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Clinical Years / Progress Test > Dermatology > Flashcards

Dermatology Flashcards

1
Q

features of eczema

A

defects in the skin barrier lead to inflammation
- redness
- itch
- dry
- FHx
- flexor surfaces common (cheeks in children)

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2
Q

endogenous types of eczema

A

varicose eczema

seborrheic dermatitis

discoid eczema

atopic eczema

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3
Q

signs of bacterial infection of eczema

management

A

weeping, pustules, crusts, atopic eczema failing to respond to therapy, rapidly worsening atopic eczema, fever and malaise)

Fucidin H Cream applied topically if milder

Oral Abx such as fluclox if more severe

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4
Q

eczema herpeticum

A

a viral infection of eczema involving herpes simplex virus 1 or 2

signs:
- areas of rapidly worsening, painful eczema
- clustered blisters consistent with early-stage cold sores
- punched-out erosions
- fever, lethargy or distress.

needs admission and IV aciclovir

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5
Q

treatment widespread bacterial infections originating from the skin

A

systemic antibiotics that are active against staph aureus and steptococcus e..g flucloxacillin

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6
Q

localised clinical infection of the skin treatment

A

Topical antibiotics, including those combined with topical corticosteroids

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7
Q

antibiotics to cover staph aureus and strep

A

flucloxacillin
erythromycin in fluclox allergy/resistance
3 rd line clarithromycin

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8
Q

when are Antiseptics such as triclosan or chlorhexidine used in skin infection

A

Adjunct therapy for decreasing bacterial load in cases of recurrent infected atopic eczema

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9
Q

complications of eczema herpeticum if untreated

A

Encephalitis; particularly if on immunosuppressants
Hepatitis
Pneumonitis

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10
Q

what microorgansmism are resident on the skin

A

mainly gram positive cocci which are aerobic
- staph aureus
- staph epidermis
- strep species

some anaerobic gram positive bacilli

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11
Q

main gene involved in eczema

A

fillagrin gene - loss of function mutations strongly linked to eczema

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12
Q

pathology of eczema

A

breakdown in skin barrier function and inflammation primarily involving Th2 helper cells

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13
Q

emollient regime

A

for eczema; emollient moisturiser, shower gel, bath additive

emollient regimes reduce the need for topical steroids

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14
Q

topical corticosteroids in eczema

A

steroids are second line treatment in atopic eczema not controlled by emollient regime

potency should align with severity i.e. mild potency for mild eczema and increase with severity

shouldn’t be used for longer than 14 days for flares

only mild potency to be used on the face

applied once or twice a day

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15
Q

topical calcineurin inhibitors

A

Tacrolimus and Pimecrolimus are used in eczema as they suppress T-lymphocyte responses, thereby suppressing the synthesis of pro-inflammatory cytokines

used second line after emollients where steroids are wished to be avoided or try after steroids

only in moderate or severe eczema and over 2 years old

side-effect of burning/stinging sensation on initial application

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16
Q

stepwise treatment of eczema

A
  1. topical emollient regime
  2. topical corticosteroids / immune modulators
  3. phototherapy
  4. systemic treatments e..g azathioprine, cyclosporin
  5. biologic drugs e.g. Dupilumab (injection) and other oral agents which are JAK1 and JAK2 inhibitors
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17
Q

macules

A

flat lesions <5mm

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18
Q

papules

A

raised bumps <1cm

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19
Q

pustules

A

pus filled lesions less than 5mm

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20
Q

vesicles

A

fluid filled lesions less than 5mm

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21
Q

plaques

A

raised lesions greater than 1cm in size

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22
Q

features of psoriatic nails

A

pitting
onychylosis
subungal hyperkeratosis
periungal erythema

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23
Q

types of psoriasis

A

Generalsied pustular psoriasis
Chronic plaque psoriasis
Erythrodermic psoriasis
Guttate psoriasis
Flexural psoriasis

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24
Q

guttate psoriasis

A

small pink plaques of psoriasis seen on the trunk, often after a streptococcal sore throat

about 1/3 go on to have chronic plaque psoriasis

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25
Q

flexural psoriasis

A

psoriasis affecting the genitalia or axillae

Usually the appearance is red (erythematous) and slightly shiny, but there will still be a clearly defined edge between normal and affected skin

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26
Q

erythrodermic psoriasis

A

flare up/inflammation of psoriasis

When it covers over 90% of the body surface it is described as erythroderma. The skin is red, feels hot and even painful.

