturey, cryotherapy

462
Q

What is this lesion?

A

Sebhorric wart

463
Q

How might melanocytic naevi be managed?

A

Usually asymptomatic, but if not:
May be shaved or completely excised

464
Q

What might cause a purpuric eruption?

A

Meningococcal septicemia
DIC
Vasculitis
Senile purpura

465
Q

What are senile purpura?

A

Non-palpable purpura with surrounding atrophic thin skin, occuring on the extensor surfaces of hands and forarms in the elderly population (with sun damaged skin)
Such skin is easily traumatised
Patients are systemically well
Bloods, urinalysis, skin biopsy may be undertaken
No treatment is needed

466
Q

Vasculitis (in context of derm)

A

Painful lesions
Dependent areas (e.g. legs, buttocks, flanks)
Palpable purpura (often painful)
Systemic illness
Bloods and urinalysis, skin biopsy, may be performed
Requires treatment of underlying cause (not skin lesions) such as steroids and immunosuppressants if there is skin involvement

467
Q

Disseminated intravascular coagulation (derm context)

A

History: trauma, malignancy, sepsis, obstertic complications, transfusions, or liver failure
Common sites: Spontaneous bleeding from the ear, nose and throat, GI tract, respiratory tract and wound site
Lesion: Petechiae, ecchymoses, haemorragic, bullae and/or tissue necrosis
Associated features; Systemically unwell
Management: Treat underlying cause, transfuse for coagulation deficiencies, anticoagulants for thrombosis

468
Q

Causes of a red swollen leg?

A

Cellulitis/erysipelas
Venous thrombosis
Chronic venous insufficiency

469
Q

When might an ASOT (anti-streptococcal O titre) be appropriate in dermatology?

A

Patients with suspected erysipelas/cellulitis

470
Q

Venous thrombosis (derm context)

A

Cause of red swollen leg
History: pain, swelling, redness, prolonged bed res/longhaul flight/clotting tendancy may preceed symtpoms
Lesion: Complete venous occlusion may lead to cyantoic discolouration
Associated features: Systemically unwell, PE
Possible investigations: D-dimer, Doppler ulrasound and/or venography

471
Q

Chronic venous insufficiency (derm context)

A

History: heaviness or aching of leg, which is worse on standing an relieved by walking, history of venous thrombosis
Lesion: discloured (blue-purple), odeama which improves in mornings, venous congestion and varicose veins
Associated features: Liodermatosclerosis (erythematous induratuion, creating champagne bottle’ appearance, stasis dermatitis (eczema with inflammatory papules, scaly, crusted erosions), haemosiderin deposition, venous ulcer
Possible investigations: Doppler USS and/or venography
Management: Leg elevation and compression stockings, sclerotherapy or surgery for varicose viens

472
Q

How long does it take for topical acne treatments to start working?

A
473
Q

Important risk factors of tetracyclines (common oral abx acne treatment)?

A

IIHH - warn about new severe headaches
Increased sun sensitivity - emphasise the importance of sun cream
Hives

474
Q

ECZEMA MANAGEMENT

A

Moisturisers – cetraben , epaderm, zeroderm etc ​

Soap substitutes – epaderm, hydromol , dermol 500 lotion ​

Topical Steroid – Hydrocortisone (mild) Eumovate - clobetasone (Moderate)​

Betnovate (betamethasone 0.1%) (potent) Dermovate –clobetasol (superpotent)​

Calcineurin inhibitors –steroid sparing agents. Tacrolimus oint 0.05 & 0.1% and Pimicrolimus cream (Elidel)​

Oral immunosuppressants – oral steroids , methotrexate, ciclosporin​

Phototherapy ​- UV treatment

Biologics – injectable and oral

475
Q

What immunosupressent may be used to manage whole body eczema?

A

Methotrexate

476
Q

NICE: psoriasis management first line

A

Offer a potent corticosteroid applied once daily plus vitamin D or a vitamin D analogue applied once daily (applied separately, 1 in the morning and the other in the evening) for up to 4 weeks as initial treatment for adults with trunk or limb psoriasis.

477
Q

NICE guidence on use of phototherpay to treat psoriasis?

A

Offer narrowband ultraviolet B (UVB) phototherapy to people with plaque or guttate-pattern psoriasis that cannot be controlled with topical treatments alone. Treatment with narrowband UVB phototherapy can be given 3 or 2 times a week depending on patient preference. Tell people receiving narrowband UVB that a response may be achieved more quickly with treatment 3 times a week.

