Dermatology Flashcards

1
Q

What is melanoma and why is it the most serious skin cancer?

A

• Malignant tumour of melanocytes
• This is the most serious skin cancer due to potential to metastasise as melanocytes are motile cells

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2
Q

What is the ABCDE criteria to tell if a mole is abnormal?

A

A= asymmetry of mole
B= border irregularity
C= colour variation
D= diameter more than 6mm
E= elevation

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3
Q

Four types of melanoma?

A

superficial spreading
lentigo maligna melanoma
nodular melanoma
acral lentiginous melanoma

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4
Q

What is the most common type of melanoma in fair skinned people?

A

superficial spreading

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5
Q

Describe the four types of melanoma?

A

Superficial Spreading
• This is the most common type of melanoma in fair skinned people
• Large, flat, irregularly pigmented lesion that grows laterally before vertical invasion

Lentigo Maligna Melanoma
• A patch of lentigo maligna (a pigmented macule on the face) that develops a papule or nodule signaling invasive melanoma

Nodular Melanoma
• This is the most aggressive type
• It presents as a rapidly growing pigmented nodule which bleeds or ulcerates
• This is invasive from the start

Acral Lentiginous Melanoma
• Arises as pigmented lesions on the palms or soles under the nail and usually presents late
• May not be related to sun exposure

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6
Q

What is Breslow thickness?

A

criteria used to determine prognosis in melanoma defined as: Breslow thickness= deepest part of the tumour from the granular layer in mm
• A Breslow < 1 mm = 5yr survival of 95-100%
• A Breslow > 4mm= 5yr survival of 50%

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7
Q

Describe spread of melanoma?

A

Melanoma tends to spread to local dermal lymphatics (satellite deposits), then to regional lymph nodes and blood spread to the skin, soft tissue, heart, lungs, GI tract, liver and brain

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8
Q

Explain what is meant by sentinel node?

A

first lymph node a tumour drains to, often biopsied to assess spread

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9
Q

Describe management of melanoma?

A

• Primary excision is done to give clear margins
• In thicker tumours a sentinel node biopsy is done and if this is positive a regional lymphadenectomy will be done
• (sentinel nodes= first nodes that a tumour drains to)
• Treatment of advanced disease is difficult
• For advanced disease some treatments include removal of regional lymph nodes, isolated limb perfusion, radiotherapy, immunotherapy and chemotherapy (unfortunately not a lot of these cause much improvement)
• There are new targeted gene therapies such as BRAF inhibitors and MEK inhibitors that have improved prognosis (BRAF is a common gene change in melanoma so these drugs target tumour cells with BRAF mutations, unfortunately the cancer may have multiple mutations so these drugs work for a short while and then the cells with other mutations keep growing and the cancer returns)

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10
Q

What is the most common malignant skin tumour?

A

basal cell carcinoma

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11
Q

Who does basal carcinoma tend to arise in? What type of sun exposure increases risk?

A

• They generally arise in fair middle-aged people with sun exposed skin
• The sun exposure is peak sun exposure so due to periods where skin has been burned (vs chronic which is to do with lifetime cumulative UV exposure)

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12
Q

Describe the 3 types of basal cell carcinoma?

A

Nodular
• Typically appears as a shiny, pearly nodule with central ulceration

Superficial
• Spreads superficially

Infiltrative/ Morpheic
• Most important type as this can infiltrate tissues widely
• Prominent desmoplastic fibrous stroma (stroma is a covering of connective tissue, desmoplasmic stroma means abnormal covering of connective tissue created/ caused by the tumour)
• Margins are poorly defined and resection can be difficult as it can spread along nerves

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13
Q

Describe treatment for basal cell carcinoma?

A

• In most cases treatment of choice is a wide excision with histology to ensure clear and adequate tumour margins
• BCCs rarely ever metastasise so the main reason to remove them is that they are locally invasive
• For superficial BCCs may do cryotherapy, phototherapy or topical imiquimod instead (imiquimod is an immune response modifier)
• Vismodegib is a new oral therapy for inoperable BCCs that inhibits the hedgehog signaling pathway (abnormalities in hedgehog signaling due to mutations in a tumour suppressor gene are thought to exist in BCCs)

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14
Q

Does SCC or BCC have higher risk of metastases?

A

SCC has higher risk, BCC virtually never metastasises (it is malignant because it is locally invasive)

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15
Q

What type of sun exposure is SCC due to?

