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BRS YEAR2 > Dermatology > Flashcards

Dermatology Flashcards

1
Q

How would Lupus Erythmatosus present

A

Proteinuria, High ESR/CRP, dsDNA positive, pancytopenia, has fever and fatigue
Photodistributed erythematous rash
Chilblains: itchy swelling
Livedo reticularis: net like redness
Cutaneous vasculitis: inflamed blood vessels
Alopecia

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2
Q

What are the two types of Lupus

A

Systemic LE:
Cutaneous/Discoid LE

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3
Q

How is SLE dignosed

A

Mucocutaneous: cutaneous lupus- spiderlike rash, oral ulcers
Haematological: haemolytic anaemia, thrombocytopenia, leukopenia
Immunological: ANA, anti-dsDNA, anti-SM

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4
Q

How can SLE and CLE be diffrentiated between

A

CLE causes scarring , SLE doesnt

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5
Q

What type of lupus is present in children and what antibody is present and what test should be done

A

Neonatal lupus
Ro positive
Test ECG as risk of heart block

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6
Q
A
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7
Q

What is the autoimmune connective tissue disease which caused proximal extensor inflammatory myopathy, a photodistributed pink violet rash on the extensors, eyes and scalp

A

Dermatomyositis

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8
Q

What signs are seen in dermatomyositis

A

High ALT, high CK, antinuclear antibody(ANA) and lots of other antibodies,
weakness, weight loss, fatigue

Heliotrope rash: on eyelids
Gottrons papules: papules on interphalangeal and metacarpal joints
Ragged cuticles
Shawl sign: rash on upper back
Photosensitive erythma

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9
Q

How would a patient with vasculitis present

A

IgA vasclitis
abdominal pain, GI bleeding,

Small vessel problems:
purapura - macular and palpable, non blanching

Medium vessel problem:
Digital necrosis
Retiform purapura ulcers
Subcutaneous nodules along blood vessels

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10
Q

What is the name of the systemic granulomatous disorder

A

Sarcoidosis

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11
Q

How does sarcoidosis present

A

Affects many systems: lungs, skin. LUNGS: cough with ?

Reactive oxygen species, joint pain
Red to brown violaceous papules
lupus pernio: blue to violet nodules and papules
disfiguring lesions on nose, lips,
Ulcerative
scar sarcoid
Granulatomous plaques

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12
Q

What symptoms does DRESS cause and what does DRESS stand for

A

Drug reaction with eosinophilia and systemic symptoms: taken an antibiotic, anti epileptic, ibuprofen or medication 2-6 weeks before

multiple myeloma
Rash, fever, tachycardia, renal (interstitial neprhitis), heart (myocarditis) and liver (hepatitis) starting to fail
Lymphadenopathy, high eosinophils

RASH: widespread papules, maculopapular, erythroderma, head/neck oedema

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13
Q

How is DRESS treated

A

take away the cause, corticosteroids

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14
Q

What is graft versus host disease

A

if face involvement, acral involvement and diarrhoea then GvHD rather than DRESS

Reaction to stem cell transplant or new drugs: a multiple organ disease. Donor T lymphocyte activity against antigens.
Skin, liver, GI tract

Erythmatous macules and papules, scleral icteus

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15
Q

what is the condition called when it is a constant itch without a rash

A

Pruritus

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16
Q

What is pruritus suggestive of and what investigations should be done

A

Renal failure, iron deficiency, Hep, HIV, cancer

GBC, rnal tets, LFT, ferritin, XR chest, BLoods for Hep ABC and HIV

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17
Q

What skin sign can occur in pruritis

A

Nodular prurigo: chronic scratichin causing nodules to form

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18
Q

What causes scurvy

A

Vit C (ascorbic acid) deficiency

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19
Q

What are the symptoms of scurvy

A

Spongey gingivae with bleeding and erosion
Petechiae, ecchymoses, follicilar hyperkaratosis, corkscrew hairs with perifollicular haemorrhage

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20
Q

What is the name of the protein deficiency and what are the skin signs

A

Kwashiorkor
Sparse dry hair
soft thin nails
cheilitis- inflam of lips
desquamation (peeling skin) large areas of erosion

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21
Q

How doe zinc deficiency present

A

dermatitis, diarhhoea, depression
perioral, acral and perineal skin with scaly erosive erythmea

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22
Q

What is carcinoid syndrome and how does it present

A

Metastases of malignant carcinoid tumour, 5HT secretion.
Flushing, diarrhoea, wheezing, dizziness, usually started on amlodipine, hypotension

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23
Q

What skin illness begins with flu, sore eyes and oral ulcers and develops into an extensive painful rash

A

Stevens Johnson Syndrom/ Toxic Epidermal Necrolysis

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24
Q

How does Stevens Johnson Syndrome develop into Toxic epidermal Necrolysis

A

flu like, abrupt lesions on trunk first then face and limbs. Get macules, blisters and erythme. blisters then merge to make sheets of skin detatchment (wet wallpaper)

Full thickness epidermal necrosis in less than 2-3 days
called TEN when more than 30% skin detachment

