SLA 4 & 8 - Dermatology (A & B) Flashcards

1
Q

Give some functions of skin.

A
  • physical barrier to protect against mechanical, chemical, osmotic, thermal and UV damage
  • physical barrier to prevent microbial infection
  • synthesis of vitamin D
  • thermostasis
  • psychosexual communication
  • major sensory organ for touch, temperature, pain, and other stimuli
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2
Q

Give the three layers of skin.

A
  1. Epidermis
  2. Dermis
  3. Hypodermis
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3
Q

Outline the ultrastructure of the epidermis.

A

Largely formed by layers of keratinocytes undergoing terminal mutation, including increase keratin production and migration toward the external surface (ie. cornification).

There are also several non-keratinocyte cells that inhabit the epidermis:

  1. Melanocytes - produce melanin and pigment formation
  2. Langerhans cells - antigen-presenting dendritic cells
  3. Merkel cells - sensory mechanoreceptors
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4
Q

Give the layers of the epidermis (outermost to innermost).

A

Stratum corneum - cells lose all organelles, continue to produce keratin

Stratum lucidum - cells lose nuclei and drastically increase keratin production

Stratum granulosum - cells secrete lipids and other waterproofing molecules

Stratum spinosum - keratinocytes are joined by desmosomes

Stratum basale - mitosis of keratinocytes

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5
Q

How long does it take for a keratinocyte to travel from the Stratum basale to the Stratum corneum?

A

30-40 days

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6
Q

Outline the ultrastructure of the dermis.

A

Immediately deep to the epidermis and tightly connected to it via the dermo-epidermal junction.

The following cells and structures can be found in the dermis:

  1. Fibroblasts - synthesise the extracellular matrix, predominantly composed of collagen and elastin.
  2. Mast cells - histamine granule-containing cells of the innate immune system
  3. Blood vessels and cutaneous sensory nerves
  4. Skin appendages - for example, hair follicles, nails, sebaceous glands and sweat glands.
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7
Q

The pilosebaceous unit is composed of what?

A

Hair follicle and sebaceous glands.

Sebaceous glands release their glandular secretions via holocrine mechanism into the hair follicle shaft. The hair follicle is associated with an arrector pili muscle, which contracts to stand the follicle upright.

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8
Q

What are the two types of sweat glands?

A
  1. Eccrine glands - major sweat glands that release a clear, odourless substance comprised of sodium chloride and water. This substance has a role in thermoregulation.
  2. Apocrine glands - larger sweat glands located in the axillary and genital regions. The products can be broken down by cutaneous microbes, producing body odour.
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9
Q

Outline the ultrastructure of the hypodermis.

A

Innermost layer of skin, deep the dermis. It acts as a major body store of adipose tissue.

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10
Q

Define ‘lesion’.

A

A single small diseased area.

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11
Q

Define ‘macule’.

A

A circumscribed area of change without elevation.

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12
Q

Define ‘rash’.

A

A skin eruption that is more extensive than a single lesion.

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13
Q

Define ‘papule’.

A

A solid and raised lesion <1cm diameter.

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14
Q

Define ‘nodule’.

A

A solid and raised lesion >1cm diameter.

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15
Q

Define ‘plaque’.

A

A raised confluence of papules >1cm diameter.

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16
Q

Define ‘pustule’.

A

A fluid-filled area containing purulence.

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17
Q

Define ‘vesicle’.

A

A fluid-filled area <1cm containing clear fluid.

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18
Q

Define ‘bullae’.

A

A fluid-filled area >1cm containing clear fluid.

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19
Q

Define ‘petechiae’.

A

Pinpoint flat spots <3mm diameter, caused by intradermal bleeding that do not blanch.

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20
Q

Define ‘purpura’.

A

Haemorrhagic areas >3mm diameter that do not blanch.

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21
Q

Define ‘exanthem’.

A

A rash outside the body (ie. skin).

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22
Q

Define ‘enanthem’.

A

A rash inside the body (ie. mucous membranes).

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23
Q

Give some examples of bacterial skin infections.

A
  • cellulitis
  • impetigo
  • Hansen’s disease (leprosy)
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24
Q

Give some examples of viral skin infections.

A
  • shingles
  • chickenpox
  • warts
  • measles
  • hand, foot and mouth disease
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25
Q

Give some examples of fungal skin infections.

