Skin Flashcards

1
Q

What should be asked in a basic rash history?

A
Where did the rash begin
How has it evolved 
Previous skin diagnosis 
Does sun exposure worsen (lupus) or improve rash (eczema/psoriasis) 
Symptoms - itch, pain weeping 
Occupation/hobbies - contact dermatitis 
Drugs 
Family history
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2
Q

What are the clinical features of an epidermis skin pathology?

A

Often fractures, fluid can seep out of cracks, oozing or dryness (scales)

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3
Q

What are the clinical features of a dermis skin pathology?

A

Skin stays smooth, raised surface e.g. uticaria (nettle rash)

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4
Q

When describing a surface, what is

a) Macule
b) Papule
c) Patch
d) Nodule
e) Vesicle
f) Bulla

A

a) Little <0.5cm and flat
b) Little and raised
c) Big >0.5cm and flat
d) Big and raised
e) Small and fluid filled
f) Large and fluid filled

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5
Q

What other physical signs should be used when describing a lesion?

A

Colour:
Redness - increased blood flow, Pigmentation - haemosiderin yellow/brown from blood, femelanin (ginger), u-melanin (brown)

Surface changes:
Crust and scale

Thickness of skin

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6
Q

What is crust? What can it be confused with?

A

Dried serum - orange/yellow colour

May be confused with keratin (white/yellow) - always remove crust to reveal underlying pathology

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7
Q

What is scale?

A

Abnormal stratum corneum
Accumulation of keratin
‘Hyperkeratotic’

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8
Q

Why can skin become thickened at the epidermal layer and the dermal layer?

A
Epidermal = lichenification and warty processes 
Dermal = scarring/infiltrative processes
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9
Q

What is an erosion?

A

Partial loss of epidermins
Heals without scarring
Usually secondary i.e. weepy eczema, burst intra-epidermal blister

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10
Q

What is an ulcer?

A

Full thickness loss of epidermis and some dermis
Heals with scarring
Surface: orange/yellow = exudate/crust, yellow = pus, necrotic tissue/slough = grey/green

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11
Q

What is excoriation?

A

Localised damage due to scratching

Linear crusts or erosions

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12
Q

If the pattern of a rash is unilateral or bilateral, what does this suggest?

A
Unilateral = external cause e.g. athletes foot 
Bilateral = internal cause e.g. eczema
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13
Q

What are the most abundant cells in the epithelial layer?

A

Keratinocytes and then melanocytes

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14
Q

What is the dermis made up of?

A

Collagen, elastic fibres, hair follicules, seberaceous glands, sweat glands, vascular supply

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15
Q

What is in the subcutaneous layer?

A

Adipocytes

Neurovascular bundles

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16
Q

What are the risk factors for basal cell carcinoma?

A
UV exposure
Fair skin 
Genetics 
Immunosuppression 
Radiotherapy
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17
Q

What are the clinical features of basal cell carcinoma?

A
Pearly 
Telangiectasia
Ulcerated (rolled edge) 
Pigmentation 
Common on head and neck
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18
Q

What are the clinical variants of BCCs?

A

Superficial BCC - less than 0.3mm into dermis
Pigmented BCC
Morphoeic BCC - high risk looks like a scar
Nodulocystic BCC

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19
Q

What are the histological features of a basal cell carcinoma?

A

Deep purply basal squamous cells against basement membrane expected but should not be in dermis - nests of BCs
Cleft between abnormal cells and stroma of dermis

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20
Q

What are the clinical features of SCC?

A
Typically hyperkeratotic (scaly) 
Sometimes ulcerated 
Not typically pearly or telangiectatic 
Sometimes painful 
Grow rapidly 
Common on scalp, pinna dorsal hand
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21
Q

What are the risk factors for SCC?

A
UV exposure
Skin type fair 
Genetics 
Immunosuppression
Radiation 
Chronic inflammation 
Scar tissue 
Arsenic
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22
Q

What are the histological features of squamous cell carcinoma?

A

Epidermis thickened with dysplastic squamous cells
Dermis has nests of squamous cells producing pearls of keratin
Inflammatory infiltrate

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23
Q

What are the clinical variants of a malignant melanoma?