478
Q

When should, according to NICE, systemic therapy be offered for psoriasis?

A

Offer systemic non-biological therapy to people with any type of psoriasis if:

it cannot be controlled with topical therapy and

it has a significant impact on physical, psychological or social wellbeing and

1 or more of the following apply:

psoriasis is extensive (for example, more than 10% of body surface area affected or a Psoriasis Area and Severity Index (PASI) score of more than 10) or

psoriasis is localised and associated with significant functional impairment and/or high levels of distress (for example, severe nail disease or involvement at high-impact sites) or

phototherapy has been ineffective, cannot be used or has resulted in rapid relapse (rapid relapse is defined as greater than 50% of baseline disease severity within 3 months).

479
Q

What is the first line systemic treatment for psoriasis?

A

Methotrexate

480
Q

Classification of the severity of eczema?

A

Clear — if there is normal skin and no evidence of active eczema.
Mild — if there are areas of dry skin, and infrequent itching (with or without small areas of redness)
Moderate — if there are areas of dry skin, frequent itching, and redness (with or without excoriation and localized skin thickening).
Severe — if there are widespread areas of dry skin, incessant itching, and redness
Infected — if eczema is weeping, crusted, or there are pustules, with fever or malaise.

481
Q

How to assess QOL in terms of dermatological conditions?

A

None — no impact on quality of life.
Mild — little impact on everyday activities, sleep, and psychosocial well-being.
Moderate — moderate impact on everyday activities and psychosocial well-being, and frequently disturbed sleep.
Severe — severe limitation of everyday activities and psychosocial functioning, and loss of sleep every night.

482
Q

Management of mile eczema?

A
483
Q

Management of mild eczema (areas of dry skin, and infrequent itching (with or without small areas of redness))

A

Prescribe generous amounts of emollients, and advise frequent and liberal use.

Consider prescribing a mild topical corticosteroid (such as hydrocortisone 1%) for areas of red skin. Treatment should be continued for 48 hours after the flare has been controlled.

484
Q

Management of moderate eczema (if there are areas of dry skin, frequent itching, and redness (with or without excoriation and localized skin thickening)?

A

Prescribe a generous amount of emollients, and advise frequent and liberal use (more than usual).

If the skin is inflamed, prescribe a moderately potent topical corticosteroid (for example betamethasone valerate 0.025% or clobetasone butyrate 0.05%) to be used on inflamed areas. Treatment should be continued for 48 hours after the flare has been controlled.

For delicate areas of skin (such as the face and flexures), consider starting with a mild potency topical corticosteroid (such as hydrocortisone 1%) and increase to a moderate potency corticosteroid only if necessary. Aim for a maximum of 5 days’ use.

Occlusive dressings or dry bandages may be of benefit; however, treatment should only be started by a healthcare professional trained in their use (otherwise consider referral).

If there is severe itch or urticaria, consider prescribing a one-month trial of a non-sedating antihistamine (such as cetirizine, loratadine, or fexofenadine).

If there are areas of infected skin, antibiotics may be required

Consider prescribing a maintenance regimen:

1)of topical corticosteroids to control areas of skin prone to frequent flares (not recommended for the face, genitals, or axillae). Options include a ‘step down approach’ or ‘intermittent treatment’.

2)Topical calcineurin inhibitors (tacrolimus and pimecrolimus) are a second-line option. However, they should only be prescribed by a specialist (including GPs with a specialist interest in dermatology).

485
Q

NICE management of severe eczema (weeping, crusted, or there are pustules, with fever or malaise)

A

Prescribe a generous amount of emollients and advise frequent and liberal use (more than usual).

If the skin is inflamed, prescribe a potent topical corticosteroid (for example betamethasone valerate 0.1%) to be used on inflamed areas.

For delicate areas of skin such as the face and flexures, use a moderate potency corticosteroid (such as betamethasone valerate 0.025% or clobetasone butyrate 0.05%). Aim for a maximum of 5 days’ use.

Do not use potent corticosteroids in children under 12 months old, or very potent corticosteroids in children of any age, without specialist dermatological advice.

Occlusive dressings or dry bandages may be of benefit; however, treatment should only be started by a healthcare professional trained in their use (otherwise consider referral).

If there is severe itch or urticaria, consider prescribing a one-month trial of a non-sedating antihistamine (such as cetirizine, loratadine, or fexofenadine).

