Derm Flashcards

1
Q

What is acne vulgaris ?

A

Acne vulgaris (acne) is an extremely common condition, often affecting people during puberty and adolescence. Most people are affected at some point during their lives, and symptoms can range from mild to severe.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Explain the pathophysiology of acne vulgaris?

A

Acne is caused by chronic inflammation, with or without localised infection, in pockets within the skin known as the pilosebaceous unit. The pilosebaceous units are the tiny dimples in the skin that contain the hair follicles and sebaceous glands. The sebaceous glands produce the natural skin oils and a waxy substance known as sebum.

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Presentation of acne

A

There is significant variation in the severity of acne. It presents with red, inflamed and sore “spots” on the skin, typically distributed across the face, upper chest and upper back.

There are few terms used to describe the appearance of the lesions:

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Aim of treatment of acne

A

The aim of treatment is to reduce the symptoms of acne, reduce the risk of scarring and minimise the psychosocial impact of the condition. Always explore the psychosocial burden and any potential anxiety and depression that may be associated with the condition.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Acne Treatment is initiated in a stepwise fashion based on the severity and response to treatment:

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 (chemicals related to vitamin A) slow the production of sebum (women of childbearing age need effective contraception)
Topical antibiotics such as clindamycin (prescribed with benzoyl peroxide to reduce bacterial resistance)
Oral antibiotics such as lymecycline
Oral contraceptive pill can help female patients stabilise their hormones and slow the production of sebum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Acne Tx: Oral retinoids

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the most effective combined oral contraceptive for acne?

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Tx for acne; Oral isotretinon

A

Oral isotretinoin (Roaccutane) is very effective at clearing the skin. It is a retinoid, and works by reducing production of sebum, reducing inflammation and reducing bacterial growth. It can only be prescribed under expert supervision by a dermatologist. It is strongly teratogenic (harmful to the fetus during pregnancy). Patients need to have effective and reliable contraception and must stop isotretinoin for at least a month before becoming pregnant.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

SE of Isotretinoin

A

Dry skin and lips
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Complications for acne

A

post-inflammatory scarring, hyperpigmentation, psychosocial impact (self-esteem, depression).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Epidemiology of acne

A

affects around 80-90% of teenagers, 60% of whom seek medical advice
acne may also persist beyond adolescence, with 10-15% of females and 5% of males over 25 years old being affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is atopic dermatitis (eczema)?

A

A chronic, relapsing inflammatory skin condition characterized by pruritus, erythema, and dry skin, often associated with atopy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the difference between atopic dermatitis and eczema?

A

Eczema is a general term for skin inflammation, while atopic dermatitis is a specific type of eczema linked to atopy (e.g., asthma, allergic rhinitis).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Atopic dermatitis is most commonly seen in __________ but can persist into adulthood.

A

children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the common triggers for atopic dermatitis?

A

Irritants (e.g., soaps, detergents), allergens (e.g., dust mites, pollen), weather changes, stress, infections, and certain fabrics.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Atopic dermatitis has a strong genetic component and is commonly associated with mutations in the __________ gene.

A

filaggrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the underlying pathophysiology of atopic dermatitis?

A

Dysfunction of the skin barrier (filaggrin mutation) leads to increased transepidermal water loss, immune dysregulation, and inflammation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

The two key immune pathways involved in atopic dermatitis are the __________ and __________ pathways.

A

Th2, Th22

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the key features of atopic dermatitis?

A

Pruritus, dry skin, erythema, excoriation, lichenification, and sometimes weeping or crusting lesions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does the distribution of atopic dermatitis differ between infants, children, and adults?

A

Infants: Face and extensor surfaces.

Children: Flexural areas (e.g., elbows, knees).

Adults: Hands, face, and flexural areas.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

A hallmark symptom of atopic dermatitis is intense __________, leading to the itch-scratch cycle.

A

pruritus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the main diagnostic approach for atopic dermatitis?

A

Clinical diagnosis based on history and examination; no specific tests required.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

In severe or atypical cases, __________ testing may be used to identify allergens.

A

patch or IgE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the four main principles of atopic dermatitis management?

A
  1. Emollients, 2. Topical corticosteroids, 3. Avoiding triggers, 4. Treating infections.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Emollients should be applied __________ to maintain skin hydration.

A

frequently (at least twice daily)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the stepwise approach for treating atopic dermatitis in the UK?

A

First-line: Emollients + mild topical steroids (e.g., hydrocortisone).

Second-line: Moderate or potent steroids (e.g., betamethasone) for flares.