A
  • athlete’s foot
  • ringworm
  • nail fungus
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26
Q

Give some examples of parasitic skin infections.

A
  • lice
  • scabies
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27
Q

Outline the pathophysiology of cellulitis.

A

Bacteria (Streptococcus or Staphylococcus) causes infection of the dermis and subcutaneous tissue, with poorly demarcated borders.

Most infections that affect intact skin are thought to be due to streptococci, although other organisms may be responsible if the integrity of the skin is compromised.

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28
Q

Presentation of cellulitis.

A
  • commonly seen in lower limbs (unilateral)
  • obvious precipitating skin lesion (e.g. traumatic wound or ulcer)
  • erythema
  • pain
  • swelling
  • warmth
  • oedema
  • bullae may form
  • systemic symptoms (e.g. fever / malaise) may occur

Note red lines streaking away from a cellulitic area represent progression of the infection into the lymphatic system.

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29
Q

Management of cellulitis.

A

Conservative measures include rest, elevation of affected limbs, and analgesia (paracetamol or ibuprofen).

Use of an emollient to keep the skin well hydrated.

Draw around the margins of infection to help identify the spread or resolution.

Abx therapy:
1. Flucloxacillin in uncomplicated infection and not penicillin allergic
2. Clarithromycin if penicillin allergic and not pregnant
3. Erythromycin if penicillin allergic and pregnant

Note if MRSA is suspected or the infection is severe, admission to hospital for IV abx therapy may be necessary.

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30
Q

Give 5 features of cellulitis infection that indicate hospital admission.

A
  1. Facial infection
  2. Necrotising fasciitis
  3. Systemic illness or vomiting
  4. Lymphoedema present
  5. Child <1yr
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31
Q

Presentation of non-bollous impetigo.

A
  • begins as small pustules > honey-coloured crusted plaques
  • usually on face
  • satellite lesions may occur
  • itching
  • regional lymphadenopathy
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32
Q

Presentation of bollous impetigo.

A
  • bullae with a thin roof and may rupture
  • common in neonates
  • painful
  • systemic symptoms (e.g. malaise)
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33
Q

Management of impetigo.

A

Skin swab if extensive or severe or MRSA is suspected.

Conservative measures include hygiene advice.

Topical abx can be prescribed in localised infection - may consider oral abx if systemic symptoms or if bullous impetigo.

34
Q

What is the causative organism of leprosy?

A

Mycobacterium leprae

35
Q

Outline the pathogenesis of leprosy.

A

Mycobacterium leprae destroy Schwann cells, resulting in demyelination of nerve cells. This results in permanent neurological damage.

36
Q

Management of leprosy.

A

Seek specialist advice from the Panel of Leprosy Opinion at the Department of Health.

Notifiable disease so must be reported to PHE.

37
Q

Pathogenesis of shingles.

A

Primary infection by varicella-zoster virus causes chickenpox. The virus subsequently lies dormant in the dorsal root ganglion of a nerve.

At periods of immunosuppression, the virus travels down the affected nerve causing a dermatomal reactivation of the virus.

38
Q

Presentation of shingles.

A
  • burning, itching or paraesthesia in a single dermatome
  • skin lesions that crust and dry
39
Q

What is Hutchingson’s sign?

A

A sight-threatening sign whereby the shingles rash involves the side or tip of nose

40
Q

Management of shingles.

A

Conservative measures include keeping the rash dry and clean, and use of regular analgesia.

Oral antiviral therapy and oral corticosteroids can be considered, but use is controversial and so should be prescribed with clinical caution.

41
Q

Give 3 features of shingle infection that would indicate admission to hospital.

A
  1. Hutchingson’s sign
  2. Pregnancy
  3. Complication of shingles (e.g. meningitis or encephalitis) suspected
42
Q

What is post-herpetic neuralgia?

A

PHN is persistent pain at the site of the shingles infection that extends beyond the period of the rash.

It usually lasts from three to six months, but can last longer. It occurs when the reactivated virus causes damage to nerve fibres, and does not respond to simple analgesia (e.g. paracetamol / ibuprofen).

43
Q

Pathophysiology of warts.

A

Infection by HPV 1-4, 10, 27 and 57 result in wart formation.

44
Q

Management of warts.

