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high yield- year 2 > derm > Flashcards

derm Flashcards

1
Q

what is the treatment for syphilis?

A

IM benzylpenicillin

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2
Q

how does lymes disease present?

A 
early= erythema migrant (expanding 'bullseye' target lesion)
late= arthritis, neuropathy and encephalopathy
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3
Q

what is the treatment Lyme disease?

A

doxycycline

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4
Q

who is chickenpox more severe in and what should they be given?

A
  • extremes of age, pregnant and immunocompromised

- These groups may be given zoster immune globin (ZIG) and acyclovir

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5
Q

what causes chicken pox?

A

-varicella zoster

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6
Q

what is shingles treated with?

A

-acyclovir

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7
Q

who is shingles more common in?

A

-elderly

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8
Q

what causes shingles and chicken pox?

A

varicella zoster

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9
Q

what is this?

A

shingles

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10
Q

what is the treatment for herpes simplex virus (HSV)?

A

topical/ oral acyclovir

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11
Q

what is the treatment for human pappilomavirus (viral warts)?

A

-regular topical keratolytic (salicylic acid) or cryotherapy

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12
Q

what is molluscum contagious?

A
  • pexvirus, fleshy, pearlescent nodules
  • contagious
  • common in children
  • can be sexually transmitted
  • self limiting/ cryotherapy is the treatment
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13
Q

what is herpangina, investigations and treatment?

A
  • a sudden viral illness commonly seen in children
  • causes painful oral mucosal blistering
  • diagnosed using swab/stool PCR diagnosis
  • is self limiting
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14
Q

what causes herpangina?

A

coxsackie virus

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15
Q

what causes hand, foot and mouth disease?

A

coxsackie enterovirus

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16
Q

how does hand, foot and mouth present?

A
  • discolored lesions on hands, feet and mouth

- presents in children and family outbreaks

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17
Q

what is erythema infectiosum also known as?

A

slapped cheek disease

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18
Q

how does erythema infectiosum (slapped cheek disease) present?

A

-slapped cheek appearance and macular rash

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19
Q

what causes erythema infectiosum and how is it diagnosed?

A
  • Parovirus B19

- diagnosed with IgM blood test, can also cause chronic anaemia which may be seen in blood test

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20
Q

what is orf?

A

-self limiting infection from farm animals-causes a firm fleshy nodule and is common in farmers

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21
Q

what is this?

A

ring worm

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22
Q

how is different types of ring worm named?

A 
named according to site:
Tinea corpis= body
Tinea barbae= beard
Tinea cruris= groin
Tinea pedis= feet
Tinea capitis= head
Tinea unguium= nails
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23
Q

what is candida and how does it present?

A
  • GI commensal which grows in moist skin
  • irritating, peeling, erythematous rash with satellite lesions

oral candidiasis= white, creamy, pseudomembranous plaques, common after oral antibiotics

thrush= vaginal candidiasis

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24
Q

who is vaginal candidiasis common in?

A

diabetics

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25
Q

what is used to treat ring worm?

A

topical terbinifine

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26
Q

what is used to treat candidiasis?

A

topical azole/ nystatin

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27
Q

how does scabies present?

A
  • widespread itchy rash that is worse at night

- curved burrows

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28
Q

what is scabies?

A

-infestation with sarcoptes scabiei

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29
Q

what is the treatment for scabies?

A

-topical permethrin overnight

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30
Q

what is the treatment for lice?

A

-dimeticone wash

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31
Q

are melanocytes naevi malignant or benign?

A

-benign proliferation of melanocytes

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32
Q

describe a junctional melanocytes naevi?

A
  • involves the DEJ

- pigmented macule

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33
Q

describe a compound melanocytic naevi?

A
  • involves the DEJ and dermis

- raised/pigmented

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34
Q

describe a intradermal melanocytes naevi?

A
  • involves the dermis

- raised non pigmented

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35
Q

describe an atypical melanocytes naevi?

A

-large/irregular/varies pigment

36
Q

what is sebhorrhoeic keratosis?

A

-common benign lesion in elderly that has a rough/warty, stuck on appearance

37
Q

what are solar lentignes?

A
  • common benign lesion in the elderly

- pigmented patches on sun exposed sites

38
Q

what are some pre malignant lesions that can progress to a SCC?

A
  • bowen’s disease

- actinic keratosis

39
Q

what is actinic keratosis?

A

-rough/scaly/erythematous patch that can progress to BCC/SCC

40
Q

what is Bowen’s disease?

A

-slowly enlarging erythematous, scaly patch that can progress to SCC (SSC in situ)

41
Q

what is the treatment for actinic keratosis and Bowen’s disease?

A

-removal (cryotherapy/curettage)+/- topical 5 fluorouracil/imiquimod

42
Q

what is lentigo maligna?

A

-changing pigmented macule with irregular border/pigmentation that can lead to a melanoma (melanoma in situ)

43
Q

what is the treatment for lentigo maligna?

A

-excision

44
Q

what cells do basal cell carcinomas arise from?

A

basal cells

45
Q

what is a risk factor for BCC?

A

-repeated sunburn

46
Q

how do BCC present?

A
  • nodular-painless
  • slow growing
  • pearly
  • aborising vessels
  • central ulceration
47
Q

are BCC or SCC more likely to metastasise?

