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Clinical Practice > Dermatology > Flashcards

Dermatology Flashcards

1
Q

describe the epidermis

A

multiple layer of keratinocyte cells
outermost layer; cornified layer of dead cells responsible for the barrier function
innermost layer; basal cells (single layer of keratinocytes)
melanocytes can be found between these layers

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2
Q

what are the functions of skin?

A 
protective barrier 
sensation (multiple nerve endings)
thermoregulation
immunological surveillance (Langerhans cells)
vitamin D production
psychosocial
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3
Q

what should be asked in a dermatology history?

A 
time of onset
where/how the skin problem started
evolution of change
associated symptoms - itch, pain, swelling, bleeding
aggravating and relieving factors
any treatments tried so far
how fair the skin is
sun exposure
previous skin problems
anticoagulants (biopsy)
work, school, quality of life
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4
Q

what are you looking for in a skin examination?

A 
location
localised/generalised
distribution
symmetrical
size
shape
colour
well/ill-defined
other associated locations - scalp, nails, mucosa
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5
Q

describe macules and patches

A

flat to the surface
macule <5mm
patch >5mm

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6
Q

describe papule and plaques

A

raised lesion
papule <5mm
plaque >5mm

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7
Q

describe a nodule

A

raised and round-topped

may be superficial or deep

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8
Q

describe vesicles, bulla and pustules

A

vesicles; <5mm with clear fluid
bullae/blisters; >5mm with clear fluid
pustule; opaque fluid

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9
Q

describe a cutaneous horn

A

abnormally thick cornified layer

overlying a pre-malignant lesion causing actinic keratosis or a squamous cell carcinoma

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10
Q

what features of a pigmented lesion indicate malignant melanoma?

A 
asymmetrical
irregular border
2 or more colours
diameter >6mm
evolution
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11
Q

describe acute eczema

A

high level of inflammation
red oedematous skin
papules and vesicles often present
wet eczema appearance

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12
Q

describe chronic eczema

A 
dry
slightly less red changes
some thickening of the skin
lichenification and fissuring
post-inflammatory hypo/hyperpigmentation may also occur
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13
Q

describe the pathophysiology of eczema

A

genetic predisposition
primary defect; skin barrier dysfunction, water loss, sensitivity
inflammation and pruritus reduce the skin barrier
scratching exacerbates the inflammation
itch-scratch cycle

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14
Q

what are the clinical subtypes of eczema?

A

intrinsic (eczema); atopic seborrhoeic, discoid, pompholyx, varicose, venous eczema
extrinsic (dermatitis); an extrinsic factor brings about the skin barrier problem, contact irritant and contact allergic dermatitis

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15
Q

describe atopic eczema

A 
most common form
particularly in children
genetic predisposition
chronic relapsing course
pattern can vary; face and flexural aspects in children, flexural areas and hands in adults
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16
Q

what are the triggers of atopic eczema?

A

stress
scratching
secondary infections (staphylococcus, herpes, molluscum)
hot and sweaty conditions
irritants (wool, dust, soap, bubble bath)
allergens (fragrance, preservative in topicals agents or cosmetics, pet dander)

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17
Q

what are the complications of eczema?

A 
due to the defective skin barrier;
secondary bacterial infection
secondary viral infection
contact allergy
itch
sleep deprivation
growth impairment
depression
social isolation
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18
Q

what is the pharmacological management of eczema?

A

emollients and soap substitutes; maintenance
anti-inflammatories
topical steroids
calcineurin inhibitors (anti-inflammatory agent) 2nd line after steroids
antibiotics/virals
sedative antihistamines
severe refractory disease; phototherapy
ciclosporin, azathioprine, mycophenolate require side effect counselling

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19
Q

what is the non-pharmacological management of eczema?

A

dermatology nurse
education in application of cream
wet wraps
clinical psychologist; break the itch-scratch cycle

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20
Q

describe seborrhoeic eczema

A

classic distribution over the scalp
associated with minimal itch due to an overgrowth of commensal yeast organisms (malassezia)
high prevalence in those with HIV

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21
Q

what is the treatment of seborrhoeic eczema?

A

mild topical steroids; hydrocortisone
anti-fungals; canesten, daktarin
or a combination of both

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22
Q

describe the presentation and differential diagnosis of discoid eczema

A

intensely itchy plaques of wet eczema
often on the limbs
often difficult to treat; require potent topical steroids

differential diagnosis; Bowen’s disease (pre-malignant lesions), fungal infection, psoriasis

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23
Q

describe pompholyx eczema

A 
very small blisters on the palmar-plantar surface; hands and feet
intensely itchy
lateral borders of the fingers
within the web spaces
can be linked to sweating
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24
Q

describe varicose eczema

A

bilateral
chronic
may be a Hx of varicose veins, DVT
eczematous change (acute or chronic) develops on a background of lipodermatosclerosis; inverted Champagne bottle leg
haemosiderin; brown, patchy appearance over lower legs
at risk of venous ulceration

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25
Q

what is the treatment of varicose eczema?

A

lots of emollient

compression stockings

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26
Q

describe asteatotic eczema

A

very common in hospital and elderly patients
very dry skins
cracks develop in a typical crazy paving pattern
aggravated by soaps and poor nutrition

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27
Q

describe contact allergic dermatitis

A

extrinsic eczema
delayed hypersensitivity reaction to substances in contact with the skin
causes; nickel, fragrance, hair dye
diagnosis; patch testing

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28
Q

describe contact irritant dermatitis

A

extrinsic eczema
skin is irritated by noxious agents
common on the hands
treatment; very careful hand care, soap substitutes, frequent emollients

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29
Q

describe psoriasis

A 
benign inflammatory condition
FHx
significant itch
nail changes
fluctuating
associated potentially destructive arthropathy
bimodal peak onset; 20, 50-60yrs
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30
Q

what are the triggers of psoriasis?