A

cumulative sun exposure

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16
Q

What are 2 pre-malignant lesions that SCC could arise in?

A

Actinic keratoses or Bowens

(bowens is essentially SCC in situ although arguments over whether it has to be on a sun exposed site to call it bowens)

(AK essentially refers to varying forms of squamous dysplasia)

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17
Q

Management of squamous cell carcinoma?

A

• Complete surgical excision with a minimal margin of 5mm
• Radiotherapy is also used

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18
Q

What is the most common inflammatory skin disease worldwide?

A

atopic eczema

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19
Q

Risk factors/ what groups get atopic eczema?

A

• It is associated with other atopic diseases i.e., Asthma, hayfever and food allergy
• Genetic and environmental factors plus the filaggrin gene are thought to be important
• Usually if eczema develops early in babies it will clear by adulthood
• If occurs in late childhood or adulthood the disease is more likely to be chronic

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20
Q

Presentation of atopic eczema?

A

• Presents as ill-defined erythema as well as generalized dry skin
• There is usually a flexural distribution (unless in babies where it can be found more on extensor areas)
• Chronic changes to the skin can occur in atopic eczema such as lichenification, excoriation and secondary infections
• Usually if eczema develops early in babies it will clear by adulthood
• If occurs in late childhood or adulthood the disease is more likely to be chronic

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21
Q

Management of atopic eczema?

A

• Emollients for everyone with eczema, they should be applied even when no flare up and skin is comfortable
• Can also get bath and shower emollients to use instead of normal products with frangrances that might aggravate the eczema
• Topical steroids are main treatment for mild to moderate eczema
• Weakest steroid for the shortest amount of time should be used
• If eczema keeps recurring after steroids stopped then can do “weekend treatment” where you do 2 days steroid, 5 days rest
• Topical calcineurin inhibitors may help in treating sensitive sites
• Long term control of severe disease may require immunosuppressive or anti-inflammatory agents

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22
Q

Describe eczema herpeticum?

A

• Infection of eczema rash by herpes virus
• This usually happens in children
• And presents a very painful monomorphic punched out lesions, in a systemically unwell child

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23
Q

Explain what acne is and pathogenesis?

A

• Chronic inflammatory disease of the pilosebaceous unit
• Lesions arise in the pilosebaceous follicle which becomes blocked due to abnormal keratinization and increased production of sebum
• This leads to overgrowth or Propionibacterium acnes which triggers a inflammatory response by activation of Toll-like receptors and induction of pro-inflammatory mediators

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24
Q

What groups tend to get acne?

A

• Generally, occurs in 14-17yrs old in females and 16-19yrs old in males
• However, it can persist into adulthood

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25
Q

Presentation of acne?

A

• Acne tends to occur in the face and upper torso where sebaceous glands are very dense
• Non inflammatory features include blackheads (open comodones) and white heads (closed comodones)
• Inflammatory features include papules, pustules, nodules and cysts
• Secondary features include scarring

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26
Q

Management of acne?

A

• Avoidance of oily substances

1) Topical benzoyl peroxide (this is keratolytic and antibacterial)
2) Topical retinoid (this has a drying effect)
3) Topical antibiotic (antibacterial and anti-inflammatory)
4) Systemic antibiotics usually tetracyclines
5) Isotretinoin (oral retinoid)

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27
Q

What is it important to note about isotretinoin?

A

Isotretinoin has a large amount of side effects and is also teratogenic

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28
Q

Define parakeratosis

A

persistence of nuclei in the keratin layer (epidermis is turning over too quickly for nuclei to be lost or may be premalignant)

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29
Q

Define hyperkeratosis?

A

increased thickness of the keratin layer

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30
Q

Define acanthosis?

A

increased thickness of the epidermis and elongation of rete ridges due to hyperplasia of the prickle cell layer

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31
Q

What are rete ridges?

A

the epithelial extensions that project into the underlying connective tissue in both skin and mucous membranes

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32
Q

Define papillomatosis?

A

irregular epithelial thickening

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33
Q

Define spongiosis?

A

oedema in the epidermis

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34
Q

Describe the four classifications of inflammatory skin disease in pathology?