If itching is severe and affecting sleep, consider prescribing a short course (maximum of two weeks) of a sedating antihistamine (such as chlorphenamine).

If there is severe, extensive eczema causing psychological distress, consider prescribing a short course of an oral corticosteroid (refer children under 16 years of age). There are no data from controlled trials, but 30 mg prednisolone taken in the morning for 1 week should be sufficient.

If there are signs of infection, abx may be required.

Consider prescribing a maintenance regimen:
1) Topical corticosteroids to control areas of skin prone to frequent flares (not recommended for the face, genitals, or axillae). Options include a ‘step down approach’ or ‘intermittent treatment’.
2) Topical calcineurin inhibitors (tacrolimus and pimecrolimus) are a second-line option. However, they should only be prescribed by a specialist (including GPs with a specialist interest in dermatology).

486
Q

Acne first line management according to NICE

A

ANY SEVERITY: Fixed combination of topical adapalene with topical benzoyl peroxide, applied once daily in the evening
Fixed combination of topical tretinoin with topical clindamycin, applied once daily in the evening

MILD TO MODERATE:
Fixed combination of topical benzoyl peroxide with topical clindamycin, applied once daily in the evening

MODERATE TO SEVERE:
Fixed combination of topical adapalene with topical benzoyl peroxide, applied once daily in the evening, plus either oral lymecycline or oral doxycycline taken once daily
Topical azelaic acid applied twice daily, plus either oral lymecycline or oral doxycycline taken once daily

487
Q

After how long should second line options be considered to treat acne and what should be done?(NICE)

A

If acne fails to respond adequately to a 12‑week course of a first-line treatment option and at review the severity is:

mild to moderate: offer another option from the table of treatment choices (see table 1)

moderate to severe, and the treatment did not include an oral antibiotic: offer another option which includes an oral antibiotic from the table of treatment choices (see table 1)

moderate to severe, and the treatment included an oral antibiotic: consider referral to a consultant dermatologist-led team.

488
Q

KELOID SCARS

A

Overgrowth of scar tissue which tends to be larger than the original wound itself
Thought to be due to overproduction of the collagen during wound healing after: minor injuries, insect bites, skin surgery, acne spots in generically predispostiioned individuals
More common in darker skin types
Presents as firm, smooth hard nodule which may be itchy and/or painful
Topical treatments such as steroids and silocone gel can potentially flatten the scar and improve symptoms - intralesional steroid injection if not effective, surgery as last resort as may result in largery keloid scar

489
Q

In which patients with eczema would specific serum IgE tests or pin prick testing be useful?

A

Patients with eczema thats difficult to control, especially children

490
Q

Advice for baths/showers in eczema flares?

A

Avoid soaps
Avoid using only water
Utilise moisturisers as a soap substitute

491
Q

How should patients be advised to apply emmolients?

A

Gently
Generously
2-4 times a day
On entire skin surface

492
Q

Why can eczema be worse in winter?

A

Low humidity in the winter can exacerbate skin dryness and then the eczema is more likely to flare

493
Q

Describe what is typically seen in drug erruption

A

Widespread erythematous macules and papules which are confluent in many areas, symetrical

494
Q

What infections may appear similar to a drug erruption?

A

Measels
Rubella
EBV
HIV

495
Q

Timing of maculopapular drug erruption?

A

New drug: 1-3 weeks
A drug that has been given before: 1-3 days

496
Q

What drugs should beused with caution in strep throat and why?

A

Ampicillin/amoxicillin - as is infectious mononucleosis (similar presentation) rather than strep, a serious reaction may occur - ie. maculopapular drug erruption

497
Q

What should a patient be advised following a drug reaction?

A

Avid drug and drugs of same class
Make sure allergy is recorded in pts notes and inform GP
Encourage pt to inform NOK
Re-exposure may result in a more severe reaction
Consider medic alert bracelet if severe cutaneous reaction

498
Q

Pityriasis rosea vs pityriasis vesicolor - affect of sunlight?

A

PR unaffected PV worse

499
Q

Conditions that may improve in sunlight?

A

Guttate psoriasis
Acne

500
Q

Examination of pityriasis versicolor in a dark room with Wood’s light (UV A)

A

Yellow green flouresence demonstrated not seen in other conditions

501
Q

Fungal scraping of pityriasis versicolor on microscopy?