A 
stress
alcohol
physical trauma; burns, repeated rubbing, cuts, abrasions, surgical operation sites (koebner phenomenon)
lithium
beta blockers
ACEi
anti-malarials
abrupt cessation of oral/topical steroids; substantial flare
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31
Q

describe the pathogenesis of psoriasis

A

interaction of genetic, immunological and environmental factors
genetic factors; influence subtype and treatment response
predominately driven by T-cells within the epidermis
pro-inflammatory cytokines; TNF, IL-12, 23, 17 cause the hyperproliferation of keratinocytes and angiogenesis

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32
Q

describe chronic plaque psoriasis

A

most common subtype
symmetrical
well defined
salmon pink plaques
on extensor sites; elbows, knees, sacrum, scalp
thick, silvery scale
auspitz sign; removed/scratched off, pinpoint bleeding
dermal blood vessels become much more close to the skin surface

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33
Q

describe subacute psoriasis

A

when chronic plaque psoriasis becomes inflamed or fiery red

less obvious scale

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34
Q

what is the treatment of chronic plaque psoriasis?

A

vitamin D analogues
tar preparations
topical steroids; used in short bursts only
narrow-band UVB; if topicals are ineffective
systemic medications; UVB ineffective
biologics; fail first line systemic agents, sc injection, immunosuppressive

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35
Q

describe erythrodermic psoriasis

A

deep red appearance
>90% body surface
widespread, exfoliative scaling
extremely unwell; fever, malaise, raised WCC

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36
Q

what are the complications and treatment of erythrodermic psoriasis?

A

defective thermoregulation
fluid and protein loss
high output HF
secondary cutaneous infection

supportive care; fluids, emollients, skin care
systemic treatment

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37
Q

describe pustular psoriasis

A 
extensive sheets of small pustules
skin red and painful
well-demarcated patches and plaques
mortality of up to 10%
significant systemic symptoms; fever, malaise
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38
Q

what is the treatment of pustular psoriasis?

A

supportive; fluids, emollients, skin care

systemic therapy required to control the skin

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39
Q

describe palmoplantar psoriasis

A 
exclusively affects the palms and soles
pustules on a background of erythema; instep of soles, heels of palms
symmetrical
painful
itchy
significant functional impairment
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40
Q

what is the treatment of palmoplantar psoriasis?

A

tar
potent topical steroids
hand and foot PUVA
systemic agents

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41
Q

describe guttate psoriasis

A

common in teenagers
classically follows a streptococcal throat infection
small teardrop plaques
particularly over the trunk
may clear in 4-6 weeks or cause chronic psoriasis

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42
Q

what is the treatment of guttate psoriasis?

A

vitamin D
topical steroid preparation
tar preparations
phototherapy; UVB, responds extremely well

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43
Q

describe flexural psoriasis

A

reflects the flexures; axilla, sub-mammy areas, groins
very well demarcated red, glistening plaques
minimal scale
due to occlusion of the areas
associated with secondary candidiasis infection; seen as satellite lesions, papule and pustules situated away from the plaques

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44
Q

what is the treatment of flexural psoriasis?

A

mild topical steroid and anti fungal mix

topical calcineurin inhibitor; causes local irritation in the first few days

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45
Q

what is the treatment of psoriasis?

A 
topical; vitamin D analogues
phototherapy; narrow-band UVB, PUVA
widespread; oral psoralen
local; topical psoralen
limit of total lifetime exposures of PUVA, significant risk factors for skin cancer
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46
Q

what are the systemic agents that are used to treat psoriasis?

A

methotrexate; inhibits dihydrofolate reductase, used in skin and joint disease, immunosuppressive (monitor blood count and LFTs)
ciclosporin; only skin disease, immunosuppressive, renal complications and hypertension
acitretin; vitamin A analogue, non-immunosuppressive
biologics; anti-TNF, IL12/23, IL17, those who have failed standard systemic treatment options
apremilast; oral inhibitor of phosphodiesterase four, non-immunosuppressive

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47
Q

what are the complications of psoriasis?

A

psoriatic arthropathy; can be destructive, lead to enthesitis, requires early intervention with systemic agents
metabolic syndrome; increased risk of CVD (could be improved by methotrexate)
psychological/psychiatric impairment; depressed, anxious, unemployed, socially isolated

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48
Q

describe psoriatic nail dystrophy

A

pitting; coarse, >5
oil-drop spots
oncholysis; may be caused by subungal hyperkeratosis
more prone to secondary fungal nail infection

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49
Q

describe psoriatic arthropathy

A 
often asymmetrical
can affect small or large joints, sacroiliac and spinal joints
enthesitis
sausage deformity of the fingers
arthritis mutilans
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50
Q

describe psoriatic scalp disease and its treatment

A 
can be very extensive
can cause significant distress
itch
excessive scaling
falling onto clothing

treatment; shampoos, pomades, steroid shampoos or gels, olive oils, coconut oils, systemic therapy

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51
Q

describe acne vulgaris

A

chronic inflammation of the pilosebaceous unit

onset usually in adolescence

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52
Q

describe the pathophysiology of acne

A

increased sebum production
blockage/plugging of the pilosebaceous unit; obstruction of the outflow of sebum
abnormal microbial colonisation of the unit; propionibacterium acnes
inflammation

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53
Q

what are the clinical signs of acne?

A 
open comedones; blackheads
closed comedones; whiteheads
papules and pustules; blocked follicle ruptures into the skin
nodules
cysts
scarring
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54
Q

what is the difference between open and closed comedones?

A

open; blockage of the follicular opening, still open to the surrounding skin
closed; follicle remains closed over the swollen sebaceous gland

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55
Q

describe papules and pustules in acne

A

increased inflammation
development of pus
often following the rupture of a wall of a closed comedone

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56
Q

describe nodules and cysts in acne

A

larger and deeper within the skin
significant inflammatory component
can be very painful
at the most risk of leaving severe scarring

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57
Q

describe scarring in acne

A

usually improve 6-12 months after the inflammatory phase has been resolved
ice pick scarring
hypertrophic scarring
exacerbated by excessive picking or squeezing

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58
Q

what are the aggravating factors for acne?