A

1) Spongiotic Intraepidermal oedema > Eczema
2) Psoriasiform- elongation of the rete ridges > Psoriasis
3) Lichenoid basal layer damage > Lichen Planus and Lupus
4) Vesiculo-bullous disorders > dermatitis herpetiforms, bullous pemphigoid and bullous pemphigus

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35
Q

What is psoriasis?

A

• Psoriasis is a chronic inflammatory skin condition characterized by clearly defined red, scaly plaques
• The skin becomes inflamed and hyper-proliferates at about 10x the normal rate

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36
Q

What groups tend to get psoriasis?

A

• It can start at any age
• However, there are 2 main peaks of onset: age 16-22 and age 55-60
• There is a genetic basis of psoriasis, but it is not fully understood, it is a multifactorial condition

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37
Q

How does

A
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38
Q

How can hyperkeratosis be described?

A

as parakeratotic - increased thickness and nuclei in the keratin layer
as orthokeratotic - increased thickness but maturation preserved so no nuclei

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39
Q

What is psoriasis?

A

• Psoriasis is a chronic inflammatory skin condition characterized by clearly defined red, scaly plaques
• The skin becomes inflamed and hyper-proliferates at about 10x the normal rate

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40
Q

Risk factors and who tends to get psoriasis?

A

• It can start at any age
• However, there are 2 main peaks of onset: age 16-22 and age 55-60
• There is a genetic basis of psoriasis, but it is not fully understood, it is a multifactorial condition
• Psoriasis is classified as an immune mediated inflammatory disease

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41
Q

How does psoriasis typically present?

A

Psoriasis usually presents with symmetrically distributed red scaly plaques with well-defined edges, the scales are typically silvery white

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42
Q

What is the most common subtype of psoriasis?

A

chronic plaque psoriasis

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43
Q

What is the Koebner phenomenon?

A

new psoriasis plaques occur at sites of trauma

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44
Q

List 7 classifications of psoriasis?

A

chronic plaque psoriasis
flexural psoriasis
guttate psoriasis
erythrodermic and pustular psoriasis
palmoplantar psoriasis
psoriatic nail disease
scalp psoriasis

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45
Q

Describe psoriatic nail disease?

A
  • Onycholysis (painless detachment of the nail from the nail bed)
  • Nail pitting (dents in the nails)
  • Subungal hyperkeratosis (the skin under the nail becomes thicker)
  • Dystrophy (destroyed parts of the nail)
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46
Q

How is psoriasis usually diagnosed?

A

usually by clinical features alone but if in doubt a biopsy can be done

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47
Q

Psoriasis pathology?

A

• Epidermal acanthosis and parakeratosis due to increased skin turnover
• The granular cell layer is often absent
• The epidermal rete ridges appear elongated and clubbed as they fold down into the dermis

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48
Q

List some health conditions associated with psoriasis?

A

• Psoriatic Arthritis – this is particularly common in those with psoriatic nail disease
• Inflammatory bowel disease
• Uveitis
• Coeliac Disease
• Metabolic Syndrome (those with psoriasis have a higher prevalence of cardiometabolic diseases)

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49
Q

Describe management of psoriasis?

A

• There is no cure for psoriasis, first line treatment varies depending on the patient
• Everyone should use emollients every day

Mild psoriasis is generally treated with topical agents alone:
• Vitamin D analogues: e.g. calipotrol or calcitrol, it is an anti-proliferative agent, need to be careful of systemic absorption and development of hypercalcaemia
• Coal Tar: no limits to use, however not cosmetically acceptable to most and generally just used in hospital
• Dithranol: this is a really effective treatment however it is irritant if applied to normal skin and also stains skin, it therefore generally needs to be left on affected skin for 10-30 mins and then washed off, need patient to be willing to apply twice a day and wash off etc which is a lot of work
• Steroids: in psoriasis these are usually given in combination because there is a risk of rebound disease

In moderate to severe disease:
• Treatment with systemic agents e.g. methotrexate, ciclosporin, acitretin
• Phototherapy

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50
Q

What is scabies?

A

• Transmissible skin disease caused by ectoparasitic mite Sarcoptes Scabiei var hominis
• This variant of scabies is only caught by humans and is not spread to other animals

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51
Q

Risk factors/ groups of people who tend to get scabies?