A

Fungal hyphae and spores in a distinctive ‘spaghetti and meatball’ appearence

502
Q

Management of pityriasis versicolour?

A

Selenium sulfid shampoo or ketoconazole shampoo applied to SKIN and left on for 10 minuites in affected area before showering off

Topical azole creams including clotrimazole, miconazole, econazole and ketoconazole or terbinafine
These should be applied to the affected areas in the evening and may require several weeks of treatment

Pigmentary changes can take months to return to normal after sucsessful treatment

503
Q

What can exaccerbate pityriasis versicolor?

A

Sweating and humidity

504
Q

What is granuloma annulare?

A

Erythematous annular ring with a slightly depressed centre
Asymptomatic
Can be differntiated from ringworm with biopsy if unsure, although lack of itchiness and scales gives a clue
Usually resolves on its own, if causing distress can use potent of very potent corticosteroid or even cryotherapy

505
Q

How long might topical corticosteroid cream be required to treat a severe eczema flare?

A

2-3 weeks, followed by shorter bursts

506
Q

What topical therapies may be used in impetigo?

A

Mupirocin
Fusidic acid

507
Q

After what time period does the risk of staph aureus becoming resistant to fusidic acid particulalry increase?

A

2 weeks

508
Q

Why might a family have recurrent cases of impetigo occuring?

A

Nasal carriage of SA is common and may not be irradicated by oral or topical treatment of lesions - may require erradicatoon using antibacterial nasal ointments (usually mupirocin) and antiseptic skinwashes

509
Q

Advice for patients suffering from contact dermititis?

A

Protect hands with gloves where possible (caution in latex/rubber)
Avoid direct contact with irritating chemicals (e.g. detergents, soaps, but also foods such as citrus fruits, potato, onion, etc.)
Regular use of emmolients.
Potentially topical steroids for flares

510
Q

What can happen if patients with occupation dermatitis do not make changes?

A

Can develop an intractable hand dermititis

511
Q

\What other skin condition often occurs alongside venous ulcers?

A

Stasis eczema

512
Q

What type of common rash can come and go during a period of hours?

A

Urticarial rashes

513
Q

Testing in patients with acute urticaria (chronic- over 6 weeks - tends to be futile)

A

Total IgE + IgE to specific suspected allergens
Pinprick testing for allergies

514
Q

If an urticurial rash last for longer than 48 hours and fades to leave a bruise what does this indicate may be occuring?

A

Urticarial vasculitis

515
Q

AI conditions associated with unusual urticaria?

A

COeliac diease
SLE
Thyroid disease
Urticarial vasculitis

516
Q

Pruritis

A

Itching without rash to account for it, does not respond to use of emmolients
Can be drug induce, endocrine related (thyroid, DM), metabolic (kidney and liver failure), or haematological (lymphoma, iron def aneamia, polycythemia )

517
Q

When should a topical coal preparation be offered in psoriasis

A

A topical coal tar preparation is recommended if no improvement is seen within 8-12 weeks of using the topical corticosteroid and topical vitamin D preparation.

518
Q

When should a topical tar preparation be offered in psoriasis?

A

A topical coal tar preparation is recommended if no improvement is seen within 8-12 weeks of using the topical corticosteroid and topical vitamin D preparation.

519
Q

What can be used to prevent sebhorric dermatitis ?

A

. Ketoconazole 2% shampoo can be applied to the skin every 1-2 weeks to prevent seborrheic dermatitis. The patient should be advised to leave the preparation on for 3-5 minutes before rinsing.

520
Q

What is recognised by NICE to be the gold standard test when diagnosing contact dermatitis in certain circumstances (e.g. when there is no obvious cause for the dermatitis or it is resistant to corticosteroids).

A

Skin patch testing is recognised by NICE to be the gold standard test when diagnosing contact dermatitis in certain circumstances (e.g. when there is no obvious cause for the dermatitis or it is resistant to corticosteroids).

521
Q

Pattern of hair loss in patchy alopeca areta

A

Sudden hair loss in a patchy distribution
Enlargement of patches
Hair regrowth.

522
Q

When might skin lesion culture be warranted in acne vulgaris and why

A

Usually in cases of acne vulgaris, a simple visual inspection is usually enough to make the diagnosis. However, skin lesion culture may be warranted in patients who do not respond to escalating treatment, to exclude Gram-negative folliculitis.

