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General practice > Derm > Flashcards

Derm Flashcards

1
Q

What is impetigo

A

Superficial bacterial skin infection usually caused by either Staphylcoccus aureus or Streptococcus pyogenes

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2
Q

Who is impetigo common in

A

common in children, particularly during warm weather

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3
Q

Where do impetigo lesions tend to occur

A

The infection can develop anywhere on the body but lesions tend to occur on the face, flexures and limbs not covered by clothing.

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4
Q

How is impetigo spread

A

Spread is by direct contact with discharges from the scabs of an infected person.

The bacteria invade the skin through minor abrasions and then spread to other sites by scratching.

Infection is spread mainly by the hands, but indirect spread via toys, clothing, equipment and the environment may occur.

The incubation period is between 4 to 10 days.

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5
Q

Appearance of impetigo

A

‘golden’, crusted skin lesions typically found around the mouth

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6
Q

Mx of limited localised impetigo

A

Hydrogen peroxide 1% cream

Topical antibiotic creams(fusidic acid)

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7
Q

What should be used in localised impetigo if there is resistance to fusidic acid

A

Topical mupirocin

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8
Q

Mx of extensive impetigo

A

Oral flucloxacillin

Oral erythromycin if penicillin-allergic

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9
Q

Advice regarding school exclusion for patients with impetigo

A

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

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10
Q

Areas typically affected by rosacea

A

Nose, cheeks and forehead

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11
Q

Appearance of rosacea

A

Flushing is often first symptom

Telangiectasia are common

Later develops into persistent erythema with papules and pustules

rhinophyma

ocular involvement: blepharitis

sunlight may exacerbate symptoms/

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12
Q

General advice for rosacea

A

Reduce common triggers that cause facial flushing.

Avoid oil-based facial creams. Use water-based make-up.

Never apply a topical steroid to the rosacea as although short-term improvement may be observed (vasoconstriction and anti-inflammatory effect), it makes the rosacea more severe over the next weeks (possibly by increased production of nitric oxide).

Protect yourself from the sun

Keep your face cool to reduce flushing: minimise your exposure to hot or spicy foods, alcohol, hot showers, hot baths, and warm rooms.

Some people find they can reduce facial redness for short periods by holding an ice block in their mouth, between the gum and cheek

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13
Q

Management of mild symptoms of rosacea

A

Topical metronidazole

Topical brimonidine gel may be considered for patients with predominant flushing but limited telangiectasia

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14
Q

Management of severe rosacea

A

Systemic antibiotics(oxytetracycline)

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15
Q

What is shingles

A

Shingles is an acute, unilateral, painful blistering rash caused by reactivation of the Varicella Zoster Virus (VZV) in the dorsal root ganglion or cranial nerve ganglia

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16
Q

Triggers for shingles

A 
Emotional stress
Immunosuppression
Chemotherapy
High dose steroid therapy
Recent illness or surgery
Skin injury
Sunburn
Trauma)
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17
Q

What type of nerves are affected in shingles

A

As the VZV affects the dorsal and/or cranial nerve ganglia, the sensory nerves are what are affected in the course of the disease, hence the characteristic single dermatome distribution

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18
Q

Phases of shingles

A

prodromal phase, the infectious rash, and the resolution phase

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19
Q

Rash features in shingles

A

Usually affecting a single dermatome in a band-like distribution
Unilateral, rarely crossing the midline
Initially is erythematous and macular in nature
Progression to erythematous papules, and eventually vesicles or bullae by day 7(lasts 7-10 days)
Vesicles become pustular or haemorrhagic near the end of this phase, right before crusting over

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20
Q

Supportive mx of shingles

A 
Mild analgesia 
Amitrptyline/duloxetine/gabapentin in moderate-severe pain 
Calamine lotion 
Topical capsaicin 
Cool compress
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21
Q

When do NICE recommend anti-virals in shingles

A

Within 72 hrs of rash if:

Immunocompromised patients
Non-truncal rash involvement (e.g. affecting face, neck, limbs, perineum)
Moderate-severe pain or rash

age>50

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22
Q

How long after a shingles rash onset can antivirals still be considered an option

A

one week after rash onset

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23
Q

Use of corticosteroids in shingles

A

If a patient is on anti-viral treatment –> oral corticosteroids
Used in the first 2 weeks following rash onset

This should only be used in conjunction with anti-viral treatment, and in immunocompetent adults with localised shingles if the pain is severe

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24
Q

Most common complication of shingles

A

Post-herpetic neuralgia

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25
Q

When should patients with shingles be referred/admitted

A

Herpes zoster ophthalmicus or eye involvement

Immunocompromised people

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26
Q

Risk factors for shingles

A

increasing age
HIV: strong risk factor, 15 times more common
other immunosuppressive conditions (e.g. steroids, chemotherapy)

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27
Q

Most common form of skin cancer

A

BCC

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28
Q

Subtypes of BCC

A

Sub types include nodular, morphoeic, superficial and pigmented.

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29
Q

Growth of BCC

A

Typically slow growing with low metastatic potential

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30
Q

Mx of BCC

A

Standard surgical excision, topical chemotherapy and radiotherapy are all successful.

As a minimum a diagnostic punch biopsy should be taken if treatment other than standard surgical excision is planned.

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31
Q

Most common type of BCC

A

Nodular

32
Q

Appearance of BCC

A

sun-exposed sites, especially the head and neck account for the majority of lesions
initially a pearly, flesh-coloured papule with telangiectasia

may later ulcerate leaving a central ‘crater’

33
Q

Mx options for BCC

A 
Surgical removal 
Curettage 
Cryotherapy 
Topical creams 
Radiotherapy
34
Q

Topical cream options for BCC

A

Imiquimod

Fluorouracil

35
Q

Risk factors for SCC

A 
Sunlight exposure/UVA
Actinic keratoses 
Immunosuppression(organ transplant/HIV)  
Smoking 
Long-standing leg ulcers 
Genetic conditions
36
Q

Mx of SCC

A

Surgical excision - wide local excision

Mohs micrographic surgery in high-risk patients and in cosmetically important sites

37
Q

What is Bowen’s disease

A

Squamous cell carcinoma in situ - erythematous scaling patch or elevated plaque arising on sun-exposed skin in an elderly patient

38
Q

What is a pyogenic granuloma

A

These present as friable overgrowths of granulation at sites of minor trauma.

They may be ulcerated and bleeding on contact is common.

39
Q

Mx of pyogenic granuloma

A

They may be treated with curettage and cautery, formal excision may be used if there is diagnostic doubt.

40
Q

Major criteria for diagnosis of malignant melanoma

A

Change in size
Change in shape
Change in colour

41
Q

Mx of malignant melanoma

A

Excision biopsy

Further treatments include sentinel lymph node mapping, isolated limb perfusion and block dissection of regional lymph node groups

42
Q

How are margins of excision determined in melanoma excision

A

Linked to breslow thickness

43
Q

What is dermatitis herpetiformis

A

Chronic itchy clusters of blisters.

Linked to underlying gluten enteropathy (coeliac disease).

44
Q

Features of dermatofibroma

A

Benign lesion.
Firm elevated nodules.
Usually history of trauma.
Lesion consists of histiocytes, blood vessels and fibrotic changes.

45
Q

Most common cause of acanthuses nigricans

A

Insulin resistance

46
Q

Features of dermatitis herpetiformis

A

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

47
Q

Causes of erythroderma

A 
eczema
psoriasis
drugs e.g. gold
lymphomas, leukaemias
idiopathic
48
Q

Two main types of contact dermatitis

A

Irritant contact dermatitis

Allergic contact dermatitis

49
Q

What type of hypersensitivity is allergic contact dermatitis

A

Type IV

50
Q

Features of allergic contact dermatitis

A

Uncommon - often seen on the head following hair dyes. Presents as an acute weeping eczema which predominately affects the margins of the hairline rather than the hairy scalp itself.