A

Global disease and anyone can be affected but more common in children, adolescents and elderly
Risk factors for scabies include:
- Crowded conditions
- Poor hygiene
- Poverty
- Malnutrition
- Homelessness
- Immunodeficiency

These risk factors are more relevant for low/ middle income countries, in high income countries scabies outbreaks can occur as a family outbreak as children acquire it from school or sleepovers, outbreaks in places like care homes or student halls is not uncommon.

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52
Q

How is scabies spread?

A

• Transmitted through close bodily skin contact e.g. holding hands for prolonged period, between sexual partners
• Brief handshake or hug is generally not long enough unless the patient has crusted scabies

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53
Q

Presentation of scabies?

A

• Classical itchy rash
• Lesions are symmetrical and mainly affect the hands, wrists, axillae, thighs, buttocks, waist, soles or feet, areola and vulva in females and penis and scrotum in males
• The neck and above are usually spared
• Itch is generalised, occurs 4-6 weeks following initial infection, worse at night time, may persist for several weeks after completion of treatment
• The rash can appear as erythematous papules, excoriations, linear scratch marks, dermatitis, nodules, crusting, vesicles (secondary to bacterial infection)
• Pathognomonic features are burrows (thread like tracks of 5-10mm mainly in web spaces, inner wrists, elbows, umbilicus and beltline) and nodules

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54
Q

Management of scabies?

A

General Measures
• Launder sheets, towels and clothes. Non washable things e.g. jackets, duvets etc. should be aired for 72 hours
• Vacuum soft furnishings if possible
• Clip nails and clean debris

Specific Measures
• All close contacts of case need to complete eradication therapy because they can be asymptomatic for weeks but still infect others and reinfect the index case
• Topical permethrin cream is first line (topical insecticide), needs applied from jawline downwards and left overnight for 8-12 hours, must reapply if wash hands, should also apply under nails and between toes
• Oral ivermectin (antiparasitic drug) is indicated in cases where topical treatment fails
• Should provide written instructions to patients, assemble beddings and clothing for laundry and apply cream before dressing and remaking beds
• Itching can last for several weeks and does not represent persistent infection or treatment failure

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55
Q

Pharma management of scabies?

A

1st line - permethrin topical cream
2nd line - oral ivermectin

56
Q

What are head lice?

A

• Small wingless insects that infest the human scalp
• They are the most common of the 3 human lice species

57
Q

What are some risk factors / common groups who get head lice?

A

• Can affect people all over the world
• Most common in children age 4-14
• Risk factors include long hair, female sex, greater number of children in a family, sharing beds, clothing and hair brushes

58
Q

How do head lice spread?

A

• They can’t jump or fly so only spread by crawling along hair shafts by head to head contact

59
Q

Features of head lice infestation?

A

• Cause itch and irritation in the scalp (can take several weeks to develop after initial infestation)
• Lice favour the nape of the neck and skin behind the ears
• Nits (empty egg cases attached to hair that the lice hatch from) are easier to see and appear as white grains on the hair shaft
• There may be red-brown spots on the skin due to excreted digested blood

60
Q

Diagnosis of head lice?

A

• They can be difficult to diagnosis but should look for clinical features
• Can identify and remove live lice by wet coming using a lice comb

61
Q

Treatment of head lice?

A

• Treat all members of family at same time, schools/ nurseries should be informed
• Usually involves at least 2 applications of insecticide and physical methods to remove nits and lice e.g. combs in wet hair
• Suffocating silicate agents are best now, 4% dimethicone is the main one
• Chemical insecticides e.g. malathion are of less use now because there are high levels of resistance

62
Q

What is folliculitis?

A

• Folliculitis means an inflamed hair follicle due to any cause
• The result is a tender red spot, often with a surface pustule
• Folliculitis can be superficial or deep
• It can affect anywhere there are hairs, including chest, back, buttocks, arms and legs
• Acne and its variants are also types of folliculitis

63
Q

List some causes of folliculitis?

A

infection
irritation from regrowing hairs
contact reactions
drugs
inflammatory skin conditions

64
Q

List some infective causes of folliculitis?

A

bacterial - commonly staph A also pseudomonas for spa pool folliculitis
yeast - pittosporum ovale
fungal - ringworm
viral - HSV or herpes zoster
parasitic - in immunosuppressed the demodex mite known as demodicosis

65
Q

Give some examples of drugs that can cause folliculitis?

A

steroids, androgens, ACTH, lithium, isoniazid, phenytoin and B-complex vitamins

66
Q

Describe the difference in pathogenesis of irritant, contact and atopic dermatitis?