A

PCOS
CAH; endocrine causes of hyperandrogenism
drugs; steroids, hormones, anti-convulsants
pregnancy
occlusive oil-based cosmetics
smoking

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59
Q

define mild acne

A

classically involves comedones and a few small pustules

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60
Q

define moderate acne

A

papulopustular lesions in a wider area or failure of mild acne to respond to therapy

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61
Q

define severe acne

A

widespread nodular cystic lesions, or a failure of moderate acne to response to treatment, or a patient with significant psychological upset associated with their acne

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62
Q

what is the treatment of mild acne?

A

topical agents; benzoyl peroxidase
topical retinoid; derived from vitamin A, particularly effective for comedonal
cream formulation; least irritant
second line topicals; combine benzoyl peroxidase with an antibiotic or a retinoid
topical antibiotics; never used as a mono therapy
topical treatment; synergistic with oral therapy

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63
Q

what is the treatment of moderate acne?

A

systemic antibiotics; tetracyclines, 6-12 weeks, tetralysal and doxycycline
OCP
topical agents; synergistic with systemic treatments

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64
Q

what is the treatment of severe acne

A 
isotretinoin; roaccutane
vitamin A derivative/retinoid
4-6 month course
40%; excellent response
40%; minimal recurrence
20%; may require a second course
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65
Q

what is the mechanism of action of isotretinoin?

A

dramatic reduction in sebum production
inhibition of P. acnes
anti-inflammatory

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66
Q

what are the side effects of isotretinoin?

A 
dry skin and mucosae
nose bleeds
flare of eczema
muscle aches
hepatitis
elevated triglycerides
photosensitivity
teratogenicity
depression
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67
Q

describe rosacea

A 
chronic inflammatory skin disorder
crops of papules and pustules
background of erythema and telangiectasia
affects convexities
increased age group
females
fairer skin type
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68
Q

what are the causes of rosacea?

A 
multifactorial;
UV exposure
demodex mite and skin peptide activation
genetic factors
vascular abnormalities
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69
Q

what are the clinical features of pustular rosacea?

A

papules and pustules on the convexities; nose, cheeks, chin, forehead
no comedones
rhinophyma
lymphedema of the skin of the nose
ocular involvement; up to 50%, most commonly blepharitis

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70
Q

what are the clinical features of erythematous rosacea?

A

frequent facial flushing
over months-years, may become persistent
triggers; alcohol, spicy food, UV, caffeine, topical steroids
extremely sensitive skin to any topical applications or cosmetics
may have ocular involvement

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71
Q

what is the treatment of pustular rosacea?

A

UV protection
topical ivermectin 1st line
topical metronidazole
orał tetracyclines; 4-6 month course, failing or adjunct to topical agents
eye involvement; lid hygiene, refer to ophthalmology

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72
Q

what is the treatment of erythematous rosacea?

A

UV protection
emollients; settle the highly sensitive skin
trigger avoidance
laser therapy
cosmetic camouflage
topical brimonidine gel/mirvaso; severe flushing, alpha-2 agonist, vasoconstriction temporarily, some pallor
eye involvement; lid hygiene, refer to ophthalmology

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73
Q

describe impetigo

A

a common superficial bacterial skin infection
pustules
heavy-coloured crusted erosions
usually caused by staph aureus
non-bulbous; caused by group A beta-haemolytic strep
acutely contagious; avoid using the same face cloth and towels

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74
Q

what is the treatment of impetigo?

A

relatively localised
simple antiseptics; chlorhexidine to wash
topical antibiotics; fucidic acid or fucidin
more widespread, resistant to topical treatment, patient is unwell; swab, initiate antibiotics (flucloxacillin or erythromycin)

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75
Q

what are the clinical features of venous stasis?

A 
afebrile
itch
Hx of DVT or varicose veins
bilateral
light pink/red
crusting, weeping
not tender
varicose veins
skin pigmentation and fibrosis
inverted Champagne bottle leg
normal inflammatory markers
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76
Q

what are the clinical features of cellulitis?

A 
febrile
pain
usually unilateral
intense erythema
tender
no crusting
occasionally blisters
lymphadenopathy/lymphadenitis
necrosis if severe
athletes foot/ulceration; blood sugar, HbA1c
raised inflammatory markers
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77
Q

define cellulitis

A

acute, subacute or chronic area of inflammation and infection of subcutaneous tissue

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78
Q

describe erysipelas

A 
similar to cellulitis
sometimes in the face
acute
well defined
more superficial; affecting the dermis and upper subcutaneous tissue
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79
Q

what is the treatment of cellulitis and erysipelas?

A

antibiotics
analgesia
blood cultures; if they are systemically unwell with a pyrexia
swab in areas of skin that may be broken

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80
Q

describe necrotising fasciitis

A

medical and surgical emergency
cellulitic-looking process
pain out of keeping with what you initially see
can become systemically unwell; septic shock

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81
Q

what are the causes and treatment of necrotising fasciitis?

A

typically polymicrobial
group A haemolytic strep
clostridium perfringens

if progresses; will most likely require surgical debridement, high mortality rate
initiate IV antibiotics, swab any areas that are broken

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82
Q

describe chicken pox

A 
caused by varicella zoster
acute fever
prodrome; feeling unwell
subsequent vesicular eruption
incubation period; 10-21 days
vesicles can take 3 weeks to clear and can leave residual scars
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83
Q

what is the management of chicken pox?

A 
usually symptomatic
mild analgesia
rest at home
fluids
calamine lotion; relief, topical
immunocompromised; antivirals, acyclovir, varicella zoster globulin
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84
Q

describe shingles

A

herpes zoster
localised, vesicular, painful rash
reactivation of the varicella zoster virus
typically unilateral
dermatomal distribution; will not cross the midline

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85
Q

what is the treatment of shingles

A

antivirals; acyclovir
simple analgesia
secondary infection; treat with antibiotics

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86
Q

what happens if shingles affects the facial nerve?

