16 - Common Dermatological Conditions Flashcards

1
Q

What are some of the different types of eczema?

A

DIFFERENT TYPES CAN CO-EXIST

Endogenous:

  • Atopic dermatitis (children)
  • Seborrhoeic (more so in adults)
  • Varicose
  • Discoid

Exogenous:

  • Contact dermatitis
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2
Q

What is the pathophysiology of eczema?

A

- Chronic atopic condition

- Defects in the barrier that the skin provides so there is an entrance for irritants, microbes and allergens that create an immune response (exaggerated IgE response), resulting in inflammation

  • Often genetic due to inheritance of FLG (fillagrin) gene that is a protein needed for the skin barrier
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3
Q

How does atopic eczema typically present and what is the disease pattern?

A
  • Relapsing and remitting in infants
  • Scaly, itchy, dry and erythematous patches commonly affecting the flexures. Can affect cheeks of infants and in black patients can affect extensors
  • Excoriation and lichenification (thickening of skin)

- Areas of hypo/hyperpigmentation after rash

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4
Q

What are some differential diagnoses for atopic eczema?

A
  • Psoriasis (not itchy)
  • Seborrhoeic dermatitis
  • Fungal infections
  • Contact dermatitis
  • Scabies
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5
Q

What are some risk factors for developing eczema?

A
  • Family history of atopy
  • Personal history of atopy (hayfever, asthma), food allergies or allergic conjunctivitis
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6
Q

How is atopic eczema different in Asian, Black Caribbean and Black African children?

A
  • Often affects extensors rather than flexors
  • Discoid and Follicular patterns more common
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7
Q

How is atopic eczema diagnosed?

A

Under 12s. Have itchy skin plus at least 3 of the following:

  • Onset of symptoms was before 2 years old
  • Past flexural symptoms
  • History of dry skin in the last 12 months
  • Personal or first degree family history of atopy
  • Visible flexural dermatitis or on cheeks
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8
Q

What area does atopic eczema usually spare?

A
  • Nappy area
  • Most children grow out of this eczema by 13 years old
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9
Q

What is an important question to ask in the history when a patient has eczema?

A
  • Is it affecting your sleep?
  • How does it affect your life?

Always need to consider if they need a referral to a psychologist for their mental health

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10
Q

How is atopic dermatitis managed in general terms?

A

Advice to give:

  • Identify and avoid triggers e.g soaps, hormones, pets, foods
  • Discourage elimination diet
  • Report any weeping/oozing rashes as could be eczema herpeticum
  • Keep nails short to prevent scratching

Treatment:

  • Emollients and Soap substitutes: as maintenance
  • Topical corticosteroids: for flares
  • Sedating antihistamine: for itch at night
  • Oral antibiotics: if secondary infection
  • Topical tacrolimus: if not controlled by above
  • Systemic immunosuppressants: if severe e.g methotrexate, azathioprine
  • Phototherapy: if severe
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11
Q

How would you advise a patient with eczema to use emollients?

A
  • Need to be applying at least 3 times a day very liberally even when eczema not active as provides a barrier
  • Use emollients as a soap substitute as normal soaps strip skins oils
  • Best emollient is the one the patient likes the most
  • Apply 30 minutes before application of steroid
  • AVOID NAKED FLAMES DUE TO PARAFFIN CONTENTS
  • Wet wrap when severe flare
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12
Q

What are the different preparations of emollient and what are some examples of each?

A

- Lotions (e.g. Dermol 500, E45): High water content. Spread easily and absorb quick. Not effective at moisturising very dry skin.

- Creams (e.g. Diprobase, Epaderm): Mixture of fat and water. Spread easily. Not as greasy so often preferred by patients

- Sprays (e.g. Emollin): Useful for hard to reach areas.

- Ointments (e.g. Diprobase, Epaderm): Contain minimal water making them thick and greasy. Patients may find them cosmetically displeasing. Very effective at holding water and repairing skin

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13
Q

What advice would you give to an eczema patient when prescribing them topical corticosteroids?

A
  • Apply thin layer 30 minutes after emollient application
  • Explain they are safe if used as prescribed
  • Only use in active eczema/flares and only up to a week at a time
  • 1 Fingertip is enough to cover two adult hands worth of skin

STEP UP AND DOWN DEPENDING ON RESPONSE TO EACH STEROID

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14
Q

What are some side effects of topical steroids?

A
  • Burning sensation
  • Thinning of skin
  • Contact dermatitis
  • Acne
  • Depigmentation
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15
Q

What is the steroid ladder?