A

atopic - not fully understood mechanism
contact - type 4 hypersensitivity - immune mediated
irritant - not immune mediated

everyone if exposed enough to right chemical will get irritant dermatitis but not everyone will get contact dermatitis, important to note that those with atopic dermatitis are at higher risk of contact and irritant dermatitis, often they can all occur together

67
Q

How do you find the responsible agent in allergic contact dermatitis?

A

patch testing

68
Q

Management of allergic contact and irritant dermatitis?

A

avoidance of whatever is causing it or wearing protective clothing to minimise contact
the actual rash is managed similarly to atopic dermatitis ie. emollients and steroids

69
Q

What is the commonest form of hand dermatitis?

A

irritant dermatitis

70
Q

What is urticaria?

A

• Urticaria is characterised by very itchy weals
• Generally, a type 1 hypersensitivity reaction
• Weals are superficial skin coloured or pale skin swelling usually surrounded by erythema that last anything from a few minutes to 24 hours
• Weals are compressible

71
Q

What can urticaria co-exist with?

A

angioedema which is a deeper swelling within the skin or mucous membranes

72
Q

Classifications of urticaria?

A

• Urticaria can be acute (<6 weeks duration and often gone within hours to days) or chronic (> 6 weeks duration with daily or episodic weals)
• Chronic urticaria may be spontaneous or inducible or both types may co-exist

73
Q

Risk factors/ groups that tend to get urticaria?

A

• One in five children or adults has an episode of acute urticaria during their lifetime, it can affect anyone
• Acute urticaria in children is usually caused by infection even if afebrile
• In older children, food, medication and inhaled allergens are also important causes
• In adults urticaria is usually idiopathic and spontaneous

74
Q

Diagnosis of urticaria?

A

• Generally diagnosed by history/ examination
• Skin prick tests and radioallergosorbent tests (RAST) or CAP fluoroimmunoassay may be done if allergy is suspected in acute urticaria
• There are no routine diagnostic tests in chronic spontaneous urticaria apart from blood count or CRP
• Chronic inducible urticaria is often confirmed by inducing the reaction e.g. scratching the skin in dermographism or applying an ice cube in suspected cold urticaria

75
Q

What is RAST testing?

A

blood test that looks for IgE antibodies for things someone might be allergic to, alternative to a skin prick test

76
Q

Management of urticaria?

A

• The main treatment of all forms of urticaria in adults and children is with an oral second generation H1-antihistamine such as cetirizine or loratadine
• If the standard 10mg dose is not effective then dose can be increased up to 40mg
• They are stopped when the acute urticaria has settled down

77
Q

What are the most common HPV types infecting the skin?

A

types 1, 2, 3, 4, 10, 27, 29 and 57

78
Q

How is HPV spread?

A

direct skin to skin contact or autoinoculation if already infected and pick the wart etc and touch other parts of skin

79
Q

Describe clinical features of cutaneous viral warts?

A

• Cutaneous viral warts have a hard, keratinous surface
• Tiny red or black dots visible in the wart are papillary capillaries
• Common warts present as cauliflower like papules with a rough papillomatous and hyperkeratotic surface ranging from 1mm to 1cm or more
• They can be solitary or multiple
• Common warts are found most on knees, backs of fingers or toes and around the nails
• Plantar warts include tender inwardly growing myrmecia caused by HPV1 and clusters of superficial less painful mosaic warts due to HPV 2
• Myrmecial warts are typically tender with lateral and direct pressure

80
Q

Explain how warts caused by HPV 1 infection present differently?

A

tend to grow inwardly and are typically tender with lateral and direct pressure

81
Q

Diagnosis of cutaneous warts?

A

Cutaneous warts are usually diagnosed clinically:

  • Pinpoint red or black dots are revealed when wart is pared down, patent capillaries cause pinpoint bleeding
  • Location of plantar wart is not restricted to pressure sites unlike callus or corn and tenderness is maximal with lateral pressure as opposed to direct

Dermoscopy assists visualisation of the papillary capillaries of a viral wart and can help distinguish from other lesions e.g. seborrheic keratosis

82
Q

Management of cutaneous warts?