A

Ramsay-Hunt syndrome

can cause a degree of facial paralysis and hearing loss in the affected ear

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87
Q

describe the pain that occurs after the resolution of the shingles rash

A

post-herpetic neuralgia

treatment; amitriptyline, can have a significant impact on patient

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88
Q

describe cold sores

A

herpes simplex virus
localised vesicular eruption
often triggered by a preceding illness, generally being run down, UV light

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89
Q

what are the causes of cold sores?

A

HSV1; oral and facial cold sores

HSV2; genital and rectal infections, anogenital herpes

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90
Q

what are the complications of herpes simplex virus?

A

eye involvement; dendritic ulcers
disseminated eczema herpeticum; if the patient has pre-existing eczema
erythema multiforme; classic targeted lesions

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91
Q

what is the treatment of cord sores?

A

acyclovir oral
prophylactic dose if recurrent
viral swab of any vesicular eruption; exclude underlying HSV

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92
Q

describe the different types of tinea fungal infections

A 
tinea pedis; foot
tinea corporis; body
tinea capitus; scalp
tinea cruris; groin
tinea unguium; nails
tinea incognita; masked by steroids
tinea manuum; hand
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93
Q

what are the investigations and treatment of cutaneous fungal infections?

A

swab for fungal O&S
skin scrapings
woods light
nail clippings; tinea unguium

stop topical steroid
topical (lamisul) or oral terbinafine, itraconazole or fluconazole
duration depends on site
monitor LFTs if long course

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94
Q

describe pityriasis versicolor and its treatment

A

scaly hypo or hyper pigmented patches on the chest and back
common yeast infection
associated with humid environments, travelling

should respond to a 5 day course of ketoconazole shampoo
persistent; oral antifungals, itraconazole, fluconazole

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95
Q

describe scabies

A

caused by a mite
common in travellers, use of hostels
intensely itchy rash, particularly between the fingers
mite burrow sites; web spaces, wrists, areola, genitalia
can present as a vesicular eruption
excoriations
inflammatory nodules adults; face usually spared
severe; peripheral eosinophilia, raised eosinophil count

96
Q

what is the differential diagnosis of scabies?

A

contact eczema

delusions of parasitosis; nothing to see in the skin

97
Q

what is the treatment of scabies?

A

patient and all household contacts
permethrin 5%, or other suitable alternatives
applied to the entire body
8-12 hours
repeated after 1 week
clothes and bed linen washed at a high temperature; capture any evolving mites or erupting from legs

98
Q

describe erythema migrans

A

lyme disease
rash occurring 3-30 days after being bitten by a tick of the borrella-carrying bacteria
lyme serology
before serology/if suspicious; doxycycline 100mg BD

99
Q

what are the causes and signs of skin ageing?

A

intrinsic genetic factors
age
smoking
UV radiation

wrinkling
loss of elasticity
telangiectasia
pigmentary change; freckling, fragility, bruising
skin cancers
100
Q

what advice should be given to patients regarding UV protection?

A 
avoid burning
seek shade between 11 and 3
clothing; long sleeves, long legs, hats, sun glasses
plentiful sun cream; reapply, >30 SPF
avoid tanning beds/lamps
keep babies and children out of the sun
see their GP about new/changing moles
high risk groups; children, fair skin, outdoor workers, outdoor habits, immunosuppressed
101
Q

what questions should be asked when a patient presents with a lesion?

A 
risk factors for skin cancer;
skin type
history of UV exposure; work or hobbies
living abroad
using sunbeds
immunosuppression
previous history of skin cancer
lesion history; duration, evolution, associated symptoms
102
Q

how should a lesion be examined?

A 
inspection of the site; sun exposed location
site
shape
colour
specific morphological description
well/ill defined
assess for a second lesion
lymph node examination

melanocytic; ABCDE

103
Q

describe seborrhoeic keratoses

A 
very common >30yrs
usually asymptomatic
can be multiple
start as small lesions
very waxy
skin coloured or yellow, over time can become brown or black
warty texture
stuck-on appearance
often well-demarcated
usually occur on the trunk and face
benign, no treatment required
104
Q

describe viral warts

A

caused by human papillomavirus
finely-formed surface
can sometimes see pinpoint haemorrhages within the lesions
slow growing
children; hands and face
adults; hands and feet
90% will resolve within 2 years, may not require treatment
wart paint/cryotherapy; painful or particularly distressing

105
Q

what is the differential diagnosis of a viral wart?

A

squamous cell carcinoma; a new wart develops in a older patient

106
Q

describe vascular lesion

A

include pyogenic granulomas
rapidly developing nodules that grow over 1-2 weeks
site of trauma; prick of finger on a thorn
bleed easily
Campbell-de-morgan spots common; seen also in liver disease
venous lakes common; soft, compressible blue nodules, usually on lip

107
Q

what is the differential diagnosis of a vascular lesion?

A

melanotic melanoma
squamous cell carcinoma

require histology

108
Q

describe infantile haemangiomas

A

grow rapidly after birth
benign
slowly resolve from 6-12 months or may take years
can leave a scar
site; important, require treatment if obstructing any vital functions, vision, breathing, feeding
deeper, segmental distribution; associated with underlying abnormalities or complications

109
Q

what is the treatment of infantile haemangiomas?