There may no longer be clearly defined plaques. Patients can feel unwell and become hypotensive. These patients should be admitted to hospital for treatment.

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27
Q

chronic plaque psoriasis

A

40% of presentations

typical distribution:
elbows and knees
nails
scalp
genitalia and natal cleft

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28
Q

Generalised Pustular Psoriasis

A

psoriasis can flare, become red, hot, painful and develop pustules within the plaques

emergency requiring hospital admission. The trigger is often WITHDRAWAL of use of a superpotent topical or systemic corticosteroids

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29
Q

psoriatic arthropathy

A

Between 5- 20% of patients with psoriasis have arthropathy affecting their joints. Arthropathy can precede (50%) or post-date (15%) the development of skin lesions. The patterns of arthropathy fall into five subtypes:

-distal interphalangeal alone
-symmetrical polyarthritis (commonest)
-asymmetrical oligoarthritis
-arthritis mutilans
-spondyloarthropathy

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30
Q

triggers/risk factors for psoriasis

A

family history

psychological stress

medications; antimalarial, NSAIDs, beta blockers, lithium

alcohol

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31
Q

management of psoriasis stepwise

A

emollients for all + reduce alcohol and smoking and lose weight

1st line: a potent corticosteroid applied once daily plus vitamin D analogue applied once daily (applied different times of day)
2nd line: if no improvement after 8 weeks a vitamin D analogue twice daily
3rd line: a potent corticosteroid applied twice daily for up to 4 weeks, or
a coal tar preparation applied once or twice daily

short-acting dithranol can also be used

phototherapy and systemic therapy can be considered by secondary care
biologics last step

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32
Q

cells involved in pathogenesis of psoriasis

A

Th1 cells

increased rate of keratinocyte proliferation

inflammatory angiogenesis

TNF-a and Psors genes also involved

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33
Q

tool to determine severity of skin disease

A

DLQI (Dermatology of Life Index) is a subjective assessment of the impact of the disease on the patient’s life. The DLQI questionnaire is completed by the patient and is calculated by summing the score of each question resulting in a score between 0 – 30

34
Q

tool to assess psoriasis severity

A

PASI (Psoriasis Area Severity Index) is an objective measure of the disease severity and is completed by the clinician. It is a numerical score with 0=no disease and 72=maximum disease

often used to objectively monitor patients

35
Q

how does phototherapy work for psoriasis

A

narrow-band UVB or PUVA which slows down the excessive growth of keratinocytes and is considered to be partially immunosuppressive

given 2-3 times a week for 10 weeks

36
Q

systemic agents that can be used in psoriasis

A

ciclosporin
methotrexate
Acitretin (oral retinoid)
Fumaric acid esters
Apremilast

37
Q

biologics used in dermatology

A

TNF inhibitors
IL-12/23 inhibitors
IL-17 inhibitors

38
Q

acne vulgaris

A

Acne vulgaris is an inflammatory condition where lesions develop from the sebaceous glands around hair follicles on the skin of the face, chest , back and anogenital region

39
Q

what are open comedones

A

blackheads

40
Q

APSEA scale

A

validated tool used to assess psychological impact of acne on work, personal life, relationships confidence etc.

