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4th year everything > Dermatology > Flashcards

Dermatology Flashcards

1
Q

What is cellulitis?

A

A spreading infection of the deep subcutaneous layer of the skin. It is the most common skin infection leading to admission to hospital

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2
Q

What preferential anatomical distribution does cellulitis demonstrate?

A

Cellulitis preferentially involves the lower limbs and extremities

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3
Q

What is erysipleas? What anatomical proclivity does it show?

A

Similar to cellulitis; it is an infection of the deep dermis and subcutaneous tissues and has a proclivity for involvement of the face

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4
Q

What are the most common bacterias causing cellulitis/erysipleas?

A

Streptococcus spp. most commonly

Rarely staphylococcus

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5
Q

What is the clinical presentation of cellulitis?

A

Tender erythematous patch with poorly demarcated borders, swelling, warmth and potentially a low grade fever

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6
Q

What is the clinical presentation of erysipleas?

A

Raised erythematous area with sharply demarcated borders, warmth, tenderness and potentially a low grade fever.

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7
Q

What is the major differential diagnosis to be ruled out in the case of suspected cellulitis of the lower limb?

A

Deep vein thrombosis

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8
Q

What is the antibiotic of choice for treatment of cellulitis/erysipleas?

A

Flucloxacillin (erythromycin if penicillin allergic)

If disease is diffuse then intravenous therapy for 3-5 days followed by at least two weeks of oral therapy

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9
Q

What is necrotising fasciitis?

A

A deep-seated infection of the subcutaneous tissue that results in fulminant and spreading destruction of the fascia and fat.

May initially spare the skin, leading to delayed diagnosis

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10
Q

What are the clinical features of necrotising fasciitis?

A

Spreading erythema and underlying crepitus with severe pain and system toxicity (disproportionate to skin findings)

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11
Q

Outline the difference between type 1 and type 2 necrotising fasciitis

A

Type 1 - mixed anaerobic and aerobic bacteria

Type 2 - mono-microbial (group A streptococci)

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12
Q

What profile of people are most likely to get type 1 necrotising fasciitis? (2)

A

Patients who have had recent abdominal surgery

Type 2 diabetics

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13
Q

How is necrotising fasciitis managed?

A

Surgical debridement followed by aggressive use of broad-spectrum antibiotics (usually benzylpenicillin and clindamycin)

With the addition of metronidazole in type 1 to cover anaerobic microorganisms

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14
Q

What is gas gangrene?

A

A specific deep-seated infection with clostridium spp. (especially clostridium perfringens) contaminating penetrating wounds

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15
Q

What clinical picture does gas gangrene present with?

A

Muscle necrosis with severe pain and swelling and crepitus on deep palpation (due to gas in subcutaneous tissue as a result of necrosis)

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16
Q

How is gas gangrene treated?

A

Surgical debridement and combination antimicrobial therapy of benzylpenicillin and clindamycin

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17
Q

What does the dermamatophytes refer to?

A

Three types of fungi commonly responsible for infections of the superficial skin layers.

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18
Q

How are dermatophytes transmissible?

A

Direct contact with infected humans/animals or by indirect contact with exfoliated hair/skin

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19
Q

What type of dermatophyte infection affects the body?

A

Tinea corporis

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20
Q

What type of dermatophyte infection affects the face?

A

Tinea faciei

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21
Q

What type of dermatophyte infection affects the groin?

A

Tinea cruris

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22
Q

What type of dermatophyte infection affects the feet?

A

Tinea pedis

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23
Q

What type of dermatophyte infection affects the hands?

A

Tinea manuum

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24
Q

What type of dermatophyte infection affects the nailbed?

A

Tinea unguium

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25
Q

What type of dermatophyte infection affects the scalp?

A

Tinea capitis

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26
Q

How does tinea corporis present?

A

Mildly itchy patches with central clearing and an advancing, scaly edge

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27
Q

How does tinea faciei present?

A

Erythematous annular lesion on the face; may or may not be itchy

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28
Q

How does tinea cruris present?

A

Intensely itchy rash in the groin with scaly edges and often extends on the inner thigh

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29
Q

How does tinea pedis present?

A

White, macerated/fissured skin around toe clefts with more scaly erythema extending onto the soles and sides of the feet

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30
Q

How does tinea manuum present?

A

Diffuse erythematous scaling of the palmar surface of the hands

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31
Q

How does tinea capitis present?