A

propanolol

110
Q

describe lipomas

A

benign fat tumours
soft, jelly-like texture
definable border
multiple within a single patient

111
Q

describe dermatofibromas

A

asymptomatic
usually on lower leg
very firm
can dimple in the centre when gently squeezed
can be pigmented, with a ring around the periphery of the lesion
thought to be a healing response to trauma; insect bite

112
Q

describe epidermoid cysts

A 
benign lesions
skin coloured
firm but fluctuant
mobile above the underlying structures
frequently seen in the scalp, face and trunk
113
Q

describe chondrodermatitis nodularis helicis

A 
painful nodule on the rim of the ear
benign
caused by recurrent pressure on the ear cartilage as they always lie on the same side at night
need to be distinguished from SCC
require histology
114
Q

describe keloid scarring

A

a scar that extends beyond the original wound
often occur after trauma; ear piercing, tattoo, skin surgery, or spontaneously
usually occur in the head and neck region, or upper torso

115
Q

describe an incisional biopsy

A

small sample

usually carried out using a punch biopsy

116
Q

describe an excision

A

small; punch biopsy

larger; elliptical excision

117
Q

describe shave or curettage

A

removal of a lesion flush with the skin surface
leave the roots of the deeper part of the lesion behind
should only be used for benign lesions
convenient; no suturing, heal with good cosmetic result

118
Q

describe mohs micro graphically controlled surgery

A

a specialist surgery carried out in stages to ensure that the margins of a difficult tumour are clear
used for difficult cases of BCC

119
Q

describe premalignant lesions

A

precursors of squamous cell carcinoma

most common; actinic keratosis, Bowens disease

120
Q

describe actinic keratosis

A

focally abnormal areas
within the epidermis
dysplasia within keratinocytes, partial thickness; brought about by UV-induced cellular DNA damage
ill-defined
sun exposed sites
surrounded by sun damaged skin; pigmentary change, wrinkles, fragility, telangiectasia
10-15% chance of developing a future SCC

121
Q

describe the grading of actinic keratoses

A

1; macular erythema that is barely visible, slight gritty feel
2; easy to see and feel
3; fleshy and hyperkeratotic lesions, highest risk for converting into SCC

122
Q

describe feel change

A

describes an area of skin that has extensive confluent actinic damage
may include actinic keratosis of various grades

123
Q

what features indicate conversion of actinic keratoses to SCC?

A 
tenderness
non-responsiveness to treatment
recent/rapid growth
induration
ulceration
lip lesions
multiple lesions
124
Q

what is the treatment of a single AK?

A

cryotherapy

curettage; thick lesion

125
Q

what is the treatment of field AK?

A

topical treatment; diclofenac gel (low grade)
patients should expect significant local irritation
inflammation; effective and lasting response
photo dynamic therapy; combination approach
sun protection and vitamin D advice

126
Q

describe Bowens disease

A

SCC in situ
keratinocyte dysplasia is evident throughout the full thickness of the epidermis
mostly on the lower legs
single or multiple
very well-defined erythematous plaques with overlying scale
5% risk of progressing to SCC
higher risk of developing a subsequent skin cancer elsewhere

127
Q

what is the differential diagnosis of Bowens disease?

A

inflammatory rashes; psoriasis, eczema, tinea
SCC
superficial BCC
amelanotic melanoma

128
Q

what is the treatment of Bowens disease?

A

photodynamic therapy
topical therapy; 5-fluorouracial, imiquimod
cryotherapy
curettage
excision
full body examination; looking for second or third lesions
sun protection advice
vitamin D replacement
no response to treatment, concerns about developing SCC; refer using the 2-week wait rule

129
Q

name the types of non-melanotic skin cancers

A

basal cell carcinoma

squamous cell carcinoma

130
Q

describe a basal cell carcinoma

A

most common form of skin cancer
develop from the basal layer of cells in the epidermis
very slow growing
develop over months-years
local invasive
irregular sub-clinical finger-like projections that grow into the dermis

131
Q

what are the clinical features of a BCC?

A

usually grow on sun-exposed sites

nodular BCC; pearly surface, rolled edge, ulceration, arborising telangiectasis

132
Q

what happens when basal cells are incompletely excised or neglected?

A

can become very destructive

especially in the head and neck region

133
Q

describe nodular BCCs

A 
usually appear on sun damaged skin
nodular or plaque like
shiny/pearly surface
telangiectasia
often ulcerate
high risk in central facial location
134
Q

describe superficial/multifocal BCCs

A 
usually appear on trunk
scaly erythematous plaque
raised rim
rarely ulcerate
low risk
135
Q

describe morphoeic /infiltrative BCCs

A 
usually appear on the face
shiny white plaque with ulceration
may intermittently heal/recur initially
often ulcerate
very high risk
136
Q

what is the treatment of BCCs?

A

most treated by standard excision with adequate margin; usually curative
more difficult/recurrent tumours may be referred for Mohs surgery

137
Q

describe squamous cell carcinomas

A

red flag cancer; locally invasive and metastatic potential
develop when dysplastic cells in the epidermis invade into the dermis
features; fleshy nodule, sometimes with a keratotic surface, grow rapidly (over weeks), painful

138
Q

what are the risk factors for developing a SCC?

A

sun exposure
fair skin
immunosuppression
chronic inflammation; chronic ulcers, Bowens disease

139
Q

which factors indicate aggressive behaviour of a tumour?

A

size; >2cm
depth; >4mm
invading beyond the depth of subcutaneous fat
location; scalp, ear, lip
presence of immunosuppression
histology; poor differentiation, perineurial invasion

140
Q

what is the treatment of a SCC?

A

excision with a clear margin

follow up; looking for signs of local/metastatic recurrence and other primary tumours

141
Q

what is the differential diagnosis of a nodular lesion on a sun exposed site?

A 
BCC
SCC
dermal naevi
dermatofibroma
cysts
molluscum contagiosum
lipoma
keloid
142
Q

what is the differential diagnosis of a lesion covered in scale?

A 
SCC
actinic keratosis
Bowens disease
superficial BCC
chondrodermatitis
viral warts
tinea
psoriasis
143
Q

what is the differential diagnosis of a fleshy/bleeding lesions?

A

SCC
amelanotic melanoma
vascular lesions; pyogenic granuloma

144
Q

describe a cutaneous lymphoma

A

most commonly seen when a systemic lymphoma involves the skin as a secondary site
primary cutaneous formal mycosis fungoides
T-cell lymphoma of the skin
patches and plaques on su protected sites; buttocks

145
Q

describe sezary syndrome

A

a systemic variant of T-cell lymphoma

presents with erythroderma

146
Q

what is the treatment of a cutaneous lymphoma?