A

- Mildly potent: Hydrocortisone

- Moderately potent: Clobetasone (Eumovate)

- Potent: Betamethasone (Betnovate)

- Very potent: Clobetasol propionate (Dermovate)

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16
Q

If eczema is not controlled by emollients and potent topical steroids, what is the next option to try within dermatology?

A

Topical calcineurin inhibitors (stops activation of T-Lymphocytes) as steroid sparing agents

Tacrolimus: Used aged >2 if moderate-severe and topical corticosteroids have not controlled symptoms and there is a risk of adverse effects from further steroids

Pimecrolimus: Used aged >2 for same reasons as above but on face and/or neck

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17
Q

If topical calcineurin inhibitors are still not controlling eczema, what is the next stage of treatment?

A
  • Phototherapy
  • Oral immunosuppressants e.g Azathioprine, ciclosporin, or methotrexate
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18
Q

What are some complications of atopic eczema and what is the prognosis?

A

Complications:

  • Secondary bacterial infections (crusting, oozing, weeping)
  • Eczema herpeticum
  • Secondary viral infections e.g molluscum
  • Poor mental health

Prognosis:

  • Tends to improve as child grows up and most grow out of it by 16
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19
Q

What is seborrheic dermatitis and how does it present?

A

Chronic dermatitis thought to be caused by an inflammatory reaction related to a proliferation of a normal skin inhabitant, a fungus called Malassezia furfur - It is common, affecting around 2% of the general population.

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

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20
Q

How is the presentation of seborrhoeic dermatitis different to atopic dermatitis?

A

Red, scaly rash affects scalp (dandruff), eyebrows, nasolabial folds, cheeks, and flexures

Due to overgrowth of fungus not atopy

Both can co-exist together

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21
Q

How is seborrhoeic dermatitis treated?

A
  • Mild topical steroid/antifungal preparations, eg Daktacort
  • Ketoconazole shampoo
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22
Q

How is irritant and contact dermatitis treated?

A

Irritant:

  • Avoid all irritants
  • Hand care (soap substitutes; regular emollients; careful drying)
  • Topical steroids for acute flare-up

Contact: (e.g nickel, rubber)

  • Consider patch testing and avoidance of allergens
  • Topical steroid appropriate for severity (decrease strength and stop as it settles)
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23
Q

What is the pathophysiology of acne vulgaris?

A

Inflammation of the pilosebaceous unit

- Basal keratinocyte proliferation in pilosebaceous unit (androgen driven)

- Increased sebum production

- Propionibacterium acnes colonisation

- Inflammation

  • Comedones (white- & black-head) blocking secretions so papules, nodules, cysts, and scars form
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24
Q

What are the clinical features of acne?

A

Non-inflammatory lesions (mild): open and closed comedones

Inflammatory lesions (moderate/severe): papules, pustules, nodules, cysts

May have scarring (e.g ice pick, rolling) and post-inflammatory depigmentation and hyperpigmentation

(Comedone = A plug in a sebaceous follicle containing altered sebum, bacteria, and cellular debris. Can present as open (blackheads) or closed (whiteheads))

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25
Q

What is Acne Conglobata and Acne Fulminans?

A

Conglobata: Inflammatory nodulocystic disease with interconnecting sinuses and abscesses. Can cause severe scarring. Associated with androgen-producing tumours and steroid use. Mainly affects men

Fulminans: Form of acne conglobata with systemic features such a fever, arthralgia and lymphadenopathy. Needs same day urgent referral to dermatology

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26
Q

Classifying the severity of acne is importnat to help guide the management. How is the severity of acne classified?

A

Mild to Moderate Acne:

  • Any number of non-inflammatory lesions (comedones)
  • Up to 34 inflammatory lesions
  • Up to 2 nodules

Moderate to Severe Acne:

  • 35 or more inflammatory lesions (with or without non-inflammatory lesions)
  • 3 or more nodules
27
Q

When should you refer someone with acne to a dermatologist?

28
Q

What is the general management of acne vulgaris? (bottom three medicines only for moderate to severe)

A
  • Skin care advice (see future flashcard)
  • Advise will take 6-8 weeks for any treatment to start working

Medicine: (use for 12 weeks before review)

  • Topical adapalene (retinoid) with topical benzoyl peroxide
  • Topical tretinoin with topical clindamycin
  • Topical benzoyl peroxide with topical clindamycin
  • Topical azelaic acid plus either oral lymecycline or oral doxycycline
  • Oral lymecycline or doxycycline (if >12)
  • Oral isotretinoin
29
Q

How do each of the medications for acne vulgaris treatment work?