41
Q

grading clinical severity of acne

A

The Leeds Scoring system counts and categorises lesions into inflammatory and non-inflammatory ranging from 0 for mild acne to 12 for the severest form (nodules, cysts, scars

42
Q

indications for treatment with oral retinoids (isotretoin) for acne

A
  • Moderate acne, unresponsive to conventional therapy or relapsing after conventional therapy
  • Severe acne
  • Acne scarring
  • Psychological effects resulting from acne and scarring
  • Unusual form of acne
43
Q

different types of drugs for acne (how they work)

A

drugs that inhibit sebaceous gland function
- anti-androgens
- oestrogens
- isotretinion

drugs that normalise pattern of follicular keratinisation
- topical retinoids

drugs with anti-inflammatory/anti-bacterial effects
- antibiotics
- benzoyl peroxide

44
Q

acne pathophysiology

A

blockage and inflammation of the pilosebaceous unit (the hair follicle, hair shaft and sebaceous gland). It presents with lesions which can be non-inflammatory (comedones), inflammatory (papules, pustules and nodules) or a mixture of both.

45
Q

treatment of acne

A

first line 12 week course of one of:
- topical adapalene with topical benzoyl peroxide
- topical tretinoin with topical clindamycin
- topical benzoyl peroxide with topical clindamycin

if moderate to severe consider oral antibiotics and Topical azelaic acid as other first line options

single antibitoic should be used for 12 weeks to assess response

combined oral contraceptives may be considered in women as treatment

46
Q

what is acne fulminans

A

Acne fulminans is a sudden severe inflammatory reaction that precipitates deep ulcerations and erosions, sometimes with systemic effects (such as fever and arthralgia).

47
Q

risk factors for BCC compared to SCC

A

both
- chronic UV exposure
- skin types I and II
- chemicals
- immunosuppressants

SCC also cigarette smoking and chronic ulcers

48
Q

Fitzpatrick skin types

A

Type I - always burns never tans very pale
Type II - usually burns tans poorly pale
Type III - tans after initial burn darker white
Type IV - tans easily burns minimally light brown
Type V - tans darker brown skin
Type VI - always tans darker never burns dark brown/black skin

49
Q

squamous cell carcinoma
- what is it
- does it spread?

A

malignant tumour arising from keratinocytes of the epidermis
can invade locally and has metastatic potential

50
Q

how does an SCC present

A

fast growing and can be painful
often on face, scalp and hands
rare under 60 years unless immunosuppressed

indurated nodular lesions often have crusted or hyperkeratotic surfaces

can develop de novo or from precursor leisons

51
Q

pathophysiology of SCC

A

malignant transformation of normal keratinocytes by apoptotic resistance via loss of TP53

52
Q

what lesions can be precursors to SCC

A

actinic/solar keratoses - multiple lesions often head and neck non painful. dysplastic keratinocytes
Bowen’s disease - single plaque of epidermal dysplasia. can be managed with cryotherapy

53
Q

poor prognostic features SCC

A

tumours >2cm
lesions on lip or ear
immunosuppression

54
Q

what options may be used to manage a BCC

A
  • imiquimod cream 5%
  • radiotherapy
  • photodynamic therapy
  • surgical excision; can be done as a day case
  • watchful waiting
55
Q

how can actinic keratosis be managed

A

5% 5-FU (efudix) cream

56
Q

how is prognosis of SCC determined

A

depth invasion of the skin

57
Q

high risk BCCs

A

lesions on eyelid margins, ear, lip

perineurial invasion on histology

recurrent lesion

lesions in immunocompromised

58
Q

BCC presentation

A

slow growing

typical features; telangiectasia, pearly translucent nodule

59
Q

types of moles

A

junctional naevus - brown and flat

intradermal naevus - skin coloured and raised

compound naevus - brown and raised

60
Q

what are the criteria for 2WW referral

A
  • new mole quickly growing in an adult
  • long standing mole changing in shape and colour
  • a mole with 3 or more colours or lost its symmetry
  • any new nodule growing and pigmented or vascular
  • new pigmented line in a nail or something growing under the nail
61
Q

looking for evidence of metastasis in melanoma

A

localised: cutaneous/subcutaneous nodules around the lesions
regional: lymphadenopathy
distant: hepatomegaly +/- splenomegaly