A

topical steroids

UV light

147
Q

describe acanthosis nigricans

A

may indicate an underlying GI malignancy

can be benign; more common, related to diabetes

148
Q

describe serpiginous erythema

A

may indicate an underlying lung malignancy

149
Q

describe Pagets disease

A

of the nipple; underlying breast disease
acquired ichthyosis, dermatomyositis, new onset pruritus, erythroderma, pemphigus, scaling of the palms and soles (tylosis)

150
Q

describe cutaneous secondary deposits

A

may be the presenting feature of an underlying carcinoma
usually presents as pink or blue firm nodules
solitary or multiple
common sites; scalp, umbilicus, upper trunk
usually occur late and indicate poor prognosis

151
Q

describe the ABCDE algorithm

A 
differentiate potentially benign lesions from those that are concerning for malignancy
asymmetry
inconsistent borders
2 or more colours
>6mm diameter
history of evolution
152
Q

what is the differential diagnosis for pigmented lesions?

A

melanocytic; naevi, moles, freckles, lentigo, melanoma in situ, melanoma
non-melanocytic; seborrhoeic keratosis, dermatofibroma, vascular lesions (haemangioma, pigmented BCC)

153
Q

describe melanocytes

A

pigment producing lesions; melanin
within the basal layer of the epidermis
melanin; acts as a protective barrier against UV exposure

154
Q

what is seen after an increase in melanin

A

freckling

155
Q

what is seen after an increase in clusters of melanocytes

A

naevi

156
Q

what is seen after an increase in individual melanocytes

A

lentigo

157
Q

describe melanoma

A

occurs when melanocyte proliferation becomes upregulated
50%; from pre-existing moles
50%; de novo

158
Q

describe congenital naevi

A

may develop coarse hairs later in life

giant/>20cm; increased risk of melanoma developing, should be routinely screened

159
Q

describe acquired naevi

A

junctional; epidermis only, flat, dark brown
compound; epidermis and dermis, light brown, raised
dermal; raised, flesh coloured, dermis only
halo; teenagers, usually benign if it is regular and symmetrical

160
Q

describe atypical naevi

A

moles with atypical clinical appearance
benign on histological assessment
clinically similar to a superficial spreading melanoma
usually large, variegated colour, ill defined borders
increased risk of melanoma
may be inherited; AD

161
Q

describe lentigo

A

in adults
permanent increase in individual melanocytes in the epidermis
scattered, small macules, usually across the shoulders
larger, light brown homogenous patches on sun exposed sites; face, lower arms
background skin damaged
benign

162
Q

describe pre-malignant melanocytes lesions

A

melanoma in situ, lentigo maligna
can occur when melanocytes become dysplastic and contained in the epidermis
high risk of lentigo maligna to progress to lentigo maligna melanoma
treatment; excision with a clear margin

163
Q

name the subtypes of melanoma

A

nodular; grow vertically, can quickly metastasise
superficial spreading; most common, grows laterally
acral; on palms, subungal areas, predominantly non-white population
lentigo maligna; exposed sites, elderly, large, difficult to manage, can be cosmetically sensitive

164
Q

describe breslow depth

A

best prognostic indicator for melanoma
depth of the tumour on histological assessment
thin tumours, <8mm; prognosis very good
depth >4mm; 50% 5 year survival

165
Q

describe the management of suspicious pigmented lesions in primary care

A

red flag pathway
3/7 point checklist, 2 on ABCDE; referred under 2 week wait rule
refer when you have strong concerns about any individual features; new pigmented or vascular nodules, new nail changes
excision of suspicious pigmented lesions should be avoided in primary care
high risk individuals should be referred for screening; giant congenital melanocytes naevi, atypical moles, FHx of 3+ melanomas, >100 normal moles

166
Q

describe the management of suspicious pigmented lesions in secondary care

A

full body examination
identifying all pigmented lesions; examine with the naked eye and dermoscopy
initial excision; narrow margin (diagnosis, breslow depth)
second procedure; achieve appropriate wide margins
regular follow up; local/metastatic recurrence
PET scanning
sentinel lymph node biopsy

167
Q

describe the new melanoma-targeted therapies available

A

BRAF targeted therapy; BRAF is a gene involved in cell growth and mutations
significant side effects

168
Q

describe lupus erythematous

A 
a group of autoimmune disorders
caused by antibodies against components of cell nuclei
systemic
discoid, subacute (primarily cutaneous)
cutaneous features
often provoked by sun exposure
worse in smokers
169
Q

describe discoid LE

A

most common form of cutaneous LE
single/multiple scaly plaques
sun exposed distribution
scarring or pigmentary change; very common
scalp may be affected; permanent hair loss
5% go on to develop SLE

170
Q

describe subacute LE

A

presents with annular/polycystic scaly plaques on the trunk
often follows an episode of sun exposure
higher proportion go on to develop SLE

171
Q

describe SLE

A

multi-systemic autoimmune disorders
neurological and renal disease; most serious problems
common cutaneous features; butterfly rash (photosensitivity), mouth ulcers, hair thinning, vasculitis
show features of DLE and subacute LE
f>m

172
Q

describe the management of SLE

A

patient education
topical therapies
sun protection
potent topical steroids; prevention of scarring
systemic treatments; hydroxychloroquine, oral prednisolone (vitamin D replacement)

173
Q

describe dermatomyositis

A

inflammatory condition of proximal muscles
accompanied by a characteristic rash
skin changes can develop several months prior to muscle weakness

174
Q

what are the risk factors for dermatomyositis?

A 
autoimmunity
infection
medications
underlying malignancy
age
175
Q

what are the features of dermatomyositis?

A

heliotrope rash (light purple) on the eyelids
purplish patches on sun exposed sites; back of the hands, bony prominences, become scaly (gottrons papules)
prominent nail-fold capillaries
calcinosis on the fingers

176
Q

what investigations should be performed to diagnose dermatomyositis?