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25
Q

How does Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis occur

A

cell mediated cytotoxic reaction against epidermal cells
Drugs usually cause anti epileptics, NSAIDs, ABs,

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26
Q

What score is used to assess severity of Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis

A

SCORTEN: over 40yrs, % epidermal detatchment, serum urea glucose and bicarbonate, malignancy

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27
Q

What are the complications of Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis

A

Death, blindness

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28
Q

How does erythroderma present

A

Erythema affecting more than 90% of body
can get oedema, loss of fluid and proteins, sepsis risk, tachy

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29
Q

What is the cause of erythroderma

A

Drug reactions
Psoriasis
Atopic eczema

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30
Q

How is erythrodema treated

A

Treat underlying cause
restore fluid and electrolytes and body temp
Emollients to help skin barrier
Topical steroids and Abs

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31
Q

What are the different signs of chronic kidney disease

A

Excoriations/prurigo
Xerosis: dryness
Half and half nails
Calciphylaxis: cow print looking
Anaemia

Signs to the primary cause like SLE or immunosuppression like viral warts

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32
Q

What are the different signs of chronic liver disease

A

Excoriations/prurigo
Jaundice
Muehrckes lines of nails
Terrys nails ( white nail then a line of normal coloured nail right before the white)
Palmar erythema
Spider telangiectasia: red blob with spider capillary lines as legs
Clubbing

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33
Q

How may Diabetes mellitus manifest cutaneously

A

Necrobiosis Lipoidica: plaques with red-brown raied edge, a yellow/brown atrophic centre
Teerys nails, Xerosis, Xanthelesma and xanthom, Granuloma annulare (ring of pink), skin infection, neuropathic ulceration

34
Q

How does graves disease present cutaneously

A

Pre tiial myxoedema

35
Q

How may acromegaly manifest cutaneously

A

Cutis gyrata verticis: scalp lines
Acne

36
Q

How may HIV manifest cutaneously

A

Morbilliform rash
Urticaria
Erythema multifome: red round marks looks like a target
oral/genital ulceration

37
Q

How does GI disorders affect the skin

A

Orofacial granulomatosis- swelling in mouth/face lips
panniculitis
psoriasis

38
Q

How does celiac disease manifest

A

Dermatitis herpetiformis : blistering vesicles on skin

39
Q

What sign is associated with IBD, obesity and smoking

A

Hidradenitis superitiva: inflamed nodes- sterile absecces, hypertrophic scars : underarms, genitals and inframammory

40
Q

What is the name for skin folds

A

Intertriginous areas

41
Q

What is the sign associated with IBD, leukaemia, seronegative arthritis

A

Pyoderma gangrenosum: pustule on erythmatous base which ulcerates and extends with a necrotic border, is painful

looks like a chunk of fat and skin has been taken out

42
Q

What test would you do for SLE

A

FBC, U&E, ANA, anti-dsDNA, complement an urinalysis

43
Q

When would you do a lipid panel

A

Xanthelesma

44
Q

What presentation is associated with scurvy

A

Corkscrew hairs and perofillicular purapura

45
Q

What symptoms is associated with crhonic kidney disease

A

calciphylaxis

46
Q

What is he difference between nail changes in chronic kidney and chronic liver disease

A

Chronic liver: Terrys nails, Muerches nails
Chronic kidney: Half and half, terrys

47
Q

What is melanoma

A

malignant tumour from melanocytes
Pigmented, asymmetrical lesion, colour variation, irregular border

48
Q

What are the risk factors of melanoma

A

FHx, fair skin, red hair
Sun exposure, subeds, immunosuppressed

49
Q

What is the pathogenesis of melanoma

A

MAP kinase messaging pathways that are important for cell migration during embryogenesis but are also important in melanoma generations. MAP kinase pathway can lead to NRAS and BRAf mutations which can can lead to activation of the pathway leading to melanocyte reproduction leading to melanoma

50
Q

How does the body respond to melanoma formation

A

CD8 Tcell recognise mealnoma antigens and are able to kill
CTLA-4 inhibits T cell abctivation by removing B7 on APC so T Cells CD28 has nothing to bind to

51
Q

What immunotherapy is based on blocking CTLA-4 so that T cells can be activated

A

Ipilimumab

52
Q

What are the subtypes of melanoma

A

Superficial spreading
Nodular
Lentigo maligna : o face
Acral lentiginous : on elbows
Unclassifyale

53
Q

How does superficial spreading melanoma present

A

fair skin, trunk of men and womens legs, (sometimes white/depigmentation in centre as immune cells fight)
Symmetry, border irregularity, large diameter because of Horizontal/radial growth phase then Vertical/downwards (nodule like if goes downwards)

54
Q

How do nodular melanomas present

A

in fair skinned individuals, trunk head and neck
blu to black or pink to red nodule
Only vertical growth which makes it more aggressive

55
Q

How does lentigo maligna melanoma present

A

over 60 yrs, chronicall sun damaged skin, usually face
slow growwing, asymmetric brown/black macule, irregular border