A
  • BCC has low metastatic risk but invades local tissue (‘rodent ulcer’)
  • SCC higher metastatic risk
48
Q

what is the treatment for a BCC?

A

-excisional biopsy

49
Q

what is the treatment for SCC?

A

excisional biopsy (+/- chemo/radiotherapy)

50
Q

what cells do SCC arise from?

A

suprabasal cells

51
Q

what are risk factors for SCC?

A
  • chronic sun exposure

- transplant

52
Q

how do SCC present?

A
  • painful
  • fast growing
  • hyperkeratotic
  • bleeding
  • inflamed
  • poorly defined
53
Q

where do melanomas arise from?

A

melanocytes

54
Q

what are risk factors for melanoma?

A
  • sun damage
  • family history
  • immunosuppression
55
Q

what are the two phases of melanoma growth?

A
  1. Radial where it grows horizontally

2. Vertical where it grows vertically (this allows metastasis)

56
Q

how is malignant melanoma diagnosed?

A 
ABCDE approach
Assymetrical
Border irregular
Colour variable
Diameter >6mm
Evolution/change
57
Q

what are the different types of malignant melanoma?

A
  • superficial spreading (most common)
  • lentigo maligna melanoma (arises wihin lentigo maligna)
  • nodular melanoma
  • acral lentiginous (affects nails/palms/soles)
58
Q

what is used to determine prognoses of malignant melanoma?

A

-Breslow thickness (top of granular layer to base of tumour measured in mm)

59
Q

what is erythema nodosum associated with?

A

Sarcoidosis

-tender, erythematous nodules on legs

60
Q

what is necrobiosis lipodica?

A

yellow/brown/red patches on legs associated with diabetes

61
Q

what is acanthosis nigricans?

A

-skin thickening/pigmentation in flexural area associated with diabetes

62
Q

what is dermatitis herpetiformis?

A

-immunobullous disease characterised by itchy vesicular rash and is associated with coeliac

63
Q

what is a heliotrope rash?

A

-red/purple rash around the eyelids associated with dermatomyositis

64
Q

what is sclerodactyly?

A

-digit skin thickening associated with systemic sclerosis

65
Q

what is a malar/butterfly rash?

A

-erythema on cheeks and bridge of nose associated with SLE

66
Q

what causes an arterial ulcer?

A

poor arterial blood supply

  • hypertension
  • smoking
  • obesity
  • PVD
67
Q

how does an arterial ulcer present differently than a venous ulcer?

A

arterial ulcer= punched out and painful

venous ulcer= commoner, painless and on medial malleolus

68
Q

what is the treatment for an arterial ulcer?

A
  • hygiene, analgesia, vascular surgery

- should avoid compression!!

69
Q

what causes a venous ulcer?

A
  • poor oxygenation secondary to venous hypertension

- peripheral oedema, stasis dermatisis, lipodermatosclerosis

70
Q

what is the treatment for a venous ulcer?

A
  • compression
  • diuretic
  • support stockings for life
71
Q

what is the pathophysiology of pemphigus vulgaris?

A
  • IgG autoantobodies attack desmoglein 3
  • desmogleins responsible for desmosomal attachments
  • affects epidermis
72
Q

what does histology show for pemphigus vulgaris?

A

-blisters within the epidermis

73
Q

what will immunoflourescence show for premphigus vulgaris?

A
  • honeycomb arrangement

- corresponds to desmoglein on outer cell surface

74
Q

how does pemphigus vulgaris present?

A
  • itchy rash and superficial blisters/erosions and mucosal ulcers
  • Nikolskys sign positive (top layers slip away when rubbed)
  • potentially fatal
  • usually presents in adulthood
75
Q

what is the treatment for pemphigus vulgaris?

A
  • prednisone and immunomodulators

- immunomodulators are methotrexate, azathioprine, ciclosporin

76
Q

what is the pathophysiology behind bullous pemphigoid?

A
  • IgG autoantibodies attack hemidesmosomes

- hemidesmosomes anchor basal cells to the basement membrane

77
Q

what is the histology of bullous pemphigoif?

A

sub epidermal blisters

78
Q

what would the immunoflourescence show for bullous pemphigoid?

A

linear arrangement

79
Q

how does bullous pemphigoid present?

A

Causes large, itchy tense bullae. Usually presents in elderly. Nikolsky’s negative.

80
Q

what is the treatment for bullous pemphigoid?

A

Localised:topical superpotent steroids
Widespread: prednisolone +/- immunomodulators

81
Q

what type of mutation is NF1?

A

-autosomal dominant mutation of NF1 gene

82
Q

what are skin signs for NF1?

A
  • neurofibromas
  • cafe au lait patches

Eyes- lisch nodules, optic glioma

83
Q

what mutation is tuberous sclerosis?

A

-autosomal dominant/sporadic mutation of TSC1 or TSC2

84
Q

what type of tumours does NF1 cause?

A

benign tumours of nervous tissue

85
Q

what type of tumours does tuberous sclerosis cause?

A

-benign tumours of various organs

86
Q

how does tuberous sclerosis present?

A
  • ash leaf macule, periungal fibromas, shagreen patches
  • cortical tubers can cause epilepsy
  • can cause kidney, heart and lung tumours
87
Q

what is associated with IBD?

A

erythema nodusum

high yield- year 2 (20 decks)

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