A 
CK
ANA; + in 70%, low specificity
anti-Jo antibodies
EMG
muscle MRI
skin or muscle biopsy
177
Q

what is the treatment of dermatomyositis?

A

identify and treat any malignancy
high dose oral prednisolone
steroid bearing agents; methotrexate, azathioprine, mycophenolate

178
Q

describe systemic sclerosis/scleroderma

A

multi-system disease
caused by autoimmunity to endothelial cells
resulting in excessive fibrosis
mostly cutaneous, cardiac, renal, respiratory and GI
vascular changes; raynauds, telangiectasia
limited systemic sclerosis; distal limbs, lower chance of significant organ involvement
localised scleroderma; skin only, isolated fibrotic plaques

179
Q

what are the cutaneous features of systemic sclerosis?

A

bird-like facial appearance; beaked nose, pursed lips
tight skin over the hands
sclerodactyly
calcinosis over the fingertips; can be painful
ulceration over bony prominences and calcinosis
prominent nail-fold capillaries
telangiectasia; often in the face and hands

180
Q

what are the investigations and treatment of systemic sclerosis?

A

anti-centromere antibodies
scl-70 antibodies
ANA

symptomatic treatment
high dose oral prednisolone
difficult and often gets a poor response

181
Q

describe erythema nodosum

A

painful erythematous nodular eruption
extensor aspect of the lower limbs
hypersensitivity reaction to a number of stimuli

182
Q

what are the causes of erythema nodosum?

A 
sarcoidosis
TB
streptococcal infection
mycoplasma infection
some medications
IBD
idiopathic >50%
183
Q

what investigations are required to diagnose erythema nodosum?

A 
CXR; most important
history; drug history
examination
throat swabs
ASO titre (group A streptococcus)
mantoux (TB) and mycoplasma serology
ace levels (sarcoidosis)
184
Q

what is the treatment of erythema nodosum?

A

treat the underlying cause
rarely oral steroids required
mostly respond to conservative therapy

185
Q

describe erythema multiforme

A

hypersensitivity reaction
to an infection; HSV (>30%), mycoplasma, hepatitis, HIV
to a drug
signs can last for 1-4 weeks and can recur
less severe than Stevens Johnson syndrome and toxic epidermal necrolysis

186
Q

what are the clinical signs of erythema multiforme?

A

target lesion; dusky, red central area, pale surround, outer dusky ring
localised to acral or distal sites; hands and feet
often symmetrical
can involve the face
may have mucosal lesions; some may be very extensive

187
Q

what is the treatment of erythema multiforme?

A 
symptomatic
topical steroid analgesics
antihistamines
oral steroids; very severe
recurrence; linked to HSV, prophylactic oral acyclovir
188
Q

describe pyoderma gangrenosum

A

ulceration
often on the lower leg
extremely painful
rapidly progressive

189
Q

what are the clinical features of pyoderma gangrenous?

A

irregular ulcers
with a purple undermined edge
necrotic base
single or multiple

190
Q

what other conditions are associated with pyoderma gangrenous?

A

IBD
inflammatory arthritis; RA
haematological malignancies; behcets disease

191
Q

what is the treatment of pyoderma gangrenous?

A

identify and treat the underlying cause
analgesia
appropriate dressing
super potent topical steroids; ulcer edges
oral steroids
steroid sparing agents; ciclosporin, mycophenolate, azathioprine, dapsone
anti-TNF agents

192
Q

describe necrobiosis lipoidica

A

presents with sharply demarcated plaques
red-brown edge
central, atrophic area with a yellow hue
usually on anterior shins
strong association with DM; microvasculature problems
can progress over many years before it stabilises
can become ulcerative

193
Q

what is the treatment of necrobiosis lipoidica?

A

topical steroids; early disease

aspirin

194
Q

describe drug eruptions

A

wide variety of clinical presentations
onset usually 7-10 days after starting
can be similar to an infectious exanthem
often caused by antibiotics; stop and switch to another class

195
Q

what are the clinical features of a drug eruption?

A

rash
fever
raised inflammatory markers

196
Q

describe a mild drug exanthem

A

maculopapular/morbilliform rash; measles-like
usually starts on the trunk and spreads to the proximal limbs
can mimic a viral or bacterial exanthem
patient systemically well

197
Q

describe Stevens Johnson syndrome

A

usually start with painful, targeted lesions
>2 mucosal surfaces involved
haemorrhage crusting
affects <10% of body surface

198
Q

describe toxic epidermal necrolysis

A 
affects >30% of body surface
blistering and separation of the epidermis from the dermis
risk of skin failure
nikolsky's sign may be positive
mortality <40%
199
Q

describe drug rash with eosinophilia and systemic symptoms (DRESS)

A

can mimic an exanthema initially
may have a maculopapular rash
tends to regress to confluent erythema
generally more unwell

200
Q

what are the symptoms and signs of DRESS?

A 
peripheral eosinophilia; FBC
facial swelling
lymphadenopathy
systemic symptoms; high fever
raised LFTs
renal impairment; increased creatinine
dyspnoea
201
Q

what drugs are more likely to cause DRESS?

A

anticonvulsants
penicillins
vancomycin

202
Q

describe acue generalised eruptive pustulosis (AGEP)

A 
acute onset of erythema and pustules
high fever
usually start in the flexures
appear 2-3 days after starting and resolve 1-3 weeks after stopping
elevated WCC
can be confused with pustular psoriasis
203
Q

what is the management of drug eruptions?

A

withdrawal of the causative agent
emollients; maintain the skin barrier integrity
topical steroids and antihistamines; mild eruptions
severe eruptions; management in HDU or ICU, careful monitoring of fluid and electrolyte balance
monitor and treat for sepsis; high risk of infection due to loss of skin barrier
mucosal care; high importance, eyes may scar
involve dermatology at an early stage

204
Q

what are the signs of a life-threatening drug eruption?