Third-line: Calcineurin inhibitors (e.g., tacrolimus) for sensitive areas.

Severe cases: Systemic immunosuppressants (e.g., ciclosporin, dupilumab).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

When should topical steroids be applied in relation to emollients?

A

Topical steroids should be applied after emollients, with a 30-minute gap.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Wet wrap therapy can be used in __________ cases to enhance treatment absorption and reduce scratching.

A

severe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are common complications of atopic dermatitis?

A

Skin infections (e.g., Staphylococcus aureus, herpes simplex), lichenification, psychological distress, and sleep disturbance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Eczema herpeticum is a serious complication caused by __________ infection in atopic dermatitis patients

A

herpes simplex virus (HSV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the most common type of contact dermatitis?

A

Irritant contact dermatiits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is irritant contact dermatitis?

A

non-allergic reaction due to weak acids or alkalis (e.g. detergents).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the presentation of irritant contact dermatitis?

A

Often seen on the hands. Erythema is typical, crusting and vesicles are rare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What type of hypersensitivity reaction is allergy contact dermatiits?

A

type IV hypersensitivity reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is 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. Topical treatment with a potent steroid is indicated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How does cement cause contact dermatitis?

A

Cement is a frequent cause of contact dermatitis. The alkaline nature of cement may cause an irritant contact dermatitis whilst the dichromates in cement also can cause an allergic contact dermatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is contact dermatitis?

A

Contact dermatitis is an inflammatory skin reaction caused by direct contact with an irritant or allergen, leading to erythema, pruritus, and skin damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the two main types of contact dermatitis?

A

Irritant contact dermatitis (ICD): Caused by direct damage to the skin from irritants (e.g., soaps, detergents).

Allergic contact dermatitis (ACD): Delayed hypersensitivity reaction to allergens (e.g., nickel, latex).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are common causes of irritant contact dermatitis?

A

Soaps, detergents, solvents, prolonged water exposure, acids, alkalis, and frequent handwashing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are common allergens that cause allergic contact dermatitis?

A

Nickel (jewellery), fragrances, latex, hair dyes (paraphenylenediamine), and preservatives.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

he most common occupational cause of contact dermatitis is exposure to __________.

A

wet work (e.g., healthcare, hairdressing)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the underlying mechanism of irritant contact dermatitis?

A

Direct damage to the skin barrier by irritants, leading to inflammation and disruption of the epidermis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Allergic contact dermatitis typically takes __________ hours to develop after allergen exposure.

A

24–72

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How does the appearance of irritant vs. allergic contact dermatitis differ?

A

Irritant: More localized, burning sensation, often seen on hands.

Allergic: Well-demarcated, pruritic, often with vesicles or weeping.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Chronic contact dermatitis can lead to skin thickening and __________.

A

lichenification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How is contact dermatitis diagnosed?

A

Mainly clinical, but patch testing can confirm allergic contact dermatitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the key principles of managing contact dermatitis?

A

Avoidance of the irritant/allergen.

Emollients to restore the skin barrier.

Topical steroids for inflammation.

Education on skin protection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Mild contact dermatitis is managed with topical __________ steroids such as hydrocortisone.

A

corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

When are systemic treatments used for contact dermatitis?

A

In severe cases, oral corticosteroids (e.g., prednisolone) or immunosuppressants (e.g., azathioprine) may be needed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What preventative strategies can reduce the risk of occupational contact dermatitis?

A

Wearing gloves, using barrier creams, minimizing irritant exposure, and applying frequent emollients.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are potential complications of contact dermatitis?

A

Secondary bacterial infection (e.g., Staphylococcus aureus)

Chronic lichenification and skin thickening

Psychosocial impact (e.g., stress, work-related issues)

52
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.

53
Q

Presentation of psoriasis

A

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.

54
Q

Plaque psoriasis

A

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.

55
Q

Guttate psoriasis

A

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.

56
Q

Pustular psoriasis

A

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.

57
Q

Erythrodermic psoriasis

A

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.

58
Q

___ psoriasis is more common in children.

A

In children the distribution and presentation of psoriasis may differ from adults. Guttate psoriasis is more common in children, often triggered by a throat infection. Plaques of psoriasis are likely to be smaller, softer and less prominent.

There are a few specific signs suggestive of psoriasis:

Auspitz sign
Koebner phenomenon
Residual pigmentation
The diagnosis can be made based on the clinical appearance of the lesions.

59
Q

What is Auspitz sign?

A

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

60
Q

What is Koebner phennomenon?

A

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

61
Q

What is Residual Pigmentation?