A

Warts eventually resolve without therapy, so if they are asymptomatic they may not require treatment.

Treatment options involve salicylic acid application (at least 12 weeks) or cryotherapy (available OTC or in general practice).

45
Q

How is measles prevented?

A

Part of MMR childhood immunisation programme in UK.

46
Q

Management of measles.

A

Uncomplicated measles is usually self-limiting and treatment is conservative, including simple analgesia (ie. paracetamol / ibuprofen) and fluid intake.

Notifiable disease so must inform PHE. Contact tracing will ensue and patient must remain at home to prevent spread.

47
Q

What is the common causative organism of hand, foot and mouth disease?

A

Coxsackieviruses (CA16)

48
Q

Presentation of hand, foot and mouth disease.

A
  • mouth lesions - yellow ulcers surrounded by red haloes
  • skin lesions (palms, soles and between fingers and toes)
  • systemic features (e.g. fever, malaise) may be present
49
Q

Management of hand, foot and mouth disease.

A
  • encourage adequate fluid intake
  • suggest soft diet
  • antipyretic analgesia (e.g. paracetamol or ibuprofen)

If the mouth is very painful, topical agents can be considered. For example, mouth rinses with warm salty solutions or oral analgesic gel.

50
Q

Presentation of tinea pedis (Athlete’s foot).

A
  • erythema, vesicles and pustules occurring on the plantar surface of the foot and the webs of toes
51
Q

Management of tinea pedis.

A

Conservative hygiene advice:
- keep skin cool and dry
- avoid scratching affected skin
- do not share towels

OTC antifungal creams or sprays can be purchased from a pharmacist.

52
Q

Give some risk factors of fungal nail infection.

A
  • adults
  • immunosuppression
  • diabetes mellitus
  • athletic / sporting background
  • trauma to nail
53
Q

Presentation of fungal nail infection.

A
  • discolouration of nail
  • thickened nail
  • flaky surface to nail bed
54
Q

Management of fungal nail infection.

A

Nail trimmings sent for microscopy.

Self-care measures include keeping nails trimmed short and sustaining good foot hygiene.

Topical antifungal creams can be prescribed but treatment time is many months. If topical antifungal creams fail to resolve the issue, an oral antifungal can be prescribed alongside topical therapy.

55
Q

What are the components of the triad of atopy?

A
  1. Eczema
  2. Allergic rhinitis
  3. Asthma
56
Q

Give some trigger factors of eczema.

A
  • irritants (e.g. soaps or detergents)
  • skin infection
  • contact allergens
  • extremes of temperature / humidity
  • inhaled allergens
  • stress
  • hormonal changes (e.g. premenstrual flare-ups, deterioration in pregnancy)
57
Q

Presentation of eczema.

A
  • itchiness
  • history of asthma or allergic rhinitis
  • dry skin
  • erythematous rash
  • localised to flexure surfaces of limbs
58
Q

Management of eczema.

A
  • liberal and frequent (TDS - QDS) application of emollient (rehydration of skin)
  • topical mild corticosteroids (e.g. 1% hydrocortisone) to be used sparingly (OD - BDS) and for as short time as possible to control flare-ups

Referral to dermatology may be necessary if topical treatments are not working.

Note prolonged corticosteroid application can result in TCS withdrawal syndrome, whereby the eczema symptoms worsen and may take months to years to resolve.

TCS Withdrawal Syndrome
59
Q

What is lichenification?

A

A secondary skin lesion to eczema due to excessive scratching, wherein the characteristic features of skin thickening, hyperpigmentation and exaggerated skin lines are notes.

60
Q

Outline the presentation of acne vulgaris.

A
  • greasy skin
  • open comedones (blackheads)
  • closed comedones (whiteheads)
  • papules
  • pustules

Most commonly face, neck and back afected.

61
Q

Management of acne vulgaris.

A

Acne is usually mild and self-limiting, and can be controlled conservatively by keeping the face clean and adopting a low-sugar diet.

Can give topical lotions to control acne, and if unsuccessful can prescribe oral antibiotics.

Review every 12 weeks - if symptoms become severe and disfiguring, referral to dermatology may be required.

Note COCP can help to control acne, so used preferably in female patients wishing to use hormonal contraception over POP.

62
Q

Give some common complications of acne vulgaris.