A

• Note: viral warts are infectious to the patient and others
• Most warts especially in children resolve spontaneously however some patients may prefer treatment and those who are immunosuppressed or have complications e.g. foot pain from the wart should be treated
• Topical treatment can be done with salicylic acid or podophyllin or similar compounds which work by removing the surface skin cells, it is applied once daily, can take weeks to resolve, patience is key
• Cryotherapy with liquid nitrogen is another option and repeated at 1-2 week intervals to cause peeling of the surface layer, it is uncomfortable and again takes weeks to months

83
Q

What is tinea/ ring worm?

A

Tinea refers to a skin infection with a dermatophyte (ringworm) fungus

84
Q

List parts of body with types of ring worm/ tinea?

A

• Tinea barbae (beard)
• Tinea capitis (head)
• Tinea cruris (groin)
• Tinea faciei (face)
• Tinea manuum (hand)
• Tinea pedis (foot) – athlete’s foot – most common dermatophyte infection
• Tinea unguium (nail)

85
Q

How is tinea spread/ passed on?

A

It is spread easily from person to person and the spores can live in warm moist environments
Can be spread in showers and changing rooms (hence the name athlete’s foot for tinea pedis)

86
Q

What is the most common dermatophyte infection?

A

tinea pedis - athletes foot

87
Q

Clinical features of tinea?

A

• Tend to form expanding annular lesion due to lateral growth
• Clinical appearance can change depending on site and type of dermatophyte
• Generally, causes asymmetrical scaly itchy rashes

88
Q

Management of tinea?

A

• Topical antifungal cream is used in most cases e.g., clotrimazole
• Should note that you can spread it to others and others to you and can also live in warm moist environments i.e. wash towels, bedding etc.

89
Q

What is candida?

A

• Group of yeasts (a type of fungus) that commonly infects the skin
• It is a normal inhabitant of the GI tract but can overgrow on occluded moist skin
• It can cause infection of the mucosa and of the skin

90
Q

Risk factors for candida?

A

Cutaneous candidiasis is more likely in the following circumstances:
- Infancy or old age
- Warm climate
- Occlusion e.g. plastic pants in babies, nylon tights
- Broad spectrum antibiotic treatment
- COCP or pregnancy
- Diabetes, cushings, and other endocrine disorders
- Iron deficiency
- General debility e.g. from cancer or malnutrition
- Underlying skin disease e.g. psoriasis or lichen planus
- Immunodeficiency
- Chemotherapy or immunosuppressive medications

91
Q

Clinical features and diagnosis of candida infection?

A

• Clinical features depend on area infected e.g. oral candidiasis (thrush), angular cheilitis, vulvovaginal candidiasis, intertrigo (skin fold infection), napkin dermatitis etc.
• Candida intertrigo (skin folds) causes irritation and soreness, affected areas are glazed and inflamed with a ragged peeling edge that may contain a few small pustules
• In infection of the oral mucosa affected mucosal surfaces are inflamed with superficial white or creamy pseudomembranous plaques which can be easily scraped away
• Microscopy and culture of skin swabs and scrapings aid in diagnosis but need correlated with clinical presentation and candida can live on mucosal surfaces harmlessly

92
Q

Management of candida infection?

A

topical clotrimazole

93
Q

What is impetigo and what is it caused by?

A

• Impetigo is a superficial skin infection
• It is generally caused by Staph Aureus but can also be caused by Strep Pyogenes

94
Q

How is impetigo spread and who is it common in?

A

highly infectious, spread by direct contact, most commonly affects children

95
Q

What are the 2 subtypes of impetigo?

A

non-bullous and bulbous

96
Q

Clinical features of non-bullous impetigo?

A

• Most commonly found on face or extremities but skin on any part of the body can be involved
• Begins with a single erythematous macule which evolves into a pustule or vesicle
• Pustule or vesicle rupture releasing serous contents which dries leaving a typical honey-coloured crust
• Patients are typically otherwise well

97
Q

Honey coloured crust?

A

impetigo

98
Q

Clinical features of bullous impetigo?

A

• Usually found on the face, trunk, extremities, buttocks and perineal regions
• Presents as quickly appearing superficial, small or large thin roofed bullae which spontaneously rupture and ooze yellow fluid leaving scaley rim
• Patients more likely to have systemic symptoms of malaise fever or lymphadenopathy in this form

99
Q

Diagnosis of impetigo?

A

• Usually, a clinical diagnosis but skin swab for culture and sensitivity may be beneficial in recurrent, widespread or concern of MRSA

100
Q

Management of impetigo?