A

Residual pigmentation of the skin after the lesions resolve

62
Q

Tx options for 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)
Topical dithranol
Topical calcineurin inhibitors (tacrolimus) are usually only used in adults
Phototherapy with narrow band ultraviolet B light is particularly useful in extensive guttate psoriasis

63
Q

What can you try if inital tx doesnt work for psoriasis?

A

Rarely, where topical treatments fail with severe and difficult to control psoriasis, children may be started on unlicensed systemic treatment under the guidance of an experienced specialist. This might include methotrexate, cyclosporine, retinoids or biologic medications.

There are two products that contain both a potent steroid and vitamin D analogue that are commonly prescribed and worth being aware of. These not licensed in children and will be guided by a specialist.

Dovobet
Enstilar

64
Q

What are some associations with psoriasis?

A

Nail psoriasis describes the nail changes that can occur in patients with psoriasis. These include nail pitting, 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.

65
Q

What are fungal skin infections?

A

Fungal skin infections are caused by dermatophytes, yeasts, or moulds, leading to inflammation, itching, and scaling of the skin.

66
Q

What are the three main types of fungi responsible for fungal skin infections?

A

Dermatophytes (e.g., Trichophyton, Microsporum, Epidermophyton) – cause tinea infections.

Yeasts (e.g., Candida, Malassezia) – cause candidiasis and pityriasis versicolor.

Moulds – rare, usually affect immunocompromised individuals.

67
Q

Dermatophyte infections are commonly known as __________ infections.

68
Q

What are common risk factors for fungal skin infections?

A

Warm, moist environments, poor hygiene, immunosuppression, diabetes, obesity, prolonged antibiotic or corticosteroid use.

69
Q

How do dermatophyte fungi cause skin infections?

A

They invade and digest keratin in the skin, hair, and nails, leading to inflammation and characteristic scaling.

70
Q

Yeast infections, such as candidiasis, occur due to overgrowth of __________, which is a normal commensal organism.

A

Candida albicans

71
Q

What are the different types of tinea infections and their affected areas?

A

Tinea pedis (Athlete’s foot): Feet, particularly between toes.

Tinea corporis (Ringworm): Trunk, arms, legs.

Tinea capitis: Scalp.

Tinea cruris (Jock itch): Groin and inner thighs.

Tinea unguium (Onychomycosis): Nails.

72
Q

What are the typical features of tinea infections?

A

Annular (ring-shaped) erythematous plaques with central clearing, scaling, and itching.

73
Q

Tinea capitis often presents with __________ hair loss and scaling on the scalp.

74
Q

What are common sites affected by cutaneous candidiasis?

A

Skin folds (axilla, groin, under breasts), intertriginous areas, and nails.

75
Q

What are the key features of candidiasis?

A

Red, moist patches with satellite lesions, often with maceration in skin folds.

76
Q

Oral candidiasis presents as white, curd-like plaques on the __________ that can be scraped off.

77
Q

What are the key clinical features of pityriasis versicolor?

A

Hypopigmented or hyperpigmented macules on the trunk, with fine scaling and mild itching.

78
Q

Pityriasis versicolor is caused by overgrowth of __________ yeast on the skin.

A

Malassezia

79
Q

What diagnostic tests can confirm fungal skin infections?

A

Microscopy with KOH preparation – Identifies fungal hyphae.

Fungal culture – Identifies specific fungal species.

Wood’s lamp examination – Some fungi fluoresce under UV light.

80
Q

A Wood’s lamp examination can help diagnose __________, as some species fluoresce green.

A

tinea capitis

81
Q

What are the first-line treatments for most fungal skin infections?

A

Topical antifungals (e.g., clotrimazole, terbinafine, miconazole).

82
Q

When are systemic antifungals required for fungal skin infections?

A

In severe, widespread, or nail/scalp infections (e.g., oral terbinafine or itraconazole for tinea capitis and onychomycosis).

83
Q

Tinea capitis requires systemic treatment, usually oral __________.

A

terbinafine

84
Q

What lifestyle measures help prevent recurrence of fungal infections?

A

Keeping skin dry, wearing breathable clothing, avoiding shared towels, and treating asymptomatic carriers in households.

85
Q

What are potential complications of untreated fungal skin infections?

A

Secondary bacterial infections (e.g., cellulitis), chronic inflammation, nail dystrophy (onychomycosis), and scarring alopecia (tinea capitis).

86
Q

Chronic, untreated fungal infections can lead to secondary __________ infections.

87
Q

What is ringworm

A

Ringworm is a common superficial fungal infection which affects the skin.