A

Oral isotretinoin: Retinoid, (Vit A analogue). Reduces production of sebum, reducing inflammation and reducing bacterial growth

30
Q

What are some of the side effects of the following acne treatments?

  • Topical benzoyl peroxide/clindamycin/adapalene
  • Oral tetracyclines
  • Oral isotretinoin
A

Topical: burning sensation, bleaching of hair and clothes, photosensitivity, skin irritation

Oral Abx: photosensitivity, cannot be used if pregnant or breast feeding

Oral Isotretinoin: HIGHLY TERATOGENIC, dry skin and lips, photosensitivity, depression, anxiety, aggression and suicidal ideation, TEN/SJS

31
Q

Which patients should you consider oral isotretinoin in? (Vit A derivative/Retinoid)

A

Aged over 12 and topical treatments and systemic antibiotics have failed with:

  • Nodulocystic acne
  • Acne conglobata
  • Acne fulminans
  • Acne at risk of permanent scarring
32
Q

What do you need to counsel patients on before starting isotretinoin?

A

- Risk of suicidal ideation, need to mental health screen them first

- Highly teratogenic so need to be on contraception and stop taking at least a month before trying to get pregnant

- May cause initial flare when starting, can start short course of oral steroids if this happens

  • Other side effects
33
Q

What patients is oral isotretinoin contraindicated in?

A
  • Hypervitaminosis A
  • Hyperlipidaemia
  • Liver dysfunction
  • Pregnancy

It must be used with caution in those with renal impairment, diabetes and dry-eye syndrome.

34
Q

What are some complications of acne vulgaris?

A
  • Scarring
  • Hyper/hypopigmentation
  • Psychological distress
35
Q

What general skin-care measures can you give to a patient who is suffering with acne?

A
  • Use a non-alkaline (skin pH neutral or slightly acidic) cleansing product twice daily
  • Avoid oil-based and comedogenic preparations of sunscreen and moisturisers

- Avoid oil-based and comedogenic makeup products, and remove make-up at the end of the day.

- Persistent picking or scratching of acne lesions can increase the risk of scarring

36
Q

What are some signs of rosacea?

A

Pre-rosacea: flushing triggered by stress/blushing, alcohol & spices.

Signs:

  • Central facial rash (usually symmetrical) with erythema, teleangi- ectasia, papules & pustules (without comedones) that is PERIORAL SPARING
  • Blepharitis/conjunctivitis (ocular rosacea)
  • Rhinophyma (swelling + soft tissue overgrowth of the nose)
37
Q

How is Rosacea treated?

A
  • Avoid sun overexposure
  • Sun glasses
  • Topical ivermecting or metronidazole for papules
  • Brimonidine for redness
  • Eyelid hygeine, ocular lubricants ± ciclosporin for ocular rosacea
  • Oral doxycycline for phymatous disease
  • Moderate-severe: topical ivermectin + oral doxycycline
38
Q

What is the epidemiology of psoriasis?

A
  • Two peaks, 20-30 and 50-60
  • Affects caucasians mostly
39
Q

What are some trigger factors for Psoriasis?

A
  • FHx
  • Streptococcal Throat infections (Guttate psoriasis)
  • Trauma (Koebner Phenomenon)
  • Hormone changes (puberty, menopause)
  • Drugs e.g beta-blockers, lithium, chloroquine and ACEi
  • HIV
  • Smoking and Alcohol
  • Stress
40
Q

What is the pathophysiology of psoriasis?

A

Autoimmune condition due to hyperproliferation of keratinocytes

41
Q

What are some associated conditions with psoriasis?

A
  • Psoriatic arthritis
  • IBD
  • Metabolic syndrome
  • CVD
  • Psoriatic nail disease
  • Other autoimmune conditions
  • Uveitis and blepharitis
  • DEPRESSION!!!!
42
Q

What are the different subtypes of psoriasis and how do they present?

A

Chronic Plaque Psoriasis (most common)

  • Well demarcated thickened erythematous plaques with silver scales usually in extensor surfaces or scalp
  • Post inflammatory hyperpigmentation

Flexural/Inverse

Guttate Psoriasis (second most common - Raindrop Psoriasis)

  • Papular rash that occurs about 2 weeks after a strep throat infection
  • Usually self limiting after 3 weeks but a third will go on to develop chronic plaque psoriasis

Erythrodermic Psoriasis

  • Widespread erythema and psoriasis affecting a large portion of the bodies surface area (at least 75-90%)
  • Recent infection, drugs or stress can induce it
  • Often needs hospital admission as emergency
  • Needs biologics

Pustular Psoriasis

  • Pustules form under areas of erythematous skin
  • Develop plaques with peripheral pustules
  • Dermatological emergency and patients are often systemically unwell with fever, malaise and arthralgia
43
Q

What are some features of psoriatic nails (strongly associated with psoriatic arthritis)?