523
Q

What will be seen on histology in eczema

A

This disruption of the skin barrier can result in spongiosis being seen histologically; this refers to the abnormal accumulation of fluid within the epidermis, resulting in increasing space between adjacent squamous cells.

524
Q

In what condition may colloid bodies be seen on histology

A

Colloid bodies may be seen histologically in the setting of lichen planus; a common skin condition that can give pruritic, raised, violaceous lesions, most commonly over the wrists or trunk.

525
Q

What may be seen on biopsy of SCC

A

Keratinisation refers to the production of keratin, most commonly carried out by squamous cells. An excessive level of keratinisation may be seen on biopsy in the setting of squamous cell carcinoma.

526
Q

With the use of topical corticosteroids regular review is required, after how long?

A

With the use of topical corticosteroids regular review is required, usually at around 3 months, and a step-down management plan put in place to manage symptoms

527
Q

Eczema plaques are typically poorly demarkated except when?

A

In discoid type eczema

528
Q

What questionaires can be used to assess the management of a patients dermatological condition?

A

DLQI
PASI

529
Q

Treatment to consider for extensive or severe psoriasis?

A

Phototherapy (UVB or PUVA)
Systemic retinoids (Acitretin)
Methotrexate
Ciclosporin
Dimethyl fumarate
Biological agents

530
Q

How should patients with scabies use Permethrin 5% dermal cream?

A

Used twice with applications a week apart
Treat whole body from chin downwards including web spaces of toes and fingers
In children aged up to 2 years and in elderly and immunocompromised people application should be extended to the scalp, neck, face and ears

531
Q

What is the pathognomic sign in scabies?

A

Burrow: a short, wavy, scaly grey line on the skin surface
These can easily be missed if the skin has been scratched, has become secondarily infected or if eczema is also present

532
Q

What dermatological condition may cause rhinophyma?

A

Rosacea may cause rhinophyma (enlarged, swollen nose), swoleen forehead, eyelides, earlobes and chin as a result of sebaceous gland hyperplasia.
This is more commonly observed in men

533
Q

How might rosacea affect a patients eyes?

A

May cause blephritis, conjuncitvitis,episcleritis and sebaceous gland hyperplasia leading to swollen eyelids.

534
Q

What is tacrolimus ointment? When is it advised patients do not use it?

A

Immunosupressive drug, used as topical second line preperation in the treatment of eczema affecting the face and neck

Patients should stop using it if they develop a coldsore as it increases the risk of eczema herpeticum

535
Q

Potential complications of BCC exicsion?

A

Bruising, swelling, minor bleeding, black-eye post-op (if lesion near eye)
Minor discomfort
Scar - contraction may cause local problems - ie. ectropian if below eyelid leading to watery eye
Wound infection
Numbeness around scar
Incomplete surgical removal causing a local recurrence

536
Q

During what times is sun exposure most hazerdous?

A

Between 11am and 3PM

537
Q

What diagnostic finding of bullous phlemigoid would be seen on direct immunoflouresnce of a biopsied lesion?

A

IgG antibodies along the basement membrane zone (dermo-epidermal junction)

538
Q

Management of bullous phlemigoid?

A

Non-adherent dressings to any eroded skin which has been caused by burst blisters
Deflate large intact blisteres with a sterile needles
Topical very potent corticosteroids
Systemic corticosteroids (mainstay of treatment)
Oral doxycline can be used for anti-inflammatory effects
Other immunosupressants may be required as steroid sparing agents

539
Q

Potential side effects of systemic corticosteroids?

A

Peptic ulceration
DM
HTN
Weight gain
Fat redistribution (moon facies and buffalo hump)
Osteoperosis
Skin atrophy and fragility leading to easy burising and tearing
Striae
Cataracts
Increased risk of infection
Proximal myopathy
Growth suppression in children
Mood changes

540
Q

Dermatological conditions that commonly produce nail changes?

A

Psoriasis
Lichen planus
Eczema
Alopecia areta

541
Q

What does a the mouth presence of Wickham’s striae suggest

A

Lichen planus

542
Q

What nail changes might be seen in association with alopecia areata?

A

Most common change is pitting, other changes include brittle nails with vertical ridging and splitting, onycholysis

543
Q

What sites have the highest rate of recurrence of SCC?

A

Lips, ears

544
Q

Most cases of guttate psoriasis resolve within 6 months, what can be trialled if it persists?