The infection is colloquially called “ringworm” because lesions are often circular-shaped. Despite this name, ringworm is not a parasitic worm infection.

Ringworm can also be referred to as tinea or dermatophytosis. Ringworm is more common in hot and humid environments.

88
Q

causes of ringworm

A

Ringworm (tinea) is caused by dermatophytes (a type of fungus).

Depending on the location, the condition can be referred to as:1,2,3

Tinea capitis (affecting the scalp)
Tinea pedis (affecting the feet)
Tinea cruris (affecting the groin)
Tinea corporis (affecting any other skin site)
In the community, ringworm of the feet may be called “athlete’s foot”, while ringworm of the groin may be called “jock itch”.

Common species of dermatophyte include T. rubrum, T. interdigitale and T. tonsurans.

Zoonotic species such as M. canis, T. verrucosum, T. equinum and T. erinacei may be present in those that interact with animals.1

89
Q

risk factors for ringworm

A

Ringworm is spread by skin-skin contact or contact with an infected surface.

Risk factors include:

Male sex
Contact with an infected person
Frequent use of communal shower facilities
Not drying feet adequately (risk of tinea pedis)
The most at-risk groups include children attending daycare and early school and households of an infected person.

Medical risk factors are those primarily relating to an immunocompromised state or skin condition affecting the skin’s barrier, and include:1,2

Previous tinea infections
Diabetes mellitus
Hyperhidrosis
Xerosis (dry skin)
Ichthyosis

90
Q

Symptoms for ringworm

A

Itch: An asymmetrical rash consisting of solitary circular erythematous patches with a raised scaly leading edge and a clearing centre (hypopigmentation within the ring)

91
Q

Ix for ringworm

A

Ringworm is a clinical diagnosis.

A skin scraping of the leading edge may be taken to confirm the diagnosis, especially in cases which do not respond to initial anti-fungal treatment. Skin scrapings can be sent for microscopy, culture and sensitivities. Any topical therapy must be removed before collecting scrapings. Hair and nail cuttings may also be used.

A Wood’s lamp can examine hair as affected hairs will fluoresce green.

Treatment-resistant or atypical presentations may require a skin biopsy.

92
Q

Tx for ringworm

A

The first line of management is topical therapy:

Topical terbinafine 1%: formulated as a cream (body, scalp, feet, nails), gel (body, scalp, groin), spray (interdigital, body, scalp) or liquid (interdigital). Used once or twice daily for one to two weeks.
Econazole (or a similar azole) cream: applied once or twice daily for two weeks.

93
Q

Oral therapy for ringworm

A

Oral therapy is the next-line treatment option if the infection is severe, affecting multiple sites, recurrent, or not responding to topical treatment.4

The first option is oral terbinafine 250mg daily for adults. For children under 20kg, the dose is 62.5mg daily. For those 20 – 40 kgs, it is 125mg daily.

The length of treatment is dependent on the site of infection:

Scalp: four weeks
Fingernails: six weeks
Toenails: 12 weeks
Other body sites: two weeks
The next option is griseofulvin (for tinea of the hair and scalp only) for 4-6 weeks and up to 1 year:

Scalp/hair/groin: 500mg daily
Feet/nails: 1 g daily
The last line of therapy is oral fluconazole or itraconazole.

94
Q

What are warts?

A

Warts are benign epidermal growths caused by human papillomavirus (HPV) infection, leading to hyperkeratosis and papillomatosis.

95
Q

What virus causes warts?

A

Human papillomavirus (HPV).

96
Q

How are warts transmitted?

A

Direct skin-to-skin contact, autoinoculation, and contact with contaminated surfaces (e.g., communal showers, swimming pools).

97
Q

What are risk factors for developing warts?

A

Immunosuppression (e.g., HIV, organ transplant patients).

Skin trauma (e.g., shaving, nail-biting).

Prolonged moisture exposure.

Young age (common in children and adolescents).

98
Q

How does HPV cause warts?

A

HPV infects basal keratinocytes, leading to uncontrolled keratinocyte proliferation, hyperkeratosis, and formation of a raised lesion.

99
Q

What are the different types of warts and their typical locations?

A

Common warts (Verruca vulgaris): Hands, fingers, knees.

Plantar warts (Verruca plantaris): Soles of feet, often painful.

Flat warts (Verruca plana): Face, hands, legs (smooth, flat-topped).

Genital warts (Condylomata acuminata): Anogenital region.

Periungual warts: Around fingernails and toenails.

100
Q

How do common warts typically appear?

A

Firm, rough, hyperkeratotic papules with a cauliflower-like surface.