A
  • Superficial spreading melanoma
  • Nodular melanoma
  • Acral lentiginous melanoma
  • Lentigo maligna (melanoma)
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24
Q

What is Hutchinson’s sign in acral lentiginous melanoma?

A

Pigmentation on proximal nail fold. Splitting of nail plate

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25
Q

What are the histological features of malignant melanomas?

A

Nests of malignant melanocytes just above basement membrane and invading into dermis
Dense inflammatory cell infiltrate

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26
Q

What is the ABCDE for melanomas?

A
Asymmetry - colour and shape 
Border irregularity 
Colour variation (often 3+ colours
Diameter (usually >6mm) 
Evolving - change in size colour shape over months/years 
Ugly duckling
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27
Q

What is the treatment for BCCs?

A

Excision
Mohs micrographic surgery
Curettage and cautery (small nodular/superficial and low risk BCC)
Cryotherapy (superficial BCC)
Topical therapy - aldara cream
Photodynamic therapy - photosensitive drug applied to lesion to destroy cells
Radiotherapy - if BCC large and difficult to excise
Vismodegib (oral drug designed to inhibit signalling and hedgehog pathway - if not a candidate for surgery

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28
Q

What is Mohs micrographic surgery (used in the treatment of BCCs)?

A

2mm clinical margin around BCC excised and specimin prepared in frozen sections for histology. Identify positive margins for further resection for clearance. Keep analysing until margin negative.

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29
Q

What is the treatment for SCCs?

A
Surgery 
Curettage and cautery 
Cryotherapy 
Lymph node dissection 
Adjuvant radiotherapy 
Chemotherapy 
Immunotherapy
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30
Q

What is the treatment for melanomas Stage 1 or 2?

A

Surgery and monitor for 5 years. If stage 1c-2b biopsy

31
Q

What is the treatment for melanomas Stage 3?

A

Lymph node dissection and biopsy

32
Q

What is the treatment for melanomas Stage 4?

A

Immunotherapy - Nivolumab, pembrolizumab, ipilimubab
Targeted treatments - Vemurafenib, Dabrafenib - not a cure but reduces symptoms and extends life expectancy
Radiotherapy and chemotherapy seldom used

33
Q

What is the treatment for lentigo maligna?

A

Surgery preffered option - excision, mohs micrographic surgery excision
Imiquimod topically
Radiotherapy
Cryotherapy

34
Q

What is merkel cell carcinoma?

A

Rare skin cancer is usually older and sun damaged pts. Rapidly enlarging pink nodule with high metastatic potential - poor prognosis

35
Q

What is atypical fibroxanthoma?

A

Rare skin cancer often in head and neck, sun damaged and elderly

36
Q

What is extramemory Pagets disease?

A

An uncommon adenocarcinoma of the anogenital region

37
Q

Name 3 sarcomas that are rare skin cancers

A
  • Dermatofibrosarcoma protuberans = in dermis, high risk of recurrence, presents early life and rarely metastasises
  • Angiosarcoma
  • Leiomyosarcoma
38
Q

What is scabies?

A

Scabies mites burrow into skin (0.3mm) forming small tunnel, sometimes with a blister. Mainly on hands, genitalia, flexural area. Allergy to mite and secretions causes generalised erythematous rash

39
Q

What is eczema?

A

Dermatitis - inflammatory condition of the skin - a reaction pattern not a disease

40
Q

What clinical signs indicate whether eczema is acute or chronic?

A

Acute - severe and weeping

chronic - scaly

41
Q

What is irritant contact eczema?

A

From substances that have a direct noxious effect on skin barrier function, may be due to repetitive and cumulative exposure e.g. detergents, gloves, nappy rash from ammonia in breakdown of urea

42
Q

What is Type 1 hypersensitivity / allergic contact uticaria?

A

Not really eczema - caused by mast cell histamine release triggered by IgE.
Immediate e,g, contact urticaria, anaphylaxis etc for latex gloves

43
Q

What is Type IV hypersensitivity / allergic contact eczema

A

By T cells proliferating - delayed type as takes days. Must patch test

44
Q

What are the common causes of allergic contact eczema?

A

Nickel e.g. earrings
Elastoplast
Suncream
Dental acrylates in dentures and denture composites

45
Q

What is lichen simplex?

A

Eczema due to scratching

46
Q

What is endogenous eczema?