62
Q

treatment of suspected melanoma

A

excision with a margin of normal skin
same day or same week

after excision follow up 3 monthly for a year

immune and targeted therapies are also now used improving survival

63
Q

melanoma presentation

A

50% from existing moles

normally asymptomatic but occasionally bleeding and itching reported

existing or new mole than changes rapidly, irregular, different shades, larger, reddish outline

64
Q

what are dysplastic naevi

A

moles that are on a continuum from benign naves to melanoma
some people have several in a genetic condition and this predisposes to melanoma

65
Q

types of melanomas

A

superficial spreading

nodular

lentigo maligna

aural lentiginous melanoma

66
Q

risk factors melanoma

A

UV exposure +++
sunburns
people with many typical moles
immunosuppression
family history
link to IBD

67
Q

what is Breslow thickness

A

distance in mm from the granular layer in the epidermis to the deepest level of invasion

major prognostic indicator

TNM based on this + some other features (mitotic index, ulceration, LN involvement and metastasis)

68
Q

chronic pruritus

A

chronic pruritus is > 6 weeks which can lead to characteristic skin lesions including excoriations, lichenification and hyperpigmentation pr hypopigmentation

69
Q

itching without skin change/rash (pruritus)

A

unlikely to be dermatological if itch came first

  • malignancy and haematological (NHL, leukaemia, metastasis of solid tumours)
  • multisystem inflammatory (dermatomyositis, scleroderma) or infectious (HIV, Hep C)
  • psychogenic
  • metabolic (hyperT, CKD, diabetes)
  • GI cholestasis
  • drugs
70
Q

bullous pemphigoid

A

autoimmune condition causing sub-epidermal blistering of the skin

oral corticosteroids are mainstay of treatment

71
Q

contact dermatitis

A

two main types:
- irritant contact dermatitis
- allergic contact dermatitis; type IV hypersensitivity reaction. needs topical potent steroid

72
Q

Dermatitis herpetiformis

A

autoimmune blistering skin disorder associated with coeliac disease caused by deposition if IgA in the dermis

73
Q

Erythema multiforme

A

hypersensitivity reaction that is most commonly triggered by viruses but also bacteria and drugs

in its most severe form can involve mucosa such as mouth

74
Q

erythema nodosum

A

inflammation of subcutaneous fat causing tender, erythematous, nodular lesions usually on the shins

many causes including infection, sarcoid, malignancy, drugs and pregnancy

75
Q

lichen planus

A

itchy, papular rash most common on the palms, soles, genitalia and flexor surfaces of arms
oral involvement in 50%

needs potent topical steroids

76
Q

Lichen sclerosus

A

condition of white patches typically affecting the genitalia of elderly females

managed with topical steroids and emollients

note increased risk of vulval cancer

77
Q

examples of topical steroids and potency

A

Mild: Hydrocortisone 0.5%, 1% and 2.5%
Moderate: Eumovate (clobetasone butyrate 0.05%)
Potent: Betnovate (betamethasone 0.1%)
Very potent: Dermovate (clobetasol propionate 0.05%)

78
Q

psoriasis Treatment options

A

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

79
Q

isotretinoin side effects

A

teratogenic - need effective contraception

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

80
Q

scabies presentation and treatment

A

incredibly itchy small red spots, possibly with track marks where the mites have burrowed. The classic location of the rash is between the finger webs, but it can spread to the whole body.

treatment is with permethrin cream which should be left on for 8-12 hours all over for

81
Q

Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN)

A

spectrum of the same pathology of epidermal necrosis due to an immune response
caused by medications or infections

needs admission, good supportive care as well as medical management including steroids, immunoglobulins and immunosuppressant

can lead to eye damage, permanent skin damage and secondary infection

Clinical Years / Progress Test (24 decks)

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