101
Q

What is a distinguishing feature of plantar warts compared to corns?

A

Plantar warts disrupt skin lines, whereas corns do not.

102
Q

What symptoms may be associated with warts?

A

Generally asymptomatic, but plantar warts can be painful with walking.

103
Q

How are warts diagnosed?

A

Clinical diagnosis based on characteristic appearance.

104
Q

When should a biopsy be considered for a wart?

A

f there is suspicion of malignancy, rapid growth, ulceration, or atypical features.

105
Q

What are the first-line treatments for common warts?

A

Topical salicylic acid (keratolytic).

Cryotherapy (liquid nitrogen).

106
Q

How does salicylic acid work in wart treatment?

A

It breaks down keratin, softening the wart and promoting exfoliation.

107
Q

How does cryotherapy work for warts?

A

Freezes the wart, causing cell damage and an immune response to clear HPV.

108
Q

When are more invasive treatments used for warts?

A

For persistent or resistant warts, options include:

Electrocautery.

Laser therapy.

Surgical excision.

109
Q

Why is surgical excision not commonly used for wart removal?

A

High recurrence rate and risk of scarring.

110
Q

What are alternative treatments for resistant warts?

A

Topical immunotherapy (e.g., imiquimod, diphencyprone).

Intralesional bleomycin.

Photodynamic therapy.

111
Q

What are potential complications of warts?

A

Pain and discomfort (especially plantar warts).

Secondary bacterial infection.

Recurrence.

Psychological distress (e.g., embarrassment, social stigma).

112
Q

What is urticaria?

A

Urticaria are also known as hives. 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.

113
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.

114
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)

115
Q

Chronic urticaria

A

Chronic urticaria is an autoimmune condition, where autoantibodies target mast cells and trigger them to release histamines and other chemicals. It can be sub-classified depending on the cause:

Chronic idiopathic urticaria
Chronic inducible urticaria
Autoimmune urticaria

116
Q

Chronic idiopathic urticaria

A

Chronic idiopathic urticaria describes recurrent episodes of chronic urticaria without a clear underlying cause or trigger.

117
Q

Chronic inducible urticaria

A

Chronic inducible urticaria describes episodes of chronic urticaria that can be induced by certain triggers, such as:

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

118
Q

Autoimmune urticaria

A

Autoimmune urticaria describes chronic urticaria associated with an underlying autoimmune condition, such as systemic lupus erythematosus.

119
Q

Management of urticaria

A

Antihistamines are the main treatment for urticaria. Fexofenadine is usually the antihistamine of choice for chronic urticaria. Oral steroids may be considered as a short course for severe flares.

In very problematic cases referral to a specialist may be required to consider treatment with:

Anti-leukotrienes such as montelukast
Omalizumab, which targets IgE
Cyclosporin

120
Q

Why do venous ulcers occur?

A

Venous ulcers occur due to the pooling of blood and waste products in the skin secondary to venous insufficiency.

121
Q

Where do venous ulcers occur?

A

Occur in the gaiter area (between the top of the foot and bottom of the calf muscle)

122
Q

What are venous ulcers associated with?

A

Are associated with chronic venous changes, such as hyperpigmentation, venous eczema and lipodermatosclerosis

123
Q

When do venous ulcers occur?

A

Occur after a minor injury to the leg

124
Q

How do venous ulcers compare to arterial ulcers?

A

Are larger than arterial ulcers
Are more superficial than arterial ulcers Are less painful than arterial ulcers

125
Q

Presentation of venous ulcers

A

Have irregular, gently sloping border
Are more likely to bleed

126
Q

Tx of venous ulcers

A

Have pain relieved by elevation and worse on lowering the leg

127
Q

Management of venous ulcers

A

The management here is based on the NICE CKS (last updated January 2021). Patients may require referral to:

Vascular surgery where mixed or arterial ulcers are suspected
Tissue viability / specialist leg ulcer clinics in complex or non-healing ulcers
Dermatology where an alternative diagnosis is suspected, such as skin cancer
Pain clinics if the pain is difficult to manage
Diabetic ulcer services (for patients with diabetic ulcers)

Patients require input from experienced nurses, such as the district nurses or tissue viability nurses. Good wound care involves:

Cleaning the wound
Debridement (removing dead tissue)
Dressing the wound

Compression therapy is used to treat venous ulcers (after arterial disease is excluded with an ABPI).

Pentoxifylline (taken orally) can improve healing in venous ulcers (but is not licensed).

Antibiotics are used to treat infection.

Analgesia is used to manage pain (avoid NSAIDs as they can worsen the condition).