A

• For localised no-bullous impetigo can apply antiseptic 2-3 a day for 5-7 days e.g. hydrogen peroxide 1% or povidone – iodine 10% ointment
• Topical antibiotics can be considered if antiseptic treatment has not worked or not appropriate, fusidic acid is first line
• Oral antibiotics can be used when topical treatments fail, a person is at high risk of complications or when a person is systemically unwell, oral flucloxacillin is often first line antibiotic of choice
• Patients should avoid touching affected areas, practice good hand hygiene, use clean cloths when washing and drying affected areas, clean clothes and bedding and avoid close contact with others until lesions have crusted over or 24 hours of treatment

101
Q

What are mosaic warts?

A

cluster of warts caused by HPV

102
Q

What type of injection can be used for persistent warts?

A

bleomycin injections

103
Q

What is paronychia?

A

inflammation around the nail
can be caused by staph or strep infection

104
Q

Rashes with amoxicillin are not uncommon especially in _________ and _________ and this doesn’t indicate a true penicillin allergy but ________

A

glandular fever
chronic lymphocytic leukaemia
still have to stop treatment

105
Q

List 4 differences between pemphigoid and pemphigus?

A

PEMPHIGOID:
sub epidermal - deep tense blisters
attack on hemidesmosomes
blisters are nikolsky sign negative
no involvement of mucosa

PEMPHIGUS:
intraepidermal - superficial blisters that rupture easily
attack on desmosomes
blisters are nikolsky sign positive
can be mucosal involvement

106
Q

What is Nikolsky sign?

A

nikolsky sign positive means the top layer of skin slops away from the lower layers when rubbed

107
Q

What can often proceed the development of blisters in bullous pemphigoid?

A

itch

108
Q

Treatment of pemphigoid?

A

• Most people are initially given steroid tablets and then dose reduced until blisters stop appearing which could take several weeks
• May be given steroid sparing agents such as tetracycline antibiotics
• Tetracycline antibiotics e.g. doxycycline can be used on their own in mild disease
• The blisters tend to heal without scarring

109
Q

Treatment of pemphigus?

A

• Systemic corticosteroids are the main stay of treatment usually as high dose oral prednisolone or IV prednisolone in the form of methylprednisolone
• Other immunosuppressive agents may be used if pemphigus lasts long term

110
Q

What is the difference between desmosomes and hemidesmosomes and what is the relevance to pemphigoid and pemphigus?

A

• Desmosomes form cell to cell adhesions
• Hemidesmosomes form adhesions between cells and the basement membrane
• It is the desmosomes that are attacked in pemphigus vulgaris but the hemidesmosomes in bullous pemphigoid

111
Q

What is dermatitis herpetiformes?

A

• A rare but persistent immunobullus disease that has been linked to coeliac disease

112
Q

What groups tend to get dermatitis herpetiformes?

A

• It predominantly affects Caucasians 15-40
• More females than males
• Genetic predisposition with HLA DQ2 and DQ8
• Some patients have personal or family history of other autoimmune diseases e.g. thyroid, pernicious anaemia, type 1 diabetes, alopecia areata, vitiligo or Addison disease

113
Q

Clinical features of dermatitis herpetiformes?

A

• Symmetrical distribution
• Mainly on scalp, shoulders, buttocks, elbows and knees
• Itchy papules and vesicles on normal or reddened skin

114
Q

Diagnosis and investigations for dermatitis herpetiformes?

A

• Skin biopsy is usually necessary to confirm it
• Should check for tissue transglutaminase antibodies
• Should screen for nutritional deficiencies that can be present in coeliac disease

115
Q

Management of dermatitis herpetiformes?

A

• Gluten free diet
• Dapsone (a type of antibiotic) is medicine of choice as can reduce itch quickly
• Majority of patients respond well to medication and a gluten free diet

116
Q

What is cellulitis and what are the most common causes?

A

• This is a common bacterial skin infection of the lower dermis and subcutaneous tissue
• Most common infective organisms are Staph Aureus and Strep Pyogenes

117
Q

Clinical features of cellulitis?

A

• Localised area of red, painful, swollen skin and systemic symptoms
• Skin swabs are usually negative unless taken from broken skin

118
Q

Management of cellulitis?

A

• Oral flucloxacillin for 5 days
• Doxycycline if penicillin allergic

119
Q

Define what an ulcer is?