A

A spectrum of presentation from mild scaling and no hair loss to circular patches of scale and alopecia

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32
Q

How does tinea unguium present?

A

Asymmetrical white/yellow/black discolouration of the nails with nail plate thickening and white residue under the nail.

33
Q

How are dermatophyte infections treated differently on a local and more diffuse scale?

A

Local disease - topical antifungal creams (e.g. clotrimazole)

Diffuse disease - oral antifungal therapy (e.g. terbinafine)

34
Q

Where can cutaneous candida infection present on the body?

A

Can occur in the groin, interdigital/toe clefts or around nails

35
Q

What are the clinical features of acne vulgaris?

A

Increased sebum production
Blockage of pilosabaceous units
Follicular epidermal hyperproliferation

All leading to formation of open/closed comedones, inflammatory papulaes/pustules, hypertrophic/keloidal scarring and hyperpigmentation

36
Q

What is the first line therapy for acne vulgaris?

A

Topical agents; e.g.

Keratolytics (benzyl peroxide)
Topical retinoids (isotretinoin)
Antibiotics (clindamycin)

37
Q

What is the second line therapy for acne vulgaris?

A 
Low-dose oral antibiotics for 3-4 months (e.g. erythromycin) 
Hormonal treatment (e.g. cyproterone acetate)
38
Q

What is the third line therapy for acne vulgaris?

A

Oral retinoid (isotretinoin)

39
Q

What is the absolute contraindication of using retinoids?

A

Teratogenicity therefore contraindicated in pregnancy

40
Q

What is psoriasis?

A

A chronic hyperproliferative disorder typically characterised by well-defined scaly plaques on extensor surfaces of the body

41
Q

What are the two peak age ranges for psoriasis?

A

16-22 years old

55-60 years old

42
Q

What four different entities of psoriasis are there?

A
  1. Chronic plaque psoriasis
  2. Flexural psoriasis
  3. Guttae
  4. Erythrodermic and pustular
43
Q

Outline the features of chronic plaque psoriasis

A

Most common form.

Erythematous and scaly plaques form on extensor surfaces .

Scalp involvement is also common

44
Q

Outline the features of flexural psoriasis

A

Erythematous non-sclay plaques confined to flexures such as the groin and under breasts

45
Q

Outline the features of guttae

A

Most commonly in children

Explosive eruption of small discoid plaques over the trunk proceeding after a streptococcal throat infection

46
Q

Outline the features of erythrodermic and pustular psoriasis

A

Most severe form

Widespread intense inflammation and systemic upset including malaise, pyrexia and potentially haemodynamic instability

47
Q

Outline the different treatment modalities for psoriasis?

A

Topical treatement - emmolients, vitamin D3 analogues, corticosteroids

Phototherpay - UVA with photosensitising agent

Systemic therapy - oral retinoid, biologics

48
Q

What is eczema (dermatitis)?

A

A condition characterised by superficial skin inflammation with vesicles in the acute phase; along with erythema, oedema, scaling and intense itching

49
Q

What is the primary defect in skin function in eczema?

A

Abnormal barrier function of skin leading to antigenic presentation to immune cells causing an immune reaction leading to inflammation

50
Q

How is eczema managed?

A

Known irritants should be avoided

Regular use of emollients

Topical steroids are the mainstay of treatment. Mild steroids (e.g. hydrocortisone) used for face and more potent steroids (e.g. betamethasone) for the body.

Topical immunomodulators e.g. tacrolimus are particularly useful for treatment of sensitive areas such as face and eyelids

51
Q

What is contact dermatitis? What clinical features would make you think of it as a diagnosis?

A

Sharply demarcated inflammation (both acute and chronic) produced by substances which irritate the skin (irritants)

Unusually sharply defined borders to the lesions should rouse suspicion

52
Q

What is erythema nodosum?

A

Acute panniculitis (inflammation of subcutaneous adipose tissues) producing painful blue/red nodules over the limbs

53
Q

What systemic features are often seen concurrently with erythema nodosum?

A

Malaise, fever and arthralgia

54
Q

How is non-resistant erythema nodosum treated?

A

NSAIDs

Light compression and bedrest for up to a number of weeks.

55
Q

How is resistant erythema nodosum treated?