A

Photophobia

545
Q

Nail changes in Lichen planus

A

Lichen plans. The inflammatory process
can sometimes lead to fusion between
the nail fold and underlying nail bed and
matrix (pterygium). Lichen plans of the
skin typically presents as itchy shiny
violaceous flat-topped plaques. Lichen
plans can also affect mucous
membranes

546
Q

Management of nail disease in lichen planus

A

Potent topical steroids rubbed into the
nail fold in active disease
Triamcinolone injection into the proximal
nail fold could be considered but can be
very painful even under local
anaesthesia.
Prednisolone or ciclosporin for severe
scarring disease as this can result in
permanent nail loss or dystrophy.

547
Q

Dermatofibroma

A

A Well circumscribed pink nodule with peripheral pigmentation with smooth surface with lack of scaling suggesting a dermal lesion.
The lesion will be firm on palpation and when gently pressed on the lateral edges will demonstrate central dimpling

This is a benign lesion with no malignant potential. Treatment is therefore not routinely required. On occasions lesions may become itchy, tender or bleed if traumatised (e.g. by shaving). Excision under local anaesthetic can be considered.

548
Q

Plantar pustulosis

A

Plantar pustulosis. There is usually involvement of the palms too, and this disorder is generally known as palmoplantar pustulosis or palmoplantar pustular psoriasis.
The presence of pustules should always prompt consideration of infection, particularly by Staphylococcus aureus or (here) dermatophyte infection (Trichophyton species) causing tinea pedis. If in doubt, burst a pustule with a sterile needle and take a swab of pus for bacteriological investigation or take a skin scraping for mycology.
In this case, the presence of multiple 2-5mm pustules, which evolve to leave brown macules on red, scaly palms and soles is typical of
palmoplantar psoriasis. These pustules are sterile. This condition may occur in isolation, or there may be psoriasis

549
Q

How can extensive persisten extensive alopecia areata?

A

Extensive alopecia areata that persists
for longer than 6 months can be treated
with diphencyprone topical
immunotherapy, though efficacy is
limited.

550
Q

Fungal nail treatment?

A

typically terbinafine for 6 weeks for fingernails and 12 weeks for toenails

551
Q

What antibodies ar associated with dermatomyositis

A

Anti-Jo1 antibodies would be detected

552
Q

Pathophysiology of venous ulcer formation

A

Oedema in the subcutaneous tissue with poor lymphatic and capillary drainage, leading to inadequate nutrients and oxygen reaching the skin. This causes skin to die and ulcers to arise.

552
Q

Pathophysiology of venous ulcer formation

A

Oedema in the subcutaneous tissue with poor lymphatic and capillary drainage, leading to inadequate nutrients and oxygen reaching the skin. This causes skin to die and ulcers to arise.

552
Q

Pathophysiology of venous ulcer formation

A

Oedema in the subcutaneous tissue with poor lymphatic and capillary drainage, leading to inadequate nutrients and oxygen reaching the skin. This causes skin to die and ulcers to arise.

553
Q

Complete correction of visual acuity with a pinhole means that the cause of the patients blurred vision is due to what and who should these patients be reffered to?

A

Refractive error

Optometrist

554
Q

What is lagopthalmos

A

Lagophthalmos is the inability to fully close the eyelids, secondary to the proptosis

555
Q

What is Henoch Scholein Purpura

A

Henoch-Schonlein purpura is a vasculitic disorder that results in a purpuric rash, abdominal pain and arthralgia

556
Q

Ciclosporin is used commonly to manage psoriasis, what are its side effects?

A

The side effects of ciclosporin can be remembered by the 5 H’s: hypertrophy of the gums, hypertrichosis, hypertension, hyperkalaemia and hyperglycaemia

557
Q

What is bullous pemphigoid

A

Bullous pemphigoid occurs more commonly in the elderly and is characterised by numerous tense bullae which may be preceded by a pruritic urticarial eruption. IgG autoantibodies bind to bullous pemphigoid antigens in the hemidesmosomes at the basement membrane zone. The disease is self-limiting in many cases and usually treated with low dose steroids.

558
Q

What is this and when is it seen?

A

Typical palpable purpura of Henoch Schönlein Purpura

Henoch-Schonlein Purpura
Henoch-Schonlein purpura (HSP) is a small vessel vasculitis that usually affects children.

It is an IgA mediated disease that is thought to be triggered by a viral upper respiratory tract infection.

HSP usually presents with a classical triad of purpura over the extensor surfaces of the lower limb, abdominal pain and arthritis. Renal involvement is often present- usually haematuria, proteinuria, nephritic syndrome or nephrotic syndrome. In young children, intussusception may also occur.