A

full thickness skin loss

120
Q

List some causes of leg ulcers?

A

• Most ulcers are venous in nature
• Other causes include arterial, diabetes and rheumatoid ulcers

121
Q

What causes venous ulcers?

A

These are due to venous insufficiency (improper functioning of the one way valves). This results in pooling of blood around lower part of the leg to just below the ankle, increased venous pressure causes fibrin deposits around the capillaries which then act as a barrier to the flow of oxygen and nutrients to the muscle and skin tissue, death of tissue leads to ulceration

122
Q

Where are venous ulcers generally found vs arterial ulcers?

A

venous: gaiter area (below knee, inner aspects of legs)
arterial: on the feet, heels or toes

123
Q

Are venous ulcers painful?

A

usually not - unless infected

124
Q

Clinical features of venous ulcers?

A

• These are generally found below the knee in the gaiter area (inner aspects of legs)
• Usually relatively painless unless infected
• There may be oedema of the lower leg, varicose veins, venous eczema, brown pigmentation from haemosiderin staining and lipodermatosclerosis (inflammation of fat under the epidermis)

125
Q

What causes arterial ulcers?

A

Arterial insufficiency causing poor blood circulation to the lower leg and foot and is usually due to atherosclerosis, the arteries fail to deliver oxygen and nutrients to the leg and foot so get tissue breakdown and ulcer formation

usually a precipitating injury

126
Q

Clinical features of arterial ulcers?

A

• These are usually found on the feet, heels or toes
• They are frequently painful, particularly at night in bed or when the legs are at rest and elevated
• The borders of the ulcer appear “punched out”
• Clinically there are signs of peripheral vascular disease ie. Diminished pulses, pallor, hair loss
• Patient may have a history of claudication, hypertension, angina or smoking

127
Q

Investigations for ulcers?

A

• Ankle Brachial Pressure Index will allow you to determine if arterial disease is present
• A normal value is o 0.92-1.3
• If ABPI is less than 0.9 there is likely arterial disease, if less than 0.5 then this indicates severe arterial disease
• Can also do a doppler to look at blood flow through the vessels

128
Q

Management of venous ulcers?

A

• Non-adherent dressing
• De-sloughing agent
• 4 layer compression bandaging, may need to increase pressure gradually if pain is a problem
• Leg elevation
• Once the ulcer has healed prevention needs to be done with continual wearing of compression stockings

129
Q

Management of arterial ulcers?

A

• No compression bandages!
• Keep the ulcer clean and covered, adequate analgesia and vascular reconstruction done if appropriate

130
Q

What is a pressure ulcer?

A

• A pressure ulcer is an area of reddened skin that progresses to breakdown of skin and underlying tissue to form an erosion or ulcer and is due to persistent pressure on the affected area

131
Q

What causes a pressure ulcer?

A

• A pressure ulcer is due to lack of blood flow due to mechanical stress on the skin and tissues over a bony area that has been under pressure for a prolonged period
• If blood supply is cut off to an area of skin for more than 2-3 hours then the skin is deprived of oxygen and begins to die
• In addition: friction from wrinkled bedding or clothing and exposure to moisture, e.g. sweat or urine increase likelihood of developing an ulcer

132
Q

Who is at risk of a pressure ulcer?

A

• People immobile due to illness, injury or disability are at greatest risk

133
Q

Management of a pressure ulcer?

A

• They can be difficult to treat once skin is no longer intact
• If skin is still intact it usually heals by itself if pressure removed
• If skin is broken need to prevent infection and protect the sore, special dressings and honey preparations can be used to help the healing process and may need debridement of any dead tissue

134
Q

Prevention of a pressure ulcer?

A

• Identify those at risk
• Avoid and correct malnutrition
• Daily inspection of skin to detect early redness
• Frequent repositioning every 2 hours
• Maintaining skin hygiene
• Special foam, fibre and gels used as padding materials on chairs and beds to relive pressure on bony prominences
• Powered alternating pressure mattresses and overlays

135
Q

Treatment of choice for a fungal nail infection?

A

need oral terbinafine to clear a fungal nail infection usually
often leave the infection in elderly as its really bad for the liver and having a fungal nail isn’t a big deal

136
Q

Treatment of choice for pyoderma gangrenosum?

A

oral steroids - it is not an infection but necrosis from inflammatory reaction!