A
  • psychological and social morbidity, leading to severe depression and suicidal ideation
  • scarring from deep lesions
  • post-inflammatory hyperpigmentation (esp. in people with darker skin)
63
Q

Give some risk factors for plaque psoriasis.

A
  • family history
  • Streptococcal infection
  • HIV infection and AIDS
  • postpartum hormonal changes
  • smoking and alcohol
  • trauma
64
Q

Give 3 associated diseases of plaque psoriasis.

A
  1. Psoriatic arthritis
  2. Inflammatory bowel disease
  3. Metabolic syndrome
65
Q

Presentation of plaque psoriasis.

A
  • scaly plaques over extensor surfaces (e.g. knees, elbows)
  • nail changes, including pitting
  • new lesions often appear at sites of injury or trauma (Kobner’s reaction)
66
Q

Management of plaque psoriasis.

A

Conservative management includes smoking cessation and a reduction in alcohol consumption.

Topical emollients to be applied liberally (TDS / QDS) to reduce scales and itching.

Topical corticosteroids and vitamin D analogues.

67
Q

Give 3 features of plaque psoriasis that indicate referral to dermatology.

A
  1. Topical therapy offering inadequate control
  2. Psoriasis is severe and extensive (covering >10% body surface area)
  3. Psoriasis having a major impact on a person’s physical, psychological or social well-being
68
Q

What is psoriatic arthritis?

A

An inflammatory arthropathy, associated with plaque psoriasis.

Note affects approx. 30% of people with plaque psoriasis.

69
Q

Which genetic mutation is specifically linked to an increased incidence of psoriatic arthritis?

A

HLA-B27

70
Q

Presentation of psoriatic arthritis.

A
  • symmetrical polyarthritis
  • wrists, hands, feet and ankles usually affected
  • negative rheumatoid factor (RF) test
71
Q

Management of psoriatic arthritis.

A
  • physiotherapy
  • smoking cessation
  • weight loss
  • physical exercise
  • NSAIDs to relieve MSK symptoms

Urgent referral to rheumatology, who will consider DMARDs or biological treatments to help control psoriatic arthritis.

72
Q

What are the three most common skin cancers?

A
  1. Basal cell carcinoma
  2. Squamous cell carcinoma
  3. Malignant melanoma
73
Q

Risk factors for basal cell carcinomas

A
  • genetic predisposition
  • exposure to UV radiation
  • increasing age
  • male sex
  • Skin types 1 and 2
74
Q

Give the presentation of a nodular basal cell cacinoma.

A
  • solitary, shiny, red nodule with large talangeictatic vessels
  • commonly on face
  • cystic, pearly, telangiectasia
  • ?ulceration
75
Q

Management of basal cell cacinoma.

A

Although metastases and death from BCC remain rare, urgent referral to dermatology is still required.

Surgical intervention is preferrable treatment.

76
Q

Presentation of squamous cell carcinoma.

A
  • non-healing ulcer or growth in photosensitive areas
  • small nodule with a necrotic centre, developing into an ulcer
  • ulcerated lesion with hard, raised edges
  • bleeding may occur from the tumour
77
Q

Management of squamous cell carcinoma.

A

Suspected cancer pathway referral (appt within 2 weeks) for treatment options to be decided.

78
Q

Presentation of malignant melanoma.

A

A mole that is:
- asymmetrical
- border irregularities
- colour (hyperpigmented)
- diameter >7mm
- evolving

79
Q

Management of malignant melanoma.

A

Refer via 2/52 suspected cancer pathway if 7-point checklist score >3.

Major features (+2):
- change in shape
- irregular shape
- irregular colour

Minor features (+1):
- diameter >7mm
- inflammation
- oozing
- change in sensation

80
Q

What is the prognosis like for malignant melanome?

A

Approx 80% 5-year survival

81
Q

Presentation of seborrhoeic keratoses?

A

A common sign of ageing, that can occur on any area of the skin, characterised by a benign hyperketatotic skin lesion.

They can be flat or raised papules or plaques, and may be skin-coloured, yellow, grey, light brown, dark brown or mixed colours.

Often itchy and interfere with clothing or jewellery.

82
Q

Management of seborrhoeic keratoses?

A

If the lesions cause no problems, it is preferable to be left alone (benign).

Can be removed via liquid nitrogen treatment.