A 
angiodema
blistering
positive nikolsky sign
mucosal involvement; could indicate Steven Johnson syndrome
extensive purpura
pustules; could be AGEP
high eosinophil count; could be DRESS
extensive confluent erythema
205
Q

describe urticaria

A

can be acute or chronic
chronic idiopathic urticaria; urticaria alone, persists for >6 weeks
can appear as hives, wheals
wheals; intensely itchy, usually resolve within 24hrs, come in waves
extensive urticaria; responds well to oral antihistamines

206
Q

define angiodema

A

swelling of the deep dermis subcutaneous tissues and mucosa

207
Q

define anaphylaxis

A

severe life-threatening systemic hypersensitivity reaction

develops quickly; within half an hour of ingesting the causative agent

208
Q

describe purpura

A 
non-blanching palpable rash
can appear red, purple or black
usually on the lower legs but can be anywhere
can be painful or bullous
clinical finding, not a diagnosis
209
Q

describe petechiae

A

pinpoint haemorrhages

causes; low platelets, pressure from BP cuff

210
Q

what are the embolic causes of purpura?

A

DIC
septic emboli
meningococcaemia
infective endocarditis

211
Q

what are the coagulopathy causes of purpura?

A

thrombocytopenia
liver disorder
anticoagulant medication
vitamin C deficiency

212
Q

what are the vascular causes of purpura?

A

senile purpura; often related to oral steroids

vasculitis

213
Q

describe vasculitis

A

can be classified based on the inflammation of small, medium or large vessels
often due to medication or infection
cutaneous vasculitis; only limited to the skin
usually self-limiting if confined to the skin

214
Q

describe henoch Schonlein purpura

A

usually affects a younger age group
post streptococcal throat infection
extensor surface and buttock involvement
systemic involvement; arthritis, renal, GI, churg strauss, wegeners, PAN, giant cell arteritis
at risk of progressive renal disease; close follow up

215
Q

what are the investigations required if purpura is found?

A 
history
examination
vasculitic screen
ASOT titres
throat swab
antinuclear antibodies, other rheumatological investigations
vitamin C; nutritional status
organ-specific inflammation; inflammatory markers, BP, urinalysis, urine microscopy, CK, LFTs, amylase
216
Q

describe bullous pemphigoid

A 
relatively common blistering condition
autoimmune
IgG auto-antibodies against BP180 and BP230 in the basement membrane
loss of hemidesmosomes
sub-epidermal blister formation
217
Q

what are the symptoms and signs of bullous pemphigoid?

A 
typically elderly patient
sever itch
tense blisters on erythematous skin
sub-epidermal blister on histology slide
stain skin for immunofluorescence
treatment; oral steroids, doxycycline
218
Q

describe pemphigus

A

autoimmune
relatively rare blistering
IgG auto-antibodies against desmoglein 3 in the epidermis
this protein binds the cells together
loss of protein; separation of the skin cells and intra-epithelial blisters

219
Q

what are the signs and symptoms of pemphigus?

A

blisters and erosions on the skin and mucous membranes
pathology slide; blister within the epidermis
immunofluorescence; IgG antibodies in the epidermis
treatment; steroids, steroid-sparing systemic agents

220
Q

describe dermatitis herpetiformis

A

more common in caucasian males
linked to coeliac disease
caused by gluten intolerance
IgA antibodies target the skin and gut; sup-epidermal blister formation

221
Q

what are the signs and symptoms of dermatitis herpetiformis?

A

intensely itchy papules and vesicles on extensor surfaces
histology; sub-epidermal separation, micro abscesses
treatment; gluten free diet, dapsone

222
Q

describe erythroderma

A

a true skin emergency
erythema affecting 90% of the body surface area
almost entirely red
only small sparing of normal skin

223
Q

what re the causes of erythroderma?

A 
eczema
psoriasis
drugs
cutaneous T-cell lymphoma
pityriasis rubra pillaris
no underlying cause
224
Q

define skin failure

A

sudden and widespread impairment of normal skin function

225
Q

what are the complications of skin failure?

A 
cutaneous pain and itching
impaired temperature regulation
infection risk
fluid loss
loss of electrolytes and proteins
increased energy requirements
oedema
risk of high output cardiac failure
mucosal ulceration
later complications; hair and nail loss
226
Q

what is the management of erythroderma?

A

stop any unnecessary drugs
admission; further treatment and investigation
bland emollients; soft white paraffin
soap substitutes
adequate pain relief
antihistamines
monitor for infections
managing food balance and body temperature
skin biopsy; establish the underlying cause
further treatment depends on the underlying cause

227
Q

describe rashes flat with skin

A

<1cm; macule

>1cm; papule

228
Q

describe raised rashes

A

fluid filled;
pus; pustule
clear fluid; <1cm; vesicle, >1cm; bullae

not fluid filled
<1cm; papule
>1cm; plaque

229
Q

describe a skin examination

A

inspection
describe
palpate
systematic check

230
Q

describe the inspection section of a skin examination

A 
distribution;
flexors/extensors
generalised/localised
photosensitive
dermatomal
confirmation;
koebner phenomenon
annular
targetoid
discoid/nummular
231
Q

describe the description section of a skin examination

A 
size
shape
colour
morphological term
surface change
232
Q

describe the palpation section of a skin examination

A 
texture;
gritty; keratin
tenderness
firm; dimple sign
heat
233
Q

name the types of pigmented lesions

A

benign; naevus
pre-malignant; melanoma-in-situ
malignant; melanoma

234
Q

name the types of non-pigmented lesions

A

benign; seborrhoeic keratosis
pre-malignant; actinic keratosis, Bowen’s disease
malignant; SCC, BCC

235
Q

what are the treatment options for actinic keratosis?

A 
good sun proection
solaraze
cryotherapy
efudix
actikerall
imiquimod
photo dynamic therapy
curettage
excision

Clinical Practice (14 decks)

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