56
Q

How does acral lentiginous melanoma present

A

palms and soles or around nails
deep pigmentation can get ulceration

57
Q

What sign on the nails can be indicative of melanoma

A

Melanonychia

58
Q

What is the name of the melanoma that doesnt produce pigment

A

Amelanotic melanoma

59
Q

What is indicative of a poor prognosis in melanomas

A

Inc breslow thickness
ulceration
age
men
lymph node

60
Q

How are melanomas nvestigated

A

Dermoscopy
Biopsy

61
Q

How are melanomas managed

A

Excision to subcutaneous fat , 2mm peripheral margin unless lentigo maligna.
wide excision : 5mm if in situ , 10mm for 1mm breslow depth
Sentinel lymphoma node biopsy: pT1b (less than 0.8mm but ulcerated)
Imaging in stage 3 or 4 (2-4mm,>4mm)
PET-CT, MRI

62
Q

Prognostic factor for metastatic melanoma

A

LDH

63
Q

If a melanoma is metastatic or unresectable what is the next step

A

Immunotherapy
CTLA-4 inhibition Ipilimumab (in BRAF negative)
PD-L1 Nivolumab
together is better

Mutated oncogene targeted therapy
BRAF and MEK inhibitor

64
Q

What types of keratinocyte dysplasia are there

A

Actinic keratoses : some dysplastic cells in the epidermis
Bowens disease: SCC in situ (same place)
Squamous cell carcinoma: SCC (mets likely)
Basal cell carcinoma: locally invades no mets

65
Q

Pathogenesis of basal cell carcinoma (3 points)

A

Basal Cell carcinoma:
- UV radiation, receptors for PDGF upregulated in mesencyhmal cells of stroma, PDGF upregulated in tumour cells.
- Proteolytic activity (metalloproteinases, collagenases) that degrade dermal tissue so can spread
- Chromosome 8q loses function (PTCH gene), p53 mutations usually there too

66
Q

Pathogenesis of squamous cell carcinoma and how it may present

A

-UV radiation is a risk factor
- addition of genetic alterations - alterations in p53 and CDKN2A
- NOTCH1 and NOTCH2

present: erythmematous/skin coloured, papule or plaque, exophytic (mushroom looking), hyperkeratotic, ulcers

67
Q

What are the risk factors of keratinocyte carcinomas

A

BCC more common than SCC
pale ppl
men
old - 68

RF: UV (PUVA), fair skin, genetic syndromes, immunosuppresant drugs, non-healing wounds,

68
Q

What is actinic keratosis

A

Atypical keratinocytes confined to epidermis
sundamaged skin
macules (flat) or papules (raised)
red or pink
scale
(looks like scaley sundamage that older people have)

69
Q

What is bowens disease

A

SCC in situ
erythmatous scaly pathc/ elevlated plaque
looks like actinic keratoses, eczema, psoriasis

70
Q

What is the treatment of actinic keratoses and bowens disease

A

5-fluorouracil
cryotherapy
imiquimod cream
photodynamic therapy
curettage and cautery (scrape and burn)
excision

71
Q

What are some high risk factors of SCC

A

more than 1cm on head and neck
more than 2cm on trunk and lim
in immunosuppressed or ppl whove had radiotherapy

poorly differentiated
PERINEURAL( around a nerve) LYMPHATIC OR VASCULAR INVASION

72
Q

A patient presents with a rapidly enlargeing papule, a circumscribed crateriform nodule with a keratotic core what is the diagnosis and how is it managed

A

Keratoacanthoma
will go away by itself

73
Q

How is SCC investigated

A

clinical diagnosis, biopsy if uncertain, US of lymph nodes if think mets

74
Q

How is SCC treated

A

Excision
radiotherapy if unresectable or perineural invasion
Cemiplimab if metastatic
skin monitoring and sun protection advice

75
Q

What are the types of BCC and how to identify

A

Nodular : pearly papule, shiny
Superficial : pink flat lesions, plaque, thin papule
Morphoeic: light pink to white colour, elevated or depressed area
Infiltrative
Basisquamous : combination of both
Micronodular: nodular but destructive and usually spreads

76
Q

How to diagnose BCC

A

biopsy

77
Q

How to treat BCC

A

surgical excision
mohs micrographic surgery (if recurrent, aggressive or in critical site)
can do topical 5-Fluorouraci or Imiquimod, or photodynamic therapy all the same things as SCC

78
Q

What are cutaenous T cell lymphomas

A

Neoplasms of T cells that attack skin

79
Q

What are the two types of cutaenous T cell lymphomas

A

Sezary syndrome : erythroderma, generalised lymphadenopathy, neoplastic T cells

Mycosis fungoides: looks like patch then plaque at first, may take 4-6 years to become a tumour.

80
Q

What is kaposi sarcoma

A

HHV8 : bruised coloured noduled/papules,
systemic disease
may be related to immunosuppression

81
Q

What is merkel cell carcinoma

A

Cells that resemble merkel cells
highly anaplastic
rapidly growing nodule, pink to red to violet, firm and domed shaped

BRS YEAR2 (11 decks)

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