A
  • Subungual hyperkeratosis
  • Nail pitting
  • Oil drop discolouration (yellow/pink patches)
  • Leukonychia (white discolouration)
  • Onycholysis (detachment of the nail from the nail bed)
  • Splinter haemorrhages
44
Q

What are some ‘signs’ of psoriasis?

A

- Auspitz sign: small points of bleeding when plaques are scraped off

- Koebner phenomenon: development of psoriatic lesions to areas of skin affected by trauma

- Residual pigmentation of the skin after the lesions resolve

45
Q

What is the general management of psoriasis?

A

EDUCATE IT IS CONTROL NOT CURE

- Emollients

- Topical steroids

- Vitamin D analogues

- Tar preparations (helps to reduce scaling and slow plaque formation)

- Short contact dithranol: (10-30 minutes then rinse) (Applied to chronic extensor plaques only, avoiding normal skin. It stains objects and skin)

- Phototherapy: usually UVB

- Systemic: methotrexate, ciclosporin, acitretin, biologics

46
Q

What is the secondary care management of psoriasis?

A

Phototherapy
• Narrowband ultraviolet B light is now the treatment of choice. If possible this should be given 3 times a week
• photochemotherapy is also used - psoralen + ultraviolet A light (PUVA)

Adverse effects: skin ageing, squamous cell cancer (not melanoma)

Systemic therapy
• oral methotrexate is used first-line. It is particularly useful if there is associated joint disease
• ciclosporin
• systemic retinoids
biological agents: infliximab, etanercept and adalimumab
• ustekinumab (IL-12 and IL-23 blocker) is showing promise in early trials

47
Q

What is Dovobet and Enstilar?

A

A mixture of Vitamin D and a potent steroid used to treat severe psoriasis

48
Q

What are the different types of phototherapy that are used to treat psoriasis?

A

- UVB: narrow-band ultraviolet B therapy. Used in plaque psoriasis that has not responded to topical therapy.

- PUVA (Psoralen + UVA): is a form of photochemotherapy, combination of a photosensitising drug and UV therapy. Complications include skin irritation, damage and SCC skin cancer (a risk that is compounded if given ciclosporin)

49
Q

What are some of the different types of psoriatic arthritis?

A
  • Monoarthritis or oligomonoarthritis
  • Psoriatic spondylitis
  • Asymmetrical polyarthritis
  • Arthritis mutilans (destructive)
  • Rheumatoid-like polyarthritis.
50
Q

What are some of the systemic therapies for psoriasis and how do you decide which therapy is best for the patient?

A

- Methotrexate (1st line): Antifolate immunosuppressant, teratogenic so need contraception whilst using and for 6 months after (both men and women).

Preferred in elderly or arthropathy as long term use can cause hepatic fibrosis

- Ciclosporin: Can raise blood pressure and drop renal function but can be used in pregnancy. Rapid control can be gained

-Acitretin: Is a retinoid. Need to avoid pregnancy whilst using and for 3 years after stopping. Dry skin and mucosae, rasied lipids, glucose rasied, raised LFTs (reversible)

- Infliximab/Biologics: given as IV injection for severe, treatment resistant disease

- Mycophenalate Mofetil

51
Q

What are some complications of psoriasis?

A

- Psychological issues like depression and anxiety

- Systemic upset with erythrodermic psoriasis and generalised pustular psoriasis can cause organ damage

- Side effects from treatment e.g skin irritation, malignancies

52
Q

Is psoriasis itchy?

A

Not really, should consider eczema if itchy!!!

53
Q

What is lichen planus?

A

Fairly common non infectious rash in adults

Lichen - small bumps on the skin, planus - flat
As flat topped papules

a chronically inflammatory condition affecting the skin and mucosal surfaces.

Pathology: t-cell mediated autoimmune disorder inflammatory cells attack an unknown protein within the skin and mucosal keratinocytes.

54
Q

How can you tell the difference between rosacea and acne?