A

Dapsone (antibiotic cream) or
Colchicine or
Oral prednisolone

56
Q

List some common causes of erythema nodosum (5)

A 
Inflammatory bowel disease
Sarcoidosis 
Tuberculosis 
Streptococcal infection
Drugs (e.g. oral contraceptive pill)
57
Q

What is erythema multiforme?

A

An acute, self-limiting rash characterised by multiple ‘target lesions’ on the distal limbs

58
Q

What is the most common cause of erythema multiforme?

A

Herpes simplex infection

Other causes include herpes simplex or autoimmune conditions such as lupus

59
Q

What is pyodermic gangrenosum? What is the classical presentation?

A

Ulcerating condition presenting with erythematous nodules/ pustules which go on to ulcerate.

The ulcers typically have a blue/black appearance and a purulent surface.

60
Q

What are the main causes of pyodermic gangrenosum?

A

Inflammatory bowel disease, rheumatoid arthritis, haematological malignancy and biliary cirrhosis

61
Q

How is pyrodermic gangrenosum managed?

A

High-dose topical and/or oral steroids to prevent further ulceration

Debridement is contraindicated as it worsens the condition

62
Q

What is acthanosis nigrans?

A

Thickened and hyperpigmented skin of flexures associated with obesity, diabetes, underlying malignancy (especially gastrointestinal) and hyperandrogenism in females

63
Q

Outline the genetics of Type 1 Neurofibromatosis (Von Ricklinghausen’s Disease)

A

Autosomal dominant condition caused by an NF1 gene mutation on chromosome 17

64
Q

Outline the genetics of Type 2 Neurofibromatosis

A

Autosomal dominant condition caused by an merlin/schwannonin conding gene mutation on chromosome 22

65
Q

What are the features indicative of Type 1 Neurofibromatosis?

A

Multiple fleshy skin tags and deeper soft tissue tumours (neurofibromas)

Café-au-lait spots (light brown macules)

Scoliosis

Increased incidence of meningiomas or gliomas

66
Q

What are the features indicative of Type2 Neurofibromatosis?

A

Presents with bilateral acoustic neuromas and cutaneous neurofibromas

67
Q

What is the inheritance pattern demonstrated in tuberous sclerosis?

A

Autosomal dominant

Due to mutations in either the TSC1 or TSC2 gene coding for hamartin or tuberin respectively

68
Q

What are the clinical features of tuberous sclerosis?

A

Mental retardation, epilepsy and cutaneous abnormalities including adenoma sebaceum (red papules around the nose), periungual fibroma and café-au-lait spots

69
Q

What is Ehlers-Danlos Syndrome?

A

Inherited defect in collagen leading to hyperelastic skin, hypermobile joints and progressive gut/aorta wall weakening

70
Q

What is pemphigus vulgaris?

A

Autoimmune condition leading to formation of cutaneous and mucosal blisters which evolve into erosions.

Can be fatal.

Treatment with high-dose oral prednisolone and immunosuppression

71
Q

What is bullous pemphigoid?

A

Autoimmune condition leading to the formation of large tense blisters on limbs and torso.

It is a disease of the elderly and is treated with high-dose oral prednisolone and immunosuppression

72
Q

What is the most common form of skin malignancy?

A

Basal Cell Carcinoma

73
Q

How do Basal Cell Carcinomas present?

A

Shiny, pearly nodule typically on sun exposed areas which may go on to ulcerate

They rarely metastasise but are locally invasive

Treated by surgical excision or topical immunomodulators e.g. imiquimod

74
Q

How do Squamous Cell Carcinomas present?

A

More aggressive than BCCs. Poorly-defined nodules that can grow rapidly and ulcerate

Treated with wide margin excision or radiotherapy (less commonly)

75
Q

What is the most severe form of skin malignancy?

A

Malignant melanoma

76
Q

Why is melanoma the most severe form of skin malignancy?

A

It can metastasise early to sites such as the bones, lung and brain

77
Q

What are the four clinical entities of malignant melanoma?

A
  1. Lentigo meligna melanoma
  2. Superficial spreading melanoma
  3. Nodule malignant melanoma
  4. Acral lentiginous malignant melanoma
78
Q

What is Kaposi sarcoma?

A

A tumour of vascular and lymphatic endothelium presenting as purple nodules/plaques in elderly males

79
Q

What groups of people are more disposed to developing Kaposi sarcoma?

A

Ashkenazi Jews
Central African natives
Patients with HIV infection

4th year everything (43 decks)

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