A

Genetic component often childhood into adult - lichenification, thickened skin and accentuated skin markings. Phototherapy or immunosuppressants e.g. methotrexate if severe and persistent

47
Q

How can you prevent hand eczema?

A

Avoid irritants - 3-6 months to heal as lipid accumulation slow
Less allergenic gloves
Minimise skin contacts with acrylates
Treat with topical steroids

48
Q

What is seborrheic eczema?

A

Dandruff

49
Q

What is eczema herpeticum?

A

Herpes simplex virus, coldsores in eczema with discrete erosions. Treated with aciclovir

50
Q

What is the histological features of lichenoid inflammation?

A

Keratinocyte death especially at basal layer
Civatte/colloid bodies (dead cells)
Inflammatory cell infiltrate beneath epithelium

51
Q

What are the clinical features of lichen planus?

A

Purplish rash - flat topped shiny papules
Usually in flexural areas
In mucosa - whitish, reticulate, wicken striae

52
Q

Although there is no satisfactory treatment for oral lichen planus, what is sometimes used?

A
  • Topical/systemic immunosuppression e.g. prednisalone or cyclosporin
  • Topical sterouds e.g. clobetazol/dermavate
53
Q

What 3 conditions are due to lichenoid inflammation (autoimmune destruction of the epithelium)?

A

Lichen planus
Lupus
Erythema multiforme

54
Q

What are the clinical features of systemic lupus erythematous?

A

Butterfly rash

Widespread oral ulcerations

55
Q

What are the clinical features of discoid lupus?

A

Disc shaped plaques

Causes scarring and permanent pigmentary change

56
Q

What is erythema multiforme?

A

Spectrum of different diseases with the same pathology: death of dermal cells
Target lesion characteristic

57
Q

What is the most severe form of erythema multiforme?

A

Toxic epidermal necrolysis (TEN) - life threatening mortality 20-50%. Once the surface area is over 10-30% the mortality increases as water and protein leak

58
Q

What is the Steven Johnsons Syndrome varient of erythema multiforme (often affecting oral mucosa) often triggered by?

A

Atypical pneumonia

59
Q

What drugs can trigger erythema multiforme?

A
  • Sulphonamindes e.g. Septrin and trimethoprim
  • Allopurinol (for gout)
  • Anticonvulsants (lamotrigine, phenytoin, carbamazepine)
60
Q

What can the target lesions in erythema multiforme be triggered by?

A

Herpes simplex

61
Q

Where in the mouth does orofacial granulomatosis occur?

A

Facial swelling particularly in lips
In dermis of submucosal layer
May be variant of Crohns - cobblestoning

62
Q

What is an inherited mechanobullous (mechanical trauma) disorder that causes deep blistering affecting the dermal layers following trauma and digits can fuse together?

A

Epidermolysis bullosa

63
Q

Of the autoimmune bullous disorders, which is the worst?

A

Pemphigus

64
Q

What are the intraepidermal blisters that are seen in pemphigus called?

A

Acantholysis

65
Q

In pempigus what happens on a cellular level?

A

Anti-desmosome antibodies - desmosome that holds dermal and mucosa cells together detaches and crumbles

66
Q

What is the age group pemphigus often presents in?

A

50-70 years

67
Q

How is pemphigus treated

A

Immunosupression:100mg prednisolone

Rituximab - CD20 on B cells

68
Q

What is bullous pemphigoid?

A

Autoimmune subepidermal bullous disease

69
Q

What are the characteristics of a bullous pemphigoid blister?

A
Intact epidermal layer
Firm and don't break easily when touched 
Can get widespread itchy rash first 
Haemorrhagic blisters 
Occasionally presents in mouth
70
Q

What does the immunofluorescence look like in bullous pemphigoid?

A

No immunofluoresence at the top (epidermis)
but green line separating dermis from epidermis
Basement membrane splits and epidermis detaches

71
Q

What is characteristic of mucous membrane pemphigoid?

A

Subepidermal blisters that lead to scarring affecting the mucous membranes - oral, occular, skin, genital, nasopharynx, oesophageal, laryngeal

72
Q

What is slightly different between mucous membrane pemphigoid and bullous pemphigoid?

A

MMP - deeper antigens closer to dermis

73
Q

What is an early sign of mucous membrane pemphigoid?

A

Desquamative gingivitis