A

ROSACEA HAS NO COMEDONES

55
Q

Lichen planus presentation

A

Most common on flexural aspects of wrists, ankles, lumbar region

Linear grouped lesions in scratch marks - Koebner’s

Papules flatten over few months, replaced by hyperpigmentation

Clinical features: may cause small number or an extensive amount of lesions on the skin and mucosal surfaces.
 papules
 polygonal plaques – shiny flat topped and firm on palpation
 plaques crossed with white lines – whickham striae
 location can be anywhere but most often on the wrists , lower back and
ankles.

50% have oral involvement

56
Q

Lichen planus presentation

A

Most common on flexural aspects of wrists, ankles, lumbar region

Linear grouped lesions in scratch marks - Koebner’s

Papules flatten over few months, replaced by hyperpigmentation

Clinical features: may cause small number or an extensive amount of lesions on the skin and mucosal surfaces.
 papules
 polygonal plaques – shiny flat topped and firm on palpation
 plaques crossed with white lines – whickham striae
 location can be anywhere but most often on the wrists , lower back and
ankles.

50% have oral involvement

57
Q

Lichen planus management

A

Dx: Clinical features → Skin biopsy to confirm

Management:
 potent topical steroids – mainstay of treatment
 topical calcineurin inhibitors e.g tacrolimus ointment
 topical retinoids

for widespread infections – 1-3 month course of oral pred while commencing one of:

hydroxychloroquine
methotrexate
azathioprine
mycophenolate mofet

58
Q

What is seborrheic keratosis? (presentation and management)

A

Benign overgrowth of epidermal keratinocytes

a harmless warty spot that appears during adult life as a common sign of skin ageing. Some will have hundreds of them.

Clinical features: arise on skin only , never on mucous membranes. highly variable appearance:
* flat or raised papules or plaque - might itch
* 1cm > several
* colour: skin coloured , yellow , gray , dark brown
* waxy/wary surface.
* maybe grouped in some areas

Management
reassurance about the benign nature of the lesion is an option
options for removal include curettage, cryosurgery and shave biopsy

59
Q

What is bullous pemphimgoid?

A

Autoimmune Blistering skin disorder
Autoantibodies against antigens between epidermis and dermis, causes sub-epidermal split in the skin

pathology:
 autoantibodies against the epidermis and dermis
 proteolytic destruction of adhesives e.g hemidesmosomes.
 leads to sub-epidermal split in the skin

Bullous pemphigoid is more common in elderly patients. Features include:
* itchy, tense blisters typically around flexures
* the blisters usually heal without scarring
* there is stereotypically no mucosal involvement (i.e. the mouth is spared)
* in reality around 10-50% of patients have a degree of mucosal involvement. It would, however, be unusual for an exam question to mention mucosal involvement as it is seen as a classic differentiating feature between pemphigoid and pemphigus.

60
Q

What investigation and management for bullous pemphimoid?

A

Skin biopsy
immunofluorescence shows IgG and C3 at the dermoepidermal junction

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

61
Q

What is Pemphigus Vulgaris?

A

Features
* mucosal ulceration is common and often the presenting symptom.
* Oral involvement is seen in 50-70% of patients
* skin blistering - flaccid, easily ruptured vesicles and bullae. Lesions are typically painful but not itchy.
* These may develop months after the initial mucosal symptoms. Nikolsky’s describes the spread of bullae following application of horizontal, tangential pressure to the skin
* acantholysis on biopsy

Pemphigus vulgaris is an autoimmune disease caused by antibodies directed against desmoglein 3, a cadherin-type epithelial cell adhesion molecule. It is more common in the Ashkenazi Jewish population.

62
Q

What is the management for pemphigus vulgaris?

A

General management:
good skin care ERS - good oral care - wound dressing

Medical management: aims to reduce the formation of blisters.
 Systemic oral steroids , high dose
 Immunosuppressive agents – azathioprine/methotrexat

63
Q

What is Pityriasis Rosea? (presentation, management)

A

Pityriasis rosea describes an acute, self-limiting rash which tends to affect young adults. The aetiology is not fully understood but is thought that herpes hominis virus 7 (HHV-7) may play a role.

Features
* in the majority of patients there is no prodrome, but a minority may give a history of a recent viral infection
* herald patch (usually on trunk)
* followed by erythematous, oval, scaly patches which follow a characteristic distribution with the longitudinal diameters of the oval lesions running parallel to the line of Langer. This may produce a ‘fir-tree’ appearance

Management: Self limiting

64
Q

What is seborrheic dermatitis and how does it present?

A

Chronic dermatitis thought to be caused by an inflammatory reaction related to a proliferation of a normal skin inhabitant, a fungus called Malassezia furfur - It is common, affecting around 2% of the general population.

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