559
Q

What is hidradenitis suppurativa

A

Hidradenitis suppurativa is a chronic, painful, inflammatory skin disorder is characterized by nodules, pustules, sinus tracts, and scars in intertriginous areas

560
Q

Blisters/Bullae

A

no mucosal involvement (in exams at least*): bullous pemphigoid
mucosal involvement: pemphigus vulgaris

561
Q

Hirsutism vs hypertrichosis

A

Hirsutism is androgen dependent
Hypertrichosis androgen independent

562
Q

Most common causative fungal species in nail infections and what treatment

A

Trichophyton rubrum

For Trichophyton rubrum infection, NICE guidelines say that the first line oral treatment should be oral terbinafine. Before commencing terbinafine, it is important to check liver function before and at regular intervals as it can cause hepatotoxicity.

563
Q

What is used to treat headlice?

A

Malathion

564
Q

Symptomatic dermatophyte nail infections should be treated how?

A

with oral terbinafine, if there are no contraindications.

565
Q

Spider naevi vs telangiectasia

A

Spider naevi can be differentiated from telangiectasia by pressing on them and watching them fill. Spider naevi fill from the centre, telangiectasia from the edge

566
Q

According to the current NICE guidance, the first-line treatment for a flare of plaque psoriasis affecting extensors is what?

A

A potent topical corticosteroid plus a topical vitamin D preparation (both applied once a day, but at different times of day).

567
Q

When does impetigo occur?

A

Impetigo occurs when bacteria enter via a break in the skin. This may be in otherwise healthy skin or may be related to eczema or dermatitis.

568
Q

What is non bullous impetigo?

A

Non-bullous impetigo typically occurs around the nose or mouth.

The exudate from the lesions dries to form a “golden crust”.

They are often unsightly but do not usually cause systemic symptoms or make the person unwell.

569
Q

Management of non-bullous impetigo?

A

Topical fusidic acid can be used to treat localised non-bullous impetigo. Draft NICE guidelines from August 2019 suggest using antiseptic cream (hydrogen peroxide 1% cream) first line rather than antibiotics for localised non-bullous impetigo.

Oral flucloxacillin is used to treat more wide spread or severe impetigo. Flucloxacillin is the antibiotic of choice for staphylococcal infections.

Advise about measure to avoid spreading the impetigo. Patients should be given advice about not touching or scratching the lesions, hand hygiene and avoiding sharing face towels and cutlery. They need to be off school until all the lesions have healed or they have been treated with antibiotics for at least 48 hours.

570
Q

What is bullous impetigo and how does it differ from non-bullous impetigo?

A

Bullous impetigo is always caused by the staphylococcus aureus bacteria. These bacteria can produce epidermolytic toxins that break down the proteins that hold skin cells together. This causes 1 – 2 cm fluid filled vesicles to form on the skin. These vesicles grow in size and then burst, forming a “golden crust”. Eventually they heal without scarring. These lesions can be painful and itchy.

This type of impetigo is more common in neonates and children under 2 years, however it can occur in older children and adults. It is more common for patients to have systemic symptoms. They may be feverish and generally unwell. In severe infections when the lesions are widespread, it is called staphylococcus scalded skin syndrome.

The condition is very contagious and patients should be isolated where possible.

571
Q

Treatment of non-bullous impetigo?

A

Treatment of bullous impetigo is with antibiotics, usually flucloxacillin. This may be given orally or intravenously if they are very unwell or at risk of complications

572
Q

How might you investigate bullous impetigo?

A

Swabs of the vesicles can confirm the diagnosis, bacteria and antibiotic sensitivities.

573
Q

Impetigo usually responds well to treatment without any long term adverse effects. Rarely there can be complications, such as what?

A

Cellulitis if the infection gets deeper in the skin
Sepsis
Scarring
Post streptococcal glomerulonephritis
Staphylococcus scalded skin syndrome
Scarlet fever

574
Q

Aim for what duration of break in between courses of topical corticosteroids in patients with psoriasis

A

Aim for a 4 week break in between courses of topical corticosteroids in patients with psoriasis

575
Q

Bowens disease on biopsy

A

‘windblown’ appearance of the keratinocytes and the presence of Pagetoid cells.

576
Q

Keloid scars are most common on where?

A

Keloid scars are most common on the sternum