Cement is a common cause

51
Q

Features of toxic epidermal necrolysis(TEN)

A

systemically unwell e.g. pyrexia, tachycardic

positive Nikolsky’s sign: the epidermis separates with mild lateral pressure

52
Q

Drugs known to induce TEN

A 
phenytoin
sulphonamides
allopurinol
penicillins
carbamazepine
NSAIDs
53
Q

Mx of TEN

A

Stop precipitating factor
Supportive care
IV immunoglobulins first line

54
Q

What is bullous pemphigoid

A

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

55
Q

Features of bullous pemphigoid

A

itchy, tense blisters typically around flexures
the blisters usually heal without scarring
there is usually no mucosal involvement (i.e. the mouth is spared)*

56
Q

What does a skin biopsy show in bullous pemphigoid

A

immunofluorescence shows IgG and C3 at the dermoepidermal junction

57
Q

Mx of bullous pemphigoid

A

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

58
Q

What is pyoderma gangrenosum

A

Pyoderma gangrenosum is a rare, non-infectious, inflammatory disorder. It is an uncommon cause of very painful skin ulceration. It may affect any part of the skin, but the lower legs are the most common site.

59
Q

What might be seen on biopsy in pyoderma gangrenosum

A

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

60
Q

Causes of pyoderma gangrenosum

A 
Idiopathic(50%)
IBDs 
Rheumatological(RA,SLE)
Haem(MDS, lymphoma)
PBC
61
Q

Mx of pyoderma gangrenosum

A

Oral steroids as 1st line

Other immunosuppressive therapy(ciclosporin)

62
Q

What is seborrhoeic dermatitis thought to be due to

A

Seborrhoeic dermatitis in adults is a chronic dermatitis thought to be caused by an inflammatory reaction related to a proliferation of a normal skin inhabitant, a fungus called Malassezia furfur

63
Q

Features of seborrhoeic dermatitis

A

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

64
Q

Conditions associated with seborrhoeic dermatitis

A

HIV

Parkinson’s disease

65
Q

Management of seborrhoeic dermatitis on scalp

A

over the counter preparations containing zinc pyrithione (‘Head & Shoulders’) and tar (‘Neutrogena T/Gel’) are first-line
the preferred second-line agent is ketoconazole
selenium sulphide and topical corticosteroid may also be useful

66
Q

Management of face and body seborrhoeic dermatitis

A

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

67
Q

Which factors can exacerbate psoriasis

A

trauma
alcohol
drugs
steroid withdrawal

68
Q

Drugs which can exacerbate psoriasis

A

beta blockers, lithium, antimalarials (chloroquine and hydroxychloroquine), NSAIDs and ACE inhibitors, infliximab

69
Q

Indicators of atopic dermatitis/eczema

A

Visible flexural eczema involving the skin creases, such as the bends of the elbows or behind the knees

Personal history of flexural eczema

Personal history of asthma or allergic rhinitis

70
Q

Mx of mild eczema

A

Generous amounts of emollients

Topical hydrocortisone 1%

71
Q

Mx of moderate eczema

A

Emollients
Betamethasone valerate 0.025%
Consider trial of cetirizine if itch or urticaria

72
Q

Preventative treatment in eczema

A

Maintenance regimen of topical corticosteroids

Topical calcineurin inhibitors(tacrolimus) as second line

73
Q

When should hospital admission be made for eczema

A

Eczema herpeticum(widespread herpes simplex virus)

74
Q

Antibiotic of choice in infected eczema

A

Flucloxacillin

75
Q

Causes of folliculitis

A

Bacteria - staph aureus

Hot tub folliculitis (pseudomonas)

Eosinophilic folliculitis(HIV/AIDS)

General practice (26 decks)

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